PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
9122182-8	1997	The PARP coactivator function is suppressed by NAD+, probably as a result of auto-ADP-ribosylation.	NAD	47-51	poly(ADP-ribose) polymerase 1	Homo sapiens	4-8
9065765-1	1997	Photoaffinity labelling of the human poly(ADP-ribose) polymerase (PARP) catalytic domain (40 kDa) with the NAD+ photoaffinity analogue 2-azido-[alpha-32P]NAD+ has been used to identify NAD+-binding residues.	NAD	107-111	poly(ADP-ribose) polymerase 1	Homo sapiens	37-64
9050836-0	1997	Unexpected genetic and structural relationships of a long-forgotten flavoenzyme to NAD(P)H:quinone reductase (DT-diaphorase) A mammalian cytosolic FAD-dependent enzyme that catalyzes the reduction of quinones by N-ribosyl- and N-alkyldihydronicotinamides, but not by NADH, NADPH, or NMNH (reduced nicotinamide mononucleotide), was isolated from bovine kidney more than 30 years ago [S. Liao, J. T. Dulaney and H. G. Williams-Ashman (1962) J. Biol.	NAD	267-271	NAD(P)H quinone dehydrogenase 1	Homo sapiens	110-123
9050836-10	1997	The x-ray crystal structure of rat QR1 shows that the 43 amino acid C-terminal tail of QR1 provides the binding site for the hydrophilic portions of NADH and NADPH.	NAD	149-153	NAD(P)H quinone dehydrogenase 1	Rattus norvegicus	35-38
9050836-10	1997	The x-ray crystal structure of rat QR1 shows that the 43 amino acid C-terminal tail of QR1 provides the binding site for the hydrophilic portions of NADH and NADPH.	NAD	149-153	NAD(P)H quinone dehydrogenase 1	Rattus norvegicus	87-90
9135130-6	1997	These data show that calmodulin is a target of calcium fluxes in response to elicitor or environmental stress, and provide the first evidence that plant NAD kinase may be a downstream target which potentiates AOS production by altering NAD(H)/NADP(H) homeostasis.	NAD	236-242	calmodulin	Nicotiana tabacum	21-31
9065765-1	1997	Photoaffinity labelling of the human poly(ADP-ribose) polymerase (PARP) catalytic domain (40 kDa) with the NAD+ photoaffinity analogue 2-azido-[alpha-32P]NAD+ has been used to identify NAD+-binding residues.	NAD	154-158	poly(ADP-ribose) polymerase 1	Homo sapiens	66-70
9065765-7	1997	The close positioning of Lys893 near the adenine ring of NAD+ has been confirmed by the recently solved crystallographic structure of the chicken PARP catalytic domain [Ruf, Menissier-de Murcia, de Murcia and Schulz (1996) Proc.	NAD	57-61	poly(ADP-ribose) polymerase 1	Homo sapiens	146-150
9065765-1	1997	Photoaffinity labelling of the human poly(ADP-ribose) polymerase (PARP) catalytic domain (40 kDa) with the NAD+ photoaffinity analogue 2-azido-[alpha-32P]NAD+ has been used to identify NAD+-binding residues.	NAD	107-111	poly(ADP-ribose) polymerase 1	Homo sapiens	66-70
9065765-1	1997	Photoaffinity labelling of the human poly(ADP-ribose) polymerase (PARP) catalytic domain (40 kDa) with the NAD+ photoaffinity analogue 2-azido-[alpha-32P]NAD+ has been used to identify NAD+-binding residues.	NAD	154-158	poly(ADP-ribose) polymerase 1	Homo sapiens	37-64
9030766-1	1997	Nicotinamide 1-beta-D-riboside (Nir), the cationic, reducible moiety of the coenzyme NAD+, has been confirmed as an unusual substrate for purified purine-nucleoside phosphorylase (PNP) from a mammalian source (calf spleen).	NAD	85-89	purine nucleoside phosphorylase	Homo sapiens	147-178
8995394-14	1997	ATX also catalyzes the hydrolysis of GTP to GDP and GMP, of either AMP or PPi to Pi, and the hydrolysis of NAD to AMP, and each of these substrates can serve as a phosphate donor in the phosphorylation of ATX.	NAD	107-110	ectonucleotide pyrophosphatase/phosphodiesterase 2	Homo sapiens	0-3
9193650-0	1997	Mouse RT6 locus 1 and rat RT6.2 are NAD+.	NAD	36-40	ADP-ribosyltransferase 2b	Rattus norvegicus	26-31
9063440-1	1997	Poly(ADP-ribosyl)ation is a posttranslational modification of nuclear proteins catalyzed by poly(ADP-ribose) polymerase (PARP), an enzyme which uses NAD+ as substrate.	NAD	149-153	poly(ADP-ribose) polymerase 1	Homo sapiens	92-119
9063440-1	1997	Poly(ADP-ribosyl)ation is a posttranslational modification of nuclear proteins catalyzed by poly(ADP-ribose) polymerase (PARP), an enzyme which uses NAD+ as substrate.	NAD	149-153	poly(ADP-ribose) polymerase 1	Homo sapiens	121-125
9193654-5	1997	Enzymatic release of ADPRT results in inability of NAD to modulate CTL function.	NAD	51-54	poly(ADP-ribose) polymerase 1	Homo sapiens	21-26
9193654-8	1997	The question how ADPRT regulates T cell functions was investigated by incubating CTL with radioactively labeled NAD which causes modification of several proteins, pointing to potential candidates in these regulatory processes.	NAD	112-115	poly(ADP-ribose) polymerase 1	Homo sapiens	17-22
9193654-10	1997	ADP-ribosylation of this protein is mediated by the arginine specific protein mono-ADPRT, presumably utilizing ecto-NAD as substrate.	NAD	116-119	poly(ADP-ribose) polymerase 1	Homo sapiens	83-88
8973191-14	1996	NAD afforded some protection against the NO inactivation of ADH.	NAD	0-3	aldo-keto reductase family 1 member A1	Rattus norvegicus	60-63
9029730-6	1997	Initially crystallized with NAD, the crystal structure of type 1 17 beta-HSD has just been determined as a complex with 17 beta-estradiol, thereby illustrating the conformation of the substrate-binding site.	NAD	28-31	hydroxysteroid 17-beta dehydrogenase 1	Homo sapiens	65-76
8958158-4	1997	Furthermore, the results reported herein show that, in the presence of nicotinamide adenine dinucleotide (NADH) and DT-diaphorase, ubiquinol-containing multilamellar vesicles exposed to a lipophilic azocompound did not undergo lipid peroxidation, whereas in vesicles lacking either NADH or DT-diaphorase, thiobarbituric acid reactive substances (TBARS) formation occurred.	NAD	106-110	NAD(P)H quinone dehydrogenase 1	Homo sapiens	290-303
9029733-5	1997	3 beta-HSD I, II, and III function as NAD(+)-dependent dehydrogenaselisomerases, and IV and V function as NADPH-dependent 3-keto steroid reductases.	NAD	38-44	hydroxy-delta-5-steroid dehydrogenase, 3 beta- and steroid delta-isomerase 1	Mus musculus	0-12
8941705-0	1996	NAD+ analogs substituted in the purine base as substrates for poly(ADP-ribosyl) transferase.	NAD	0-4	poly(ADP-ribose) polymerase 1	Homo sapiens	62-91
8941705-1	1996	Poly(ADP-ribosyl) transferase (pADPRT) catalyzes the transfer of the ADP-ribose moiety from NAD+ onto proteins as well as onto protein-bound ADP-ribose.	NAD	92-96	poly(ADP-ribose) polymerase 1	Homo sapiens	0-29
8941705-1	1996	Poly(ADP-ribosyl) transferase (pADPRT) catalyzes the transfer of the ADP-ribose moiety from NAD+ onto proteins as well as onto protein-bound ADP-ribose.	NAD	92-96	poly(ADP-ribose) polymerase 1	Homo sapiens	31-37
8780571-6	1996	Neutrophil depletion or antibodies to either ICAM-1 or CD11/CD18 blunted the gut I/R-induced increases in NADH autofluorescence in the pericentral region, leukocyte adherence, and nonperfused sinusoids.	NAD	106-110	integrin subunit beta 2	Rattus norvegicus	60-64
8969940-2	1996	Two isoforms of this enzyme have been characterized; a low affinity NADP(H)-dependent enzyme (11 beta-HSD1) and a high affinity NAD-dependent dehydrogenase (11 beta-HSD2).	NAD	68-71	hydroxysteroid 11-beta dehydrogenase 1	Rattus norvegicus	94-106
8912669-0	1996	Nitric oxide-dependent NAD linkage to glyceraldehyde-3-phosphate dehydrogenase: possible involvement of a cysteine thiyl radical intermediate.	NAD	23-26	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	38-78
8912669-1	1996	Previous studies have demonstrated that glyceraldehyde-3-phosphate dehydrogenase (GAPDH) undergoes NAD(H) linkage to an active site thiol when it comes into contact with .NO-related oxidants.	NAD	99-105	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	40-80
8912669-1	1996	Previous studies have demonstrated that glyceraldehyde-3-phosphate dehydrogenase (GAPDH) undergoes NAD(H) linkage to an active site thiol when it comes into contact with .NO-related oxidants.	NAD	99-105	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	82-87
8938587-3	1996	Two kinetically distinct isoforms of this enzyme have been characterized in both rodents and man; a low-affinity NADP(H)-dependent enzyme (11 beta-HSD1) which predominantly acts as an oxoreductase and, more recently, a high-affinity NAD-dependent uni-directional dehydrogenase (11 beta-HSD2).	NAD	113-116	hydroxysteroid 11-beta dehydrogenase 1	Homo sapiens	139-151
8938587-12	1996	Ingestion of the 11 beta-HSD inhibitor, glycyrrhizic acid (> 100 mg/kg body weight per day for 4 days) resulted in significant inhibition of adrenal NADP-dependent (98.0 +/- 1.4 vs 42.5 +/- 0.4) and NAD-dependent (97.0 +/- 9.0 vs 73.2 +/- 6.7) 11 beta-dehydrogenase activity and 11-oxoreductase activity (187.7 +/- 31.2 vs 67.7 +/- 15.3).	NAD	152-155	hydroxysteroid 11-beta dehydrogenase 1	Rattus norvegicus	17-24
8790427-5	1996	Mitochondria from Bcl-2 expressors were also much more resistant to inhibition of NADH-dependent respiration caused by sequestration of large Ca2+ loads.	NAD	82-86	BCL2 apoptosis regulator	Homo sapiens	18-23
8912669-6	1996	All the .NO-related oxidants were able to induce the linkage of NAD(H) to GAPDH and the formation of a protein free-radical identified as a thiyl radical (inhibited by N-ethylmaleimide).	NAD	64-70	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	74-79
8912669-8	1996	Thiyl radical formation was decreased by the reconstitution of GAPDH with NAD+.	NAD	74-78	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	63-68
8912669-9	1996	Apo-GAPDH was a strong scavenger of AAPH radicals, but its scavenging ability was decreased when its cysteine residues were alkylated or when it was reconstituted with NAD+.	NAD	168-172	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	4-9
8912669-11	1996	We suggest that the NAD(H) linkage to GAPDH is mediated by a thiyl radical intermediate not specific to .NO or .NO-related oxidants.	NAD	20-26	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	38-43
8912669-12	1996	The cysteine residue located at the active site of GAPDH (Cys-149) is oxidized by free radicals to a thiyl radical, which reacts with the neighbouring coenzyme to form Cys-NAD(H) linkages.	NAD	172-178	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	51-56
8912669-13	1996	Studies with the NAD+ molecule radio-labelled in the nicotinamide or adenine portion revealed that both portions of the NAD+ molecule are linked to GAPDH.	NAD	17-21	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	148-153
8912669-13	1996	Studies with the NAD+ molecule radio-labelled in the nicotinamide or adenine portion revealed that both portions of the NAD+ molecule are linked to GAPDH.	NAD	120-124	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	148-153
8883403-3	1996	Using p-hydroxymercuribenzoate (pHMB) as an inhibitor of B5R, we have quantified the contribution of B5R to the NADH-dependent reduction of cytochrome c and to the overall reduction of cytochrome c in the DT-diaphorase assay.	NAD	112-116	cytochrome c, somatic	Homo sapiens	140-152
8883403-3	1996	Using p-hydroxymercuribenzoate (pHMB) as an inhibitor of B5R, we have quantified the contribution of B5R to the NADH-dependent reduction of cytochrome c and to the overall reduction of cytochrome c in the DT-diaphorase assay.	NAD	112-116	cytochrome c, somatic	Homo sapiens	185-197
8883403-3	1996	Using p-hydroxymercuribenzoate (pHMB) as an inhibitor of B5R, we have quantified the contribution of B5R to the NADH-dependent reduction of cytochrome c and to the overall reduction of cytochrome c in the DT-diaphorase assay.	NAD	112-116	NAD(P)H quinone dehydrogenase 1	Homo sapiens	205-218
8883403-5	1996	Thus, simply measuring the NADH-dependent reduction of cytochrome c consistently overestimated B5R activity.	NAD	27-31	cytochrome c, somatic	Homo sapiens	55-67
8883403-7	1996	Therefore, we have developed a spectrophotometric assay for measuring B5R activity as the pHMB-inhibitable NADH-dependent reduction of cytochrome c.	NAD	107-111	cytochrome c, somatic	Homo sapiens	135-147
8987594-10	1996	This result shows that clofibrate enhanced the conversion ratio without any side-effects under the conditions used and supports again the claim that the activity of ACMSDase exerts a critical influence on the tryptophan-NAD conversion.	NAD	220-223	aminocarboxymuconate semialdehyde decarboxylase	Rattus norvegicus	165-173
8752134-7	1996	In addition, the NAD+/NADH ratio of bcl-2-expressing PC12 and GT1-7 cells was two- to threefold less than that of control cell lines.	NAD	17-21	BCL2, apoptosis regulator	Rattus norvegicus	36-41
8752134-7	1996	In addition, the NAD+/NADH ratio of bcl-2-expressing PC12 and GT1-7 cells was two- to threefold less than that of control cell lines.	NAD	22-26	BCL2, apoptosis regulator	Rattus norvegicus	36-41
8759717-4	1996	Two other nucleotide-hydrolyzing activities were induced on the T cell surface concomitantly with CD38: the human PC-1 molecule, a nucleotide phosphodiesterase/pyrophosphatase that produces AMP from NAD or ADP-ribose, and a nucleotidase that produces adenosine from AMP, but which may be distinct from the CD73 5"-nucleotidase.	NAD	199-202	ectonucleotide pyrophosphatase/phosphodiesterase 1	Homo sapiens	114-118
8889808-1	1996	Mouse lung carbonyl reductase, a member of the short-chain dehydrogenase/reductase (SDR) family, shows a strong coenzyme preference for NADP(H) over NAD(H), and is uniquely activated by fatty acids.	NAD	149-155	carbonyl reductase 2	Mus musculus	6-29
8811894-1	1996	Using 1,N6-etheno NAD, a fluorescent analog of NAD, we extended an existing assay for NAD glycohydrolase to the measurement of mono-ADP-ribosyltransferase (mADP-RT) activity using agmatine as acceptor for ADP-ribose.	NAD	18-21	ADP-ribosyltransferase 1	Mus musculus	156-163
21619301-7	1996	Perfusion with 30 muM glutamate in the presence of 3 mM NAD(+) resulted in a strong increase in fluorescence, with a response time of 450 ms.	NAD	56-62	latexin	Homo sapiens	18-21
8660945-7	1996	Consistently with these results, the addition of PARP inhibitors, such as thymidine and 3-aminobenzamide, during the preincubation with AA, prevents NAD+ depletion and abolishes the protective effect of AA against apoptosis.	NAD	149-153	poly(ADP-ribose) polymerase 1	Homo sapiens	49-53
8615810-1	1996	Deoxyhypusine synthase is an NAD(+)-dependent enzyme that catalyses the formation of a deoxyhypusine residue on the eukaryotic initiation factor 5A (eIF-5A) precursor by transferring an aminobutyl moiety from spermidine to the epsilon-amino group of a unique lysine residue.	NAD	29-35	deoxyhypusine synthase	Homo sapiens	0-22
8663122-7	1996	The enzymatic characteristics of the expressed 11beta-HSD2/GFP fusion protein were undistinguishable from those of the native enzyme: high affinity for corticosterone (KM 8-10 nM), NAD dependence, and lack of reductase activity.	NAD	181-184	11-beta-hydroxysteroid dehydrogenase type 2	Oryctolagus cuniculus	47-58
8818686-1	1996	Poly(ADP-ribose) polymerase catalyses the formation of ADP-ribose polymers covalently attached to various nuclear proteins, using NAD+ as substrate.	NAD	130-134	poly(ADP-ribose) polymerase 1	Homo sapiens	0-27
8613464-10	1996	Kinetic measurements revealed that the pl 7.8 form of malate dehydrogenase has the lowest affinity for NADH.	NAD	103-107	malic enzyme 2	Homo sapiens	54-74
8620022-1	1996	Oscillatory kinetics in the peroxidase-oxidase reaction catalyzed by structurally different peroxidases were investigated using NADH as a substrate.	NAD	128-132	peroxidase	Glycine max	28-38
8620022-7	1996	Substituting NADH with dihydroxyfumaric acid as a substrate, oscillations in the oxygen concentration were observed for about 1.5 h when a concentrated solution of this substrate was continuously fed to a solution containing horseradish peroxidase.	NAD	13-17	peroxidase	Glycine max	237-247
8811669-2	1996	Two different 17 beta-HSDs were discovered in human placenta: one highly estrogen specific and using NADP+/NADPH as cofactors (type-1 17 beta-HSD), and a second one that utilizes both androgens and estrogens as substrates with NAD+/NADH (type-2 17 beta-HSD).	NAD	227-231	hydroxysteroid 17-beta dehydrogenase 1	Homo sapiens	14-25
8811669-2	1996	Two different 17 beta-HSDs were discovered in human placenta: one highly estrogen specific and using NADP+/NADPH as cofactors (type-1 17 beta-HSD), and a second one that utilizes both androgens and estrogens as substrates with NAD+/NADH (type-2 17 beta-HSD).	NAD	227-231	hydroxysteroid 17-beta dehydrogenase 1	Homo sapiens	134-145
8811669-2	1996	Two different 17 beta-HSDs were discovered in human placenta: one highly estrogen specific and using NADP+/NADPH as cofactors (type-1 17 beta-HSD), and a second one that utilizes both androgens and estrogens as substrates with NAD+/NADH (type-2 17 beta-HSD).	NAD	232-236	hydroxysteroid 17-beta dehydrogenase 1	Homo sapiens	14-25
8811669-2	1996	Two different 17 beta-HSDs were discovered in human placenta: one highly estrogen specific and using NADP+/NADPH as cofactors (type-1 17 beta-HSD), and a second one that utilizes both androgens and estrogens as substrates with NAD+/NADH (type-2 17 beta-HSD).	NAD	232-236	hydroxysteroid 17-beta dehydrogenase 1	Homo sapiens	134-145
8698091-3	1996	This assay employs phosphoglycerate kinase to catalyse the formation 1,3- bisphosphoglycerate which is then used to oxidise NADH in the presence of glyceraldehyde 3-phosphate dehydrogenase.	NAD	124-128	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	148-188
18966494-6	1996	The diaphorase electrode thus obtained responds to NADH at 0 V. The sensitivity and detection limit of this biosensor are 11.2 mA M(-1) cm(-2) and 1 muM respectively.	NAD	51-55	latexin	Homo sapiens	149-152
8636981-3	1996	Binding of GAPDH to the TNF-alpha-Rz and its derivatives was inhibited by NAD+ and ATP, suggesting that the GAPDH Rossmann fold structure is a part of the ribozyme binding site.	NAD	74-78	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	11-16
8636981-3	1996	Binding of GAPDH to the TNF-alpha-Rz and its derivatives was inhibited by NAD+ and ATP, suggesting that the GAPDH Rossmann fold structure is a part of the ribozyme binding site.	NAD	74-78	tumor necrosis factor	Homo sapiens	24-33
8636981-3	1996	Binding of GAPDH to the TNF-alpha-Rz and its derivatives was inhibited by NAD+ and ATP, suggesting that the GAPDH Rossmann fold structure is a part of the ribozyme binding site.	NAD	74-78	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	108-113
8617745-2	1996	pertussis toxin (PTX) (100 ng/ml) + NAD (1 mM) + ATP (1 mM) treatment of ORCC and CFTR in bilayers resulted in a 2-fold increase in single channel open probability (Po) of ORCC but not of CFTR.	NAD	36-41	CF transmembrane conductance regulator	Homo sapiens	82-86
8617745-2	1996	pertussis toxin (PTX) (100 ng/ml) + NAD (1 mM) + ATP (1 mM) treatment of ORCC and CFTR in bilayers resulted in a 2-fold increase in single channel open probability (Po) of ORCC but not of CFTR.	NAD	36-41	CF transmembrane conductance regulator	Homo sapiens	188-192
8621776-0	1996	Angiotensin II-mediated hypertension in the rat increases vascular superoxide production via membrane NADH/NADPH oxidase activation.	NAD	102-106	angiotensinogen	Rattus norvegicus	0-14
8621776-5	1996	Studies using various enzyme inhibitors and vascular homogenates suggested that the predominant source of .O2- activated by angiotensin II infusion is an NADH/NADPH-dependent, membrane-bound oxidase.	NAD	154-158	angiotensinogen	Rattus norvegicus	124-138
8642645-6	1996	Nuclear changes were accompanied by activation of the DNA repair enzyme poly(ADP-ribose) polymerase (PARP), resulting in increased consumption of NAD which was apparent by 10 h after infection.	NAD	146-149	poly(ADP-ribose) polymerase 1	Homo sapiens	72-99
8642645-6	1996	Nuclear changes were accompanied by activation of the DNA repair enzyme poly(ADP-ribose) polymerase (PARP), resulting in increased consumption of NAD which was apparent by 10 h after infection.	NAD	146-149	poly(ADP-ribose) polymerase 1	Homo sapiens	101-105
8676756-3	1996	As such, PrP contains a putative nicotinamide adenine dinucleotide (NADH)-binding site.	NAD	33-66	prion protein	Homo sapiens	9-12
8676756-3	1996	As such, PrP contains a putative nicotinamide adenine dinucleotide (NADH)-binding site.	NAD	68-72	prion protein	Homo sapiens	9-12
8626764-0	1996	Posttranslational modification of glyceraldehyde-3-phosphate dehydrogenase by S-nitrosylation and subsequent NADH attachment.	NAD	109-113	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	34-74
8611577-1	1996	The reduction kinetics of coenzyme Q (CoQ, ubiquinone) by NADH:ubiquinone oxidoreductase (complex I, EC 1.6.99.3) was investigated in bovine heart mitochondrial membranes using water-soluble homologs and analogs of the endogenous ubiquinone acceptor CoQ10 [the lower homologs from CoQ0 to CoQ3, the 6-pentyl (PB) and 6-decyl (DB) analogs, and duroquinone].	NAD	58-62	coenzyme Q3, methyltransferase	Bos taurus	289-293
8626764-1	1996	Nitric oxide (NO)-related activity has been associated with an NAD+-dependent modification of the glycolytic enzyme, glyceraldehyde-3-phosphate dehydrogenase (GAPDH).	NAD	63-67	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	117-157
8626764-1	1996	Nitric oxide (NO)-related activity has been associated with an NAD+-dependent modification of the glycolytic enzyme, glyceraldehyde-3-phosphate dehydrogenase (GAPDH).	NAD	63-67	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	159-164
8611027-4	1996	Spectroscopic studies indicated NADH:molecular oxygen reductase activity resulted in the production of the superoxide radical, detected as the formation of adrenochrome from epinephrine and by the formation of adrenochrome from epinephrine and by the reduction of nitroblue tetrazolium, both of which could be inhibited by the addition of superoxide dismutase and were unaffected by the addition of catalase.	NAD	32-36	catalase	Homo sapiens	399-407
8881035-2	1996	The deduced amino acid sequence of Bp3 cDNA shares significant similarity to human and mouse CD38 and molluscan ADP-ribosyl cyclase, enzymes that generate the calcium mobilizing agent cyclic ADP-ribose from NAD.	NAD	207-210	BP3	Homo sapiens	35-38
8627159-0	1996	Biochemical pathways of apoptosis: nicotinamide adenine dinucleotide-deficient cells are resistant to tumor necrosis factor or ultraviolet light activation of the 24-kD apoptotic protease and DNA fragmentation.	NAD	35-68	tumor necrosis factor	Homo sapiens	102-123
8627159-2	1996	The present study examined the role of intracellular NAD in tumor necrosis factor (TNF) and ultraviolet (UV) light-induced activation of the 24-kD apoptotic protease (AP24) leading to internucleosomal DNA fragmentation and death.	NAD	53-56	tumor necrosis factor	Homo sapiens	60-81
8627159-2	1996	The present study examined the role of intracellular NAD in tumor necrosis factor (TNF) and ultraviolet (UV) light-induced activation of the 24-kD apoptotic protease (AP24) leading to internucleosomal DNA fragmentation and death.	NAD	53-56	tumor necrosis factor	Homo sapiens	83-86
8627159-8	1996	We confirmed a requirement for intracellular NAD, activation of ADPRT, and subsequent NAD depletion during apoptosis in KG1a, YAC-1, and BW1547 leukemia cell lines.	NAD	86-89	ADP-ribosyltransferase 1	Mus musculus	126-131
8627159-11	1996	Rather, NAD-dependent reactions which may involve mono-ADPRT, function in signal transduction leading to activation of AP24, with subsequent DNA fragmentation and cell death.	NAD	8-11	poly(ADP-ribose) polymerase 1	Homo sapiens	55-60
8907197-2	1996	When the recombinant glutathione S-transferase-RhoA fusion protein (GST-RhoA) was incubated with C3 and [adenylate-32P]NAD, incorporation of radioactivity into the recombinant RhoA increased in the presence of KCl.	NAD	119-122	ras homolog family member A	Homo sapiens	47-51
7492595-0	1995	The ATPase activity of purified CDC48p from Saccharomyces cerevisiae shows complex dependence on ATP-, ADP-, and NADH-concentrations and is completely inhibited by NEM.	NAD	113-117	AAA family ATPase CDC48	Saccharomyces cerevisiae S288C	32-38
8554320-1	1995	The NADH-dependent microsomal electron transfer system consists of NADH-cytochrome b5 reductase and cytochrome b5, which donates reducing equivalents to fatty acyl desaturase, cytochrome P450, and other reactions.	NAD	4-8	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	176-191
8547178-1	1995	17 beta-Hydroxysteroid dehydrogenase (17 beta-HSD) type 2 catalyzes the NAD(+)-dependent oxidation of androgens, estrogens and progestins, predominantly in the secretory endometrium, placenta, liver and small intestine.	NAD	72-78	hydroxysteroid 17-beta dehydrogenase 7	Homo sapiens	0-36
8533007-2	1996	The latter are exemplified by protein thiol modification followed by subsequent NAD(+)-dependent automodification of the glycolytic enzyme GAPDH, or by mechanisms inducing accumulation of the tumor suppressor gene p53 and causing apoptotic cell death.	NAD	80-86	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	139-144
8530457-4	1995	NADH consumption by these cells was stimulated by TGF-beta 1 while that of NADPH remained unchanged.	NAD	0-4	transforming growth factor beta 1	Homo sapiens	50-60
8530457-5	1995	NADPH oxidase activity as measured by diphenyliodonium (DPI)-inhibitable NADH consumption in TGF-beta 1-treated cells followed a time course similar to that of H2O2 release.	NAD	73-77	transforming growth factor beta 1	Homo sapiens	93-103
7493646-1	1995	We have recently described that poly(ADP-ribosyl)-polymerase (PARP) inhibitors rescue U937 cells from apoptosis induced by 1 mM H2O2 oxidative stress; PARP activation leads to a reversible drop in NAD level, which could be blocked by PARP inhibitors (Nos-seri et al., 1994, Exp.	NAD	197-200	poly(ADP-ribose) polymerase 1	Homo sapiens	62-66
7493646-1	1995	We have recently described that poly(ADP-ribosyl)-polymerase (PARP) inhibitors rescue U937 cells from apoptosis induced by 1 mM H2O2 oxidative stress; PARP activation leads to a reversible drop in NAD level, which could be blocked by PARP inhibitors (Nos-seri et al., 1994, Exp.	NAD	197-200	poly(ADP-ribose) polymerase 1	Homo sapiens	151-155
7493646-1	1995	We have recently described that poly(ADP-ribosyl)-polymerase (PARP) inhibitors rescue U937 cells from apoptosis induced by 1 mM H2O2 oxidative stress; PARP activation leads to a reversible drop in NAD level, which could be blocked by PARP inhibitors (Nos-seri et al., 1994, Exp.	NAD	197-200	poly(ADP-ribose) polymerase 1	Homo sapiens	151-155
7493646-7	1995	These cells (LN+) behaved as HN U937: oxidative stress induced a NAD drop, the extent of which is dependent on the cells" basal NAD level; moreover, PARP inhibitors could rescue LN+ cells from peroxide-induced apoptosis.	NAD	65-68	poly(ADP-ribose) polymerase 1	Homo sapiens	149-153
7493646-7	1995	These cells (LN+) behaved as HN U937: oxidative stress induced a NAD drop, the extent of which is dependent on the cells" basal NAD level; moreover, PARP inhibitors could rescue LN+ cells from peroxide-induced apoptosis.	NAD	128-131	poly(ADP-ribose) polymerase 1	Homo sapiens	149-153
8547172-9	1995	It is 37% identical in amino acid sequence to an NAD(+)-dependent isozyme of 17 beta-hydroxysteroid dehydrogenase.	NAD	49-55	hydroxysteroid 17-beta dehydrogenase 7	Homo sapiens	77-113
8547176-7	1995	Useful parameters for the detection of multiple forms of 17 beta-HSD appear to be the E2/T activity ratio, NAD/NADP activity ratios, steroid inhibitor specificity and inhibition patterns over a wide range of putative inhibitor concentrations.	NAD	107-110	hydroxysteroid 17-beta dehydrogenase 1	Homo sapiens	57-68
7499345-8	1995	Similar to microsomal RoDH and RoDH(I), RoDH(II) had higher activity with NADP rather than NAD, was stimulated by ethanol and phosphatidyl choline, was not inhibited by the medium-chain alcohol dehydrogenase inhibitor 4-methylpyrazole, but was inhibited by phenylarsine oxide and the short-chain dehydrogenase/reductase inhibitor carbenoxolone.	NAD	74-77	retinol dehydrogenase 16	Rattus norvegicus	40-48
7590361-2	1995	The protein has homology to the rabbit and human skeletal muscle (50% identity) and two chicken heterophil (52% identity) NAD+:arginine MADPRT.	NAD	122-126	ADP-ribosyltransferase 1 like 2	Gallus gallus	136-142
7578039-8	1995	Hydride transfer from alcohol to NADP+ (0.6 s-1), however, is at least 100- to 1000-fold slower than NAD(+)-dependent alcohol oxidation mediated by these two enzymes, resulting in a bound-state equilibrium constant for aldose reductase which greatly favors the forward reaction.	NAD	101-107	aldo-keto reductase family 1 member B	Homo sapiens	219-235
7568279-6	1995	The activity of hepatic gamma-GCS was 1.6 times higher in the copper-deficient than in the copper-adequate rats (58.0 vs 35.9 nmol NADH/min.mg protein).	NAD	131-135	glutamate-cysteine ligase, catalytic subunit	Rattus norvegicus	24-33
7578008-1	1995	Anaerobic titrations of the two-electron-reduced NADH peroxidase (EH2) with NADH and 3-acetylpyridine adenine dinucleotide (AcPyADH) yield the respective complexes without significant formation of the four-electron-reduced enzyme (EH4).	NAD	49-53	epoxide hydrolase 4	Homo sapiens	231-234
7573405-5	1995	Although under certain conditions both GSNO and the NO donor, sodium nitroprusside (SNP), led to the covalent NAD(+)-dependent modification of GAPDH, this putative ADP ribosylation was unlikely to be the primary mechanism for inhibition, since the stoichiometry was extremely low, and, in the case of GSNO, inhibition was completely reversed by thiol reagents.	NAD	110-116	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	143-148
8673015-1	1995	In vitro experiments are reported showing that NAD(P)H:(quinone acceptor) oxidoreductase (QR), purified from Glycine max seedlings, reduces Leu- and Met-enkephalin-tyrosinase oxidation products, in the presence of NADH or NADPH.	NAD	214-218	proopiomelanocortin	Homo sapiens	149-163
8593536-6	1995	Catalase different significantly with respect to NADPH and NADH oxidation during reduction of adrenochrome catalyzed by NADPH-cytochrome P450 reductase and DT-diaphorase.	NAD	59-63	catalase	Homo sapiens	0-8
8593536-6	1995	Catalase different significantly with respect to NADPH and NADH oxidation during reduction of adrenochrome catalyzed by NADPH-cytochrome P450 reductase and DT-diaphorase.	NAD	59-63	cytochrome p450 oxidoreductase	Homo sapiens	120-151
8593536-6	1995	Catalase different significantly with respect to NADPH and NADH oxidation during reduction of adrenochrome catalyzed by NADPH-cytochrome P450 reductase and DT-diaphorase.	NAD	59-63	NAD(P)H quinone dehydrogenase 1	Homo sapiens	156-169
8593536-7	1995	Catalase increased NADPH oxidation slightly, while NADH oxidation was inhibited during reduction of adrenochrome by NADPH cytochrome P450 reductase and DT-diaphorase, respectively.	NAD	51-55	cytochrome p450 oxidoreductase	Homo sapiens	116-147
8593536-7	1995	Catalase increased NADPH oxidation slightly, while NADH oxidation was inhibited during reduction of adrenochrome by NADPH cytochrome P450 reductase and DT-diaphorase, respectively.	NAD	51-55	NAD(P)H quinone dehydrogenase 1	Homo sapiens	152-165
7559400-0	1995	NAD(+)-dependent ADP-ribosylation of T lymphocyte alloantigen RT6.1 reversibly proceeding in intact rat lymphocytes.	NAD	0-6	ADP-ribosyltransferase 2b	Rattus norvegicus	62-67
7559400-1	1995	Rat T lymphocyte alloantigen 6.1 (RT6.1), which was synthesized as the fusion protein with a maltose-binding protein in Escherichia coli, displayed NAD(+)-dependent auto-ADP-ribosylation in addition to an enzyme activity of NAD+ glycohydrolase.	NAD	148-154	ADP-ribosyltransferase 2b	Rattus norvegicus	34-39
7559400-6	1995	These results suggested that the NAD(+)-dependent modification of the 31-kDa protein was due to ADP-ribosylation of glycosylphosphatidylinositol-anchored RT6.1 at an arginine residue.	NAD	33-39	ADP-ribosyltransferase 2b	Rattus norvegicus	154-159
7559400-10	1995	Moreover, readdition of NAD+ caused the ADP-ribosylation of RT6.1 again.	NAD	24-28	ADP-ribosyltransferase 2b	Rattus norvegicus	60-65
7562915-2	1995	Compound 1 was recently designed using the NAD:GAPDH complexes of the human enzyme and that of Trypanosoma brucei, the causative agent of sleeping sickness.	NAD	43-46	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	47-52
7565631-0	1995	Nicotinamide adenine dinucleotide (phosphate): quinone oxidoreductase (DT-diaphorase) as a target for bioreductive antitumor quinones: quinone cytotoxicity and selectivity in human lung and breast cancer cell lines.	NAD	0-33	NAD(P)H quinone dehydrogenase 1	Homo sapiens	71-84
7639707-0	1995	Oxygen free radicals enhance the nitric oxide-induced covalent NAD(+)-linkage to neuronal glyceraldehyde-3-phosphate dehydrogenase.	NAD	63-69	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	90-130
7639707-3	1995	In the present study, we show that 3-morpholino-sydnonimine (SIN-1) is much more efficient than sodium nitroprusside (SNP) in stimulating the covalent labelling of GAPDH from cultured striatal neurones in the presence of [adenylate-32P]NAD+ (877 +/- 110 and 266 +/- 33% increase in NAD(+)-labelling induced by maximally effective concentrations of SIN-1 and SNP respectively).	NAD	282-288	MAPK associated protein 1	Homo sapiens	61-66
7639707-4	1995	The difference in the efficacy of both NO-generating compounds could be due to the additional release of superoxide by SIN-1, since superoxide dismutase and the nitrone 5,5"-dimethyl pyrroline-1-oxide markedly inhibited the SIN-1-induced covalent binding of NAD+ to GAPDH.	NAD	258-262	MAPK associated protein 1	Homo sapiens	119-124
7639707-6	1995	Supporting further a role of oxygen free radicals in the NAD+ linkage to GAPDH, pyrogallol, a superoxide generator, which alone was ineffective, potentiated the SNP-evoked response.	NAD	57-61	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	73-78
7639539-1	1995	NAD(P)H: quinone-acceptor oxidoreductase (EC 1.6.99.2), also referred to as DT-diaphorase, is a flavoprotein that catalyzes the two-electron reduction of quinones and quinonoid compounds to hydroquinones, using either NADH or NADPH as the electron donor.	NAD	218-222	NAD(P)H quinone dehydrogenase 1	Homo sapiens	76-89
7639707-3	1995	In the present study, we show that 3-morpholino-sydnonimine (SIN-1) is much more efficient than sodium nitroprusside (SNP) in stimulating the covalent labelling of GAPDH from cultured striatal neurones in the presence of [adenylate-32P]NAD+ (877 +/- 110 and 266 +/- 33% increase in NAD(+)-labelling induced by maximally effective concentrations of SIN-1 and SNP respectively).	NAD	282-288	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	164-169
7639707-7	1995	The NAD+ linkage to neuronal GAPDH measured in the presence of NO and superoxide probably involves sulphydryl groups, since the radiolabelling of the protein was reversed by exposure to HgCl2 and prevented by pretreatment with the alkylating agent N-ethylmaleimide.	NAD	4-8	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	29-34
7639707-9	1995	In conclusion, the present study indicates that superoxide anions potentiate NO-induced covalent NAD(+)-linkage to GAPDH and enzyme inactivation.	NAD	97-103	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	115-120
7664797-4	1995	This automodification of RT6.2 is covalent, requires intact NAD as substrate, and displays characteristics typical for linkage of ADP-ribose to arginine.	NAD	60-63	ADP-ribosyltransferase 2b	Rattus norvegicus	25-30
7622508-2	1995	Aldose reductase (ALR2) shows a strong specificity for its nucleotide coenzyme, binding NADPH much more tightly than NADH (KD of < 1 microM versus 1.2 mM respectively).	NAD	117-121	aldo-keto reductase family 1 member B	Homo sapiens	0-16
7630349-8	1995	These findings suggest that the disease severity in our patients may be related to the degree of NADH reoxidation by glycerol 3-phosphate dehydrogenase substituting for LDH.	NAD	97-101	lactate dehydrogenase A	Homo sapiens	169-172
7628449-3	1995	In addition, mdh3-disrupted cells were unable to grow on oleate whereas growth on other non-fermentable carbon sources was normal, suggesting that MDH3 is involved in the reoxidation of NADH generated during fatty acid beta-oxidation rather than functioning as part of the glyoxylate cycle.	NAD	186-190	malate dehydrogenase MDH3	Saccharomyces cerevisiae S288C	13-17
7628449-3	1995	In addition, mdh3-disrupted cells were unable to grow on oleate whereas growth on other non-fermentable carbon sources was normal, suggesting that MDH3 is involved in the reoxidation of NADH generated during fatty acid beta-oxidation rather than functioning as part of the glyoxylate cycle.	NAD	186-190	malate dehydrogenase MDH3	Saccharomyces cerevisiae S288C	147-151
7477744-8	1995	NO activates poly(ADP-ribose) synthetase (PARS), a nuclear enzyme that synthesizes poly(ADP-ribose) from NAD.	NAD	105-108	poly(ADP-ribose) polymerase 1	Homo sapiens	13-40
7477744-8	1995	NO activates poly(ADP-ribose) synthetase (PARS), a nuclear enzyme that synthesizes poly(ADP-ribose) from NAD.	NAD	105-108	poly(ADP-ribose) polymerase 1	Homo sapiens	42-46
7477744-9	1995	Prolonged activation of PARS depletes NAD and lowers cellular energy levels.	NAD	38-41	poly(ADP-ribose) polymerase 1	Homo sapiens	24-28
7622508-2	1995	Aldose reductase (ALR2) shows a strong specificity for its nucleotide coenzyme, binding NADPH much more tightly than NADH (KD of < 1 microM versus 1.2 mM respectively).	NAD	117-121	aldo-keto reductase family 1 member B	Homo sapiens	18-22
7793986-7	1995	The enzyme contained about one flavin adenine dinucleotide (FAD) per 45-kDa subunit as determined by fluorescence spectroscopy, was specific for the beta-hydrogen of NADH, preferred NADH over NADPH as electron donor, and preferred hexacyanoferrate(III) as electron acceptor, e.g., it reduced Fe3+-EDTA, cytochrome c, oxygen, and duroquinone at < 10% of the rate with hexacyanoferrate(III).	NAD	166-170	cytochrome c, somatic	Homo sapiens	303-315
7619045-3	1995	The Km values for NAD+ and PFK-2/FBPase-2 were 14 microM and 0.4 microM respectively.	NAD	18-22	fructose-bisphosphatase 2	Rattus norvegicus	33-41
7793986-7	1995	The enzyme contained about one flavin adenine dinucleotide (FAD) per 45-kDa subunit as determined by fluorescence spectroscopy, was specific for the beta-hydrogen of NADH, preferred NADH over NADPH as electron donor, and preferred hexacyanoferrate(III) as electron acceptor, e.g., it reduced Fe3+-EDTA, cytochrome c, oxygen, and duroquinone at < 10% of the rate with hexacyanoferrate(III).	NAD	182-186	cytochrome c, somatic	Homo sapiens	303-315
7626443-4	1995	Mouse 3 beta HSD I and III function as 3 beta-hydroxysteroid dehydrogenases and 5-en-->4-en isomerases using NAD+ as a cofactor.	NAD	112-116	hydroxy-delta-5-steroid dehydrogenase, 3 beta- and steroid delta-isomerase 1	Mus musculus	6-18
7786036-3	1995	3-Aminobenzamide (ABA), an inhibitor of PARP, spared the depletion of NAD and ATP and prevented the cell killing.	NAD	70-73	poly(ADP-ribose) polymerase 1	Homo sapiens	40-44
7628865-1	1995	Poly(ADPR) polymerase (PARP; EC 2.4.2.30) is a nuclear enzyme, which, when activated by oxygen- and nitrogen-radical-induced DNA strand breaks, transfers ADP ribose units to nuclear proteins and initiates apoptosis by depletion of cellular NAD and ATP pools.	NAD	240-243	poly(ADP-ribose) polymerase 1	Homo sapiens	23-27
8592522-1	1995	Basic fibroblast growth factor (FGF-2) is posttranslationally modified by the enzymatic transfer of ADP-ribose from nicotinamide adenine dinucleotide (NAD).	NAD	116-149	fibroblast growth factor 2	Homo sapiens	32-37
8592522-1	1995	Basic fibroblast growth factor (FGF-2) is posttranslationally modified by the enzymatic transfer of ADP-ribose from nicotinamide adenine dinucleotide (NAD).	NAD	151-154	fibroblast growth factor 2	Homo sapiens	32-37
8592522-2	1995	When sonicated nuclei of adrenal capillary endothelial or SK-Hep1 cells are incubated with [32P]NAD, FGF-2 is rapidly ADP-ribosylated in a dose- and time-dependent fashion.	NAD	96-99	fibroblast growth factor 2	Homo sapiens	101-106
8592522-8	1995	As such, an immunoreactive ADP-ribosylated FGF-2 is detected in extracts of SK-Hep1 nuclei when they are incubated with [32P]NAD.	NAD	125-128	fibroblast growth factor 2	Homo sapiens	43-48
7755589-5	1995	It is 55, 43 and 44% identical with yeast NAD(+)-specific IDH2, yeast NAD(+)-specific IDH1 and monkey NAD(+)-specific IDH gamma-subunit (IDH gamma) respectively.	NAD	70-76	isocitrate dehydrogenase (NAD(+)) IDH1	Saccharomyces cerevisiae S288C	86-90
7758579-3	1995	The pathway of NO induced islet cell death involves DNA damage and excessive activation of poly(ADP-ribose)polymerase leading to irreversible depletion of intracellular NAD+.	NAD	169-173	poly(ADP-ribose) polymerase 1	Homo sapiens	91-117
7771804-1	1995	Recently we have proposed and presented evidence suggesting the existence of a "bi-trans-membrane" electron transport chain, located at the contact sites between outer and inner mitochondrial membranes, which can be utilized to promote either the oxidation of exogenous NADH in the presence of catalytic amounts of added cytochrome c or the reduction of exogenous cytochrome c supported by the oxidation of respiratory substrates present inside the mitochondria.	NAD	270-274	cytochrome c, somatic	Homo sapiens	321-333
7771804-1	1995	Recently we have proposed and presented evidence suggesting the existence of a "bi-trans-membrane" electron transport chain, located at the contact sites between outer and inner mitochondrial membranes, which can be utilized to promote either the oxidation of exogenous NADH in the presence of catalytic amounts of added cytochrome c or the reduction of exogenous cytochrome c supported by the oxidation of respiratory substrates present inside the mitochondria.	NAD	270-274	cytochrome c, somatic	Homo sapiens	364-376
7771804-6	1995	In the out-->in electron transport pathway the components involved appear to be cytosolic reduced substrates-->NADH produced by cytosolic dehydrogenases activity-->NADH-cytochrome b5 oxidoreductase complex leaning out the external side of the external membrane-->exogenous cytochrome c-->cytochrome oxidase of contact sites-->molecular oxygen.	NAD	117-121	cytochrome c, somatic	Homo sapiens	285-297
7771788-6	1995	Similarly, the enzymes of the mitochondrial matrix in the presence of either NADH or NADPH are able to reduce DTNB.	NAD	77-81	dystrobrevin, beta	Rattus norvegicus	110-114
7755589-5	1995	It is 55, 43 and 44% identical with yeast NAD(+)-specific IDH2, yeast NAD(+)-specific IDH1 and monkey NAD(+)-specific IDH gamma-subunit (IDH gamma) respectively.	NAD	70-76	isocitrate dehydrogenase (NAD(+)) IDH1	Saccharomyces cerevisiae S288C	86-90
7531693-4	1995	The AUUUA-specific RNA binding activity of GAPDH was inhibited by NAD+, NADH, and ATP in a concentration-dependent manner, suggesting that RNA binding of GAPDH might involve the NAD(+)-binding region, or dinucleotide-binding (Rossmann) fold.	NAD	178-184	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	43-48
7726572-0	1995	Evidence for free radical generation due to NADH oxidation by aldehyde oxidase during ethanol metabolism.	NAD	44-48	aldehyde oxidase 1	Homo sapiens	62-78
7726572-4	1995	In this study we demonstrated that AO acts not only upon acetaldehyde but also upon NADH, with superoxide anion radical (O2.-) formation.	NAD	84-88	aldehyde oxidase 1	Homo sapiens	35-37
7726572-5	1995	The apparent Km of NADH for AO was approximately 28 microM, a much smaller value than the one reported for acetaldehyde (1 mM).	NAD	19-23	aldehyde oxidase 1	Homo sapiens	28-30
7726572-6	1995	The NADH oxidation by AO promoted the O2.- generation and the ADP-Fe(3+)-dependent microsomal lipid peroxidation in a NADH and AO concentration-dependent manner.	NAD	4-8	aldehyde oxidase 1	Homo sapiens	22-24
7726572-6	1995	The NADH oxidation by AO promoted the O2.- generation and the ADP-Fe(3+)-dependent microsomal lipid peroxidation in a NADH and AO concentration-dependent manner.	NAD	4-8	aldehyde oxidase 1	Homo sapiens	127-129
7726572-6	1995	The NADH oxidation by AO promoted the O2.- generation and the ADP-Fe(3+)-dependent microsomal lipid peroxidation in a NADH and AO concentration-dependent manner.	NAD	118-122	aldehyde oxidase 1	Homo sapiens	22-24
7726572-8	1995	To explain this observation a vicious cycle which increases the oxyradical production is suggested: ADH reduces NAD+ to NADH, which is oxidized by AO, generating reactive oxidative species plus NAD+ available again for reduction by ADH.	NAD	112-116	aldehyde oxidase 1	Homo sapiens	147-149
7726572-8	1995	To explain this observation a vicious cycle which increases the oxyradical production is suggested: ADH reduces NAD+ to NADH, which is oxidized by AO, generating reactive oxidative species plus NAD+ available again for reduction by ADH.	NAD	120-124	aldehyde oxidase 1	Homo sapiens	147-149
7726572-8	1995	To explain this observation a vicious cycle which increases the oxyradical production is suggested: ADH reduces NAD+ to NADH, which is oxidized by AO, generating reactive oxidative species plus NAD+ available again for reduction by ADH.	NAD	194-198	aldehyde oxidase 1	Homo sapiens	147-149
7726572-10	1995	Our studies indicate that the NADH oxidation by AO may play a role in ethanol-induced generation of reactive oxygen species, contributing to its hepatotoxicity.	NAD	30-34	aldehyde oxidase 1	Homo sapiens	48-50
7850801-1	1995	We have recently demonstrated that cell lines deficient in poly(ADP-ribose) synthesis due to deficiency in the enzyme poly(ADP-ribose) polymerase (PADPRP) or depletion of its substrate NAD+ overexpress GRP78.	NAD	185-189	heat shock protein family A (Hsp70) member 5	Homo sapiens	202-207
7850801-3	1995	Thus, our studies suggest that interference with NAD+-PADPRP metabolism could provide an important approach to (a) define pathways of GRP78 induction, (b) study the effect of GRP78 on other cellular processes, (c) elucidate the mechanism of GRP78-dependent resistance to topoisomerase II targeted drugs, and (d) modulate responses to chemotherapy in normal and tumor tissues.	NAD	49-53	poly(ADP-ribose) polymerase 1	Homo sapiens	54-60
7850801-3	1995	Thus, our studies suggest that interference with NAD+-PADPRP metabolism could provide an important approach to (a) define pathways of GRP78 induction, (b) study the effect of GRP78 on other cellular processes, (c) elucidate the mechanism of GRP78-dependent resistance to topoisomerase II targeted drugs, and (d) modulate responses to chemotherapy in normal and tumor tissues.	NAD	49-53	heat shock protein family A (Hsp70) member 5	Homo sapiens	134-139
7850801-3	1995	Thus, our studies suggest that interference with NAD+-PADPRP metabolism could provide an important approach to (a) define pathways of GRP78 induction, (b) study the effect of GRP78 on other cellular processes, (c) elucidate the mechanism of GRP78-dependent resistance to topoisomerase II targeted drugs, and (d) modulate responses to chemotherapy in normal and tumor tissues.	NAD	49-53	heat shock protein family A (Hsp70) member 5	Homo sapiens	175-180
7850801-3	1995	Thus, our studies suggest that interference with NAD+-PADPRP metabolism could provide an important approach to (a) define pathways of GRP78 induction, (b) study the effect of GRP78 on other cellular processes, (c) elucidate the mechanism of GRP78-dependent resistance to topoisomerase II targeted drugs, and (d) modulate responses to chemotherapy in normal and tumor tissues.	NAD	49-53	heat shock protein family A (Hsp70) member 5	Homo sapiens	175-180
7850801-4	1995	However, in the in vivo situation, it is impractical to interfere with NAD+-PADPRP metabolism by mutational inactivation of PADPRP or by depletion of its substrate NAD+.	NAD	71-75	poly(ADP-ribose) polymerase 1	Homo sapiens	76-82
7850801-5	1995	Therefore, we have examined several inhibitors of NAD+-PADPRP metabolism including 3-aminobenzamide, PD128763, and 6-aminonicotinamide for their ability to reproduce the results obtained with cell lines deficient in NAD+-PADPRP metabolism relative to the induction of GRP78 and subsequent development of resistance to VP-16.	NAD	50-54	poly(ADP-ribose) polymerase 1	Homo sapiens	55-61
7733870-11	1995	The stimulation of NADH-dependent microsomal DNA strand cleavage was completely blocked by catalase, superoxide dismutase, GSH and a variety of hydroxyl-radical-scavenging agents, but not by anti-oxidants that prevent microsomal lipid peroxidation.	NAD	19-23	catalase	Rattus norvegicus	91-99
7698643-1	1995	Poly(ADP-ribosyl)ation is catalyzed by NAD+: protein(ADP-ribosyl) transferase (ADPRT), a chromatin-associated enzyme which, in the presence of DNA breaks, transfers ADP-ribose from NAD+ to nuclear proteins.	NAD	39-42	ADP-ribosyltransferase 1	Mus musculus	79-84
7698643-1	1995	Poly(ADP-ribosyl)ation is catalyzed by NAD+: protein(ADP-ribosyl) transferase (ADPRT), a chromatin-associated enzyme which, in the presence of DNA breaks, transfers ADP-ribose from NAD+ to nuclear proteins.	NAD	39-43	ADP-ribosyltransferase 1	Mus musculus	79-84
7531691-1	1995	NAD(P)H:quinone oxidoreductase (EC 1.6.99.2) (DT-diaphorase) is an FAD-containing enzyme that catalyzes the 2-electron reduction of quinones to hydroquinones using either NADH or NADPH as the electron donor.	NAD	171-175	NAD(P)H quinone dehydrogenase 1	Homo sapiens	46-59
7531693-4	1995	The AUUUA-specific RNA binding activity of GAPDH was inhibited by NAD+, NADH, and ATP in a concentration-dependent manner, suggesting that RNA binding of GAPDH might involve the NAD(+)-binding region, or dinucleotide-binding (Rossmann) fold.	NAD	178-184	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	154-159
7531693-6	1995	The direct demonstration of ARE-specific binding protein activity localized to the NAD(+)-binding region of GAPDH supports the general concept that enzymes containing this domain may exhibit specific RNA binding activity and play additional roles in nucleic acid metabolism.	NAD	83-89	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	108-113
7578427-1	1995	Two approaches have been used to elucidate the role of the nuclear polymerizing NAD+:protein(ADP-ribosyl)-transferase (ADPRT): i) comparison of the primary structure of Dictyostelium discoideum ADPRT derived from a 2 kb, partial cDNA sequence with the mammalian, fish, amphibian and insect counterparts revealed an overall homology of 25%.	NAD	80-84	ADP-ribosyltransferase 1	Mus musculus	119-124
7551811-3	1995	These results contrast with the almost complete inhibition of autoxidation (NADH oxidation) of ortho-hydroquinone during reduction of aminochrome catalyzed by DT-diaphorase in the presence of both superoxide dismutase and catalase.	NAD	76-80	NAD(P)H quinone dehydrogenase 1	Homo sapiens	159-172
7551811-3	1995	These results contrast with the almost complete inhibition of autoxidation (NADH oxidation) of ortho-hydroquinone during reduction of aminochrome catalyzed by DT-diaphorase in the presence of both superoxide dismutase and catalase.	NAD	76-80	catalase	Homo sapiens	222-230
7822273-2	1995	The COOH-terminal domain of the 10-FTHFDH (residues 417-902) shows a 46% identity with a series of NAD(+)-dependent aldehyde dehydrogenases (EC 1.2.1.3).	NAD	99-105	aldehyde dehydrogenase 1 family, member L1	Rattus norvegicus	32-41
7578422-3	1995	While PARP-mono(ADP-ribose) conjugates were the predominant products of automodification at 200 nM NAD (initiation), highly branched and complex polymers were synthesized at 200 microM NAD (polymerization).	NAD	99-102	poly(ADP-ribose) polymerase 1	Homo sapiens	6-10
7578422-8	1995	In addition, the auto-poly(ADP-ribosyl)ation reaction of PARP increased with second order kinetics as a function of the NAD concentration at nanomolar levels (0.2-106 microM).	NAD	120-123	poly(ADP-ribose) polymerase 1	Homo sapiens	57-61
7578422-9	1995	Therefore, the dimeric structure of PARP also requires two molecules of bound NAD for efficient ADP-ribose polymerization.	NAD	78-81	poly(ADP-ribose) polymerase 1	Homo sapiens	36-40
7703274-1	1995	The NADPH-adrenodoxin complex with adrenodoxin is responsible for the transformation of the two-electron flow from NADH to the mono-electron flow to cytochrome P-450 in the steroid-hydroxyl enzyme system of mitochondria of kidney crust.	NAD	115-119	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	149-165
7578427-0	1995	On the biological role of the nuclear polymerizing NAD+: protein(ADP-ribosyl) transferase (ADPRT): ADPRT from Dictyostelium discoideum and inactivation of the ADPRT gene in the mouse.	NAD	51-55	ADP-ribosyltransferase 1	Mus musculus	91-96
7578427-0	1995	On the biological role of the nuclear polymerizing NAD+: protein(ADP-ribosyl) transferase (ADPRT): ADPRT from Dictyostelium discoideum and inactivation of the ADPRT gene in the mouse.	NAD	51-55	ADP-ribosyltransferase 1	Mus musculus	99-104
7578427-0	1995	On the biological role of the nuclear polymerizing NAD+: protein(ADP-ribosyl) transferase (ADPRT): ADPRT from Dictyostelium discoideum and inactivation of the ADPRT gene in the mouse.	NAD	51-55	ADP-ribosyltransferase 1	Mus musculus	99-104
7540026-2	1995	The latter are exemplified by the NAD(+)-dependent automodification of the glycolytic enzyme glyceraldehyde-3-phosphate dehydrogenase (GAPDH).	NAD	34-40	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	93-133
7918631-2	1994	Poly(ADP-ribose) polymerase (EC 2.4.2.30) synthesizes the polymer from NAD, and poly(ADP-ribose) glycohydrolase (PARG) is the major enzyme responsible for its catabolism (Thomassin et al.	NAD	71-74	poly(ADP-ribose) polymerase 1	Homo sapiens	0-27
7540026-2	1995	The latter are exemplified by the NAD(+)-dependent automodification of the glycolytic enzyme glyceraldehyde-3-phosphate dehydrogenase (GAPDH).	NAD	34-40	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	135-140
7540026-3	1995	The experimental post-translational, covalent modification of the enzyme by [32P]NAD+ is achieved using NO-releasing compounds and an active constitutive or inducible NO-synthase.	NAD	81-85	nitric oxide synthase 2	Homo sapiens	157-178
7540026-4	1995	Potential roles for NO in this covalent enzyme modification can be grouped as follows: S-Nitrosylation of GAPDH by NO+ NAD(+)-dependent, post-translational covalent automodification of GAPDH.	NAD	119-125	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	106-111
7540026-4	1995	Potential roles for NO in this covalent enzyme modification can be grouped as follows: S-Nitrosylation of GAPDH by NO+ NAD(+)-dependent, post-translational covalent automodification of GAPDH.	NAD	119-125	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	185-190
7540026-17	1995	Because some of these alternative functions of GAPDH, just like NO-mediated modification of the enzyme, are related to the NAD+ binding site of the protein, we are interested in searching for the significance of these activities in relation to NO actions.	NAD	123-127	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	47-52
8750613-2	1995	Such reduced ATP concentrations are correlated with reduced poly(ADP-ribose) synthetase (polyADPRT; EC 2.4.2.30) activity; this reduces the breakdown of nicotinamide-adenine dinucleotide coenzymes and thus explains their normal intracellular concentrations.	NAD	153-186	poly(ADP-ribose) polymerase 1	Homo sapiens	60-87
7603529-5	1995	The metabolic background of exertional myoglobinuria was demonstrated as a result of the impaired reoxidation of NADH produced by glyceraldehyde-3-phosphate-dehydrogenase (G3PD) action.	NAD	113-117	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	130-170
7603529-5	1995	The metabolic background of exertional myoglobinuria was demonstrated as a result of the impaired reoxidation of NADH produced by glyceraldehyde-3-phosphate-dehydrogenase (G3PD) action.	NAD	113-117	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	172-176
8082230-6	1994	The addition of DETAPAC resulted in a strong inhibition of NADH oxidation (65% inhibition) during the reduction of cDoQ by DT-diaphorase, suggesting that manganese was responsible for 65% of the autoxidation of cDoQH2.	NAD	59-63	NAD(P)H quinone dehydrogenase 1	Homo sapiens	123-136
8082230-7	1994	The addition of SOD to the incubation mixture resulted in the inhibition of NADH oxidation (79%) during the reduction of cDoQ by DT-diaphorase.	NAD	76-80	superoxide dismutase 1	Homo sapiens	16-19
8082230-7	1994	The addition of SOD to the incubation mixture resulted in the inhibition of NADH oxidation (79%) during the reduction of cDoQ by DT-diaphorase.	NAD	76-80	NAD(P)H quinone dehydrogenase 1	Homo sapiens	129-142
8082230-8	1994	In the presence of DETAPAC, the addition of SOD inhibited NADH oxidation during cDoQH2 autoxidation 75%, suggesting that superoxide radicals are responsible for 75% of the oxygen-dependent autoxidation.	NAD	58-62	superoxide dismutase 1	Homo sapiens	44-47
7531693-0	1995	Glyceraldehyde-3-phosphate dehydrogenase selectively binds AU-rich RNA in the NAD(+)-binding region (Rossmann fold).	NAD	78-84	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	0-40
7531693-4	1995	The AUUUA-specific RNA binding activity of GAPDH was inhibited by NAD+, NADH, and ATP in a concentration-dependent manner, suggesting that RNA binding of GAPDH might involve the NAD(+)-binding region, or dinucleotide-binding (Rossmann) fold.	NAD	66-70	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	43-48
7531693-4	1995	The AUUUA-specific RNA binding activity of GAPDH was inhibited by NAD+, NADH, and ATP in a concentration-dependent manner, suggesting that RNA binding of GAPDH might involve the NAD(+)-binding region, or dinucleotide-binding (Rossmann) fold.	NAD	66-70	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	154-159
7531693-4	1995	The AUUUA-specific RNA binding activity of GAPDH was inhibited by NAD+, NADH, and ATP in a concentration-dependent manner, suggesting that RNA binding of GAPDH might involve the NAD(+)-binding region, or dinucleotide-binding (Rossmann) fold.	NAD	72-76	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	43-48
7531693-4	1995	The AUUUA-specific RNA binding activity of GAPDH was inhibited by NAD+, NADH, and ATP in a concentration-dependent manner, suggesting that RNA binding of GAPDH might involve the NAD(+)-binding region, or dinucleotide-binding (Rossmann) fold.	NAD	72-76	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	154-159
7988726-5	1994	Here we report the effect of replacing Ala-46 with an argine residue, and A46R mutant, on binding of NADP+ to ADH and its catalytic efficiency with the NADP+ cofactor, and a modeling of the three-dimensional structure of the NAD(+)-binding region of ADH.	NAD	225-231	Alcohol dehydrogenase	Drosophila melanogaster	110-113
7988726-5	1994	Here we report the effect of replacing Ala-46 with an argine residue, and A46R mutant, on binding of NADP+ to ADH and its catalytic efficiency with the NADP+ cofactor, and a modeling of the three-dimensional structure of the NAD(+)-binding region of ADH.	NAD	225-231	Alcohol dehydrogenase	Drosophila melanogaster	250-253
7988726-7	1994	For the A46R mutant, the ratio of kcat/Km of NAD+ to NADP+ is 85, over ten-fold lower than that for wild-type ADH.	NAD	45-49	Alcohol dehydrogenase	Drosophila melanogaster	110-113
7988726-8	1994	Our model of the 3D structure of the NAD(+)-binding region of ADH shows that Ala-46 is over 10 A from the ribose moiety of NAD+, which would suggest that there is little interaction between this residue and NAD+ and explain why its mutation to arginine has little effect on NAD+ binding.	NAD	37-43	Alcohol dehydrogenase	Drosophila melanogaster	62-65
7988726-8	1994	Our model of the 3D structure of the NAD(+)-binding region of ADH shows that Ala-46 is over 10 A from the ribose moiety of NAD+, which would suggest that there is little interaction between this residue and NAD+ and explain why its mutation to arginine has little effect on NAD+ binding.	NAD	123-127	Alcohol dehydrogenase	Drosophila melanogaster	62-65
7988726-8	1994	Our model of the 3D structure of the NAD(+)-binding region of ADH shows that Ala-46 is over 10 A from the ribose moiety of NAD+, which would suggest that there is little interaction between this residue and NAD+ and explain why its mutation to arginine has little effect on NAD+ binding.	NAD	207-211	Alcohol dehydrogenase	Drosophila melanogaster	62-65
7988726-8	1994	Our model of the 3D structure of the NAD(+)-binding region of ADH shows that Ala-46 is over 10 A from the ribose moiety of NAD+, which would suggest that there is little interaction between this residue and NAD+ and explain why its mutation to arginine has little effect on NAD+ binding.	NAD	207-211	Alcohol dehydrogenase	Drosophila melanogaster	62-65
7988726-10	1994	We also constructed a double mutant, D39N/A46R mutant, which we find has a 30-fold lower Km(app)NADP+ and 8-fold higher kcat with NADP+ as a cofactor compared to wild-type ADH; binding of NAD+ to this double mutant was lowered by 5-fold and kcat was increased by 1.5-fold.	NAD	188-192	Alcohol dehydrogenase	Drosophila melanogaster	172-175
7988726-12	1994	The principle effect of the two mutations in ADH is to alter its affinity for the nucleotide cofactor; kcat decreases slightly in A46R with NAD+ and remains unchanged or increases in the other mutants.	NAD	140-144	Alcohol dehydrogenase	Drosophila melanogaster	45-48
7986093-1	1994	The interaction between muscle-type lactate dehydrogenase (LDHm) and tubulin was investigated by monitoring the combined effect of NADH and tubulin on steady-state kinetics and the combined effect of NADH and pH on complex formation between tubulin and the enzyme.	NAD	131-135	lactate dehydrogenase A	Homo sapiens	59-63
7986093-1	1994	The interaction between muscle-type lactate dehydrogenase (LDHm) and tubulin was investigated by monitoring the combined effect of NADH and tubulin on steady-state kinetics and the combined effect of NADH and pH on complex formation between tubulin and the enzyme.	NAD	200-204	lactate dehydrogenase A	Homo sapiens	59-63
7986093-7	1994	In contrast to the absence of tubulin, its presence induced a modification of the kinetic behavior of LDHm; i.e., the velocity dependence on NADH concentration displayed a marked sigmoid response.	NAD	141-145	lactate dehydrogenase A	Homo sapiens	102-106
7986093-11	1994	NAD+ was much less effective than NADH in dissociating LDHm from immobilized tubulin.	NAD	0-4	lactate dehydrogenase A	Homo sapiens	55-59
7986093-11	1994	NAD+ was much less effective than NADH in dissociating LDHm from immobilized tubulin.	NAD	34-38	lactate dehydrogenase A	Homo sapiens	55-59
7918631-2	1994	Poly(ADP-ribose) polymerase (EC 2.4.2.30) synthesizes the polymer from NAD, and poly(ADP-ribose) glycohydrolase (PARG) is the major enzyme responsible for its catabolism (Thomassin et al.	NAD	71-74	poly(ADP-ribose) glycohydrolase	Homo sapiens	80-111
7918631-2	1994	Poly(ADP-ribose) polymerase (EC 2.4.2.30) synthesizes the polymer from NAD, and poly(ADP-ribose) glycohydrolase (PARG) is the major enzyme responsible for its catabolism (Thomassin et al.	NAD	71-74	poly(ADP-ribose) glycohydrolase	Homo sapiens	113-117
8062255-1	1994	Poly(ADP-ribose) polymerase (PADPRP) catalyzes the transfer of multiple ADP-ribose units from NAD to nuclear histone and nonhistone proteins, a reaction that appears to be important in the rejoining of DNA strand breaks during DNA repair and replication.	NAD	94-97	poly(ADP-ribose) polymerase 1	Homo sapiens	0-27
7534225-6	1994	Purified DT diaphorase, in the presence of either NADPH or NADH as electron donor, produced mutagenic derivatives from IQ and Trp-P-2.	NAD	59-63	NAD(P)H quinone dehydrogenase 1	Homo sapiens	9-22
7534225-6	1994	Purified DT diaphorase, in the presence of either NADPH or NADH as electron donor, produced mutagenic derivatives from IQ and Trp-P-2.	NAD	59-63	polycystin 2, transient receptor potential cation channel	Homo sapiens	126-133
7824086-4	1994	In contrast, the mitochondrial-microsomal 17 beta-HSD II catalyzes both the estrogenic as well as the androgenic substrates of the 17 beta-HSD and uses NAD+ and NADH as cofactors.	NAD	152-156	hydroxysteroid 17-beta dehydrogenase 1	Homo sapiens	42-53
7824086-4	1994	In contrast, the mitochondrial-microsomal 17 beta-HSD II catalyzes both the estrogenic as well as the androgenic substrates of the 17 beta-HSD and uses NAD+ and NADH as cofactors.	NAD	152-156	hydroxysteroid 17-beta dehydrogenase 1	Homo sapiens	131-142
7824086-4	1994	In contrast, the mitochondrial-microsomal 17 beta-HSD II catalyzes both the estrogenic as well as the androgenic substrates of the 17 beta-HSD and uses NAD+ and NADH as cofactors.	NAD	161-165	hydroxysteroid 17-beta dehydrogenase 1	Homo sapiens	42-53
7824086-4	1994	In contrast, the mitochondrial-microsomal 17 beta-HSD II catalyzes both the estrogenic as well as the androgenic substrates of the 17 beta-HSD and uses NAD+ and NADH as cofactors.	NAD	161-165	hydroxysteroid 17-beta dehydrogenase 1	Homo sapiens	131-142
7945247-4	1994	GAPDH is completely inactivated at 0.3 M GdmCl but at this GdmCl concentration it still binds NAD+ with negative co-operativity.	NAD	94-98	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	0-5
7989219-1	1994	In order to clarify the cause of null mutations in enzyme loci, the molecular structure of six null mutations in the Gpdh locus (encoding alpha GPDH: alpha glycerol-3-phosphate dehydrogenase (NAD+), E.C.	NAD	192-196	Glycerol-3-phosphate dehydrogenase 1	Drosophila melanogaster	117-121
7945297-4	1994	The activity of ADH, not MEOS, was significantly inhibited by acetylcarnitine at NAD: acetylcarnitine < or = 1.	NAD	81-84	aldo-keto reductase family 1 member A1	Rattus norvegicus	16-19
8062255-1	1994	Poly(ADP-ribose) polymerase (PADPRP) catalyzes the transfer of multiple ADP-ribose units from NAD to nuclear histone and nonhistone proteins, a reaction that appears to be important in the rejoining of DNA strand breaks during DNA repair and replication.	NAD	94-97	poly(ADP-ribose) polymerase 1	Homo sapiens	29-35
7985780-3	1994	Deoxyhypusine synthase, an NAD(+)-dependent enzyme, catalyzes the first step of hypusine formation on the eIF-5A precursor.	NAD	27-33	deoxyhypusine synthase	Homo sapiens	0-22
7898463-1	1994	ADP-ribosylation reaction, that is the transfer of the ADP-ribose moiety of NAD+ to acceptor protein, is catalyzed by two classes of ADP-ribosyltransferases, i.e., poly(ADP-ribose) synthetase and mono(ADP-ribosyl)transferases.	NAD	76-80	poly(ADP-ribose) polymerase 1	Homo sapiens	164-191
7898464-3	1994	The NO-stimulated, NAD-dependent modification of GAPDH was recently characterized as covalent binding of the whole NAD molecule to the enzyme, not ADP-ribosylation.	NAD	19-22	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	49-54
7898464-3	1994	The NO-stimulated, NAD-dependent modification of GAPDH was recently characterized as covalent binding of the whole NAD molecule to the enzyme, not ADP-ribosylation.	NAD	115-118	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	49-54
7898464-4	1994	With this result, along with the knowledge that GAPDH is stoichiometrically S-nitrosylated, the role of NO in protein modification with NAD may be viewed as the conferring of an unexpected chemical reactivity upon GAPDH, possibly due to nitrosylation of a cysteine in the enzyme active site.	NAD	136-139	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	48-53
7898464-4	1994	With this result, along with the knowledge that GAPDH is stoichiometrically S-nitrosylated, the role of NO in protein modification with NAD may be viewed as the conferring of an unexpected chemical reactivity upon GAPDH, possibly due to nitrosylation of a cysteine in the enzyme active site.	NAD	136-139	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	214-219
7898466-3	1994	Instead, it was a non-competitive inhibitor of beta NAD+ in the ADP-ribose polymerization reaction catalyzed by PARP.	NAD	47-56	poly(ADP-ribose) polymerase 1	Homo sapiens	112-116
7898480-1	1994	Poly(ADP-ribosyl)ation is a eukaryotic posttranslational protein modification catalyzed by poly(ADP-ribose) polymerase (PARP), a highly conserved nuclear enzyme which uses NAD as substrate.	NAD	172-175	poly(ADP-ribose) polymerase 1	Homo sapiens	91-118
7898480-1	1994	Poly(ADP-ribosyl)ation is a eukaryotic posttranslational protein modification catalyzed by poly(ADP-ribose) polymerase (PARP), a highly conserved nuclear enzyme which uses NAD as substrate.	NAD	172-175	poly(ADP-ribose) polymerase 1	Homo sapiens	120-124
8034046-1	1994	Previous studies have suggested that glyceraldehyde-3-phosphate dehydrogenase (GAPDH) undergoes covalent modification of an active site thiol by a NO.-induced [32P]NAD(+)-dependent mechanism.	NAD	164-170	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	37-77
8034046-1	1994	Previous studies have suggested that glyceraldehyde-3-phosphate dehydrogenase (GAPDH) undergoes covalent modification of an active site thiol by a NO.-induced [32P]NAD(+)-dependent mechanism.	NAD	164-170	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	79-84
8031841-5	1994	However, the hydroquinone formed proved to be unstable in the presence of oxygen, since reduction of cyclized norepinephrine o-quinone by DT-diaphorase was accompanied by continuous oxidation of NADH and oxygen consumption.	NAD	195-199	NAD(P)H quinone dehydrogenase 1	Homo sapiens	138-151
8031841-7	1994	Elimination of the effects of superoxide radicals, manganese and H2O2 on autoxidation of hydroquinone by addition of SOD, catalase and DETAPAC to the incubation mixture resulted in a 79% inhibition of NADH oxidation, suggesting that 21% of the autoxidation is oxygen-dependent.	NAD	201-205	superoxide dismutase 1	Homo sapiens	117-120
8031841-7	1994	Elimination of the effects of superoxide radicals, manganese and H2O2 on autoxidation of hydroquinone by addition of SOD, catalase and DETAPAC to the incubation mixture resulted in a 79% inhibition of NADH oxidation, suggesting that 21% of the autoxidation is oxygen-dependent.	NAD	201-205	catalase	Homo sapiens	122-130
8031116-1	1994	The kinetic mechanism of NAD-dependent glyceraldehyde-3-phosphate dehydrogenase [D-glyceraldehyde-3-phosphate:NAD+ oxidoreductase (phosphorylating), EC 1.2.1.12] from the host cytosolic fraction of soybean (Glycine max L. Merr.	NAD	25-28	putative NADH-dependent hydroxypyruvate reductase	Glycine max	115-129
8038764-1	1994	Poly(ADP-ribose) synthetase catalyses the synthesis of poly(ADP-ribose) from NAD+, thereby releasing the DNA from histones to a transcriptionally and reparationally active form.	NAD	77-81	poly(ADP-ribose) polymerase 1	Homo sapiens	0-27
8013376-8	1994	The addition of excess NAD increased 17 beta HSD oxidative activity in control and RA-treated cells, but the addition of NADH had no effect on 17 beta HSD reductive activity.	NAD	23-26	hydroxysteroid 17-beta dehydrogenase 1	Homo sapiens	37-48
7958397-5	1994	In intact islets, this nuclear response was observed after 18 h culture in medium containing rIL-1 beta, with a concomitant decrease in NAD (88.5%).	NAD	136-139	interleukin 1 beta	Rattus norvegicus	93-103
8003475-2	1994	Accompanying NAD-dependent automodification of poly(ADP-ribose) polymerase is required for effective DNA rejoining.	NAD	13-16	poly(ADP-ribose) polymerase 1	Homo sapiens	47-74
8003475-5	1994	In response to addition of gamma-irradiated plasmid DNA, rapid and heavy automodification of poly(ADP-ribose) polymerase occurred in NAD-containing human cell extracts.	NAD	133-136	poly(ADP-ribose) polymerase 1	Homo sapiens	93-120
8187280-0	1994	Angiotensin II stimulates NADH and NADPH oxidase activity in cultured vascular smooth muscle cells.	NAD	26-30	angiotensinogen	Homo sapiens	0-14
8187831-4	1994	3-Aminobenzamide (3-ABA), a specific inhibitor of poly(ADP-ribosyl) polymerase (PARP), a nuclear enzyme which is activated by breaks in DNA to catabolize intracellular NAD, is capable of relieving such a drop.	NAD	168-171	poly(ADP-ribose) polymerase 1	Homo sapiens	50-78
8187831-4	1994	3-Aminobenzamide (3-ABA), a specific inhibitor of poly(ADP-ribosyl) polymerase (PARP), a nuclear enzyme which is activated by breaks in DNA to catabolize intracellular NAD, is capable of relieving such a drop.	NAD	168-171	poly(ADP-ribose) polymerase 1	Homo sapiens	80-84
8187831-7	1994	At 20 h, when the apoptotic ladder-like pattern of DNA is visible, NAD concentration has dropped again, probably because of a second PARP activation due to the extensive DNA degradation that accompanies apoptosis.	NAD	67-70	poly(ADP-ribose) polymerase 1	Homo sapiens	133-137
8187831-9	1994	All apoptotic U937 cells have a reduced NAD content, independently of the inducing agent; however, upon treatments which do not cause immediate DNA breaks, the drop in NAD concentration occurs only after the apoptotic ladder is detectable and can be ascribed to the activation of PARP by the free ends of DNA formed during the endonucleolytic degradation.	NAD	168-171	poly(ADP-ribose) polymerase 1	Homo sapiens	280-284
8187831-10	1994	Moreover, in these instances the inhibition of PARP, although effective in blocking the drop in NAD concentration, has no effect on apoptosis, thus being only circumstantial.	NAD	96-99	poly(ADP-ribose) polymerase 1	Homo sapiens	47-51
8201009-1	1994	Sorbitol (aldose reductase) pathway flux in diabetes perturbs intracellular metabolism by two putative mechanisms: reciprocal osmoregulatory depletion of other organic osmolytes e.g., myo-inositol, and alterations in NADPH/NADP+ and/or NADH/NAD+.	NAD	236-240	aldo-keto reductase family 1 member B	Homo sapiens	10-26
8201009-1	1994	Sorbitol (aldose reductase) pathway flux in diabetes perturbs intracellular metabolism by two putative mechanisms: reciprocal osmoregulatory depletion of other organic osmolytes e.g., myo-inositol, and alterations in NADPH/NADP+ and/or NADH/NAD+.	NAD	241-245	aldo-keto reductase family 1 member B	Homo sapiens	10-26
8307191-2	1994	ADP-ribose moiety containing digoxigenin was transferred by pertussis toxin (IAP) to the alpha subunit of Gi (Gi alpha) from digoxigenin-conjugated NAD (DIG-NAD) in a beta gamma subunit-dependent manner.	NAD	148-151	alkaline phosphatase, intestinal	Homo sapiens	77-80
8193132-1	1994	With an in vitro DNA repair system, Satoh and Lindah [(1992) Nature 356, 356-358] demonstrated that unmodified poly(ADP-ribose) polymerase (PADPRP) binds to radiation-damaged DNA and inhibits repair in the absence of NAD.	NAD	217-220	poly(ADP-ribose) polymerase 1	Homo sapiens	111-138
8193132-1	1994	With an in vitro DNA repair system, Satoh and Lindah [(1992) Nature 356, 356-358] demonstrated that unmodified poly(ADP-ribose) polymerase (PADPRP) binds to radiation-damaged DNA and inhibits repair in the absence of NAD.	NAD	217-220	poly(ADP-ribose) polymerase 1	Homo sapiens	140-146
8193132-2	1994	However, in the presence of NAD, PADPRP undergoes automodification and the DNA is repaired.	NAD	28-31	poly(ADP-ribose) polymerase 1	Homo sapiens	33-39
8125121-3	1994	The similarities to the human PARP in amino acid sequence were relatively low in the DNA-binding and auto-modification domains, but very high in the C-terminal catalytic domain: identity of amino acids is 34% in the N-terminal DNA-binding domain (residues 1-369), 27% in the auto-modification domain (residues 370-507), and 56% in the C-terminal NAD-binding domain (residues 508-996).	NAD	346-349	poly(ADP-ribose) polymerase 1	Homo sapiens	30-34
8258703-3	1993	PARP, which binds to and is activated by DNA strand breaks, catalyzes the removal of ADP-ribose from NAD+ and poly(ADP-ribosylation) of chromatin-associated acceptor proteins.	NAD	101-105	poly(ADP-ribose) polymerase 1	Homo sapiens	0-4
7929613-3	1994	In cells in which glucose oxidation is switched off during starvation, fatty acids are used as fuel, and acetyl CoA and NADH formed by beta-oxidation promote phosphorylation of PDH complex by activation of PDH kinase.	NAD	120-124	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	177-180
7929613-3	1994	In cells in which glucose oxidation is switched off during starvation, fatty acids are used as fuel, and acetyl CoA and NADH formed by beta-oxidation promote phosphorylation of PDH complex by activation of PDH kinase.	NAD	120-124	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	206-209
8262916-0	1993	The crystallographic structure of a human dihydropteridine reductase NADH binary complex expressed in Escherichia coli by a cDNA constructed from its rat homologue.	NAD	69-73	quinoid dihydropteridine reductase	Homo sapiens	42-68
7507826-4	1994	Islet NAD levels were also sharply reduced to 43% of the control value after 24-h exposure to IL-1 beta, but not after 1 or 3 h, demonstrating the same time course as that for inhibition of insulin secretion.	NAD	6-9	interleukin 1 beta	Rattus norvegicus	94-103
7507826-7	1994	Nicotinamide and thymidine prevented the IL-1 beta-induced loss of cell viability and suppression of NAD, but had no effect on sustaining insulin secretion.	NAD	101-104	interleukin 1 beta	Rattus norvegicus	41-50
8006974-3	1994	Further studies suggested that the basis for this observation was a high molecular weight compound which consumes the XDH cofactor, NAD+.	NAD	132-136	xanthine dehydrogenase/oxidase	Oryctolagus cuniculus	118-121
8130648-7	1994	Increasingly enough, patients with NAD displayed high IL-5 but low IL-4 levels.	NAD	35-38	interleukin 4	Homo sapiens	67-71
8216206-10	1993	Acid-resistant binding of ADPR, as well as of NAD+, to Ga3PDH was confirmed for the enzyme purified from human erythrocytes.	NAD	46-50	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	55-61
7902582-8	1993	Under the same conditions, koningic acid also inhibited basal and SNP- SNAP-, and SIN-1-stimulated NAD-dependent modification of GAPDH and its enzymatic activity.	NAD	99-102	MAPK associated protein 1	Homo sapiens	82-87
7902582-8	1993	Under the same conditions, koningic acid also inhibited basal and SNP- SNAP-, and SIN-1-stimulated NAD-dependent modification of GAPDH and its enzymatic activity.	NAD	99-102	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	129-134
8218263-0	1993	Immediate reduction of cytochrome c by photoexcited NADH: reaction mechanism as revealed by flow-flash and rapid-scan studies.	NAD	52-56	cytochrome c, somatic	Homo sapiens	23-35
8218263-1	1993	Upon exposure of an aqueous solution of NADH and cytochrome c to a laser pulse at 355 nm under anaerobic conditions, cytochrome c is reduced within 1-2 ms to a maximal extent of 90%.	NAD	40-44	cytochrome c, somatic	Homo sapiens	117-129
8218263-4	1993	As the oxygen concentration approaches 20% saturation, the cytochrome c reduction by NAD is abolished first and then the reduction by hydrated electrons, since molecular oxygen competes with cytochrome c for NAD and hydrated electrons.	NAD	85-88	cytochrome c, somatic	Homo sapiens	59-71
8218263-4	1993	As the oxygen concentration approaches 20% saturation, the cytochrome c reduction by NAD is abolished first and then the reduction by hydrated electrons, since molecular oxygen competes with cytochrome c for NAD and hydrated electrons.	NAD	85-88	cytochrome c, somatic	Homo sapiens	191-203
8218263-4	1993	As the oxygen concentration approaches 20% saturation, the cytochrome c reduction by NAD is abolished first and then the reduction by hydrated electrons, since molecular oxygen competes with cytochrome c for NAD and hydrated electrons.	NAD	208-211	cytochrome c, somatic	Homo sapiens	59-71
8218263-4	1993	As the oxygen concentration approaches 20% saturation, the cytochrome c reduction by NAD is abolished first and then the reduction by hydrated electrons, since molecular oxygen competes with cytochrome c for NAD and hydrated electrons.	NAD	208-211	cytochrome c, somatic	Homo sapiens	191-203
8218263-6	1993	The second-order rate constants for the reduction of cytochrome c at pH 7.4 and 20 degrees C by NAD and the superoxide anion are 2.0 x 10(9) and 4.0 x 10(6) M-1 s-1, respectively.	NAD	96-99	cytochrome c, somatic	Homo sapiens	53-65
8288159-1	1993	Thyroxine and other iodothyronines (concentrations in the nanomolar range) stimulated the oxidation of NADH in the myeloperoxidase-H2O2-Cl- system.	NAD	103-107	myeloperoxidase	Homo sapiens	115-130
8288159-5	1993	Pre-incubation of thyroxine in the myeloperoxidase system showed that thyroxine was oxidized to a product capable of stimulating NADH oxidation.	NAD	129-133	myeloperoxidase	Homo sapiens	35-50
8226768-3	1993	Thus, the initiation, elongation, and branching reactions catalyzed by PARP appear to be [NAD]-dependent.	NAD	90-93	poly(ADP-ribose) polymerase 1	Homo sapiens	71-75
8226768-4	1993	Initial rates of automodification increased with second order kinetics as a function of [PARP] at both 200 nM and 200 microM NAD.	NAD	125-128	poly(ADP-ribose) polymerase 1	Homo sapiens	89-93
8274146-8	1993	The inhibition of ALDH and the resulting decrease in the redox effect on the NAD system bound to alcohol dehydrogenase (EC 1.1.1.1) could explain the protective effect of methylene blue against metabolic redox effects of ethanol.	NAD	77-80	aldo-keto reductase family 1 member A1	Rattus norvegicus	97-118
8269627-8	1993	Ribosylated poly(ADP-ribose)polymerase has been isolated by affinity chromatography on boronate column from cells permeabilized and labelled with [32P]NAD.	NAD	151-154	poly(ADP-ribose) polymerase 1	Homo sapiens	12-38
8264549-6	1993	A higher molecular mass product (60 kDa) was detected by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and Western blot analysis of DT-diaphorase preincubated with NADH and mitomycin C at pH 7.8, suggesting that mitomycin C is capable of cross-linking DT-diaphorase.	NAD	176-180	NAD(P)H quinone dehydrogenase 1	Homo sapiens	144-157
8216372-4	1993	Whereas NAD(P)H:quinone reductase (NAD(P)H:(quinone acceptor) oxidoreductase; DT diaphorase; EC 1.6.99.2) was the predominant 4NQO reductase present in liver cytosol from Sprague-Dawley rats, dicumarol-resistant NADH:4NQO nitroreductase specific activities were comparable with those of mouse liver cytosols.	NAD	212-216	NAD(P)H quinone dehydrogenase 1	Rattus norvegicus	78-91
8409103-2	1993	Poly(ADP-ribose) polymerase, an enzyme activated by DNA strand breaks, is the ADP-ribosyltransferase of greatest interest with regard to effects on the niacin status of cells since its Km for NAD is high, and its activity can deplete NAD.	NAD	192-195	poly(ADP-ribose) polymerase 1	Homo sapiens	0-27
8237468-1	1993	We have developed a chemiluminescent flow injection method for analysis of bile acid, glucose and ATP using the chemiluminescent assay of NADH using 1-methoxy-5-methylphenazinium methyl sulphate (1-MPMS)/isoluminol(IL)/microperoxidase (m-POD) system and immobilized enzyme reactors such as 3 alpha-hydroxysteroid dehydrogenase, glucose-dehydrogenase, hexokinase and glucose-6-phosphate dehydrogenase.	NAD	138-142	hexokinase 1	Homo sapiens	351-361
8409103-2	1993	Poly(ADP-ribose) polymerase, an enzyme activated by DNA strand breaks, is the ADP-ribosyltransferase of greatest interest with regard to effects on the niacin status of cells since its Km for NAD is high, and its activity can deplete NAD.	NAD	234-237	poly(ADP-ribose) polymerase 1	Homo sapiens	0-27
8511877-1	1993	Insulin-stimulated synthesis of plasma membraneous "signal" ATP (psATP) from ADP and P(i) in oxidation coupled with that of NADH was detected in a preparation of plasma membranes from human erythrocytes; psATP was formed at concentrations of 10(-8)-10(-9) M. Effect of medicinal plasmapheresis on ability of erythrocyte membranes to produce psATP was studied.	NAD	124-128	insulin	Homo sapiens	0-7
8391315-3	1993	The activities with ferricyanide, menadione and cytochrome c were lost synchronously during preincubation of the enzyme in the presence of NADH or dithionite under either aerobic or anaerobic conditions.	NAD	139-143	cytochrome c, somatic	Homo sapiens	48-60
8327504-0	1993	Stimulation by nitric oxide of an NAD linkage to glyceraldehyde-3-phosphate dehydrogenase.	NAD	34-37	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	49-89
8327504-1	1993	Nitric oxide-stimulated modification of glyceraldehyde-3-phosphate dehydrogenase (GAPDH) by [adenylate-32P]NAD has been interpreted in recent reports as ADP-ribosylation.	NAD	107-110	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	40-80
8327504-1	1993	Nitric oxide-stimulated modification of glyceraldehyde-3-phosphate dehydrogenase (GAPDH) by [adenylate-32P]NAD has been interpreted in recent reports as ADP-ribosylation.	NAD	107-110	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	82-87
8327504-2	1993	Incubations of GAPDH with the NO-releasing agent sodium nitroprusside (SNP) and NAD resulted, however, in essentially equal incorporation of radiolabel from the adenine, phosphate, and nicotinamide moieties to the extent of approximately 0.02 mol of NAD.mol of GAPDH-1.	NAD	80-83	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	15-20
8327504-2	1993	Incubations of GAPDH with the NO-releasing agent sodium nitroprusside (SNP) and NAD resulted, however, in essentially equal incorporation of radiolabel from the adenine, phosphate, and nicotinamide moieties to the extent of approximately 0.02 mol of NAD.mol of GAPDH-1.	NAD	80-83	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	261-266
8327504-2	1993	Incubations of GAPDH with the NO-releasing agent sodium nitroprusside (SNP) and NAD resulted, however, in essentially equal incorporation of radiolabel from the adenine, phosphate, and nicotinamide moieties to the extent of approximately 0.02 mol of NAD.mol of GAPDH-1.	NAD	250-253	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	15-20
8327504-3	1993	Modification of GAPDH by free adenosine 5"-diphosphoribose (ADP-ribose) was only 10% of that by NAD.	NAD	96-99	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	16-21
8327504-4	1993	Exposure of GAPDH modified by NAD in the presence of SNP to HgCl2, which acts at thiol linkages, released two products.	NAD	30-33	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	12-17
8327504-6	1993	GAPDH activity was inhibited by SNP in a dose-dependent manner in the presence of NAD.	NAD	82-85	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	0-5
8327504-8	1993	This result is consistent with the conclusion that inhibition of GAPDH activity by SNP in the presence of NAD is due primarily to active-site nitrosylation, as reported by other workers, and is not due to the minor modification with NAD.	NAD	106-109	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	65-70
8327504-8	1993	This result is consistent with the conclusion that inhibition of GAPDH activity by SNP in the presence of NAD is due primarily to active-site nitrosylation, as reported by other workers, and is not due to the minor modification with NAD.	NAD	233-236	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	65-70
8327504-9	1993	These results demonstrate that NO-stimulated modification of GAPDH with NAD is not ADP-ribosylation as previously reported but rather is covalent binding of NAD through a NO-dependent thiol intermediate, possibly providing an example of an unexpected, altered reactivity of a nitrosylated protein.	NAD	72-75	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	61-66
8327504-9	1993	These results demonstrate that NO-stimulated modification of GAPDH with NAD is not ADP-ribosylation as previously reported but rather is covalent binding of NAD through a NO-dependent thiol intermediate, possibly providing an example of an unexpected, altered reactivity of a nitrosylated protein.	NAD	157-160	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	61-66
8473297-4	1993	The consequences of conservative substitution of Lys-893 and Asp-993 on the kinetic properties of human poly(ADP-ribose) polymerase enzyme and the polymer it synthesizes suggest that these 2 amino acids are directly involved in the covalent attachment of the first ADP-ribosyl residue from NAD+ onto the acceptor amino acid.	NAD	290-294	poly(ADP-ribose) polymerase 1	Homo sapiens	104-131
8385945-4	1993	The Km for NAD of the ADP-ribosylation of rhoA was decreased by SDS from about 10 to 0.6 microM.	NAD	11-14	ras homolog family member A	Homo sapiens	42-46
8498157-2	1993	Interferon-gamma and tumor necrosis factor-alpha reduced the nicotinamide adenine dinucleotide content of mouse islet cells; the combination of interferon-gamma (4 x 10(5) U/l) and tumor necrosis factor-alpha (4 x 10(5) U/l) caused nicotinamide adenine dinucleotide reduction by approximately 40%.	NAD	61-94	interferon gamma	Mus musculus	0-48
8498157-2	1993	Interferon-gamma and tumor necrosis factor-alpha reduced the nicotinamide adenine dinucleotide content of mouse islet cells; the combination of interferon-gamma (4 x 10(5) U/l) and tumor necrosis factor-alpha (4 x 10(5) U/l) caused nicotinamide adenine dinucleotide reduction by approximately 40%.	NAD	232-265	interferon gamma	Mus musculus	0-48
8498157-2	1993	Interferon-gamma and tumor necrosis factor-alpha reduced the nicotinamide adenine dinucleotide content of mouse islet cells; the combination of interferon-gamma (4 x 10(5) U/l) and tumor necrosis factor-alpha (4 x 10(5) U/l) caused nicotinamide adenine dinucleotide reduction by approximately 40%.	NAD	232-265	tumor necrosis factor	Mus musculus	144-208
8390449-7	1993	The results of inhibition studies on the NADH oxidation with SOD and catalase suggested that the reaction mixture containing stannum (IV) chloride contained a greater amount of H2O2 and a lower amount of O2- than that containing only vanadium (IV).	NAD	41-45	superoxide dismutase 1	Homo sapiens	61-64
8390449-7	1993	The results of inhibition studies on the NADH oxidation with SOD and catalase suggested that the reaction mixture containing stannum (IV) chloride contained a greater amount of H2O2 and a lower amount of O2- than that containing only vanadium (IV).	NAD	41-45	catalase	Homo sapiens	69-77
7680646-4	1993	Selective depletion of poly(ADP-ribose) polymerase from cell extracts improved the repair of DNA exposed to a variety of DNA-damaging agents by removing the NAD+ dependence of the repair reaction.	NAD	157-161	poly(ADP-ribose) polymerase 1	Homo sapiens	23-50
8323298-1	1993	Photoaffinity labeling of ovine prolactin with the NAD+ photoaffinity analog [alpha-32P]nicotinamide-2-azidoadenine dinucleotide has been used to identify an NADH/NADPH binding site.	NAD	51-55	prolactin	Homo sapiens	32-41
8323298-1	1993	Photoaffinity labeling of ovine prolactin with the NAD+ photoaffinity analog [alpha-32P]nicotinamide-2-azidoadenine dinucleotide has been used to identify an NADH/NADPH binding site.	NAD	158-162	prolactin	Homo sapiens	32-41
8323298-7	1993	The adenine ring binding domain of NADH/NADPH binding site was identified by trypsin and chymotrypsin digestion of the photolabeled prolactin and purification of the photolabeled peptide by boronate affinity chromatography and immobilized Fe3+ affinity chromatography.	NAD	35-39	prolactin	Homo sapiens	132-141
8323298-9	1993	These studies demonstrate that prolactin contains an NADH/NADPH binding site which may be significant in the mechanism of action of this hormone.	NAD	53-57	prolactin	Homo sapiens	31-40
8395934-0	1993	Formation of a hydroxyl radical by the myeloperoxidase-NADH-oxygen system.	NAD	55-59	myeloperoxidase	Homo sapiens	39-54
8395934-4	1993	The tyrosine formation by the MPO-NADH system was greatly reduced under anaerobic conditions, and significantly inhibited by hydroxyl radical scavengers.	NAD	34-38	myeloperoxidase	Homo sapiens	30-33
8395934-6	1993	Even though the superoxide radical (O2-)-producing ability of the MPO-NADH system was about 29% of that of the hypoxanthine-xanthine oxidase system, under the experimental conditions employed, the rate of tyrosine formation from phenylalanine by two systems was found to be a similar.	NAD	70-74	myeloperoxidase	Homo sapiens	66-69
8395934-8	1993	may occur in the MPO-NADH system under aerobic conditions and a superoxide radical may be involved in the OH.	NAD	21-25	myeloperoxidase	Homo sapiens	17-20
8463342-0	1993	Cytochrome P-450 55A1 (P-450dNIR) acts as nitric oxide reductase employing NADH as the direct electron donor.	NAD	75-79	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	0-16
8463342-2	1993	The cytochrome P-450 (P-450) exhibited a potent nitric oxide (NO) reductase activity to form nitrous oxide (N2O) employing NADH but not NADPH as the sole effective electron donor.	NAD	123-127	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	4-20
8510671-4	1993	The burst of NADH oxidation and oxygen uptake which occurs in phosphate, but not in Tris buffer, was prevented by SOD, catalase, histidine, EDTA, MnCl2 and CuSO4, but not by the hydroxyl radical quenchers, ethanol, methanol, formate and mannitol.	NAD	13-17	catalase	Rattus norvegicus	119-127
8390449-6	1993	The inhibition of the vanadium (IV) catalyzed NADH oxidation in the presence of stannum (IV) chloride by catalase, superoxide dismutase (SOD), and hydroxyl radical scavengers indicated that the stannum (IV) chloride stimulated NADH oxidation consisted of almost the same reaction steps as that in the absence of stannum (IV) chloride.	NAD	46-50	catalase	Homo sapiens	105-113
8390449-6	1993	The inhibition of the vanadium (IV) catalyzed NADH oxidation in the presence of stannum (IV) chloride by catalase, superoxide dismutase (SOD), and hydroxyl radical scavengers indicated that the stannum (IV) chloride stimulated NADH oxidation consisted of almost the same reaction steps as that in the absence of stannum (IV) chloride.	NAD	46-50	superoxide dismutase 1	Homo sapiens	115-135
8390449-6	1993	The inhibition of the vanadium (IV) catalyzed NADH oxidation in the presence of stannum (IV) chloride by catalase, superoxide dismutase (SOD), and hydroxyl radical scavengers indicated that the stannum (IV) chloride stimulated NADH oxidation consisted of almost the same reaction steps as that in the absence of stannum (IV) chloride.	NAD	46-50	superoxide dismutase 1	Homo sapiens	137-140
8420004-4	1993	The cofactor nicotinamide adenine dinucleotide disrupted complex formation between tRNA and GAPDH and thus may share a common binding site with the RNA.	NAD	13-46	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	92-97
8442754-9	1993	The redox effect appears to result primarily from rapid elimination of acetaldehyde and equilibration with the NAD system on the alcohol dehydrogenase, but is not enhanced by further decreases in acetaldehyde concentration.	NAD	111-114	aldo-keto reductase family 1 member A1	Rattus norvegicus	129-150
8382051-9	1993	This kinase probably corresponds to CaM kinase III and the 102 kDa peptide to elongation factor 2 (EF-2), since the 102 kDa peptide was shown to undergo ADP-ribosylation in the presence of diphtheria toxin and NAD+.	NAD	210-214	eukaryotic translation elongation factor 2	Rattus norvegicus	78-97
8382051-9	1993	This kinase probably corresponds to CaM kinase III and the 102 kDa peptide to elongation factor 2 (EF-2), since the 102 kDa peptide was shown to undergo ADP-ribosylation in the presence of diphtheria toxin and NAD+.	NAD	210-214	eukaryotic translation elongation factor 2	Rattus norvegicus	99-103
1295007-0	1992	[Microdetermination methods for deoxyglucose and beta-NGF using NADP and NAD enzymatic cyclings].	NAD	64-67	nerve growth factor	Homo sapiens	49-57
1482396-4	1992	However, NADH-Fe(III) oxidoreductive activity was very weak when Fe(III)-ammonium citrate or diferric transferrin was used as electron acceptor in the presence of bathophenanthroline disulfonate as an indicator of the reaction.	NAD	9-13	transferrin	Homo sapiens	102-113
1639779-2	1992	Comparison of kcat and Km values measured employing quinonoid 6,7-dimethyldihydropteridine (q-PtH2) as substrate indicate that the native enzyme has a considerable preference for NADH with an optimum kcat/Km of 12 microM-1 s-1 compared with a figure of 0.25 microM-1 s-1 for NADPH.	NAD	179-183	parathyroid hormone 2	Rattus norvegicus	94-98
1449531-5	1992	The toxicity experienced by human cell lines after exposure to CB 1954 and NADH was proportional to their levels of the enzyme DT diaphorase NAD(P)H dehydrogenase (quinone), EC 1.6.99.2.	NAD	75-79	NAD(P)H quinone dehydrogenase 1	Homo sapiens	127-140
1419892-2	1992	A rapid and simple method for measuring the 3 beta-HSD activity has been developed, in which the NADH, generated by 3 beta-HSD, reduced nitroblue tetrazolium to a product with absorption maximum at 560 nm.	NAD	97-101	hydroxy-delta-5-steroid dehydrogenase, 3 beta- and steroid delta-isomerase 1	Rattus norvegicus	44-54
1419892-2	1992	A rapid and simple method for measuring the 3 beta-HSD activity has been developed, in which the NADH, generated by 3 beta-HSD, reduced nitroblue tetrazolium to a product with absorption maximum at 560 nm.	NAD	97-101	hydroxy-delta-5-steroid dehydrogenase, 3 beta- and steroid delta-isomerase 1	Rattus norvegicus	116-126
1435769-7	1992	Catalase inhibited the effect of NADH partly.	NAD	33-37	catalase	Mus musculus	0-8
16652965-1	1992	Ferric leghemoglobin reductase (FLbR) from soybean (Glycine max [L.] Merr) nodules catalyzed oxidation of NADH, reduction of ferric leghemoglobin (Lb(+3)), and reduction of dichloroindophenol (diaphorase activity).	NAD	106-110	leghemoglobin A	Glycine max	7-20
1644826-0	1992	Cloning and characterization of the gene encoding the IDH1 subunit of NAD(+)-dependent isocitrate dehydrogenase from Saccharomyces cerevisiae.	NAD	70-76	isocitrate dehydrogenase (NAD(+)) IDH1	Saccharomyces cerevisiae S288C	54-58
1644826-8	1992	To examine the function of the IDH1 subunit and to determine the metabolic role of NAD(+)-dependent isocitrate dehydrogenase the IDH1 gene was disrupted in a wild type haploid yeast strain and in a haploid strain lacking IDH2.	NAD	83-89	isocitrate dehydrogenase (NAD(+)) IDH1	Saccharomyces cerevisiae S288C	129-133
1644826-11	1992	Growth phenotype analysis of the IDH1 disruption strains revealed that they grew at a reduced rate on the nonfermentable carbon sources examined (glycerol, lactate, and acetate), consistent with NAD(+)-dependent isocitrate dehydrogenase performing a critical role in oxidative function of the citric acid cycle.	NAD	195-201	isocitrate dehydrogenase (NAD(+)) IDH1	Saccharomyces cerevisiae S288C	33-37
1409644-7	1992	ADP-ribosylation appears to involve the cysteine where NAD interacts with GAPDH so that ADP-ribosylation likely inhibits enzymatic activity.	NAD	55-58	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	74-79
1522600-1	1992	The alcohol dehydrogenase (ADHase) enzyme catalyses the oxidation of alcohols to aldehydes or ketones using NAD+ as a cofactor.	NAD	108-112	Alcohol dehydrogenase	Drosophila melanogaster	4-25
1522600-1	1992	The alcohol dehydrogenase (ADHase) enzyme catalyses the oxidation of alcohols to aldehydes or ketones using NAD+ as a cofactor.	NAD	108-112	Alcohol dehydrogenase	Drosophila melanogaster	27-33
1502187-1	1992	6-Nitroso-1,2-benzopyrone and 3-nitrosobenzamide, two C-nitroso compounds that inactivate the eukaryotic nuclear protein poly(ADP-ribose) polymerase [NAD+:poly(adenosine diphosphate D-ribose) ADP-D-ribosyltransferase, ADPRT, EC 2.4.2.30] at one zinc-finger site, completely suppressed the proliferation of leukemic and other malignant human cells and subsequently produced cell death.	NAD	150-154	poly(ADP-ribose) polymerase 1	Homo sapiens	121-148
1502187-1	1992	6-Nitroso-1,2-benzopyrone and 3-nitrosobenzamide, two C-nitroso compounds that inactivate the eukaryotic nuclear protein poly(ADP-ribose) polymerase [NAD+:poly(adenosine diphosphate D-ribose) ADP-D-ribosyltransferase, ADPRT, EC 2.4.2.30] at one zinc-finger site, completely suppressed the proliferation of leukemic and other malignant human cells and subsequently produced cell death.	NAD	150-154	poly(ADP-ribose) polymerase 1	Homo sapiens	218-223
1324690-3	1992	This method is based on the ability of anthraquinones to decrease the amount of enzymatic cytochrome c reduction at low concentrations of NADH.	NAD	138-142	cytochrome c, somatic	Homo sapiens	90-102
1642637-2	1992	DNA damage and activation of poly(ADP-ribose)polymerase are often associated with a decrease in NAD+.	NAD	96-100	poly(ADP-ribose) polymerase 1	Homo sapiens	29-55
1518531-4	1992	NADH-dependent H2O2 production (16 +/- 1 nmol min-1 (mg protein)-1) was confirmed using cytochrome c peroxidase.	NAD	0-4	cytochrome c, somatic	Homo sapiens	88-100
1518531-7	1992	No inhibition by antimycin was observed when NADH replaced succinate as an electron donor, indicating that the electrons from NADH oxidation reduced cytochrome c through a different route.	NAD	126-130	cytochrome c, somatic	Homo sapiens	149-161
1497678-0	1992	Ceruloplasmin stimulates NADH oxidation of pig liver plasma membrane.	NAD	25-29	ceruloplasmin	Sus scrofa	0-13
1497678-1	1992	NADH oxidation by pig liver plasma membranes is stimulated by ceruloplasmin (CUP) reaching a maximal value at 50 U/ml of CUP.	NAD	0-4	ceruloplasmin	Sus scrofa	62-75
1497678-1	1992	NADH oxidation by pig liver plasma membranes is stimulated by ceruloplasmin (CUP) reaching a maximal value at 50 U/ml of CUP.	NAD	0-4	ceruloplasmin	Sus scrofa	77-80
1497678-1	1992	NADH oxidation by pig liver plasma membranes is stimulated by ceruloplasmin (CUP) reaching a maximal value at 50 U/ml of CUP.	NAD	0-4	ceruloplasmin	Sus scrofa	121-124
1497678-2	1992	NADH oxidation activated by CUP is proportional to the amount of protein.	NAD	0-4	ceruloplasmin	Sus scrofa	28-31
1497678-3	1992	Concanavalin A (Con A) which recognizes the glucidic residues of the CUP required for binding to the receptor inhibits the NADH oxidation in a dose-responsive manner.	NAD	123-127	ceruloplasmin	Sus scrofa	69-72
1497678-4	1992	Both adriamycin and bathophenantroline disulfonate (BPS), previously reported as transplasma membrane electron transport inhibitors, also inhibit the CUP-stimulated NADH oxidation of pig liver plasma membranes.	NAD	165-169	ceruloplasmin	Sus scrofa	150-153
1385952-1	1992	The enzyme DT diaphorase (NAD(P)H dehydrogenase (quinone), EC 1.6.99.2) is unusual in that it can utilize either NADH or NADPH as a co-factor for the reduction of its substrates.	NAD	113-117	NAD(P)H quinone dehydrogenase 1	Homo sapiens	11-47
1586150-4	1992	In contrast, NADH-dependent C-nitrosoreductase activity was inhibited 70-80% by pyrazole and thus may be attributed mainly to alcohol dehydrogenase(s).	NAD	13-17	aldo-keto reductase family 1 member A1	Rattus norvegicus	126-147
1512561-6	1992	While the Km of the TyrA* dehydrogenase for NAD+ remained unaltered, the Km for prephenate was fourfold greater and the Vmax was almost twofold greater than observed for the parental T-protein dehydrogenase.	NAD	44-48	tyrA	Pantoea agglomerans	20-24
1586150-7	1992	Increased NADPH-dependent reduction is mediated by the induction of cytosolic NQOR while an NADH-dependent pathway responds to the increased availability of reduced cofactor upon ethanol ingestion and involves mainly the alcohol dehydrogenase-mediated reduction of such compounds.	NAD	92-96	aldo-keto reductase family 1 member A1	Rattus norvegicus	221-242
1317004-1	1992	The oxidation of NADH and accompanying reduction of oxygen to H2O2 stimulated by polyvanadate was markedly inhibited by SOD and cytochrome c.	NAD	17-21	superoxide dismutase 1	Homo sapiens	120-123
1601310-6	1992	The purified enzyme has the same affinity for NAD+ and turnover number as the human placental PARP.	NAD	46-50	poly(ADP-ribose) polymerase 1	Homo sapiens	94-98
1329447-4	1992	On the other hand, low H2O2 concentrations cause ATP depletion by an activation of the DNA repair enzyme, poly(ADP-ribose)polymerase (pADPRP), leading to consumption of NAD+, an essential cofactor for G3PDH.	NAD	169-173	poly(ADP-ribose) polymerase 1	Homo sapiens	106-132
1329447-4	1992	On the other hand, low H2O2 concentrations cause ATP depletion by an activation of the DNA repair enzyme, poly(ADP-ribose)polymerase (pADPRP), leading to consumption of NAD+, an essential cofactor for G3PDH.	NAD	169-173	poly(ADP-ribose) polymerase 1	Homo sapiens	134-140
1329447-4	1992	On the other hand, low H2O2 concentrations cause ATP depletion by an activation of the DNA repair enzyme, poly(ADP-ribose)polymerase (pADPRP), leading to consumption of NAD+, an essential cofactor for G3PDH.	NAD	169-173	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	201-206
1526963-1	1992	Externally added ascorbate or NADH effectively reduced ferricyanide and promoted the exit of Fe3+ originated from acid-destabilized transferrin contained inside endocytic vesicles.	NAD	30-34	transferrin	Homo sapiens	132-143
1526963-3	1992	At physiological concentrations of both ascorbate and NADH, the ascorbate transport and the NADH-oxidoreductase system were additive as measured by the rate of reduction of ferricyanide and by the mobilization of transferrin-associated iron.	NAD	54-58	transferrin	Homo sapiens	213-224
1317004-1	1992	The oxidation of NADH and accompanying reduction of oxygen to H2O2 stimulated by polyvanadate was markedly inhibited by SOD and cytochrome c.	NAD	17-21	cytochrome c, somatic	Homo sapiens	128-140
1549180-1	1992	The abundant nuclear enzyme poly(ADP-ribose) polymerase catalyses the synthesis of poly(ADP-ribose) from nicotinamide adenine dinucleotide (NAD+).	NAD	105-138	poly(ADP-ribose) polymerase 1	Homo sapiens	28-55
1549180-1	1992	The abundant nuclear enzyme poly(ADP-ribose) polymerase catalyses the synthesis of poly(ADP-ribose) from nicotinamide adenine dinucleotide (NAD+).	NAD	140-144	poly(ADP-ribose) polymerase 1	Homo sapiens	28-55
1735985-10	1992	Tissue homogenates were assayed for 5"-nucleotidase by the linked formation of nicotinamide-adenine dinucleotide at 340 nm (Arkesteijn method).	NAD	79-112	LOW QUALITY PROTEIN: 5'-nucleotidase	Oryctolagus cuniculus	36-51
1312087-11	1992	Analysis of the mitochondrial electron flow revealed that TNF treatment led to a rapid inhibition of the mitochondria to oxidize succinate and NADH-linked substrates.	NAD	143-147	tumor necrosis factor	Mus musculus	58-61
1557029-1	1992	Constitutive expression of human nuclear NAD+: protein ADP-ribosyltransferase (polymerizing) [pADPRT; poly(ADP-ribose)polymerase; EC 2.4.2.30] as an active enzyme in Saccharomyces cerevisiae, under the control of the alcohol dehydrogenase promoter, was only possible with simultaneous inhibition of ADP-ribosylation by 3-methoxybenzamide.	NAD	41-45	poly(ADP-ribose) polymerase 1	Homo sapiens	102-128
1731641-4	1992	Based on the observations that (a) the alcohol did not interact with GSH in the presence or absence of cytosol, (b) the spectral manifestation of the interaction between GSH and the alcohol occurred only when NAD+ was added to the reaction mixture containing the cytosol and reactants, and (c) a similar absorbance spectrum was obtained following the interaction between aldehyde and GSH, it was concluded that dec-2-ynol is converted to an electrophile, dec-2-ynal, which causes depletion of GSH.	NAD	209-213	basic helix-loop-helix family, member e41	Rattus norvegicus	411-416
1731641-4	1992	Based on the observations that (a) the alcohol did not interact with GSH in the presence or absence of cytosol, (b) the spectral manifestation of the interaction between GSH and the alcohol occurred only when NAD+ was added to the reaction mixture containing the cytosol and reactants, and (c) a similar absorbance spectrum was obtained following the interaction between aldehyde and GSH, it was concluded that dec-2-ynol is converted to an electrophile, dec-2-ynal, which causes depletion of GSH.	NAD	209-213	basic helix-loop-helix family, member e41	Rattus norvegicus	455-460
1370824-0	1992	Characterization of lysyl residues of NADH-cytochrome b5 reductase implicated in charge-pairing with active-site carboxyl residues of cytochrome b5 by site-directed mutagenesis of an expression vector for the flavoprotein.	NAD	38-42	cytochrome b5 type A	Bos taurus	43-56
1370824-0	1992	Characterization of lysyl residues of NADH-cytochrome b5 reductase implicated in charge-pairing with active-site carboxyl residues of cytochrome b5 by site-directed mutagenesis of an expression vector for the flavoprotein.	NAD	38-42	cytochrome b5 type A	Bos taurus	134-147
1530940-1	1992	Two classes of enzymes, poly(ADP-ribose) synthetase and mono(ADP-ribosyl)transferases, catalyze covalent attachment of multiple or single residues, respectively, of the ADP-ribose moiety of NAD+ to various proteins.	NAD	190-194	poly(ADP-ribose) polymerase 1	Homo sapiens	24-51
1317324-8	1992	The ESR signal attributable to the hydroxyl radical spin adduct requires the presence of NADH and is completely abolished by catalase and to a lesser extent superoxide dismutase (SOD).	NAD	89-93	catalase	Homo sapiens	125-133
1345201-13	1992	Such intermediary steps can be the phospholipase A2 activation, accumulation of lysophosphatides, poly-ADP-ribose polymerase repair enzyme activation, following oxidative damage of DNA, with subsequent NAD and ATP depletion.	NAD	202-205	phospholipase A2 group IB	Homo sapiens	35-51
1309351-2	1992	When homogenate from cells transfected with a plasmid vector containing type I 3 beta-HSD is incubated in the presence of DHT using NAD+ as cofactor, a somewhat unexpected metabolite is formed, namely 5 alpha-androstanedione (A-dione), thus indicating an intrinsic androgenic 17 beta-hydroxysteroid dehydrogenase (17 beta-HSD) activity of this 3 beta-HSD isoform.	NAD	132-136	hydroxy-delta-5-steroid dehydrogenase, 3 beta- and steroid delta-isomerase 1	Rattus norvegicus	79-89
1309351-2	1992	When homogenate from cells transfected with a plasmid vector containing type I 3 beta-HSD is incubated in the presence of DHT using NAD+ as cofactor, a somewhat unexpected metabolite is formed, namely 5 alpha-androstanedione (A-dione), thus indicating an intrinsic androgenic 17 beta-hydroxysteroid dehydrogenase (17 beta-HSD) activity of this 3 beta-HSD isoform.	NAD	132-136	hydroxy-delta-5-steroid dehydrogenase, 3 beta- and steroid delta-isomerase 1	Rattus norvegicus	344-354
1317324-8	1992	The ESR signal attributable to the hydroxyl radical spin adduct requires the presence of NADH and is completely abolished by catalase and to a lesser extent superoxide dismutase (SOD).	NAD	89-93	superoxide dismutase 1	Homo sapiens	157-177
1317324-8	1992	The ESR signal attributable to the hydroxyl radical spin adduct requires the presence of NADH and is completely abolished by catalase and to a lesser extent superoxide dismutase (SOD).	NAD	89-93	superoxide dismutase 1	Homo sapiens	179-182
1873300-3	1991	The generation of H2O2 and reduction of Fe-complex were mainly dependent on the activity of NADH: menadione oxidoreductase in the plasma membrane and cytosol fractions.	NAD	92-96	oxidoreductase	Saccharomyces cerevisiae S288C	108-122
1660479-6	1991	These results indicate that: 1) .OH radical was most likely the ultimate O2 species responsible for DNA damage and activation of poly(ADP)ribose polymerase; 2) both H2O2 and .OH radicals were involved in the other cytotoxic effects (inhibition of protein synthesis and reduction of NAD and ATP stores); and 3) NAD and ATP depletion did not result solely from activation of poly(ADP)ribose polymerase, but other mechanisms are likely to be involved.	NAD	282-285	poly(ADP-ribose) polymerase 1	Homo sapiens	129-155
1660479-6	1991	These results indicate that: 1) .OH radical was most likely the ultimate O2 species responsible for DNA damage and activation of poly(ADP)ribose polymerase; 2) both H2O2 and .OH radicals were involved in the other cytotoxic effects (inhibition of protein synthesis and reduction of NAD and ATP stores); and 3) NAD and ATP depletion did not result solely from activation of poly(ADP)ribose polymerase, but other mechanisms are likely to be involved.	NAD	310-313	poly(ADP-ribose) polymerase 1	Homo sapiens	129-155
1959619-0	1991	Electron transfer properties of NADH:ubiquinone reductase in the ND1/3460 and the ND4/11778 mutations of the Leber hereditary optic neuroretinopathy (LHON).	NAD	32-36	mitochondrially encoded NADH dehydrogenase 1	Homo sapiens	65-68
1815509-3	1991	Aldose reductase activity is expressed with either NADH or NADPH as cofactor, whereas aldehyde reductase utilizes only NADPH.	NAD	51-55	aldo-keto reductase family 1 member B	Homo sapiens	0-16
1661222-4	1991	With dihydronicotinamide adenine dinucleotide (NADH), we verified it was aldose reductase but not aldehyde reductase II that was activated in the erythrocytes of the patients with NIDDM.	NAD	5-45	aldo-keto reductase family 1 member B	Homo sapiens	73-89
1661222-4	1991	With dihydronicotinamide adenine dinucleotide (NADH), we verified it was aldose reductase but not aldehyde reductase II that was activated in the erythrocytes of the patients with NIDDM.	NAD	47-51	aldo-keto reductase family 1 member B	Homo sapiens	73-89
1924300-1	1991	Replacing Leu-182 by Ala in yeast alcohol dehydrogenase (YADH; alcohol:NAD+ oxidoreductase, EC 1.1.1.1) yields a mutant that retains 34% of its kcat value and makes one stereochemical "mistake" every 850,000 turnovers (instead of approximately 1 error every 7,000,000,000 turnovers in native YADH) in its selection of the 4-Re hydrogen of NADH.	NAD	339-343	oxidoreductase	Saccharomyces cerevisiae S288C	76-90
1909571-8	1991	On the basis of the amino acid sequence, the NQO2 gene was found to be located 1.7 kilobase pairs upstream of the gene for NADH-binding subunit (NQO1).	NAD	123-127	NAD(P)H quinone dehydrogenase 1	Homo sapiens	145-149
1813060-5	1991	The induced FL cells were demonstrated to activate common promutagens/procarcinogens in UDS and ADPRT-mediated decrease of NAD content assay systems.	NAD	123-126	poly(ADP-ribose) polymerase 1	Homo sapiens	96-101
1931966-7	1991	An initial analysis by deletion mutagenesis of pADPRP"s functional domains revealed that deletions in the NAD binding domain eliminated all activity; however, partial polymerase activity resulted from deletion in the DNA binding or automodification domains.	NAD	106-109	poly(ADP-ribose) polymerase 1	Homo sapiens	47-53
1873300-6	1991	These facts suggest that menadione-catalyzed H2O2 production and chemiluminescence are used as the indicators of cell activity to keep the NADH concentration and NADH: menadione oxidoreductase activity which may be sensitive to the change in pH and ion concentrations.	NAD	162-166	oxidoreductase	Saccharomyces cerevisiae S288C	178-192
1892541-6	1991	Activities of 17 beta-HSD were measured in particulate and soluble fractions from normal breast adipose and non-adipose tissues, and from breast tumours obtained from post-menopausal women, in the oxidative direction with NAD+ and NADP+ as coenzymes and in the reductive direction with NADH and NADPH as coenzymes.	NAD	222-226	hydroxysteroid 17-beta dehydrogenase 1	Homo sapiens	14-25
1752628-0	1991	Differential binding of NAD+ to acyl glyceraldehyde-3-phosphate dehydrogenase and its role in the acyl group transfer reaction.	NAD	24-28	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	37-77
1752628-1	1991	Enzyme protein fluorescence of di-furylacryloyl-glyceraldehyde-3-phosphate dehydrogenase (di-FA-GPDH:lambda max.excitation 290 nm, lambda max.emission 338 nm) is quenched about 28% on saturation with NAD+.	NAD	200-204	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	48-88
1892541-6	1991	Activities of 17 beta-HSD were measured in particulate and soluble fractions from normal breast adipose and non-adipose tissues, and from breast tumours obtained from post-menopausal women, in the oxidative direction with NAD+ and NADP+ as coenzymes and in the reductive direction with NADH and NADPH as coenzymes.	NAD	286-290	hydroxysteroid 17-beta dehydrogenase 1	Homo sapiens	14-25
1944305-10	1991	Using [3 alpha-3H]dehydroepiandrosterone as substrate for 3 beta HSD activity, we determined the apparent Km for liver microsomal NAD(+)-dependent 3 beta HSD activity to be 20 microM in both adult male and female liver and was much greater than the Km of rat Leydig tumor 3 beta HSD activity (0.2 microM).	NAD	130-136	hydroxy-delta-5-steroid dehydrogenase, 3 beta- and steroid delta-isomerase 1	Rattus norvegicus	58-68
1650217-4	1991	Chloride stimulated the oxidation of NADH in the MPO-H2O2 system in a concentration-dependent manner (50-fold at 150 mM NaCl).	NAD	37-41	myeloperoxidase	Homo sapiens	49-52
1650217-6	1991	Observations demonstrating the effect of the drugs on the MPO system, are: (1) Inhibition of Cl(-)-stimulated oxidation of NADH.	NAD	123-127	myeloperoxidase	Homo sapiens	58-61
1944305-13	1991	The enzyme obtained upon expression of this cDNA had properties characteristic of male-specific NAD(+)-dependent liver microsomal 3 beta HSD (i.e. high apparent Km for dehydroepiandrosterone) and distinct from those of the high affinity gonadal type I 3 beta HSD.	NAD	96-102	hydroxy-delta-5-steroid dehydrogenase, 3 beta- and steroid delta-isomerase 1	Rattus norvegicus	130-140
1944305-13	1991	The enzyme obtained upon expression of this cDNA had properties characteristic of male-specific NAD(+)-dependent liver microsomal 3 beta HSD (i.e. high apparent Km for dehydroepiandrosterone) and distinct from those of the high affinity gonadal type I 3 beta HSD.	NAD	96-102	hydroxy-delta-5-steroid dehydrogenase, 3 beta- and steroid delta-isomerase 1	Rattus norvegicus	252-262
1944305-10	1991	Using [3 alpha-3H]dehydroepiandrosterone as substrate for 3 beta HSD activity, we determined the apparent Km for liver microsomal NAD(+)-dependent 3 beta HSD activity to be 20 microM in both adult male and female liver and was much greater than the Km of rat Leydig tumor 3 beta HSD activity (0.2 microM).	NAD	130-136	hydroxy-delta-5-steroid dehydrogenase, 3 beta- and steroid delta-isomerase 1	Rattus norvegicus	147-157
1944305-10	1991	Using [3 alpha-3H]dehydroepiandrosterone as substrate for 3 beta HSD activity, we determined the apparent Km for liver microsomal NAD(+)-dependent 3 beta HSD activity to be 20 microM in both adult male and female liver and was much greater than the Km of rat Leydig tumor 3 beta HSD activity (0.2 microM).	NAD	130-136	hydroxy-delta-5-steroid dehydrogenase, 3 beta- and steroid delta-isomerase 1	Rattus norvegicus	147-157
1956581-3	1991	The presence of DHPR, in addition to BH4 and NADH, greatly prolongs the lag period, which increases with increasing concentrations of each of BH4, NADH and DHPR.	NAD	45-49	quinoid dihydropteridine reductase	Homo sapiens	16-20
1367242-3	1991	Mercuric reductase activity was assayed from the Escherichia coli clone carrying pZH5 and it was Hg(2+)-inducible, NADH dependent and also required 2-mercaptoethanol for its activity.	NAD	115-119	mercuric reductase	Escherichia coli	0-18
1956581-0	1991	Inhibition of dopamine autoxidation by tetrahydrobiopterin and NADH in the presence of dihydropteridine reductase.	NAD	63-67	quinoid dihydropteridine reductase	Homo sapiens	87-113
1956581-1	1991	Dihydropteridine reductase (DHPR) catalyzes the regeneration of tetrahydrobiopterin (BH4) from quinonoid dihydrobiopterin by using NADH as a hydrogen donor.	NAD	131-135	quinoid dihydropteridine reductase	Homo sapiens	0-26
1956581-3	1991	The presence of DHPR, in addition to BH4 and NADH, greatly prolongs the lag period, which increases with increasing concentrations of each of BH4, NADH and DHPR.	NAD	45-49	quinoid dihydropteridine reductase	Homo sapiens	156-160
1956581-1	1991	Dihydropteridine reductase (DHPR) catalyzes the regeneration of tetrahydrobiopterin (BH4) from quinonoid dihydrobiopterin by using NADH as a hydrogen donor.	NAD	131-135	quinoid dihydropteridine reductase	Homo sapiens	28-32
1956581-3	1991	The presence of DHPR, in addition to BH4 and NADH, greatly prolongs the lag period, which increases with increasing concentrations of each of BH4, NADH and DHPR.	NAD	147-151	quinoid dihydropteridine reductase	Homo sapiens	16-20
1922097-6	1991	The protein expressed in bacteria was highly active in androsterone reduction in the presence of NAD as cofactor, and this activity was inhibited by indomethacin, a potent inhibitor of 3 alpha HSD.	NAD	97-100	dehydrogenase/reductase 9	Bos taurus	185-196
1817814-8	1991	DAN showed a significantly smaller HF during deep breathing (49 +/- 49) and a significantly smaller LF during tilting (54 +/- 52) than DPN.	NAD	135-138	NBL1, DAN family BMP antagonist	Homo sapiens	0-3
1943652-9	1991	This effect is due to the NAD(+)-dependent glycerol 3-phosphate dehydrogenase step being inhibited in the chronic ethanol-treated rats.	NAD	26-32	glycerol-3-phosphate dehydrogenase 1	Rattus norvegicus	43-77
2025253-2	1991	Expression of the fusion protein is toxic to the host cells, however yields of the released proteinase have been improved by optimising induction nad harvest times to increase culture biomass, and decrease degradation of the proteinase.	NAD	146-149	endogenous retrovirus group K member 25	Homo sapiens	92-102
1654805-6	1991	Based on kinetic analysis and the use of the diagnostic inhibitors--superoxide dismutase, catalase, albumin, mannitol, ethanol, and anaerobic conditions--we have assigned two major mechanisms of NADH oxidation.	NAD	195-199	catalase	Homo sapiens	90-98
2004328-2	1991	Previous studies found that hyperthermia alters the metabolism of adenosine diphosphate (ADP)-ribose polymers required for recovery from DNA damage and that poly(ADP-ribose) polymerase activity is very sensitive to cellular nicotinamide-adenine dinucleotide (NAD) levels.	NAD	224-257	poly(ADP-ribose) polymerase 1	Homo sapiens	157-184
2004328-2	1991	Previous studies found that hyperthermia alters the metabolism of adenosine diphosphate (ADP)-ribose polymers required for recovery from DNA damage and that poly(ADP-ribose) polymerase activity is very sensitive to cellular nicotinamide-adenine dinucleotide (NAD) levels.	NAD	259-262	poly(ADP-ribose) polymerase 1	Homo sapiens	157-184
1901170-3	1991	Two inhibitors of ADPRT, benzamide, competing with NAD at the nicotinamide binding site, and 6-amino-1,2-benzopyrone, which competes with DNA at the DNA binding site(s), both selectively arrest differentiation at the prodissoconch stage.	NAD	51-54	poly [ADP-ribose] polymerase 1	Bos taurus	18-23
1654786-0	1991	Reactive oxygen injury to cultured pulmonary artery endothelial cells: mediation by poly(ADP-ribose) polymerase activation causing NAD depletion and altered energy balance.	NAD	131-134	poly(ADP-ribose) polymerase 1	Homo sapiens	84-111
2009275-1	1991	NADH oxidase of purified plasma membranes (electron transfer from NADH to oxygen) was stimulated by the growth factor diferric transferrin.	NAD	0-4	transferrin	Homo sapiens	127-138
1908195-2	1991	Poly(ADP ribose) polymerase activity levels have been frequently assayed by incubating permeabilized cells with radioactively labeled NAD+ as substrate.	NAD	134-138	poly(ADP-ribose) polymerase 1	Homo sapiens	0-27
1908195-6	1991	The activating effect of oligonucleotides was also evident when ethanol-fixed HeLa cells were postincubated with NAD+ to allow poly(ADP ribose) synthesis to occur in situ, which was detected as specific anti-poly (ADP ribose) immunofluorescence.	NAD	113-117	poly(ADP-ribose) polymerase 1	Homo sapiens	208-213
1828277-11	1991	Glycolysis was markedly retarded in the patient"s muscle in the glyceraldehyde 3-phosphate dehydrogenase (GA3PD) step, possibly due to the impaired reoxidation of NADH produced by GA3PD activity.	NAD	163-167	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	64-104
2038500-4	1991	Respiratory assay, by reduction of exogenous cytochrome c, showed NADH, alpha-glycerophosphate and succinate to be the substrates with the greatest potential for metabolism.	NAD	66-70	cytochrome c, somatic	Homo sapiens	45-57
2038500-7	1991	The NADH-dependent reduction of cytochrome c was insensitive to rotenone and antimycin A.	NAD	4-8	cytochrome c, somatic	Homo sapiens	32-44
2038500-8	1991	Fumarate inhibited the NADH-dependent reduction of cytochrome c and stimulated the oxidation of NADH, suggestive of an NADH-fumarate reductase pathway.	NAD	23-27	cytochrome c, somatic	Homo sapiens	51-63
1828277-11	1991	Glycolysis was markedly retarded in the patient"s muscle in the glyceraldehyde 3-phosphate dehydrogenase (GA3PD) step, possibly due to the impaired reoxidation of NADH produced by GA3PD activity.	NAD	163-167	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	106-111
1828277-11	1991	Glycolysis was markedly retarded in the patient"s muscle in the glyceraldehyde 3-phosphate dehydrogenase (GA3PD) step, possibly due to the impaired reoxidation of NADH produced by GA3PD activity.	NAD	163-167	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	180-185
1856112-6	1991	Therefore, only the NAD-independent GPDH which is stimulated by menadione, can be selectively demonstrated in the histochemical procedure applied.	NAD	20-23	glycerol-3-phosphate dehydrogenase 1	Rattus norvegicus	36-40
1999293-1	1991	The structural organization of the entire nuclear gene (NMDMC) encoding the mitochondrial (mt) NAD-dependent methylenetetrahydrofolate dehydrogenase-methenyltetrahydrofolate cyclohydrolase enzyme (NMDMC) was determined by analysis of clones obtained from a lambda EMBL3 murine genomic DNA library.	NAD	95-98	methylenetetrahydrofolate dehydrogenase (NAD+ dependent), methenyltetrahydrofolate cyclohydrolase	Mus musculus	56-61
1999293-1	1991	The structural organization of the entire nuclear gene (NMDMC) encoding the mitochondrial (mt) NAD-dependent methylenetetrahydrofolate dehydrogenase-methenyltetrahydrofolate cyclohydrolase enzyme (NMDMC) was determined by analysis of clones obtained from a lambda EMBL3 murine genomic DNA library.	NAD	95-98	methylenetetrahydrofolate dehydrogenase (NAD+ dependent), methenyltetrahydrofolate cyclohydrolase	Mus musculus	197-202
2070435-2	1991	The cytotoxicities of these agents are greatly reduced by the simultaneous presence of 0.1 mM tetrahydrobiopterin (BH4), 3 units/ml horseradish peroxidase, 0.2 mM NADH, and 0.1 units/ml sheep liver dihydropteridine reductase (DHPR).	NAD	163-167	quinoid dihydropteridine reductase	Homo sapiens	226-230
2070435-6	1991	The reactions responsible for the BH4-antioxidation system may consist of the non-enzymatic and the peroxidase-catalyzed reduction of H2O2 to H2O by BH4 and the regeneration of BH4 by DHPR using NADH as the cofactor.	NAD	195-199	quinoid dihydropteridine reductase	Homo sapiens	184-188
1899380-6	1991	263, 13572-13578] and provided preliminary evidence that this enzyme may correspond to diaphorase 4, an enzymatic activity present in various tissues that catalyzes the reduction of a variety of quinones by both NADH and NADPH [Edwards et al.	NAD	212-216	NAD(P)H quinone dehydrogenase 1	Homo sapiens	87-99
1856112-11	1991	It is concluded that using menadione histochemical methods are suited to determine the mitochondrial GPDH activities in brain sections whereas using PMS a coreaction of GPDH takes place in the demonstration of NAD-GPDH, so that a histochemical quantification of NAD-GPDH cannot be recommended.	NAD	210-213	glycerol-3-phosphate dehydrogenase 1	Rattus norvegicus	169-173
1856112-11	1991	It is concluded that using menadione histochemical methods are suited to determine the mitochondrial GPDH activities in brain sections whereas using PMS a coreaction of GPDH takes place in the demonstration of NAD-GPDH, so that a histochemical quantification of NAD-GPDH cannot be recommended.	NAD	210-213	glycerol-3-phosphate dehydrogenase 1	Rattus norvegicus	169-173
1856112-11	1991	It is concluded that using menadione histochemical methods are suited to determine the mitochondrial GPDH activities in brain sections whereas using PMS a coreaction of GPDH takes place in the demonstration of NAD-GPDH, so that a histochemical quantification of NAD-GPDH cannot be recommended.	NAD	210-213	glycerol-3-phosphate dehydrogenase 1	Rattus norvegicus	169-173
16667745-6	1990	NADH:ascorbate free-radical reductase comigrated with NADH:ferricyanide and cytochrome c reductases when glyoxy-somal membranes were solubilized with detergent and subjected to rate-zonal centrifugation.	NAD	0-4	cytochrome c	Ricinus communis	76-88
1794453-11	1991	Kinetic studies performed with lung reductase by varying NADH and cytochrome b5 concentrations at different fixed concentrations at cytochrome b5 or NADH showed a series of parallel lines indicating a "ping-pong" type of kinetic mechanism for interaction of NADH and cytochrome b5 with lung cytochrome b5 reductase.	NAD	57-61	cytochrome b5	Ovis aries	132-145
1794453-11	1991	Kinetic studies performed with lung reductase by varying NADH and cytochrome b5 concentrations at different fixed concentrations at cytochrome b5 or NADH showed a series of parallel lines indicating a "ping-pong" type of kinetic mechanism for interaction of NADH and cytochrome b5 with lung cytochrome b5 reductase.	NAD	57-61	cytochrome b5	Ovis aries	132-145
1794453-11	1991	Kinetic studies performed with lung reductase by varying NADH and cytochrome b5 concentrations at different fixed concentrations at cytochrome b5 or NADH showed a series of parallel lines indicating a "ping-pong" type of kinetic mechanism for interaction of NADH and cytochrome b5 with lung cytochrome b5 reductase.	NAD	57-61	cytochrome b5	Ovis aries	132-145
1794453-11	1991	Kinetic studies performed with lung reductase by varying NADH and cytochrome b5 concentrations at different fixed concentrations at cytochrome b5 or NADH showed a series of parallel lines indicating a "ping-pong" type of kinetic mechanism for interaction of NADH and cytochrome b5 with lung cytochrome b5 reductase.	NAD	149-153	cytochrome b5	Ovis aries	66-79
1794453-11	1991	Kinetic studies performed with lung reductase by varying NADH and cytochrome b5 concentrations at different fixed concentrations at cytochrome b5 or NADH showed a series of parallel lines indicating a "ping-pong" type of kinetic mechanism for interaction of NADH and cytochrome b5 with lung cytochrome b5 reductase.	NAD	149-153	cytochrome b5	Ovis aries	66-79
1964814-5	1990	The particulate E1 17-KSR appeared capable of utilizing NADH or NADPH, whereas both the cytosolic form of this enzyme and the soluble DHEA 17-KSR activity showed a strict requirement for NADPH.	NAD	56-60	kinase suppressor of ras 1	Homo sapiens	22-25
1901806-8	1991	Aldose reductase utilized both NADPH and NADH as coenzymes, whereas aldehyde reductase only NADPH.	NAD	41-45	aldo-keto reductase family 1 member B	Homo sapiens	0-16
2037868-1	1991	Kinetic analysis has shown that isoquinoline, papaverine and berberine act as reversible competitive inhibitors to muscle lactate dehydrogenase and mitochondrial malate dehydrogenase with respect to the coenzyme NADH.	NAD	212-216	malic enzyme 2	Homo sapiens	162-182
1703398-8	1990	It utilized either NADPH or NADH as electron donor at equal efficiency and displayed high activities in reduction of menadione, 1,4-benzoquinone, and 2,6-dichlorophenolindophenol which are typical substrates for DT-diaphorase.	NAD	28-32	NAD(P)H quinone dehydrogenase 1	Homo sapiens	212-225
2121335-1	1990	Reduction of 2,5-diaziridinyl-3,6-bis(carboethoxyamino)-1,4-benzoquinone (diaziquone; AZQ) by purified rat hepatic DT-diaphorase was NADH and enzyme dependent and was inhibited by prior boiling of the enzyme or by dicumarol.	NAD	133-137	NAD(P)H quinone dehydrogenase 1	Rattus norvegicus	115-128
2120135-6	1990	There was a concomitant decrease in NAD levels, the substrate for poly-ADPRT.	NAD	36-39	poly(ADP-ribose) polymerase 1	Homo sapiens	71-76
2249975-6	1990	The supernatant retained over 60% of the NADH-dehydrogenase activity, tested with either DCIP2 or ferricyanide as substrates, together with NADH.	NAD	41-45	regulator of calcineurin 2	Rattus norvegicus	89-94
2277034-0	1990	Significance of catalase in peroxisomal fatty acyl-CoA beta-oxidation: NADH oxidation by acetoacetyl-CoA and H2O2.	NAD	71-75	catalase	Rattus norvegicus	16-24
2223769-3	1990	Mutations to neutralize the basic charge at Arg 72 (R72Q) and to both neutralize and reverse the charge at Lys 344 (K344Q, K344E) resulted in alteration of NADH oxidation rates in the reconstituted physiological electron-transfer system, which is rate limited by putidaredoxin-cytochrome P-450cam electron transfer.	NAD	156-160	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	277-293
2390286-5	1990	NADH-catalyzed CCl4 metabolism occurred to a similar extent in control and PB microsomes, amounting to 9-10% and 5-6% of the NADPH rate in control and PB microsomes, respectively.	NAD	0-4	C-C motif chemokine ligand 4	Rattus norvegicus	15-19
2390286-8	1990	Thus, the synergistic increase in CCl4 metabolism produced by NADH may occur in part from an increased availability of NADPH, as a result of decreased degradation, rather than by electron donation from NADH.	NAD	62-66	C-C motif chemokine ligand 4	Rattus norvegicus	34-38
2390286-8	1990	Thus, the synergistic increase in CCl4 metabolism produced by NADH may occur in part from an increased availability of NADPH, as a result of decreased degradation, rather than by electron donation from NADH.	NAD	202-206	C-C motif chemokine ligand 4	Rattus norvegicus	34-38
2382959-1	1990	Some NADH-linked aspartate aminotransferase (AST) assay systems may produce significant errors due to endogenous pyruvate because the pre-incubation time employed is too short and/or because the reagent lactate dehydrogenase (LD) activity is inadequate.	NAD	5-9	solute carrier family 17 member 5	Homo sapiens	17-43
2372948-1	1990	This coupled-enzyme method for determining the activity of catalase (EC 1.11.1.6) in erythrocyte lysates is based on measuring the absorbance at 340 nm of NADH produced from the peroxidic reaction between ethanol, hydrogen peroxide, and catalase.	NAD	155-159	catalase	Homo sapiens	59-67
2372948-1	1990	This coupled-enzyme method for determining the activity of catalase (EC 1.11.1.6) in erythrocyte lysates is based on measuring the absorbance at 340 nm of NADH produced from the peroxidic reaction between ethanol, hydrogen peroxide, and catalase.	NAD	155-159	catalase	Homo sapiens	237-245
2126460-1	1990	Directed mutagenesis has been used to study the nicotinamide subsite of the glycolytic NAD-dependent glyceraldehyde-3-phosphate dehydrogenase (GAPDH).	NAD	87-90	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	101-141
2126460-1	1990	Directed mutagenesis has been used to study the nicotinamide subsite of the glycolytic NAD-dependent glyceraldehyde-3-phosphate dehydrogenase (GAPDH).	NAD	87-90	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	143-148
2382959-1	1990	Some NADH-linked aspartate aminotransferase (AST) assay systems may produce significant errors due to endogenous pyruvate because the pre-incubation time employed is too short and/or because the reagent lactate dehydrogenase (LD) activity is inadequate.	NAD	5-9	solute carrier family 17 member 5	Homo sapiens	45-48
2371231-5	1990	The apparent first order rate constant for the reverse ADH reaction, assuming the reactants to be acetaldehyde and the ADH-NADH complex, was determined by two methods giving comparable results.	NAD	123-127	aldo-keto reductase family 1 member A1	Rattus norvegicus	119-122
2328693-0	1990	The methyltrienolone binding protein of human placenta requires nicotinamide adenine dinucleotide cofactor(s) for steroid binding.	NAD	64-97	MDM2 binding protein	Homo sapiens	4-36
2328693-2	1990	Purification and characterization of the modulating activity showed that NAD+ is the endogenous substance responsible for activating MTBP to a form capable of steroid binding.	NAD	73-77	MDM2 binding protein	Homo sapiens	133-137
2157501-4	1990	Oxidation of NADH was stimulated by diferric transferrin.	NAD	13-17	transferrin	Rattus norvegicus	45-56
2371231-5	1990	The apparent first order rate constant for the reverse ADH reaction, assuming the reactants to be acetaldehyde and the ADH-NADH complex, was determined by two methods giving comparable results.	NAD	123-127	aldo-keto reductase family 1 member A1	Rattus norvegicus	55-58
2295642-4	1990	Both effects of butanol were blocked by an inhibitor of ADH, 4-methylpyrazole, consistent with the hypothesis that elevation of the NADH redox state by butanol inhibited H2O2 production via NAD+-requiring peroxisomal beta-oxidation, leading indirectly to diminished rates of catalase-dependent methanol uptake.	NAD	132-136	catalase	Rattus norvegicus	275-283
2345545-5	1990	Phenobarbital/hydrocortisone showed a consistent, but not always significant increase in the NADPH and NADH cyt c reduction and benzanthracene an increase in the NADH cyt c reducing activity and cyt b5 content.	NAD	103-107	cytochrome c, somatic	Homo sapiens	108-113
2345545-6	1990	Griseofulvin lowered the NADH cyt c reducing activity.	NAD	25-29	cytochrome c, somatic	Homo sapiens	30-35
2108672-1	1990	Adenosine Diphosphoribosyl Transferase is a eucaryotic nuclear protein that catalyses the transfer of ADP-ribose moiety of NAD+ to itself and other cellular proteins.	NAD	123-127	poly(ADP-ribose) polymerase 1	Homo sapiens	0-38
2105502-0	1990	Photoaffinity labeling of ATP and NAD+ binding sites on recombinant human interleukin 2.	NAD	34-38	interleukin 2	Homo sapiens	74-87
2295642-4	1990	Both effects of butanol were blocked by an inhibitor of ADH, 4-methylpyrazole, consistent with the hypothesis that elevation of the NADH redox state by butanol inhibited H2O2 production via NAD+-requiring peroxisomal beta-oxidation, leading indirectly to diminished rates of catalase-dependent methanol uptake.	NAD	190-194	catalase	Rattus norvegicus	275-283
2109080-2	1990	Therefore, Gs alpha was radiolabeled by cholera toxin-catalzyed (32P)ADP-ribosylation with (32P)NAD as substrate.	NAD	96-99	GNAS complex locus	Homo sapiens	11-19
2072980-1	1990	Monoclonal antibodies (MAb 1-7-1) directed against the isoenzymes of rat liver cytochrome P-450 induced by methylcholanthrene, inhibited benzo(a)pyrene hydroxylase less strongly at low (0.04 mM) than at high (2 mM) NADH concentration.	NAD	215-219	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	79-95
2072980-5	1990	It is postulated that different cytochrome P-450 isoenzymes participate in benzo(a)pyrene hydroxylation, whereas the second one acts at high concentration of both NADH and NADPH.	NAD	163-167	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	32-48
2354811-4	1990	In contrast, 3-aminobenzamide inhibited the loss of NAD+ and viability caused by dimethyl sulphate so implicating poly(ADP-ribose)polymerase in its toxicity but not that of the quinones.	NAD	52-56	poly(ADP-ribose) polymerase 1	Homo sapiens	114-140
2105732-3	1990	Both reductions had the classic characteristics of DT-diaphorase: they were equally supported by NADPH and NADH and almost entirely inhibited by dicumarol.	NAD	107-111	NAD(P)H quinone dehydrogenase 1	Rattus norvegicus	51-64
2073786-14	1990	Possible mechanisms for beta cell destruction by these chemicals include (a) generation of oxygen free radicals and alteration of endogenous scavengers of these reactive species; (b) breakage of DNA and a consequent increase in the activity of poly-ADP-ribose synthetase, an enzyme depleting nicotinamide adenine dinucleotide in beta cells; and (c) inhibition of active calcium transport and calmodulin-activated protein kinase activity.	NAD	292-325	poly(ADP-ribose) polymerase 1	Homo sapiens	244-270
2182564-4	1990	According to the only acceptable model, when the acetaldehyde concentration is kept low by the action of aldehyde dehydrogenase, NADH no longer binds to alcohol dehydrogenase, but acetaldehyde still competes with ethanol for the active site of the enzyme.	NAD	129-133	aldo-keto reductase family 1 member A1	Rattus norvegicus	153-174
33944777-1	2021	SARM1 regulates axonal degeneration through its NAD-metabolizing activity and is a drug target for neurodegenerative disorders.	NAD	48-51	sterile alpha and HEAT/Armadillo motif containing 1	Mus musculus	0-5
2332989-2	1990	This was confirmed by either an increased uptake of radio-labelled NAD into the acid-insoluble fraction or a fall in cellular NAD levels, which was counteracted by 3-aminobenzamide, an inhibitor of poly(ADP-ribose) polymerase.	NAD	67-70	poly(ADP-ribose) polymerase 1	Homo sapiens	198-225
2332989-2	1990	This was confirmed by either an increased uptake of radio-labelled NAD into the acid-insoluble fraction or a fall in cellular NAD levels, which was counteracted by 3-aminobenzamide, an inhibitor of poly(ADP-ribose) polymerase.	NAD	126-129	poly(ADP-ribose) polymerase 1	Homo sapiens	198-225
2115165-0	1990	ADPRT-mediated decrease of cellular NAD content and the detection of chemically induced DNA damage--development of a new short-term screening test for mutagens.	NAD	36-39	poly(ADP-ribose) polymerase 1	Homo sapiens	0-5
2115165-2	1990	The reduction of NAD after DNA damage could be partially or completely prevented by ADPRT inhibitors, 3-aminobenzamide or nicotinamide, which showed no influence on reduction of NAD induced by metabolic blocking agents.	NAD	17-20	poly(ADP-ribose) polymerase 1	Homo sapiens	84-89
2115165-3	1990	Therefore, a simple and specific method to detect DNA-damaging mutagens by measuring ADPRT-mediated decrease of cellular NAD content was explored.	NAD	121-124	poly(ADP-ribose) polymerase 1	Homo sapiens	85-90
3615341-1	1987	Chloral hydrate (CH), an intermediate metabolite of trichloroethylene, is reduced to trichloroethanol (TCE) by alcohol dehydrogenase and aldehyde reductase, and is also oxidized to trichloroacetic acid (TCA) by the nicotinamide adenine dinucleotide (NAD)-dependent enzyme, CH dehydrogenase.	NAD	215-248	aldo-keto reductase family 1 member A1	Rattus norvegicus	111-132
3615341-1	1987	Chloral hydrate (CH), an intermediate metabolite of trichloroethylene, is reduced to trichloroethanol (TCE) by alcohol dehydrogenase and aldehyde reductase, and is also oxidized to trichloroacetic acid (TCA) by the nicotinamide adenine dinucleotide (NAD)-dependent enzyme, CH dehydrogenase.	NAD	250-253	aldo-keto reductase family 1 member A1	Rattus norvegicus	111-132
3615341-2	1987	Alcohol dehydrogenase requires reduced NAD (NADH), aldehyde reductase requires reduced nicotinamide adenine dinucleotide phosphate (NADPH) and CH dehydrogenase requires NAD to complete the reaction.	NAD	39-42	aldo-keto reductase family 1 member A1	Rattus norvegicus	0-21
3615341-2	1987	Alcohol dehydrogenase requires reduced NAD (NADH), aldehyde reductase requires reduced nicotinamide adenine dinucleotide phosphate (NADPH) and CH dehydrogenase requires NAD to complete the reaction.	NAD	44-48	aldo-keto reductase family 1 member A1	Rattus norvegicus	0-21
3615341-2	1987	Alcohol dehydrogenase requires reduced NAD (NADH), aldehyde reductase requires reduced nicotinamide adenine dinucleotide phosphate (NADPH) and CH dehydrogenase requires NAD to complete the reaction.	NAD	44-47	aldo-keto reductase family 1 member A1	Rattus norvegicus	0-21
33788980-4	2021	Here, we aimed to assess whether genetic deletion of nicotinamide phosphoribosyltransferase (Nampt), a rate-limiting enzyme in NAD+ production, affects AgRP neuronal function to impact whole-body metabolism and food intake.	NAD	127-131	nicotinamide phosphoribosyltransferase	Mus musculus	53-91
33811702-1	2021	Hyperactivation of PARP1 is known to be a major cause of necrotic cell death by depleting NAD+ /ATP pools during Ca2+ overload which is associated with many ischemic diseases.	NAD	90-94	poly(ADP-ribose) polymerase 1	Homo sapiens	19-24
33788980-4	2021	Here, we aimed to assess whether genetic deletion of nicotinamide phosphoribosyltransferase (Nampt), a rate-limiting enzyme in NAD+ production, affects AgRP neuronal function to impact whole-body metabolism and food intake.	NAD	127-131	nicotinamide phosphoribosyltransferase	Mus musculus	93-98
33810973-2	2021	Intracellular nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme in nicotinamide adenine dinucleotide (NAD) salvage pathway, is involved in many inflammatory disorders.	NAD	90-123	nicotinamide phosphoribosyltransferase	Mus musculus	14-52
33818184-1	2021	Nicotinamide phosphoribosyltransferase (NAMPT) is the key enzyme for the synthesis of nicotinamide adenine dinucleotide (NAD) in the salvaging pathway.	NAD	86-119	nicotinamide phosphoribosyltransferase	Mus musculus	0-38
33818184-1	2021	Nicotinamide phosphoribosyltransferase (NAMPT) is the key enzyme for the synthesis of nicotinamide adenine dinucleotide (NAD) in the salvaging pathway.	NAD	86-119	nicotinamide phosphoribosyltransferase	Mus musculus	40-45
33818184-1	2021	Nicotinamide phosphoribosyltransferase (NAMPT) is the key enzyme for the synthesis of nicotinamide adenine dinucleotide (NAD) in the salvaging pathway.	NAD	121-124	nicotinamide phosphoribosyltransferase	Mus musculus	0-38
33818184-1	2021	Nicotinamide phosphoribosyltransferase (NAMPT) is the key enzyme for the synthesis of nicotinamide adenine dinucleotide (NAD) in the salvaging pathway.	NAD	121-124	nicotinamide phosphoribosyltransferase	Mus musculus	40-45
33810973-2	2021	Intracellular nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme in nicotinamide adenine dinucleotide (NAD) salvage pathway, is involved in many inflammatory disorders.	NAD	90-123	nicotinamide phosphoribosyltransferase	Mus musculus	54-59
33810973-2	2021	Intracellular nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme in nicotinamide adenine dinucleotide (NAD) salvage pathway, is involved in many inflammatory disorders.	NAD	125-128	nicotinamide phosphoribosyltransferase	Mus musculus	14-52
33810973-2	2021	Intracellular nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme in nicotinamide adenine dinucleotide (NAD) salvage pathway, is involved in many inflammatory disorders.	NAD	125-128	nicotinamide phosphoribosyltransferase	Mus musculus	54-59
31427442-3	2019	In this study, we explored how NAD+ affects TLR4 and NOD-like receptor with a PYD-domain 3 (NLRP3) inflammasome activation, two key innate immune responses.	NAD	31-35	NLR family pyrin domain containing 3	Homo sapiens	92-97
33817415-4	2021	Sirtuin3, an NAD+-dependent deacetylase of mitochondria, regulates the function of mitochondria in diverse activities.	NAD	13-16	sirtuin 3	Homo sapiens	0-8
33779763-5	2021	We showed that PGDH3 exerts high NAD(H)-specificity and is active in photosynthesizing chloroplasts.	NAD	33-39	D-3-phosphoglycerate dehydrogenase	Arabidopsis thaliana	15-20
33779763-8	2021	pgdh3 loss-of-function mutants revealed an overreduced NADP(H) redox pool but a more oxidized plastid NAD(H) pool compared to wild-type plants.	NAD	102-108	D-3-phosphoglycerate dehydrogenase	Arabidopsis thaliana	0-5
32858528-6	2020	Moreover, the genes involved in nicotinamide adenine dinucleotide metabolism were negatively correlated with the expression of BRAF in the high-risk group.	NAD	32-65	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	127-131
33804735-2	2021	Poly ADP-ribose polymerases (PARP) are specialized enzymes that catalyze the addition of ADP ribose units from "nicotinamide adenine dinucleotide-donor molecules" to their target substrates.	NAD	112-145	poly(ADP-ribose) polymerase 1	Homo sapiens	0-27
33804735-2	2021	Poly ADP-ribose polymerases (PARP) are specialized enzymes that catalyze the addition of ADP ribose units from "nicotinamide adenine dinucleotide-donor molecules" to their target substrates.	NAD	112-145	poly(ADP-ribose) polymerase 1	Homo sapiens	29-33
28832634-5	2017	NKA enzyme activity was determined by NADH-linked methods and immunoblotting of NKA alpha1-, beta1-isoform, and E-cadherin were performed to evaluate protein expression.	NAD	38-42	tachykinin precursor 1	Homo sapiens	0-3
18814027-2	2009	PAR modification of VEGF was found to be related with the changes in NAD(+) associated with a shift in LDH isoenzymes.	NAD	69-75	vascular endothelial growth factor A	Homo sapiens	20-24
34919819-2	2021	Binding of PARP1 to damaged DNA leads to activation wherein PARP1 uses NAD+ to add chains of poly(ADP-ribose) onto itself and other nuclear proteins.	NAD	71-75	poly(ADP-ribose) polymerase 1	Homo sapiens	11-16
2194572-0	1990	Immunological detection of NADH-specific enoyl-ACP reductase from rape seed (Brassica napus)--induction, relationship of alpha and beta polypeptides, mRNA translation and interaction with ACP.	NAD	27-31	enoyl-[acyl-carrier-protein] reductase [NADH], chloroplastic-like	Brassica napus	41-60
34861210-3	2022	In this study, we found that the expression of Sirtuin 1 (SIRT1), a nicotinamide adenine dinucleotide (NAD+)-dependent histone deacetylase, was downregulated significantly in the hippocampus of streptozotocin (STZ)-induced diabetic cognitive impairment rats.	NAD	68-101	sirtuin 1	Rattus norvegicus	47-56
34861210-3	2022	In this study, we found that the expression of Sirtuin 1 (SIRT1), a nicotinamide adenine dinucleotide (NAD+)-dependent histone deacetylase, was downregulated significantly in the hippocampus of streptozotocin (STZ)-induced diabetic cognitive impairment rats.	NAD	68-101	sirtuin 1	Rattus norvegicus	58-63
34861210-3	2022	In this study, we found that the expression of Sirtuin 1 (SIRT1), a nicotinamide adenine dinucleotide (NAD+)-dependent histone deacetylase, was downregulated significantly in the hippocampus of streptozotocin (STZ)-induced diabetic cognitive impairment rats.	NAD	103-107	sirtuin 1	Rattus norvegicus	47-56
34861210-3	2022	In this study, we found that the expression of Sirtuin 1 (SIRT1), a nicotinamide adenine dinucleotide (NAD+)-dependent histone deacetylase, was downregulated significantly in the hippocampus of streptozotocin (STZ)-induced diabetic cognitive impairment rats.	NAD	103-107	sirtuin 1	Rattus norvegicus	58-63
34926116-2	2022	It plays a crucial role in post-translational modification by adding poly (ADP-ribose) (PAR) groups to various proteins and PARP1 itself by utilizing nicotinamide adenine dinucleotide (NAD +) as a substrate.	NAD	150-183	poly(ADP-ribose) polymerase 1	Homo sapiens	124-129
34926116-2	2022	It plays a crucial role in post-translational modification by adding poly (ADP-ribose) (PAR) groups to various proteins and PARP1 itself by utilizing nicotinamide adenine dinucleotide (NAD +) as a substrate.	NAD	185-190	poly(ADP-ribose) polymerase 1	Homo sapiens	124-129
34656796-3	2022	In this study, we identified a novel variant, m.3955G>A, in mitochondrially encoded NADH:ubiquinone oxidoreductase core subunit 1 (MT-ND1) in two unrelated LS patients, manifesting as infancy-onset frequent seizures, neurodegeneration, elevated lactate levels, and bilateral symmetrical lesions in the brainstem, basal ganglia, and thalamus.	NAD	84-88	mitochondrially encoded NADH dehydrogenase 1	Homo sapiens	131-137
34928817-0	2021	NAD+ improved experimental autoimmune encephalomyelitis by regulating SIRT1 to inhibit PI3K/Akt/mTOR signaling pathway.	NAD	0-4	thymoma viral proto-oncogene 1	Mus musculus	92-95
34928817-10	2021	RESULTS: Enrichment analysis showed PI3K-Akt-mTOR and autophagy pathway were main terms in EAE diseases, and the relationship between NAD+ and SIRT1.	NAD	134-138	thymoma viral proto-oncogene 1	Mus musculus	41-44
34928817-13	2021	CONCLUSIONS: NAD+ exerted a protective effect on EAE mice by inhibiting PI3K/Akt/mTOR signaling pathway through SIRT1 in TECs, and prevented EAE mice from sustained damage.	NAD	13-17	thymoma viral proto-oncogene 1	Mus musculus	77-80
34919052-5	2021	Mechanistic analysis suggests that NMNAT interferes with DNA damage-p53-caspase-3 apoptosis signaling pathway by enhancing NAD+-dependent posttranslational modifications (PTMs) poly(ADP-ribosyl)ation (PARylation) and deacetylation of p53.	NAD	123-127	tumor protein p53	Homo sapiens	68-71
34919052-5	2021	Mechanistic analysis suggests that NMNAT interferes with DNA damage-p53-caspase-3 apoptosis signaling pathway by enhancing NAD+-dependent posttranslational modifications (PTMs) poly(ADP-ribosyl)ation (PARylation) and deacetylation of p53.	NAD	123-127	caspase 3	Homo sapiens	72-81
34919052-7	2021	Our findings reveal a novel tumorigenic mechanism involving protein complex formation of p53 with NAD+ synthetic enzyme NMNAT and NAD+-dependent PTM enzymes that regulates glioma growth.	NAD	98-102	tumor protein p53	Homo sapiens	89-92
34919052-7	2021	Our findings reveal a novel tumorigenic mechanism involving protein complex formation of p53 with NAD+ synthetic enzyme NMNAT and NAD+-dependent PTM enzymes that regulates glioma growth.	NAD	130-134	tumor protein p53	Homo sapiens	89-92
34843934-10	2022	Moreover, compared with M3 and M5 groups, the higher NAD+/NADH ratio in the liver of M1 group activated SIRT1, which stimulated the AMPK signaling associated pathways by up-regulating the LKB1 gene.	NAD	53-57	serine/threonine kinase 11	Sus scrofa	188-192
34843934-10	2022	Moreover, compared with M3 and M5 groups, the higher NAD+/NADH ratio in the liver of M1 group activated SIRT1, which stimulated the AMPK signaling associated pathways by up-regulating the LKB1 gene.	NAD	58-62	serine/threonine kinase 11	Sus scrofa	188-192
34961895-3	2022	Extracellular NAD+ also serves as substrate for mono-ADP-ribosylation of cell surface proteins, which in human cells is mediated by ecto-ADP-ribosyltransferase 1 (ARTC1).	NAD	14-18	ADP-ribosyltransferase 1	Homo sapiens	163-168
34961895-10	2022	Thus, in settings with enhanced release of NAD+ as substrate for ARTC1, assessment of CD73 protein expression in human tissues may not be predictive of adenosine formation resulting in anti-inflammatory activity.	NAD	43-47	ADP-ribosyltransferase 1	Homo sapiens	65-70
34919819-2	2021	Binding of PARP1 to damaged DNA leads to activation wherein PARP1 uses NAD+ to add chains of poly(ADP-ribose) onto itself and other nuclear proteins.	NAD	71-75	poly(ADP-ribose) polymerase 1	Homo sapiens	60-65
34880123-10	2022	Implications: PARP1 inhibitors augment the DNA damage-induced killing of ALL cells by limiting the opposing effects of cAMP-mediated autophagy, which involves ROS-induced PARP1-activation and depletion of cellular NAD-levels.	NAD	214-218	poly(ADP-ribose) polymerase 1	Homo sapiens	14-19
34948094-9	2021	It was found that high glucose in HK-2 cells incubated under normoxic conditions: (1) activated transcription of HIF-1 target genes, elevated HIF-1alpha and ChREBP content, and increased the efficacy of ChREBP binding to promoter region of HIF1A gene; and (2), although it lowered NAD+/NADH ratio, it affected neither sirtuin activity nor HIF-1alpha acetylation level.	NAD	286-290	hypoxia inducible factor 1 subunit alpha	Homo sapiens	113-118
34959937-9	2021	Also, TGPN and PNY stimulated NAD-dependent deacetylase sirtuin-1(SIRT1), peroxisome proliferator-activated receptor gamma coactivator-1 alpha (PGC-1alpha), nuclear respiratory factor 1,2, mitochondrial transcription factor A, along with mitochondrial DNA content via SIRT1/PGC-1alpha signaling.	NAD	30-33	nuclear respiratory factor 1	Mus musculus	157-187
34893614-0	2021	Acute RyR1 Ca2+ leak enhances NADH-linked mitochondrial respiratory capacity.	NAD	30-34	ryanodine receptor 1, skeletal muscle	Mus musculus	6-10
34880123-6	2022	Furthermore, we reveal that cAMP-mediated PARP1-activation is preceded by induction of reactive oxygen species (ROS) and results in depletion of nicotinamide adenine dinucleotide (NAD), both of which are autophagy-promoting events.	NAD	145-178	poly(ADP-ribose) polymerase 1	Homo sapiens	42-47
34880123-6	2022	Furthermore, we reveal that cAMP-mediated PARP1-activation is preceded by induction of reactive oxygen species (ROS) and results in depletion of nicotinamide adenine dinucleotide (NAD), both of which are autophagy-promoting events.	NAD	180-183	poly(ADP-ribose) polymerase 1	Homo sapiens	42-47
34956283-3	2021	The enzyme S-nitrosoglutathione reductase (GSNOR) is a major route of NADH-dependent GSNO catabolism and is critical to NO homeostasis.	NAD	70-74	GroES-like zinc-binding dehydrogenase family protein	Arabidopsis thaliana	11-41
34880332-4	2021	Here, we discovered a novel role for the NAD+-dependent deacylase SIRT3 in kidney development.	NAD	41-44	sirtuin 3	Homo sapiens	66-71
34839666-7	2021	The reason is that PARP-1 polymerized nicotinamideadenine dinucleotide (NAD+) into large and hyperbranched poly(ADP-ribose) polymer (PAR) on the surface of Au@Ag NRs, preventing the Ag shell from being etched by H2O2.	NAD	38-70	poly(ADP-ribose) polymerase 1	Homo sapiens	19-25
34839666-7	2021	The reason is that PARP-1 polymerized nicotinamideadenine dinucleotide (NAD+) into large and hyperbranched poly(ADP-ribose) polymer (PAR) on the surface of Au@Ag NRs, preventing the Ag shell from being etched by H2O2.	NAD	72-76	poly(ADP-ribose) polymerase 1	Homo sapiens	19-25
34956283-3	2021	The enzyme S-nitrosoglutathione reductase (GSNOR) is a major route of NADH-dependent GSNO catabolism and is critical to NO homeostasis.	NAD	70-74	GroES-like zinc-binding dehydrogenase family protein	Arabidopsis thaliana	43-48
34956283-9	2021	These data uncover a new, NADPH-dependent component of NO metabolism that may be integrated with NADH-dependent GSNOR activity to control NO homeostasis in plants.	NAD	97-101	GroES-like zinc-binding dehydrogenase family protein	Arabidopsis thaliana	112-117
34923754-0	2021	NAD+ repletion attenuates obesity-induced oocyte mitochondrial dysfunction and offspring metabolic abnormalities via a SIRT3-dependent pathway.	NAD	0-4	sirtuin 3	Homo sapiens	119-124
34425214-2	2021	Sirtuin 6 (Sirt6), an NAD+-dependent deacetylase, has been implicated in hepatic glucose and lipid metabolism; however, the underlying mechanisms are incompletely understood.	NAD	22-25	sirtuin 6	Mus musculus	0-9
34425214-2	2021	Sirtuin 6 (Sirt6), an NAD+-dependent deacetylase, has been implicated in hepatic glucose and lipid metabolism; however, the underlying mechanisms are incompletely understood.	NAD	22-25	sirtuin 6	Mus musculus	11-16
34752167-0	2021	NAMPT-mediated NAD+ biosynthesis suppresses activation of hepatic stellate cells and protects against CCl4-induced liver fibrosis in mice.	NAD	15-19	nicotinamide phosphoribosyltransferase	Mus musculus	0-5
34724256-6	2021	Ectopic NDUFA4L2 expression resulted in reduced mitochondrial respiration and reactive oxygen species followed by lowered AMP, ADP, ATP, and NAD+ levels without affecting the overall protein content of the mitochondrial electron transport chain.	NAD	141-145	Ndufa4, mitochondrial complex associated like 2	Mus musculus	8-16
34724256-11	2021	Specifically, induced NDUFA4L2 reduces mitochondrial activity leading to lower levels of important intramuscular metabolites, including adenine nucleotides and NAD+ , which are hallmarks of mitochondrial dysfunction and hence shows that dysfunctional mitochondrial activity may drive muscle wasting.	NAD	160-164	Ndufa4, mitochondrial complex associated like 2	Mus musculus	22-30
34752167-11	2021	Tgfbeta1 treatment decreases intracellular NAD+ levels and NAMPT expression in LX2 cells.	NAD	43-47	transforming growth factor beta 1	Homo sapiens	0-8
34752167-14	2021	Conclusions: NAMPT-mediated NAD+ biosynthesis inhibits HSC activation and protects against CCl4-induced liver fibrosis.	NAD	28-32	nicotinamide phosphoribosyltransferase	Mus musculus	13-18
34762911-1	2021	Nicotinamide phosphoribosyltransferase (NAMPT) converts nicotinamide to nicotinamide adenine dinucleotide (NAD+).	NAD	72-105	nicotinamide phosphoribosyltransferase	Mus musculus	0-38
34762911-1	2021	Nicotinamide phosphoribosyltransferase (NAMPT) converts nicotinamide to nicotinamide adenine dinucleotide (NAD+).	NAD	72-105	nicotinamide phosphoribosyltransferase	Mus musculus	40-45
34762911-1	2021	Nicotinamide phosphoribosyltransferase (NAMPT) converts nicotinamide to nicotinamide adenine dinucleotide (NAD+).	NAD	107-111	nicotinamide phosphoribosyltransferase	Mus musculus	0-38
34762911-1	2021	Nicotinamide phosphoribosyltransferase (NAMPT) converts nicotinamide to nicotinamide adenine dinucleotide (NAD+).	NAD	107-111	nicotinamide phosphoribosyltransferase	Mus musculus	40-45
34115723-7	2021	The benefit of olaparib and other clinically approved PARP inhibitors has already been demonstrated in several experimental models of human diseases, such as neurodegeneration and neuroinflammation, acute hepatitis, skeletal muscle disorders, aging and acute ischemic stroke, protecting, for example, from the deterioration of the blood-brain barrier, restoring the cellular levels of NAD+, improving mitochondrial function and biogenesis and, among other effects, reducing oxidative stress and pro-inflammatory mediators, such as TNF-alpha, IL1-beta, IL-6 and VCAM1.	NAD	385-389	poly(ADP-ribose) polymerase 1	Homo sapiens	54-58
34811544-4	2021	Shortage of mitochondrial aspartate disrupted the regeneration of the metabolic cofactor nicotinamide adenine dinucleotide, causing ADP deribosylation of the endoplasmic reticulum (ER) sensor GRP78/BiP.	NAD	89-122	heat shock protein family A (Hsp70) member 5	Homo sapiens	192-197
34811544-4	2021	Shortage of mitochondrial aspartate disrupted the regeneration of the metabolic cofactor nicotinamide adenine dinucleotide, causing ADP deribosylation of the endoplasmic reticulum (ER) sensor GRP78/BiP.	NAD	89-122	heat shock protein family A (Hsp70) member 5	Homo sapiens	198-201
34647721-1	2021	Poly(ADP-ribose) polymerases, PARPs, transfer ADP-ribose onto target proteins from nicotinamide adenine dinucleotide (NAD+).	NAD	83-116	poly(ADP-ribose) polymerase 1	Homo sapiens	30-35
34517598-3	2021	The determination relies on the oxidation of NADH cofactor, which is used by SDH reacting with its substrates.	NAD	45-49	sorbitol dehydrogenase	Homo sapiens	77-80
34517598-5	2021	The concentration of cofactors (NADH, NAD+) and substrates (fructose, sorbitol) for SDH determination at a strip was optimized via internally-calibrated amperometric assays at a chitosan/nitrogen-doped carbon nanotube electrode.	NAD	32-36	sorbitol dehydrogenase	Homo sapiens	84-87
34517598-5	2021	The concentration of cofactors (NADH, NAD+) and substrates (fructose, sorbitol) for SDH determination at a strip was optimized via internally-calibrated amperometric assays at a chitosan/nitrogen-doped carbon nanotube electrode.	NAD	38-42	sorbitol dehydrogenase	Homo sapiens	84-87
34517598-7	2021	The assays yielded kinetic parameters Km and kcat and demonstrated higher apparent affinity of SDH for NADH and fructose than NAD+ and sorbitol.	NAD	103-107	sorbitol dehydrogenase	Homo sapiens	95-98
34647721-1	2021	Poly(ADP-ribose) polymerases, PARPs, transfer ADP-ribose onto target proteins from nicotinamide adenine dinucleotide (NAD+).	NAD	118-122	poly(ADP-ribose) polymerase 1	Homo sapiens	30-35
34636650-10	2021	Additionally, IFN-gamma resulted in a 23% depletion of intracellular NAD+ in HCAEC.	NAD	69-73	interferon gamma	Homo sapiens	14-23
34799586-4	2021	In the early phase, NR was directly absorbed and contributed to NAD+ generation through the NR salvage pathway, while in the late phase, NR was hydrolyzed to nicotinamide (NAM) by bone marrow stromal cell antigen 1 (BST1), and was further metabolized by the gut microbiota to nicotinic acid, contributing to generate NAD+ through the Preiss-Handler pathway.	NAD	64-68	bone marrow stromal cell antigen 1	Homo sapiens	216-220
34806016-0	2021	NAD+ bioavailability mediates PARG inhibition-induced replication arrest, intra S-phase checkpoint and apoptosis in glioma stem cells.	NAD	0-4	poly(ADP-ribose) glycohydrolase	Homo sapiens	30-34
34806016-3	2021	Supplementation with the NAD+ precursor dihydronicotinamide riboside (NRH) rapidly increased NAD+ levels in GSCs and glioma cells, inducing PARP1 activation and mild suppression of replication fork progression.	NAD	25-29	poly(ADP-ribose) polymerase 1	Homo sapiens	140-145
34806016-3	2021	Supplementation with the NAD+ precursor dihydronicotinamide riboside (NRH) rapidly increased NAD+ levels in GSCs and glioma cells, inducing PARP1 activation and mild suppression of replication fork progression.	NAD	93-97	poly(ADP-ribose) polymerase 1	Homo sapiens	140-145
34636650-13	2021	Conclusions: IFN-gamma impairs endothelial glucose metabolism via altered tryptophan catabolism destabilizing HIF1, depletes NAD+, and results in a metabolic shift toward increased fatty acid oxidation.	NAD	125-129	interferon gamma	Homo sapiens	13-22
34636650-14	2021	This work suggests a novel mechanistic basis for pathologic T-lymphocyte-endothelial interactions in atherosclerosis mediated by IFN-gamma, linking endothelial glucose, tryptophan, and fatty acid metabolism with NAD(H) and ATP generation, and their adverse endothelial functional consequences.	NAD	212-218	interferon gamma	Homo sapiens	129-138
34769515-0	2021	Modulation of Cellular NAD+ Attenuates Cancer-Associated Hypercoagulability and Thrombosis via the Inhibition of Tissue Factor and Formation of Neutrophil Extracellular Traps.	NAD	23-27	coagulation factor III	Mus musculus	113-126
34520170-12	2021	Furthermore, miR-34a-5p knockdown increased the Nampt protein expression levels as well as NAD+ levels, indicating that miR-34a-5p regulates Nampt during BBP exposure.	NAD	91-95	nicotinamide phosphoribosyltransferase	Mus musculus	141-146
34520170-14	2021	BBP exposure demonstrated the involvement of epigenetic regulation by altering the expression patterns of miR-34a-5p and its target Nampt, which may perturb the energy homeostasis of the differentiating adipocytes by altering NAD+ levels and sirtuin activity, resulting in increased adipogenesis.	NAD	226-230	nicotinamide phosphoribosyltransferase	Mus musculus	132-137
34827652-8	2021	This oxidation leads to a release of the coenzyme NAD+ from the active center of GAPDH, followed by the dissociation of the tetramer into subunits, which move to the nucleus due to passive transport and induce apoptosis.	NAD	50-54	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	81-86
34750509-1	2021	PARP enzymes utilise NAD+ as a co-substrate for their enzymatic activity.	NAD	21-25	poly(ADP-ribose) polymerase 1	Homo sapiens	0-4
34748530-0	2021	NAMPT-derived NAD+ fuels PARP1 to promote skin inflammation through parthanatos cell death.	NAD	14-18	poly(ADP-ribose) polymerase 1	Homo sapiens	25-30
34748530-6	2021	In conclusion, hyperactivation of PARP1 in response to ROS-induced DNA damage, fueled by NAMPT-derived NAD+, mediates skin inflammation through parthanatos cell death.	NAD	103-107	poly(ADP-ribose) polymerase 1	Homo sapiens	34-39
34769515-2	2021	NAD(P)H quinone oxidoreductase 1 (NQO1) increases the cellular nicotinamide adenine dinucleotide (NAD+) levels by accelerating the oxidation of NADH to NAD+, thus playing important roles in cellular homeostasis, energy metabolism, and inflammatory responses.	NAD	63-96	NAD(P)H quinone dehydrogenase 1	Homo sapiens	34-38
34769515-2	2021	NAD(P)H quinone oxidoreductase 1 (NQO1) increases the cellular nicotinamide adenine dinucleotide (NAD+) levels by accelerating the oxidation of NADH to NAD+, thus playing important roles in cellular homeostasis, energy metabolism, and inflammatory responses.	NAD	98-102	NAD(P)H quinone dehydrogenase 1	Homo sapiens	34-38
34769515-2	2021	NAD(P)H quinone oxidoreductase 1 (NQO1) increases the cellular nicotinamide adenine dinucleotide (NAD+) levels by accelerating the oxidation of NADH to NAD+, thus playing important roles in cellular homeostasis, energy metabolism, and inflammatory responses.	NAD	144-148	NAD(P)H quinone dehydrogenase 1	Homo sapiens	34-38
34769515-2	2021	NAD(P)H quinone oxidoreductase 1 (NQO1) increases the cellular nicotinamide adenine dinucleotide (NAD+) levels by accelerating the oxidation of NADH to NAD+, thus playing important roles in cellular homeostasis, energy metabolism, and inflammatory responses.	NAD	152-156	NAD(P)H quinone dehydrogenase 1	Homo sapiens	34-38
34769515-5	2021	Dunnione increases the cellular NAD+ levels in lung tissues of tumor-bearing mice to restore the declining sirtuin 1 (SIRT1) activity, thus deacetylating nuclear factor-kappa B (NF-kappaB) and preventing the overexpression of tissue factor in bronchial epithelial and vascular endothelial cells.	NAD	32-36	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	154-176
34731617-0	2021	Temporal dynamics of base excision/single-strand break repair protein complex assembly/disassembly are modulated by the PARP/NAD+/SIRT6 axis.	NAD	125-129	poly(ADP-ribose) polymerase 1	Homo sapiens	120-124
34618449-2	2021	The approach relies on the in situ reduction of Co(II) by H-BPin in the presence of bisphosphine ligands generating catalytically active Co(I) hydride complexes.	NAD	137-142	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	48-54
34732825-2	2021	The histone PARylation factor 1 (HPF1) discovered recently to form a joint active site with PARP1 and PARP2 was shown to limit the PARylation activity of PARPs and stimulate their NAD+-hydrolase activity.	NAD	180-184	histone PARylation factor 1	Homo sapiens	4-31
34732825-2	2021	The histone PARylation factor 1 (HPF1) discovered recently to form a joint active site with PARP1 and PARP2 was shown to limit the PARylation activity of PARPs and stimulate their NAD+-hydrolase activity.	NAD	180-184	histone PARylation factor 1	Homo sapiens	33-37
34732825-2	2021	The histone PARylation factor 1 (HPF1) discovered recently to form a joint active site with PARP1 and PARP2 was shown to limit the PARylation activity of PARPs and stimulate their NAD+-hydrolase activity.	NAD	180-184	poly(ADP-ribose) polymerase 1	Homo sapiens	92-97
34732825-2	2021	The histone PARylation factor 1 (HPF1) discovered recently to form a joint active site with PARP1 and PARP2 was shown to limit the PARylation activity of PARPs and stimulate their NAD+-hydrolase activity.	NAD	180-184	poly(ADP-ribose) polymerase 2	Homo sapiens	102-107
34731617-6	2021	These findings highlight coordinated yet independent roles for PARP1, PARP2, and SIRT6 and their regulation by NAD+ bioavailability to facilitate BER.	NAD	111-115	poly(ADP-ribose) polymerase 1	Homo sapiens	63-68
34731617-6	2021	These findings highlight coordinated yet independent roles for PARP1, PARP2, and SIRT6 and their regulation by NAD+ bioavailability to facilitate BER.	NAD	111-115	poly(ADP-ribose) polymerase 2	Homo sapiens	70-75
34559251-6	2021	As examples, the present commentary tries to integrate responses of AHR and NAD+-consuming enzymes (PARP7/TiPARP, CD38 and sirtuins) into infectious and stress-induced inflammatory responses, the latter exemplified by nonalcoholic fatty liver disease (NAFLD).	NAD	76-80	TCDD inducible poly(ADP-ribose) polymerase	Homo sapiens	100-105
34559251-6	2021	As examples, the present commentary tries to integrate responses of AHR and NAD+-consuming enzymes (PARP7/TiPARP, CD38 and sirtuins) into infectious and stress-induced inflammatory responses, the latter exemplified by nonalcoholic fatty liver disease (NAFLD).	NAD	76-80	TCDD inducible poly(ADP-ribose) polymerase	Homo sapiens	106-112
34514931-1	2021	OBJECTIVE: Sirtuin3 (SIRT3) is a NAD+-dependent major mitochondrial deacetylase.	NAD	33-37	sirtuin 3	Homo sapiens	11-19
34728642-3	2021	The repressor activity of CtBP2 is reciprocally regulated by NADH and acyl-CoAs.	NAD	61-65	C-terminal binding protein 2	Homo sapiens	26-31
34831209-4	2021	We demonstrate that impairment of DNMT1 enzymatic activity by NAD-promoted ADP-ribosylation leads to demethylation and transcriptional activation of the CEBPA gene, suggesting the existence of an unknown NAD-controlled region within the locus.	NAD	62-65	CCAAT enhancer binding protein alpha	Homo sapiens	153-158
34831209-4	2021	We demonstrate that impairment of DNMT1 enzymatic activity by NAD-promoted ADP-ribosylation leads to demethylation and transcriptional activation of the CEBPA gene, suggesting the existence of an unknown NAD-controlled region within the locus.	NAD	204-207	CCAAT enhancer binding protein alpha	Homo sapiens	153-158
34529977-4	2021	Binding of NADH appears to require protonation of a group with a pK value of ~7.4 in wild-type ADH1, but the pK value for T45G ADH1 appears to be less than 5.	NAD	11-15	alcohol dehydrogenase ADH1	Saccharomyces cerevisiae S288C	95-99
34514931-1	2021	OBJECTIVE: Sirtuin3 (SIRT3) is a NAD+-dependent major mitochondrial deacetylase.	NAD	33-37	sirtuin 3	Homo sapiens	21-26
34116232-4	2021	METHODS: Using targeted and isotope tracing high-resolution liquid chromatography-mass spectrometry, dual stable isotope tracer nuclear magnetic resonance spectroscopy-based metabolic flux modeling, and complementary physiological approaches in novel cell type-specific knockout mice, we quantified the roles of hepatocyte D-beta-hydroxybutyrate dehydrogenase (BDH1), a mitochondrial enzyme required for NAD+/NADH-dependent oxidation/reduction of ketone bodies.	NAD	404-408	3-hydroxybutyrate dehydrogenase, type 1	Mus musculus	361-365
34403688-4	2021	However, with injury or disease the levels of the NAD+ biosynthetic enzyme NMNAT2 drop, increasing the NMN/ NAD+ ratio and thereby promoting NMN binding to the SARM1 allosteric site, which in turn induces a conformational change activating the SARM1 NAD+ hydrolase.	NAD	50-54	nicotinamide nucleotide adenylyltransferase 2	Homo sapiens	75-81
34403688-4	2021	However, with injury or disease the levels of the NAD+ biosynthetic enzyme NMNAT2 drop, increasing the NMN/ NAD+ ratio and thereby promoting NMN binding to the SARM1 allosteric site, which in turn induces a conformational change activating the SARM1 NAD+ hydrolase.	NAD	108-112	nicotinamide nucleotide adenylyltransferase 2	Homo sapiens	75-81
34116232-4	2021	METHODS: Using targeted and isotope tracing high-resolution liquid chromatography-mass spectrometry, dual stable isotope tracer nuclear magnetic resonance spectroscopy-based metabolic flux modeling, and complementary physiological approaches in novel cell type-specific knockout mice, we quantified the roles of hepatocyte D-beta-hydroxybutyrate dehydrogenase (BDH1), a mitochondrial enzyme required for NAD+/NADH-dependent oxidation/reduction of ketone bodies.	NAD	409-413	3-hydroxybutyrate dehydrogenase, type 1	Mus musculus	361-365
34116232-5	2021	RESULTS: Exogenously administered AcAc is reduced to D-betaOHB, and increases hepatic NAD+/NADH ratio, reflecting hepatic BDH1 activity.	NAD	86-90	3-hydroxybutyrate dehydrogenase, type 1	Mus musculus	122-126
34116232-5	2021	RESULTS: Exogenously administered AcAc is reduced to D-betaOHB, and increases hepatic NAD+/NADH ratio, reflecting hepatic BDH1 activity.	NAD	91-95	3-hydroxybutyrate dehydrogenase, type 1	Mus musculus	122-126
34119711-2	2021	Nicotinamide phosphoribosyltransferase (NAMPT) controls NAD+ synthesis, and in skeletal muscle, NAD+ is important for muscle integrity.	NAD	56-60	nicotinamide phosphoribosyltransferase	Mus musculus	0-38
34548209-4	2021	HCbl is known to be a transient species where the oxidation state of the Co is variable; Co(I)-H+   Co(II)-H   Co(III)-H-.	NAD	89-94	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	100-106
34119711-2	2021	Nicotinamide phosphoribosyltransferase (NAMPT) controls NAD+ synthesis, and in skeletal muscle, NAD+ is important for muscle integrity.	NAD	56-60	nicotinamide phosphoribosyltransferase	Mus musculus	40-45
34509617-4	2021	D-ring-fused triazolyl estrone analog 24 showed potent inhibition of NADH-complexed 17beta-HSD1, with a binding affinity similar to that of the substrate estrone; its inhibition against NADPH-complexed 17beta-HSD1 was markedly weaker.	NAD	69-73	hydroxysteroid 17-beta dehydrogenase 1	Homo sapiens	84-95
34119711-2	2021	Nicotinamide phosphoribosyltransferase (NAMPT) controls NAD+ synthesis, and in skeletal muscle, NAD+ is important for muscle integrity.	NAD	96-100	nicotinamide phosphoribosyltransferase	Mus musculus	0-38
34119711-2	2021	Nicotinamide phosphoribosyltransferase (NAMPT) controls NAD+ synthesis, and in skeletal muscle, NAD+ is important for muscle integrity.	NAD	96-100	nicotinamide phosphoribosyltransferase	Mus musculus	40-45
34119711-4	2021	Thus, the objective of the current study was to delineate the role of NAMPT-mediated NAD+ biosynthesis in skeletal muscle development and function.	NAD	85-89	nicotinamide phosphoribosyltransferase	Mus musculus	70-75
34718610-7	2022	In transfected HepG2 cells, both variants significantly increased MDH2 enzymatic activity, thereby decreasing the NAD+/NADH ratio - a change known to affect insulin signaling and secretion.	NAD	114-118	insulin	Homo sapiens	157-164
34725423-1	2021	Lactate dehydrogenase (LDH) catalyses the conversion of pyruvate to lactate and NADH to NAD+; it has two isoforms, LDHA and LDHB.	NAD	80-84	lactate dehydrogenase A	Homo sapiens	115-119
34725423-1	2021	Lactate dehydrogenase (LDH) catalyses the conversion of pyruvate to lactate and NADH to NAD+; it has two isoforms, LDHA and LDHB.	NAD	88-92	lactate dehydrogenase A	Homo sapiens	115-119
34727004-6	2021	Furthermore, the IC50 values of ATP, ADP, NAD+, and NADP+ were approximately 15 muM.In our previous study, ATP was the strongest inhibitor of UGT activity in RLM.	NAD	42-46	solute carrier family 35 (UDP-galactose transporter), member A2	Mus musculus	142-145
34727004-8	2021	Furthermore, AMP antagonised the inhibitory effects of ATP and ADP.These results suggest that ATP, ADP, NAD+, and NADP+ are common endogenous inhibitors of UGT beyond species.	NAD	104-108	solute carrier family 35 (UDP-galactose transporter), member A2	Mus musculus	156-159
34584567-11	2021	These results suggested that 3-HK generated by KMO activity may be involved in the regulation of DLBCL cell viability via NAD+ synthesis.	NAD	122-126	kynurenine 3-monooxygenase (kynurenine 3-hydroxylase)	Mus musculus	47-50
34619528-8	2021	Doxorubicin and IR caused metabolic changes with nicotinamide adenine dinucleotide depletion and ensuing mitochondrial stunning (reversible mitochondria dysfunction without showing any cell death under ATP depletion) via p90RSK-ERK5 modulation and poly (ADP-ribose) polymerase (PARP) activation, which formed a nucleus-mitochondria positive feedback loop.	NAD	49-82	poly(ADP-ribose) polymerase 1	Homo sapiens	248-276
34619528-8	2021	Doxorubicin and IR caused metabolic changes with nicotinamide adenine dinucleotide depletion and ensuing mitochondrial stunning (reversible mitochondria dysfunction without showing any cell death under ATP depletion) via p90RSK-ERK5 modulation and poly (ADP-ribose) polymerase (PARP) activation, which formed a nucleus-mitochondria positive feedback loop.	NAD	49-82	poly(ADP-ribose) polymerase 1	Homo sapiens	278-282
34718610-7	2022	In transfected HepG2 cells, both variants significantly increased MDH2 enzymatic activity, thereby decreasing the NAD+/NADH ratio - a change known to affect insulin signaling and secretion.	NAD	119-123	insulin	Homo sapiens	157-164
34708231-1	2021	SIRT6, a member of the silencing information regulatory protein family, is a nicotinamide adenine dinucleotide-dependent histone deacetylase and an ADP-ribose transferase enzyme.	NAD	77-110	sirtuin 6	Mus musculus	0-5
34666848-1	2022	OBJECTIVE: Since the NAD+-dependent histone deacetylases sirtuin-1 (SIRT1) and sirtuin-2 (SIRT2) are critically involved in epigenetics, endocrinology and immunology and affect the longevity in model organisms, we investigated their expression in brains of 3 month old and 14-15 month old rat model of depression Flinders Sensitive Line (FSL) and control Flinders Resistant Line (FRL) rats.	NAD	21-24	sirtuin 1	Rattus norvegicus	57-66
34745158-9	2021	In part, it explains the existence of the light-independent NAD-specific malate dehydrogenase in the stroma.	NAD	60-63	malic enzyme 2	Homo sapiens	73-93
34686345-2	2021	SARM1 is activated by an increased ratio of NMN to NAD+, which competes for binding to an allosteric activating site.	NAD	51-55	sterile alpha and HEAT/Armadillo motif containing 1	Mus musculus	0-5
34686345-4	2021	The discovery of this allosteric activating site led us to hypothesize that other NAD+-related metabolites might activate SARM1.	NAD	82-86	sterile alpha and HEAT/Armadillo motif containing 1	Mus musculus	122-127
34686345-5	2021	Here, we show the nicotinamide analog 3-acetylpyridine (3-AP), first identified as a neurotoxin in the 1940s, is converted to 3-APMN, which activates SARM1 and induces SARM1-dependent NAD+ depletion, axon degeneration, and neuronal death.	NAD	184-188	sterile alpha and HEAT/Armadillo motif containing 1	Mus musculus	168-173
34692783-4	2021	The significant alteration of the component (E1 component subunit alpha and subunit beta) and the activity-regulating enzyme (pyruvate dehydrogenase kinase 2 and pyruvate dehydrogenase kinase 4) of pyruvate dehydrogenase complex and poly (ADP-ribose) polymerase 3, a nicotinamide adenine dinucleotide(+)-consuming enzymes, was further verified in targeted analysis.	NAD	267-300	poly (ADP-ribose) polymerase family, member 3	Mus musculus	233-263
34708032-2	2021	PARP1 functions by adding ADP-ribose polymers (PAR) to proteins including itself, using NAD+ as a donor.	NAD	88-92	poly(ADP-ribose) polymerase 1	Homo sapiens	0-5
34803499-10	2021	More importantly, Ex527 (Sirt1 inhibitor) and 3-TYP (Sirt3 inhibitor) significantly enhanced OA-induced lipid accumulation and oxidative stress in CD38-/- primary hepatocytes, suggesting that the anti-lipid accumulation of CD38 deficiency might be dependent on NAD/Sirtuins-mediated enhancement of FAA beta-oxidation and suppression of oxidative stress in hepatocytes.	NAD	261-264	protein tyrosine phosphatase, non-receptor type 20	Mus musculus	48-51
34500765-2	2021	Furthermore, all compounds were investigated in silico for their ability to inhibit mitochondrial NADH: ubiquinone oxidoreductase (complex I) by targeting the AMPK/mTOR signaling pathway and inhibiting hexokinase, a key glycolytic enzyme to prevent the Warburg effect in cancer cells.	NAD	98-102	mechanistic target of rapamycin kinase	Homo sapiens	164-168
34746707-6	2021	SIRT1 was deactivated with a decline in NAD+/NADH, which further aggravated inflammation.	NAD	40-44	NAD-dependent protein deacetylase sirtuin-1	Larimichthys crocea	0-5
34746707-6	2021	SIRT1 was deactivated with a decline in NAD+/NADH, which further aggravated inflammation.	NAD	45-49	NAD-dependent protein deacetylase sirtuin-1	Larimichthys crocea	0-5
34410304-2	2021	Here, we screened related LS-specific TCRs for antigen specificity and identified a peptide derived from NAD-dependent histone deacetylase hst4 (NDPD) of Aspergillus nidulans that stimulated these CD4+ T cells in an HLA-DR3-restricted manner.	NAD	105-108	CD4 molecule	Homo sapiens	197-200
34390780-8	2021	Global and targeted metabolites analysis revealed a fundamental role of PPARalpha in regulating the tryptophan-NAD pathway.	NAD	111-114	peroxisome proliferator activated receptor alpha	Mus musculus	72-81
34390780-13	2021	Catalase-mediated hydrogen peroxide removal represents an underlying mechanism of how PPARalpha preserves the NAD pool.	NAD	110-113	catalase	Mus musculus	0-8
34390780-13	2021	Catalase-mediated hydrogen peroxide removal represents an underlying mechanism of how PPARalpha preserves the NAD pool.	NAD	110-113	peroxisome proliferator activated receptor alpha	Mus musculus	86-95
34464722-5	2021	ERbeta agonists DPN and ERB-041 attenuated P2X7R expression in macrophages from colitis rats and in a murine macrophage cell line (RAW264.7) in response to either lipopolysaccharide (LPS) or adenosine triphosphate (ATP).	NAD	16-19	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	43-48
34464722-6	2021	DPN and ERB-041 also blocked increased production of TNF-alpha, IL-6, and IL-1beta in the rectocolon of colitis rats.	NAD	0-3	tumor necrosis factor	Rattus norvegicus	53-62
34464722-6	2021	DPN and ERB-041 also blocked increased production of TNF-alpha, IL-6, and IL-1beta in the rectocolon of colitis rats.	NAD	0-3	interleukin 6	Rattus norvegicus	64-68
34464722-6	2021	DPN and ERB-041 also blocked increased production of TNF-alpha, IL-6, and IL-1beta in the rectocolon of colitis rats.	NAD	0-3	interleukin 1 alpha	Rattus norvegicus	74-82
34663976-5	2021	In the nucleus, the altered PHGDH activity restricts NAD+ level and compartmentally repressed NAD+-dependent PARP1 activity for poly(ADP-ribosyl)ation of c-Jun, thereby leading to impaired c-Jun transcriptional activity linked to cell growth inhibition.	NAD	94-97	poly(ADP-ribose) polymerase 1	Homo sapiens	109-114
34397061-5	2021	To this end, electrochemical reactivity studies performed using (Cp*CoIII(P2BCy4)Cl)+ or an "all-akyl" model, (Cp*CoIII(dnppe)Cl)+ (dnppe = 1,2-bis(di-n-propylphosphino)ethane) with benzoic or 4-pyridylbenzoic acid show divergent responses for protonation of electrochemically-generated Co(i) to give a Co(iii) hydride.	NAD	287-292	mitochondrially encoded cytochrome c oxidase III	Homo sapiens	68-73
34497121-0	2021	NAD+ supplementation reduces neuroinflammation and cell senescence in a transgenic mouse model of Alzheimer"s disease via cGAS-STING.	NAD	0-4	cyclic GMP-AMP synthase	Mus musculus	122-126
34497121-12	2021	Our findings suggest a role for NAD+ depletion-mediated activation of cGAS-STING in neuroinflammation and cellular senescence in AD.	NAD	32-36	cyclic GMP-AMP synthase	Mus musculus	70-74
34638458-5	2021	Both, classical NAD-like and non-NAD-like PARP-1 inhibitors reduced viability and clonogenic potential of ccRCC cell lines and suppressed growth of ccRCC xenograft tumors.	NAD	33-36	poly(ADP-ribose) polymerase 1	Homo sapiens	42-48
34638458-6	2021	However, classical NAD-like PARP-1 inhibitors affected viability of normal kidney epithelial cells at high concentrations, while novel non-NAD-like PARP-1 inhibitors exhibited activity against malignant cells only.	NAD	19-22	poly(ADP-ribose) polymerase 1	Homo sapiens	28-34
34638458-6	2021	However, classical NAD-like PARP-1 inhibitors affected viability of normal kidney epithelial cells at high concentrations, while novel non-NAD-like PARP-1 inhibitors exhibited activity against malignant cells only.	NAD	139-142	poly(ADP-ribose) polymerase 1	Homo sapiens	148-154
34464722-9	2021	Blockade of JAK2 or STAT3 phosphorylation significantly reduced the ability of DPN to down-regulate P2X7R expression and the ability of ERB-041 and DPN to inhibit IL-1beta release from RAW264.7 cells.	NAD	79-82	signal transducer and activator of transcription 3	Mus musculus	20-25
34464722-9	2021	Blockade of JAK2 or STAT3 phosphorylation significantly reduced the ability of DPN to down-regulate P2X7R expression and the ability of ERB-041 and DPN to inhibit IL-1beta release from RAW264.7 cells.	NAD	79-82	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	100-105
34562089-6	2022	DOX activates nicotinamide adenine dinucleotide phosphate NADPH oxidase (NOX) in the heart, resulting in excessive reactive oxygen species that can induce cardiomyocyte apoptosis through phosphorylation of p53, DNA damage and/or mitogen-activated protein kinases-mediated cardiomyocyte apoptosis.	NAD	14-47	tumor protein p53	Homo sapiens	206-209
34603081-13	2021	Moreover, the expression of NAD+-consuming enzymes sirtuin 3 (SIRT3) and CD38 decreased significantly in CKD rats.	NAD	28-32	CD38 molecule	Rattus norvegicus	73-77
34530866-0	2021	NAD+ improves cognitive function and reduces neuroinflammation by ameliorating mitochondrial damage and decreasing ROS production in chronic cerebral hypoperfusion models through Sirt1/PGC-1alpha pathway.	NAD	0-4	sirtuin 1	Rattus norvegicus	179-184
34530866-0	2021	NAD+ improves cognitive function and reduces neuroinflammation by ameliorating mitochondrial damage and decreasing ROS production in chronic cerebral hypoperfusion models through Sirt1/PGC-1alpha pathway.	NAD	0-4	PPARG coactivator 1 alpha	Rattus norvegicus	185-195
34530866-10	2021	Results of mechanistic pathway analysis indicated that the detrimental effects of CCH might be associated with decreased gene expression of PPAR-gamma co-activator1alpha (PGC-1alpha) and its upstream transcription factor Sirt1, while NAD+ treatment markedly reversed their decrease.	NAD	234-238	PPARG coactivator 1 alpha	Rattus norvegicus	140-169
34530866-10	2021	Results of mechanistic pathway analysis indicated that the detrimental effects of CCH might be associated with decreased gene expression of PPAR-gamma co-activator1alpha (PGC-1alpha) and its upstream transcription factor Sirt1, while NAD+ treatment markedly reversed their decrease.	NAD	234-238	PPARG coactivator 1 alpha	Rattus norvegicus	171-181
34530866-10	2021	Results of mechanistic pathway analysis indicated that the detrimental effects of CCH might be associated with decreased gene expression of PPAR-gamma co-activator1alpha (PGC-1alpha) and its upstream transcription factor Sirt1, while NAD+ treatment markedly reversed their decrease.	NAD	234-238	sirtuin 1	Rattus norvegicus	221-226
34530866-11	2021	In vitro study confirmed that NAD+ administration had protective effects on hypoxia-induced neuroinflammation and mitochondrial damage, as well as ROS production in BV2 microglia via Sirt1/PGC-1alpha pathway.	NAD	30-34	sirtuin 1	Rattus norvegicus	183-188
34530866-11	2021	In vitro study confirmed that NAD+ administration had protective effects on hypoxia-induced neuroinflammation and mitochondrial damage, as well as ROS production in BV2 microglia via Sirt1/PGC-1alpha pathway.	NAD	30-34	PPARG coactivator 1 alpha	Rattus norvegicus	189-199
34530866-12	2021	Sirt1 overexpression mimicked the protective effects of NAD+ treatment in BV2 microglia.	NAD	56-60	sirtuin 1	Rattus norvegicus	0-5
34530866-13	2021	CONCLUSIONS: NAD+ ameliorated cognitive impairment and dampened neuroinflammation in CCH models in vivo and in vitro, and these beneficial effects were associated with mitochondrial protection and ROS inhibition via activating Sirt1/PGC-1alpha pathway.	NAD	13-17	sirtuin 1	Rattus norvegicus	227-232
34530866-13	2021	CONCLUSIONS: NAD+ ameliorated cognitive impairment and dampened neuroinflammation in CCH models in vivo and in vitro, and these beneficial effects were associated with mitochondrial protection and ROS inhibition via activating Sirt1/PGC-1alpha pathway.	NAD	13-17	PPARG coactivator 1 alpha	Rattus norvegicus	233-243
34567409-16	2021	Mechanically, these beneficial effects were attributed to the inhibition of NLRP3 inflammasome activation and myocardial inflammatory response by regulating the NAD+-Sirtuin3-MnSOD signaling pathway.	NAD	161-165	superoxide dismutase 2, mitochondrial	Mus musculus	175-180
34265417-2	2021	Sirtuin 1(SIRT1) is an NAD+-dependent histone deacetylase and transcriptional enhancer of GR.	NAD	23-26	sirtuin 1	Rattus norvegicus	0-9
34265417-2	2021	Sirtuin 1(SIRT1) is an NAD+-dependent histone deacetylase and transcriptional enhancer of GR.	NAD	23-26	sirtuin 1	Rattus norvegicus	10-15
34314389-5	2021	Furthermore, LSD1 regulates gene expression and protein methylation of nicotinamide mononucleotide adenylyltransferase 1 (NMNAT1), which controls the final step of NAD+ synthesis and limits NAD+ availability in nucleus.	NAD	164-168	lysine (K)-specific demethylase 1A	Mus musculus	13-17
34314389-5	2021	Furthermore, LSD1 regulates gene expression and protein methylation of nicotinamide mononucleotide adenylyltransferase 1 (NMNAT1), which controls the final step of NAD+ synthesis and limits NAD+ availability in nucleus.	NAD	190-194	lysine (K)-specific demethylase 1A	Mus musculus	13-17
34314389-6	2021	Lsd1 knockout reduces NAD+-dependent SIRT1 and SIRT7 deacetylase activity, leading to hyperacetylation and hypofunctioning of GABPbeta and PGC-1alpha, the major transcriptional factor/cofactor for nuclear-encoded mitochondrial genes.	NAD	22-25	lysine (K)-specific demethylase 1A	Mus musculus	0-4
34314389-8	2021	Thus, LSD1 orchestrates a core regulatory network involving epigenetic modifications and NAD+ synthesis to control mitochondrial function and hepatokine production.	NAD	89-93	lysine (K)-specific demethylase 1A	Mus musculus	6-10
34571963-9	2021	Importantly, estradiol prevented TNFalpha-induced pericyte migration and this effect was mimicked by PPT (ER-alpha agonist) and DPN (ER-beta agonist), but not by G1 (GPR30 agonist).	NAD	128-131	tumor necrosis factor	Homo sapiens	33-41
34571963-9	2021	Importantly, estradiol prevented TNFalpha-induced pericyte migration and this effect was mimicked by PPT (ER-alpha agonist) and DPN (ER-beta agonist), but not by G1 (GPR30 agonist).	NAD	128-131	estrogen receptor 1	Homo sapiens	133-140
34500765-2	2021	Furthermore, all compounds were investigated in silico for their ability to inhibit mitochondrial NADH: ubiquinone oxidoreductase (complex I) by targeting the AMPK/mTOR signaling pathway and inhibiting hexokinase, a key glycolytic enzyme to prevent the Warburg effect in cancer cells.	NAD	98-102	hexokinase 1	Homo sapiens	202-212
34382917-0	2021	NAD+ metabolism controls growth inhibition by HIF1 in normoxia and determines differential sensitivity of normal and cancer cells.	NAD	0-4	hypoxia inducible factor 1 subunit alpha	Homo sapiens	46-50
34382917-7	2021	Antiproliferative effects of hypoxia response were alleviated by inhibition of lactate dehydrogenase and more effectively, by boosting cellular production of NAD+, which was decreased by HIF1 activation.	NAD	158-162	hypoxia inducible factor 1 subunit alpha	Homo sapiens	187-191
34382917-10	2021	Thus, metabolic changes in cancer cells, such as enhanced NAD+ production, create resistance to growth-inhibitory activity of HIF1 permitting manifestation of its tumor-promoting properties.AbbreviationsDMOG: dimethyloxalylglycine, DM-NOFD: dimethyl N-oxalyl-D-phenylalanine, NMN: beta-nicotinamide mononucleotide.	NAD	58-62	hypoxia inducible factor 1 subunit alpha	Homo sapiens	126-130
34183378-7	2021	Supplementing NMN as an NAD+ donor inhibited p65 acetylation, decreased p65 nuclear translocation, and restored cyp3a transcription in both HepG2 cells and mouse hepatocytes.	NAD	24-28	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	112-117
34332984-6	2021	Moreover, in SAA1-deficient MDA-MB-231 and HCC70 cells, metabolism (NADH oxidation) continually increased while cell migration (% wound closure and the rate of wound closure) decreased.	NAD	68-72	serum amyloid A1	Homo sapiens	13-17
34403696-6	2021	Pre-incubation of TRF1 with its regulator protein Tankyrase 1 and the cofactor NAD+ significantly reduced TRF1-TIN2 mediated DNA-DNA bridging, whereas TIN2 protected the disassembly of TRF1-TIN2 mediated DNA-DNA bridging upon Tankyrase 1 addition.	NAD	79-83	telomeric repeat binding factor 1	Homo sapiens	18-22
34403696-6	2021	Pre-incubation of TRF1 with its regulator protein Tankyrase 1 and the cofactor NAD+ significantly reduced TRF1-TIN2 mediated DNA-DNA bridging, whereas TIN2 protected the disassembly of TRF1-TIN2 mediated DNA-DNA bridging upon Tankyrase 1 addition.	NAD	79-83	telomeric repeat binding factor 1	Homo sapiens	106-110
34439319-3	2021	Cells overexpressing NQO1 subsequently die rapidly through an NAD+-keresis mechanism.	NAD	62-66	NAD(P)H quinone dehydrogenase 1	Homo sapiens	21-25
34180254-2	2022	As the metabolic and redox hub, mitochondria provide numerous links to the plasma membrane channels, insulin granule vesicles (IGVs), cell redox, NADH, NADPH, and Ca2+-homeostasis, all affecting insulin secretion.	NAD	146-150	insulin	Homo sapiens	195-202
34460049-5	2021	The current study focuses on the functional characterization of nicotinamidase 3 (NIC3) gene, which is involved in the biochemical conversion of nicotinamide (NAM) to nicotinic acid (NA) in the salvage pathway of NAD biosynthesis.	NAD	213-216	nicotinamidase 3	Arabidopsis thaliana	64-80
34460049-5	2021	The current study focuses on the functional characterization of nicotinamidase 3 (NIC3) gene, which is involved in the biochemical conversion of nicotinamide (NAM) to nicotinic acid (NA) in the salvage pathway of NAD biosynthesis.	NAD	213-216	nicotinamidase 3	Arabidopsis thaliana	82-86
34380043-0	2021	NAD+ supplement potentiates tumor-killing function by rescuing defective TUB-mediated NAMPT transcription in tumor-infiltrated T cells.	NAD	0-4	nicotinamide phosphoribosyltransferase	Mus musculus	86-91
34445574-7	2021	The reduced NAD+ content in NMNAT1 KO cells was further decreased by ActD, which partially inhibited NAD+-dependent enzymes, including the DNA nick sensor enzyme PARP1 and the NAD+-dependent deacetylase SIRT1.	NAD	101-105	poly(ADP-ribose) polymerase 1	Homo sapiens	162-167
34485381-4	2021	In particular, emergent data show viral infection stimulates activation of poly (ADP-ribose) polymerase (PARP) mediated NAD+ depletion and stimulates hydrolysis of existing ADP-ribosylation modifications.	NAD	120-124	poly(ADP-ribose) polymerase 1	Homo sapiens	75-103
34485381-4	2021	In particular, emergent data show viral infection stimulates activation of poly (ADP-ribose) polymerase (PARP) mediated NAD+ depletion and stimulates hydrolysis of existing ADP-ribosylation modifications.	NAD	120-124	poly(ADP-ribose) polymerase 1	Homo sapiens	105-109
34380612-5	2021	PARP inhibitors do not affect the level of condensation of undamaged DNA but act to block condensation reversal for damaged DNA in the presence of NAD+ Our findings suggest a mechanism for PARP1 in the organization of chromatin structure.	NAD	147-151	poly(ADP-ribose) polymerase 1	Homo sapiens	0-4
34380612-5	2021	PARP inhibitors do not affect the level of condensation of undamaged DNA but act to block condensation reversal for damaged DNA in the presence of NAD+ Our findings suggest a mechanism for PARP1 in the organization of chromatin structure.	NAD	147-151	poly(ADP-ribose) polymerase 1	Homo sapiens	189-194
34380043-4	2021	The intracellular level of NAD+, whose synthesis is dependent on the NAMPT-mediated salvage pathway, is also decreased in TILs.	NAD	27-31	nicotinamide phosphoribosyltransferase	Mus musculus	69-74
34380043-7	2021	Collectively, this study reveals that an impaired TCR-TUB-NAMPT-NAD+ axis leads to T cell dysfunction in the tumor microenvironment, and an over-the-counter nutrient supplement of NAD+ could boost T-cell-based immunotherapy.	NAD	64-68	nicotinamide phosphoribosyltransferase	Mus musculus	58-63
34380043-7	2021	Collectively, this study reveals that an impaired TCR-TUB-NAMPT-NAD+ axis leads to T cell dysfunction in the tumor microenvironment, and an over-the-counter nutrient supplement of NAD+ could boost T-cell-based immunotherapy.	NAD	180-184	nicotinamide phosphoribosyltransferase	Mus musculus	58-63
34370789-0	2021	NAD+ pool depletion as a signal for the Rex regulon involved in Streptococcus agalactiae virulence.	NAD	0-4	rex	Mus musculus	40-43
34370789-1	2021	In many Gram-positive bacteria, the redox-sensing transcriptional repressor Rex controls central carbon and energy metabolism by sensing the intra cellular balance between the reduced and oxidized forms of nicotinamide adenine dinucleotide; the NADH/NAD+ ratio.	NAD	206-239	rex	Mus musculus	76-79
34370789-8	2021	However, GBS Rex is unique compared to Rex regulators previously characterized because of its sensing mechanism: we show that it primarily responds to NAD+ levels (or growth rate) rather than to the NADH/NAD+ ratio.	NAD	204-208	rex	Mus musculus	39-42
34370789-1	2021	In many Gram-positive bacteria, the redox-sensing transcriptional repressor Rex controls central carbon and energy metabolism by sensing the intra cellular balance between the reduced and oxidized forms of nicotinamide adenine dinucleotide; the NADH/NAD+ ratio.	NAD	245-249	rex	Mus musculus	76-79
34370789-1	2021	In many Gram-positive bacteria, the redox-sensing transcriptional repressor Rex controls central carbon and energy metabolism by sensing the intra cellular balance between the reduced and oxidized forms of nicotinamide adenine dinucleotide; the NADH/NAD+ ratio.	NAD	250-254	rex	Mus musculus	76-79
34370789-3	2021	We present structures of Rex bound to NAD+ and to a DNA operator which are the first structures of a Rex-family member from a pathogenic bacterium.	NAD	38-42	rex	Mus musculus	25-28
34370789-3	2021	We present structures of Rex bound to NAD+ and to a DNA operator which are the first structures of a Rex-family member from a pathogenic bacterium.	NAD	38-42	rex	Mus musculus	101-104
34370789-4	2021	The structures reveal the molecular basis of DNA binding and the conformation alterations between the free NAD+ complex and DNA-bound form of Rex.	NAD	107-111	rex	Mus musculus	142-145
34370789-7	2021	Mechanistically, NAD+ stabilizes Rex as a repressor in the absence of NADH.	NAD	17-21	rex	Mus musculus	33-36
34370789-8	2021	However, GBS Rex is unique compared to Rex regulators previously characterized because of its sensing mechanism: we show that it primarily responds to NAD+ levels (or growth rate) rather than to the NADH/NAD+ ratio.	NAD	151-155	rex	Mus musculus	13-16
34370789-8	2021	However, GBS Rex is unique compared to Rex regulators previously characterized because of its sensing mechanism: we show that it primarily responds to NAD+ levels (or growth rate) rather than to the NADH/NAD+ ratio.	NAD	151-155	rex	Mus musculus	39-42
34370789-8	2021	However, GBS Rex is unique compared to Rex regulators previously characterized because of its sensing mechanism: we show that it primarily responds to NAD+ levels (or growth rate) rather than to the NADH/NAD+ ratio.	NAD	199-203	rex	Mus musculus	13-16
34370789-8	2021	However, GBS Rex is unique compared to Rex regulators previously characterized because of its sensing mechanism: we show that it primarily responds to NAD+ levels (or growth rate) rather than to the NADH/NAD+ ratio.	NAD	199-203	rex	Mus musculus	39-42
34370789-8	2021	However, GBS Rex is unique compared to Rex regulators previously characterized because of its sensing mechanism: we show that it primarily responds to NAD+ levels (or growth rate) rather than to the NADH/NAD+ ratio.	NAD	204-208	rex	Mus musculus	13-16
34091287-2	2021	Twelve compounds were identified as inhibitors of moderate to high potency on an inhouse MCF-7 cell line, of which 2 compounds (5 and 6) were capable of reducing NAD level in MCF-7 cells in concentrations equivalent to half of their IC50s, potentially due to NAD(P)H quinone oxidoreductase (NQO1) inhibition.	NAD	162-165	NAD(P)H quinone dehydrogenase 1	Homo sapiens	291-295
34348217-5	2022	Recent advances include the realization that NADH, the most common natural cofactor for reverse FDH catalysis, is an inefficient electron donor for FDH catalyzed CO2 conversion.	NAD	45-49	aldehyde dehydrogenase 1 family member L1	Homo sapiens	96-99
34374300-13	2021	Importantly, elevation of cardiac NAD+ levels by NAMPT normalized NAD+ redox balance, alleviated cardiac dysfunction (fractional shortening: 40.2% versus 24.8% in cKO:NAMPT versus cKO, P<0.05; early-to-late ratio of peak diastolic velocity: 1.32 versus 1.04, P<0.05), and reversed pathogenic mechanisms in diabetic mice.	NAD	34-38	nicotinamide phosphoribosyltransferase	Mus musculus	49-54
34374300-13	2021	Importantly, elevation of cardiac NAD+ levels by NAMPT normalized NAD+ redox balance, alleviated cardiac dysfunction (fractional shortening: 40.2% versus 24.8% in cKO:NAMPT versus cKO, P<0.05; early-to-late ratio of peak diastolic velocity: 1.32 versus 1.04, P<0.05), and reversed pathogenic mechanisms in diabetic mice.	NAD	66-70	nicotinamide phosphoribosyltransferase	Mus musculus	49-54
34348217-5	2022	Recent advances include the realization that NADH, the most common natural cofactor for reverse FDH catalysis, is an inefficient electron donor for FDH catalyzed CO2 conversion.	NAD	45-49	aldehyde dehydrogenase 1 family member L1	Homo sapiens	148-151
34342816-8	2021	Temporal nicotinamide adenine dinucleotide (NAD+) assay was done to show the inhibition of PARP1.	NAD	9-42	poly(ADP-ribose) polymerase 1	Homo sapiens	91-96
34130091-7	2021	We showed that poly(ADP-ribose) polymerase (PARP) inhibitor rescued the NAD+ depletion in UVA/B-irradiated human keratinocytes, confirming that PAPR transiently exhausts cellular NAD+ to repair DNA damage.	NAD	72-76	poly(ADP-ribose) polymerase 1	Homo sapiens	15-42
34130091-7	2021	We showed that poly(ADP-ribose) polymerase (PARP) inhibitor rescued the NAD+ depletion in UVA/B-irradiated human keratinocytes, confirming that PAPR transiently exhausts cellular NAD+ to repair DNA damage.	NAD	72-76	poly(ADP-ribose) polymerase 1	Homo sapiens	44-48
34130091-7	2021	We showed that poly(ADP-ribose) polymerase (PARP) inhibitor rescued the NAD+ depletion in UVA/B-irradiated human keratinocytes, confirming that PAPR transiently exhausts cellular NAD+ to repair DNA damage.	NAD	179-183	poly(ADP-ribose) polymerase 1	Homo sapiens	15-42
34130091-7	2021	We showed that poly(ADP-ribose) polymerase (PARP) inhibitor rescued the NAD+ depletion in UVA/B-irradiated human keratinocytes, confirming that PAPR transiently exhausts cellular NAD+ to repair DNA damage.	NAD	179-183	poly(ADP-ribose) polymerase 1	Homo sapiens	44-48
34130091-9	2021	Moreover, the NAMPT inhibitor abrogated the sirtuin-1 (SIRT1)-mediated deacetylation of p53 and significantly inhibited the proliferation of UVA/B-irradiated cells, suggesting that the NAMPT-NAD+-SIRT1 axis regulates p53 functions upon UVA/B stress.	NAD	191-195	tumor protein p53	Homo sapiens	88-91
34130091-9	2021	Moreover, the NAMPT inhibitor abrogated the sirtuin-1 (SIRT1)-mediated deacetylation of p53 and significantly inhibited the proliferation of UVA/B-irradiated cells, suggesting that the NAMPT-NAD+-SIRT1 axis regulates p53 functions upon UVA/B stress.	NAD	191-195	tumor protein p53	Homo sapiens	217-220
34130091-0	2021	Restoring NAD+ by NAMPT is essential for the SIRT1/p53-mediated survival of UVA- and UVB-irradiated epidermal keratinocytes.	NAD	10-14	tumor protein p53	Homo sapiens	51-54
34342816-8	2021	Temporal nicotinamide adenine dinucleotide (NAD+) assay was done to show the inhibition of PARP1.	NAD	44-48	poly(ADP-ribose) polymerase 1	Homo sapiens	91-96
34187548-2	2021	It demonstrates pre-clinical efficacy toward a broad spectrum of acute myeloid leukemia (AML) subtypes by inhibiting NAMPT-dependent NAD+ production.	NAD	133-137	nicotinamide phosphoribosyltransferase	Mus musculus	117-122
34307460-3	2021	This is an axonal NAD-related signaling mechanism mainly regulated by the two key proteins with opposing roles: the NAD-synthesizing enzyme NMNAT2, and SARM1, a protein with NADase and related activities.	NAD	18-21	nicotinamide nucleotide adenylyltransferase 2	Homo sapiens	140-146
34307460-3	2021	This is an axonal NAD-related signaling mechanism mainly regulated by the two key proteins with opposing roles: the NAD-synthesizing enzyme NMNAT2, and SARM1, a protein with NADase and related activities.	NAD	116-119	nicotinamide nucleotide adenylyltransferase 2	Homo sapiens	140-146
34097876-8	2021	Interestingly, silencing the NAD+-sensor enzyme SIRT1 prevented eNAD+-dependent transcriptional repression of CD73, Slc12a8, and NRK1, as well as iNAD+ resetting.	NAD	29-33	solute carrier family 12 member 8	Homo sapiens	116-123
34097876-8	2021	Interestingly, silencing the NAD+-sensor enzyme SIRT1 prevented eNAD+-dependent transcriptional repression of CD73, Slc12a8, and NRK1, as well as iNAD+ resetting.	NAD	29-33	nicotinamide riboside kinase 1	Homo sapiens	129-133
34356514-5	2021	MacroH2A1.1 and macroH2A1.2 isoforms differ only in a few amino acids and their ability to bind NAD-derived metabolites, a property allegedly conferring their different functions in vivo.	NAD	96-99	macroH2A.1 histone	Homo sapiens	0-11
34233170-3	2021	(2021) now provide the clinical evidence that an NAD+ booster increases muscle insulin sensitivity in postmenopausal prediabetic women, validating the therapeutic promises of NAD+ boosters in humans.	NAD	49-53	insulin	Homo sapiens	79-86
34087956-4	2021	Here, we demonstrate that molecular hallmarks involved in aging biology including NAD+ decline, and activation of mTOR, p53, and p16INK4A are significantly enhanced in NLRX1 deficiency in vitro.	NAD	82-86	NLR family member X1	Mus musculus	168-173
34087956-5	2021	Mechanistic studies of replicative cellular senescence in the presence or absence of NLRX1 in vitro reveal that NLRX1-deficient fibroblasts fail to maintain optimal NAD+ /NADH ratio, which instigates the decline of SIRT1 and the activation of mTOR, p16INK4A , and p53, leading to the increase in senescence-associated beta-galactosidase (SA-beta-gal)-positive cells.	NAD	165-169	NLR family member X1	Mus musculus	85-90
34087956-5	2021	Mechanistic studies of replicative cellular senescence in the presence or absence of NLRX1 in vitro reveal that NLRX1-deficient fibroblasts fail to maintain optimal NAD+ /NADH ratio, which instigates the decline of SIRT1 and the activation of mTOR, p16INK4A , and p53, leading to the increase in senescence-associated beta-galactosidase (SA-beta-gal)-positive cells.	NAD	165-169	NLR family member X1	Mus musculus	112-117
34087956-5	2021	Mechanistic studies of replicative cellular senescence in the presence or absence of NLRX1 in vitro reveal that NLRX1-deficient fibroblasts fail to maintain optimal NAD+ /NADH ratio, which instigates the decline of SIRT1 and the activation of mTOR, p16INK4A , and p53, leading to the increase in senescence-associated beta-galactosidase (SA-beta-gal)-positive cells.	NAD	165-169	cyclin dependent kinase inhibitor 2A	Mus musculus	249-257
34087956-5	2021	Mechanistic studies of replicative cellular senescence in the presence or absence of NLRX1 in vitro reveal that NLRX1-deficient fibroblasts fail to maintain optimal NAD+ /NADH ratio, which instigates the decline of SIRT1 and the activation of mTOR, p16INK4A , and p53, leading to the increase in senescence-associated beta-galactosidase (SA-beta-gal)-positive cells.	NAD	171-175	NLR family member X1	Mus musculus	85-90
34087956-5	2021	Mechanistic studies of replicative cellular senescence in the presence or absence of NLRX1 in vitro reveal that NLRX1-deficient fibroblasts fail to maintain optimal NAD+ /NADH ratio, which instigates the decline of SIRT1 and the activation of mTOR, p16INK4A , and p53, leading to the increase in senescence-associated beta-galactosidase (SA-beta-gal)-positive cells.	NAD	171-175	NLR family member X1	Mus musculus	112-117
34187548-3	2021	NAMPT is the rate-limiting enzyme in the salvage metabolic pathway leading to NAD+ generation.	NAD	78-82	nicotinamide phosphoribosyltransferase	Mus musculus	0-5
34249897-2	2021	Sperm-specific glyceraldehyde-3-phosphate dehydrogenase (GAPDHS) switches glyceraldehyde-3-phosphate to 1,3-bisphosphoglycerate by coupling with the reduction of NAD+ to NADH.	NAD	162-166	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	15-55
34249897-2	2021	Sperm-specific glyceraldehyde-3-phosphate dehydrogenase (GAPDHS) switches glyceraldehyde-3-phosphate to 1,3-bisphosphoglycerate by coupling with the reduction of NAD+ to NADH.	NAD	162-166	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	57-63
34249897-2	2021	Sperm-specific glyceraldehyde-3-phosphate dehydrogenase (GAPDHS) switches glyceraldehyde-3-phosphate to 1,3-bisphosphoglycerate by coupling with the reduction of NAD+ to NADH.	NAD	170-174	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	15-55
34249897-2	2021	Sperm-specific glyceraldehyde-3-phosphate dehydrogenase (GAPDHS) switches glyceraldehyde-3-phosphate to 1,3-bisphosphoglycerate by coupling with the reduction of NAD+ to NADH.	NAD	170-174	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	57-63
34199944-2	2021	The deletion of PARP2 induces mitochondrial biogenesis and mitochondrial activity by increasing NAD+ levels and inducing SIRT1 activity.	NAD	96-100	poly(ADP-ribose) polymerase 2	Homo sapiens	16-21
34142751-5	2021	In stenotic valves (n = 50), due to reduced CD73 activity, NAD+ was degraded predominantly by CD38 and additionally by ALP and eNPP1.	NAD	59-63	ectonucleotide pyrophosphatase/phosphodiesterase 1	Homo sapiens	127-132
34195227-9	2021	Correlating NADH lifetime delta with overexpression strength of Abeta-related proteins on the single-cell level, we could verify the important role of intracellular Abeta-mediated mitochondrial toxicity.	NAD	12-16	amyloid beta precursor protein	Homo sapiens	64-69
34195227-9	2021	Correlating NADH lifetime delta with overexpression strength of Abeta-related proteins on the single-cell level, we could verify the important role of intracellular Abeta-mediated mitochondrial toxicity.	NAD	12-16	amyloid beta precursor protein	Homo sapiens	165-170
34108479-5	2021	In this conformation, PARP2 is capable of binding substrate NAD+ and histone PARylation factor 1 that changes PARP2 residue specificity from glutamate to serine when initiating DNA repair processes.	NAD	60-64	poly(ADP-ribose) polymerase 2	Homo sapiens	22-27
34108479-5	2021	In this conformation, PARP2 is capable of binding substrate NAD+ and histone PARylation factor 1 that changes PARP2 residue specificity from glutamate to serine when initiating DNA repair processes.	NAD	60-64	poly(ADP-ribose) polymerase 2	Homo sapiens	110-115
34234670-2	2021	The requirement of NAD+ for SIRT1 activity led us to assume that NQO1, an NADH oxidoreductase producing NAD+, regulates SIRT1 activity.	NAD	19-23	NAD(P)H quinone dehydrogenase 1	Homo sapiens	65-69
34234670-2	2021	The requirement of NAD+ for SIRT1 activity led us to assume that NQO1, an NADH oxidoreductase producing NAD+, regulates SIRT1 activity.	NAD	104-108	NAD(P)H quinone dehydrogenase 1	Homo sapiens	65-69
34112762-5	2021	In addition, we observed that CD38 deficiency or NAD supplementation remarkably mitigated Ang II-induced vascular senescence by suppressing the biogenesis, secretion, and internalization of senescence-associated small extracellular vesicles (SA-sEVs), which facilitated the senescence of neighboring non-damaged VSMCs.	NAD	49-52	angiotensinogen (serpin peptidase inhibitor, clade A, member 8)	Mus musculus	90-96
34112762-7	2021	In conclusion, our findings demonstrated that CD38 and its associated intracellular NAD decline are critical for Ang II-induced VSMC senescence and vascular remodeling.	NAD	84-87	angiotensinogen (serpin peptidase inhibitor, clade A, member 8)	Mus musculus	113-119
34073600-3	2021	Enzymatic activity of NNMT is important for the prevention of NAM-mediated inhibition of NAD+-consuming enzymes poly-adenosine -diphosphate (ADP), ribose polymerases (PARPs), and sirtuins (SIRTs).	NAD	89-93	poly(ADP-ribose) polymerase 1	Homo sapiens	167-172
34070758-7	2021	In vitro data confirmed that SFRP2 promotes NFATc3, CD38 and PD-1 expression in T-cells, while hSFRP2 mAb treatment counteracts these effects and increases NAD+ levels.	NAD	156-160	secreted frizzled related protein 2	Homo sapiens	95-101
34073600-5	2021	Largely overlooked, in the context of cancer, is the inhibitory effect of 2-PY on PARP-1 activity, which abrogates NNMT"s positive effect on cellular NAD+ flux by stalling liberation of NAM and reducing NAD+ synthesis in the salvage pathway.	NAD	150-154	poly(ADP-ribose) polymerase 1	Homo sapiens	82-88
34073600-5	2021	Largely overlooked, in the context of cancer, is the inhibitory effect of 2-PY on PARP-1 activity, which abrogates NNMT"s positive effect on cellular NAD+ flux by stalling liberation of NAM and reducing NAD+ synthesis in the salvage pathway.	NAD	203-207	poly(ADP-ribose) polymerase 1	Homo sapiens	82-88
34066057-5	2021	Modulation of their activity using PARP inhibitors occupying the NAD+ binding site has proven successful in cancer therapies.	NAD	65-69	poly(ADP-ribose) polymerase 1	Homo sapiens	35-39
34079576-9	2021	Among the 26 genes within the 16p11.2 region, as a key enzyme for nicotinamide adenine dinucleotide (NAD+) biosynthesis, QPRT was distinctly localized in renal tubules but was barely observed in renal interstitial and glomeruli in fetal kidneys.	NAD	66-99	quinolinate phosphoribosyltransferase	Homo sapiens	121-125
34079576-9	2021	Among the 26 genes within the 16p11.2 region, as a key enzyme for nicotinamide adenine dinucleotide (NAD+) biosynthesis, QPRT was distinctly localized in renal tubules but was barely observed in renal interstitial and glomeruli in fetal kidneys.	NAD	101-105	quinolinate phosphoribosyltransferase	Homo sapiens	121-125
34082111-11	2021	CONCLUSION: This study demonstrated that AhR activation is a protective response to counteract alcohol-induced hepatic NAD+ depletion through induction of NQO1 and targeting hepatic AhR-NQO1 pathway may serve as a novel therapeutic approach for ALD.	NAD	119-123	aryl-hydrocarbon receptor	Mus musculus	41-44
35504092-0	2022	Inhibition of NAD kinase elevates the hepatic NAD+ pool and alleviates acetaminophen-induced acute liver injury in mice.	NAD	46-50	NAD kinase	Mus musculus	14-24
34102973-0	2021	Codonopsis pilosula Polysaccharides Alleviate Abeta1-40-Induced PC12 Cells Energy Dysmetabolism via CD38/NAD+ Signaling Pathway.	NAD	105-109	CD38 molecule	Rattus norvegicus	100-104
34102973-6	2021	Additionally, it was found that Abeta1-40 increased CD38 expres- sion related to NAD+ homeostasis, whereas Silent Information Regulation 2 homolog1 (SIRT1), SIRT3, Peroxisome proliferator-activated receptor gamma coactivator-1 alpha (PGC-1alpha) and SIRT3 activity were decreased.	NAD	81-85	CD38 molecule	Rattus norvegicus	52-56
34102973-7	2021	Codonopsis pilosula polysaccharides increased NAD+, NAD+/NADH, SIRT3, SIRT1, and PGC-1alpha related to NAD+, thus partially recovering ATP.	NAD	103-107	PPARG coactivator 1 alpha	Rattus norvegicus	81-91
34629354-2	2021	The diabetogenic agents, alloxan and streptozotocin, caused DNA strand breaks, which in turn activated poly(ADP-ribose) polymerase/synthetase (PARP) to deplete NAD+, thereby inhibiting islet beta-cell functions such as proinsulin synthesis and ultimately leading to beta-cell necrosis.	NAD	160-164	poly(ADP-ribose) polymerase 1	Homo sapiens	103-141
34629354-2	2021	The diabetogenic agents, alloxan and streptozotocin, caused DNA strand breaks, which in turn activated poly(ADP-ribose) polymerase/synthetase (PARP) to deplete NAD+, thereby inhibiting islet beta-cell functions such as proinsulin synthesis and ultimately leading to beta-cell necrosis.	NAD	160-164	poly(ADP-ribose) polymerase 1	Homo sapiens	143-147
34629354-2	2021	The diabetogenic agents, alloxan and streptozotocin, caused DNA strand breaks, which in turn activated poly(ADP-ribose) polymerase/synthetase (PARP) to deplete NAD+, thereby inhibiting islet beta-cell functions such as proinsulin synthesis and ultimately leading to beta-cell necrosis.	NAD	160-164	insulin	Homo sapiens	219-229
34629354-4	2021	Inhibitors of PARP prevented the NAD+ depletion, inhibition of proinsulin synthesis and beta-cell death.	NAD	33-37	poly(ADP-ribose) polymerase 1	Homo sapiens	14-18
35447104-5	2022	Under normal condition in the absence of exogenous DNA-damaging agent, PAR turnovers with a half-life of <40 s; consistent with significant decrease of NAD+ levels in S phase, which is recovered by PARP inhibitors, and, substantiating the observed rapid turnover of PAR.	NAD	152-156	poly(ADP-ribose) polymerase 1	Homo sapiens	198-202
34719594-1	2021	Nicotinamide phosphoribosyltransferase (NAMPT) catalyzes the rate-limiting step of the nicotinamide adenine dinucleotide (NAD+) salvage pathway.	NAD	87-120	nicotinamide phosphoribosyltransferase	Mus musculus	0-38
34719594-1	2021	Nicotinamide phosphoribosyltransferase (NAMPT) catalyzes the rate-limiting step of the nicotinamide adenine dinucleotide (NAD+) salvage pathway.	NAD	87-120	nicotinamide phosphoribosyltransferase	Mus musculus	40-45
34719594-1	2021	Nicotinamide phosphoribosyltransferase (NAMPT) catalyzes the rate-limiting step of the nicotinamide adenine dinucleotide (NAD+) salvage pathway.	NAD	122-126	nicotinamide phosphoribosyltransferase	Mus musculus	0-38
34719594-1	2021	Nicotinamide phosphoribosyltransferase (NAMPT) catalyzes the rate-limiting step of the nicotinamide adenine dinucleotide (NAD+) salvage pathway.	NAD	122-126	nicotinamide phosphoribosyltransferase	Mus musculus	40-45
34719594-2	2021	Because NAD+ plays a pivotal role in energy metabolism and boosting NAD+ has positive effects on metabolic regulation, activation of NAMPT is an attractive therapeutic approach for the treatment of various diseases, including type 2 diabetes and obesity.	NAD	8-12	nicotinamide phosphoribosyltransferase	Mus musculus	133-138
34719594-2	2021	Because NAD+ plays a pivotal role in energy metabolism and boosting NAD+ has positive effects on metabolic regulation, activation of NAMPT is an attractive therapeutic approach for the treatment of various diseases, including type 2 diabetes and obesity.	NAD	68-72	nicotinamide phosphoribosyltransferase	Mus musculus	133-138
35504092-4	2022	Herein, we firstly investigated the protein expression of NAD kinase (NADK), as the rate-limiting enzyme converting NAD+ to nicotinamide adenine dinucleotide phosphate (NADP+), and found it was positively correlated with APAP-induced ALI in a dose- and time-dependent manner.	NAD	116-120	NAD kinase	Mus musculus	58-68
35504092-4	2022	Herein, we firstly investigated the protein expression of NAD kinase (NADK), as the rate-limiting enzyme converting NAD+ to nicotinamide adenine dinucleotide phosphate (NADP+), and found it was positively correlated with APAP-induced ALI in a dose- and time-dependent manner.	NAD	116-120	NAD kinase	Mus musculus	70-74
35504092-6	2022	Moreover, pretreatment with methotrexate (MTX), the inhibitor of NADK, attenuated the levels of transaminases, alleviated morphological abnormalities, and improved oxidative stress triggered by APAP overdose, which was attributed to elevated hepatic NAD+ pool.	NAD	250-254	NAD kinase	Mus musculus	65-69
35504092-7	2022	Subsequently, the increased NAD+ upregulated the expression of Sirt1, SOD2 and attenuated DNA damage.	NAD	28-32	superoxide dismutase 2, mitochondrial	Mus musculus	70-74
35504092-8	2022	Collectively, elevated expression of NADK is related to APAP-induced ALI, and inhibition of NADK alleviates the ALI through elevating liver NAD+ level and improving antioxidant capacity.	NAD	140-144	NAD kinase	Mus musculus	37-41
35504092-8	2022	Collectively, elevated expression of NADK is related to APAP-induced ALI, and inhibition of NADK alleviates the ALI through elevating liver NAD+ level and improving antioxidant capacity.	NAD	140-144	NAD kinase	Mus musculus	92-96
35490894-11	2022	CONCLUSION: In view of the findings, crocin ameliorates depression in mice, which may be associated with regulating NAMPT-NAD+-SIRT1 pathway.	NAD	122-126	nicotinamide phosphoribosyltransferase	Mus musculus	116-121
35413388-0	2022	Inhibition of Nicotinamide adenine dinucleotide phosphate oxidase 4 attenuates cell apoptosis and oxidative stress in a rat model of polycystic ovary syndrome through the activation of Nrf-2/HO-1 signaling pathway.	NAD	14-47	NFE2 like bZIP transcription factor 2	Rattus norvegicus	185-190
35385807-1	2022	NAMPT is the rate-limiting enzyme in the NAD salvage pathway, which makes it an attractive target for the treatment of many diseases associated with NAD exhaustion such as neurodegenerative diseases.	NAD	41-44	nicotinamide phosphoribosyltransferase	Mus musculus	0-5
35385807-1	2022	NAMPT is the rate-limiting enzyme in the NAD salvage pathway, which makes it an attractive target for the treatment of many diseases associated with NAD exhaustion such as neurodegenerative diseases.	NAD	149-152	nicotinamide phosphoribosyltransferase	Mus musculus	0-5
35585057-0	2022	Involvement of FSP1-CoQ10-NADH and GSH-GPx-4 pathways in retinal pigment epithelium ferroptosis.	NAD	26-30	atlastin GTPase 1	Homo sapiens	15-19
35624865-7	2022	In stretched macrophages, H2S prevented MIP-2 release by limiting nicotinamide adenine dinucleotide phosphate oxidase-derived superoxide radicals (ROS).	NAD	66-99	chemokine (C-X-C motif) ligand 2	Mus musculus	40-45
34994384-10	2022	Moreover, it was demonstrated that H2S derived from CBS activated SIRT1 via increasing the NAD +/NADH ratio and promoting the phosphorylation of SIRT1.	NAD	91-96	cystathionine beta-synthase	Homo sapiens	52-55
34994384-10	2022	Moreover, it was demonstrated that H2S derived from CBS activated SIRT1 via increasing the NAD +/NADH ratio and promoting the phosphorylation of SIRT1.	NAD	97-101	cystathionine beta-synthase	Homo sapiens	52-55
35585057-5	2022	Here, we report that both FSP1-CoQ10-NADH and GSH-GPx-4 pathways inhibit retinal ferroptosis in sodium iodate (SIO)-induced retinal degeneration pathologies in human primary RPE cells (HRPEpiC), ARPE-19 cell line, and mice.	NAD	37-41	atlastin GTPase 1	Homo sapiens	26-30
35602287-2	2022	ART1 utilizes free nicotinamide adenine dinucleotide (NAD+) in the tumor microenvironment (TME) to mono-ADP-ribosylate (MARylate) the P2X7 receptor (P2X7R) on CD8 T cells, resulting in NAD-induced cell death (NICD) and tumor immune resistance.	NAD	19-52	ADP-ribosyltransferase 1	Homo sapiens	0-4
35602287-2	2022	ART1 utilizes free nicotinamide adenine dinucleotide (NAD+) in the tumor microenvironment (TME) to mono-ADP-ribosylate (MARylate) the P2X7 receptor (P2X7R) on CD8 T cells, resulting in NAD-induced cell death (NICD) and tumor immune resistance.	NAD	19-52	purinergic receptor P2X 7	Homo sapiens	149-154
35625870-6	2022	A negative correlation between age and the NAD levels among the control group was observed, however among the patients the relationship was diminished.	NAD	43-46	renin binding protein	Homo sapiens	31-34
35602287-2	2022	ART1 utilizes free nicotinamide adenine dinucleotide (NAD+) in the tumor microenvironment (TME) to mono-ADP-ribosylate (MARylate) the P2X7 receptor (P2X7R) on CD8 T cells, resulting in NAD-induced cell death (NICD) and tumor immune resistance.	NAD	54-58	ADP-ribosyltransferase 1	Homo sapiens	0-4
35602287-2	2022	ART1 utilizes free nicotinamide adenine dinucleotide (NAD+) in the tumor microenvironment (TME) to mono-ADP-ribosylate (MARylate) the P2X7 receptor (P2X7R) on CD8 T cells, resulting in NAD-induced cell death (NICD) and tumor immune resistance.	NAD	54-58	purinergic receptor P2X 7	Homo sapiens	134-147
35602287-2	2022	ART1 utilizes free nicotinamide adenine dinucleotide (NAD+) in the tumor microenvironment (TME) to mono-ADP-ribosylate (MARylate) the P2X7 receptor (P2X7R) on CD8 T cells, resulting in NAD-induced cell death (NICD) and tumor immune resistance.	NAD	54-58	purinergic receptor P2X 7	Homo sapiens	149-154
35602287-2	2022	ART1 utilizes free nicotinamide adenine dinucleotide (NAD+) in the tumor microenvironment (TME) to mono-ADP-ribosylate (MARylate) the P2X7 receptor (P2X7R) on CD8 T cells, resulting in NAD-induced cell death (NICD) and tumor immune resistance.	NAD	185-188	ADP-ribosyltransferase 1	Homo sapiens	0-4
35602287-2	2022	ART1 utilizes free nicotinamide adenine dinucleotide (NAD+) in the tumor microenvironment (TME) to mono-ADP-ribosylate (MARylate) the P2X7 receptor (P2X7R) on CD8 T cells, resulting in NAD-induced cell death (NICD) and tumor immune resistance.	NAD	185-188	purinergic receptor P2X 7	Homo sapiens	134-147
35602287-2	2022	ART1 utilizes free nicotinamide adenine dinucleotide (NAD+) in the tumor microenvironment (TME) to mono-ADP-ribosylate (MARylate) the P2X7 receptor (P2X7R) on CD8 T cells, resulting in NAD-induced cell death (NICD) and tumor immune resistance.	NAD	185-188	purinergic receptor P2X 7	Homo sapiens	149-154
35610161-11	2022	SLC12A6 was the most highly expressed gene among the SLC12A family members in melanocytes and was significantly influenced by NMN or NAD+ treatment, indicating that SLC12A6 protein is an NMN transporter in melanocytes.	NAD	133-137	solute carrier family 12 member 6	Homo sapiens	0-7
35545049-3	2022	Here we show that tumor-secreted lactate downregulates p62 transcriptionally through a mechanism involving reduction of the NAD+/NADH ratio, which impairs poly(ADP-ribose)-polymerase 1 (PARP-1) activity.	NAD	124-128	poly(ADP-ribose) polymerase 1	Homo sapiens	155-184
35545049-3	2022	Here we show that tumor-secreted lactate downregulates p62 transcriptionally through a mechanism involving reduction of the NAD+/NADH ratio, which impairs poly(ADP-ribose)-polymerase 1 (PARP-1) activity.	NAD	124-128	poly(ADP-ribose) polymerase 1	Homo sapiens	186-192
35545049-3	2022	Here we show that tumor-secreted lactate downregulates p62 transcriptionally through a mechanism involving reduction of the NAD+/NADH ratio, which impairs poly(ADP-ribose)-polymerase 1 (PARP-1) activity.	NAD	129-133	poly(ADP-ribose) polymerase 1	Homo sapiens	155-184
35545049-3	2022	Here we show that tumor-secreted lactate downregulates p62 transcriptionally through a mechanism involving reduction of the NAD+/NADH ratio, which impairs poly(ADP-ribose)-polymerase 1 (PARP-1) activity.	NAD	129-133	poly(ADP-ribose) polymerase 1	Homo sapiens	186-192
35610161-11	2022	SLC12A6 was the most highly expressed gene among the SLC12A family members in melanocytes and was significantly influenced by NMN or NAD+ treatment, indicating that SLC12A6 protein is an NMN transporter in melanocytes.	NAD	133-137	solute carrier family 12 member 6	Homo sapiens	165-172
35500221-8	2022	These data identify an IFNgamma-induced, NAMPT-dependent, NAD+ salvage pathway that is critical for IFNgamma activation of human monocytes.	NAD	58-62	interferon gamma	Homo sapiens	23-31
35491967-1	2022	Congenital nicotinamide adenine dinucleotide (NAD) deficiency disorders are associated with pathogenic variants in the genes NADSYN1, HAAO, and KYNU.	NAD	11-44	kynureninase	Homo sapiens	144-148
35500221-8	2022	These data identify an IFNgamma-induced, NAMPT-dependent, NAD+ salvage pathway that is critical for IFNgamma activation of human monocytes.	NAD	58-62	interferon gamma	Homo sapiens	100-108
35500221-0	2022	IFNgamma Regulates NAD+ Metabolism to Promote the Respiratory Burst in Human Monocytes.	NAD	19-23	interferon gamma	Homo sapiens	0-8
35571098-3	2022	As a major mitochondrial NAD+-dependent deacetylase, sirtuin3 (SIRT3) deacetylates and regulates the enzymes involved in regulating mitochondrial energy metabolism, including fatty acid oxidation, the Krebs cycle, and the respiratory chain to maintain metabolic homeostasis.	NAD	25-28	sirtuin 3	Homo sapiens	53-61
35500221-4	2022	Transcriptional profiling revealed that this oxidative phenotype was driven by IFNgamma-induced reprogramming of NAD+ metabolism, which is dependent on nicotinamide phosphoribosyltransferase (NAMPT)-mediated NAD+ salvage to generate NADH and NADPH for oxidation by mitochondrial complex I and NADPH oxidase, respectively.	NAD	113-117	interferon gamma	Homo sapiens	79-87
35500221-4	2022	Transcriptional profiling revealed that this oxidative phenotype was driven by IFNgamma-induced reprogramming of NAD+ metabolism, which is dependent on nicotinamide phosphoribosyltransferase (NAMPT)-mediated NAD+ salvage to generate NADH and NADPH for oxidation by mitochondrial complex I and NADPH oxidase, respectively.	NAD	208-212	interferon gamma	Homo sapiens	79-87
35500221-4	2022	Transcriptional profiling revealed that this oxidative phenotype was driven by IFNgamma-induced reprogramming of NAD+ metabolism, which is dependent on nicotinamide phosphoribosyltransferase (NAMPT)-mediated NAD+ salvage to generate NADH and NADPH for oxidation by mitochondrial complex I and NADPH oxidase, respectively.	NAD	233-237	interferon gamma	Homo sapiens	79-87
35227738-8	2022	Biochemical assays confirmed depletion of NAD in WT and Nrf2 KO cells due to H2O2 treatment.	NAD	42-45	NFE2 like bZIP transcription factor 2	Homo sapiens	56-60
35227738-9	2022	These data support that although Nrf2 deficiency caused baseline activation of the pentose phosphate pathway and sugar alcohol synthesis, a brief exposure to none-lethal doses of H2O2 caused NAD depletion in an Nrf2 independent manner.	NAD	191-194	NFE2 like bZIP transcription factor 2	Homo sapiens	33-37
35227738-9	2022	These data support that although Nrf2 deficiency caused baseline activation of the pentose phosphate pathway and sugar alcohol synthesis, a brief exposure to none-lethal doses of H2O2 caused NAD depletion in an Nrf2 independent manner.	NAD	191-194	NFE2 like bZIP transcription factor 2	Homo sapiens	211-215
35563783-2	2022	Sirt6 is an NAD+-dependent deacetylase and mono-ADP ribosyltransferase known to play diverse roles in the processes attendant to aging, metabolism, and carcinogenesis.	NAD	12-15	sirtuin 6	Mus musculus	0-5
35571098-3	2022	As a major mitochondrial NAD+-dependent deacetylase, sirtuin3 (SIRT3) deacetylates and regulates the enzymes involved in regulating mitochondrial energy metabolism, including fatty acid oxidation, the Krebs cycle, and the respiratory chain to maintain metabolic homeostasis.	NAD	25-28	sirtuin 3	Homo sapiens	63-68
35479740-3	2022	NAD+ also serves as the substrate for poly(ADP-ribose) polymerase (PARP) and sirtuins, and regulates various biological processes, such as metabolism, DNA repair, gene expression, and stress responses.	NAD	0-4	poly(ADP-ribose) polymerase 1	Homo sapiens	38-65
35629880-11	2022	Once formed, cis-3MGCylated proteins can be deacylated by the NAD+-dependent enzyme, sirtuin 4.	NAD	62-65	sirtuin 4	Homo sapiens	85-94
35410407-6	2022	Under both weak and strong H2O2 stimulation, intracellular nicotinamide adenine dinucleotide (NAD+) was depleted to a similar extent by poly (ADP-ribose) (PAR) polymerase 1 (PARP1)-dependent consumption.	NAD	59-92	poly(ADP-ribose) polymerase 1	Homo sapiens	174-179
35410407-6	2022	Under both weak and strong H2O2 stimulation, intracellular nicotinamide adenine dinucleotide (NAD+) was depleted to a similar extent by poly (ADP-ribose) (PAR) polymerase 1 (PARP1)-dependent consumption.	NAD	94-98	poly(ADP-ribose) polymerase 1	Homo sapiens	174-179
35410407-10	2022	Collectively, these findings suggest that NAD+ dynamics balanced by PARP1-dependent consumption and NAMPT-dependent production are important to determine the form of cell death activated under oxidative stress.	NAD	42-46	poly(ADP-ribose) polymerase 1	Homo sapiens	68-73
35445486-6	2022	The SJ 6-nFe3 O4 system performed the light reaction of photosynthesis as confirmed by the reduction of 1 mM NAD+ to 0.180 mM NADH upon exposure to visible light (Xe lamp lambda > 420 nm) for 1 h. The photochemical regeneration of NADH using the SJ 6-nFe3 O4 system was coupled to glutamate dehydrogenase-catalyzed conversion of alpha-ketoglutarate to L-glutamate.	NAD	109-113	nuclear receptor subfamily 2 group F member 2	Homo sapiens	9-13
35445486-6	2022	The SJ 6-nFe3 O4 system performed the light reaction of photosynthesis as confirmed by the reduction of 1 mM NAD+ to 0.180 mM NADH upon exposure to visible light (Xe lamp lambda > 420 nm) for 1 h. The photochemical regeneration of NADH using the SJ 6-nFe3 O4 system was coupled to glutamate dehydrogenase-catalyzed conversion of alpha-ketoglutarate to L-glutamate.	NAD	109-113	nuclear receptor subfamily 2 group F member 2	Homo sapiens	251-255
35445486-6	2022	The SJ 6-nFe3 O4 system performed the light reaction of photosynthesis as confirmed by the reduction of 1 mM NAD+ to 0.180 mM NADH upon exposure to visible light (Xe lamp lambda > 420 nm) for 1 h. The photochemical regeneration of NADH using the SJ 6-nFe3 O4 system was coupled to glutamate dehydrogenase-catalyzed conversion of alpha-ketoglutarate to L-glutamate.	NAD	126-130	nuclear receptor subfamily 2 group F member 2	Homo sapiens	9-13
35445486-6	2022	The SJ 6-nFe3 O4 system performed the light reaction of photosynthesis as confirmed by the reduction of 1 mM NAD+ to 0.180 mM NADH upon exposure to visible light (Xe lamp lambda > 420 nm) for 1 h. The photochemical regeneration of NADH using the SJ 6-nFe3 O4 system was coupled to glutamate dehydrogenase-catalyzed conversion of alpha-ketoglutarate to L-glutamate.	NAD	126-130	nuclear receptor subfamily 2 group F member 2	Homo sapiens	251-255
35445486-6	2022	The SJ 6-nFe3 O4 system performed the light reaction of photosynthesis as confirmed by the reduction of 1 mM NAD+ to 0.180 mM NADH upon exposure to visible light (Xe lamp lambda > 420 nm) for 1 h. The photochemical regeneration of NADH using the SJ 6-nFe3 O4 system was coupled to glutamate dehydrogenase-catalyzed conversion of alpha-ketoglutarate to L-glutamate.	NAD	231-235	nuclear receptor subfamily 2 group F member 2	Homo sapiens	9-13
35479740-3	2022	NAD+ also serves as the substrate for poly(ADP-ribose) polymerase (PARP) and sirtuins, and regulates various biological processes, such as metabolism, DNA repair, gene expression, and stress responses.	NAD	0-4	poly(ADP-ribose) polymerase 1	Homo sapiens	67-71
35455963-0	2022	NAD+ Modulates the Proliferation and Differentiation of Adult Neural Stem/Progenitor Cells via Akt Signaling Pathway.	NAD	0-4	AKT serine/threonine kinase 1	Homo sapiens	95-98
35547746-8	2022	These beneficial effects of NAD+ precursors, however, were attenuated in mast cell-specific Sirt6 knockout mice, indicating a Sirt6 dependency for their action.	NAD	28-32	sirtuin 6	Mus musculus	92-97
35547746-8	2022	These beneficial effects of NAD+ precursors, however, were attenuated in mast cell-specific Sirt6 knockout mice, indicating a Sirt6 dependency for their action.	NAD	28-32	sirtuin 6	Mus musculus	126-131
35455963-6	2022	NAD+ exposure significantly decreases the expression of multiple genes related to ATP metabolism and the PI3k-Akt signaling pathway.	NAD	0-4	AKT serine/threonine kinase 1	Homo sapiens	110-113
35453414-7	2022	The SOD and POX activities appeared closely related, and related to the NADH oxidation and the amount of O2-.	NAD	72-76	superoxide dismutase 1	Homo sapiens	4-7
35393510-0	2022	Tumor growth of neurofibromin-deficient cells is driven by decreased respiration and hampered by NAD+ and SIRT3.	NAD	97-101	neurofibromin 1	Homo sapiens	16-29
35393510-2	2022	Here we report that neurofibromin ablation dampens expression and activity of NADH dehydrogenase, the respiratory chain complex I, in an ERK-dependent fashion, decreasing both respiration and intracellular NAD+.	NAD	206-210	mitogen-activated protein kinase 1	Homo sapiens	137-140
35393510-2	2022	Here we report that neurofibromin ablation dampens expression and activity of NADH dehydrogenase, the respiratory chain complex I, in an ERK-dependent fashion, decreasing both respiration and intracellular NAD+.	NAD	206-210	neurofibromin 1	Homo sapiens	20-33
35114390-6	2022	We next demonstrate that AAV2 intravitreal injection-mediated overexpression of long half-life NMNAT2 mutant driven by RGC-specific mouse gamma-synuclein (mSncg) promoter restores decreased NAD+ levels in glaucomatous RGCs and ONs.	NAD	190-194	nicotinamide nucleotide adenylyltransferase 2	Homo sapiens	95-101
35463964-1	2022	Human alpha-amino-beta-carboxymuconate-epsilon-semialdehyde decarboxylase (ACMSD) stands at a branch point of the de novo NAD+ synthesis pathway and plays an important role in maintaining NAD+ homeostasis.	NAD	122-126	aminocarboxymuconate semialdehyde decarboxylase	Homo sapiens	75-80
35463964-1	2022	Human alpha-amino-beta-carboxymuconate-epsilon-semialdehyde decarboxylase (ACMSD) stands at a branch point of the de novo NAD+ synthesis pathway and plays an important role in maintaining NAD+ homeostasis.	NAD	188-192	aminocarboxymuconate semialdehyde decarboxylase	Homo sapiens	75-80
35385122-4	2022	Here, we demonstrate the important role of NADP+ supply for the biogenesis of PSI by examining the nad kinase 2 (nadk2) mutant in Arabidopsis (Arabidopsis thaliana), which demonstrates disrupted synthesis of NADP+ from NAD+ in chloroplasts.	NAD	219-223	NAD kinase 2	Arabidopsis thaliana	99-111
35385122-4	2022	Here, we demonstrate the important role of NADP+ supply for the biogenesis of PSI by examining the nad kinase 2 (nadk2) mutant in Arabidopsis (Arabidopsis thaliana), which demonstrates disrupted synthesis of NADP+ from NAD+ in chloroplasts.	NAD	219-223	NAD kinase 2	Arabidopsis thaliana	113-118
35393510-5	2022	These findings shed light on bioenergetic adaptations of tumors lacking neurofibromin, linking complex I inhibition to mitochondrial NAD+/NADH unbalance and SIRT3 inhibition, as well as to down-regulation of succinate dehydrogenase.	NAD	133-137	neurofibromin 1	Homo sapiens	72-85
35393510-5	2022	These findings shed light on bioenergetic adaptations of tumors lacking neurofibromin, linking complex I inhibition to mitochondrial NAD+/NADH unbalance and SIRT3 inhibition, as well as to down-regulation of succinate dehydrogenase.	NAD	138-142	neurofibromin 1	Homo sapiens	72-85
35114390-6	2022	We next demonstrate that AAV2 intravitreal injection-mediated overexpression of long half-life NMNAT2 mutant driven by RGC-specific mouse gamma-synuclein (mSncg) promoter restores decreased NAD+ levels in glaucomatous RGCs and ONs.	NAD	190-194	synuclein, gamma	Mus musculus	138-153
35114390-8	2022	Collectively, our studies suggest that the weakening of NMNAT2 expression in glaucomatous RGCs contributes to a deleterious NAD+ decline and that modulating RGC intrinsic NMNAT2 levels by AAV2-mSncg vector is a promising gene therapy for glaucomatous neurodegeneration.	NAD	124-128	nicotinamide nucleotide adenylyltransferase 2	Homo sapiens	56-62
35453391-6	2022	In human umbilical vein endothelial cells, SIRT3 silencing potentiated the induction of inflammatory factors by IL-1beta, including VCAM-1, ICAM-1, and MCP1, and the impairment of mitochondrial respiration, both of which were alleviated by NAD+ treatment.	NAD	240-244	sirtuin 3	Homo sapiens	43-48
35139656-0	2022	NAD+ Levels Are Augmented in Aortic Tissue of ApoE-/- Mice by Dietary Omega-3 Fatty Acids.	NAD	0-4	apolipoprotein E	Mus musculus	46-50
35218657-2	2022	Here, we tested the hypothesis that nicotinamide phosphoribosyltransferase (NAMPT), which mediates the biosynthesis of nicotinamide adenine dinucleotide (NAD +), a key regulator of cellular energy metabolism, plays a critical role in obesity-associated intestinal pathophysiology and systemic metabolic complications.	NAD	119-152	nicotinamide phosphoribosyltransferase	Mus musculus	36-74
35443857-2	2022	It was reported that macrophages have an important function in synovial inflammation, and our team revealed that the amounts of Sirt6, a nicotinamide adenine dinucleotide (NAD)+-dependent histone deacetylase, decrease during synovial inflammation and osteoarthritis.	NAD	137-170	sirtuin 6	Mus musculus	128-133
35443857-2	2022	It was reported that macrophages have an important function in synovial inflammation, and our team revealed that the amounts of Sirt6, a nicotinamide adenine dinucleotide (NAD)+-dependent histone deacetylase, decrease during synovial inflammation and osteoarthritis.	NAD	172-175	sirtuin 6	Mus musculus	128-133
35218657-2	2022	Here, we tested the hypothesis that nicotinamide phosphoribosyltransferase (NAMPT), which mediates the biosynthesis of nicotinamide adenine dinucleotide (NAD +), a key regulator of cellular energy metabolism, plays a critical role in obesity-associated intestinal pathophysiology and systemic metabolic complications.	NAD	119-152	nicotinamide phosphoribosyltransferase	Mus musculus	76-81
35218657-2	2022	Here, we tested the hypothesis that nicotinamide phosphoribosyltransferase (NAMPT), which mediates the biosynthesis of nicotinamide adenine dinucleotide (NAD +), a key regulator of cellular energy metabolism, plays a critical role in obesity-associated intestinal pathophysiology and systemic metabolic complications.	NAD	154-159	nicotinamide phosphoribosyltransferase	Mus musculus	36-74
35218657-2	2022	Here, we tested the hypothesis that nicotinamide phosphoribosyltransferase (NAMPT), which mediates the biosynthesis of nicotinamide adenine dinucleotide (NAD +), a key regulator of cellular energy metabolism, plays a critical role in obesity-associated intestinal pathophysiology and systemic metabolic complications.	NAD	154-159	nicotinamide phosphoribosyltransferase	Mus musculus	76-81
35218657-6	2022	We also found that diet-induced obese mice had compromised intestinal NAMPT-mediated NAD + biosynthesis and the Wnt signaling pathway, associated with impaired GLP-1 production and whole-body glucose metabolism, resembling the INKO mice.	NAD	85-90	nicotinamide phosphoribosyltransferase	Mus musculus	70-75
35060352-1	2022	BACKGROUND: Nicotinamide phosphoribosyltransferase (Nampt), a key enzyme in NAD salvage pathway is decreased in metabolic diseases, and its precise role in skeletal muscle function is not known.	NAD	76-79	nicotinamide phosphoribosyltransferase	Mus musculus	12-50
35060352-1	2022	BACKGROUND: Nicotinamide phosphoribosyltransferase (Nampt), a key enzyme in NAD salvage pathway is decreased in metabolic diseases, and its precise role in skeletal muscle function is not known.	NAD	76-79	nicotinamide phosphoribosyltransferase	Mus musculus	52-57
35318613-5	2022	In this report, we identify a crucial role for the NAD+-dependent histone deacetylase Sirtuin 1 (Sirt1) downstream of PKA and CREB in dmPGE2-dependent radioprotection of hematopoietic cells.	NAD	51-55	cAMP responsive element binding protein 1	Mus musculus	126-130
35137552-7	2022	Inhibition of SIRT1 blunted the protective effect of NAD+ and up-regulated the activity of glycogen synthase kinase-3beta (GSK-3beta) that was concomitant with mitigated Nrf2 nuclear accumulation, thereby exacerbates AKI.	NAD	53-57	NFE2 like bZIP transcription factor 2	Homo sapiens	170-174
35063804-1	2022	Nicotinamide phosphoribosyltransferase (NAMPT) is the rate-limiting enzyme in the nicotinamide adenine dinucleotide (NAD+) salvage pathway and plays a crucial role in the maintenance of the NAD+ pool during inflammation.	NAD	82-115	nicotinamide phosphoribosyltransferase	Mus musculus	40-45
35063804-1	2022	Nicotinamide phosphoribosyltransferase (NAMPT) is the rate-limiting enzyme in the nicotinamide adenine dinucleotide (NAD+) salvage pathway and plays a crucial role in the maintenance of the NAD+ pool during inflammation.	NAD	117-121	nicotinamide phosphoribosyltransferase	Mus musculus	0-38
35063804-1	2022	Nicotinamide phosphoribosyltransferase (NAMPT) is the rate-limiting enzyme in the nicotinamide adenine dinucleotide (NAD+) salvage pathway and plays a crucial role in the maintenance of the NAD+ pool during inflammation.	NAD	117-121	nicotinamide phosphoribosyltransferase	Mus musculus	40-45
35063804-1	2022	Nicotinamide phosphoribosyltransferase (NAMPT) is the rate-limiting enzyme in the nicotinamide adenine dinucleotide (NAD+) salvage pathway and plays a crucial role in the maintenance of the NAD+ pool during inflammation.	NAD	190-194	nicotinamide phosphoribosyltransferase	Mus musculus	0-38
35063804-1	2022	Nicotinamide phosphoribosyltransferase (NAMPT) is the rate-limiting enzyme in the nicotinamide adenine dinucleotide (NAD+) salvage pathway and plays a crucial role in the maintenance of the NAD+ pool during inflammation.	NAD	190-194	nicotinamide phosphoribosyltransferase	Mus musculus	40-45
35063804-4	2022	Nampt-deficient macrophages exhibit reduced phagocytic activity due to insufficient NAD+ abundance, which is required to produce NADPH for the oxidative burst.	NAD	84-88	nicotinamide phosphoribosyltransferase	Mus musculus	0-5
35063804-8	2022	Collectively, our findings suggest that activation of the NAMPT-dependent NAD+ biosynthetic pathway, via NMN administration, is a potential therapeutic strategy for managing inflammatory diseases.	NAD	74-78	nicotinamide phosphoribosyltransferase	Mus musculus	58-63
35137552-0	2022	NAD+ ameliorates endotoxin-induced acute kidney injury in a sirtuin1-dependent manner via GSK-3beta/Nrf2 signalling pathway.	NAD	0-4	NFE2 like bZIP transcription factor 2	Homo sapiens	100-104
35134563-6	2022	ATP and NADH, derivatives of adenosine, inhibit insulin signaling inside cells by downregulation of activities of AMPK and SIRT1, respectively.	NAD	8-12	insulin	Homo sapiens	48-55
35134563-8	2022	Current evidence suggests that ATP, NADH, cGAMP and uridine are potential biomarkers of insulin resistance.	NAD	36-40	insulin	Homo sapiens	88-95
35063804-1	2022	Nicotinamide phosphoribosyltransferase (NAMPT) is the rate-limiting enzyme in the nicotinamide adenine dinucleotide (NAD+) salvage pathway and plays a crucial role in the maintenance of the NAD+ pool during inflammation.	NAD	82-115	nicotinamide phosphoribosyltransferase	Mus musculus	0-38
35354042-5	2022	Interestingly, we find that PTIP deletion impairs the proinflammatory response of primary murine and human macrophages, promotes their metabolic switch from glycolysis to oxidative phosphorylation, and alters NAD+ metabolism via downregulating CD38 expression.	NAD	209-213	PAX interacting (with transcription-activation domain) protein 1	Mus musculus	28-32
35143783-3	2022	The kinetic expression for alcohol dehydrogenase takes into account inhibition by ethanol and NADH.	NAD	94-98	aldo-keto reductase family 1 member A1	Rattus norvegicus	27-48
35298165-3	2022	Glucose dehydrogenase (GDH) with 18.13-fold higher activity than FDH was used for reconstructing a cofactor self-sufficient system, which was combined with the overexpression of the rate-limiting genes involved in NAD+ salvage metabolic flow to expand the available intracellular NAD(H) pool.	NAD	214-218	aldehyde dehydrogenase 1 family member L1	Homo sapiens	65-68
35298165-3	2022	Glucose dehydrogenase (GDH) with 18.13-fold higher activity than FDH was used for reconstructing a cofactor self-sufficient system, which was combined with the overexpression of the rate-limiting genes involved in NAD+ salvage metabolic flow to expand the available intracellular NAD(H) pool.	NAD	280-286	aldehyde dehydrogenase 1 family member L1	Homo sapiens	65-68
35296687-5	2022	The Spt-Ada-Gcn5 acetyltransferase (SAGA) complex and NAD+-dependent histone deacetylase Hst2 could function as the writer and eraser of histone Kbz, respectively.	NAD	54-57	histone deacetylase HST2	Saccharomyces cerevisiae S288C	89-93
35399501-8	2022	Interestingly, AZD5153 treatment upregulated NAMPT, whose product is the rate-limiting enzyme for NAD+ synthesis from nicotinamide.	NAD	98-102	nicotinamide phosphoribosyltransferase	Mus musculus	45-50
35408818-4	2022	Here our study found that the disruption of NAD+ anabolism homeostasis caused an elevation in both oxidative stress and fibronectin expression, along with a decrease in Sirt1 and an increase in both NF-kappaB P65 expression and acetylation, culminating in extracellular matrix deposition and globular fibrosis in DN.	NAD	44-48	fibronectin 1	Homo sapiens	120-131
35388296-2	2022	We aimed to investigate the association between human whole blood NAD+ contents and aging in a relative large-scale community-based population and further to address the gender impact on this association.	NAD	66-70	ATPase H+ transporting V0 subunit a2	Homo sapiens	93-94
35388296-13	2022	We observed a decline trend of NAD+ contents with aging before 50 years in total participants with significant level in 40-49 years old group (beta coefficients with 95% confidence interval (95% CI): -1.12 (-2.18, -0.06)), while this trend disappeared after the 50 years.	NAD	31-35	ATPase H+ transporting V0 subunit a2	Homo sapiens	12-13
35419389-4	2022	Here, we identify PPARalpha as a deacetylation target of the NAD-dependent deacetylase sirtuin-1 (SIRT1) and link this to the decrease in PPARalpha protein levels in undernourished liver.	NAD	61-64	peroxisome proliferator activated receptor alpha	Mus musculus	18-27
35419389-4	2022	Here, we identify PPARalpha as a deacetylation target of the NAD-dependent deacetylase sirtuin-1 (SIRT1) and link this to the decrease in PPARalpha protein levels in undernourished liver.	NAD	61-64	peroxisome proliferator activated receptor alpha	Mus musculus	138-147
35369299-4	2022	Sirtuin 3 (SIRT3) is one of the seven mammalian sirtuins (SIRT1 to SIRT7), with NAD+ dependent deacetylase activity.	NAD	80-83	sirtuin 3	Homo sapiens	0-9
35369299-4	2022	Sirtuin 3 (SIRT3) is one of the seven mammalian sirtuins (SIRT1 to SIRT7), with NAD+ dependent deacetylase activity.	NAD	80-83	sirtuin 3	Homo sapiens	11-16
35294260-2	2022	Nicotinamide adenine dinucleotide (NAD)-induced cell death (NICD) of P2X7 receptor (P2X7R)-expressing T cells regulates immune homeostasis in inflamed tissues.	NAD	0-33	purinergic receptor P2X 7	Homo sapiens	69-82
35294260-2	2022	Nicotinamide adenine dinucleotide (NAD)-induced cell death (NICD) of P2X7 receptor (P2X7R)-expressing T cells regulates immune homeostasis in inflamed tissues.	NAD	0-33	purinergic receptor P2X 7	Homo sapiens	84-89
35294260-2	2022	Nicotinamide adenine dinucleotide (NAD)-induced cell death (NICD) of P2X7 receptor (P2X7R)-expressing T cells regulates immune homeostasis in inflamed tissues.	NAD	35-38	purinergic receptor P2X 7	Homo sapiens	69-82
35294260-2	2022	Nicotinamide adenine dinucleotide (NAD)-induced cell death (NICD) of P2X7 receptor (P2X7R)-expressing T cells regulates immune homeostasis in inflamed tissues.	NAD	35-38	purinergic receptor P2X 7	Homo sapiens	84-89
35264567-5	2022	We show that the effects on myelination are mediated via the NAD+-SIRT2-H3K18Ac-ID4 axis, and SIRT2 is required for rejuvenating OPCs.	NAD	61-65	inhibitor of DNA binding 4	Mus musculus	80-83
35294260-6	2022	In vitro, P2X7R+ CD8 T cells were susceptible to ART1-mediated ADP-ribosylation and NICD, which was exacerbated upon blockade of the NAD+-degrading ADP-ribosyl cyclase CD38.	NAD	133-137	purinergic receptor P2X 7	Homo sapiens	10-15
35277554-7	2022	Our results show that metabolomic defects occur early in ALS motor cortex and establishing NAD+ balance could offer therapeutic benefit to UMNs with TDP-43 pathology.	NAD	91-95	TAR DNA binding protein	Mus musculus	149-155
35386537-4	2022	During the innate immune response, poly-ADP-ribose polymerase hyperactivated due to virus entry and extensive DNA damage sequentially, leading to nicotinamide adenine dinucleotide (NAD)+ depletion, adenosine triphosphate depletion, and finally cell death.	NAD	146-179	poly(ADP-ribose) polymerase 1	Homo sapiens	35-61
35269514-4	2022	The HO-1-Tom20 axis induced an increase in mitochondrial functions, detected with cytochrome c oxidase subunit 2 and cytochrome c. HO-1 crosstalk with nicotinamide phosphoribosyltransferase was concomitant with the upregulated nicotinamide adenine dinucleotide (NAD)/NADH ratio, thereby upregulating NAD-dependent class I sirtuins.	NAD	300-303	translocase of outer mitochondrial membrane 20	Mus musculus	9-14
35269514-4	2022	The HO-1-Tom20 axis induced an increase in mitochondrial functions, detected with cytochrome c oxidase subunit 2 and cytochrome c. HO-1 crosstalk with nicotinamide phosphoribosyltransferase was concomitant with the upregulated nicotinamide adenine dinucleotide (NAD)/NADH ratio, thereby upregulating NAD-dependent class I sirtuins.	NAD	300-303	heme oxygenase 1	Mus musculus	131-135
35269514-4	2022	The HO-1-Tom20 axis induced an increase in mitochondrial functions, detected with cytochrome c oxidase subunit 2 and cytochrome c. HO-1 crosstalk with nicotinamide phosphoribosyltransferase was concomitant with the upregulated nicotinamide adenine dinucleotide (NAD)/NADH ratio, thereby upregulating NAD-dependent class I sirtuins.	NAD	227-260	heme oxygenase 1	Mus musculus	4-8
35269514-4	2022	The HO-1-Tom20 axis induced an increase in mitochondrial functions, detected with cytochrome c oxidase subunit 2 and cytochrome c. HO-1 crosstalk with nicotinamide phosphoribosyltransferase was concomitant with the upregulated nicotinamide adenine dinucleotide (NAD)/NADH ratio, thereby upregulating NAD-dependent class I sirtuins.	NAD	227-260	translocase of outer mitochondrial membrane 20	Mus musculus	9-14
35269514-4	2022	The HO-1-Tom20 axis induced an increase in mitochondrial functions, detected with cytochrome c oxidase subunit 2 and cytochrome c. HO-1 crosstalk with nicotinamide phosphoribosyltransferase was concomitant with the upregulated nicotinamide adenine dinucleotide (NAD)/NADH ratio, thereby upregulating NAD-dependent class I sirtuins.	NAD	227-260	heme oxygenase 1	Mus musculus	131-135
35269514-4	2022	The HO-1-Tom20 axis induced an increase in mitochondrial functions, detected with cytochrome c oxidase subunit 2 and cytochrome c. HO-1 crosstalk with nicotinamide phosphoribosyltransferase was concomitant with the upregulated nicotinamide adenine dinucleotide (NAD)/NADH ratio, thereby upregulating NAD-dependent class I sirtuins.	NAD	262-265	heme oxygenase 1	Mus musculus	4-8
35269514-4	2022	The HO-1-Tom20 axis induced an increase in mitochondrial functions, detected with cytochrome c oxidase subunit 2 and cytochrome c. HO-1 crosstalk with nicotinamide phosphoribosyltransferase was concomitant with the upregulated nicotinamide adenine dinucleotide (NAD)/NADH ratio, thereby upregulating NAD-dependent class I sirtuins.	NAD	262-265	translocase of outer mitochondrial membrane 20	Mus musculus	9-14
35269514-4	2022	The HO-1-Tom20 axis induced an increase in mitochondrial functions, detected with cytochrome c oxidase subunit 2 and cytochrome c. HO-1 crosstalk with nicotinamide phosphoribosyltransferase was concomitant with the upregulated nicotinamide adenine dinucleotide (NAD)/NADH ratio, thereby upregulating NAD-dependent class I sirtuins.	NAD	262-265	heme oxygenase 1	Mus musculus	131-135
35269514-4	2022	The HO-1-Tom20 axis induced an increase in mitochondrial functions, detected with cytochrome c oxidase subunit 2 and cytochrome c. HO-1 crosstalk with nicotinamide phosphoribosyltransferase was concomitant with the upregulated nicotinamide adenine dinucleotide (NAD)/NADH ratio, thereby upregulating NAD-dependent class I sirtuins.	NAD	267-271	heme oxygenase 1	Mus musculus	4-8
35269514-4	2022	The HO-1-Tom20 axis induced an increase in mitochondrial functions, detected with cytochrome c oxidase subunit 2 and cytochrome c. HO-1 crosstalk with nicotinamide phosphoribosyltransferase was concomitant with the upregulated nicotinamide adenine dinucleotide (NAD)/NADH ratio, thereby upregulating NAD-dependent class I sirtuins.	NAD	267-271	translocase of outer mitochondrial membrane 20	Mus musculus	9-14
35269514-4	2022	The HO-1-Tom20 axis induced an increase in mitochondrial functions, detected with cytochrome c oxidase subunit 2 and cytochrome c. HO-1 crosstalk with nicotinamide phosphoribosyltransferase was concomitant with the upregulated nicotinamide adenine dinucleotide (NAD)/NADH ratio, thereby upregulating NAD-dependent class I sirtuins.	NAD	267-271	heme oxygenase 1	Mus musculus	131-135
35269514-4	2022	The HO-1-Tom20 axis induced an increase in mitochondrial functions, detected with cytochrome c oxidase subunit 2 and cytochrome c. HO-1 crosstalk with nicotinamide phosphoribosyltransferase was concomitant with the upregulated nicotinamide adenine dinucleotide (NAD)/NADH ratio, thereby upregulating NAD-dependent class I sirtuins.	NAD	300-303	heme oxygenase 1	Mus musculus	4-8
35386537-4	2022	During the innate immune response, poly-ADP-ribose polymerase hyperactivated due to virus entry and extensive DNA damage sequentially, leading to nicotinamide adenine dinucleotide (NAD)+ depletion, adenosine triphosphate depletion, and finally cell death.	NAD	181-184	poly(ADP-ribose) polymerase 1	Homo sapiens	35-61
35250263-9	2022	MG can significantly inhibit the activity of AChE and increase the level of NAD+, thereby further up-regulated the expression levels of alpha7nAChR and SIRT1.	NAD	76-80	sirtuin 1	Rattus norvegicus	152-157
35228549-2	2022	Nicotinamide phosphoribosyltransferase (NAMPT) is rate-limiting in NAD+ salvage, yet hepatocyte NAMPT actions during fasting and metabolic duress remain unclear.	NAD	67-71	nicotinamide phosphoribosyltransferase	Mus musculus	0-38
35228549-2	2022	Nicotinamide phosphoribosyltransferase (NAMPT) is rate-limiting in NAD+ salvage, yet hepatocyte NAMPT actions during fasting and metabolic duress remain unclear.	NAD	67-71	nicotinamide phosphoribosyltransferase	Mus musculus	40-45
35228549-2	2022	Nicotinamide phosphoribosyltransferase (NAMPT) is rate-limiting in NAD+ salvage, yet hepatocyte NAMPT actions during fasting and metabolic duress remain unclear.	NAD	67-71	nicotinamide phosphoribosyltransferase	Mus musculus	96-101
35337091-8	2022	To explain the underlying pharmacological actions of YJT, we focused on a representative epigenetic regulator, a nicotinamide adenine dinucleotide + (NAD+)-dependent chromatin enzyme, Sirtuin 6 (Sirt6).	NAD	113-146	sirtuin 6	Mus musculus	184-193
35337091-8	2022	To explain the underlying pharmacological actions of YJT, we focused on a representative epigenetic regulator, a nicotinamide adenine dinucleotide + (NAD+)-dependent chromatin enzyme, Sirtuin 6 (Sirt6).	NAD	113-146	sirtuin 6	Mus musculus	195-200
35337091-8	2022	To explain the underlying pharmacological actions of YJT, we focused on a representative epigenetic regulator, a nicotinamide adenine dinucleotide + (NAD+)-dependent chromatin enzyme, Sirtuin 6 (Sirt6).	NAD	150-154	sirtuin 6	Mus musculus	184-193
35337091-8	2022	To explain the underlying pharmacological actions of YJT, we focused on a representative epigenetic regulator, a nicotinamide adenine dinucleotide + (NAD+)-dependent chromatin enzyme, Sirtuin 6 (Sirt6).	NAD	150-154	sirtuin 6	Mus musculus	195-200
35281060-6	2022	Our results show that only NRH supplementation strongly increased NAD+ levels in both bone marrow-derived and THP-1 macrophages.	NAD	66-70	GLI family zinc finger 2	Homo sapiens	110-115
35085893-5	2022	The co-treatment of alpha-syn/MPP+ can cause aberrant mitochondrial homeostasis to diminish the concentration of the coenzyme nicotinamide adenine dinucleotide (NAD+), mediate accumulation of ac-alpha-tubulin, and induce mitochondrial perinuclear aggregation, navigating the co-localization of NLRP3 and apoptosis-associated speck-like protein containing a CARD domain (ASC).	NAD	161-165	PYD and CARD domain containing	Mus musculus	370-373
35281060-9	2022	The effect of NRH in NAD+ boosting and gene expression was blocked by inhibitors of adenosine kinase, equilibrative nucleoside transporters (ENT), and IkappaB kinase (IKK).	NAD	21-25	adenosine kinase	Homo sapiens	84-100
35137036-7	2022	Expression of S. cerevisiae GPD2, which encodes NAD+-dependent glycerol-3-phosphate dehydrogenase, and GPP1 supported increased glycerol production by oxygen-limited chemostat cultures of O. parapolymorpha.	NAD	48-51	glycerol-1-phosphatase RHR2	Saccharomyces cerevisiae S288C	103-107
35203360-1	2022	Nicotinamide adenine dinucleotide (NAD) is a versatile chemical compound serving as a coenzyme in metabolic pathways and as a substrate to support the enzymatic functions of sirtuins (SIRTs), poly (ADP-ribose) polymerase-1 (PARP-1), and cyclic ADP ribose hydrolase (CD38).	NAD	0-33	poly(ADP-ribose) polymerase 1	Homo sapiens	192-222
35168992-7	2022	The glucose- induced high NADH/NAD+ ratio upregulates the hypoxia-inducible factor-1 gene, which stimulates not only the glucose transporter-1 gene, but also many profibrotic genes like TGFbeta, VEGF, PAI-1 and CTGF, all known to be involved in the development of peritoneal fibrosis.	NAD	26-30	vascular endothelial growth factor A	Homo sapiens	195-199
35168992-7	2022	The glucose- induced high NADH/NAD+ ratio upregulates the hypoxia-inducible factor-1 gene, which stimulates not only the glucose transporter-1 gene, but also many profibrotic genes like TGFbeta, VEGF, PAI-1 and CTGF, all known to be involved in the development of peritoneal fibrosis.	NAD	31-35	vascular endothelial growth factor A	Homo sapiens	195-199
35195252-5	2022	Specifically, FoxOs regulate mitochondrial biogenesis by dampening NRF1-Tfam and c-Myc-Tfam cascades directly, and inhibiting NAD-Sirt1-Pgc1alpha cascade indirectly by inducing Hmox1 or repressing Fxn and Urod.	NAD	126-129	PPARG coactivator 1 alpha	Homo sapiens	136-145
35203360-1	2022	Nicotinamide adenine dinucleotide (NAD) is a versatile chemical compound serving as a coenzyme in metabolic pathways and as a substrate to support the enzymatic functions of sirtuins (SIRTs), poly (ADP-ribose) polymerase-1 (PARP-1), and cyclic ADP ribose hydrolase (CD38).	NAD	0-33	poly(ADP-ribose) polymerase 1	Homo sapiens	224-230
35203360-1	2022	Nicotinamide adenine dinucleotide (NAD) is a versatile chemical compound serving as a coenzyme in metabolic pathways and as a substrate to support the enzymatic functions of sirtuins (SIRTs), poly (ADP-ribose) polymerase-1 (PARP-1), and cyclic ADP ribose hydrolase (CD38).	NAD	35-38	poly(ADP-ribose) polymerase 1	Homo sapiens	192-222
35203360-1	2022	Nicotinamide adenine dinucleotide (NAD) is a versatile chemical compound serving as a coenzyme in metabolic pathways and as a substrate to support the enzymatic functions of sirtuins (SIRTs), poly (ADP-ribose) polymerase-1 (PARP-1), and cyclic ADP ribose hydrolase (CD38).	NAD	35-38	poly(ADP-ribose) polymerase 1	Homo sapiens	224-230
35138247-3	2022	Whereas PFOR reduces ferredoxin, the PDH complex utilizes NAD+.	NAD	58-62	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	37-40
35115484-7	2022	In addition to inducing increased NAD+ levels, NDUFV1 interacts with Src to attenuate LDHA phosphorylation at tyrosine 10 and reduce lactate production.	NAD	34-38	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	69-72
35029256-7	2022	Notably, HPLC analysis indicates that cytochrome c accelerates reduction (or activation) of the Pt(IV) prodrug in the presence of the electron donor nicotinamide adenine dinucleotide (NADH).	NAD	149-182	cytochrome c, somatic	Homo sapiens	38-50
35029256-7	2022	Notably, HPLC analysis indicates that cytochrome c accelerates reduction (or activation) of the Pt(IV) prodrug in the presence of the electron donor nicotinamide adenine dinucleotide (NADH).	NAD	184-188	cytochrome c, somatic	Homo sapiens	38-50
35207470-13	2022	Cytosolic NAD+ concentration is diminished by PA-induced ER stress, leading to decreased Sirt1 activity.	NAD	10-14	sirtuin 1	Rattus norvegicus	89-94
34260721-9	2022	Our preclinical results provide a rationale for targeting the NAMPT-dependent alternative NAD biosynthesis pathway as a novel clinical strategy against gliomas.	NAD	90-93	nicotinamide phosphoribosyltransferase	Mus musculus	62-67
35173682-6	2021	NAD+-increasing interventions improved capacity to exercise, decreased blood pressure, increased the anti-inflammatory profile and insulin-stimulated glucose disposal, and reduced the fat-free mass.	NAD	0-4	insulin	Homo sapiens	131-138
34981121-0	2022	Overexpression of NMNAT3 improves mitochondrial function and enhances anti-oxidative stress of bone marrow mesenchymal stem cells via the NAD+-Sirt3 pathway.	NAD	138-142	sirtuin 3	Homo sapiens	143-148
34981121-6	2022	We increased the level of nicotinamide adenine dinucleotide (NAD+) by overexpressing NMNAT3 in BMSCs and found that it could significantly increase the activity of silent mating type information regulation 2 homolog 3 (Sirt3) and significantly decrease the acetylation levels of Sirt3-dependent deacetylation-related proteins isocitrate dehydrogenase 2 (Idh2) and Forkhead-box protein O3a (FOXO3a).	NAD	26-59	sirtuin 3	Homo sapiens	219-224
34981121-6	2022	We increased the level of nicotinamide adenine dinucleotide (NAD+) by overexpressing NMNAT3 in BMSCs and found that it could significantly increase the activity of silent mating type information regulation 2 homolog 3 (Sirt3) and significantly decrease the acetylation levels of Sirt3-dependent deacetylation-related proteins isocitrate dehydrogenase 2 (Idh2) and Forkhead-box protein O3a (FOXO3a).	NAD	26-59	sirtuin 3	Homo sapiens	279-284
34981121-6	2022	We increased the level of nicotinamide adenine dinucleotide (NAD+) by overexpressing NMNAT3 in BMSCs and found that it could significantly increase the activity of silent mating type information regulation 2 homolog 3 (Sirt3) and significantly decrease the acetylation levels of Sirt3-dependent deacetylation-related proteins isocitrate dehydrogenase 2 (Idh2) and Forkhead-box protein O3a (FOXO3a).	NAD	26-59	isocitrate dehydrogenase (NADP(+)) 2	Homo sapiens	326-352
34981121-6	2022	We increased the level of nicotinamide adenine dinucleotide (NAD+) by overexpressing NMNAT3 in BMSCs and found that it could significantly increase the activity of silent mating type information regulation 2 homolog 3 (Sirt3) and significantly decrease the acetylation levels of Sirt3-dependent deacetylation-related proteins isocitrate dehydrogenase 2 (Idh2) and Forkhead-box protein O3a (FOXO3a).	NAD	26-59	isocitrate dehydrogenase (NADP(+)) 2	Homo sapiens	354-358
34981121-6	2022	We increased the level of nicotinamide adenine dinucleotide (NAD+) by overexpressing NMNAT3 in BMSCs and found that it could significantly increase the activity of silent mating type information regulation 2 homolog 3 (Sirt3) and significantly decrease the acetylation levels of Sirt3-dependent deacetylation-related proteins isocitrate dehydrogenase 2 (Idh2) and Forkhead-box protein O3a (FOXO3a).	NAD	26-59	forkhead box O3	Homo sapiens	390-396
34981121-6	2022	We increased the level of nicotinamide adenine dinucleotide (NAD+) by overexpressing NMNAT3 in BMSCs and found that it could significantly increase the activity of silent mating type information regulation 2 homolog 3 (Sirt3) and significantly decrease the acetylation levels of Sirt3-dependent deacetylation-related proteins isocitrate dehydrogenase 2 (Idh2) and Forkhead-box protein O3a (FOXO3a).	NAD	61-65	sirtuin 3	Homo sapiens	219-224
34981121-6	2022	We increased the level of nicotinamide adenine dinucleotide (NAD+) by overexpressing NMNAT3 in BMSCs and found that it could significantly increase the activity of silent mating type information regulation 2 homolog 3 (Sirt3) and significantly decrease the acetylation levels of Sirt3-dependent deacetylation-related proteins isocitrate dehydrogenase 2 (Idh2) and Forkhead-box protein O3a (FOXO3a).	NAD	61-65	sirtuin 3	Homo sapiens	279-284
34981121-6	2022	We increased the level of nicotinamide adenine dinucleotide (NAD+) by overexpressing NMNAT3 in BMSCs and found that it could significantly increase the activity of silent mating type information regulation 2 homolog 3 (Sirt3) and significantly decrease the acetylation levels of Sirt3-dependent deacetylation-related proteins isocitrate dehydrogenase 2 (Idh2) and Forkhead-box protein O3a (FOXO3a).	NAD	61-65	isocitrate dehydrogenase (NADP(+)) 2	Homo sapiens	326-352
34981121-6	2022	We increased the level of nicotinamide adenine dinucleotide (NAD+) by overexpressing NMNAT3 in BMSCs and found that it could significantly increase the activity of silent mating type information regulation 2 homolog 3 (Sirt3) and significantly decrease the acetylation levels of Sirt3-dependent deacetylation-related proteins isocitrate dehydrogenase 2 (Idh2) and Forkhead-box protein O3a (FOXO3a).	NAD	61-65	isocitrate dehydrogenase (NADP(+)) 2	Homo sapiens	354-358
34981121-6	2022	We increased the level of nicotinamide adenine dinucleotide (NAD+) by overexpressing NMNAT3 in BMSCs and found that it could significantly increase the activity of silent mating type information regulation 2 homolog 3 (Sirt3) and significantly decrease the acetylation levels of Sirt3-dependent deacetylation-related proteins isocitrate dehydrogenase 2 (Idh2) and Forkhead-box protein O3a (FOXO3a).	NAD	61-65	forkhead box O3	Homo sapiens	390-396
34981121-7	2022	These findings show that NMNAT3 may increase the activity of Sirt3 by increasing NAD+ levels.	NAD	81-85	sirtuin 3	Homo sapiens	61-66
34981121-8	2022	Our results confirm that the NMNAT3-NAD+-Sirt3 axis is a potential mechanism for improving mitochondrial function and enhancing anti-oxidative stress of BMSCs.	NAD	36-40	sirtuin 3	Homo sapiens	41-46
34997967-0	2022	NADH/NAD+ binding and linked tetrameric assembly of the oncogenic transcription factors CtBP1 and CtBP2.	NAD	0-4	C-terminal binding protein 2	Homo sapiens	98-103
34997967-0	2022	NADH/NAD+ binding and linked tetrameric assembly of the oncogenic transcription factors CtBP1 and CtBP2.	NAD	5-9	C-terminal binding protein 2	Homo sapiens	98-103
35101076-3	2022	METHODS: The effects of TRPM7 silencing on transcriptome profile, glucose uptake, lactic acid production, extracellular acidification rate (ECAR), oxygen consumption rate (OCR), intracellular ROS and ATP levels, and NAD+/NADH ratios in ovarian cancer cells were examined.	NAD	221-225	transient receptor potential cation channel, subfamily M, member 7	Mus musculus	24-29
35308855-0	2022	Discovery of an NAD+ analogue with enhanced specificity for PARP1.	NAD	16-20	poly(ADP-ribose) polymerase 1	Homo sapiens	60-65
35308855-1	2022	Among various protein posttranslational modifiers, poly-ADP-ribose polymerase 1 (PARP1) is a key player for regulating numerous cellular processes and events through enzymatic attachments of target proteins with ADP-ribose units donated by nicotinamide adenine dinucleotide (NAD+).	NAD	240-273	poly(ADP-ribose) polymerase 1	Homo sapiens	51-79
35308855-1	2022	Among various protein posttranslational modifiers, poly-ADP-ribose polymerase 1 (PARP1) is a key player for regulating numerous cellular processes and events through enzymatic attachments of target proteins with ADP-ribose units donated by nicotinamide adenine dinucleotide (NAD+).	NAD	240-273	poly(ADP-ribose) polymerase 1	Homo sapiens	81-86
35308855-1	2022	Among various protein posttranslational modifiers, poly-ADP-ribose polymerase 1 (PARP1) is a key player for regulating numerous cellular processes and events through enzymatic attachments of target proteins with ADP-ribose units donated by nicotinamide adenine dinucleotide (NAD+).	NAD	275-279	poly(ADP-ribose) polymerase 1	Homo sapiens	51-79
35308855-1	2022	Among various protein posttranslational modifiers, poly-ADP-ribose polymerase 1 (PARP1) is a key player for regulating numerous cellular processes and events through enzymatic attachments of target proteins with ADP-ribose units donated by nicotinamide adenine dinucleotide (NAD+).	NAD	275-279	poly(ADP-ribose) polymerase 1	Homo sapiens	81-86
34793337-1	2022	The biosynthetic routes leading to de novo Nicotinamine Adenine Dinucleotide (NAD+) production are involved in acute kidney injury (AKI) with a critical role for Quinolinate Phosphoribosyl Transferase (QPRT), a bottleneck enzyme of de novo NAD+ biosynthesis.	NAD	78-82	quinolinate phosphoribosyltransferase	Homo sapiens	162-200
35077680-4	2022	Mechanistically, Notch acts in an unconventional manner to regulate RET by interacting with specific RC-I proteins containing electron-transporting Fe-S clusters and NAD(H)-binding sites.	NAD	166-172	Notch	Drosophila melanogaster	17-22
35077680-6	2022	Our results identify Notch as a regulator of RET and RET-induced NAD+/NADH balance, a critical mechanism of metabolic reprogramming and a metabolic vulnerability of cancer that may be exploited for therapeutic purposes.	NAD	65-69	Notch	Drosophila melanogaster	21-26
35077680-6	2022	Our results identify Notch as a regulator of RET and RET-induced NAD+/NADH balance, a critical mechanism of metabolic reprogramming and a metabolic vulnerability of cancer that may be exploited for therapeutic purposes.	NAD	70-74	Notch	Drosophila melanogaster	21-26
34793337-1	2022	The biosynthetic routes leading to de novo Nicotinamine Adenine Dinucleotide (NAD+) production are involved in acute kidney injury (AKI) with a critical role for Quinolinate Phosphoribosyl Transferase (QPRT), a bottleneck enzyme of de novo NAD+ biosynthesis.	NAD	78-82	quinolinate phosphoribosyltransferase	Homo sapiens	202-206
34793337-1	2022	The biosynthetic routes leading to de novo Nicotinamine Adenine Dinucleotide (NAD+) production are involved in acute kidney injury (AKI) with a critical role for Quinolinate Phosphoribosyl Transferase (QPRT), a bottleneck enzyme of de novo NAD+ biosynthesis.	NAD	240-244	quinolinate phosphoribosyltransferase	Homo sapiens	162-200
34793337-4	2022	We also provide evidence that the Endoplasmic Reticulum (ER) stress response impairs de novo NAD+ biosynthesis by repressing QPRT transcription.	NAD	93-97	quinolinate phosphoribosyltransferase	Homo sapiens	125-129
34793337-5	2022	In conclusion, NAD+ biosynthesis impairment is an early event in AKI embedded with the ER stress response, and persistent reduction of QPRT expression is associated with AKI to CKD progression.	NAD	15-19	quinolinate phosphoribosyltransferase	Homo sapiens	135-139
35012648-12	2022	Mechanistic studies showed that NAD+ and NAMPT levels were rescued in AT2 cells co-cultured with MSCs and MSCs could suppress AT2 cells senescence mainly via suppressing lysosome-mediated NAMPT degradation.	NAD	32-36	nicotinamide phosphoribosyltransferase	Mus musculus	188-193
35491023-8	2022	The analysis supports existence of the NADH/NAD+ driven regulatory feedback loop between SIRT3, complex I (MRC), and acetyl-CoA synthetases, and existence of the nuclear substrates of SIRT3.	NAD	39-43	sirtuin 3	Homo sapiens	89-94
35491023-8	2022	The analysis supports existence of the NADH/NAD+ driven regulatory feedback loop between SIRT3, complex I (MRC), and acetyl-CoA synthetases, and existence of the nuclear substrates of SIRT3.	NAD	44-48	sirtuin 3	Homo sapiens	89-94
2792373-2	1989	Five spots were always detected, all of Mr 95,000, which were not artefactual for their amount varied when EF-2 was specifically ADP-ribosylated by diphtheria toxin in the presence of NAD+, and/or phosphorylated on a threonine residue by a Ca2+/calmodulin-dependent protein kinase (most likely Ca2+/calmodulin-dependent protein kinase III described by others [(1987) J. Biol.	NAD	184-188	eukaryotic translation elongation factor 2	Rattus norvegicus	107-111
34981667-12	2022	Mechanistically, mitochondrial fission increased the acetylation level of sterol regulatory element-binding protein 1 (SREBP1) and peroxisome proliferator-activated receptor coactivator 1 alpha (PGC-1alpha) by suppressing nicotinamide adenine dinucleotide (NAD+)/Sirtuin 1 (SIRT1) signaling.	NAD	257-261	PPARG coactivator 1 alpha	Homo sapiens	195-205
35242674-12	2022	In the GSEA results for pancreatic cancer patients, DUOX2 was significantly associated with oxidoreductase activity acting on nicotinamide adenine dinucleotide hydrogen (NADH) or NADPH and uridine 5"-diphospho-glucuronosyltansferase (UDP) glycosyltransferase activity.	NAD	170-174	dual oxidase 2	Homo sapiens	52-57
2628174-7	1989	This alignment clearly identifies the three catalytic domains of NR, namely, a molybdopterin cofactor-binding domain, a heme domain and a FAD/NADH domain.	NAD	142-146	nitrate reductase [NADH]	Solanum lycopersicum	65-67
2511329-1	1989	Poly(ADP-ribose)polymerase is a chromatin-associated enzyme of eukaryotic cell nuclei that catalyses the covalent attachment of ADP-ribose units from NAD+ to various nuclear acceptor proteins.	NAD	150-154	poly(ADP-ribose) polymerase 1	Homo sapiens	0-26
2506850-1	1989	Poly(ADP-ribose) polymerase (ADPRP) is a nuclear enzyme that transfers ADP-ribose from NAD+ to diverse nuclear proteins.	NAD	87-91	poly(ADP-ribose) polymerase 1	Homo sapiens	0-27
2506850-1	1989	Poly(ADP-ribose) polymerase (ADPRP) is a nuclear enzyme that transfers ADP-ribose from NAD+ to diverse nuclear proteins.	NAD	87-91	poly(ADP-ribose) polymerase 1	Homo sapiens	29-34
34981667-12	2022	Mechanistically, mitochondrial fission increased the acetylation level of sterol regulatory element-binding protein 1 (SREBP1) and peroxisome proliferator-activated receptor coactivator 1 alpha (PGC-1alpha) by suppressing nicotinamide adenine dinucleotide (NAD+)/Sirtuin 1 (SIRT1) signaling.	NAD	222-255	PPARG coactivator 1 alpha	Homo sapiens	195-205
35036692-4	2022	Comparisons of this structure with malate dehydrogenase enzymes from other species confirm that the human enzyme adopts similar secondary, tertiary, and quaternary structures and that the enzyme retains a similar conformation even when nicotinamide adenine dinucleotide (NAD+) is not bound.	NAD	236-269	malic enzyme 2	Homo sapiens	35-55
2598931-2	1989	The results show that initial velocities determined by the standard method of coupling bisphosphoglycerate production to NADH reduction in the presence of glyceraldehyde-3-phosphate dehydrogenase do not differ significantly from those determined in the absence of the latter enzyme.	NAD	121-125	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	155-195
2598932-7	1989	Previously reported evidence that the binary complex of bisphosphoglycerate and phosphoglycerate kinase may act (in the presence of NADH) as a substrate for glyceraldehyde-3-phosphate dehydrogenase according to Michaelis-Menten kinetics is based on a misinterpretation of the experimental observations that can be attributed to neglect of the autocatalytic effect of NAD+ produced during the reaction.	NAD	132-136	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	157-197
2598932-7	1989	Previously reported evidence that the binary complex of bisphosphoglycerate and phosphoglycerate kinase may act (in the presence of NADH) as a substrate for glyceraldehyde-3-phosphate dehydrogenase according to Michaelis-Menten kinetics is based on a misinterpretation of the experimental observations that can be attributed to neglect of the autocatalytic effect of NAD+ produced during the reaction.	NAD	367-371	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	157-197
2506854-3	1989	The partially purified poly(ADP-ribose) polymerase expressed in E. coli had the same molecular weight and enzymological properties as human placental poly(ADP-ribose) polymerase, including affinity for NAD, turnover number and DNA-dependency for activity.	NAD	202-205	poly(ADP-ribose) polymerase 1	Homo sapiens	23-50
2506854-3	1989	The partially purified poly(ADP-ribose) polymerase expressed in E. coli had the same molecular weight and enzymological properties as human placental poly(ADP-ribose) polymerase, including affinity for NAD, turnover number and DNA-dependency for activity.	NAD	202-205	poly(ADP-ribose) polymerase 1	Homo sapiens	150-177
2503544-9	1989	ADP-RT catalyzes the incorporation of the ADP moiety of nicotinamide adenine dinucleotide (NAD) into proteins and causes depletion of intracellular NAD.	NAD	56-89	poly(ADP-ribose) polymerase 1	Homo sapiens	0-6
2673040-8	1989	Further, comparisons of the kinetic parameters of the bacterially produced enzyme and ADH activity in larval fly extracts indicate similar substrate preferences, pH dependencies, and Km values for 2-propanol and NAD.	NAD	212-215	Alcohol dehydrogenase	Drosophila melanogaster	86-89
2503544-0	1989	Inhibition of tumor cell growth by interferon-gamma is mediated by two distinct mechanisms dependent upon oxygen tension: induction of tryptophan degradation and depletion of intracellular nicotinamide adenine dinucleotide.	NAD	189-222	interferon gamma	Homo sapiens	35-51
2503544-9	1989	ADP-RT catalyzes the incorporation of the ADP moiety of nicotinamide adenine dinucleotide (NAD) into proteins and causes depletion of intracellular NAD.	NAD	91-94	poly(ADP-ribose) polymerase 1	Homo sapiens	0-6
2503544-9	1989	ADP-RT catalyzes the incorporation of the ADP moiety of nicotinamide adenine dinucleotide (NAD) into proteins and causes depletion of intracellular NAD.	NAD	148-151	poly(ADP-ribose) polymerase 1	Homo sapiens	0-6
2503544-10	1989	All tumor cell lines tested had reduced levels of intracellular NAD after treatment with IFN-gamma and loss of NAD preceded inhibition of cell growth by 12-24 h. Inhibitors of IFN-gamma-mediated inhibition of cell growth prevented loss of levels of intracellular NAD.	NAD	64-67	interferon gamma	Homo sapiens	89-98
2503544-10	1989	All tumor cell lines tested had reduced levels of intracellular NAD after treatment with IFN-gamma and loss of NAD preceded inhibition of cell growth by 12-24 h. Inhibitors of IFN-gamma-mediated inhibition of cell growth prevented loss of levels of intracellular NAD.	NAD	64-67	interferon gamma	Homo sapiens	176-185
2503544-10	1989	All tumor cell lines tested had reduced levels of intracellular NAD after treatment with IFN-gamma and loss of NAD preceded inhibition of cell growth by 12-24 h. Inhibitors of IFN-gamma-mediated inhibition of cell growth prevented loss of levels of intracellular NAD.	NAD	111-114	interferon gamma	Homo sapiens	176-185
2503544-10	1989	All tumor cell lines tested had reduced levels of intracellular NAD after treatment with IFN-gamma and loss of NAD preceded inhibition of cell growth by 12-24 h. Inhibitors of IFN-gamma-mediated inhibition of cell growth prevented loss of levels of intracellular NAD.	NAD	111-114	interferon gamma	Homo sapiens	176-185
16667010-11	1989	Enzyme distribution studies revealed that both NADH and NADPH-dependent HPR and GR activities were predominantly localized in the bundle sheath compartment.	NAD	47-51	glyoxylate reductase	Zea mays	80-82
2745445-11	1989	By this criterion, NADH is transferred directly from glutamate dehydrogenase to malate dehydrogenase and alpha-ketoglutarate is channeled from the aminotransferase to both glutamate dehydrogenase and the alpha-ketoglutarate dehydrogenase complex.	NAD	19-23	malic enzyme 2	Homo sapiens	80-100
2546562-1	1989	We have shown that (i) the cytochrome c reductase activity of the commercial NADH dehydrogenase does not perturb its ability to catalyse the reduction of various antitumor compounds of the anthracycline class, (ii) the reduction of these compounds by NADH, catalysed by commercial NADH dehydrogenase, correlates with their reduction by NADH catalysed by microsomes.	NAD	77-81	cytochrome c, somatic	Homo sapiens	27-39
2546562-1	1989	We have shown that (i) the cytochrome c reductase activity of the commercial NADH dehydrogenase does not perturb its ability to catalyse the reduction of various antitumor compounds of the anthracycline class, (ii) the reduction of these compounds by NADH, catalysed by commercial NADH dehydrogenase, correlates with their reduction by NADH catalysed by microsomes.	NAD	251-255	cytochrome c, somatic	Homo sapiens	27-39
2743579-1	1989	Measurements of the activity of transketolase in human erythrocyte lysates by an assay coupled to NADH oxidation indicate that interactions of assay substrates with hemoglobin can give rise to overestimations of transketolase activity.	NAD	98-102	transketolase	Homo sapiens	32-45
2543970-0	1989	Import of cytochrome c into mitochondria: reduction of heme, mediated by NADH and flavin nucleotides, is obligatory for its covalent linkage to apocytochrome c. The covalent attachment of heme to apocytochrome c, and therefore the import of cytochrome c into mitochondria, is dependent on both NADH plus a cytosolic cofactor that has been identified to be FMN or FAD.	NAD	73-77	cytochrome c, somatic	Homo sapiens	10-22
2543970-0	1989	Import of cytochrome c into mitochondria: reduction of heme, mediated by NADH and flavin nucleotides, is obligatory for its covalent linkage to apocytochrome c. The covalent attachment of heme to apocytochrome c, and therefore the import of cytochrome c into mitochondria, is dependent on both NADH plus a cytosolic cofactor that has been identified to be FMN or FAD.	NAD	73-77	cytochrome c, somatic	Homo sapiens	147-159
2543970-0	1989	Import of cytochrome c into mitochondria: reduction of heme, mediated by NADH and flavin nucleotides, is obligatory for its covalent linkage to apocytochrome c. The covalent attachment of heme to apocytochrome c, and therefore the import of cytochrome c into mitochondria, is dependent on both NADH plus a cytosolic cofactor that has been identified to be FMN or FAD.	NAD	294-298	cytochrome c, somatic	Homo sapiens	10-22
2543970-0	1989	Import of cytochrome c into mitochondria: reduction of heme, mediated by NADH and flavin nucleotides, is obligatory for its covalent linkage to apocytochrome c. The covalent attachment of heme to apocytochrome c, and therefore the import of cytochrome c into mitochondria, is dependent on both NADH plus a cytosolic cofactor that has been identified to be FMN or FAD.	NAD	294-298	cytochrome c, somatic	Homo sapiens	147-159
2540716-4	1989	In all reactions, superoxide dismutase and catalase completely inhibit the vanadium-stimulated oxidation of NADH.	NAD	108-112	catalase	Homo sapiens	43-51
2703701-7	1989	Various analogues of beta-NADPH could be used by the enzyme; however, beta-NADH, which can be used by DT-diaphorase, was ineffective.	NAD	70-79	NAD(P)H quinone dehydrogenase 1	Rattus norvegicus	102-115
2649501-8	1989	In isolated ghosts, some G3PD was tightly bound to the membrane and was resistant to elution with phosphate-buffered saline and NAD+/arsenate.	NAD	128-132	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	25-29
2743579-3	1989	Thus, in lysates containing methemoglobin, NADH oxidation can be due firstly to methemoglobin reductase activity or secondly to the monooxygenase activity of methemoglobin, for which the substrate can be ribose 5-phosphate, a substrate also of transketolase.	NAD	43-47	transketolase	Homo sapiens	244-257
2522691-2	1989	Presumably, this NAD+ loss is due to activation of the enzyme NAD:protein ADP-ribosyltransferase (ADPRT) and may lead to glycolysis inhibition, disturbance of energy metabolism, and eventually cell death.	NAD	17-21	poly(ADP-ribose) polymerase 1	Homo sapiens	74-96
16347898-4	1989	The specific activities of NADH- and NADPH-dependent butanol dehydrogenase and butyraldehyde dehydrogenase as well as those of acetoacetyl-coenzyme A:acetate/butyrate:coenzyme A-transferase (butyrate-acetoacetate coenzyme A-transferase [EC 2.8.3.9]) (CoA-transferase), butyrate kinase, and phosphotransbutyrylase were measured at the onset of stationary phase.	NAD	27-31	CA_C1423	Clostridium acetobutylicum ATCC 824	61-74
16347898-4	1989	The specific activities of NADH- and NADPH-dependent butanol dehydrogenase and butyraldehyde dehydrogenase as well as those of acetoacetyl-coenzyme A:acetate/butyrate:coenzyme A-transferase (butyrate-acetoacetate coenzyme A-transferase [EC 2.8.3.9]) (CoA-transferase), butyrate kinase, and phosphotransbutyrylase were measured at the onset of stationary phase.	NAD	27-31	CA_C1423	Clostridium acetobutylicum ATCC 824	93-106
2498460-9	1989	Dietary ethanol alone and in combination with isopropanol stimulated an increase in the size of the NAD-pool in larvae, a condition that may favor the activity of ADH.	NAD	100-103	Alcohol dehydrogenase	Drosophila melanogaster	163-166
2522691-2	1989	Presumably, this NAD+ loss is due to activation of the enzyme NAD:protein ADP-ribosyltransferase (ADPRT) and may lead to glycolysis inhibition, disturbance of energy metabolism, and eventually cell death.	NAD	17-21	poly(ADP-ribose) polymerase 1	Homo sapiens	98-103
2537100-5	1989	Exogenous soluble cytochrome c can be both reduced by NADH- and succinate-linked systems and oxidized by cytochrome aa3 present in membranes of the mutant strain.	NAD	54-58	cytochrome c, somatic	Homo sapiens	18-30
2704236-7	1989	In the same fraction, the ADP-ribosylated protein of Mr 100,000 was detected in the presence of diphtheria toxin (fragment A) and (adenylate-32P) NAD, indicating the presence of EF-2 in the cytosol from rat adrenal glomerulosa cells.	NAD	146-149	eukaryotic translation elongation factor 2	Rattus norvegicus	178-182
2492526-4	1989	ALR2 catalyzes the primarily NADPH-dependent reduction of a wide variety of aldehydes, although the enzyme can also utilize NADH.	NAD	124-128	aldo-keto reductase family 1 member B	Homo sapiens	0-4
2558980-6	1989	The oxidation of NADH, mediated by a catalytically low concentration of phenazine(+O2), was augmented two-fold by SOD.	NAD	17-21	superoxide dismutase 1	Homo sapiens	114-117
2930467-1	1989	Cytoplasmic aldehyde dehydrogenase catalyses the hydrolysis of methyl p-nitrophenyl (PNP) carbonate at an appreciable rate that is markedly stimualted by NAD+ or NADH.	NAD	154-158	purine nucleoside phosphorylase	Homo sapiens	85-88
2930467-1	1989	Cytoplasmic aldehyde dehydrogenase catalyses the hydrolysis of methyl p-nitrophenyl (PNP) carbonate at an appreciable rate that is markedly stimualted by NAD+ or NADH.	NAD	162-166	purine nucleoside phosphorylase	Homo sapiens	85-88
2930467-5	1989	The presence of NAD+, NADH, propionaldehyde, chloral hydrate, diethylstilboestrol or disulfiram slows the reaction of enzyme with PNP dimethylcarbamate.	NAD	16-20	purine nucleoside phosphorylase	Homo sapiens	130-133
2930467-5	1989	The presence of NAD+, NADH, propionaldehyde, chloral hydrate, diethylstilboestrol or disulfiram slows the reaction of enzyme with PNP dimethylcarbamate.	NAD	22-26	purine nucleoside phosphorylase	Homo sapiens	130-133
3170585-8	1988	Although chicken exons VIII-XI have been fused into human exon 8, introns which separate exons encoding the NAD binding, catalytic, and helical domains of the GAPDH protein have been retained.	NAD	108-111	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	159-164
2463266-4	1989	All sera with autoantibodies to ADPRP recognized the NAD-binding domain of the enzyme, as demonstrated by either immunoblotting or immunoprecipitation of partially proteolyzed ADPRP.	NAD	53-56	poly(ADP-ribose) polymerase 1	Homo sapiens	32-37
2463266-4	1989	All sera with autoantibodies to ADPRP recognized the NAD-binding domain of the enzyme, as demonstrated by either immunoblotting or immunoprecipitation of partially proteolyzed ADPRP.	NAD	53-56	poly(ADP-ribose) polymerase 1	Homo sapiens	176-181
2521933-6	1989	Because activation of the DNA-repairing enzyme poly ADP-ribose polymerase can consume NAD sufficient to interfere with ATP synthesis, we studied NAD and ATP levels after oxidant injury when ADP-ribose polymerase was inhibited with 3-aminobenzamide and nicotinamide.	NAD	86-89	poly(ADP-ribose) polymerase 1	Homo sapiens	47-73
2521933-6	1989	Because activation of the DNA-repairing enzyme poly ADP-ribose polymerase can consume NAD sufficient to interfere with ATP synthesis, we studied NAD and ATP levels after oxidant injury when ADP-ribose polymerase was inhibited with 3-aminobenzamide and nicotinamide.	NAD	145-148	poly(ADP-ribose) polymerase 1	Homo sapiens	47-73
2521933-7	1989	When poly ADP-ribose polymerase was inhibited, NAD levels remained normal, but ATP depletion was not prevented.	NAD	47-50	poly(ADP-ribose) polymerase 1	Homo sapiens	5-31
2521933-9	1989	NAD depletion results from activation of poly ADP-ribose polymerase, but this phenomenon is not the mechanism of ATP depletion in human umbilical vein endothelial cells.	NAD	0-3	poly(ADP-ribose) polymerase 1	Homo sapiens	41-67
3182815-5	1988	2) Hepatocyte plasma membrane NADH:ferricyanide oxidoreductase activity and uptake of iron from transferrin are stimulated by low oxygen concentration and inhibited by iodoacetate.	NAD	30-34	transferrin	Rattus norvegicus	96-107
2531893-1	1989	The cell cycle dependent fluctuation of adenosine diphosphoribosyl transferase (ADPRT) activity was demonstrated by both nicotinamide adenine dinucleotide (3H-NAD+) incorporation into the acid insoluble fraction of permeabilized cells and changes in the cellular content of NAD, the only substrate of ADPRT, in intact FL cells.	NAD	121-154	poly(ADP-ribose) polymerase 1	Homo sapiens	80-85
2531893-1	1989	The cell cycle dependent fluctuation of adenosine diphosphoribosyl transferase (ADPRT) activity was demonstrated by both nicotinamide adenine dinucleotide (3H-NAD+) incorporation into the acid insoluble fraction of permeabilized cells and changes in the cellular content of NAD, the only substrate of ADPRT, in intact FL cells.	NAD	159-162	poly(ADP-ribose) polymerase 1	Homo sapiens	80-85
3148735-2	1988	ADH-F, ADH-S, ADH-71k of D. melanogaster and the ADH of D. simulans were inhibited by NADH, but the inhibition was relieved by NAD+.	NAD	86-90	Alcohol dehydrogenase	Drosophila melanogaster	0-3
3148735-2	1988	ADH-F, ADH-S, ADH-71k of D. melanogaster and the ADH of D. simulans were inhibited by NADH, but the inhibition was relieved by NAD+.	NAD	86-90	Alcohol dehydrogenase	Drosophila melanogaster	7-10
3148735-2	1988	ADH-F, ADH-S, ADH-71k of D. melanogaster and the ADH of D. simulans were inhibited by NADH, but the inhibition was relieved by NAD+.	NAD	86-90	Alcohol dehydrogenase	Drosophila melanogaster	7-10
3148735-2	1988	ADH-F, ADH-S, ADH-71k of D. melanogaster and the ADH of D. simulans were inhibited by NADH, but the inhibition was relieved by NAD+.	NAD	86-90	Alcohol dehydrogenase	Drosophila melanogaster	7-10
3148735-2	1988	ADH-F, ADH-S, ADH-71k of D. melanogaster and the ADH of D. simulans were inhibited by NADH, but the inhibition was relieved by NAD+.	NAD	127-131	Alcohol dehydrogenase	Drosophila melanogaster	0-3
3148735-2	1988	ADH-F, ADH-S, ADH-71k of D. melanogaster and the ADH of D. simulans were inhibited by NADH, but the inhibition was relieved by NAD+.	NAD	127-131	Alcohol dehydrogenase	Drosophila melanogaster	7-10
3148735-2	1988	ADH-F, ADH-S, ADH-71k of D. melanogaster and the ADH of D. simulans were inhibited by NADH, but the inhibition was relieved by NAD+.	NAD	127-131	Alcohol dehydrogenase	Drosophila melanogaster	7-10
3148735-2	1988	ADH-F, ADH-S, ADH-71k of D. melanogaster and the ADH of D. simulans were inhibited by NADH, but the inhibition was relieved by NAD+.	NAD	127-131	Alcohol dehydrogenase	Drosophila melanogaster	7-10
3148735-3	1988	The order of sensitivity to NADH was ADH-F less than ADH-71k, ADH-S less than ADH-simulans with ADH-F being about four times less sensitive than the D. melanogaster enzymes and 12 times less sensitive than the D. simulans enzyme.	NAD	28-32	Alcohol dehydrogenase	Drosophila melanogaster	37-40
3148735-3	1988	The order of sensitivity to NADH was ADH-F less than ADH-71k, ADH-S less than ADH-simulans with ADH-F being about four times less sensitive than the D. melanogaster enzymes and 12 times less sensitive than the D. simulans enzyme.	NAD	28-32	Alcohol dehydrogenase	Drosophila melanogaster	37-40
3148735-3	1988	The order of sensitivity to NADH was ADH-F less than ADH-71k, ADH-S less than ADH-simulans with ADH-F being about four times less sensitive than the D. melanogaster enzymes and 12 times less sensitive than the D. simulans enzyme.	NAD	28-32	Alcohol dehydrogenase	Drosophila melanogaster	37-40
3148735-3	1988	The order of sensitivity to NADH was ADH-F less than ADH-71k, ADH-S less than ADH-simulans with ADH-F being about four times less sensitive than the D. melanogaster enzymes and 12 times less sensitive than the D. simulans enzyme.	NAD	28-32	Alcohol dehydrogenase	Drosophila melanogaster	37-40
2853215-0	1988	Photoexcitation of the methionine-iron bond in iron(III) cytochrome c: bimolecular reaction with NADH.	NAD	97-101	cytochrome c, somatic	Homo sapiens	57-69
2853215-1	1988	When iron(III) cytochrome c aqueous solutions containing NADH are irradiated with polychromatic light (wavelength greater than 280 nm), iron(II) cytochrome c and NAD+ in the stoichiometric ratio 2/1 are observed to be the principal reaction products, independently of the presence of oxygen; in addition, a minor process due to direct photodegradation of the nucleotide is observed.	NAD	57-61	cytochrome c, somatic	Homo sapiens	15-27
2853215-1	1988	When iron(III) cytochrome c aqueous solutions containing NADH are irradiated with polychromatic light (wavelength greater than 280 nm), iron(II) cytochrome c and NAD+ in the stoichiometric ratio 2/1 are observed to be the principal reaction products, independently of the presence of oxygen; in addition, a minor process due to direct photodegradation of the nucleotide is observed.	NAD	57-61	cytochrome c, somatic	Homo sapiens	145-157
2853215-1	1988	When iron(III) cytochrome c aqueous solutions containing NADH are irradiated with polychromatic light (wavelength greater than 280 nm), iron(II) cytochrome c and NAD+ in the stoichiometric ratio 2/1 are observed to be the principal reaction products, independently of the presence of oxygen; in addition, a minor process due to direct photodegradation of the nucleotide is observed.	NAD	162-166	cytochrome c, somatic	Homo sapiens	15-27
2853215-7	1988	radical rapidly reacts with oxygen to give NAD+ and superoxide O2- anion radical which, in turn, reduces the second iron(III) cytochrome c molecule.	NAD	43-47	cytochrome c, somatic	Homo sapiens	126-138
28398864-4	1988	When muscle PYK activity is present, NADH is oxidized resulting in a loss of fluorescence (reaction mixture spots on filter paper viewed under long-wave ultraviolet light).	NAD	37-41	phosphorylase kinase regulatory subunit alpha 2	Homo sapiens	12-15
2842191-3	1988	Glycated poly-Lys caused the oxidation of NADH in the presence of LDH at pH 7.0 which was completely inhibited by SOD.	NAD	42-46	superoxide dismutase 1	Homo sapiens	114-117
3370255-1	1988	The steady-state levels of aerobic and anaerobic reduction of cytochrome b5 by ascorbic acid and the initial rates of cytochrome b5 reduction in the presence of ascorbic acid and of anaerobic cytochrome P-450 reduction in the presence of NADH were used to calculate the rate constants for cytochrome b5 oxidation.	NAD	238-242	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	192-208
3218146-3	1988	These data suggest that reduced NAD- and NADP-containing oxidoreductases alpha-GPD and G6PD are donors of H+ used in biosynthesis of H2O2 catalyzed by SOD.	NAD	32-35	superoxide dismutase 1	Homo sapiens	151-154
3379048-2	1988	The uptake of iron from transferrin by isolated rat hepatocytes varies in parallel with plasma membrane NADH:ferricyanide oxidoreductase activity, is inhibited by ferricyanide, ferric, and ferrous iron chelators, divalent transition metal cations, and depends on calcium ions.	NAD	104-108	transferrin	Rattus norvegicus	24-35
3197763-3	1988	The relative ratio of pyridine dinucleotides (NADH/NAD) was calculated from equilibrium equations of two NAD-linked enzymes, lactate dehydrogenase (LDH) and alpha-glycerophosphate dehydrogenase (GPDH).	NAD	46-50	glycerol-3-phosphate dehydrogenase 1	Rattus norvegicus	157-193
3197763-3	1988	The relative ratio of pyridine dinucleotides (NADH/NAD) was calculated from equilibrium equations of two NAD-linked enzymes, lactate dehydrogenase (LDH) and alpha-glycerophosphate dehydrogenase (GPDH).	NAD	46-50	glycerol-3-phosphate dehydrogenase 1	Rattus norvegicus	195-199
3197763-3	1988	The relative ratio of pyridine dinucleotides (NADH/NAD) was calculated from equilibrium equations of two NAD-linked enzymes, lactate dehydrogenase (LDH) and alpha-glycerophosphate dehydrogenase (GPDH).	NAD	46-49	glycerol-3-phosphate dehydrogenase 1	Rattus norvegicus	157-193
3197763-3	1988	The relative ratio of pyridine dinucleotides (NADH/NAD) was calculated from equilibrium equations of two NAD-linked enzymes, lactate dehydrogenase (LDH) and alpha-glycerophosphate dehydrogenase (GPDH).	NAD	46-49	glycerol-3-phosphate dehydrogenase 1	Rattus norvegicus	195-199
3197763-3	1988	The relative ratio of pyridine dinucleotides (NADH/NAD) was calculated from equilibrium equations of two NAD-linked enzymes, lactate dehydrogenase (LDH) and alpha-glycerophosphate dehydrogenase (GPDH).	NAD	51-54	glycerol-3-phosphate dehydrogenase 1	Rattus norvegicus	157-193
3197763-4	1988	The change in NADH/NAD ratio based on biochemical assays correlates well with that estimated from GPDH reaction.	NAD	14-18	glycerol-3-phosphate dehydrogenase 1	Rattus norvegicus	98-102
3197763-4	1988	The change in NADH/NAD ratio based on biochemical assays correlates well with that estimated from GPDH reaction.	NAD	14-17	glycerol-3-phosphate dehydrogenase 1	Rattus norvegicus	98-102
2841217-0	1988	The effect of thyroxine and related compounds on the aerobic myeloperoxidase--catalysed oxidation of NADH.	NAD	101-105	myeloperoxidase	Homo sapiens	61-76
2841217-1	1988	Thyroxine concentrations as low as 1 microM significantly stimulate compound III formation during aerobic oxidation of NADH by highly purified myeloperoxidase.	NAD	119-123	myeloperoxidase	Homo sapiens	143-158
2968936-1	1988	A common mechanism has been proposed for the beta-cell toxins alloxan (ALX) and streptozocin (STZ) involving the formation of single-strand breaks in DNA that lead to the overactivation of the enzyme poly(ADP-ribose) synthetase and the critical depletion of its substrate NAD.	NAD	272-275	poly(ADP-ribose) polymerase 1	Homo sapiens	200-227
3383424-5	1988	The glycolysis retardation may be attributed to the impaired reoxidation of NADH produced by GA3PD action.	NAD	76-80	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	93-98
3146908-3	1988	The reconsituted system of heme oxygenase, composed of heme oxygenase, NADPH cytochrome c (P450) reductase and biliverdin reductase was equiactive with 1 mM NADPH and 4 nM NADH and showed complete dependence on added heme for catalytic activity.	NAD	172-176	cytochrome c, somatic	Homo sapiens	77-89
2907967-2	1988	Activation of poly(ADP-ribose) polymerase (ADPRP), and the resultant consumption of NAD, play an essential role in mediating the toxicity of these agents.	NAD	84-87	poly(ADP-ribose) polymerase 1	Homo sapiens	14-41
2907967-2	1988	Activation of poly(ADP-ribose) polymerase (ADPRP), and the resultant consumption of NAD, play an essential role in mediating the toxicity of these agents.	NAD	84-87	poly(ADP-ribose) polymerase 1	Homo sapiens	43-48
2907967-7	1988	Supplementation of the medium with inhibitors of poly(ADP-ribose) polymerase blocks the fall in cellular NAD and ATP, and protects the lymphocytes from the toxicity of DNA damaging agents.	NAD	105-108	poly(ADP-ribose) polymerase 1	Homo sapiens	49-76
3119366-4	1987	Treatment of HL 60 membranes with cholera toxin and NAD markedly inhibits FMLP-stimulated high affinity GTPase.	NAD	52-55	formyl peptide receptor 1	Homo sapiens	74-78
3369122-2	1988	An increase in content of diene conjugates and malonic dialdehyde as well as in activity of NADPH.H+- and NADH.H+-nitroblue tetrazolium-oxydoreductases in liver microsomes, a decrease in activity of catalase and superoxide dismutase in liver mitochondria were observed in the animals within two months of their mobility restriction.	NAD	106-110	catalase	Rattus norvegicus	199-207
3395650-4	1988	The lower content of free fatty acids and decreased rate of the oxidation of exogenic NADH in the external pathway indicate the decrease in the activity of phospholipase A2 in mitochondria from liver of hibernating ground squirrels.	NAD	86-90	phospholipase A2 group IB	Homo sapiens	156-172
2961740-4	1987	Poly(ADP-ribose) polymerase was labeled with radioactive NAD, excess precursor was removed by rapid gel filtration chromatography, and nonradioactive NAD was supplied for a second incubation.	NAD	57-60	poly(ADP-ribose) polymerase 1	Homo sapiens	0-27
2960266-5	1987	Inhibition of poly(ADP-ribose) polymerase by 3-aminobenzamide prevented both the depletion of NAD pools and the associated changes in purine nucleotide metabolism.	NAD	94-97	poly(ADP-ribose) polymerase 1	Homo sapiens	14-41
3672551-2	1987	We have proposed a biochemical hypothesis that explains HD-induced injury by linking DNA alkylation and DNA breaks with activation of poly(ADP-ribose) polymerase, resulting in depletion of cellular NAD+.	NAD	198-202	poly(ADP-ribose) polymerase 1	Homo sapiens	134-161
16665778-0	1987	beta-Oxidation and Glyoxylate Cycle Coupled to NADH: Cytochrome c and Ferricyanide Reductases in Glyoxysomes.	NAD	47-51	cytochrome c	Ricinus communis	53-65
3672551-5	1987	Inhibitors of poly(ADP-ribose) polymerase or substrates for NAD+ synthesis were able to prevent the HD-induced NAD+ decrease.	NAD	111-115	poly(ADP-ribose) polymerase 1	Homo sapiens	14-41
3329525-4	1987	Another cellular enzyme, poly(ADP-ribose) polymerase, responds to DNA strand breaks by cleaving its substrate, NAD+, and using the resultant ADP-ribose moieties to synthesize homopolymers of ADP-ribose.	NAD	111-115	poly(ADP-ribose) polymerase 1	Homo sapiens	25-52
3315367-4	1987	The possible mechanisms for the beta cell destruction by these chemicals include (a) generation of oxygen free radicals and alteration of endogenous scavengers of these reactive species; (b) breakage of DNA and consequent increase in the activity of poly ADP ribose synthetase, and enzyme depleting NAD in beta cells; and (c) inhibition of active calcium transport and calmodulin-activated protein kinase activity.	NAD	299-302	poly(ADP-ribose) polymerase 1	Homo sapiens	250-276
3115798-1	1987	A selection strategy to obtain cells deficient in poly(ADP-ribose) polymerase was developed based on the fact that treatment with high levels of N-methyl-N"-nitro-N-nitrosoguanidine results in sufficient activation of poly(ADP-ribose) polymerase to cause NAD and ATP depletion leading to cessation of all energy-dependent processes and rapid cell death.	NAD	255-258	poly(ADP-ribose) polymerase 1	Homo sapiens	50-77
3115798-1	1987	A selection strategy to obtain cells deficient in poly(ADP-ribose) polymerase was developed based on the fact that treatment with high levels of N-methyl-N"-nitro-N-nitrosoguanidine results in sufficient activation of poly(ADP-ribose) polymerase to cause NAD and ATP depletion leading to cessation of all energy-dependent processes and rapid cell death.	NAD	255-258	poly(ADP-ribose) polymerase 1	Homo sapiens	218-245
3121332-1	1987	NAD+:Protein ADP-ribosyltransferase (EC 2.4.2.30) (ADPRT) was purified from human placenta by affinity chromatography.	NAD	0-4	poly(ADP-ribose) polymerase 1	Homo sapiens	51-56
24225782-6	1987	Membranes purified by treatment with 0.2 M KCl or 0.1 M carbonate catalyzed the reduction of cytochrome-c when NADH or NADPH was provided as the electron donor.	NAD	111-115	cytochrome c	Ricinus communis	93-105
2442198-1	1987	The chromatin-bound enzyme poly(ADP-ribose) polymerase (ADPRP) is strongly stimulated by DNA with single- or double-stranded breaks, and transfers the ADP-ribose moiety of NAD to nuclear proteins.	NAD	172-175	poly(ADP-ribose) polymerase 1	Homo sapiens	27-54
2442198-1	1987	The chromatin-bound enzyme poly(ADP-ribose) polymerase (ADPRP) is strongly stimulated by DNA with single- or double-stranded breaks, and transfers the ADP-ribose moiety of NAD to nuclear proteins.	NAD	172-175	poly(ADP-ribose) polymerase 1	Homo sapiens	56-61
3622513-7	1987	In contrast, single exchanges of these residues are the ones involved in the major allelic differences (beta 1 versus beta 2 and gamma 1 versus gamma 2), which affects the overall rate of alcohol oxidation since NADH dissociation is the rate-determining step.	NAD	212-216	potassium calcium-activated channel subfamily M regulatory beta subunit 1	Homo sapiens	104-110
3622513-7	1987	In contrast, single exchanges of these residues are the ones involved in the major allelic differences (beta 1 versus beta 2 and gamma 1 versus gamma 2), which affects the overall rate of alcohol oxidation since NADH dissociation is the rate-determining step.	NAD	212-216	tryptophanyl-tRNA synthetase 1	Homo sapiens	144-151
3622513-9	1987	Both His and Arg can make a hydrogen bond to a phosphate oxygen atom of NAD; hence the lower turnover rate of beta 1 apparently derives from a charge effect.	NAD	72-75	potassium calcium-activated channel subfamily M regulatory beta subunit 1	Homo sapiens	110-116
3622513-12	1987	The important difference between gamma 1 and gamma 2 is an exchange at position 271 from Arg to Gln which can give a hydrogen bond from Gln in gamma 2 to the adenine of NAD.	NAD	169-172	tryptophanyl-tRNA synthetase 1	Homo sapiens	45-52
3622513-12	1987	The important difference between gamma 1 and gamma 2 is an exchange at position 271 from Arg to Gln which can give a hydrogen bond from Gln in gamma 2 to the adenine of NAD.	NAD	169-172	tryptophanyl-tRNA synthetase 1	Homo sapiens	143-150
3033643-1	1987	Dihydropteridine reductase (DHPR; EC 1.6.99.7) catalyzes the NADH-mediated reduction of quinonoid dihydrobiopterin and is an essential component of the pterin-dependent aromatic amino acid hydroxylating systems.	NAD	61-65	quinoid dihydropteridine reductase	Homo sapiens	0-26
3039271-4	1987	However, when the rate of oxygen uptake by mitochondria was measured in the presence of rotenone and tetramethyl-p-phenylene-diamine with NADH as substrate, the specific activity in CCl4 treated rats was lower than that of normal rats (Vmax = 345 +/- 31 (e-/s/cytochrome aa3), as compared to Vmax = 408 +/- 21) in spite of the increased activity of cytochrome c oxidase.	NAD	138-142	C-C motif chemokine ligand 4	Rattus norvegicus	182-186
2957224-3	1987	3AB inhibits the synthesis of poly(ADP-ribose) by the enzyme adenosine diphosphate ribosyl transferase (ADPRT), which requires NAD as a substrate.	NAD	127-130	poly(ADP-ribose) polymerase 1	Homo sapiens	104-109
3650694-9	1987	Addition of excess catalase or SOD abolished the oxygen uptake while retaining significant rates of NADH disappearance indicating that the two activities are delinked.	NAD	100-104	catalase	Rattus norvegicus	19-27
3650695-7	1987	Catalase and Mn2+, which inhibit oxygen consumption accompanying NADH oxidation, increased both the rate and extent of the blue color compound formed.	NAD	65-69	catalase	Rattus norvegicus	0-8
3620161-4	1987	To test whether ethanol metabolism was limited by the rate of removal of one of the end products (NADH) of alcohol dehydrogenase, fluoropyruvate was infused to reoxidize hepatic NADH and to prevent NADH generation via flux through pyruvate dehydrogenase.	NAD	98-102	aldo-keto reductase family 1 member A1	Rattus norvegicus	107-128
3663093-5	1987	The data were used to calculate the oxidation rate of NADH catalysed by lactate dehydrogenase, alcohol dehydrogenase, triosephosphate dehydrogenase and glycerol phosphate dehydrogenase.	NAD	54-58	aldo-keto reductase family 1 member A1	Rattus norvegicus	95-116
3112036-5	1987	Incubation of intact nuclei from HeLa cells with [14C]NAD resulted in the isolation of a poly(ADP-ribose)synthetase to which a definite radioactivity is bound.	NAD	54-57	poly(ADP-ribose) polymerase 1	Homo sapiens	89-115
2952875-1	1987	NAD is the substrate of a novel chromatin-associated enzyme-ADP-ribosyl transferase (ADPRT).	NAD	0-3	poly(ADP-ribose) polymerase 1	Homo sapiens	85-90
2952875-4	1987	3AB, a potent ADPRT inhibitor, can inhibit the cell cycle dependent change in cellular NAD content and also inhibit DNA synthesis in the S phase and extend the S phase.	NAD	87-90	poly(ADP-ribose) polymerase 1	Homo sapiens	14-19
2952875-7	1987	This DNA-damage-induced NAD lowering could be partially or completely prevented by the ADPRT inhibitors, 3AB or nicotinamide, which were shown to exert no influence on either the cellular NAD content of normal quiescent FL cells or the metabolic blocking agent, 2,4-DNP-induced cellular NAD lowering.	NAD	24-27	poly(ADP-ribose) polymerase 1	Homo sapiens	87-92
3436636-0	1987	Purification of rat liver alcohol dehydrogenase and studies on kinetic characteristics of thiamine, thiazole and NAD+ by the purified enzyme.	NAD	113-117	aldo-keto reductase family 1 member A1	Rattus norvegicus	26-47
3476810-7	1987	A likely mechanism for the former inhibition is that the increase in the NADH/NAD+ ratio in Leydig cells leads to inhibition of reactions catalyzed by 3 beta-hydroxy-5-ene-steroid dehydrogenase/5-ene-4-ene isomerase, but the inhibition mechanism operating at the androstenedione-to-testosterone step remains to be characterized.	NAD	73-77	hydroxy-delta-5-steroid dehydrogenase, 3 beta- and steroid delta-isomerase 5	Rattus norvegicus	151-193
3476810-7	1987	A likely mechanism for the former inhibition is that the increase in the NADH/NAD+ ratio in Leydig cells leads to inhibition of reactions catalyzed by 3 beta-hydroxy-5-ene-steroid dehydrogenase/5-ene-4-ene isomerase, but the inhibition mechanism operating at the androstenedione-to-testosterone step remains to be characterized.	NAD	78-82	hydroxy-delta-5-steroid dehydrogenase, 3 beta- and steroid delta-isomerase 5	Rattus norvegicus	151-193
3429208-2	1987	A simple rate equation for alcohol dehydrogenase was obtained by assuming independent binding sites for ethanol and NAD+ and fully competitive inhibition by the products of the reaction, acetaldehyde and NADH.	NAD	116-120	aldo-keto reductase family 1 member A1	Rattus norvegicus	27-48
3429208-2	1987	A simple rate equation for alcohol dehydrogenase was obtained by assuming independent binding sites for ethanol and NAD+ and fully competitive inhibition by the products of the reaction, acetaldehyde and NADH.	NAD	204-208	aldo-keto reductase family 1 member A1	Rattus norvegicus	27-48
3429208-6	1987	The parameters for alcohol dehydrogenase partially purified from rat liver were: Km for ethanol = 0.746 mM, Km for NAD+ = 0.0563 mM, Km for acetaldehyde = 7.07 microM, Km for NADH = 4.77 microM and Keq = 2.36 X 10(-4).	NAD	115-119	aldo-keto reductase family 1 member A1	Rattus norvegicus	19-40
3429208-6	1987	The parameters for alcohol dehydrogenase partially purified from rat liver were: Km for ethanol = 0.746 mM, Km for NAD+ = 0.0563 mM, Km for acetaldehyde = 7.07 microM, Km for NADH = 4.77 microM and Keq = 2.36 X 10(-4).	NAD	175-179	aldo-keto reductase family 1 member A1	Rattus norvegicus	19-40
3108318-5	1987	These studies suggest that steroid-induced cytotoxicity in susceptible lymphocytes is due to the presence of DNA strand breaks that activate poly(ADP-ribose) polymerase to a sufficient degree to consume cellular pools of NAD with a consequent depletion of ATP and loss of cell viability.	NAD	221-224	poly(ADP-ribose) polymerase 1	Homo sapiens	141-168
3033643-1	1987	Dihydropteridine reductase (DHPR; EC 1.6.99.7) catalyzes the NADH-mediated reduction of quinonoid dihydrobiopterin and is an essential component of the pterin-dependent aromatic amino acid hydroxylating systems.	NAD	61-65	quinoid dihydropteridine reductase	Homo sapiens	28-32
3426694-0	1987	Rate determining factors of ethanol oxidation in hepatocytes from starved and fed rats: effect of acetaldehyde concentration on the rate of NADH oxidation catalyzed by alcohol dehydrogenase.	NAD	140-144	aldo-keto reductase family 1 member A1	Rattus norvegicus	168-189
3828359-1	1987	Ferric leghemoglobin isolated from soybean root nodules was reduced nonenzymatically to ferrous leghemoglobin in vitro at pH 5.2 using either 1.0 mM NADH or NADPH as the reductant.	NAD	149-153	leghemoglobin A	Glycine max	96-109
3104902-1	1987	Aldose reductase [aldehyde reductase 2; alditol:NAD(P)+ 1-oxidoreductase, EC 1.1.1.21] catalyzes conversion of glucose to sorbitol.	NAD	48-51	aldo-keto reductase family 1 member B	Homo sapiens	0-16
3100337-1	1987	The catalytic activity of highly purified poly(ADP-ribose) polymerase was determined at constant NAD+ concentration and varying concentrations of sDNA or synthetic octadeoxyribonucleotides of differing composition.	NAD	97-101	poly(ADP-ribose) polymerase 1	Homo sapiens	42-69
3100337-8	1987	The synthetic molecule 6-amino-1,2-benzopyrone (6-aminocoumarin) competitively inhibited the coenzymic function of synthetic octadeoxyribonucleotides at constant concentration of NAD+, identifying a new inhibitory site of poly(ADP-ribose) polymerase.	NAD	179-183	poly(ADP-ribose) polymerase 1	Homo sapiens	222-249
3828359-1	1987	Ferric leghemoglobin isolated from soybean root nodules was reduced nonenzymatically to ferrous leghemoglobin in vitro at pH 5.2 using either 1.0 mM NADH or NADPH as the reductant.	NAD	149-153	leghemoglobin A	Glycine max	7-20
2950173-8	1987	Basal NAD turnover was prolonged threefold to fourfold by 3-aminobenzamide (3-ABA), an inhibitor of poly(ADP-ribose) synthetase.	NAD	6-9	poly(ADP-ribose) polymerase 1	Homo sapiens	100-127
3559036-4	1986	The concentration of radioactive 3-phosphoglycerate measured by liquid scintillation shows a good correlation (correlation coefficient: 0.997) with the spectrophotometrically determined concentration of NADH, which is formed from [U-14C]fructose-1,6-bisphosphate in equimolar concentration with 3-phosphoglycerate in aldolase and glyceraldehyde-3-phosphate dehydrogenase system.	NAD	203-207	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	330-370
3114164-3	1987	The formation of DNA strand breaks leads to activation of poly-ADP-ribose polymerase (24) which in turn causes depletion of NAD and ATP, followed by Ca++ influx and eventually by cell lysis.	NAD	124-127	poly(ADP-ribose) polymerase 1	Homo sapiens	58-84
3566771-2	1987	Reduction of external diferric transferrin is reflected in oxidation of internal NADH.	NAD	81-85	transferrin	Homo sapiens	31-42
3615421-1	1987	The highly active alcohol dehydrogenase (EC 1.1.1.1) in rat hepatic tumor cells (HTC) was purified 120-fold by chromatography on DEAE-Sepharose and AMP-Agarose to yield an enzyme with a specific activity of 88 mumole/min/mg protein, assayed with 1.7 mM NAD+ and 0.55 M ethanol at pH 9 and 30 degrees C. (By comparison, purified, normal rat liver enzyme has an activity of about 1 unit/mg.)	NAD	253-257	aldo-keto reductase family 1 member A1	Rattus norvegicus	18-39
3028476-1	1986	Homogeneous S-adenosylhomocysteinase (AdoHcyase) from rat liver is a tetrameric enzyme that contains four molecules of tightly bound NAD per mole of enzyme.	NAD	133-136	adenosylhomocysteinase	Rattus norvegicus	12-36
3028476-1	1986	Homogeneous S-adenosylhomocysteinase (AdoHcyase) from rat liver is a tetrameric enzyme that contains four molecules of tightly bound NAD per mole of enzyme.	NAD	133-136	adenosylhomocysteinase	Rattus norvegicus	38-47
3542074-2	1986	ATP was synthesized in a medium containing Tris-HCl buffer, pH 7.5, ADP, Mg2+, and Pi during NADH-dependent oxidation in the presence of cytochrome C and oxygen.	NAD	93-97	cytochrome c, somatic	Homo sapiens	137-149
3542074-4	1986	Quantitative assessment of ATP in lyophilized product was carried out by means of fluorimetry (excitation wavelength--360 nm; emission wavelength--460 nm) of NADH formed during coupled enzymatic reactions involving hexokinase and glucose-6-phosphate dehydrogenase.	NAD	158-162	hexokinase 1	Homo sapiens	215-225
3712278-9	1986	UDP-glucose dehydrogenase is subject to product inhibition by NADH and UDP-glucuronic acid and it is possible that NADH accumulates during rapid utilization of UDP-glucuronic acid.	NAD	62-66	UDP-glucose 6-dehydrogenase	Rattus norvegicus	0-25
3795046-10	1986	The mechanism is likely to be inhibition of UDP-glucose dehydrogenase activity by ethanol from increased intracellular NADH/NAD ratio accompanying ethanol oxidation.	NAD	119-123	UDP-glucose 6-dehydrogenase	Rattus norvegicus	44-69
3795046-10	1986	The mechanism is likely to be inhibition of UDP-glucose dehydrogenase activity by ethanol from increased intracellular NADH/NAD ratio accompanying ethanol oxidation.	NAD	119-122	UDP-glucose 6-dehydrogenase	Rattus norvegicus	44-69
3800997-5	1986	The data support the hypothesis that hydrogen peroxide generated by peroxidase from NADH may play a role during cell wall breakdown in plants.	NAD	84-88	peroxidase	Glycine max	68-78
3767994-3	1986	Reduction of external diferric transferrin is accompanied by oxidation of internal NADH which indicates that the transmembrane enzyme is an NADH diferric transferrin reductase.	NAD	83-87	transferrin	Homo sapiens	31-42
3767994-3	1986	Reduction of external diferric transferrin is accompanied by oxidation of internal NADH which indicates that the transmembrane enzyme is an NADH diferric transferrin reductase.	NAD	83-87	transferrin	Homo sapiens	154-165
3088445-1	1986	ADP-ribosyl transferase (ADPRT) is a DNA-dependent chromatin-associated enzyme which covalently attaches ADP-ribose moieties derived from NAD+ to protein acceptors to form poly(ADP-ribose).	NAD	138-142	poly(ADP-ribose) polymerase 1	Homo sapiens	0-23
3088445-1	1986	ADP-ribosyl transferase (ADPRT) is a DNA-dependent chromatin-associated enzyme which covalently attaches ADP-ribose moieties derived from NAD+ to protein acceptors to form poly(ADP-ribose).	NAD	138-142	poly(ADP-ribose) polymerase 1	Homo sapiens	25-30
3463506-7	1986	It was found that placental microsomal 20 alpha-HSD required NADPH as well as NADH.	NAD	78-82	hydroxysteroid 17-beta dehydrogenase 1	Homo sapiens	39-51
3530813-1	1986	NADH and NADPH accelerate the "in vitro" rate of proteolysis of glyceraldehyde-3-phosphate dehydrogenase (GAPDH) by elastase and other proteases, including lysosomal proteases.	NAD	0-4	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	64-104
3530813-1	1986	NADH and NADPH accelerate the "in vitro" rate of proteolysis of glyceraldehyde-3-phosphate dehydrogenase (GAPDH) by elastase and other proteases, including lysosomal proteases.	NAD	0-4	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	106-111
3745207-6	1986	In the presence of 0.5 mM NADH, NADP+, or NADPH, the P50 is raised to 3.8, 7.1, and 12.5 mm Hg, respectively.	NAD	26-30	nuclear factor kappa B subunit 1	Homo sapiens	53-56
16664999-4	1986	This peroxidase, which can use both NADH and NADPH as a substrate, is stimulated by low concentrations of monophenols, e.g. salicylhydroxamic acid and 2-methoxyphenol.	NAD	36-40	peroxidase 1	Zea mays	5-15
3026335-1	1986	The nicotinamide nucleotide dimers (NAD)2 and (NADP)2, obtained by electrochemical reduction of NAD+ and NADP+, are able to reduce such single-electron acceptors as the proteins cytochrome c, azurin and methaemoglobin, though at different rates.	NAD	96-100	cytochrome c, somatic	Homo sapiens	178-190
2941760-5	1986	Poly(ADP-ribose) polymerase utilizes nicotinamide adenine dinucleotide (NAD) as substrate and has been previously shown to consume NAD during exposure of cells to oxidants that was associated with inhibition of glycolysis, a decrease in cellular ATP, and cell death.	NAD	37-70	poly(ADP-ribose) polymerase 1	Homo sapiens	0-27
2941760-5	1986	Poly(ADP-ribose) polymerase utilizes nicotinamide adenine dinucleotide (NAD) as substrate and has been previously shown to consume NAD during exposure of cells to oxidants that was associated with inhibition of glycolysis, a decrease in cellular ATP, and cell death.	NAD	72-75	poly(ADP-ribose) polymerase 1	Homo sapiens	0-27
2941760-5	1986	Poly(ADP-ribose) polymerase utilizes nicotinamide adenine dinucleotide (NAD) as substrate and has been previously shown to consume NAD during exposure of cells to oxidants that was associated with inhibition of glycolysis, a decrease in cellular ATP, and cell death.	NAD	131-134	poly(ADP-ribose) polymerase 1	Homo sapiens	0-27
2941760-6	1986	In the current studies, inhibition of poly(ADP-ribose) polymerase by 3-aminobenzamide, nicotinamide, or theophylline in cells exposed to lethal concentrations of H2O2 prevented the sequence of events that eventually led to cell lysis--i.e., the decrease in NAD, followed by depletion of ATP, influx of extracellular Ca2+, actin polymerization and, finally, cell death.	NAD	257-260	poly(ADP-ribose) polymerase 1	Homo sapiens	38-65
3712278-9	1986	UDP-glucose dehydrogenase is subject to product inhibition by NADH and UDP-glucuronic acid and it is possible that NADH accumulates during rapid utilization of UDP-glucuronic acid.	NAD	115-119	UDP-glucose 6-dehydrogenase	Rattus norvegicus	0-25
2424480-1	1986	Monoclonal antibodies were developed against poly(ADP-ribose) polymerase and analyzed for their reactivity against the NAD+- and DNA-binding fragments.	NAD	119-123	poly(ADP-ribose) polymerase 1	Homo sapiens	45-72
3011109-1	1986	The interaction of heme nonapeptide (a proteolytic product of cytochrome c) with purified NADH:cytochrome b5 (EC 1.6.2.2) and NADPH:cytochrome P-450 (EC 1.6.2.4) reductases was investigated.	NAD	90-94	cytochrome c, somatic	Homo sapiens	62-74
3753651-10	1986	13, 121-134), the cytochrome b-558 in complex II was also reduced with NADH and reoxidized with fumarate.	NAD	71-75	CYTB	Ascaris suum	18-30
3956735-2	1986	A high rate of ADP-independent (non-coupled with ATP synthesis) respiration is observed during oxidation of succinate, NADH and ascorbate + cytochrome c, but not with NAD-dependent substrates.	NAD	119-123	cytochrome c, somatic	Homo sapiens	140-152
3956735-2	1986	A high rate of ADP-independent (non-coupled with ATP synthesis) respiration is observed during oxidation of succinate, NADH and ascorbate + cytochrome c, but not with NAD-dependent substrates.	NAD	119-122	cytochrome c, somatic	Homo sapiens	140-152
3956735-3	1986	It increases in the presence of cytochrome c during oxidation of succinate and NADH and is also revealed during oxidation of NAD-dependent substrates in the presence of NAD+ and cytochrome c.	NAD	79-83	cytochrome c, somatic	Homo sapiens	32-44
3956735-3	1986	It increases in the presence of cytochrome c during oxidation of succinate and NADH and is also revealed during oxidation of NAD-dependent substrates in the presence of NAD+ and cytochrome c.	NAD	79-83	cytochrome c, somatic	Homo sapiens	178-190
3956735-3	1986	It increases in the presence of cytochrome c during oxidation of succinate and NADH and is also revealed during oxidation of NAD-dependent substrates in the presence of NAD+ and cytochrome c.	NAD	79-82	cytochrome c, somatic	Homo sapiens	32-44
3956735-3	1986	It increases in the presence of cytochrome c during oxidation of succinate and NADH and is also revealed during oxidation of NAD-dependent substrates in the presence of NAD+ and cytochrome c.	NAD	79-82	cytochrome c, somatic	Homo sapiens	178-190
3956735-3	1986	It increases in the presence of cytochrome c during oxidation of succinate and NADH and is also revealed during oxidation of NAD-dependent substrates in the presence of NAD+ and cytochrome c.	NAD	169-173	cytochrome c, somatic	Homo sapiens	32-44
3954760-0	1986	Decrease of NADH in HeLa cells in the presence of transferrin or ferricyanide.	NAD	12-16	transferrin	Homo sapiens	50-61
3954760-1	1986	The short-term incubation of HeLa cells in the presence of diferric transferrin or ferricyanide, which are reduced externally by the transplasma membrane reductase, produces a stoichiometric decrease in NADH and increase in NAD+, which is stimulated by insulin.	NAD	203-207	transferrin	Homo sapiens	68-79
3954760-1	1986	The short-term incubation of HeLa cells in the presence of diferric transferrin or ferricyanide, which are reduced externally by the transplasma membrane reductase, produces a stoichiometric decrease in NADH and increase in NAD+, which is stimulated by insulin.	NAD	224-228	transferrin	Homo sapiens	68-79
3954760-6	1986	It appears that oxidation of NADH by the transmembrane electron transport using ferricyanide or iron transferrin as external electron acceptors is sufficient to stimulate growth in HeLa cells.	NAD	29-33	transferrin	Homo sapiens	101-112
3633190-7	1986	Oxidation of NADH, but not xanthine, was inhibited by KCN, ascorbate, MnCl2, cytochrome c, mannitol, Tris, epinephrine, norepinephrine, and triiodothyronine.	NAD	13-17	cytochrome c, somatic	Homo sapiens	77-89
3000966-8	1986	These data indicate that the radiosensitizing effect of heat and nicotinamide could both be explained by effects on the enzyme ADPRT, i.e. nicotinamide by directly blocking the enzyme and hyperthermia by limiting the co-substrate (NAD+).	NAD	231-235	poly(ADP-ribose) polymerase 1	Homo sapiens	127-132
3101408-1	1986	Poly(ADP-ribose) synthetase is a chromatin-bound enzyme which synthesizes a protein-bound homopolymer of ADP-ribose utilizing NAD as a substrate.	NAD	126-129	poly(ADP-ribose) polymerase 1	Homo sapiens	0-27
3467630-3	1986	By opposing some of the effects of estrogen, the progestogen alters the utilization of NAD in the endometrium to induce an increase in NADP+ production, elevation of the NADP+/NADPH ratio, and inhibition of the rate of degradation of NAD to NAM and ADP-ribose.	NAD	87-90	SH3 and cysteine rich domain 3	Homo sapiens	241-244
3468920-1	1986	Hepatic microsomal H2O2 production (oxidase function of microsomal cytochrome P-450) is strongly dependent on NADPH or NADH concentration.	NAD	119-123	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	67-83
3789876-1	1986	Ethanol metabolism to acetaldehyde by NAD+-dependent alcohol dehydrogenase (ADH) activity reduces, in part, androgen secretion by rat Leydig cells.	NAD	38-41	aldo-keto reductase family 1 member A1	Rattus norvegicus	53-74
3789876-1	1986	Ethanol metabolism to acetaldehyde by NAD+-dependent alcohol dehydrogenase (ADH) activity reduces, in part, androgen secretion by rat Leydig cells.	NAD	38-41	aldo-keto reductase family 1 member A1	Rattus norvegicus	76-79
3789876-2	1986	ADH in Leydig cells is proposed to decrease the NAD+/NADH ratio and thereby inhibit NAD+-dependent delta 5-3 beta hydroxysteroid dehydrogenase-isomerase activity and increase NADH-dependent 5 alpha-androstane-3 beta-hydroxysteroid dehydrogenase activity.	NAD	48-52	aldo-keto reductase family 1 member A1	Rattus norvegicus	0-3
3789876-2	1986	ADH in Leydig cells is proposed to decrease the NAD+/NADH ratio and thereby inhibit NAD+-dependent delta 5-3 beta hydroxysteroid dehydrogenase-isomerase activity and increase NADH-dependent 5 alpha-androstane-3 beta-hydroxysteroid dehydrogenase activity.	NAD	53-57	aldo-keto reductase family 1 member A1	Rattus norvegicus	0-3
3789876-2	1986	ADH in Leydig cells is proposed to decrease the NAD+/NADH ratio and thereby inhibit NAD+-dependent delta 5-3 beta hydroxysteroid dehydrogenase-isomerase activity and increase NADH-dependent 5 alpha-androstane-3 beta-hydroxysteroid dehydrogenase activity.	NAD	48-51	aldo-keto reductase family 1 member A1	Rattus norvegicus	0-3
3789876-2	1986	ADH in Leydig cells is proposed to decrease the NAD+/NADH ratio and thereby inhibit NAD+-dependent delta 5-3 beta hydroxysteroid dehydrogenase-isomerase activity and increase NADH-dependent 5 alpha-androstane-3 beta-hydroxysteroid dehydrogenase activity.	NAD	175-179	aldo-keto reductase family 1 member A1	Rattus norvegicus	0-3
3732224-0	1986	Purification and properties of NADH-specific dihydropteridine reductase from human erythrocytes.	NAD	31-35	quinoid dihydropteridine reductase	Homo sapiens	45-71
3732224-3	1986	The enzyme reacted with antiserum against NADH-specific dihydropteridine reductase from bovine liver and formed a single immunoprecipitin line in the Ouchterlony double-diffusion system.	NAD	42-46	quinoid dihydropteridine reductase	Homo sapiens	56-82
3732224-7	1986	The average activity of NADH-specific dihydropteridine reductase of 9 human blood samples from healthy males (20-25 years old) was calculated to be approximately 600 mU/g of hemoglobin, 1.8 mU per 20 microliters of blood, or 1.9 mU per 10(8) erythrocytes.	NAD	24-28	quinoid dihydropteridine reductase	Homo sapiens	38-64
4091803-7	1985	NADPH (1 mM) and NADH (1 mM) completely [2-mercaptoethanol (5 mM) almost completely] inhibited the 5,6-epoxidation catalysed by haemoglobin, but catalase, superoxide dismutase and mannitol showed no inhibitory effect.	NAD	17-21	catalase	Homo sapiens	145-153
3935115-1	1985	This study compared the NADH- and NADPH-supported p-nitrophenetole (NP) O-deethylase, ethylmorphine (EM) O-deethylase and EM N-demethylase activities of rat hepatic microsomes with respect to dioxygen requirement, inhibition by carbon monoxide, inhibition by classical inhibitors of cytochrome P-450 systems, and the involvement of NADH-cytochrome b5, cytochrome b5 reductase and NADPH-cytochrome P-450 reductase.	NAD	24-28	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	283-299
2419197-12	1985	The participation of poly(ADP-ribose)polymerase activity in the HD-induced NAD+ loss was substantiated by prevention of this loss in the presence of inhibitors of the enzyme.	NAD	75-79	poly(ADP-ribose) polymerase 1	Homo sapiens	21-47
4054226-3	1985	It is also shown that binding of the 34K-ssb protein to ssDNA is fully inhibited by NADH but not by NAD+ or by several other nucleotides.	NAD	84-88	lupus La protein homolog	Oryctolagus cuniculus	41-44
3101158-1	1986	The response of cellular NAD+ metabolism to DEN and/or ABA and the carcinogenesis of the liver initiated by DEN and ABA were studied in rats.	NAD	25-29	dendrin	Rattus norvegicus	44-47
3101158-2	1986	The liver NAD+ level was depleted by an ip injection of 20 mg or 200 mg/kg body weight of DEN.	NAD	10-14	dendrin	Rattus norvegicus	90-93
3101158-3	1986	ABA, administered ip at a dose of 600 mg/kg simultaneously with or 4 hours after DEN, prevented the depletion of NAD+ by DEN.	NAD	113-117	dendrin	Rattus norvegicus	121-124
4065147-5	1985	The action of thiol oxidants on the in vitro biosynthesised and microsomally processed prolactin were both dose-dependent and catalytic; non-thiol oxidants such as NAD+ and NADP+ were ineffective.	NAD	164-168	prolactin	Bos taurus	87-96
4054226-3	1985	It is also shown that binding of the 34K-ssb protein to ssDNA is fully inhibited by NADH but not by NAD+ or by several other nucleotides.	NAD	100-104	lupus La protein homolog	Oryctolagus cuniculus	41-44
4054226-4	1985	Enzymatic tests on the possible NADH/NAD+-dependent dehydrogenase activity of the 34K-ssb protein have demonstrated that it has lactic dehydrogenase activity (LDH) with a specific activity comparable to that of rabbit muscle.	NAD	32-36	lupus La protein homolog	Oryctolagus cuniculus	86-89
2417997-5	1985	Next the D-glyceraldehyde-3-phosphate is oxidized by exogenous and endogenous glyceraldehyde-3-phosphate dehydrogenase and the electrons are transported concomitantly via NAD+, phenazine methosulphate and menadione to nitro-BT.	NAD	171-175	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	78-118
4054226-4	1985	Enzymatic tests on the possible NADH/NAD+-dependent dehydrogenase activity of the 34K-ssb protein have demonstrated that it has lactic dehydrogenase activity (LDH) with a specific activity comparable to that of rabbit muscle.	NAD	32-35	lupus La protein homolog	Oryctolagus cuniculus	86-89
2995995-5	1985	Similar correlations are found in the bipartite NAD-binding domains of alcohol dehydrogenase and glyceraldehyde-3-phosphate dehydrogenase.	NAD	48-51	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	97-137
4074778-6	1985	NADH may also serve as an electron donor for cytochrome P-450scc.	NAD	0-4	cytochrome P450 family 11 subfamily A member 1	Homo sapiens	45-64
3928401-1	1985	We propose that the activation of poly(ADP-ribose) synthetase by DNA damage serves to decrease rapidly and transiently the cellular level of NAD (by production therefrom of poly ADP-ribose).	NAD	141-144	poly(ADP-ribose) polymerase 1	Homo sapiens	34-61
4005852-8	1985	Similarly, cytosolic reduction of chromium(VI) was partially inhibited by selective metabolic depletors of both coenzymes of DT-diaphorase, i.e., NADPH and NADH.	NAD	156-160	NAD(P)H quinone dehydrogenase 1	Rattus norvegicus	125-138
4074667-3	1985	With purified, phospholipid-reconstituted BDH and NAD as the variable substrate, the apparent Km and Vmax values were respectively 0.25 mM and 62.5 mumol min-1 (mg of protein)-1.	NAD	50-53	CD59 molecule (CD59 blood group)	Homo sapiens	154-177
4014446-9	1985	These results suggest that one mechanism by which the cytosolic modifier protein stimulates G3PD activity is to decrease product inhibition by NADH.	NAD	143-147	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	92-96
4044832-6	1985	LTB4 omega-hydroxylase activity in isolated PMN membranes was linear with respect to duration of incubation and protein concentration, was maximal at pH 7.4, had a Km for LTB4 of 0.6 microM, and was dependent on oxygen and on reduced pyridine nucleotides (apparent Km for NADPH = 0.5 microM; apparent Km for NADH = 223 microM).	NAD	308-312	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	0-22
4052043-4	1985	The kinetics of these inhibitions was competitive with cytochrome b5, and non-competitive with NADH, indicating that these anions inhibit the interaction of the enzyme with cytochrome b5.	NAD	95-99	cytochrome b5 type A	Bos taurus	173-186
2988642-1	1985	Heme-nonapeptide, derived from cytochrome c, inhibited both the NADPH- and NADH-dependent lipid peroxidation of brain microsomes but, in the case of liver microsomes, this inhibitory effect manifested itself in the presence of SKF-525A (a specific blocker of cytochrome P-450) only.	NAD	75-79	cytochrome c, somatic	Homo sapiens	31-43
3875625-1	1985	High-performance liquid chromatographic techniques were developed for the simultaneous detection of metabolites in a cytochrome P-450 model system composed of NADH, haemoglobin and methylene blue.	NAD	159-163	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	117-133
16664269-5	1985	These studies indicate that the methylation state of lysine 115 may be important in the maximal NAD kinase activator activity of calmodulin and support the concept that calmodulin has multiple functional domains in addition to multiple structural domains.	NAD	96-99	calmodulin 1	Homo sapiens	129-139
16664269-5	1985	These studies indicate that the methylation state of lysine 115 may be important in the maximal NAD kinase activator activity of calmodulin and support the concept that calmodulin has multiple functional domains in addition to multiple structural domains.	NAD	96-99	calmodulin 1	Homo sapiens	169-179
2986713-1	1985	The reactivities of myeloperoxidase-H2O2-Cl- and sodium hypochlorite with amino acids, uric acid, NADH, ascorbic acid, ADP, albumin, haemoglobin, alpha 1-antitrypsin and some hydroxyl radical scavengers have been compared.	NAD	98-102	myeloperoxidase	Homo sapiens	20-35
4007074-2	1985	The DHPR activity was higher in the retina [120.56 +/- 12.46 nmol NADH oxidized min-1 (mg soluble protein)-1] than in the ciliary body--iris [46.10 +/- 7.46 nmol NADH oxidized min-1 (mg soluble protein)-1] and lens [2.79 +/- 0.15 nmol NADH oxidized min-1 (mg soluble protein)-1].	NAD	66-70	quinoid dihydropteridine reductase	Homo sapiens	4-8
4023425-6	1985	In addition, the extent of NAD-effect using acetylcholinesterase (AChE) was lesser than that of CEase, therefore, a higher susceptibility of liver microsomal CEase to organophosphorus insecticides may be explained, at least inpart, by NAD-effect.	NAD	27-30	acetylcholinesterase (Cartwright blood group)	Homo sapiens	44-64
4023425-6	1985	In addition, the extent of NAD-effect using acetylcholinesterase (AChE) was lesser than that of CEase, therefore, a higher susceptibility of liver microsomal CEase to organophosphorus insecticides may be explained, at least inpart, by NAD-effect.	NAD	27-30	acetylcholinesterase (Cartwright blood group)	Homo sapiens	66-70
3996398-7	1985	Disruption of the purified peroxisomes by the hypotonic treatment or in the alkaline conditions resulted in the release of catalase from the broken organelles, while aldehyde dehydrogenase as well as nucleoid-bound urate oxidase and the peroxisomal membrane marker NADH:cytochrome c reductase remained in the peroxisomal "ghosts".	NAD	265-269	catalase	Rattus norvegicus	123-131
3922304-6	1985	Aldose reductase activity is expressed with either NADH or NADPH as cofactors, whereas aldehyde reductase II can utilize only NADPH.	NAD	51-55	aldo-keto reductase family 1 member B	Homo sapiens	0-16
4007074-2	1985	The DHPR activity was higher in the retina [120.56 +/- 12.46 nmol NADH oxidized min-1 (mg soluble protein)-1] than in the ciliary body--iris [46.10 +/- 7.46 nmol NADH oxidized min-1 (mg soluble protein)-1] and lens [2.79 +/- 0.15 nmol NADH oxidized min-1 (mg soluble protein)-1].	NAD	66-70	CD59 molecule (CD59 blood group)	Homo sapiens	80-108
4007074-2	1985	The DHPR activity was higher in the retina [120.56 +/- 12.46 nmol NADH oxidized min-1 (mg soluble protein)-1] than in the ciliary body--iris [46.10 +/- 7.46 nmol NADH oxidized min-1 (mg soluble protein)-1] and lens [2.79 +/- 0.15 nmol NADH oxidized min-1 (mg soluble protein)-1].	NAD	162-166	quinoid dihydropteridine reductase	Homo sapiens	4-8
4007074-2	1985	The DHPR activity was higher in the retina [120.56 +/- 12.46 nmol NADH oxidized min-1 (mg soluble protein)-1] than in the ciliary body--iris [46.10 +/- 7.46 nmol NADH oxidized min-1 (mg soluble protein)-1] and lens [2.79 +/- 0.15 nmol NADH oxidized min-1 (mg soluble protein)-1].	NAD	162-166	quinoid dihydropteridine reductase	Homo sapiens	4-8
2992542-0	1985	[Reduction of cytochrome c by NADH induced by light].	NAD	30-34	cytochrome c, somatic	Homo sapiens	14-26
3856839-7	1985	In contrast to nearly all other known structures of protein-bound NADP, NAD, and FAD, the NADP molecule of beef liver catalase is folded into a right-handed helix and bound, in part, in the vicinity of the carboxyl end of two alpha-helices.	NAD	66-69	catalase	Homo sapiens	118-126
3999477-4	1985	In conclusion, NAD was enzymatically reduced to NADH, a cofactor of microsomal dehydrogenase(s), and then formation of EPNoxon through microsomal cytochrome P-450-coupled monooxygenase was accelerated.	NAD	15-18	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	146-162
4002652-2	1985	The second half of the normal pregnancy was characterized by an increase in activity of hexokinase, in content of 2,3-DPG, ADP, by a distinct decrease in ATP, NAD and the ratio ATP/ADP as well as by unaltered ratios NAD/NADH and lactate/pyruvate.	NAD	220-224	hexokinase 1	Homo sapiens	88-98
2988200-1	1985	In the particles enriched with plasmatic membranes of target cells (human erythrocytes, skeletal muscles and adipocytes of rats) ATP was steadily formed within 1 min of incubation of the particles with insulin (4 microgram/ml) in the medium containing Tris-HCl buffer, pH 7.5, ADP, Mg2+, inorganic phosphate, NaF, during NADH oxidation in presence of cytochrome c and oxygen (30 degrees).	NAD	321-325	insulin	Homo sapiens	202-209
3970930-2	1985	The biological activity of elongation factor 2 (EF-2) following NAD+ - and diphtheria-toxin-dependent ADP-ribosylation was studied (i) in translation experiments using the reticulocyte lysate system and (ii) in ribosomal binding experiments using either reconstituted empty rat liver ribosomes or programmed reticulocyte polysomes.	NAD	64-68	eukaryotic translation elongation factor 2	Rattus norvegicus	27-46
3970916-5	1985	This blockade is due to the inhibition of glyceraldehyde-3-phosphate dehydrogenase by NAD+ depletion caused by enzymatic oxidation of formaldehyde coupled to NADH production.	NAD	86-90	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	42-82
3970916-5	1985	This blockade is due to the inhibition of glyceraldehyde-3-phosphate dehydrogenase by NAD+ depletion caused by enzymatic oxidation of formaldehyde coupled to NADH production.	NAD	158-162	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	42-82
3970930-2	1985	The biological activity of elongation factor 2 (EF-2) following NAD+ - and diphtheria-toxin-dependent ADP-ribosylation was studied (i) in translation experiments using the reticulocyte lysate system and (ii) in ribosomal binding experiments using either reconstituted empty rat liver ribosomes or programmed reticulocyte polysomes.	NAD	64-68	eukaryotic translation elongation factor 2	Rattus norvegicus	48-52
3970930-17	1985	The data indicate that the inhibition of translocation caused by diphtheria toxin and NAD+ is mediated through a reduced affinity of the ADP-ribosylated EF-2 for binding to ribosomes in the pretranslocation state.	NAD	86-90	eukaryotic translation elongation factor 2	Rattus norvegicus	153-157
3155867-1	1985	Poly(ADP-ribose) polymerase is a chromatin-bound enzyme which, on activation by DNA strand breaks, catalyzes the successive transfer of ADP-ribose units from NAD to nuclear proteins.	NAD	158-161	poly(ADP-ribose) polymerase 1	Homo sapiens	0-27
3989481-3	1985	NADH, formed in the glycerol-3-phosphate and glyceraldehyde-3-phosphate dehydrogenase reactions, is subsequently determined by the bacterial luciferase system.	NAD	0-4	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	45-85
4043713-4	1985	Twenty-four hours following a potentiating dose of ethanol and CCl4 an 81 and 57% decline in NAD+-dependent microsomal and mitochondrial ALDH activity was observed, respectively.	NAD	93-97	C-C motif chemokine ligand 4	Rattus norvegicus	63-67
3018063-2	1985	The pyridine cofactors NADPH and NADH, riboflavin, and the nucleosides 2-thiouracil and 4-thiouridine were found to sensitize the transmission of photon energy from solar radiation and monochromatic radiation (290, 334, 365, and 405 nm) to oxygen, resulting in O2- formation, as detected by superoxide dismutase-inhibitable cytochrome c reduction.	NAD	33-37	cytochrome c, somatic	Homo sapiens	324-336
3155867-6	1985	Inhibitors of poly(ADP-ribose) polymerase or deficiencies of the substrate, NAD, lead to retardation of the DNA repair process.	NAD	76-79	poly(ADP-ribose) polymerase 1	Homo sapiens	14-41
3155867-8	1985	Depletion of NAD and consequent lowering of cellular ATP pools, due to activation of poly(ADP-ribose) polymerase, may account for rapid cell death before DNA repair takes place and before the genetic effects of DNA damage become manifest.	NAD	13-16	poly(ADP-ribose) polymerase 1	Homo sapiens	85-112
6093877-9	1984	The identical specific activity employing dichloroindophenol as an electron acceptor with NADH or NADPH as donor indicate a DT-diaphorase (EC 1.6.99.2) like activity in the astrocytes plasma membrane.	NAD	90-94	NAD(P)H quinone dehydrogenase 1	Homo sapiens	124-137
16663940-2	1984	The NADH-GDH purified 161-fold with ammonium sulfate, DEAE-Toyopearl, and Sephadex G-200 was also activated by Ca(2+) in the presence of 160 micromolar NADH.	NAD	4-8	glutamate dehydrogenase	Zea mays	9-12
16663940-2	1984	The NADH-GDH purified 161-fold with ammonium sulfate, DEAE-Toyopearl, and Sephadex G-200 was also activated by Ca(2+) in the presence of 160 micromolar NADH.	NAD	152-156	glutamate dehydrogenase	Zea mays	9-12
16663940-4	1984	The deamination reaction (NAD-GDH) was not influenced by the addition of Ca(2+).About 25% of the NADH-GDH activity was solubilized from purified mitochondria after a simple osmotic shock treatment, whereas the remaining 75% of the activity was associated with the mitochondrial membrane fraction.	NAD	26-29	glutamate dehydrogenase	Zea mays	30-33
16663940-4	1984	The deamination reaction (NAD-GDH) was not influenced by the addition of Ca(2+).About 25% of the NADH-GDH activity was solubilized from purified mitochondria after a simple osmotic shock treatment, whereas the remaining 75% of the activity was associated with the mitochondrial membrane fraction.	NAD	26-29	glutamate dehydrogenase	Zea mays	102-105
16663940-4	1984	The deamination reaction (NAD-GDH) was not influenced by the addition of Ca(2+).About 25% of the NADH-GDH activity was solubilized from purified mitochondria after a simple osmotic shock treatment, whereas the remaining 75% of the activity was associated with the mitochondrial membrane fraction.	NAD	97-101	glutamate dehydrogenase	Zea mays	30-33
16663940-4	1984	The deamination reaction (NAD-GDH) was not influenced by the addition of Ca(2+).About 25% of the NADH-GDH activity was solubilized from purified mitochondria after a simple osmotic shock treatment, whereas the remaining 75% of the activity was associated with the mitochondrial membrane fraction.	NAD	97-101	glutamate dehydrogenase	Zea mays	102-105
16663940-5	1984	When the lysed mitochondria, mitochondrial matrix, or mitochondrial membrane fraction was used as the source of NADH-GDH, Ca(2+) had little effect on its activity.	NAD	112-116	glutamate dehydrogenase	Zea mays	117-120
16663940-6	1984	The mitochondrial fraction contained about 155 nanomoles Ca per milligram of mitochondrial protein, suggesting that the NADH-GDH in the mitochondria is already in an activated form with regard Ca(2+).	NAD	120-124	glutamate dehydrogenase	Zea mays	125-128
6477525-6	1984	From the detritiation of labelled lactate and the labelling pattern of ethanol and glucose, we calculated the rate of reoxidation of NADH catalysed by lactate dehydrogenase, alcohol dehydrogenase and triosephosphate dehydrogenase.	NAD	133-137	aldo-keto reductase family 1 member A1	Rattus norvegicus	174-195
6477525-12	1984	The rate of reoxidation of NADH catalysed by lactate dehydrogenase was only a few per cent of the maximal activity of the enzymes, but the rate of reoxidation of NADH catalysed by alcohol dehydrogenase was equal to or higher than the maximal activity as measured in vitro, suggesting that the dissociation of enzyme-bound NAD+ as well as NADH may be rate-limiting steps in the alcohol dehydrogenase reaction.	NAD	27-31	aldo-keto reductase family 1 member A1	Rattus norvegicus	180-201
6477525-12	1984	The rate of reoxidation of NADH catalysed by lactate dehydrogenase was only a few per cent of the maximal activity of the enzymes, but the rate of reoxidation of NADH catalysed by alcohol dehydrogenase was equal to or higher than the maximal activity as measured in vitro, suggesting that the dissociation of enzyme-bound NAD+ as well as NADH may be rate-limiting steps in the alcohol dehydrogenase reaction.	NAD	27-31	aldo-keto reductase family 1 member A1	Rattus norvegicus	377-398
6477525-12	1984	The rate of reoxidation of NADH catalysed by lactate dehydrogenase was only a few per cent of the maximal activity of the enzymes, but the rate of reoxidation of NADH catalysed by alcohol dehydrogenase was equal to or higher than the maximal activity as measured in vitro, suggesting that the dissociation of enzyme-bound NAD+ as well as NADH may be rate-limiting steps in the alcohol dehydrogenase reaction.	NAD	162-166	aldo-keto reductase family 1 member A1	Rattus norvegicus	180-201
6477525-12	1984	The rate of reoxidation of NADH catalysed by lactate dehydrogenase was only a few per cent of the maximal activity of the enzymes, but the rate of reoxidation of NADH catalysed by alcohol dehydrogenase was equal to or higher than the maximal activity as measured in vitro, suggesting that the dissociation of enzyme-bound NAD+ as well as NADH may be rate-limiting steps in the alcohol dehydrogenase reaction.	NAD	162-166	aldo-keto reductase family 1 member A1	Rattus norvegicus	377-398
6477525-12	1984	The rate of reoxidation of NADH catalysed by lactate dehydrogenase was only a few per cent of the maximal activity of the enzymes, but the rate of reoxidation of NADH catalysed by alcohol dehydrogenase was equal to or higher than the maximal activity as measured in vitro, suggesting that the dissociation of enzyme-bound NAD+ as well as NADH may be rate-limiting steps in the alcohol dehydrogenase reaction.	NAD	162-166	aldo-keto reductase family 1 member A1	Rattus norvegicus	180-201
6477525-12	1984	The rate of reoxidation of NADH catalysed by lactate dehydrogenase was only a few per cent of the maximal activity of the enzymes, but the rate of reoxidation of NADH catalysed by alcohol dehydrogenase was equal to or higher than the maximal activity as measured in vitro, suggesting that the dissociation of enzyme-bound NAD+ as well as NADH may be rate-limiting steps in the alcohol dehydrogenase reaction.	NAD	162-166	aldo-keto reductase family 1 member A1	Rattus norvegicus	377-398
6326802-9	1984	A mechanism for electron transfer from NADH to cytochrome b5 is discussed on the basis of the one-electron redox potentials of the enzyme and is compared with the electron-transfer mechanism of NADPH-cytochrome P-450 reductase.	NAD	39-43	cytochrome p450 oxidoreductase	Homo sapiens	194-226
6327687-1	1984	The activity of purified Ca2+, Mg2+-dependent endonuclease was inhibited when the enzyme was incubated in a system containing poly(ADP-ribose) synthetase, NAD+, Mg2+, and DNA.	NAD	155-159	mucolipin TRP cation channel 1	Homo sapiens	31-34
6325408-8	1984	These results indicate that poly (ADP-ribose) synthetase contains three separable domains, the first possessing the site for binding of the substrate, NAD, the second containing the site for binding of DNA, and the third acting as the site(s) for accepting poly(ADP-ribose).	NAD	151-154	poly(ADP-ribose) polymerase 1	Homo sapiens	28-56
6433908-4	1984	Conversion of valproic acid to all three metabolites in microsomes required NADPH (NADH was less effective), utilized molecular oxygen, was suppressed by inhibitors of cytochrome P-450 and was stimulated (notably at C-3 and C-4) by phenobarbital pretreatment of the rats.	NAD	83-87	complement C4A	Rattus norvegicus	224-227
6087035-1	1984	ADP-ribosyl transferase (ADP-RT) is a chromatin-bound nuclear enzyme catalysing the transfer of ADP-ribose from NAD+ to chromatin proteins.	NAD	112-116	poly(ADP-ribose) polymerase 1	Homo sapiens	0-23
6233965-3	1984	Thus, in contrast to the liver, the cytosolic redox state of the NADH/NAD+ system in isolated perfused heart oxidizing external glucose or fatty acid is not amenable to optical monitoring, but can be assessed from the state of the lactate dehydrogenase or glycerol-3-phosphate dehydrogenase systems.	NAD	65-69	glycerol-3-phosphate dehydrogenase 1	Rattus norvegicus	256-290
6233965-3	1984	Thus, in contrast to the liver, the cytosolic redox state of the NADH/NAD+ system in isolated perfused heart oxidizing external glucose or fatty acid is not amenable to optical monitoring, but can be assessed from the state of the lactate dehydrogenase or glycerol-3-phosphate dehydrogenase systems.	NAD	70-74	glycerol-3-phosphate dehydrogenase 1	Rattus norvegicus	256-290
6698026-12	1984	A cytochrome of type b with an absorption maximum at 559 nm accumulates during starvation only in queuine-lacking cells; it might be a component of an NAD-independent lactic acid oxidoreductase as is cytochrome b 557 in yeast and be responsible for the reduced level of lactate in cells lacking queuine in tRNA.	NAD	151-154	oxidoreductase	Saccharomyces cerevisiae S288C	179-193
6331001-3	1984	In the same mixtures, but containing cytochrome c, oxidation of NAD-dependent substrates was decreased less distinctly and oxidation of succinate was similar to the control values.	NAD	64-67	cytochrome c, somatic	Homo sapiens	37-49
6331001-4	1984	The rate of rhothenone-sensitive oxidation of NADH as well as the activating effect of cytochrome c on oxidation of all the substrates studied, except of NADH, were increased in ischemia.	NAD	154-158	cytochrome c, somatic	Homo sapiens	87-99
6319419-9	1984	ADP-ribose-whole histones X adducts formed by ADP-ribosyltransferase served as initiators for poly(ADP-ribose) synthesis when these adducts were incubated in the presence of NAD, DNA, Mg2+, and the purified poly(ADP-ribose) synthetase, in which poly(ADP-ribose) formation can occur.	NAD	174-177	poly(ADP-ribose) polymerase 1	Homo sapiens	207-234
6546483-2	1984	The cells were cryopreserved and stored under liquid nitrogen for intervals of 2, 4, 6, 8, or 12 wk, then assayed for viability (using the trypan dye exclusion method as well as the NADH-dependent cytochrome c reductase (cytochrome c) assay) and cellular function (as documented by the measurement of in vitro aryl hydrocarbon hydroxylase (AHH) induction by benzanthracene (BA) and by quantitation of PAM particulate phagocytosis).	NAD	182-186	cytochrome c, somatic	Homo sapiens	197-209
6692539-4	1984	This increase is a result of coupling the following series of enzymes: hexokinase (EC 2.7.1.1), glucosephosphate isomerase (EC 5.3.1.9), and glucose-6-phosphate dehydrogenase (EC 1.1.1.49, NAD+-dependent).	NAD	189-193	hexokinase 1	Homo sapiens	71-81
6087035-1	1984	ADP-ribosyl transferase (ADP-RT) is a chromatin-bound nuclear enzyme catalysing the transfer of ADP-ribose from NAD+ to chromatin proteins.	NAD	112-116	poly(ADP-ribose) polymerase 1	Homo sapiens	25-31
6870945-5	1983	Addition of NADH increased the extent of activation suggesting that betamethasone facilitates transference of the second electron to cytochrome P-450.	NAD	12-16	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	133-149
6316434-1	1983	Adriamycin mediated electron transport between NADH and cytochrome c results in the formation of a new linkage between adriamycin and cardiolipin.	NAD	47-51	cytochrome c, somatic	Homo sapiens	56-68
6679347-2	1983	Thermal inactivation kinetics, employed here as a probe for site-site heterogeneity in solution, show that green gram glyceraldehyde 3-phosphate dehydrogenase (in the absence and presence of phosphate and NAD+) loses activity in two distinct phases, each of which accounts for half of the initial activity.	NAD	205-209	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	118-158
6367210-2	1983	The ATP was synthesized in a medium containing Tris-HCl buffer, pH 7.5, ADP, Mg2+ and P1 during NADH-dependent oxidation in presence of cytochrome c and oxygen; amount of the ATP was 0.1-0.3 nmole/mg/min.	NAD	96-100	cytochrome c, somatic	Homo sapiens	136-148
6407471-2	1983	Since Drosophila alcohol dehydrogenase (ADH) uses NAD+ to remove a hydrogen from ethanol in the first step of alcohol catabolism, it is possible that under alcohol stress conditions the in vivo NAD+ levels in Drosophila may decrease.	NAD	50-54	Alcohol dehydrogenase	Drosophila melanogaster	40-43
6860707-4	1983	The mechanism by which NADH and NADPH prevent lipid peroxidation may involve a reduction of the hydroperoxides mediated by cytochrome P-450 and occurring without formation of free radical forms that are usual sparkers of lipid peroxidation.	NAD	23-27	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	123-139
6305359-3	1983	NADH-synergistic effect decreased in parallel with the decrease of the ratio of cytochrome b5/cytochrome P-450 in liver microsomes.	NAD	0-4	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	94-110
6301892-2	1983	delta 5-3 beta-Hydroxysteroid dehydrogenase (delta 5-3 beta-HSD) and 17 beta-hydroxysteroid dehydrogenase (17 beta-HSD) activities were detected by Dickmann and Dey"s reaction medium consisting of 1.8 mg substrate (pregnenolone or 17 beta-estradiol [E2]), 4 mg nicotinamide-adenine dinucleotide, 2 mg nitro-blue tetrazolium, 10 ml 0.1 M phosphate buffer.	NAD	261-294	hydroxysteroid 17-beta dehydrogenase 13	Homo sapiens	69-105
6301892-2	1983	delta 5-3 beta-Hydroxysteroid dehydrogenase (delta 5-3 beta-HSD) and 17 beta-hydroxysteroid dehydrogenase (17 beta-HSD) activities were detected by Dickmann and Dey"s reaction medium consisting of 1.8 mg substrate (pregnenolone or 17 beta-estradiol [E2]), 4 mg nicotinamide-adenine dinucleotide, 2 mg nitro-blue tetrazolium, 10 ml 0.1 M phosphate buffer.	NAD	261-294	hydroxysteroid 17-beta dehydrogenase 1	Homo sapiens	107-118
6860707-1	1983	Lipid peroxidation induced through cytochrome P-450 activation of cumene hydroperoxide, linolenic acid hydroperoxide and peroxidized phosphatidylcholine in rat liver microsomes is markedly inhibited by either NADH or NADPH.	NAD	209-213	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	35-51
6414330-2	1983	The HCO-3 is reacted with phosphoenolpyruvate (PEP) in the presence of PEP carboxylase (EC 4.1.1.31) and the oxaloacetate formed reduced to malate by NADH in the reaction catalyzed by malate dehydrogenase (EC 1.1.1.37).	NAD	150-154	malic enzyme 2	Homo sapiens	184-204
6625161-1	1983	Combining ion-exchange (AG MP-1) and reversed-phase (C-18) partition chromatography accomplishes a higher degree of purification of NADH than either method can provide alone.	NAD	132-136	Bardet-Biedl syndrome 9	Homo sapiens	53-57
6407471-2	1983	Since Drosophila alcohol dehydrogenase (ADH) uses NAD+ to remove a hydrogen from ethanol in the first step of alcohol catabolism, it is possible that under alcohol stress conditions the in vivo NAD+ levels in Drosophila may decrease.	NAD	194-198	Alcohol dehydrogenase	Drosophila melanogaster	40-43
6404248-3	1983	On electrophoresis in a starch gel containing NAD or NADH, of purified AdhS which consists of the three Adh forms S-5, S-4, and S-3, five enzymatically active zones appear.	NAD	46-49	Alcohol dehydrogenase	Drosophila melanogaster	71-74
6838634-2	1983	(1) An interaction with cardiolipin (CL) resulted in the formation of an ADM-CL complex able to transfer electrons from NADH to cytochrome c (cyt.c) as well as coenzyme Q (CoQ).	NAD	120-124	cytochrome c, somatic	Homo sapiens	128-140
6838634-2	1983	(1) An interaction with cardiolipin (CL) resulted in the formation of an ADM-CL complex able to transfer electrons from NADH to cytochrome c (cyt.c) as well as coenzyme Q (CoQ).	NAD	120-124	cytochrome c, somatic	Homo sapiens	142-147
6824331-5	1983	DPNH disrupts complexes with malate dehydrogenase and has little effect on those with the aminotransferase, while oxalacetate disrupts complexes with citrate synthase but has little effect on those with glutamate dehydrogenase.	NAD	0-4	malic enzyme 2	Homo sapiens	29-49
6404248-3	1983	On electrophoresis in a starch gel containing NAD or NADH, of purified AdhS which consists of the three Adh forms S-5, S-4, and S-3, five enzymatically active zones appear.	NAD	53-57	Alcohol dehydrogenase	Drosophila melanogaster	71-74
6152729-12	1983	Other NAD utilizing enzymes, including representative dehydrogenases and poly ADP ribose polymerase, were, by comparison to mammalian IMPD, resistant to inhibition by TAD.	NAD	6-9	poly(ADP-ribose) polymerase 1	Homo sapiens	73-99
6294113-4	1983	By incubating permeabilized cells in the absence or presence of Ap4A and purified poly(ADP-ribose) polymerase auto-ADP-ribosylated with [32P]NAD+, we showed that the Mr = 96,000, 79,000, and 62,000 bands were derivatives of the prelabeled enzyme.	NAD	141-145	poly(ADP-ribose) polymerase 1	Homo sapiens	82-109
6430013-1	1983	The NAD-induced local conformational changes in the fluorescent dye-binding region of muscle glyceraldehyde-3-phosphate dehydrogenase were studied (Ovadi et al., 1982).	NAD	4-7	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	93-133
6317637-2	1983	The decrease in NAD+ is associated with the activation of poly(ADP-ribose) polymerase and the decrease in ATP is consequent to the fall in NAD+.	NAD	16-20	poly(ADP-ribose) polymerase 1	Homo sapiens	58-85
6411649-5	1983	In erythrocytes, impaired reoxidation of NADH followed by the deficiency of substrate NAD+ causes a reduction of glyceraldehyde 3-phosphate dehydrogenase activity.	NAD	41-45	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	113-153
6411649-5	1983	In erythrocytes, impaired reoxidation of NADH followed by the deficiency of substrate NAD+ causes a reduction of glyceraldehyde 3-phosphate dehydrogenase activity.	NAD	86-90	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	113-153
6317637-3	1983	Depletion of both NAD+ and ATP can be blocked or retarded by inhibitors of poly(ADP-ribose) polymerase.	NAD	18-22	poly(ADP-ribose) polymerase 1	Homo sapiens	75-102
6317637-7	1983	The use of inhibitors of poly(ADP-ribose) polymerase to prevent the depletion of NAD+ and ATP partially restores the cells" ability to conduct DNA, RNA, and protein synthesis.	NAD	81-85	poly(ADP-ribose) polymerase 1	Homo sapiens	25-52
6317641-5	1983	Exposure of cells to small alkylating agents or to radiation causes a fall in cellular NAD+ levels due to a transient activation of ADPRT and a consequent ADP-ribosylation of chromatin proteins.	NAD	87-91	poly(ADP-ribose) polymerase 1	Homo sapiens	132-137
6297484-0	1982	Induction by retinoic acid of NAD+-glycohydrolase activity of myelomonocytic cell lines HL-60, THP-1 and U-937, and fresh human acute promyelocytic leukemia cells in primary culture.	NAD	30-33	GLI family zinc finger 2	Homo sapiens	95-100
6289905-0	1982	The role of the nicotinamide moiety of NAd+ for negative cooperativity in glyceraldehyde-3-phosphate dehydrogenase as studied by spin-labeled cofactors.	NAD	39-43	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	74-114
7173200-1	1982	The steroid 9 alpha-hydroxylase from Nocardia species M117 was found to be an electron-transport chain consisting of an NADH-dependent flavoprotein reductase and two iron-sulfur proteins named protein II and protein III.	NAD	120-124	annexin A4	Homo sapiens	193-219
7173200-11	1982	Protein III catalyzes the reduction of cytochrome c in the presence of NADH and Nocardia flavoprotein reductase.	NAD	71-75	cytochrome c, somatic	Homo sapiens	39-51
7138903-5	1982	A NADH-dependent production of hydrogen peroxide was observed by measuring the difference of oxygen uptake in the presence and absence of catalase (500 units), which was not inhibited by potassium cyanide (1 mM).	NAD	2-6	catalase	Homo sapiens	138-146
6289905-1	1982	Two derivatives of NAD+ spin-labeled at N6 or C-8 of the adenine ring have been shown previously to be active coenzymes of glyceraldehyde-3-phosphate dehydrogenase (D-glyceraldehyde-3-phosphate: NAD+ oxidoreductase (phosphorylating), EC 1.2.1.12).	NAD	19-23	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	123-163
7109608-1	1982	The NADH-supported cytochrome P-450-dependent 2-hydroxylation of estradiol in rat liver microsomes has been investigated.	NAD	4-8	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	19-35
7107704-11	1982	In phospholipid-enriched membranes with randomly dispersed intramembrane particles, electron transfer activities from NADH- and succinate-dehydrogenase to cytochrome c decreased proportionally to the increase in distance between the particles.	NAD	118-122	cytochrome c, somatic	Homo sapiens	155-167
7109608-9	1982	These results strongly imply the possible involvement of a cytochrome P-450 system in the NADH-dependent 2-hydroxylation of estradiol with rat liver microsomes.	NAD	90-94	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	59-75
6806275-0	1982	Kinetic investigation of rat liver microsomal electron transport from NADH to cytochrome P-450.	NAD	70-74	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	78-94
6806275-1	1982	NADH-dependent reduction of microsomal cytochrome P-450 has been analyzed kinetically by observing formation of the ferrous-carbonyl complex.	NAD	0-4	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	39-55
6806275-6	1982	Thus, microsomal cytochrome P-450 appears to be reduced via two independent pathways of electron transport from NADH; the biphasic reduction occurs via cytochrome P-450 reductase while the slower monophasic reduction occurs via cytochrome b5.	NAD	112-116	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	17-33
6288003-3	1982	The values of the apparent maximum velocity are similar for the reduction of Fe(CN)6(3)-and mammalian cytochrome c by NADH.	NAD	118-122	cytochrome c, somatic	Homo sapiens	102-114
6292673-0	1982	Does an increase in the ratio of cytoplasmic NADPH to NADP+ accompanied by a decrease in the ratio of cytoplasmic NADH to NAD+ mediate the actions of insulin?	NAD	114-118	insulin	Homo sapiens	150-157
6292673-0	1982	Does an increase in the ratio of cytoplasmic NADPH to NADP+ accompanied by a decrease in the ratio of cytoplasmic NADH to NAD+ mediate the actions of insulin?	NAD	122-126	insulin	Homo sapiens	150-157
7115810-6	1982	The immobilized monomers of glyceraldehyde 3-phosphate dehydrogenase exhibit Vmax and Km (for NAD and substrate) values similar to those found for the immobilized tetramer.	NAD	94-97	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	28-68
6288003-5	1982	NAD+ activates NADH-dependent reduction of cytochrome c, and the apparent maximum velocity for this substrate increases more sharply with the concentration of NAD+ than for hydroxylamine.	NAD	0-4	cytochrome c, somatic	Homo sapiens	43-55
6288003-5	1982	NAD+ activates NADH-dependent reduction of cytochrome c, and the apparent maximum velocity for this substrate increases more sharply with the concentration of NAD+ than for hydroxylamine.	NAD	15-19	cytochrome c, somatic	Homo sapiens	43-55
6288003-5	1982	NAD+ activates NADH-dependent reduction of cytochrome c, and the apparent maximum velocity for this substrate increases more sharply with the concentration of NAD+ than for hydroxylamine.	NAD	159-163	cytochrome c, somatic	Homo sapiens	43-55
6288003-6	1982	The simplest explanation is that NAD+ activation of hydroxylamine reduction derives solely from activation of steps involved in the reduction of cytochrome c, a flavin-mediated reaction, but these steps are only partly rate-limiting for the reduction of hydroxylamine.	NAD	33-37	cytochrome c, somatic	Homo sapiens	145-157
6288003-7	1982	At 0.5 mM-NAD+, the apparent maximum velocity was 2.3 times higher for 0.1 mM-cytochrome c as substrate than for 100 mM-hydroxylamine, suggesting that the rate-limiting step during hydroxylamine reduction is a step that is not involved in cytochrome c reduction.	NAD	10-14	cytochrome c, somatic	Homo sapiens	78-90
6288003-7	1982	At 0.5 mM-NAD+, the apparent maximum velocity was 2.3 times higher for 0.1 mM-cytochrome c as substrate than for 100 mM-hydroxylamine, suggesting that the rate-limiting step during hydroxylamine reduction is a step that is not involved in cytochrome c reduction.	NAD	10-14	cytochrome c, somatic	Homo sapiens	239-251
6288003-8	1982	A scheme is proposed that can account for the pattern of variation with [NAD+] of the Michaelis-Menten parameters for hydroxylamine and for NADH with hydroxylamine or cytochrome c as oxidized substrate.	NAD	73-77	cytochrome c, somatic	Homo sapiens	167-179
6288003-8	1982	A scheme is proposed that can account for the pattern of variation with [NAD+] of the Michaelis-Menten parameters for hydroxylamine and for NADH with hydroxylamine or cytochrome c as oxidized substrate.	NAD	140-144	cytochrome c, somatic	Homo sapiens	167-179
6954463-1	1982	GTP and isoproterenol activation of adenylate cyclase [ATP pyrophosphate-lyase (cyclizing), EC 4.6.1.1] in washed membranes prepared from C6 gliomas cells was enhanced by incubation with islet-activating protein, one of the pertussis toxins, if the incubation mixture was supplemented with NAD and ATP.	NAD	290-293	adenylate cyclase 10	Homo sapiens	55-78
7074966-2	1982	The procedure is based on enzymic conversion of glycerol to 3-phosphoglycerate, which is irreversible in the presence of arsenate, and subsequent determination of NADH formed in the glycerol-phosphate- and glyceraldehyde-3-phosphate dehydrogenase reactions respectively.	NAD	163-167	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	206-246
7113353-1	1982	pH-titrations with NADH show two ionizable groups in mitochondrial and cytoplasmic malate dehydrogenase, the first with a pKa in the range 6.8-8.3 for the mitochondrial and 6.4-7.8 for the cytoplasmic enzyme, the second with a lower limit at 10.2 resp. 11.	NAD	19-23	malic enzyme 2	Homo sapiens	83-103
6763360-8	1982	These data indicate that CCl4-treatment significantly reduces hepatic ethanol metabolism via the inhibition of reoxidation of NADH, a rate limiting step of ethanol metabolism in the liver.	NAD	126-130	C-C motif chemokine ligand 4	Rattus norvegicus	25-29
6805478-1	1982	GTP levels were low and NAD+ levels high in purine nucleoside phosphorylase (PNP) deficient erythrocytes, in addition to the raised deoxy-GTP (dGTP) levels previously noted by others.	NAD	24-28	purine nucleoside phosphorylase	Homo sapiens	44-75
6805478-1	1982	GTP levels were low and NAD+ levels high in purine nucleoside phosphorylase (PNP) deficient erythrocytes, in addition to the raised deoxy-GTP (dGTP) levels previously noted by others.	NAD	24-28	purine nucleoside phosphorylase	Homo sapiens	77-80
7068771-4	1982	Oxalacetate production from malate (malate dehydrogenase, EC 1.1.1.37) in both the particulate and soluble fraction was strictly dependent on NAD+.	NAD	142-146	malic enzyme 2	Homo sapiens	36-56
6275889-10	1982	It is concluded that (i) oxidation of exogenous NADH in the presence of cytochrome c proceeds mostly through NADH-cytochrome b5 reductase and cytochrome b5 on the outer membrane and then through cytochrome oxidase via the cytochrome c shuttle, and (ii) ATP synthesis during oxidation of exogenous NADH is partly due to oxidation of endogenous substrates and partly to operation of cytochrome oxidase receiving electrons from the outer membrane via cytochrome c.	NAD	48-52	cytochrome c, somatic	Homo sapiens	72-84
6275889-10	1982	It is concluded that (i) oxidation of exogenous NADH in the presence of cytochrome c proceeds mostly through NADH-cytochrome b5 reductase and cytochrome b5 on the outer membrane and then through cytochrome oxidase via the cytochrome c shuttle, and (ii) ATP synthesis during oxidation of exogenous NADH is partly due to oxidation of endogenous substrates and partly to operation of cytochrome oxidase receiving electrons from the outer membrane via cytochrome c.	NAD	48-52	cytochrome c, somatic	Homo sapiens	222-234
6275889-10	1982	It is concluded that (i) oxidation of exogenous NADH in the presence of cytochrome c proceeds mostly through NADH-cytochrome b5 reductase and cytochrome b5 on the outer membrane and then through cytochrome oxidase via the cytochrome c shuttle, and (ii) ATP synthesis during oxidation of exogenous NADH is partly due to oxidation of endogenous substrates and partly to operation of cytochrome oxidase receiving electrons from the outer membrane via cytochrome c.	NAD	48-52	cytochrome c, somatic	Homo sapiens	222-234
6275889-10	1982	It is concluded that (i) oxidation of exogenous NADH in the presence of cytochrome c proceeds mostly through NADH-cytochrome b5 reductase and cytochrome b5 on the outer membrane and then through cytochrome oxidase via the cytochrome c shuttle, and (ii) ATP synthesis during oxidation of exogenous NADH is partly due to oxidation of endogenous substrates and partly to operation of cytochrome oxidase receiving electrons from the outer membrane via cytochrome c.	NAD	109-113	cytochrome c, somatic	Homo sapiens	72-84
6802189-3	1982	The addition of glutamate (but not succinate), NAD+ and amytal (or rotenone) to the reconstituted system caused a 40-50% reduction of NADPH-reducible cytochrome P-450.	NAD	47-51	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	150-166
6802189-4	1982	The inhibitor of mitochondrial NADH-cytochrome b5 reductase dicumarol prevented the cytochrome P-450 reduction in the presence of glutamate, NAD+ and amytal but did not affect the reduction of cytochrome P-450 by the added NADH.	NAD	141-145	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	84-100
6802189-4	1982	The inhibitor of mitochondrial NADH-cytochrome b5 reductase dicumarol prevented the cytochrome P-450 reduction in the presence of glutamate, NAD+ and amytal but did not affect the reduction of cytochrome P-450 by the added NADH.	NAD	31-35	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	84-100
6802189-5	1982	It was concluded that the electron transfer from the NAD-dependent substrates of the inner mitochondrial respiratory chain to the microsomal cytochrome P-450 occurs with the participation of non-bound NAD and cytochrome b5 of the outer mitochondrial membrane on the condition that the membranes of the two main oxidative systems are in tight contact.	NAD	53-56	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	141-157
6802189-5	1982	It was concluded that the electron transfer from the NAD-dependent substrates of the inner mitochondrial respiratory chain to the microsomal cytochrome P-450 occurs with the participation of non-bound NAD and cytochrome b5 of the outer mitochondrial membrane on the condition that the membranes of the two main oxidative systems are in tight contact.	NAD	201-204	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	141-157
7085238-1	1982	Photosynthetic GAPDH has been studied in chloroplast extracts, obtained in presence of physiological concentrations of NADP and NAD.	NAD	119-122	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	15-20
6284133-2	1982	By using the differential response to inhibitors of the two major enzymes that catabolize NAD in mammalian cells, it is shown that poly(ADP-ribose) polymerase is responsible for the loss of NAD.	NAD	90-93	poly(ADP-ribose) polymerase 1	Homo sapiens	131-158
6284133-2	1982	By using the differential response to inhibitors of the two major enzymes that catabolize NAD in mammalian cells, it is shown that poly(ADP-ribose) polymerase is responsible for the loss of NAD.	NAD	190-193	poly(ADP-ribose) polymerase 1	Homo sapiens	131-158
7074178-0	1982	[Increase in the phospholipase A2 activity of liver tissue during adaptation to cold and the external pathway of NADH oxidation].	NAD	113-117	phospholipase A2 group IB	Homo sapiens	17-33
7298637-2	1981	In these membranes NADH, but not NADPH, is oxidized when ferricyanide or catalytic amounts of cytochrome c were present.	NAD	19-23	cytochrome c, somatic	Homo sapiens	94-106
7317380-1	1981	Hepatic microsomal cytochrome P-450 from phenobarbital-pretreated rats is destroyed by propyne in a reduced nicotinamide adenine dinucleotide dependent process which also results in vivo in the accumulation of an abnormal green porphyrin.	NAD	108-141	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	19-35
6280677-1	1981	When permeabilized hamster fibroblasts were incubated with 4 mM-NAD+, the substrate for poly(ADP-ribose) polymerase, RNA polymerase I activity was inhibited by about 85%.	NAD	64-68	poly(ADP-ribose) polymerase 1	Homo sapiens	88-115
7317523-5	1981	The external pathway of NADH oxidation in liver mitochondria is sensitive to the inhibitors of phospholipase A2 (nupercaine, EGTA) and the inhibitor of lipid peroxidation (ionole).	NAD	24-28	phospholipase A2 group IB	Homo sapiens	95-111
6119752-7	1981	It is concluded that bromotrichloromethane and 1,2-dibromo-1,2-dichloroethane stimulate hepatic microsomal electron transfer from NADH via cytochrome b-5 by interacting with cytochrome P-450 and with stearate desaturase.	NAD	130-134	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	174-219
16662109-3	1981	Biosynthetic glutamine synthetase activity was 1.5 to 1.8 times greater in nitrogen-limited cells than cells grown at high levels of the three nitrogen sources.Conversely, glutamate dehydrogenase (both NADH- and NADPH-dependent activities) was greatest in cells grown at high levels of asparagine or ammonium, while nitrate-grown cells possessed little activity at all concentrations employed.	NAD	202-206	glutamate-ammonia ligase	Homo sapiens	13-33
7275987-7	1981	This reassociation at pH 7.5 is accompanied by a significant regain of enzymatic activity, indicating that NADH binding is able to partially overcome the negative effect of the cysteine modification on the pH-dependent subunit reassociation of mitochondrial malate dehydrogenase.	NAD	107-111	malic enzyme 2	Homo sapiens	258-278
7030742-1	1981	The oxidation of NADH in submitochondrial particles isolated from MUC1, MUC2 and MUC3 mucidin-resistant mutants of Saccharomyces cerevisiae is specifically resistant to mucidin.	NAD	17-21	Flo11p	Saccharomyces cerevisiae S288C	66-70
7275987-2	1981	In this report, an investigation of proton release and uptake upon NADH binding to the native enzyme and to the N-ethylmaleimide-modified enzyme has implicated the above cysteine residue as being directly linked to the pH-dependent subunit dissociation of mitochondrial malate dehydrogenase.	NAD	67-71	malic enzyme 2	Homo sapiens	270-290
7317032-7	1981	A complex of dihydropteridine reductase with NADH was observed on gel electrophoresis.	NAD	45-49	quinoid dihydropteridine reductase	Homo sapiens	13-39
6894850-2	1981	Histochemical staining of glyceraldehyde-3-phosphate dehydrogenase activity in fresh-frozen muscle tissue may be performed using a beta-nicotinamide adenine dinucleotide (beta-NAD) reduced-dehydrogenase tetrazolium-reductase linked reaction.	NAD	131-169	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	26-66
6894850-2	1981	Histochemical staining of glyceraldehyde-3-phosphate dehydrogenase activity in fresh-frozen muscle tissue may be performed using a beta-nicotinamide adenine dinucleotide (beta-NAD) reduced-dehydrogenase tetrazolium-reductase linked reaction.	NAD	171-179	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	26-66
6280867-9	1981	This Ca2+-calmodulin complex then activates chloroplastic NAD kinase resulting in an increased NADP/NAD ratio.	NAD	58-61	calmodulin 1	Homo sapiens	10-20
7248931-3	1981	The specific activity of nicotinamide adenine dinucleotide-dependent 15-hydroxyprostaglandin dehydrogenase in hydatidiform mole tissue (0 to 1.2 nmol 15-ketoprostaglandin E2 formed x min-1 x mg-1 cytosolic protein) and in choriocarcinoma cells (1.0 nmol 15-ketoprostaglandin E2 x min-1 x mg-1 protein) was strikingly less than that found in normal placental tissue [11.4 +/- 2.3 (S.E.)	NAD	25-58	CD59 molecule (CD59 blood group)	Homo sapiens	183-188
7248931-3	1981	The specific activity of nicotinamide adenine dinucleotide-dependent 15-hydroxyprostaglandin dehydrogenase in hydatidiform mole tissue (0 to 1.2 nmol 15-ketoprostaglandin E2 formed x min-1 x mg-1 cytosolic protein) and in choriocarcinoma cells (1.0 nmol 15-ketoprostaglandin E2 x min-1 x mg-1 protein) was strikingly less than that found in normal placental tissue [11.4 +/- 2.3 (S.E.)	NAD	25-58	CD59 molecule (CD59 blood group)	Homo sapiens	280-285
6943544-1	1981	During metabolism of (type I) drugs by cytochrome P-450-dependent monooxygenase of the endoplasmic reticulum, the NADPH/NADP+ ratio in rat liver selectively decreases to approximately one-half of the control values, whereas the NADH/NAD+ ratio remains practically unaffected [Sies, H. &amp; Brauser, B.	NAD	228-232	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	39-55
6792322-9	1981	The NADPH and NADH cofactors supply reducing equivalents ultimately to cytochrome P-450 which functions as a reductase in chromate metabolism.	NAD	14-18	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	71-87
6265441-1	1981	Addition of exogenous NADH to rotenone- and antimycin A-treated mitochondria, in 125 mM KCl, results in rates of oxygen uptake of 0.5-1 and 10-12 nanoatoms of oxygen X mg protein-1 X min-1 in the absence and presence of cytochrome c, respectively.	NAD	22-26	cytochrome c, somatic	Homo sapiens	220-232
6265441-2	1981	During oxidation of exogenous NADH there is a fast and complete reduction of cytochrome b5 while endogenous or added exogenous cytochrome c become 10-15% and 100% reduced, respectively.	NAD	30-34	cytochrome c, somatic	Homo sapiens	127-139
6265441-8	1981	It is concluded that aerobic oxidation of exogenous NADH involves the following pathway: NADH leads to NADH-cytochrome b5 reductase leads to cytochrome b5 leads to intermembrane cytochrome c leads to cytochrome oxidase leads to oxygen.	NAD	52-56	cytochrome c, somatic	Homo sapiens	178-190
6265441-8	1981	It is concluded that aerobic oxidation of exogenous NADH involves the following pathway: NADH leads to NADH-cytochrome b5 reductase leads to cytochrome b5 leads to intermembrane cytochrome c leads to cytochrome oxidase leads to oxygen.	NAD	89-93	cytochrome c, somatic	Homo sapiens	178-190
6265441-9	1981	It is suggested that the communication between the outer and inner membranes mediated by cytochrome c may affect the oxidation-reduction level of cytosolic NADH and the related oxidation-reduction reactions.	NAD	156-160	cytochrome c, somatic	Homo sapiens	89-101
6943544-1	1981	During metabolism of (type I) drugs by cytochrome P-450-dependent monooxygenase of the endoplasmic reticulum, the NADPH/NADP+ ratio in rat liver selectively decreases to approximately one-half of the control values, whereas the NADH/NAD+ ratio remains practically unaffected [Sies, H. &amp; Brauser, B.	NAD	233-237	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	39-55
6974537-2	1981	It is based on the conversion of 3-phosphoglycerate to 1,3-diphosphoglycerate catalyzed by the PGK whose activity is visually estimated by the oxidation of NADH (fluorescent) to NAD+ (non-fluorescent) in a coupled reaction with the enzyme glyceraldehyde 3-phosphate dehydrogenase.	NAD	156-160	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	239-279
7306070-0	1981	Possible involvement of the enhanced tryptophan pyrrolase activity in the corticosterone- and starvation-induced increases in concentrations of nicotinamide-adenine dinucleotides (phosphates) in rat liver.	NAD	144-178	tryptophan 2,3-dioxygenase	Rattus norvegicus	37-57
7306070-13	1981	It is suggested that liver tryptophan pyrrolase activity plays an important role in NAD+ synthesis from tryptophan in the rat.	NAD	84-88	tryptophan 2,3-dioxygenase	Rattus norvegicus	27-47
7005000-5	1981	Inhibition of alcohol dehydrogenase by triiodothyronine in vitro was found to be competitive with respect to NAD+ and uncompetitive with respect to ethanol in both contrast and thyroidectomized animals.	NAD	109-113	aldo-keto reductase family 1 member A1	Rattus norvegicus	14-35
6260474-1	1981	We tested the hypothesis that NAD plays a role in the cellular mechanism of action of parathyroid hormone (PTH) on phosphate transport.	NAD	30-33	parathyroid hormone	Rattus norvegicus	86-105
6788036-4	1981	We have shown than ADH (Alcohol: NAD oxidoreductase, E.C.1.1.1.1) also oxidizes L(+)-lactate or D(-)-lactate with the NAD, while LDH oxidizes ethanol.	NAD	33-36	Alcohol dehydrogenase	Drosophila melanogaster	19-22
6974537-2	1981	It is based on the conversion of 3-phosphoglycerate to 1,3-diphosphoglycerate catalyzed by the PGK whose activity is visually estimated by the oxidation of NADH (fluorescent) to NAD+ (non-fluorescent) in a coupled reaction with the enzyme glyceraldehyde 3-phosphate dehydrogenase.	NAD	178-182	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	239-279
7459843-5	1980	Theophylline, a known inhibitor of poly(ADP-ribose)polymerase, inhibited both the NAD reduction in cells treated with DNA damaging agents and the incorporation of [3H]thymidine into DNA.	NAD	82-85	poly(ADP-ribose) polymerase 1	Homo sapiens	35-61
7321056-3	1981	The addition of theophylline, a potent inhibitor of poly(ADP-ribose) polymerase, to the culture medium of normal cells blocked over 90% of the conversion of NAD to poly(ADP-ribose) following treatment with UV or N-methyl-N"-nitro-N-nitro-soguanidine but did not affect the rate of unscheduled DNA synthesis.	NAD	157-160	poly(ADP-ribose) polymerase 1	Homo sapiens	52-79
7408193-2	1980	The assay utilizes the tetrahydropterin-dependent reduction of ferri-cytochrome C in the presence of NADH and requires a smaller number of cells than assays described for cultured skin fibroblasts.	NAD	101-105	cytochrome c, somatic	Homo sapiens	69-81
6933064-4	1980	Enzyme activity in peak 1 was predominantly stimulated by NADH and that in peak 2 was stimulated mainly by NADPH.	NAD	58-62	pseudopodium-enriched atypical kinase 1	Rattus norvegicus	19-25
6933064-9	1980	NADH caused a very similar activation of enzyme activity in peak 1 or the prostate and epididymis (Km 50-100 micro M), whereas the enzyme in the testis was activated by much lower cofactor concentration (Km approximately 5 microM).	NAD	0-4	pseudopodium-enriched atypical kinase 1	Rattus norvegicus	60-66
7432491-1	1980	Poly (ADP-ribose) polymerase is a eukaryotic chromosomal enzyme which utilizes the ADP-ribose moiety of NAD to synthesize the nucleic acid homopolymer (ADP-ribose)n (ref.	NAD	104-107	poly(ADP-ribose) polymerase 1	Homo sapiens	0-28
7420468-6	1980	Aminopropanol dehydrogenase activity in serum of rats with acute CCl4 poisoning was determined by following the increase in absorbance at 340 nm due to the production of NADH.	NAD	170-174	C-C motif chemokine ligand 4	Rattus norvegicus	65-69
6821371-4	1980	Preincubation of the intact cells under conditions designed to increase internal NADH concentrations, leads to a lower membrane-associated activity of glyceraldehyde 3-phosphate dehydrogenase after lysis.	NAD	81-85	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	151-191
6251809-0	1980	Protection by picolinamide, a novel inhibitor of poly (ADP-ribose) synthetase, against both streptozotocin-induced depression of proinsulin synthesis and reduction of NAD content in pancreatic islets.	NAD	167-170	poly(ADP-ribose) polymerase 1	Homo sapiens	49-77
7371189-0	1980	Correction for the suppressive effect of haemoglobin on NADH absorbance in the transketolase assay.	NAD	56-60	transketolase	Homo sapiens	79-92
6246928-5	1980	The reaction of the oxidase of submitochondrial particles with the endogenous cytochrome c is stimulated by the nucleotides, as is the reduced nicotinamide adenine dinucleotide (NADH) oxidase activity.	NAD	143-176	cytochrome c, somatic	Homo sapiens	78-90
7371189-1	1980	The kinetic transketolase assay measures the absorbance change of NADH in the presence of haemoglobin.	NAD	66-70	transketolase	Homo sapiens	12-25
7378419-1	1980	By phosphorus analysis of the fluorescent derivative produced by ultraviolet irradiation of carboxymethylated glyceraldehyde-3-phosphate dehydrogenase in the presence of NAD at saturation levels, it has been shown that the photochemical reaction leading to the formation of the new fluorophore is also a "half-of-the-sites" reaction.	NAD	170-173	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	110-150
7188697-0	1980	Glyceraldehyde-3-phosphate dehydrogenase-catalyzed chain oxidation of reduced nicotinamide adenine dinucleotide by perhydroxyl radicals.	NAD	78-111	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	0-40
7188697-1	1980	The chain oxidation of glyceraldehyde-3-phosphate dehydrogenase.NADH by perhydroxyl radicals and propagated by molecular oxygen was studied by the xanthine-xanthine oxidase system, 60Co gamma-ray, and pulse radiolysis.	NAD	64-68	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	23-63
7188697-3	1980	The rate constant for the oxidation of the glyceraldehyde-3-phosphate dehydrogenase.NADH complex by HO2 was estimated to be 2 X 10(7) M-1 S-1 at ambient temperatures (23-24 degrees C).	NAD	84-88	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	43-83
7188697-4	1980	Rate studies as a function of pH indicate that O2- is unreactive toward the glyceraldehyde-3-phosphate dehydrogenase.NADH complex.	NAD	117-121	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	76-116
7357001-4	1980	The interaction of glyceraldehyde-3-phosphate dehydrogenase with DNA is strongly inhibited by NAD and NADH but not by NADP.	NAD	94-97	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	19-59
7357001-4	1980	The interaction of glyceraldehyde-3-phosphate dehydrogenase with DNA is strongly inhibited by NAD and NADH but not by NADP.	NAD	102-106	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	19-59
7357001-7	1980	These results suggest that DNA interacts through the NAD binding sites of glyceraldehyde-3-phosphate dehydrogenase.	NAD	53-56	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	74-114
7346055-5	1980	Since chronic ethanol treatment increases cellular levels of NADH and NADPH which are known to inhibit tryptophan pyrrolase activity, it is suggested that the potentiating effect of pyridoxine might be due to the maintenance of normal ratios of cellular NAD+/NADH and BADP+/NADPH.	NAD	61-65	tryptophan 2,3-dioxygenase	Rattus norvegicus	103-123
466784-4	1979	Modification of a commercially available hexokinase/glucose-6-phosphate dehydrogenase reagent system for glucose provides that the rate of production of NADH be first-order in total glucose concentration within about 30 s after sample and reagent are mixed.	NAD	153-157	hexokinase 1	Homo sapiens	41-51
6769190-0	1980	[Possible mechanism of CO2 interaction with NAD-dependent malate dehydrogenase].	NAD	44-47	malic enzyme 2	Homo sapiens	58-78
6769190-1	1980	IR spectra of NAD-dependent malate dehydrogenase in the deuterium oxide solutions were studied in the absence of CO2 and at solution saturation with it.	NAD	14-17	malic enzyme 2	Homo sapiens	28-48
43146-0	1979	Relationship between the ability of nicotinamide to maintain nicotinamide-adenine dinucleotide in rat liver cell culture and its effect on cytochrome P-450.	NAD	61-94	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	139-155
583558-2	1979	Aymaras of the high Andean Plateau are shown to have within erythrocytes: (a) increased activity of NADH2 (GAPDH) generating stages, (b) decreased activity of NADH2 (LDH) consuming steps, (c) significantly increased methaemoglobin content, and (d) a large increase in the level of reduced glutathione.	NAD	100-105	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	107-112
228934-0	1979	The involvement of poly(ADP-ribose) polymerase in the degradation of NAD caused by gamma-radiation and N-methyl-N-nitrosourea.	NAD	69-72	poly(ADP-ribose) polymerase 1	Homo sapiens	19-46
232402-0	1979	Isolation and characterization of an alkali metal ion-sensitive NAD+-dependent glyceraldehyde 3-phosphate dehydrogenase from germinating green gram (Phaseolus aurieus).	NAD	64-67	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	79-119
6243364-0	1980	Chlorination or reduced nicotinamide adenine dinucleotides by myeloperoxidase: a novel bactericidal mechanism.	NAD	24-58	myeloperoxidase	Homo sapiens	62-77
94928-2	1979	The liberated glucose is determined specifically by the hexokinase/glucose-6-phosphate dehydrogenase (NAD+-dependent) method+ by addition of pyruvate, lactate dehydrogenase and ATP.	NAD	102-106	hexokinase 1	Homo sapiens	56-66
113135-2	1979	The method is based on reduction of fructose by a commercially available preparation of sorbitol dehydrogenase (EC 1.1.1.14), with the concomitant oxidation of NADH.	NAD	160-164	sorbitol dehydrogenase	Homo sapiens	88-110
39543-9	1979	Production of O(2) (-) by NADH-ubiquinone reductase preparation (Complex I) with NADH or NADPH as an electron donor was assayed by measuring the formation of adrenochrome or the reduction of acetylated cytochrome c which does not react with the respiratory-chain components.	NAD	26-30	cytochrome c, somatic	Homo sapiens	202-214
36318-7	1979	Our data suggest that the insulin-releasing action of leucine depends on the islets" NADPH and reduced glutathione (GSH); in addition, leucine may contribute to insulin secretion by increasing the islet NADPH:NADP ratio and the NADH:NAD ratio.	NAD	228-232	insulin	Homo sapiens	26-33
36318-7	1979	Our data suggest that the insulin-releasing action of leucine depends on the islets" NADPH and reduced glutathione (GSH); in addition, leucine may contribute to insulin secretion by increasing the islet NADPH:NADP ratio and the NADH:NAD ratio.	NAD	85-88	insulin	Homo sapiens	26-33
43909-3	1979	Antiserum to cytochrome P-450 isolated from phenobarbital-treated rat liver microsomes inhibited the NADH-dependent O-demethylation activity as well as the NADPH-dependent O-demethylation activity seen in rat liver microsomes.	NAD	101-105	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	13-29
43909-4	1979	Addition of either purified cytochrome P-450 or cytochrome P-448 to an incubation mixture containing phenobarbital-treated rat liver microsomes enhanced the NADH-dependent p-nitroanisole O-demethylation activity.	NAD	157-161	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	28-44
43909-5	1979	These results suggest that NADH-dependent and, in part, NADPH-dependent O-demethylations are catalyzed by cytochrome P-448 and cytochrome P-450 receiving electrons from cytochrome b5.	NAD	27-31	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	127-143
718958-5	1978	Glyceraldehyde-3-phosphate dehydrogenase can then be specifically eluted from the ghosts by incubating them with 2 mM NADH in 5mM phosphate buffer (pH 8.0).	NAD	118-122	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	0-40
454365-5	1979	Under these conditions, tryptophan accumulates in the liver and apo-(tryptophan pyrrolase) activity is completely abolished, but could be restored by administration of regenerators of liver NAD+ and/or NADP+.	NAD	190-194	tryptophan 2,3-dioxygenase	Rattus norvegicus	69-89
216708-5	1979	Here it obtains reducing equivalents which appear to come from NADH made available at the level of glyceraldehyde 3-phosphate dehydrogenase.	NAD	63-67	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	99-139
463453-5	1979	In partially hepatectomized rats the rate of ethanol elimination was linearly correlated with the activity of alcohol dehydrogenase, which suggests that when the rate of NADH reoxidation is markedly increased, as in regenerating rat liver, the rate of ethanol elimination may be limited by the activity of alcohol dehydrogenase.	NAD	170-174	aldo-keto reductase family 1 member A1	Rattus norvegicus	110-131
463453-5	1979	In partially hepatectomized rats the rate of ethanol elimination was linearly correlated with the activity of alcohol dehydrogenase, which suggests that when the rate of NADH reoxidation is markedly increased, as in regenerating rat liver, the rate of ethanol elimination may be limited by the activity of alcohol dehydrogenase.	NAD	170-174	aldo-keto reductase family 1 member A1	Rattus norvegicus	306-327
553321-5	1979	Restriction of glycolysis is due to inhibition of glyceraldehyde-3-phosphate dehydrogenase by accumulated metabolites, such as H+, lactate and NADH.	NAD	143-147	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	50-90
9762143-3	1978	The utilization of inorganic pyrophosphate is measured by coupling the production of fructose-1,6-bisphosphate with the oxidation of NADH using fructose-bisphosphate aldolase (EC 4.1.2.13), triosephosphate isomerase (EC 5.3.1.1), and glycerol-3-phosphate dehydrogenase (NAD+)(EC 1.1.1.8).	NAD	133-137	triosephosphate isomerase 1	Homo sapiens	190-215
27211-1	1978	Reversed-phase high-pressure liquid chromatography was used to isolate acid breakdown products of reduced nicotinamide adenine dinucleotide (NADH) and products produced when NADH breakdown is catalyzed by glyceraldehyde-3-phosphate dehydrogenase (G-3-PD).	NAD	106-139	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	247-253
214425-1	1978	The oxidation of tetrahydropterin with ferri-cytochrome c was studied using a tetrahydropterin-generating system composed of dihydropteridine reductase [EC 1.6.99.7] and NADH.	NAD	170-174	cytochrome c, somatic	Homo sapiens	45-57
214425-2	1978	Under aerobic conditions, 1.5 to 1.8 mol of cytochrome c was reduced per mol of NADH, whereas 2 mol of cytochrome c was reduced under anaerobic conditions.	NAD	80-84	cytochrome c, somatic	Homo sapiens	44-56
214425-3	1978	When superoxide dismutase [EC 1.15.1.1] was added to the system under aerobic conditions, only 1 mol of cytochrome c was reduced per mol of NADH, while the pterin oxidation was scarcely affected.	NAD	140-144	cytochrome c, somatic	Homo sapiens	104-116
208069-1	1978	Treatment of pigeon erythrocyte membranes with cholera toxin and NAD(+) enhanced the GTP stimulation and suppressed the F(-) activation of the adenylate cylase [ATP pyrophosphate-lyase (cyclizing), EC 4.6.1.1].	NAD	65-71	adenylate cyclase 10	Homo sapiens	161-184
27211-1	1978	Reversed-phase high-pressure liquid chromatography was used to isolate acid breakdown products of reduced nicotinamide adenine dinucleotide (NADH) and products produced when NADH breakdown is catalyzed by glyceraldehyde-3-phosphate dehydrogenase (G-3-PD).	NAD	141-145	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	205-245
27211-1	1978	Reversed-phase high-pressure liquid chromatography was used to isolate acid breakdown products of reduced nicotinamide adenine dinucleotide (NADH) and products produced when NADH breakdown is catalyzed by glyceraldehyde-3-phosphate dehydrogenase (G-3-PD).	NAD	141-145	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	247-253
27211-1	1978	Reversed-phase high-pressure liquid chromatography was used to isolate acid breakdown products of reduced nicotinamide adenine dinucleotide (NADH) and products produced when NADH breakdown is catalyzed by glyceraldehyde-3-phosphate dehydrogenase (G-3-PD).	NAD	174-178	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	205-245
27211-1	1978	Reversed-phase high-pressure liquid chromatography was used to isolate acid breakdown products of reduced nicotinamide adenine dinucleotide (NADH) and products produced when NADH breakdown is catalyzed by glyceraldehyde-3-phosphate dehydrogenase (G-3-PD).	NAD	174-178	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	247-253
27211-3	1978	G-3-PD is shown to catalyze a reaction in which two products are formed which are also intermediates in the acid degradation of NADH (alpha- and beta-6-hydroxynicotinamide products).	NAD	128-132	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	0-6
204337-2	1978	Data on reactions with NADH-linked cytochrome c reductase (complexes I and III) are included.	NAD	23-27	cytochrome c, somatic	Homo sapiens	35-47
557464-15	1977	By inhibiting alkaline phosphomonoesterase with 0.1 mM of L-p-bromotetramisole or 16 mM of beta-glycerophosphate, 3beta-HSD was shown to be exclusively NAD-linked.	NAD	152-156	hydroxy-delta-5-steroid dehydrogenase, 3 beta- and steroid delta-isomerase 1	Rattus norvegicus	114-123
201305-3	1977	It was shown that in both cases NAD at saturating concentration exerts a far weaker stabilizing effect on the structure of glyceraldehyde-3-phosphate dehydrogenase from lamprey muscle than on that of the porcine muscle enzyme.	NAD	32-35	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	123-163
14469-3	1977	Under these conditions the 17beta-HSD was stable for several days at -20, +4 and +20 degrees C and resistant to heat denaturation at 60 degrees C. The Km-value for Oe2 with NAD or NADP as cosubstrate was 5 X 10(-6) or 2 X 10(-6) M, respectively.	NAD	173-176	hydroxysteroid 17-beta dehydrogenase 13	Homo sapiens	27-37
196649-2	1977	The Michaelis constants for EF-2 and NAD are 0.15 and 1.4 muM, respectively.	NAD	37-40	latexin	Homo sapiens	58-61
191082-7	1977	Extrapolation to saturation with NAD+ showed NADH gave linear uncompetitive inhibition of UDPG if NAD+ was saturating.	NAD	33-37	UDP-glucose pyrophosphorylase 2	Homo sapiens	90-94
191082-7	1977	Extrapolation to saturation with NAD+ showed NADH gave linear uncompetitive inhibition of UDPG if NAD+ was saturating.	NAD	45-49	UDP-glucose pyrophosphorylase 2	Homo sapiens	90-94
191082-7	1977	Extrapolation to saturation with NAD+ showed NADH gave linear uncompetitive inhibition of UDPG if NAD+ was saturating.	NAD	98-102	UDP-glucose pyrophosphorylase 2	Homo sapiens	90-94
191082-10	1977	These results are compatible with a mechanism in which UDPG binds first, followed by NAD+, which is reduced and released.	NAD	85-89	UDP-glucose pyrophosphorylase 2	Homo sapiens	55-59
14930-7	1977	The reductase, however, could not reduce cytochrome c. Michaelis constants of the reductase for NADH and calf liver cytochrome b5 were 6.3 and 1.5 micron M, respectively, and optimal pH for cytochrome b5 reduction was 5.6.	NAD	96-100	cytochrome b5 type A	Bos taurus	116-129
189803-4	1977	If, on the other hand, isolated HeLa cell nuclei were first incubated with labeled NAD, the substrate for poly(ADP-ribose) polymerase, prior to the preparation and fractionation of nuclease-digested chromatin, it was found that those chromatin fractions which possess significant poly(ADP-ribose) polymerase activity (nucleosome oligomers) are relatively deficient in the labeled product of this enzyme, and that a considerable portion of the homopolymeric product is ultimately associated with the 11S v bodies.	NAD	83-86	poly(ADP-ribose) polymerase 1	Homo sapiens	106-133
189803-4	1977	If, on the other hand, isolated HeLa cell nuclei were first incubated with labeled NAD, the substrate for poly(ADP-ribose) polymerase, prior to the preparation and fractionation of nuclease-digested chromatin, it was found that those chromatin fractions which possess significant poly(ADP-ribose) polymerase activity (nucleosome oligomers) are relatively deficient in the labeled product of this enzyme, and that a considerable portion of the homopolymeric product is ultimately associated with the 11S v bodies.	NAD	83-86	poly(ADP-ribose) polymerase 1	Homo sapiens	280-307
14930-7	1977	The reductase, however, could not reduce cytochrome c. Michaelis constants of the reductase for NADH and calf liver cytochrome b5 were 6.3 and 1.5 micron M, respectively, and optimal pH for cytochrome b5 reduction was 5.6.	NAD	96-100	cytochrome b5 type A	Bos taurus	190-203
186779-1	1976	A three-step procedure including affinity chromatography on NAD+-azobenzamidopropyl-Sepharose has been designed for the purification of yeast glyceraldehyde-3-phosphate dehydrogenase [D-glyceraldehyde-3-phosphate: NAD+ oxidoreductase (phosphorylating), EC 1.2.1.12] with maximized specific activity and maximized homogeneity with respect to affinity for the coenzyme, NAD+.	NAD	60-64	oxidoreductase	Saccharomyces cerevisiae S288C	219-233
1009935-6	1976	The results indicate that alcohol dehydrogenase and aldehyde dehydrogenase do not share a common pool of NAD, and that NADH formed during acetaldehyde oxidation is utilized for reductions in the cytosol to a smaller extent than the NADH formed in the alcohol dehydrogenase reaction.	NAD	105-108	aldo-keto reductase family 1 member A1	Rattus norvegicus	26-47
1009935-6	1976	The results indicate that alcohol dehydrogenase and aldehyde dehydrogenase do not share a common pool of NAD, and that NADH formed during acetaldehyde oxidation is utilized for reductions in the cytosol to a smaller extent than the NADH formed in the alcohol dehydrogenase reaction.	NAD	119-123	aldo-keto reductase family 1 member A1	Rattus norvegicus	26-47
1009935-6	1976	The results indicate that alcohol dehydrogenase and aldehyde dehydrogenase do not share a common pool of NAD, and that NADH formed during acetaldehyde oxidation is utilized for reductions in the cytosol to a smaller extent than the NADH formed in the alcohol dehydrogenase reaction.	NAD	119-123	aldo-keto reductase family 1 member A1	Rattus norvegicus	251-272
1009935-6	1976	The results indicate that alcohol dehydrogenase and aldehyde dehydrogenase do not share a common pool of NAD, and that NADH formed during acetaldehyde oxidation is utilized for reductions in the cytosol to a smaller extent than the NADH formed in the alcohol dehydrogenase reaction.	NAD	232-236	aldo-keto reductase family 1 member A1	Rattus norvegicus	26-47
6475-9	1976	Titration of adrenodoxin reductase with NADH, instead of NADPH, provides a curved titration plot rather than the sharp break seen with NADPH, and permits calculation of a potential for the AR/ARH2 couple of -0.291 V, close to that of NAD(P)H (-0.316 V).	NAD	40-44	low density lipoprotein receptor adaptor protein 1	Homo sapiens	192-196
10611-1	1976	Aminopeptidase activity of three fractions of human erythrocytes (membranes free of hemoglobin; hemolysate free of membranes; enzyme protein fraction made free of hemoglobin by DEAE-cellulose) was measured by a NADH dependent optical test using asparaginyl1-angiotension II-amide as substrate.	NAD	211-215	carboxypeptidase Q	Homo sapiens	0-14
183977-1	1976	Isolated human term placenta mitochondria catalyse oxidation of external NADH in the presence of cytochrome c.	NAD	73-77	cytochrome c, somatic	Homo sapiens	97-109
8041-0	1976	The regulation of rat liver tryptophan pyrrolase activity by reduced nicotinamide-adenine dinucleotide (phosphate).	NAD	69-102	tryptophan 2,3-dioxygenase	Rattus norvegicus	28-48
947364-3	1976	Reductions of juglone, ferricyanide, indophenol, coenzyme Q, duroquinone, and cytochrome c by NADH are inhibited to different extents on both sides of the membrane by the impermeant hydrophilic chelators bathophenanthroline sulfonate and orthophenanthroline.	NAD	94-98	cytochrome c, somatic	Homo sapiens	78-90
179739-0	1976	Application of nicotin amide-adenine dinucleotide analogs for clinical enzymology: alcohol dehydrogenase activity in liver injury.	NAD	15-49	aldo-keto reductase family 1 member A1	Rattus norvegicus	83-104
945314-6	1976	The apparent Km for the substrate hydroxyphosphopyruvic acid was 32.8 muM, and the apparent Km for NADH 4.8 muM similar to the Kms for other mammalian 3-PGDHs.	NAD	99-103	latexin	Homo sapiens	108-111
181090-9	1976	(5) The relation between activity and NADH concentration is sigmoidal (h = 2.0) with ferricyanide or cytochrome c as acceptor, but hyperbolic with 2,6-dichloroindophenol.	NAD	38-42	cytochrome c, somatic	Homo sapiens	101-113
178671-1	1976	The rate of turnover of nicotinamide adenine dinucleotide (NAD) in the human cell line, D98/AH2, has been estimated by measuring the rates of entry into and exit from NAD molecules of 14C-adenine.	NAD	24-57	zinc finger RANBP2-type containing 3	Homo sapiens	92-95
178671-1	1976	The rate of turnover of nicotinamide adenine dinucleotide (NAD) in the human cell line, D98/AH2, has been estimated by measuring the rates of entry into and exit from NAD molecules of 14C-adenine.	NAD	59-62	zinc finger RANBP2-type containing 3	Homo sapiens	92-95
178671-9	1976	The results from both types of experiment indicate that within D98/AH2 cells the half-life of an intact NAD molecule is 60 +/- 18 minutes.	NAD	104-107	zinc finger RANBP2-type containing 3	Homo sapiens	67-70
178671-10	1976	Thus, in a human D98/AH2 cell growing with a generation time of 24 hours, NAD is turning over at twice the rate found in Escherichia coli with a generation time of half an hour.	NAD	74-77	zinc finger RANBP2-type containing 3	Homo sapiens	21-24
8041-17	1976	It is suggested that the inhibition of tryptophan pyrrolase activity by glucose or nicotinamide is mediated by both NADPH and NADH.	NAD	126-130	tryptophan 2,3-dioxygenase	Rattus norvegicus	39-59
176191-0	1976	Letter: Hydride transfer from NADH models to sp3-hybridized carbon.	NAD	30-34	Sp3 transcription factor	Homo sapiens	45-48
1259946-6	1976	Furthermore, milimolar levels of fructose 1,6-bisphosphate eluted the enzyme from ghosts, while fructose 6-phosphate and NADH (a metabolite which elutes human erythrocyte glyceraldehyde-3-phosphate dehydrogenase (G3PD) from its binding site) were ineffectuve.	NAD	121-125	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	171-211
1259946-6	1976	Furthermore, milimolar levels of fructose 1,6-bisphosphate eluted the enzyme from ghosts, while fructose 6-phosphate and NADH (a metabolite which elutes human erythrocyte glyceraldehyde-3-phosphate dehydrogenase (G3PD) from its binding site) were ineffectuve.	NAD	121-125	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	213-217
3082-2	1976	With NADH as cofactor there was a preferential 3alpha-reduction of the C19- and C21-3-oxo-steroids and a preferential 3beta-reduction of the C24- and C27-3-oxo-steroids.	NAD	5-9	TBL1X/Y related 1	Homo sapiens	80-83
1248128-3	1976	The resulting NADH, in the presence of malate dehydrogenase, is oxidized to NAD+, and the decrease in absorbance at 340 nm is directly proportional to the amount of CO2 present in the sample.	NAD	14-18	malic enzyme 2	Homo sapiens	39-59
175293-0	1976	Magnitude and significance of NAD turnover in human cell line D98/AH2.	NAD	30-33	zinc finger RANBP2-type containing 3	Homo sapiens	66-69
2388-1	1976	The molar absorptivity of NADH at 340 nm has been determined by an indirect procedure in which high-purity glucose is phosphorylated by ATP in the presence of hexokinase, coupled to oxidation of the glucose-6-phosphate by NAD+ in the presence of glucose-6-phosphate dehydrogenase.	NAD	26-30	hexokinase 1	Homo sapiens	159-169
1248128-3	1976	The resulting NADH, in the presence of malate dehydrogenase, is oxidized to NAD+, and the decrease in absorbance at 340 nm is directly proportional to the amount of CO2 present in the sample.	NAD	76-80	malic enzyme 2	Homo sapiens	39-59
809440-6	1975	The addition of solubilized cytochrome P-450 also enhances the NADH-supported microsomal benzpyrene hydroxylation and the NADH synergism of the NADPH-supported reaction.	NAD	63-67	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	28-44
171264-3	1975	The same inactivation carried out in the presence of 80 mM coenzyme, NADH, produces malate dehydrogenase which is approximately 94% active and contains 4.6 mol of pyridoxal-5"-P per mol of enzyme.	NAD	69-73	malic enzyme 2	Homo sapiens	84-104
809440-6	1975	The addition of solubilized cytochrome P-450 also enhances the NADH-supported microsomal benzpyrene hydroxylation and the NADH synergism of the NADPH-supported reaction.	NAD	122-126	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	28-44
239964-14	1975	Ki values, with respect to prenenolone, were 7.4 muM for progesterone and 150 muM for NADH.	NAD	86-90	latexin	Homo sapiens	78-81
239964-8	1975	The Michaelis constants (Km) for NAD were 50 muM, 33 muM and 14 muM, respectively for the dehydrogenation of pregnenolone, 17alpha-hydroxypregnenolone, androstenediol and dehydroepiandrosterone.	NAD	33-36	latexin	Homo sapiens	45-48
239964-15	1975	NADH, however, acted competitively with NAD and Ki value was 30 muM.	NAD	0-4	latexin	Homo sapiens	64-67
239964-8	1975	The Michaelis constants (Km) for NAD were 50 muM, 33 muM and 14 muM, respectively for the dehydrogenation of pregnenolone, 17alpha-hydroxypregnenolone, androstenediol and dehydroepiandrosterone.	NAD	33-36	latexin	Homo sapiens	53-56
239964-8	1975	The Michaelis constants (Km) for NAD were 50 muM, 33 muM and 14 muM, respectively for the dehydrogenation of pregnenolone, 17alpha-hydroxypregnenolone, androstenediol and dehydroepiandrosterone.	NAD	33-36	latexin	Homo sapiens	53-56
239964-15	1975	NADH, however, acted competitively with NAD and Ki value was 30 muM.	NAD	0-3	latexin	Homo sapiens	64-67
166378-1	1975	NAD is a necessary cofactor for the activation of adenylate cyclase (ATP pyrophosphate-lyase (cyclizing), EC 4.6.1.1) by cholera toxin.	NAD	0-3	adenylate cyclase 10	Homo sapiens	69-92
167022-3	1975	When a small amount of NADH-cytochrome b5 reductase is bound liposomes simultaneously with cytochrome b5, the two proteins catalyze the reduction of cytochrome c by NADH.	NAD	23-27	cytochrome c, somatic	Homo sapiens	149-161
164901-7	1975	This distance decreases to 6.9 A when NADH is bound, and a Co(II) to methyne proton distance of 6.6 A is determined indicating a conformation change leading to the formation of a second sphere enzyme-Co(II)-isobutyramide complex in which a hydroxyl or water ligand intervenes between the metal and the substrate analog.	NAD	38-42	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	59-64
164901-7	1975	This distance decreases to 6.9 A when NADH is bound, and a Co(II) to methyne proton distance of 6.6 A is determined indicating a conformation change leading to the formation of a second sphere enzyme-Co(II)-isobutyramide complex in which a hydroxyl or water ligand intervenes between the metal and the substrate analog.	NAD	38-42	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	59-65
237755-4	1975	For the oxido-reduction of the steroids, the 17 beta-hydroxysteroid dehydrogenase preferred NADP(H) to NAD(h).	NAD	103-109	hydroxysteroid 17-beta dehydrogenase 13	Homo sapiens	45-81
164901-9	1975	The paramagnetic effects of Co(II), at the catalytic site, on the relaxation rates of the protons of ethanol at 100 and 220 MHz, indicate that this substrate bind at a site 12-14 A distant from the catalytic Co(II) but that this distancedecreases to 6.3 A in the abortive enzyme-NADH-ethanol complex.	NAD	279-283	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	28-34
237755-5	1975	Transhydrogenation from NADPH to NAD+ or NADH to NADP+ through the cyclic oxido-reduction of the steroids by the purified 17 beta hydroxysteroid dehydrogenase preparation was not spectrophotometrically detectable, because of selective preference of the testicular 17 beta-hydroxysteroid dehydrogenase against NADP(H).	NAD	33-37	hydroxysteroid 17-beta dehydrogenase 13	Homo sapiens	122-158
237755-5	1975	Transhydrogenation from NADPH to NAD+ or NADH to NADP+ through the cyclic oxido-reduction of the steroids by the purified 17 beta hydroxysteroid dehydrogenase preparation was not spectrophotometrically detectable, because of selective preference of the testicular 17 beta-hydroxysteroid dehydrogenase against NADP(H).	NAD	41-45	hydroxysteroid 17-beta dehydrogenase 13	Homo sapiens	122-158
47760-8	1975	A rotenone- and antimycin-insensitive, exterior pathway for NADH oxidation was demonstrated which could be artificially linked by exogenous cytochrome c to the cytochrome oxidase region of the classical electron transport system.	NAD	60-64	cytochrome c, somatic	Homo sapiens	140-152
1201750-3	1975	On the basis of binding studies with ethyl isocyanide, degradation of cytochrome P-450 to P-420, redox potential, aniline binding, and relative rates of reduction by NADPH and NADH, it is suggested that the cytochrome P-450 system is analogous to that mammalian microsomes.	NAD	176-180	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	207-223
123767-8	1975	(3) With partially inhibitory concentrations of KCN, cytochrome c in either the X- or the KC1 extracted X-fragments showed uncoupler-sensitive, biphasic reduction kinetics upon the addition of NADH to the oligomycin-supplemented system.	NAD	193-197	cytochrome c, somatic	Homo sapiens	53-65
163256-4	1975	3-Pyridinealdehyde-deamino-NAD or glyceraldehyde 3-phosphate also forms an acid-stable complex with glyceraldehyde 3-phosphate dehydrogenase; however, NAD, 3-acetylpyridine-NAD, or thionicotinamide-NAD does not produce an acid-stable complex.	NAD	27-30	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	100-140
163256-4	1975	3-Pyridinealdehyde-deamino-NAD or glyceraldehyde 3-phosphate also forms an acid-stable complex with glyceraldehyde 3-phosphate dehydrogenase; however, NAD, 3-acetylpyridine-NAD, or thionicotinamide-NAD does not produce an acid-stable complex.	NAD	151-154	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	100-140
1112783-7	1975	The presence of the coenzyme, NADH, protects the enzyme from inactivation, suggesting that pyridoxal-5-P interacts at or near the malate dehydrogenase active center.	NAD	30-34	malic enzyme 2	Homo sapiens	130-150
234977-4	1975	The microsomal 20alpha-hydroxysteroid dehydrogenase showed substrate affinity to pregnenolone and progesterone and not to 17alpha-hydroxyprogesterone and preferred NADH to NADPH as a hydrogen donor.	NAD	164-168	hydroxysteroid 17-beta dehydrogenase 1	Homo sapiens	15-51
234977-10	1975	The results indicate that the microsomal 20alpha-hydroxysteroid dehydrogenase is a different enzyme from the one in the soluble fraction of the human testis and that microsomal 17alpha-hydroxylase in the human testis is activated by NADH as well as NADPH.	NAD	233-237	hydroxysteroid 17-beta dehydrogenase 1	Homo sapiens	41-77
4371815-0	1974	Glyceraldehyde-3-phosphate dehydrogenase catalyzed hydration of the 5-6 double bond of reduced beta-nicotinamide adenine dinucleotide (betaNADH).	NAD	95-133	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	0-40
170765-1	1975	Alcohol dehydrogenase from horse (isoenzyme SS and ES, but not EE), rat and human liver were found to catalyze the NAD-dependent oxidation of 3beta-hydroxy groups in 5alpha- and 5beta-steroids of the C19, C21, and C24 series.	NAD	115-118	TBL1X/Y related 1	Homo sapiens	205-208
4374132-0	1974	Reduced nicotinamide adenine dinucleotide-cytochrome b5 reductase and cytochrome b5 as electron carriers in NADH-supported cytochrome P-450 -dependent enzyme activities in liver microsomes.	NAD	108-112	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	123-139
4377103-3	1974	The analogue of 3-phosphoglycerate oxidizes NADH under the combined action of 3-phosphoglycerate kinase and glyceraldehyde 3-phosphate dehydrogenase if ATP is added.	NAD	44-48	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	108-148
4154122-4	1974	Assays for galactose 1-phosphate uridyl transferase involving the reduction of the coenzymes NAD or NADP are unsuitable for amniotic cells whereas estimation of (14)C-UDP-galactose produced from (14)C-galactose 1-phosphate detected the homozygous mutant fetus.	NAD	93-96	galactose-1-phosphate uridylyltransferase	Homo sapiens	11-51
16658941-12	1974	Finally, the nitrate reductase will exhibit a diaphorase activity and reduce the artificial electron acceptor mammalian cytochrome c in flavin-adeninedinucleotide-dependent reaction.Inhibition studies with potassium cyanide, sodium azide, and o-phenanthroline have yielded indirect evidence for metal component (s) of the enzyme.The inhibition of the NADH-requiring enzyme activities by p-hydroxymercuribenzoate has shown that an essential sulfhydryl group is involved in the initial portion of the electron transport.	NAD	351-355	cytochrome c, somatic	Homo sapiens	120-132
16742801-6	1973	Increased picolinate carboxylase and decreased quinolinate phosphoribosyltransferase activities would result in a decrease in NAD formation from dietary tryptophan.	NAD	126-129	aminocarboxymuconate semialdehyde decarboxylase	Rattus norvegicus	10-32
4374185-1	1974	Rat skeletal-muscle elongation factor 2 was assayed by causing it to react with NAD(+) by using fragment A of diphtheria toxin as the catalyst.	NAD	80-86	eukaryotic translation elongation factor 2	Rattus norvegicus	20-39
4154306-6	1974	Since the intracellular concentration of both nucleotides is estimated to be about 50 muM, it is much more likely, from a kinetic argument, that the respiratory burst of phagocytosis is intiated by the oxidation of NADH rather than of NADPH.	NAD	215-219	latexin	Homo sapiens	86-89
4151581-0	1974	Redox properties of the reduced nicotinamide adenine dinucleotide phosphate-cytochrome P-450 and reduced nicotinamide adenine dinucleotide-cytochrome b5 reductases.	NAD	32-65	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	76-92
19396987-8	1974	(4) It is postulated that with pyruvate as substrate, recycling of carbon via pyruvate carboxylase, phosphoenolpyruvate carboxylase and pyruvate kinase (ATP: pyruvate phosphotransferase, EC 2.7.1.40) is an important, energy-requiring, mechanism for the transfer of the proportion of NADH not directly associated with gluconeogenesis.	NAD	283-287	pyruvate carboxylase	Homo sapiens	78-98
16657934-5	1972	Hydroxypyruvate reductase (NAD-linked) is present in the glyoxysomes, and at very high substrate concentrations (&gt;10 mm) this enzyme can also transfer electrons from NADH to glyoxylate.	NAD	27-30	glyoxylate and hydroxypyruvate reductase	Homo sapiens	0-25
4350261-0	1973	A peroxide-dependent reduction of cytochrome c by NADH.	NAD	50-54	cytochrome c, somatic	Homo sapiens	34-46
4341351-5	1972	The decrease in NAD(+) concentration following enolase inhibition by F is attributed to a diminished rate of formation in the reaction catalyzed by lactic dehydrogenase (LDH) with undiminished continued utilization in the reaction catalyzed by glyceraldehyde-3-phosphate dehydrogenase (GAPDH).	NAD	16-22	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	244-284
4341351-5	1972	The decrease in NAD(+) concentration following enolase inhibition by F is attributed to a diminished rate of formation in the reaction catalyzed by lactic dehydrogenase (LDH) with undiminished continued utilization in the reaction catalyzed by glyceraldehyde-3-phosphate dehydrogenase (GAPDH).	NAD	16-22	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	286-291
4341351-6	1972	It is postulated that the NAD(+) lowering limited the GAPDH step, resulting in proportionate decreases in the rates of phosphoglycerate kinase (PGK) and Na,K-dependent adenosine triphosphatase (Na,K-ATPase), a reaction sequence thought to link glycolysis with active Na extrusion.	NAD	26-32	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	54-59
4341351-7	1972	Adding pyruvate with F increased NAD(+) production at the LDH step, thus reactivating GAPDH, PGK, and Na,K-ATPase and leading to the observed restoration of (22)Na release.	NAD	33-39	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	86-91
4346743-8	1972	Subsequent elution with the cofactor NAD(+) yields glyceraldehyde 3-phosphate dehydrogenase whereas lactate dehydrogenase is eluted by applying the same molarity of the reduced cofactor.	NAD	37-43	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	51-91
16657934-5	1972	Hydroxypyruvate reductase (NAD-linked) is present in the glyoxysomes, and at very high substrate concentrations (&gt;10 mm) this enzyme can also transfer electrons from NADH to glyoxylate.	NAD	169-173	glyoxylate and hydroxypyruvate reductase	Homo sapiens	0-25
4326877-0	1971	Interaction of nicotinamide-adenine dinucleotide and its analogs with glyceraldehyde 3-phosphate dehydrogenase.	NAD	15-48	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	70-110
4392627-0	1970	Nicotinamide adenine dinucleotide as an active site director in glyceraldehyde 3-phosphate dehydrogenase modification.	NAD	0-33	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	64-104
4326747-1	1971	I. Nicotinamide mononucleotide deamidase and a new pathway for "salvage synthesis" of nicotinamide adenine dinucleotide].	NAD	86-119	cathepsin A	Homo sapiens	31-40
4316548-1	1970	By competition with lactate dehydrogenase (LDH) for nicotinamide adenine dinucleotide (NAD), commonly occurring intracellular proteins, such as glyceraldehyde-3-phosphate dehydrogenase, malate dehydrogenase, and albumin, can protect LDH-1 and LDH-5 from inhibition and ternary complex formation with NAD and pyruvate.	NAD	52-85	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	144-184
4316548-1	1970	By competition with lactate dehydrogenase (LDH) for nicotinamide adenine dinucleotide (NAD), commonly occurring intracellular proteins, such as glyceraldehyde-3-phosphate dehydrogenase, malate dehydrogenase, and albumin, can protect LDH-1 and LDH-5 from inhibition and ternary complex formation with NAD and pyruvate.	NAD	87-90	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	144-184
4316548-1	1970	By competition with lactate dehydrogenase (LDH) for nicotinamide adenine dinucleotide (NAD), commonly occurring intracellular proteins, such as glyceraldehyde-3-phosphate dehydrogenase, malate dehydrogenase, and albumin, can protect LDH-1 and LDH-5 from inhibition and ternary complex formation with NAD and pyruvate.	NAD	300-303	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	144-184
4317722-1	1970	Lactoperoxidase (EC 1.11.1.7) catalysed the oxidation of NADH by hydrogen peroxide in the presence of either thiocyanate, iodide or bromide.	NAD	57-61	lactoperoxidase	Homo sapiens	0-15
4310081-1	1969	Activities for nicotinamide adenine dinucleotide (NAD)-dependent and NAD-independent forms of lactate dehydrogenase (LDH) were measured in cell-free extracts of Staphylococcus aureus strain PS 6 for the d and l isomers of lactate.	NAD	15-48	AT695_RS04475	Staphylococcus aureus	94-115
4310081-4	1969	The fast band exhibited LDH activity that was not NAD-dependent for both isomers of lactate, whereas, the slow band had very high NAD-dependent LDH activity for the l isomer but just detectable activity or the d isomer.	NAD	130-133	AT695_RS04475	Staphylococcus aureus	144-147
4310081-1	1969	Activities for nicotinamide adenine dinucleotide (NAD)-dependent and NAD-independent forms of lactate dehydrogenase (LDH) were measured in cell-free extracts of Staphylococcus aureus strain PS 6 for the d and l isomers of lactate.	NAD	15-48	AT695_RS04475	Staphylococcus aureus	117-120
4310081-6	1969	NAD-dependent LDH, in apparent association with a nonspecific tetrazolium-reducing protein, is responsible for the production of the slow band.	NAD	0-3	AT695_RS04475	Staphylococcus aureus	14-17
4310081-1	1969	Activities for nicotinamide adenine dinucleotide (NAD)-dependent and NAD-independent forms of lactate dehydrogenase (LDH) were measured in cell-free extracts of Staphylococcus aureus strain PS 6 for the d and l isomers of lactate.	NAD	69-72	AT695_RS04475	Staphylococcus aureus	94-115
4310081-1	1969	Activities for nicotinamide adenine dinucleotide (NAD)-dependent and NAD-independent forms of lactate dehydrogenase (LDH) were measured in cell-free extracts of Staphylococcus aureus strain PS 6 for the d and l isomers of lactate.	NAD	69-72	AT695_RS04475	Staphylococcus aureus	117-120
4310081-2	1969	Data obtained for the NAD-dependent lactate dehydrogenases indicate that oxidation of both isomers of lactate is due to both an l-lactate-specific LDH and a lactate racemase.	NAD	22-25	AT695_RS04475	Staphylococcus aureus	147-150
4386919-0	1968	Glyceraldehyde-3-phosphate dehydrogenase in photosynthetic tissues: kinetic evidence for competitivity between NADP and NAD.	NAD	111-114	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	0-40
4301879-1	1968	The binding of diphosphopyridine nucleotide to glyceraldehyde 3-phosphate dehydrogenase.	NAD	15-43	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	47-87
4318272-0	1969	On the binding of mammalian cytochrome c in NADH- and succinate-cytochrome c-reductase from Rhodospirillum rubrum.	NAD	44-48	cytochrome c, somatic	Homo sapiens	28-40
4294340-3	1968	A change in heat stability accompanies the conversion of the slowest form of alcohol dehydrogenase to the fastest form; the latter becomes stable at 45 degrees C. The increased heat stability may indicate that a conformational change in the alcohol dehydrogenase occurs along with the binding of nicotinamide-adenine dinucleotide.	NAD	296-329	Alcohol dehydrogenase	Drosophila melanogaster	77-98
4295239-1	1968	The effect of growth conditions on the specific activity of nicotinamide adenine dinucleotide (NAD)-linked lactate dehydrogenase (LDH) in extracts of Staphylococcus aureus strain SG 511A was examined.	NAD	60-93	AT695_RS04475	Staphylococcus aureus	107-128
4294340-3	1968	A change in heat stability accompanies the conversion of the slowest form of alcohol dehydrogenase to the fastest form; the latter becomes stable at 45 degrees C. The increased heat stability may indicate that a conformational change in the alcohol dehydrogenase occurs along with the binding of nicotinamide-adenine dinucleotide.	NAD	296-329	Alcohol dehydrogenase	Drosophila melanogaster	241-262
4295239-1	1968	The effect of growth conditions on the specific activity of nicotinamide adenine dinucleotide (NAD)-linked lactate dehydrogenase (LDH) in extracts of Staphylococcus aureus strain SG 511A was examined.	NAD	60-93	AT695_RS04475	Staphylococcus aureus	130-133
4295239-1	1968	The effect of growth conditions on the specific activity of nicotinamide adenine dinucleotide (NAD)-linked lactate dehydrogenase (LDH) in extracts of Staphylococcus aureus strain SG 511A was examined.	NAD	95-98	AT695_RS04475	Staphylococcus aureus	107-128
4382010-2	1966	The concentrations of the nicotinamide-adenine dinucleotides in rat liver have been determined at intervals during the period 1-24hr.	NAD	26-60	period circadian regulator 1	Rattus norvegicus	119-127
4295239-1	1968	The effect of growth conditions on the specific activity of nicotinamide adenine dinucleotide (NAD)-linked lactate dehydrogenase (LDH) in extracts of Staphylococcus aureus strain SG 511A was examined.	NAD	95-98	AT695_RS04475	Staphylococcus aureus	130-133
4295239-3	1968	The aerobic level of NAD-linked LDH of S. aureus remained constant and was independent of the carbon source.	NAD	21-24	AT695_RS04475	Staphylococcus aureus	32-35
4295240-5	1968	LDH activity for these enzyme preparations was determined by the colorimetric method mentioned and also by measuring the rate of nicotinamide adenine dinucleotide reduction at 340 mmu.	NAD	129-162	AT695_RS04475	Staphylococcus aureus	0-3
4383133-5	1967	The antibiotic inhibited the reduced nicotinamide adenine dinucleotide (NADH(2)) cytochrome c reductase (EC 1.6.2.1) as well as the much slower nonenzymatic reduction of this cytochrome by the nucleotide.	NAD	37-70	cytochrome c, somatic	Homo sapiens	81-93
4383133-5	1967	The antibiotic inhibited the reduced nicotinamide adenine dinucleotide (NADH(2)) cytochrome c reductase (EC 1.6.2.1) as well as the much slower nonenzymatic reduction of this cytochrome by the nucleotide.	NAD	72-76	cytochrome c, somatic	Homo sapiens	81-93
4287841-9	1966	When the activity of glyceraldehyde 3-phosphate dehydrogenase was limited experimentally by a low concentration of NAD(+) or when it was blocked by iodoacetate, the accumulations of fructose diphosphate and triose phosphates were large and accounted for most of the carbohydrate degraded in the presence of AMP.	NAD	115-121	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	21-61
4289868-1	1966	Absorbance and fluorescence properties of reduced nicotinamide-adenine dinucleotide complexes with glyceraldehyde 3-phosphate dehydrogenase.	NAD	50-83	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	99-139
14336076-0	1965	AN ULTRAVIOLET ABSORPTION BAND DUE TO THE INTERACTION OF NAD AND GLYCERALDEHYDE-3-PHOSPHATE DEHYDROGENASE.	NAD	57-60	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	65-105
4285726-2	1965	In glycolysis the oxidation of glyceraldehyde-3-phosphate is controlled by DPNH, which inhibits glyceraldehyde-3-phosphate dehydrogenase.	NAD	75-79	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	96-136
14087009-0	1963	ADENOSINE TRIPHOSPHATE-DEPENDENT REDUCTION OF NICOTINAMIDE ADENINE DINUCLEOTIDE BY FERRO-CYTOCHROME C IN CHEMOAUTOTROPHIC BACTERIA.	NAD	46-79	cytochrome c, somatic	Homo sapiens	89-101
14325940-0	1965	THE EFFECT OF CA2+ ON DPN AND TPN INCORPORATION INTO RAT-LIVER MITOCHONDRIA.	NAD	22-25	carbonic anhydrase 2	Rattus norvegicus	14-17
13118107-7	1954	The metabolism of the outer limb is probably adequate to provide the DPN required for the maintenance of the rhodopsin concentration necessary for vision.	NAD	69-72	rhodopsin	Homo sapiens	109-118
13174589-0	1954	The action of glyceraldehyde-3-phosphate dehydrogenase on reduced diphosphopyridine nucleotide.	NAD	66-94	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	14-54
13084624-0	1953	The binding of diphosphopyridine nucleotide by glyceraldehyde-3-phosphate dehydrogenase.	NAD	15-43	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	47-87
33872694-1	2021	Dysfunction of Sirtuin 3 (SIRT3), an NAD+-dependent histone deacetylase, impairs varied mitochondrial metabolic pathways in human cancer.	NAD	37-40	sirtuin 3	Homo sapiens	15-24
18108501-17	1949	This action of DPN brings a member of the vitamin B complex, nicotinic acid amide, into an auxiliary position in the rhodopsin system.	NAD	15-18	rhodopsin	Homo sapiens	117-126
33872694-1	2021	Dysfunction of Sirtuin 3 (SIRT3), an NAD+-dependent histone deacetylase, impairs varied mitochondrial metabolic pathways in human cancer.	NAD	37-40	sirtuin 3	Homo sapiens	26-31
33011882-6	2021	The activity of CYB5R and CYPOR was assessed with lucigenin-enhanced chemiluminescence stimulated by NADH and NADPH, respectively.	NAD	101-105	cytochrome p450 oxidoreductase	Homo sapiens	26-31
34050173-2	2021	The NAD+-dependent SIRT6 deacylase regulates aging and metabolism through mechanisms that largely remain unknown.	NAD	4-8	sirtuin 6	Mus musculus	19-24
33347833-11	2021	In the absence of metastasis, in lesions with well/moderate differentiation and without muscle invasion, ET is adequate for NAD-NETs <10 mm and is a viable option for 11 to 19 mm lesions.	NAD	124-127	major facilitator superfamily domain containing 11	Homo sapiens	105-107
33739373-6	2021	In its backward direction, phosphoglycerate kinase and p-GAPDH consume ATP and NADH.	NAD	79-83	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	57-62
34050173-6	2021	To mediate these changes, mechanistically, SIRT6 increases hepatic gluconeogenic gene expression, de novo NAD+ synthesis, and systemically enhances glycerol release from adipose tissue.	NAD	106-110	sirtuin 6	Mus musculus	43-48
33990669-5	2021	In this survival response of cancer cells, MEK pathway directs melanoma cells to deregulate mitochondrial metabolism, to accumulate reduced species (NADH), and to centralize metabolism in the cytosol.	NAD	149-153	mitogen-activated protein kinase kinase 7	Homo sapiens	43-46
33991007-7	2021	ATP, ADP and AMP as well as NAD+ , NADH, NADP+ and NADPH directly interact with CIRBP, involving both the folded RNA-recognition motif and the disordered RG/RGG region.	NAD	28-32	cold inducible RNA binding protein	Homo sapiens	80-85
33991007-7	2021	ATP, ADP and AMP as well as NAD+ , NADH, NADP+ and NADPH directly interact with CIRBP, involving both the folded RNA-recognition motif and the disordered RG/RGG region.	NAD	35-39	cold inducible RNA binding protein	Homo sapiens	80-85
33749979-5	2021	Moreover, SIRT7 interacts with KCC4 in a NAD+ -dependent manner and increases its stability and activity in HEK293 cells.	NAD	41-45	solute carrier family 12 member 7	Homo sapiens	31-35
33982576-5	2021	Decreased glycolysis and citric cycle activity impair BCAA transamination to branched-chain keto acids (BCKAs) due to decreased supply of amino group acceptors (alpha-ketoglutarate, pyruvate, and oxaloacetate); increased fatty acid oxidation inhibits flux of BCKA through BCKA dehydrogenase due to increased supply of NADH and acyl-CoAs.	NAD	318-322	AT-rich interaction domain 4B	Homo sapiens	54-58
33706382-1	2021	Sirtuin 3 (SIRT3) is an NAD+-dependent deacetylase linked to a broad range of physiological and pathological processes, including aging and aging-related diseases.	NAD	24-27	sirtuin 3	Homo sapiens	0-9
33706382-1	2021	Sirtuin 3 (SIRT3) is an NAD+-dependent deacetylase linked to a broad range of physiological and pathological processes, including aging and aging-related diseases.	NAD	24-27	sirtuin 3	Homo sapiens	11-16
33976173-3	2021	Here, we identify NAMPT, the rate limiting enzyme in NAD salvage synthesis, as a target of STAT1 during cellular activation by interferon gamma, an important driver of macrophage polarization and antitumor responses.	NAD	53-56	interferon gamma	Homo sapiens	127-143
32037512-12	2021	CONCLUSIONS AND IMPLICATIONS: The NAD+ boosting agent P7C3-A20 alleviates NAFLD through stimulating FGF21 and FGF1 in an LKB1/AMPK/CRTC2-dependent manner and shaping gut microbiota.	NAD	34-37	fibroblast growth factor 1	Mus musculus	110-114
33949241-7	2021	Our findings indicated that APAP resulted in remarkable NAD+ depletion in a dose-dependent manner accompanied by NAMPT downregulation, and NAM pretreatment significantly elevated the NAD+ decline due to upregulation of NAMPT.	NAD	183-187	nicotinamide phosphoribosyltransferase	Mus musculus	219-224
32037512-12	2021	CONCLUSIONS AND IMPLICATIONS: The NAD+ boosting agent P7C3-A20 alleviates NAFLD through stimulating FGF21 and FGF1 in an LKB1/AMPK/CRTC2-dependent manner and shaping gut microbiota.	NAD	34-37	serine/threonine kinase 11	Mus musculus	121-125
33774477-6	2021	Established roles for NQO1 include a superoxide reductase activity, NAD+ generation, interaction with proteins and their stabilization against proteasomal degradation, binding and regulation of mRNA translation and binding to microtubules including the mitotic spindles.	NAD	68-72	NAD(P)H quinone dehydrogenase 1	Homo sapiens	22-26
33548217-2	2021	SARM1 is a particularly attractive therapeutic target, as it is an inducible NAD+ cleaving enzyme that is required for axon loss in multiple mouse models of traumatic and degenerative neurological disease.	NAD	77-81	sterile alpha and HEAT/Armadillo motif containing 1	Mus musculus	0-5
33636397-2	2021	Owing to its dependance on the cofactor nicotinamide adenine dinucleotide (NAD+), SIRT4 can act as a mitochondrial metabolic sensor of cellular energy status.	NAD	40-73	sirtuin 4	Rattus norvegicus	82-87
33636397-2	2021	Owing to its dependance on the cofactor nicotinamide adenine dinucleotide (NAD+), SIRT4 can act as a mitochondrial metabolic sensor of cellular energy status.	NAD	75-79	sirtuin 4	Rattus norvegicus	82-87
33636397-12	2021	Furthermore, our results verified that in addition to reducing DPC differentiation, Sirt4 knockdown could also significantly reduce ATP levels, elevate the NAD+/NADH ratio, and increase ROS levels.	NAD	156-160	sirtuin 4	Rattus norvegicus	84-89
33636397-12	2021	Furthermore, our results verified that in addition to reducing DPC differentiation, Sirt4 knockdown could also significantly reduce ATP levels, elevate the NAD+/NADH ratio, and increase ROS levels.	NAD	161-165	sirtuin 4	Rattus norvegicus	84-89
33752971-7	2021	Brain concentrations of nicotinamide adenine dinucleotide (NAD+) were lower in Ndufs4-/- mice breathing air than in WT mice, but preserved at WT levels with hypoxia treatment.	NAD	24-57	NADH:ubiquinone oxidoreductase core subunit S4	Mus musculus	79-85
33752971-7	2021	Brain concentrations of nicotinamide adenine dinucleotide (NAD+) were lower in Ndufs4-/- mice breathing air than in WT mice, but preserved at WT levels with hypoxia treatment.	NAD	59-63	NADH:ubiquinone oxidoreductase core subunit S4	Mus musculus	79-85
33925170-6	2021	Autoregulation of PAR elongation at high PARP and NAD+ concentrations is stronger for PARP2 than for PARP1, and the activity of PARP2 is more effectively inhibited by XRCC1.	NAD	50-54	poly(ADP-ribose) polymerase 2	Homo sapiens	86-91
33928788-12	2021	Conclusions:Nampt-mediated production of NAD+ protects against oxidative stress in part through the NADPH-dependent reducing system, thereby alleviating the development of diabetic cardiomyopathy in response to HFD consumption.	NAD	41-45	nicotinamide phosphoribosyltransferase	Mus musculus	12-17
33928788-2	2021	The role of nicotinamide phosphoribosyltransferase (Nampt), the rate-limiting enzyme of the salvage pathway of NAD+ synthesis, in the development of diabetic cardiomyopathy is poorly understood.	NAD	111-115	nicotinamide phosphoribosyltransferase	Mus musculus	12-50
33928788-2	2021	The role of nicotinamide phosphoribosyltransferase (Nampt), the rate-limiting enzyme of the salvage pathway of NAD+ synthesis, in the development of diabetic cardiomyopathy is poorly understood.	NAD	111-115	nicotinamide phosphoribosyltransferase	Mus musculus	52-57
33928788-7	2021	Nampt overexpression upregulated not only NAD+ but also NADP+ and NADPH in the heart and in cultured cardiomyocytes, which in turn stimulated the GSH and Trx1 systems and alleviated oxidative stress in the heart induced by HFD consumption.	NAD	42-46	nicotinamide phosphoribosyltransferase	Mus musculus	0-5
33928788-8	2021	In cultured cardiomyocytes, Nampt-induced upregulation of NADPH was abolished in the presence of NADK knockdown, whereas that of NAD+ was not.	NAD	129-133	nicotinamide phosphoribosyltransferase	Mus musculus	28-33
33925170-6	2021	Autoregulation of PAR elongation at high PARP and NAD+ concentrations is stronger for PARP2 than for PARP1, and the activity of PARP2 is more effectively inhibited by XRCC1.	NAD	50-54	poly(ADP-ribose) polymerase 1	Homo sapiens	101-106
33921561-2	2021	PARP inhibitors (PARPi) are able to interact with the binding site for PARP cofactor (NAD+) and trapping PARP on the DNA.	NAD	86-90	poly(ADP-ribose) polymerase 1	Homo sapiens	0-4
33922080-3	2021	We found that TGF-beta1 lowers NADH and NADH/NAD levels, possibly due to changes in the TCA cycle, resulting in reductions in the ATP level and oxidative phosphorylation in pulmonary fibroblasts.	NAD	31-35	transforming growth factor beta 1	Homo sapiens	14-23
33922080-3	2021	We found that TGF-beta1 lowers NADH and NADH/NAD levels, possibly due to changes in the TCA cycle, resulting in reductions in the ATP level and oxidative phosphorylation in pulmonary fibroblasts.	NAD	40-44	transforming growth factor beta 1	Homo sapiens	14-23
33922080-3	2021	We found that TGF-beta1 lowers NADH and NADH/NAD levels, possibly due to changes in the TCA cycle, resulting in reductions in the ATP level and oxidative phosphorylation in pulmonary fibroblasts.	NAD	31-34	transforming growth factor beta 1	Homo sapiens	14-23
33922080-6	2021	Consistent with the mitochondrial observations, butyrate significantly increased ADP, ATP, NADH, and NADH/NAD levels in TGF-beta1-treated pulmonary fibroblasts.	NAD	101-105	transforming growth factor beta 1	Homo sapiens	120-129
33922080-6	2021	Consistent with the mitochondrial observations, butyrate significantly increased ADP, ATP, NADH, and NADH/NAD levels in TGF-beta1-treated pulmonary fibroblasts.	NAD	91-94	transforming growth factor beta 1	Homo sapiens	120-129
33925372-0	2021	Role of PGC-1alpha in the Mitochondrial NAD+ Pool in Metabolic Diseases.	NAD	40-44	PPARG coactivator 1 alpha	Homo sapiens	8-18
33925372-3	2021	A decrease in both mitochondria biogenesis and NAD+ is a characteristic of metabolic diseases, and peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1alpha) orchestrates mitochondrial biogenesis and is involved in mitochondrial NAD+ pool.	NAD	252-256	PPARG coactivator 1 alpha	Homo sapiens	99-167
33925372-3	2021	A decrease in both mitochondria biogenesis and NAD+ is a characteristic of metabolic diseases, and peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1alpha) orchestrates mitochondrial biogenesis and is involved in mitochondrial NAD+ pool.	NAD	252-256	PPARG coactivator 1 alpha	Homo sapiens	169-179
33925372-4	2021	Here we discuss how PGC-1alpha is involved in the NAD+ synthesis pathway and metabolism, as well as the strategy for increasing the NAD+ pool in the metabolic disease state.	NAD	50-54	PPARG coactivator 1 alpha	Homo sapiens	20-30
33925372-4	2021	Here we discuss how PGC-1alpha is involved in the NAD+ synthesis pathway and metabolism, as well as the strategy for increasing the NAD+ pool in the metabolic disease state.	NAD	132-136	PPARG coactivator 1 alpha	Homo sapiens	20-30
33788551-5	2021	The reduction of Co(II) to Co(I) occurs at -2.6 V for a neutral donor but shifts to -3.4 V for an anionic donor.	NAD	27-32	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	17-23
33921561-2	2021	PARP inhibitors (PARPi) are able to interact with the binding site for PARP cofactor (NAD+) and trapping PARP on the DNA.	NAD	86-90	poly(ADP-ribose) polymerase 1	Homo sapiens	17-21
33921561-2	2021	PARP inhibitors (PARPi) are able to interact with the binding site for PARP cofactor (NAD+) and trapping PARP on the DNA.	NAD	86-90	poly(ADP-ribose) polymerase 1	Homo sapiens	17-21
33528041-6	2021	The expression of genes encoding for nicotinamide adenine dinucleotide (NAD+ ) biosynthetic enzymes-Nmnat3 and Nampt-and NAD+ levels were decreased, suggesting that NAD+ is essential for maintaining lysosomal acidification.	NAD	37-70	nicotinamide phosphoribosyltransferase	Mus musculus	111-116
33528041-6	2021	The expression of genes encoding for nicotinamide adenine dinucleotide (NAD+ ) biosynthetic enzymes-Nmnat3 and Nampt-and NAD+ levels were decreased, suggesting that NAD+ is essential for maintaining lysosomal acidification.	NAD	72-76	nicotinamide phosphoribosyltransferase	Mus musculus	111-116
33854178-7	2021	Supplementing preadipocytes with the NAD+ booster nicotinamide mononucleotide (NMN) during differentiation increased expression levels of leptin, SIRT1, and PGC-1alpha and its transcriptional targets, and reduced levels of pro-fibrotic collagens (Col6A1 and Col6A3) in a SIRT1-dependent manner.	NAD	37-41	PPARG coactivator 1 alpha	Homo sapiens	157-167
33657415-4	2021	PARP1 is aberrantly activated in many non-oncological diseases, leading to the excessive NAD+ depletion and PAR formation, thus causing cell death and tissue damage.	NAD	89-93	poly(ADP-ribose) polymerase 1	Homo sapiens	0-5
33600944-9	2021	As the substrate of NQO1, TSB induced oxidative stress, which resulted in dramatic DNA damage, poly (ADP-ribose) polymerase 1 hyperactivation, and NAD+ depletion, leading to necrotic cell death.	NAD	147-151	NAD(P)H quinone dehydrogenase 1	Homo sapiens	20-24
33850276-6	2022	PGG blocks GAPDH activity by a reversible and NAD+ and Pi competitive mechanism, suggesting that it represents a novel class of GAPDH inhibitors.	NAD	46-50	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	11-16
33831359-0	2021	An NAD+/NMN balancing act by SARM1 and NMNAT2 controls axonal degeneration.	NAD	3-7	nicotinamide nucleotide adenylyltransferase 2	Homo sapiens	39-45
33831359-3	2021	(2021) reveal a key regulatory mechanism that controls SARM1"s enzymatic activity, providing insight into how NAD+ biosynthesis by the NMNAT2 enzyme protects axons, and a new therapeutic path to tune SARM1 activity.	NAD	110-114	nicotinamide nucleotide adenylyltransferase 2	Homo sapiens	135-141
34056345-3	2021	Using the nicotinamide adenine dinucleotide (NADH)-oxaloacetic acid with the enzyme of malate dehydrogenase as an example, mixtures of different reagent concentrations were characterized to extract the ratio of remaining concentrations between NAD+ and NADH.	NAD	10-43	malic enzyme 2	Homo sapiens	87-107
34056345-3	2021	Using the nicotinamide adenine dinucleotide (NADH)-oxaloacetic acid with the enzyme of malate dehydrogenase as an example, mixtures of different reagent concentrations were characterized to extract the ratio of remaining concentrations between NAD+ and NADH.	NAD	45-49	malic enzyme 2	Homo sapiens	87-107
34056345-3	2021	Using the nicotinamide adenine dinucleotide (NADH)-oxaloacetic acid with the enzyme of malate dehydrogenase as an example, mixtures of different reagent concentrations were characterized to extract the ratio of remaining concentrations between NAD+ and NADH.	NAD	244-248	malic enzyme 2	Homo sapiens	87-107
34056345-3	2021	Using the nicotinamide adenine dinucleotide (NADH)-oxaloacetic acid with the enzyme of malate dehydrogenase as an example, mixtures of different reagent concentrations were characterized to extract the ratio of remaining concentrations between NAD+ and NADH.	NAD	253-257	malic enzyme 2	Homo sapiens	87-107
33967591-6	2021	Furthermore, our results show that culturing hMSCs in the microcarrier-based suspension bioreactor (compared to static planar culture) results in smaller cell size and higher levels of reactive oxidative species (ROS) and ROS regulator Sirtuin-3, which have implications on the nicotinamide adenine dinucleotide metabolic pathway and metabolic homeostasis.	NAD	278-311	sirtuin 3	Homo sapiens	236-245
33485900-4	2021	As a sensing or consuming enzyme of the poly (ADP-ribose) polymerase 1 (PARP1), the cyclic ADP-ribose (cADPR) synthases (CD38 and CD157), and sirtuin protein deacetylases (sirtuins, SIRTs), NAD+ participates in several key processes in cardiovascular disease.	NAD	190-194	poly(ADP-ribose) polymerase 1	Homo sapiens	40-70
33690226-3	2021	Sirtuins, including SIRT3, require nicotinamide adenine dinucleotide (NAD) as a cosubstrate.	NAD	35-68	sirtuin 3	Homo sapiens	20-25
33690226-3	2021	Sirtuins, including SIRT3, require nicotinamide adenine dinucleotide (NAD) as a cosubstrate.	NAD	70-73	sirtuin 3	Homo sapiens	20-25
33710180-3	2021	This study analyzed if BD by generating oxidative stress modulates the alteration in hepatic energy homeostasis through two important regulators of energy metabolism: the NAD+-dependent sirtuin deacetylase (SIRT1) and AMP-activated protein kinase (AMPK) and if supplementation with the antioxidant selenium (Se) improves these metabolic disorders.	NAD	171-175	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	248-252
33893948-3	2021	Photoactivation of astrocytes led to activation of neurogenesis and changes in the expression of molecules (Cx43 and CD38) that determine bioavailability of NAD+ to ensure proliferative activity of cells in the neurogenic niche.	NAD	157-161	gap junction protein, alpha 1	Mus musculus	108-112
33485900-4	2021	As a sensing or consuming enzyme of the poly (ADP-ribose) polymerase 1 (PARP1), the cyclic ADP-ribose (cADPR) synthases (CD38 and CD157), and sirtuin protein deacetylases (sirtuins, SIRTs), NAD+ participates in several key processes in cardiovascular disease.	NAD	190-194	poly(ADP-ribose) polymerase 1	Homo sapiens	72-77
33485900-4	2021	As a sensing or consuming enzyme of the poly (ADP-ribose) polymerase 1 (PARP1), the cyclic ADP-ribose (cADPR) synthases (CD38 and CD157), and sirtuin protein deacetylases (sirtuins, SIRTs), NAD+ participates in several key processes in cardiovascular disease.	NAD	190-194	bone marrow stromal cell antigen 1	Homo sapiens	130-135
33650791-3	2021	Previous reports suggest that ERalpha expression can be regulated by sirt1 (sirtuin 1), a nicotinamide adenine dinucleotide (NAD+)-dependent class III histone deacetylases that modulates activity of several substrates involved in cellular stress, metabolism, proliferation, senescence, protein degradation and apoptosis.	NAD	90-123	estrogen receptor 1	Homo sapiens	30-37
33650791-3	2021	Previous reports suggest that ERalpha expression can be regulated by sirt1 (sirtuin 1), a nicotinamide adenine dinucleotide (NAD+)-dependent class III histone deacetylases that modulates activity of several substrates involved in cellular stress, metabolism, proliferation, senescence, protein degradation and apoptosis.	NAD	125-129	estrogen receptor 1	Homo sapiens	30-37
33264605-4	2021	Here, we present the cryoelectron microscopic structures of two different constructs of CtBP2 corroborating that the native state of CtBP2 in the presence of NADH is tetrameric.	NAD	158-162	C-terminal binding protein 2	Homo sapiens	88-93
33264605-4	2021	Here, we present the cryoelectron microscopic structures of two different constructs of CtBP2 corroborating that the native state of CtBP2 in the presence of NADH is tetrameric.	NAD	158-162	C-terminal binding protein 2	Homo sapiens	133-138
33732926-2	2021	The sperm DNA mutation was observed on nicotinamide adenine dinucleotide hydride (NADH) dehydrogenase 1 (ND1) of mitochondrial Deoxyribonucleic Acid (mtDNA).	NAD	82-86	mitochondrially encoded NADH dehydrogenase 1	Homo sapiens	105-108
33683197-6	2021	This HPF1-mediated switch from polymerase to hydrolase has important implications for the PARP1-mediated response to DNA damage and raises interesting new questions about the role of intracellular ADPR and depletion of NAD+.	NAD	219-223	histone PARylation factor 1	Homo sapiens	5-9
33683197-6	2021	This HPF1-mediated switch from polymerase to hydrolase has important implications for the PARP1-mediated response to DNA damage and raises interesting new questions about the role of intracellular ADPR and depletion of NAD+.	NAD	219-223	poly(ADP-ribose) polymerase 1	Homo sapiens	90-95
33868961-4	2021	Western blot analysis showed that darbepoetin reduced the phosphorylation of c-Jun N-terminal kinases (JNK)1/2 over a period of 1 h incubation with NaD, but did not have an obvious effect on several other targets associated with cell death/survival.	NAD	148-151	mitogen-activated protein kinase 8	Homo sapiens	103-110
33621088-8	2021	Together, these experiments reveal the details of the reaction mechanism: reduction of the Co(III) species is followed by dissociation of the bound acetonitrile ligand, subsequent reduction of the unligated Co(II) species to form a Co(I) species is followed by protonation, which occurs at the Cp ring, followed by tautomerization to generate the stable Co(III)-hydride product [HCoCp(dxpe)]+.	NAD	232-237	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	207-213
33355213-9	2021	The formation velocity of atRA in the presence of NAD+ correlated significantly with the expression of ALDH1A1 and AOX protein.	NAD	50-54	aldehyde oxidase 1	Homo sapiens	115-118
33543238-2	2021	The major purpose of the present study was to test the hypothesis that NAD+ in white adipose tissue (WAT) is a regulator of whole-body metabolic flexibility in response to changes in insulin sensitivity and with respect to substrate availability and use during feeding and fasting conditions.	NAD	71-75	insulin	Homo sapiens	183-190
33543238-10	2021	These results demonstrate a novel function of WAT NAMPT-mediated NAD+ biosynthesis in regulating whole-body metabolic flexibility, and provide new insights into the role of adipose tissue NAD+ biology in metabolic health.	NAD	65-69	nicotinamide phosphoribosyltransferase	Mus musculus	50-55
33543238-10	2021	These results demonstrate a novel function of WAT NAMPT-mediated NAD+ biosynthesis in regulating whole-body metabolic flexibility, and provide new insights into the role of adipose tissue NAD+ biology in metabolic health.	NAD	188-192	nicotinamide phosphoribosyltransferase	Mus musculus	50-55
33486887-4	2021	KYNU is a pyridoxal phosphate (PLP) dependent enzyme involved in the biosynthesis of NAD cofactors from tryptophan that has been associated with the onset and development of BC.	NAD	85-88	kynureninase	Homo sapiens	0-4
33606677-5	2021	Further, additional results suggest that NAD+ conversion to a second messenger, cyclic ADP ribose (cADPR), via ADP ribosyl cyclase/cADPR hydrolase (CD38) is required for imeglimin"s effects in islets, thus representing a potential link between increased NAD+ and enhanced glucose-induced Ca2+ mobilization which-in turn-is known to drive insulin granule exocytosis.	NAD	41-45	insulin	Homo sapiens	338-345
33672651-6	2021	We treated cells with 17beta-estradiol (E2), 1,3,5-tris(4-hydroxyphenyl)-4-propyl-1H-pyrazole (PPT) an estrogen receptor (ER) alpha (ERalpha) agonist, or 2,3-bis(4-hydroxyphenyl)-propionitrile (DPN), an ERbeta agonist.	NAD	194-197	tachykinin precursor 1	Homo sapiens	95-98
33524253-5	2021	By serving as an excellent substrate for poly-ADP-ribose polymerase 1 (PARP1)-catalyzed PARylation, the generated bifunctional NAD+ enables photo-cross-linking and enrichment of PARylation-dependent interacting proteins for proteomic identification.	NAD	127-131	poly(ADP-ribose) polymerase 1	Homo sapiens	41-69
33524253-5	2021	By serving as an excellent substrate for poly-ADP-ribose polymerase 1 (PARP1)-catalyzed PARylation, the generated bifunctional NAD+ enables photo-cross-linking and enrichment of PARylation-dependent interacting proteins for proteomic identification.	NAD	127-131	poly(ADP-ribose) polymerase 1	Homo sapiens	71-76
33444675-3	2021	Sirtuins, especially SIRT3, a mitochondrial deacetylase, are NAD-dependent histone deacetylases involved in aging and longevity.	NAD	61-64	sirtuin 3	Homo sapiens	21-26
33649352-8	2021	Nonetheless, PARylation by PARP2 led to Polbeta inhibition and to significant stimulation of LigIIIalpha activities in a NAD+-dependent manner.	NAD	121-125	poly(ADP-ribose) polymerase 2	Homo sapiens	27-32
33672651-6	2021	We treated cells with 17beta-estradiol (E2), 1,3,5-tris(4-hydroxyphenyl)-4-propyl-1H-pyrazole (PPT) an estrogen receptor (ER) alpha (ERalpha) agonist, or 2,3-bis(4-hydroxyphenyl)-propionitrile (DPN), an ERbeta agonist.	NAD	194-197	estrogen receptor 1	Homo sapiens	103-131
33562281-5	2021	Moreover, exogenous NAD+ reduced senescence-associated-beta-galactosidase activity, and downregulated poly (ADP-ribose) polymerase 1 expression.	NAD	20-24	poly(ADP-ribose) polymerase 1	Homo sapiens	102-132
33606971-2	2021	(2020) demonstrate that pyruvate dehydrogenase (PDH) overactivation blunts NAD+ regeneration by overcharging the mitochondrial membrane potential and driving ATP synthesis beyond demand.	NAD	75-79	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	24-46
33606971-2	2021	(2020) demonstrate that pyruvate dehydrogenase (PDH) overactivation blunts NAD+ regeneration by overcharging the mitochondrial membrane potential and driving ATP synthesis beyond demand.	NAD	75-79	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	48-51
33387580-3	2021	NAD+ depletion resulted PARP related cell death only happened when the trial used extreme high oxidization treatment.	NAD	0-4	poly(ADP-ribose) polymerase 1	Homo sapiens	24-28
32971159-17	2021	Moreover, compared with PPT (ERalpha agonist) and DPN (ERbeta agonist), G1 could significantly increase the expression of A20.	NAD	50-53	estrogen receptor 1	Homo sapiens	55-61
33385367-4	2021	Since positively charged groove including substrate- and NAD+-binding sites is proposed as potential binding site for alpha-synuclein and RNA, GAPDH was glycated on residues in grooves and randomly distributed over the whole surface.	NAD	57-61	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	143-148
33360352-2	2021	NQO1 catalyzes the oxidation of NADH to NAD+ and may supplement levels of NAD+ near microtubules to aid SIRT2 deacetylase activity.	NAD	40-44	NAD(P)H quinone dehydrogenase 1	Homo sapiens	0-4
33524397-2	2021	We have previously shown that NAD(H) promotes the assembly of similar tetramers from either human CtBP1 and CtBP2 and that CtBP2 tetramer destabilizing mutants are defective for oncogenic activity.	NAD	30-36	C-terminal binding protein 2	Homo sapiens	108-113
33563078-1	2021	Nicotinamide phosphoribosyltransferase (NAMPT) is the rate-limiting enzyme in the NAD+ salvage pathway.	NAD	82-86	nicotinamide phosphoribosyltransferase	Mus musculus	0-38
33563078-1	2021	Nicotinamide phosphoribosyltransferase (NAMPT) is the rate-limiting enzyme in the NAD+ salvage pathway.	NAD	82-86	nicotinamide phosphoribosyltransferase	Mus musculus	40-45
33563078-4	2021	Here using steady-state metabolomics, we demonstrate that deletion of NAMPT causes a significant decrease of NAD+ metabolome and bioenergetics, a buildup of metabolic intermediates upstream of glyceraldehyde 3-phosphate dehydrogenase (GAPDH) in glycolysis, and an increase of oxidative stress.	NAD	109-113	nicotinamide phosphoribosyltransferase	Mus musculus	70-75
33563078-5	2021	RNA-seq shows that NAMPT deletion leads to the increase of mRNA levels of enzymes in NAD metabolism, in particular PARP family of NAD+ consumption enzymes, as well as glycolytic genes Glut1, Hk2 and PFBFK3 before GAPDH.	NAD	85-88	nicotinamide phosphoribosyltransferase	Mus musculus	19-24
33563078-5	2021	RNA-seq shows that NAMPT deletion leads to the increase of mRNA levels of enzymes in NAD metabolism, in particular PARP family of NAD+ consumption enzymes, as well as glycolytic genes Glut1, Hk2 and PFBFK3 before GAPDH.	NAD	130-134	nicotinamide phosphoribosyltransferase	Mus musculus	19-24
33541361-3	2021	The NAD-dependent deacetylase protein Sirtuin 3 (SIRT3) is located in the mitochondria and regulates mitochondrial function.	NAD	4-7	sirtuin 3	Homo sapiens	49-54
33038343-4	2021	In this review, we summarize the contribution of NAD+ metabolism to inflammation, with special emphasis in the major NAD+ biosynthetic enzyme, nicotinamide phosphoribosyl transferase (NAMPT), and the NAD+-consuming enzyme, poly(ADP-ribose) polymerase (PARP).	NAD	49-53	poly(ADP-ribose) polymerase 1	Homo sapiens	223-250
33038343-4	2021	In this review, we summarize the contribution of NAD+ metabolism to inflammation, with special emphasis in the major NAD+ biosynthetic enzyme, nicotinamide phosphoribosyl transferase (NAMPT), and the NAD+-consuming enzyme, poly(ADP-ribose) polymerase (PARP).	NAD	49-53	poly(ADP-ribose) polymerase 1	Homo sapiens	252-256
33360352-2	2021	NQO1 catalyzes the oxidation of NADH to NAD+ and may supplement levels of NAD+ near microtubules to aid SIRT2 deacetylase activity.	NAD	74-78	NAD(P)H quinone dehydrogenase 1	Homo sapiens	0-4
33482921-1	2021	BACKGROUND: Sirtuin 6 (SIRT6) is a NAD+-dependent deacetylase with key roles in cell metabolism.	NAD	35-38	sirtuin 6	Mus musculus	12-21
33503437-5	2021	Disruption of one of these Fos/AP-1 targets, NAD(+)-consuming mono-ADP-ribosyl-transferase 1 (Art1), in SCs delays cell cycle entry and impedes progenitor cell expansion and muscle regeneration.	NAD	45-51	ADP-ribosyltransferase 1	Homo sapiens	62-92
33503437-5	2021	Disruption of one of these Fos/AP-1 targets, NAD(+)-consuming mono-ADP-ribosyl-transferase 1 (Art1), in SCs delays cell cycle entry and impedes progenitor cell expansion and muscle regeneration.	NAD	45-51	ADP-ribosyltransferase 1	Homo sapiens	94-98
33503805-5	2021	Our results showed that the activation of ERalpha (using ERalpha-selective agonist PPT) and ERbeta (using ERbeta-selective agonist DPN) increased phosphorylation of SRC in PC-3 cells.	NAD	131-134	estrogen receptor 1	Homo sapiens	92-98
33503805-5	2021	Our results showed that the activation of ERalpha (using ERalpha-selective agonist PPT) and ERbeta (using ERbeta-selective agonist DPN) increased phosphorylation of SRC in PC-3 cells.	NAD	131-134	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	165-168
33503805-6	2021	In the presence of the selective inhibitor for SRC-family kinases PP2, the effects of DPN and PPT on transmigration and soft agar colony formation assays were decreased.	NAD	86-89	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	47-50
33482921-1	2021	BACKGROUND: Sirtuin 6 (SIRT6) is a NAD+-dependent deacetylase with key roles in cell metabolism.	NAD	35-38	sirtuin 6	Mus musculus	23-28
33481867-4	2021	A previously published two-step PARP activity assay uses biotinylated NAD+ and streptavidin labelling for this purpose.	NAD	70-74	poly(ADP-ribose) polymerase 1	Homo sapiens	32-36
33475085-4	2021	To identify the MARylated substrates of PARP-7 in ovarian cancer cells, we developed an NAD+ analog-sensitive approach, which we coupled with mass spectrometry to identify the PARP-7 ADP-ribosylated proteome in ovarian cancer cells, including cell-cell adhesion and cytoskeletal proteins.	NAD	88-92	TCDD inducible poly(ADP-ribose) polymerase	Homo sapiens	40-46
33475085-4	2021	To identify the MARylated substrates of PARP-7 in ovarian cancer cells, we developed an NAD+ analog-sensitive approach, which we coupled with mass spectrometry to identify the PARP-7 ADP-ribosylated proteome in ovarian cancer cells, including cell-cell adhesion and cytoskeletal proteins.	NAD	88-92	TCDD inducible poly(ADP-ribose) polymerase	Homo sapiens	176-182
33450210-0	2021	Mitochondrial NAD+ Controls Nuclear ARTD1-Induced ADP-Ribosylation.	NAD	14-18	poly(ADP-ribose) polymerase 1	Homo sapiens	36-41
33479917-4	2021	Importantly, CD38 stimulation with NAD accelerated ATP production along with increasing glutathione reductase (GR) and dipicolinic acid (DPA) in intracellular mitochondria.	NAD	35-38	CD38 molecule	Rattus norvegicus	13-17
33481867-5	2021	Here, we used the fluorescent NAD+ analogues epsilon-NAD+ and 6-Fluo-10-NAD+ to assess PARP activity directly on unfixed tissue sections obtained from wild-type and retinal degeneration-1 (rd1) mutant retina.	NAD	30-34	poly(ADP-ribose) polymerase 1	Homo sapiens	87-91
33482196-6	2021	To dissect the direct effect of PARP1 on mtDNA from the secondary perturbation of metabolism, we report here biochemical studies that recapitulated Pol gamma PARylation observed in cells and showed that PARP1 regulates Pol gamma activity during DNA repair in a metabolic cofactor NAD+ (nicotinamide adenosine dinucleotide)-dependent manner.	NAD	280-284	poly(ADP-ribose) polymerase 1	Homo sapiens	203-208
33478031-1	2021	Aldehyde dehydrogenase 1A3 (ALDH1A3) belongs to an enzymatic superfamily composed by 19 different isoforms, with a scavenger role, involved in the oxidation of a plethora of aldehydes to the respective carboxylic acids, through a NAD+-dependent reaction.	NAD	230-233	aldehyde dehydrogenase family 1, subfamily A3	Mus musculus	0-26
33478031-1	2021	Aldehyde dehydrogenase 1A3 (ALDH1A3) belongs to an enzymatic superfamily composed by 19 different isoforms, with a scavenger role, involved in the oxidation of a plethora of aldehydes to the respective carboxylic acids, through a NAD+-dependent reaction.	NAD	230-233	aldehyde dehydrogenase family 1, subfamily A3	Mus musculus	28-35
33440786-4	2021	In this review, we provide an overview of the current knowledge of NAD+ metabolism, highlighting the functional liaison with mono(ADP-ribosyl)ating enzymes, such as the well-known ARTD10 (also named PARP10), SIRT6, and SIRT7.	NAD	67-71	poly(ADP-ribose) polymerase family member 10	Homo sapiens	180-186
33441761-6	2021	Further studies on cytochrome b5 (CYB5), an alternative NADH-dependent electron donor indicated particularly strong support of CYP2C8-dependent amodiaquine N-deethylation by CYB5 and this was confirmed by genetic CYB5 single- and POR/CYB5 double-knockout.	NAD	56-60	cytochrome p450 oxidoreductase	Homo sapiens	230-233
33441761-8	2021	In summary our results show that POR/NADPH- and CYB5/NADH-electron transport systems influence human drug metabolizing CYPs differentially and differently than mouse Cyps.	NAD	53-57	cytochrome p450 oxidoreductase	Homo sapiens	33-36
33440786-4	2021	In this review, we provide an overview of the current knowledge of NAD+ metabolism, highlighting the functional liaison with mono(ADP-ribosyl)ating enzymes, such as the well-known ARTD10 (also named PARP10), SIRT6, and SIRT7.	NAD	67-71	poly(ADP-ribose) polymerase family member 10	Homo sapiens	199-205
32936424-7	2021	A total of 33 upregulated and 52 downregulated genes associated with HCC progression and ferroptosis were obtained, and these genes were significantly involved in the negative regulation of ERK1 and ERK2 cascades; the NAD biosynthetic process; alanine, aspartate, and glutamate metabolism; and other pathways.	NAD	218-221	mitogen-activated protein kinase 3	Homo sapiens	190-194
33406399-2	2021	Here we describe MP31, a micropeptide encoded by the upstream open reading frame (uORF) of phosphatase and tensin homolog (PTEN) acting as a "circuit breaker" that limits lactate-pyruvate conversion in mitochondria by competing with mitochondrial lactate dehydrogenase (mLDH) for nicotinamide adenine dinucleotide (NAD+).	NAD	280-313	phosphatase and tensin homolog	Mus musculus	91-121
33406399-2	2021	Here we describe MP31, a micropeptide encoded by the upstream open reading frame (uORF) of phosphatase and tensin homolog (PTEN) acting as a "circuit breaker" that limits lactate-pyruvate conversion in mitochondria by competing with mitochondrial lactate dehydrogenase (mLDH) for nicotinamide adenine dinucleotide (NAD+).	NAD	280-313	phosphatase and tensin homolog	Mus musculus	123-127
33406399-2	2021	Here we describe MP31, a micropeptide encoded by the upstream open reading frame (uORF) of phosphatase and tensin homolog (PTEN) acting as a "circuit breaker" that limits lactate-pyruvate conversion in mitochondria by competing with mitochondrial lactate dehydrogenase (mLDH) for nicotinamide adenine dinucleotide (NAD+).	NAD	315-319	phosphatase and tensin homolog	Mus musculus	91-121
33406399-2	2021	Here we describe MP31, a micropeptide encoded by the upstream open reading frame (uORF) of phosphatase and tensin homolog (PTEN) acting as a "circuit breaker" that limits lactate-pyruvate conversion in mitochondria by competing with mitochondrial lactate dehydrogenase (mLDH) for nicotinamide adenine dinucleotide (NAD+).	NAD	315-319	phosphatase and tensin homolog	Mus musculus	123-127
33645520-7	2021	In particular, the registered changes reflect a violation of the paracrine intercellular interactions of two subpopulations of cells, one of which acts as a source of NAD+, and the second as a consumer of NAD+ to ensure the processes of intracellular signal transduction; a change in the mechanisms of lactate transport due to aberrant expression of the lactate transporter MCT1 in cells forming a pool of cells developing along the neuronal path of differentiation.	NAD	167-171	solute carrier family 16 member 1	Homo sapiens	374-378
33645520-7	2021	In particular, the registered changes reflect a violation of the paracrine intercellular interactions of two subpopulations of cells, one of which acts as a source of NAD+, and the second as a consumer of NAD+ to ensure the processes of intracellular signal transduction; a change in the mechanisms of lactate transport due to aberrant expression of the lactate transporter MCT1 in cells forming a pool of cells developing along the neuronal path of differentiation.	NAD	205-209	solute carrier family 16 member 1	Homo sapiens	374-378
33049665-5	2021	Nicotinamide phosphoribosyltransferase (NAmPRTase or Nampt) catalyzes the condensation of nicotinamide with 5-phosphoribosyl-1-pyrophosphate to yield nicotinamide mononucleotide (NMN), a requisite step for production of NAD+, which is known to increase longevity.	NAD	220-224	nicotinamide phosphoribosyltransferase	Mus musculus	40-49
33049665-5	2021	Nicotinamide phosphoribosyltransferase (NAmPRTase or Nampt) catalyzes the condensation of nicotinamide with 5-phosphoribosyl-1-pyrophosphate to yield nicotinamide mononucleotide (NMN), a requisite step for production of NAD+, which is known to increase longevity.	NAD	220-224	nicotinamide phosphoribosyltransferase	Mus musculus	53-58
32936424-7	2021	A total of 33 upregulated and 52 downregulated genes associated with HCC progression and ferroptosis were obtained, and these genes were significantly involved in the negative regulation of ERK1 and ERK2 cascades; the NAD biosynthetic process; alanine, aspartate, and glutamate metabolism; and other pathways.	NAD	218-221	mitogen-activated protein kinase 1	Homo sapiens	199-203
32936424-12	2021	These genes played roles in HCC progression and ferroptosis via the negative regulation of the ERK1 and ERK2 cascades; the NAD biosynthetic process; and alanine, aspartate, and glutamate metabolism.	NAD	123-126	mitogen-activated protein kinase 3	Homo sapiens	95-99
32936424-12	2021	These genes played roles in HCC progression and ferroptosis via the negative regulation of the ERK1 and ERK2 cascades; the NAD biosynthetic process; and alanine, aspartate, and glutamate metabolism.	NAD	123-126	mitogen-activated protein kinase 1	Homo sapiens	104-108
34013691-1	2021	OBJECTIVE: Evaluation of the relationship between the activity of proteolytic enzymes (cathepsin D and calpains) and the dynamics of the fluorescence intensity of the coenzymes nicotinamide adenine dinucleotide (NADH) and flavin adenine dinucleotide (FAD) in the rats" skeletal muscles in relation to the time of death.	NAD	177-210	cathepsin D	Rattus norvegicus	87-98
33290962-9	2021	Treatment with NAD + also inhibited the expressions of NLRP3 and modulated the differentiation of Th1 and Th17 cells, reduced the expressions of the pro-inflammatory factors IL-1beta, IL-2, IL-18, IFN-gamma and IL-17, and increased the expression of anti-inflammatory IL-10.	NAD	15-20	interferon gamma	Mus musculus	197-206
33290962-9	2021	Treatment with NAD + also inhibited the expressions of NLRP3 and modulated the differentiation of Th1 and Th17 cells, reduced the expressions of the pro-inflammatory factors IL-1beta, IL-2, IL-18, IFN-gamma and IL-17, and increased the expression of anti-inflammatory IL-10.	NAD	15-20	interleukin 10	Mus musculus	268-273
33053398-12	2021	Furthermore, in DM mice, NAD+ and its precursors nicotinamide mononucleotide and nicotinamide riboside also facilitated corneal epithelial and nerve regeneration, accompanied with the recovered expression of SIRT1 and phosphorylated EGFR, AKT, and ERK1/2 in epithelium and corneal sensitivity.	NAD	25-29	thymoma viral proto-oncogene 1	Mus musculus	239-242
34013691-1	2021	OBJECTIVE: Evaluation of the relationship between the activity of proteolytic enzymes (cathepsin D and calpains) and the dynamics of the fluorescence intensity of the coenzymes nicotinamide adenine dinucleotide (NADH) and flavin adenine dinucleotide (FAD) in the rats" skeletal muscles in relation to the time of death.	NAD	212-216	cathepsin D	Rattus norvegicus	87-98
33442387-1	2020	Sirtuins, NAD + dependent proteins belonging to class III histone deacetylases, are involved in regulating numerous cellular processes including cellular stress, insulin resistance, inflammation, mitochondrial biogenesis, chromatin silencing, cell cycle regulation, transcription, and apoptosis.	NAD	10-13	insulin	Homo sapiens	162-169
33488923-3	2020	Nicotinamide phosphoribosyltransferase (NAMPT) is a rate-limiting enzyme in nicotinamide adenine dinucleotide (NAD) biosynthesis that influences the activity of NAD-dependent enzymes, such as sirtuins, which possess NAD-dependent protein deacetylase activity and cleave NAD during the deacetylation cycle.	NAD	76-109	nicotinamide phosphoribosyltransferase	Mus musculus	0-38
33488923-3	2020	Nicotinamide phosphoribosyltransferase (NAMPT) is a rate-limiting enzyme in nicotinamide adenine dinucleotide (NAD) biosynthesis that influences the activity of NAD-dependent enzymes, such as sirtuins, which possess NAD-dependent protein deacetylase activity and cleave NAD during the deacetylation cycle.	NAD	76-109	nicotinamide phosphoribosyltransferase	Mus musculus	40-45
33488923-3	2020	Nicotinamide phosphoribosyltransferase (NAMPT) is a rate-limiting enzyme in nicotinamide adenine dinucleotide (NAD) biosynthesis that influences the activity of NAD-dependent enzymes, such as sirtuins, which possess NAD-dependent protein deacetylase activity and cleave NAD during the deacetylation cycle.	NAD	111-114	nicotinamide phosphoribosyltransferase	Mus musculus	0-38
33488923-3	2020	Nicotinamide phosphoribosyltransferase (NAMPT) is a rate-limiting enzyme in nicotinamide adenine dinucleotide (NAD) biosynthesis that influences the activity of NAD-dependent enzymes, such as sirtuins, which possess NAD-dependent protein deacetylase activity and cleave NAD during the deacetylation cycle.	NAD	111-114	nicotinamide phosphoribosyltransferase	Mus musculus	40-45
33488923-3	2020	Nicotinamide phosphoribosyltransferase (NAMPT) is a rate-limiting enzyme in nicotinamide adenine dinucleotide (NAD) biosynthesis that influences the activity of NAD-dependent enzymes, such as sirtuins, which possess NAD-dependent protein deacetylase activity and cleave NAD during the deacetylation cycle.	NAD	161-164	nicotinamide phosphoribosyltransferase	Mus musculus	0-38
33488923-3	2020	Nicotinamide phosphoribosyltransferase (NAMPT) is a rate-limiting enzyme in nicotinamide adenine dinucleotide (NAD) biosynthesis that influences the activity of NAD-dependent enzymes, such as sirtuins, which possess NAD-dependent protein deacetylase activity and cleave NAD during the deacetylation cycle.	NAD	161-164	nicotinamide phosphoribosyltransferase	Mus musculus	40-45
33488923-3	2020	Nicotinamide phosphoribosyltransferase (NAMPT) is a rate-limiting enzyme in nicotinamide adenine dinucleotide (NAD) biosynthesis that influences the activity of NAD-dependent enzymes, such as sirtuins, which possess NAD-dependent protein deacetylase activity and cleave NAD during the deacetylation cycle.	NAD	161-164	nicotinamide phosphoribosyltransferase	Mus musculus	0-38
33488923-3	2020	Nicotinamide phosphoribosyltransferase (NAMPT) is a rate-limiting enzyme in nicotinamide adenine dinucleotide (NAD) biosynthesis that influences the activity of NAD-dependent enzymes, such as sirtuins, which possess NAD-dependent protein deacetylase activity and cleave NAD during the deacetylation cycle.	NAD	161-164	nicotinamide phosphoribosyltransferase	Mus musculus	40-45
33488923-3	2020	Nicotinamide phosphoribosyltransferase (NAMPT) is a rate-limiting enzyme in nicotinamide adenine dinucleotide (NAD) biosynthesis that influences the activity of NAD-dependent enzymes, such as sirtuins, which possess NAD-dependent protein deacetylase activity and cleave NAD during the deacetylation cycle.	NAD	161-164	nicotinamide phosphoribosyltransferase	Mus musculus	0-38
33488923-3	2020	Nicotinamide phosphoribosyltransferase (NAMPT) is a rate-limiting enzyme in nicotinamide adenine dinucleotide (NAD) biosynthesis that influences the activity of NAD-dependent enzymes, such as sirtuins, which possess NAD-dependent protein deacetylase activity and cleave NAD during the deacetylation cycle.	NAD	161-164	nicotinamide phosphoribosyltransferase	Mus musculus	40-45
33051211-0	2020	Coronavirus infection and PARP expression dysregulate the NAD metabolome: An actionable component of innate immunity.	NAD	58-61	poly(ADP-ribose) polymerase 1	Homo sapiens	26-30
33051211-1	2020	Poly(ADP-ribose) polymerase (PARP) superfamily members covalently link either a single ADP-ribose (ADPR) or a chain of ADPR units to proteins using NAD as the source of ADPR.	NAD	148-151	poly(ADP-ribose) polymerase 1	Homo sapiens	29-33
33051211-7	2020	These data suggest that the antiviral activities of noncanonical PARP isozyme activities are limited by the availability of NAD and that nutritional and pharmacological interventions to enhance NAD levels may boost innate immunity to coronaviruses.	NAD	124-127	poly(ADP-ribose) polymerase 1	Homo sapiens	65-69
33051211-7	2020	These data suggest that the antiviral activities of noncanonical PARP isozyme activities are limited by the availability of NAD and that nutritional and pharmacological interventions to enhance NAD levels may boost innate immunity to coronaviruses.	NAD	194-197	poly(ADP-ribose) polymerase 1	Homo sapiens	65-69
33392072-5	2020	Furthermore, knockout of the DGUOK considerably reduced expression of the NMNAT2, a key molecule controlling NAD+ synthesis, at both mRNA and protein levels.	NAD	109-113	nicotinamide nucleotide adenylyltransferase 2	Homo sapiens	74-80
33392072-6	2020	Ectopic expression of the NMNAT2 abrogated the effect of knockdown of DGUOK on NAD+.	NAD	79-83	nicotinamide nucleotide adenylyltransferase 2	Homo sapiens	26-32
33392072-9	2020	Our study suggested that DGUOK regulates NAD+ in a NMNAT2 dependent manner and DGUOK-NMNAT2-NAD+ axis could be a potential therapeutic target in lung adenocarcinoma.	NAD	41-45	nicotinamide nucleotide adenylyltransferase 2	Homo sapiens	51-57
33392072-9	2020	Our study suggested that DGUOK regulates NAD+ in a NMNAT2 dependent manner and DGUOK-NMNAT2-NAD+ axis could be a potential therapeutic target in lung adenocarcinoma.	NAD	92-96	nicotinamide nucleotide adenylyltransferase 2	Homo sapiens	85-91
33414897-3	2020	NAD+ is reduced with age at a cellular, tissue, and organismal level due to inflammation, defect in NAMPT-mediated NAD+ biosynthesis, and the PARP-mediated NAD+ depletion.	NAD	0-4	poly(ADP-ribose) polymerase 1	Homo sapiens	142-146
33326785-4	2020	Reduced NADH is not available for NAD+-dependent enzymatic reactions involving glyceraldehyde 3-phosphate dehydrogenase (GAPDH) and 3-phosphoglycerate dehydrogenase (PGDH).	NAD	8-12	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	121-126
33146386-1	2020	Poly(ADP-ribose) Polymerase 1 (PARP-1) is a nuclear enzyme that catalyse the transfer of ADP-ribose units from NAD+ to several target proteins involved in cellular stress responses.	NAD	111-115	poly(ADP-ribose) polymerase 1	Homo sapiens	0-29
33146386-1	2020	Poly(ADP-ribose) Polymerase 1 (PARP-1) is a nuclear enzyme that catalyse the transfer of ADP-ribose units from NAD+ to several target proteins involved in cellular stress responses.	NAD	111-115	poly(ADP-ribose) polymerase 1	Homo sapiens	31-37
33146386-2	2020	Using WRL68 (HeLa derivate) cells, we previously showed that PARP-1 activation induced by oxidative stress after H2O2 treatment lead to depletion of cellular NAD+ and ATP, which promoted cell death.	NAD	158-162	poly(ADP-ribose) polymerase 1	Homo sapiens	61-67
33146386-6	2020	Supplementation of NAD+ also reduced YAP1 phosphorylation, suggesting that the loss of cellular NAD+ caused by PARP-1 activation after oxidative treatment is responsible for the phosphorylation of YAP1.	NAD	19-23	poly(ADP-ribose) polymerase 1	Homo sapiens	111-117
33146386-6	2020	Supplementation of NAD+ also reduced YAP1 phosphorylation, suggesting that the loss of cellular NAD+ caused by PARP-1 activation after oxidative treatment is responsible for the phosphorylation of YAP1.	NAD	96-100	poly(ADP-ribose) polymerase 1	Homo sapiens	111-117
33146386-8	2020	Since, NAD+ supplementation reduced the phosphorylation of some AMPK substrates, we hypothesized that the loss of cellular NAD+ after PARP-1 activation may induce an energy stress that activates AMPK.	NAD	7-11	poly(ADP-ribose) polymerase 1	Homo sapiens	134-140
33146386-8	2020	Since, NAD+ supplementation reduced the phosphorylation of some AMPK substrates, we hypothesized that the loss of cellular NAD+ after PARP-1 activation may induce an energy stress that activates AMPK.	NAD	123-127	poly(ADP-ribose) polymerase 1	Homo sapiens	134-140
33146386-9	2020	In summary, we showed a new crucial role of PARP-1 in the response to oxidative stress in which PARP-1 activation reduced cell viability by promoting the phosphorylation and degradation of YAP1 through a mechanism that involves the depletion of NAD+.	NAD	245-249	poly(ADP-ribose) polymerase 1	Homo sapiens	44-50
33146386-9	2020	In summary, we showed a new crucial role of PARP-1 in the response to oxidative stress in which PARP-1 activation reduced cell viability by promoting the phosphorylation and degradation of YAP1 through a mechanism that involves the depletion of NAD+.	NAD	245-249	poly(ADP-ribose) polymerase 1	Homo sapiens	96-102
33225340-5	2020	PEI/ZIF-FMN also mediated the electron transfer from NADH to cytochrome c (Cyt c), thereby exhibiting Cyt c reductase-like activity.	NAD	53-57	cytochrome c, somatic	Homo sapiens	61-73
33225340-5	2020	PEI/ZIF-FMN also mediated the electron transfer from NADH to cytochrome c (Cyt c), thereby exhibiting Cyt c reductase-like activity.	NAD	53-57	cytochrome c, somatic	Homo sapiens	75-80
33225340-5	2020	PEI/ZIF-FMN also mediated the electron transfer from NADH to cytochrome c (Cyt c), thereby exhibiting Cyt c reductase-like activity.	NAD	53-57	cytochrome c, somatic	Homo sapiens	102-107
33297334-6	2020	Moreover, the NADH-stabilized 26S PC is efficient in degrading intrinsically disordered protein (IDP) substrates that might not require ATP-dependent unfolding, such as p27, Tau, c-Fos and more.	NAD	14-18	dynactin subunit 6	Homo sapiens	169-172
33244652-7	2021	Interestingly, although both isomers of RSV bind to TyrRS, only the cis-isomer evokes a unique structural change at the active site to promote its interaction with poly-ADP-ribose polymerase 1 (PARP1), a major determinant of cellular NAD+-dependent stress response.	NAD	234-238	poly(ADP-ribose) polymerase 1	Homo sapiens	194-199
33166073-0	2020	Cockayne syndrome proteins CSA and CSB maintain mitochondrial homeostasis through NAD+ signaling.	NAD	82-86	ERCC excision repair 6, chromatin remodeling factor	Homo sapiens	35-38
33166073-9	2020	In primary cells depleted for CSA or CSB, this dysfunction can be corrected with supplementation of NAD+ precursors.	NAD	100-104	ERCC excision repair 6, chromatin remodeling factor	Homo sapiens	37-40
33263331-1	2020	The peroxisomal multifunctional enzyme type 1 (MFE1) catalyzes two successive reactions in the beta-oxidation cycle: the 2E-enoyl-CoA hydratase (ECH) and NAD+-dependent 3S-hydroxyacyl-CoA dehydrogenase (HAD) reactions.	NAD	154-157	enoyl-CoA hydratase and 3-hydroxyacyl CoA dehydrogenase	Rattus norvegicus	47-51
33011272-7	2020	PMA-induced depletion of NAD+ in neutrophils was blocked by PKC inhibitors, but was not dependent on NOX-2, as it was not blocked by the NOX inhibitor, diphenyleneiodonium.	NAD	25-29	proline rich transmembrane protein 2	Homo sapiens	60-63
33304350-2	2020	It is commonly accepted that CD157 catalyzes NAD+ hydrolysis and acts as a component of integrin adhesion receptor complex.	NAD	45-49	bone marrow stromal cell antigen 1	Homo sapiens	29-34
33330464-0	2020	NAD+ Metabolism Regulates Preadipocyte Differentiation by Enhancing alpha-Ketoglutarate-Mediated Histone H3K9 Demethylation at the PPARgamma Promoter.	NAD	0-4	peroxisome proliferator activated receptor gamma	Homo sapiens	131-140
32998997-2	2020	Diverse genetic subtypes of malignant glioma are sensitive to selective inhibition of the NAD+ salvage pathway enzyme nicotinamide phosphoribosyltransferase (NAMPT).	NAD	90-94	nicotinamide phosphoribosyltransferase	Mus musculus	118-156
32998997-2	2020	Diverse genetic subtypes of malignant glioma are sensitive to selective inhibition of the NAD+ salvage pathway enzyme nicotinamide phosphoribosyltransferase (NAMPT).	NAD	90-94	nicotinamide phosphoribosyltransferase	Mus musculus	158-163
32998997-6	2020	NAD+ depletion and autophagy induced by NAMPT inhibitors mediated the upregulation of PD-L1 transcripts and cell surface protein levels in GBM cells.	NAD	0-4	nicotinamide phosphoribosyltransferase	Mus musculus	40-45
32998997-6	2020	NAD+ depletion and autophagy induced by NAMPT inhibitors mediated the upregulation of PD-L1 transcripts and cell surface protein levels in GBM cells.	NAD	0-4	CD274 antigen	Mus musculus	86-91
33141820-2	2020	Upon binding to DNA double-strand breaks, PARP2 uses nicotinamide adenine dinucleotide to synthesize poly(ADP-ribose) (PAR) onto itself and other proteins, including histones.	NAD	53-86	poly(ADP-ribose) polymerase 2	Homo sapiens	42-47
32839274-0	2020	Differential processing and localization of human Nocturnin controls metabolism of mRNA and nicotinamide adenine dinucleotide cofactors.	NAD	92-125	nocturnin	Homo sapiens	50-59
33144600-8	2020	We also showed that lethal UVB irradiation induces a PARP-dependent drastic loss of cellular metabolic activity caused by an overused of NAD+.	NAD	137-141	poly(ADP-ribose) polymerase 1	Homo sapiens	53-57
32920515-11	2020	Moreover, CRO caused an activation in nuclear factor erythroid-2 related factor 2, leading to enhanced Kelch-like ECH-associated protein 1, heme oxygenase-1 and nicotinamide adenine dinucleotide quinone dehydrogenase 1 expressions involved in Nrf2 signaling during ATO-induced cardiotoxicity.	NAD	161-194	NFE2 like bZIP transcription factor 2	Rattus norvegicus	38-81
32920515-11	2020	Moreover, CRO caused an activation in nuclear factor erythroid-2 related factor 2, leading to enhanced Kelch-like ECH-associated protein 1, heme oxygenase-1 and nicotinamide adenine dinucleotide quinone dehydrogenase 1 expressions involved in Nrf2 signaling during ATO-induced cardiotoxicity.	NAD	161-194	NFE2 like bZIP transcription factor 2	Rattus norvegicus	243-247
32916028-2	2020	The MAS was initially proposed as a route for the oxidation of cytosolic NADH by the mitochondria in Ehrlich ascites cell tumor lacking other routes, and to explain the need for a mitochondrial aspartate aminotransferase (glutamate oxaloacetate transaminase 2 [GOT2]).	NAD	73-77	glutamatic-oxaloacetic transaminase 2, mitochondrial	Mus musculus	180-220
32916028-2	2020	The MAS was initially proposed as a route for the oxidation of cytosolic NADH by the mitochondria in Ehrlich ascites cell tumor lacking other routes, and to explain the need for a mitochondrial aspartate aminotransferase (glutamate oxaloacetate transaminase 2 [GOT2]).	NAD	73-77	glutamatic-oxaloacetic transaminase 2, mitochondrial	Mus musculus	261-265
32606138-0	2020	Poly(ADP-ribose) glycohydrolase inhibition sequesters NAD+ to potentiate the metabolic lethality of alkylating chemotherapy in IDH mutant tumor cells.	NAD	54-58	poly(ADP-ribose) glycohydrolase	Homo sapiens	0-31
32606138-5	2020	Both in vitro and in vivo, we observe that concurrent alkylator and PARG inhibition depletes freely available NAD+ by preventing PAR breakdown, resulting in NAD+ sequestration and collapse of metabolic homeostasis.	NAD	110-114	poly(ADP-ribose) glycohydrolase	Homo sapiens	68-72
32606138-5	2020	Both in vitro and in vivo, we observe that concurrent alkylator and PARG inhibition depletes freely available NAD+ by preventing PAR breakdown, resulting in NAD+ sequestration and collapse of metabolic homeostasis.	NAD	157-161	poly(ADP-ribose) glycohydrolase	Homo sapiens	68-72
32385936-7	2020	Deconvolution of the combined NAD(H) and UDP(G) signals showed that the measured NAD+ /NAD ratio was heavily influenced by UDP(G) modeling (7.5 +- 1.8 when the UDP(G) signal was fitted as multiple doublets versus 5.3 +- 0.6 when a simplified pseudo doublet model was used).	NAD	30-36	UDP-glucose pyrophosphorylase 2	Homo sapiens	123-129
32385936-7	2020	Deconvolution of the combined NAD(H) and UDP(G) signals showed that the measured NAD+ /NAD ratio was heavily influenced by UDP(G) modeling (7.5 +- 1.8 when the UDP(G) signal was fitted as multiple doublets versus 5.3 +- 0.6 when a simplified pseudo doublet model was used).	NAD	30-36	UDP-glucose pyrophosphorylase 2	Homo sapiens	123-129
32385936-7	2020	Deconvolution of the combined NAD(H) and UDP(G) signals showed that the measured NAD+ /NAD ratio was heavily influenced by UDP(G) modeling (7.5 +- 1.8 when the UDP(G) signal was fitted as multiple doublets versus 5.3 +- 0.6 when a simplified pseudo doublet model was used).	NAD	81-85	UDP-glucose pyrophosphorylase 2	Homo sapiens	41-47
32385936-7	2020	Deconvolution of the combined NAD(H) and UDP(G) signals showed that the measured NAD+ /NAD ratio was heavily influenced by UDP(G) modeling (7.5 +- 1.8 when the UDP(G) signal was fitted as multiple doublets versus 5.3 +- 0.6 when a simplified pseudo doublet model was used).	NAD	81-85	UDP-glucose pyrophosphorylase 2	Homo sapiens	123-129
32385936-7	2020	Deconvolution of the combined NAD(H) and UDP(G) signals showed that the measured NAD+ /NAD ratio was heavily influenced by UDP(G) modeling (7.5 +- 1.8 when the UDP(G) signal was fitted as multiple doublets versus 5.3 +- 0.6 when a simplified pseudo doublet model was used).	NAD	81-85	UDP-glucose pyrophosphorylase 2	Homo sapiens	123-129
32385936-7	2020	Deconvolution of the combined NAD(H) and UDP(G) signals showed that the measured NAD+ /NAD ratio was heavily influenced by UDP(G) modeling (7.5 +- 1.8 when the UDP(G) signal was fitted as multiple doublets versus 5.3 +- 0.6 when a simplified pseudo doublet model was used).	NAD	30-33	UDP-glucose pyrophosphorylase 2	Homo sapiens	123-129
32385936-7	2020	Deconvolution of the combined NAD(H) and UDP(G) signals showed that the measured NAD+ /NAD ratio was heavily influenced by UDP(G) modeling (7.5 +- 1.8 when the UDP(G) signal was fitted as multiple doublets versus 5.3 +- 0.6 when a simplified pseudo doublet model was used).	NAD	30-33	UDP-glucose pyrophosphorylase 2	Homo sapiens	123-129
32839274-6	2020	Recent biochemical data indicate that NOCT dephosphorylates nicotinamide adenine dinucleotide (NAD) metabolites, and thus we measured the effect of NOCT on these cofactors in cells.	NAD	60-93	nocturnin	Homo sapiens	38-42
32839274-6	2020	Recent biochemical data indicate that NOCT dephosphorylates nicotinamide adenine dinucleotide (NAD) metabolites, and thus we measured the effect of NOCT on these cofactors in cells.	NAD	95-98	nocturnin	Homo sapiens	38-42
33204328-0	2020	ITGB2-mediated metabolic switch in CAFs promotes OSCC proliferation by oxidation of NADH in mitochondrial oxidative phosphorylation system.	NAD	84-88	integrin subunit beta 2	Homo sapiens	0-5
33063092-3	2020	The immunity modulators, the aryl hydrocarbon receptor (AhR) and the nuclear NAD+-consuming enzyme poly (ADP-ribose) polymerase 1 (PARP 1) may play a critical role in COVID-19 pathophysiology.	NAD	77-81	poly(ADP-ribose) polymerase 1	Homo sapiens	99-129
33063092-3	2020	The immunity modulators, the aryl hydrocarbon receptor (AhR) and the nuclear NAD+-consuming enzyme poly (ADP-ribose) polymerase 1 (PARP 1) may play a critical role in COVID-19 pathophysiology.	NAD	77-81	poly(ADP-ribose) polymerase 1	Homo sapiens	131-137
33063092-5	2020	PARP 1 activation leads to cell death mainly by depletion of NAD+ and adenosine triphosphate (ATP), especially when availability of these energy mediators is compromised.	NAD	61-65	poly(ADP-ribose) polymerase 1	Homo sapiens	0-6
33063092-9	2020	It conserves NAD+ and prevents ATP depletion by PARP 1 and Sirtuin 1 (silent mating type information regulation 2 homologue 1) inhibition, enhances NAD+ synthesis, and hence that of NADP+ which is a stronger PARP inhibitor, reverses lung injury caused by ischaemia/reperfusion, inhibits proinflammatory cytokines and is effective against HIV infection.	NAD	148-152	poly(ADP-ribose) polymerase 1	Homo sapiens	48-54
33063092-9	2020	It conserves NAD+ and prevents ATP depletion by PARP 1 and Sirtuin 1 (silent mating type information regulation 2 homologue 1) inhibition, enhances NAD+ synthesis, and hence that of NADP+ which is a stronger PARP inhibitor, reverses lung injury caused by ischaemia/reperfusion, inhibits proinflammatory cytokines and is effective against HIV infection.	NAD	148-152	poly(ADP-ribose) polymerase 1	Homo sapiens	48-52
33204328-12	2020	Accordingly, lactate derived from ITGB2-expressing CAFs was absorbed and metabolized in OSCC to generate NADH, which was then oxidized in the mitochondrial oxidative phosphorylation system (OXPHOS) to produce ATP.	NAD	105-109	integrin subunit beta 2	Homo sapiens	34-39
33204328-14	2020	Conclusions: Our study uncovered the ITGB2high pro-tumoral CAFs that activated the PI3K/AKT/mTOR axis to promote tumor proliferation in OSCC by NADH oxidation in the mitochondrial oxidative phosphorylation system.	NAD	144-148	integrin subunit beta 2	Homo sapiens	37-42
33204328-14	2020	Conclusions: Our study uncovered the ITGB2high pro-tumoral CAFs that activated the PI3K/AKT/mTOR axis to promote tumor proliferation in OSCC by NADH oxidation in the mitochondrial oxidative phosphorylation system.	NAD	144-148	AKT serine/threonine kinase 1	Homo sapiens	88-91
33204328-14	2020	Conclusions: Our study uncovered the ITGB2high pro-tumoral CAFs that activated the PI3K/AKT/mTOR axis to promote tumor proliferation in OSCC by NADH oxidation in the mitochondrial oxidative phosphorylation system.	NAD	144-148	mechanistic target of rapamycin kinase	Homo sapiens	92-96
33134468-10	2020	Conclusions: The apparent mismatch between HIF-1alpha expression and NADH fluorescence has become the basis for the design of an algorithm for monitoring malignant melanoma based on the sensing of NADH fluorescence and the determination of HIF-1alpha.	NAD	69-73	hypoxia inducible factor 1 subunit alpha	Homo sapiens	240-250
33134468-10	2020	Conclusions: The apparent mismatch between HIF-1alpha expression and NADH fluorescence has become the basis for the design of an algorithm for monitoring malignant melanoma based on the sensing of NADH fluorescence and the determination of HIF-1alpha.	NAD	197-201	hypoxia inducible factor 1 subunit alpha	Homo sapiens	43-53
32728715-3	2020	Three NADH-linked assays were tested that use alternative coupling enzymes: glyceraldehyde-3-phosphate dehydrogenase (GAPDH) and glycerolphosphate dehydrogenase (GlyPDH); phosphoenolpyruvate carboxylase (PEPC) and malate dehydrogenase (MDH); and pyruvate kinase (PK) and lactate dehydrogenase (LDH).	NAD	6-10	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	76-116
33092205-3	2020	Herein, we summarize the regulation of the most common calcium channels (TRPM2, TPCs, RyRs, and TRPML1) by NAD+ and its metabolites, with a particular focus on their roles in cancers.	NAD	107-111	mucolipin TRP cation channel 1	Homo sapiens	96-102
32890402-9	2020	Together, these findings uncovered the nature of persistent PARP1 foci and identified NAD+ interacting residues involved in the PARP1 exchange.	NAD	86-90	poly(ADP-ribose) polymerase 1	Homo sapiens	128-133
32787519-7	2020	CORM-A1 provoked an increase in concentrations of proximal (before GAPDH), but not distal glycolysis metabolites, suggesting that CO delayed glycolysis at the level of NAD+-dependent GAPDH; however, GAPDH activity was directly not inhibited.	NAD	168-172	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	183-188
32787519-7	2020	CORM-A1 provoked an increase in concentrations of proximal (before GAPDH), but not distal glycolysis metabolites, suggesting that CO delayed glycolysis at the level of NAD+-dependent GAPDH; however, GAPDH activity was directly not inhibited.	NAD	168-172	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	183-188
32553688-1	2020	BACKGROUND: Nuclear poly(ADP-ribose) polymerase-1 (PARP-1) is a well characterised protein that accounts for the majority of PARylation reactions using NAD+ as a substrate, regulating diverse cellular functions.	NAD	152-156	poly(ADP-ribose) polymerase 1	Homo sapiens	20-49
32553688-1	2020	BACKGROUND: Nuclear poly(ADP-ribose) polymerase-1 (PARP-1) is a well characterised protein that accounts for the majority of PARylation reactions using NAD+ as a substrate, regulating diverse cellular functions.	NAD	152-156	poly(ADP-ribose) polymerase 1	Homo sapiens	51-57
32390174-6	2020	Deliberate activation of P2RX7 in vivo by exogenous NAD resulted in a nearly complete iNKT cell ablation in liver and spleen in a P2RX7-dependent manner.	NAD	52-55	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	25-30
32390174-6	2020	Deliberate activation of P2RX7 in vivo by exogenous NAD resulted in a nearly complete iNKT cell ablation in liver and spleen in a P2RX7-dependent manner.	NAD	52-55	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	130-135
32890402-7	2020	Moreover, mutation analyses of the NAD+ interacting residues of PARP1 showed that PARP1 can be physically trapped at DNA damage sites, and identified H862 as a potential regulator for PARP1 exchange.	NAD	35-39	poly(ADP-ribose) polymerase 1	Homo sapiens	64-69
32890402-7	2020	Moreover, mutation analyses of the NAD+ interacting residues of PARP1 showed that PARP1 can be physically trapped at DNA damage sites, and identified H862 as a potential regulator for PARP1 exchange.	NAD	35-39	poly(ADP-ribose) polymerase 1	Homo sapiens	82-87
32890402-7	2020	Moreover, mutation analyses of the NAD+ interacting residues of PARP1 showed that PARP1 can be physically trapped at DNA damage sites, and identified H862 as a potential regulator for PARP1 exchange.	NAD	35-39	poly(ADP-ribose) polymerase 1	Homo sapiens	82-87
32728715-3	2020	Three NADH-linked assays were tested that use alternative coupling enzymes: glyceraldehyde-3-phosphate dehydrogenase (GAPDH) and glycerolphosphate dehydrogenase (GlyPDH); phosphoenolpyruvate carboxylase (PEPC) and malate dehydrogenase (MDH); and pyruvate kinase (PK) and lactate dehydrogenase (LDH).	NAD	6-10	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	118-123
33087267-4	2020	These signaling enzymes include nicotinamide adenine dinucleotide (NAD+) dependent poly(ADP-ribose) polymerases (PARP1, PARP2) and class III deacetylases (SIRT1, SIRT6) that comprise a key PARP-NAD-SIRT axis to facilitate the regulation and coordination of BER in the mammalian cell.	NAD	32-65	poly(ADP-ribose) polymerase 1	Homo sapiens	113-118
32908120-1	2020	NAMPT mediates the rate-limiting step of the NAD salvage pathway, which maintains cellular bioenergetics and provides a necessary substrate for functions essential to rapidly proliferating cancer cells.	NAD	45-48	nicotinamide phosphoribosyltransferase	Mus musculus	0-5
32908120-5	2020	On-target activity of OT-82 was confirmed with the addition of NMN, the product of NAMPT, which rescued NAD concentration and EWS cellular viability.	NAD	104-107	nicotinamide phosphoribosyltransferase	Mus musculus	83-88
32880588-8	2020	Analysis of the NAD+-bound form showed some differences between the structures of EcGAPDH1 and human GAPDH.	NAD	16-20	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	84-89
32829780-9	2020	In addition, 6PGD inhibition disrupted NADPH and NADH homeostasis in RCC cells as shown by the decreased level of NADPH and NADH, and suppressed SIRT-1 activity.	NAD	49-53	phosphogluconate dehydrogenase	Homo sapiens	13-17
32829780-9	2020	In addition, 6PGD inhibition disrupted NADPH and NADH homeostasis in RCC cells as shown by the decreased level of NADPH and NADH, and suppressed SIRT-1 activity.	NAD	124-128	phosphogluconate dehydrogenase	Homo sapiens	13-17
32946760-3	2020	(2020b) report how the NAD+-dependent ADP-ribosylation of histone H2B by PARP-1 in complex with a metabolic enzyme suppresses the phosphorylation of an adjacent residue, impacting adipogenesis.	NAD	23-27	poly(ADP-ribose) polymerase 1	Homo sapiens	73-79
32535274-2	2020	Recent findings highlight that Sirtuin-3 (SIRT3), a mitochondrial protein, is an oxidized nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase and a key modulator in maintaining integrity and functions of mitochondria.	NAD	90-123	sirtuin 3	Homo sapiens	31-40
32535274-2	2020	Recent findings highlight that Sirtuin-3 (SIRT3), a mitochondrial protein, is an oxidized nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase and a key modulator in maintaining integrity and functions of mitochondria.	NAD	90-123	sirtuin 3	Homo sapiens	42-47
32535274-2	2020	Recent findings highlight that Sirtuin-3 (SIRT3), a mitochondrial protein, is an oxidized nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase and a key modulator in maintaining integrity and functions of mitochondria.	NAD	125-129	sirtuin 3	Homo sapiens	31-40
32535274-2	2020	Recent findings highlight that Sirtuin-3 (SIRT3), a mitochondrial protein, is an oxidized nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase and a key modulator in maintaining integrity and functions of mitochondria.	NAD	125-129	sirtuin 3	Homo sapiens	42-47
32535274-9	2020	SIRT3 chemical activators and NAD + precursors can up-regulate SIRT3 activity to protect against DA neuron degeneration in PD models.	NAD	30-35	sirtuin 3	Homo sapiens	63-68
31873757-0	2020	Extracellular signal-regulated kinase 1/2 regulates NAD metabolism during acute kidney injury through microRNA-34a-mediated NAMPT expression.	NAD	52-55	nicotinamide phosphoribosyltransferase	Mus musculus	124-129
31873757-5	2020	The rate-limiting NAD biosynthesis salvage enzyme, NAMPT, decreased following AKI, and this decrease was prevented by ERK1/2 inhibition.	NAD	18-21	nicotinamide phosphoribosyltransferase	Mus musculus	51-56
32072237-5	2020	In addition, hyperglycemia-induced activation of the polyol pathway can lead to increased NADH/NAD+ ratio, which might translate into increased levels of hydrogen sulfide-via enhanced activity of cystathionine beta-synthase-that would fuel reductive stress through inhibition of mitochondrial complex I. Reductive stress may be either a potential weapon against cancer priming tumor cells to apoptosis or a cancer"s ally promoting tumor cell proliferation and making tumor cells resistant to reactive oxygen species-inducing drugs.	NAD	90-94	cystathionine beta-synthase	Homo sapiens	196-223
32072237-5	2020	In addition, hyperglycemia-induced activation of the polyol pathway can lead to increased NADH/NAD+ ratio, which might translate into increased levels of hydrogen sulfide-via enhanced activity of cystathionine beta-synthase-that would fuel reductive stress through inhibition of mitochondrial complex I. Reductive stress may be either a potential weapon against cancer priming tumor cells to apoptosis or a cancer"s ally promoting tumor cell proliferation and making tumor cells resistant to reactive oxygen species-inducing drugs.	NAD	95-99	cystathionine beta-synthase	Homo sapiens	196-223
33087267-4	2020	These signaling enzymes include nicotinamide adenine dinucleotide (NAD+) dependent poly(ADP-ribose) polymerases (PARP1, PARP2) and class III deacetylases (SIRT1, SIRT6) that comprise a key PARP-NAD-SIRT axis to facilitate the regulation and coordination of BER in the mammalian cell.	NAD	32-65	poly(ADP-ribose) polymerase 2	Homo sapiens	120-125
33087267-4	2020	These signaling enzymes include nicotinamide adenine dinucleotide (NAD+) dependent poly(ADP-ribose) polymerases (PARP1, PARP2) and class III deacetylases (SIRT1, SIRT6) that comprise a key PARP-NAD-SIRT axis to facilitate the regulation and coordination of BER in the mammalian cell.	NAD	32-65	poly(ADP-ribose) polymerase 1	Homo sapiens	113-117
33087267-4	2020	These signaling enzymes include nicotinamide adenine dinucleotide (NAD+) dependent poly(ADP-ribose) polymerases (PARP1, PARP2) and class III deacetylases (SIRT1, SIRT6) that comprise a key PARP-NAD-SIRT axis to facilitate the regulation and coordination of BER in the mammalian cell.	NAD	67-71	poly(ADP-ribose) polymerase 1	Homo sapiens	113-118
33087267-4	2020	These signaling enzymes include nicotinamide adenine dinucleotide (NAD+) dependent poly(ADP-ribose) polymerases (PARP1, PARP2) and class III deacetylases (SIRT1, SIRT6) that comprise a key PARP-NAD-SIRT axis to facilitate the regulation and coordination of BER in the mammalian cell.	NAD	67-71	poly(ADP-ribose) polymerase 2	Homo sapiens	120-125
33087267-4	2020	These signaling enzymes include nicotinamide adenine dinucleotide (NAD+) dependent poly(ADP-ribose) polymerases (PARP1, PARP2) and class III deacetylases (SIRT1, SIRT6) that comprise a key PARP-NAD-SIRT axis to facilitate the regulation and coordination of BER in the mammalian cell.	NAD	67-71	poly(ADP-ribose) polymerase 1	Homo sapiens	113-117
33015038-4	2020	Sirtuin 3 (SIRT3) is the major mitochondrial nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase, which deacetylates two critical lysine residues (lysine 68 and lysine 122) on SOD2 and promotes its antioxidative activity.	NAD	45-78	sirtuin 3	Homo sapiens	0-9
33015038-4	2020	Sirtuin 3 (SIRT3) is the major mitochondrial nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase, which deacetylates two critical lysine residues (lysine 68 and lysine 122) on SOD2 and promotes its antioxidative activity.	NAD	45-78	sirtuin 3	Homo sapiens	11-16
33015038-4	2020	Sirtuin 3 (SIRT3) is the major mitochondrial nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase, which deacetylates two critical lysine residues (lysine 68 and lysine 122) on SOD2 and promotes its antioxidative activity.	NAD	80-83	sirtuin 3	Homo sapiens	0-9
33015038-4	2020	Sirtuin 3 (SIRT3) is the major mitochondrial nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase, which deacetylates two critical lysine residues (lysine 68 and lysine 122) on SOD2 and promotes its antioxidative activity.	NAD	80-83	sirtuin 3	Homo sapiens	11-16
33015038-7	2020	Mechanistically, caffeine bound to SIRT3 with high affinity (K D = 6.858 x 10-7 M); the binding affinity between SIRT3 and its substrate acetylated p53 was also 9.03 (without NAD+) or 6.87 (with NAD+) times higher in the presence of caffeine.	NAD	195-199	sirtuin 3	Homo sapiens	113-118
32939087-7	2020	Our data suggest that active PARP2 cycles through different conformational states to exchange NAD+ and substrate, which may enable PARP enzymes to act processively while bound to chromatin.	NAD	94-98	poly(ADP-ribose) polymerase 2	Homo sapiens	29-34
32228195-3	2020	Nicotinamide adenine dinucleotide-dependent deacetylase sirtuin-1 (SIRT1)/forkhead box O3 (FOXO3a) signaling is critical for maintaining neuronal function and regulation of the apoptotic pathway.	NAD	0-33	sirtuin 1	Rattus norvegicus	56-65
32228195-3	2020	Nicotinamide adenine dinucleotide-dependent deacetylase sirtuin-1 (SIRT1)/forkhead box O3 (FOXO3a) signaling is critical for maintaining neuronal function and regulation of the apoptotic pathway.	NAD	0-33	sirtuin 1	Rattus norvegicus	67-72
32534944-11	2020	NAD+ has a direct inhibitory effect on PARP-1 and can prevent pro-inflammatory cytokines over-activation.	NAD	0-4	poly(ADP-ribose) polymerase 1	Homo sapiens	39-45
32939087-7	2020	Our data suggest that active PARP2 cycles through different conformational states to exchange NAD+ and substrate, which may enable PARP enzymes to act processively while bound to chromatin.	NAD	94-98	poly(ADP-ribose) polymerase 1	Homo sapiens	29-33
33005608-4	2020	Under reaction with hNQO1 and NADH, turn-on fluorescence appears due to in-situ formation of the organic fluorescent compound 7-diethylamino-3-cyanocoumarin, and fluorescent intensity changes significantly.	NAD	30-34	NAD(P)H quinone dehydrogenase 1	Homo sapiens	20-25
32807821-4	2020	PARP-1 activity is dependent on intracellular NAD+ concentration.	NAD	46-50	poly(ADP-ribose) polymerase 1	Homo sapiens	0-6
32802964-1	2020	Background: n-Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) catalyses the reversible NAD +-dependent oxidative phosphorylation of n-glyceraldehyde-3-phosphate to 1,3-diphospho-n-glycerate in both glycolysis and gluconeogenesis.	NAD	88-93	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	12-54
32802964-1	2020	Background: n-Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) catalyses the reversible NAD +-dependent oxidative phosphorylation of n-glyceraldehyde-3-phosphate to 1,3-diphospho-n-glycerate in both glycolysis and gluconeogenesis.	NAD	88-93	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	56-61
32846968-1	2020	The stress-inducible and senescence-associated tumor suppressor SIRT4, a member of the family of mitochondrial sirtuins (SIRT3, SIRT4, and SIRT5), regulates bioenergetics and metabolism via NAD+-dependent enzymatic activities.	NAD	190-194	sirtuin 4	Homo sapiens	64-69
32846968-1	2020	The stress-inducible and senescence-associated tumor suppressor SIRT4, a member of the family of mitochondrial sirtuins (SIRT3, SIRT4, and SIRT5), regulates bioenergetics and metabolism via NAD+-dependent enzymatic activities.	NAD	190-194	sirtuin 3	Homo sapiens	121-126
32846968-1	2020	The stress-inducible and senescence-associated tumor suppressor SIRT4, a member of the family of mitochondrial sirtuins (SIRT3, SIRT4, and SIRT5), regulates bioenergetics and metabolism via NAD+-dependent enzymatic activities.	NAD	190-194	sirtuin 4	Homo sapiens	128-133
32807821-5	2020	We therefore hypothesized that defects of the NAD+ salvage pathway might result in decreases in PARP-1 activity.	NAD	46-50	poly(ADP-ribose) polymerase 1	Homo sapiens	96-102
32601098-7	2020	However, mCAT macrophages exhibited increased glycolytic and oxidative metabolism, coupled with increased ATP production and an increased intracellular NADH/NAD+ ratio compared with BMDMs from WT mice.	NAD	152-156	catalase	Mus musculus	9-13
32524997-6	2020	In contrast to ERalpha activity, the nuclear AIF is increased with an ERbeta agonist, DPN and blocked with an ERbeta antagonist, PHTPP.	NAD	86-89	estrogen receptor 1	Homo sapiens	70-76
32601098-7	2020	However, mCAT macrophages exhibited increased glycolytic and oxidative metabolism, coupled with increased ATP production and an increased intracellular NADH/NAD+ ratio compared with BMDMs from WT mice.	NAD	157-161	catalase	Mus musculus	9-13
32601098-9	2020	Taken together, these findings point to an increased availability of reducing equivalents in the form of NADH as an important mechanism by which metabolic activity modulates inflammatory signaling through the NF-kappaB pathway.	NAD	105-109	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	209-218
32796716-1	2020	Sirtuin1 (Sirt1) has a NAD (+) binding domain and modulates the acetylation status of peroxisome proliferator-activated receptor-gamma coactivator-1alpha (PGC1alpha) and Fork Head Box O1 transcription factor (Foxo1) according to the nutritional status.	NAD	23-30	PPARG coactivator 1 alpha	Homo sapiens	155-164
32974194-5	2020	Studies have shown that NQO1 can bioactivate certain quinone molecules (e.g., ortho-naphthoquinone and beta-lapachone) to induce a futile redox cycle leading to the formation of oxidative DNA damage, hyperactivation of poly(ADP-ribose) polymerase 1 (PARP1), and catastrophic depletion of NAD+ and ATP, which culminates in cellular lethality via NAD+-Keresis.	NAD	288-292	NAD(P)H quinone dehydrogenase 1	Homo sapiens	24-28
32974194-5	2020	Studies have shown that NQO1 can bioactivate certain quinone molecules (e.g., ortho-naphthoquinone and beta-lapachone) to induce a futile redox cycle leading to the formation of oxidative DNA damage, hyperactivation of poly(ADP-ribose) polymerase 1 (PARP1), and catastrophic depletion of NAD+ and ATP, which culminates in cellular lethality via NAD+-Keresis.	NAD	345-349	NAD(P)H quinone dehydrogenase 1	Homo sapiens	24-28
32903806-4	2020	PARP-1 functions as a DNA repair enzyme but under intense DNA damage depletes the cell of NAD+ and ATP and leads to a non-apoptotic type of cell death called Parthanatos, which has been associated with the pathogenesis of neurodegenerative diseases.	NAD	90-94	poly(ADP-ribose) polymerase 1	Homo sapiens	0-6
32796716-1	2020	Sirtuin1 (Sirt1) has a NAD (+) binding domain and modulates the acetylation status of peroxisome proliferator-activated receptor-gamma coactivator-1alpha (PGC1alpha) and Fork Head Box O1 transcription factor (Foxo1) according to the nutritional status.	NAD	23-30	forkhead box O1	Homo sapiens	209-214
32778948-3	2020	In studies with primary cultured CMECs under hypoxia/reoxygenation (HR) and a rat model of I/R, our results suggested that the protective effect of NAD+ on CMECs exposed to HR or I/R is at least partially mediated by the NAD+-induced restoration of autophagic flux, especially lysosomal autophagy: NAD+ treatment markedly induced transcription factor EB (TFEB) activation and attenuated lysosomal dysfunction in the I/R or HR-exposed cells.	NAD	148-152	transcription factor EB	Rattus norvegicus	330-353
32778948-3	2020	In studies with primary cultured CMECs under hypoxia/reoxygenation (HR) and a rat model of I/R, our results suggested that the protective effect of NAD+ on CMECs exposed to HR or I/R is at least partially mediated by the NAD+-induced restoration of autophagic flux, especially lysosomal autophagy: NAD+ treatment markedly induced transcription factor EB (TFEB) activation and attenuated lysosomal dysfunction in the I/R or HR-exposed cells.	NAD	148-152	transcription factor EB	Rattus norvegicus	355-359
32778948-4	2020	Collectively, our study has provided the first in vivo and in vitro evidence that NAD+ significantly rescued the impaired autophagic flux and cell apoptosis that was induced by I/R in rat CMECs, which is mediated in part through the action of TFEB-mediated lysosomal autophagy.	NAD	82-86	transcription factor EB	Rattus norvegicus	243-247
32556414-3	2020	Especially, the highest enzyme activity towards acetaldehyde by Bdh2p(Y) was 117.95 U/mg with cofactor nicotinamide adenine dinucleotide reduced (NADH).	NAD	103-136	putative dehydrogenase BDH2	Saccharomyces cerevisiae S288C	64-69
32781630-1	2020	Silent information regulator 1 and 2 (SIRT1, 2) were NAD+-dependent histone or non-histone deacetylase, which emerged as key metabolic sensors in several tissues of mammals.	NAD	53-56	NAD-dependent protein deacetylase sirtuin-1	Ovis aries	38-43
32556414-3	2020	Especially, the highest enzyme activity towards acetaldehyde by Bdh2p(Y) was 117.95 U/mg with cofactor nicotinamide adenine dinucleotide reduced (NADH).	NAD	146-150	putative dehydrogenase BDH2	Saccharomyces cerevisiae S288C	64-69
32389638-8	2020	Surprisingly, intracellular NAD concentration increased in HAEC stimulated by IL1beta or TNFalpha and this effect was associated with upregulation of NAMPT and CD73, whereas changes in CD38 expression were less pronounced.	NAD	28-31	tumor necrosis factor	Mus musculus	89-97
32305451-0	2020	Interplay between NADH oxidation by complex I, glutathione redox state and sirtuin-3, and its role in the development of insulin resistance.	NAD	18-22	insulin	Homo sapiens	121-128
32305451-1	2020	Metabolic diseases are characterized by high NADH/NAD+ ratios due to excessive electron supply, causing defective mitochondrial function and impaired sirtuin-3 (SIRT-3) activity, the latter driving to oxidative stress and altered fatty acid beta-oxidation.	NAD	45-49	sirtuin 3	Homo sapiens	150-159
32305451-1	2020	Metabolic diseases are characterized by high NADH/NAD+ ratios due to excessive electron supply, causing defective mitochondrial function and impaired sirtuin-3 (SIRT-3) activity, the latter driving to oxidative stress and altered fatty acid beta-oxidation.	NAD	50-54	sirtuin 3	Homo sapiens	150-159
32305451-2	2020	NADH is oxidized by the complex I in the electron transport chain, thereby factors inhibiting complex I like acetylation, cardiolipin peroxidation, and glutathionylation by low GSH/GSSG ratios affects SIRT3 function by increasing the NADH/NAD+ ratio.	NAD	0-4	sirtuin 3	Homo sapiens	201-206
32389638-8	2020	Surprisingly, intracellular NAD concentration increased in HAEC stimulated by IL1beta or TNFalpha and this effect was associated with upregulation of NAMPT and CD73, whereas changes in CD38 expression were less pronounced.	NAD	28-31	nicotinamide phosphoribosyltransferase	Mus musculus	150-155
32305451-2	2020	NADH is oxidized by the complex I in the electron transport chain, thereby factors inhibiting complex I like acetylation, cardiolipin peroxidation, and glutathionylation by low GSH/GSSG ratios affects SIRT3 function by increasing the NADH/NAD+ ratio.	NAD	234-238	sirtuin 3	Homo sapiens	201-206
32305451-2	2020	NADH is oxidized by the complex I in the electron transport chain, thereby factors inhibiting complex I like acetylation, cardiolipin peroxidation, and glutathionylation by low GSH/GSSG ratios affects SIRT3 function by increasing the NADH/NAD+ ratio.	NAD	239-243	sirtuin 3	Homo sapiens	201-206
32199820-0	2020	The taming of PARP1 and its impact on NAD+ metabolism.	NAD	38-42	poly(ADP-ribose) polymerase 1	Homo sapiens	14-19
32305451-4	2020	We propose that maintenance of proper NADH/NAD+ and GSH/GSSG ratios are central to ameliorate insulin resistance, as alterations in these redox couples lead to complex I dysfunction, disruption of SIRT-3 activity, ROS production and impaired beta-oxidation, the latter two being key effectors of insulin resistance.	NAD	38-42	insulin	Homo sapiens	94-101
32533606-8	2020	Our results demonstrate that NAMPT/NAD+ axis functions to protect cells not only from replicative senescence, but also from stress-induced premature senescence in vitro.	NAD	35-39	nicotinamide phosphoribosyltransferase	Mus musculus	29-34
32540762-3	2020	The changes in the levels of transcripts of the genes Me1 and Me2 encoding NAD-malic enzyme revealed their dependence on irradiation in opposite ways.	NAD	75-78	NADP-dependent malic enzyme	Zea mays	62-65
32428596-1	2020	AIMS: Since the role of the major mitochondrial NAD+-dependent deacetylase, sirtuin 3 (Sirt3), is differential in cancer, opposite to the well-known tumor-suppressing effect of hyperoxia, this study aimed to investigate the role of Sirt3 in triple-negative breast cancer (TNBC) cell line MDA-MB-231 upon hyperoxic (95% O2) conditions.	NAD	48-51	sirtuin 3	Homo sapiens	87-92
32199820-3	2020	PARP1/ARTD1 in the nucleus is the major NAD+ consuming activity and plays a key role in maintaining genomic integrity.	NAD	40-44	poly(ADP-ribose) polymerase 1	Homo sapiens	0-5
32199820-3	2020	PARP1/ARTD1 in the nucleus is the major NAD+ consuming activity and plays a key role in maintaining genomic integrity.	NAD	40-44	poly(ADP-ribose) polymerase 1	Homo sapiens	6-11
32199820-6	2020	MAJOR CONCLUSIONS: The presence of macroH2A1.1, particularly in differentiated cells, raises the threshold for the activation of PARP1 with consequences for DNA repair, gene transcription, and NAD+ homeostasis.	NAD	193-197	macroH2A.1 histone	Homo sapiens	35-46
32472322-2	2020	ADP-ribosylation is a reversible NAD+-dependent modification, catalyzed by poly ADP-ribose polymerase (PARP) or ADP-ribosyl transferase (ADPRTs) and has been reported by us and others as a modification that reduces the biological activity of VEGF.	NAD	33-37	poly(ADP-ribose) polymerase 1	Homo sapiens	75-101
32199820-6	2020	MAJOR CONCLUSIONS: The presence of macroH2A1.1, particularly in differentiated cells, raises the threshold for the activation of PARP1 with consequences for DNA repair, gene transcription, and NAD+ homeostasis.	NAD	193-197	poly(ADP-ribose) polymerase 1	Homo sapiens	129-134
32472322-2	2020	ADP-ribosylation is a reversible NAD+-dependent modification, catalyzed by poly ADP-ribose polymerase (PARP) or ADP-ribosyl transferase (ADPRTs) and has been reported by us and others as a modification that reduces the biological activity of VEGF.	NAD	33-37	poly(ADP-ribose) polymerase 1	Homo sapiens	103-107
32678295-6	2020	Single-cell imaging methods for metabolism by fluorescence lifetime (FLIM) of NADH and signaling by kinases Akt and ERK revealed that breast cancer cells utilized oxidative phosphorylation and signaling by Akt to a greater extent both in 3D co-cultures and a mouse model of ER+ breast cancer cells in bone marrow.	NAD	78-82	thymoma viral proto-oncogene 1	Mus musculus	108-111
32472322-2	2020	ADP-ribosylation is a reversible NAD+-dependent modification, catalyzed by poly ADP-ribose polymerase (PARP) or ADP-ribosyl transferase (ADPRTs) and has been reported by us and others as a modification that reduces the biological activity of VEGF.	NAD	33-37	vascular endothelial growth factor A	Homo sapiens	242-246
32678295-6	2020	Single-cell imaging methods for metabolism by fluorescence lifetime (FLIM) of NADH and signaling by kinases Akt and ERK revealed that breast cancer cells utilized oxidative phosphorylation and signaling by Akt to a greater extent both in 3D co-cultures and a mouse model of ER+ breast cancer cells in bone marrow.	NAD	78-82	mitogen-activated protein kinase 1	Mus musculus	116-119
32678295-6	2020	Single-cell imaging methods for metabolism by fluorescence lifetime (FLIM) of NADH and signaling by kinases Akt and ERK revealed that breast cancer cells utilized oxidative phosphorylation and signaling by Akt to a greater extent both in 3D co-cultures and a mouse model of ER+ breast cancer cells in bone marrow.	NAD	78-82	thymoma viral proto-oncogene 1	Mus musculus	206-209
32752130-0	2020	Flexible NAD+ Binding in Deoxyhypusine Synthase Reflects the Dynamic Hypusine Modification of Translation Factor IF5A.	NAD	9-13	deoxyhypusine synthase	Homo sapiens	25-47
32752130-1	2020	The eukaryotic and archaeal translation factor IF5A requires a post-translational hypusine modification, which is catalyzed by deoxyhypusine synthase (DHS) at a single lysine residue of IF5A with NAD+ and spermidine as cofactors, followed by hydroxylation to form hypusine.	NAD	196-200	deoxyhypusine synthase	Homo sapiens	127-149
32396938-6	2020	Mechanistically, STAT3 transactivates MDH1 to sustain the malate-aspartate NADH shuttle activity and the HSC self-renewal and differentiation.	NAD	75-79	signal transducer and activator of transcription 3	Mus musculus	17-22
32709019-4	2020	The enzymatic activity of CD38 in the process of generating the second messenger cADPR utilizes intracellular NAD+, and thus limits its availability to different NAD+ consuming enzymes (PARP, ART, and sirtuins) inside the cells.	NAD	110-114	poly(ADP-ribose) polymerase 1	Homo sapiens	186-190
32493816-1	2020	Sirtuin 2 (Sirt2), an NAD+-dependent protein deacetylase, deacetylates tubulin, AKT, and other proteins.	NAD	22-25	AKT serine/threonine kinase 1	Homo sapiens	80-83
32711564-5	2020	We also demonstrated that ectopic expression of SIRT2, a cytoplasmic NAD+ - dependent deacetylase, suppresses the defects of HDAC6 knockdown neurons.	NAD	69-72	histone deacetylase 6	Homo sapiens	125-130
32848753-15	2020	Moreover, our study found that TMZ upregulated Sirt1 expression by increasing the expression of nicotinamide phosphoribosyl transferase (Nampt), which is a rate limiting enzyme for nicotinamide adenine dinucleotide (NAD+) generation by salvage pathway.	NAD	181-214	sirtuin 1	Rattus norvegicus	47-52
32848753-15	2020	Moreover, our study found that TMZ upregulated Sirt1 expression by increasing the expression of nicotinamide phosphoribosyl transferase (Nampt), which is a rate limiting enzyme for nicotinamide adenine dinucleotide (NAD+) generation by salvage pathway.	NAD	216-220	sirtuin 1	Rattus norvegicus	47-52
32848753-16	2020	And the increased NAD+ promoted Sirt1 expression.	NAD	18-22	sirtuin 1	Rattus norvegicus	32-37
32709019-4	2020	The enzymatic activity of CD38 in the process of generating the second messenger cADPR utilizes intracellular NAD+, and thus limits its availability to different NAD+ consuming enzymes (PARP, ART, and sirtuins) inside the cells.	NAD	162-166	poly(ADP-ribose) polymerase 1	Homo sapiens	186-190
32679093-1	2020	Poly(ADP-ribose) polymerase (PARP) enzymes use nicotinamide adenine dinucleotide (NAD+) to modify up to seven different amino acids with a single mono(ADP-ribose) unit (MARylation deposited by PARP monoenzymes) or branched poly(ADP-ribose) polymers (PARylation deposited by PARP polyenzymes).	NAD	47-80	poly(ADP-ribose) polymerase 1	Homo sapiens	0-27
32679093-1	2020	Poly(ADP-ribose) polymerase (PARP) enzymes use nicotinamide adenine dinucleotide (NAD+) to modify up to seven different amino acids with a single mono(ADP-ribose) unit (MARylation deposited by PARP monoenzymes) or branched poly(ADP-ribose) polymers (PARylation deposited by PARP polyenzymes).	NAD	47-80	poly(ADP-ribose) polymerase 1	Homo sapiens	29-33
32679093-1	2020	Poly(ADP-ribose) polymerase (PARP) enzymes use nicotinamide adenine dinucleotide (NAD+) to modify up to seven different amino acids with a single mono(ADP-ribose) unit (MARylation deposited by PARP monoenzymes) or branched poly(ADP-ribose) polymers (PARylation deposited by PARP polyenzymes).	NAD	47-80	poly(ADP-ribose) polymerase 1	Homo sapiens	193-197
32679093-1	2020	Poly(ADP-ribose) polymerase (PARP) enzymes use nicotinamide adenine dinucleotide (NAD+) to modify up to seven different amino acids with a single mono(ADP-ribose) unit (MARylation deposited by PARP monoenzymes) or branched poly(ADP-ribose) polymers (PARylation deposited by PARP polyenzymes).	NAD	47-80	poly(ADP-ribose) polymerase 1	Homo sapiens	193-197
32679093-1	2020	Poly(ADP-ribose) polymerase (PARP) enzymes use nicotinamide adenine dinucleotide (NAD+) to modify up to seven different amino acids with a single mono(ADP-ribose) unit (MARylation deposited by PARP monoenzymes) or branched poly(ADP-ribose) polymers (PARylation deposited by PARP polyenzymes).	NAD	82-86	poly(ADP-ribose) polymerase 1	Homo sapiens	0-27
32679093-1	2020	Poly(ADP-ribose) polymerase (PARP) enzymes use nicotinamide adenine dinucleotide (NAD+) to modify up to seven different amino acids with a single mono(ADP-ribose) unit (MARylation deposited by PARP monoenzymes) or branched poly(ADP-ribose) polymers (PARylation deposited by PARP polyenzymes).	NAD	82-86	poly(ADP-ribose) polymerase 1	Homo sapiens	29-33
32679093-1	2020	Poly(ADP-ribose) polymerase (PARP) enzymes use nicotinamide adenine dinucleotide (NAD+) to modify up to seven different amino acids with a single mono(ADP-ribose) unit (MARylation deposited by PARP monoenzymes) or branched poly(ADP-ribose) polymers (PARylation deposited by PARP polyenzymes).	NAD	82-86	poly(ADP-ribose) polymerase 1	Homo sapiens	193-197
32679093-1	2020	Poly(ADP-ribose) polymerase (PARP) enzymes use nicotinamide adenine dinucleotide (NAD+) to modify up to seven different amino acids with a single mono(ADP-ribose) unit (MARylation deposited by PARP monoenzymes) or branched poly(ADP-ribose) polymers (PARylation deposited by PARP polyenzymes).	NAD	82-86	poly(ADP-ribose) polymerase 1	Homo sapiens	193-197
33040724-10	2020	Simultaneously, the activities of NAD+-dependent IDH, mitochondrial aspartate aminotransferase, and two malate dehydrogenase isoenzymes, whose genes were not predicted to have the p53-binding sequences near the transcription starting points, were upregulated by cisplatin.	NAD	34-37	tumor protein p53	Homo sapiens	180-183
32668623-2	2020	P2X7 receptor activation may also be triggered by ARTC2.2-dependent ADP ribosylation in the presence of extracellular NAD.	NAD	118-121	purinergic receptor P2X 7	Homo sapiens	0-13
32685721-6	2020	Result: Serum beta-endorphin is significantly reduced in DN and DPN (*p < 0.001) compared with the control and DM group.	NAD	64-67	proopiomelanocortin	Homo sapiens	14-28
32647171-4	2020	LDHA binds to NADH and promotes reactive oxygen species (ROS) to induce catabolic changes through stabilization of IkappaB-zeta, a critical pro-inflammatory mediator in chondrocytes.	NAD	14-18	lactate dehydrogenase A	Homo sapiens	0-4
32645959-12	2020	NQO1 and cytochrome b5 reductase can neutralize ROS in the plasma membrane and induce a high NAD+/NADH ratio, which then activates SIRT1 and mitochondrial bioenergetics.	NAD	93-97	NAD(P)H quinone dehydrogenase 1	Homo sapiens	0-4
32645959-12	2020	NQO1 and cytochrome b5 reductase can neutralize ROS in the plasma membrane and induce a high NAD+/NADH ratio, which then activates SIRT1 and mitochondrial bioenergetics.	NAD	98-102	NAD(P)H quinone dehydrogenase 1	Homo sapiens	0-4
32497158-1	2020	The photocatalytic generation of an NADH synthetic analogue, i.e. 1-benzyl-1,4-dihydronicotinamide (1,4-BNAH), has been studied using the cobalt diimino-dioxime complexes and the BF2-bridged derivative as catalysts.	NAD	36-40	forkhead box G1	Homo sapiens	179-182
32636388-3	2020	Here, we find that depleting the NAD biosynthetic enzyme, nicotinamide phosphoribosyl-transferase (Nampt), in mouse oocytes results in markedly longer spindles and compromises asymmetry.	NAD	33-36	nicotinamide phosphoribosyltransferase	Mus musculus	58-97
32636388-3	2020	Here, we find that depleting the NAD biosynthetic enzyme, nicotinamide phosphoribosyl-transferase (Nampt), in mouse oocytes results in markedly longer spindles and compromises asymmetry.	NAD	33-36	nicotinamide phosphoribosyltransferase	Mus musculus	99-104
32636388-6	2020	Additionally, we find that Nampt-depletion lowers NAD and ATP levels and that reducing NAD using small molecule Nampt inhibitors also compromises asymmetry.	NAD	50-53	nicotinamide phosphoribosyltransferase	Mus musculus	27-32
32636388-6	2020	Additionally, we find that Nampt-depletion lowers NAD and ATP levels and that reducing NAD using small molecule Nampt inhibitors also compromises asymmetry.	NAD	87-90	nicotinamide phosphoribosyltransferase	Mus musculus	112-117
31896781-5	2020	OT-82 was shown to induce cell death by inhibiting nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme in the salvage pathway of NAD synthesis.	NAD	150-153	nicotinamide phosphoribosyltransferase	Mus musculus	51-89
32238439-6	2020	Quinolinic acid phosphoribosyltransferase (QPRT), the rate-determining enzyme for de novo synthesis of nicotinamide adenine dinucleotide (NAD+) from tryptophan, exhibited particularly high differential gene expression in resistant U87 cells and protein expression in all resistant lines tested.	NAD	103-136	quinolinate phosphoribosyltransferase	Homo sapiens	0-41
32238439-6	2020	Quinolinic acid phosphoribosyltransferase (QPRT), the rate-determining enzyme for de novo synthesis of nicotinamide adenine dinucleotide (NAD+) from tryptophan, exhibited particularly high differential gene expression in resistant U87 cells and protein expression in all resistant lines tested.	NAD	103-136	quinolinate phosphoribosyltransferase	Homo sapiens	43-47
32238439-6	2020	Quinolinic acid phosphoribosyltransferase (QPRT), the rate-determining enzyme for de novo synthesis of nicotinamide adenine dinucleotide (NAD+) from tryptophan, exhibited particularly high differential gene expression in resistant U87 cells and protein expression in all resistant lines tested.	NAD	138-142	quinolinate phosphoribosyltransferase	Homo sapiens	0-41
32238439-6	2020	Quinolinic acid phosphoribosyltransferase (QPRT), the rate-determining enzyme for de novo synthesis of nicotinamide adenine dinucleotide (NAD+) from tryptophan, exhibited particularly high differential gene expression in resistant U87 cells and protein expression in all resistant lines tested.	NAD	138-142	quinolinate phosphoribosyltransferase	Homo sapiens	43-47
32461692-5	2020	Using LbNOX, we demonstrate that NADH reductive stress mediates the effects of GCKR variation on many metabolic traits, including circulating triglyceride levels, glucose tolerance and FGF21 levels.	NAD	33-37	fibroblast growth factor 21	Homo sapiens	185-190
31974433-6	2020	Therapeutic application of the Nampt small-molecule inhibitor, Fk866, strongly attenuated experimental GVHD and caused NAD depletion in T-cell subsets, which displayed differential susceptibility to NAD shortage.	NAD	119-122	nicotinamide phosphoribosyltransferase	Mus musculus	31-36
31896781-5	2020	OT-82 was shown to induce cell death by inhibiting nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme in the salvage pathway of NAD synthesis.	NAD	150-153	nicotinamide phosphoribosyltransferase	Mus musculus	91-96
31974433-6	2020	Therapeutic application of the Nampt small-molecule inhibitor, Fk866, strongly attenuated experimental GVHD and caused NAD depletion in T-cell subsets, which displayed differential susceptibility to NAD shortage.	NAD	199-202	nicotinamide phosphoribosyltransferase	Mus musculus	31-36
32573651-4	2020	This includes the NAD+-dependent sirtuin family of protein deacetylases and the PARP family of DNA repair enzymes.	NAD	18-21	poly(ADP-ribose) polymerase 1	Homo sapiens	80-84
32591631-2	2020	We analyzed the mechanism of NADH-channeling from D-glyceraldehyde-3-phosphate dehydrogenase (GAPDH) to L-lactate Dehydrogenase (LDH) using enzymes from different cells.	NAD	29-33	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	50-92
32629939-0	2020	Nicotinamide Phosphoribosyltransferase (Nampt)/Nicotinamide Adenine Dinucleotide (NAD) Axis Suppresses Atrial Fibrillation by Modulating the Calcium Handling Pathway.	NAD	82-85	nicotinamide phosphoribosyltransferase	Mus musculus	40-45
32629939-2	2020	Nicotinamide phosphoribosyltransferase (Nampt) is the rate-limiting enzyme that catalyzes nicotinamide adenine dinucleotide (NAD) activity.	NAD	90-123	nicotinamide phosphoribosyltransferase	Mus musculus	0-38
32629939-2	2020	Nicotinamide phosphoribosyltransferase (Nampt) is the rate-limiting enzyme that catalyzes nicotinamide adenine dinucleotide (NAD) activity.	NAD	90-123	nicotinamide phosphoribosyltransferase	Mus musculus	40-45
32629939-2	2020	Nicotinamide phosphoribosyltransferase (Nampt) is the rate-limiting enzyme that catalyzes nicotinamide adenine dinucleotide (NAD) activity.	NAD	125-128	nicotinamide phosphoribosyltransferase	Mus musculus	0-38
32629939-2	2020	Nicotinamide phosphoribosyltransferase (Nampt) is the rate-limiting enzyme that catalyzes nicotinamide adenine dinucleotide (NAD) activity.	NAD	125-128	nicotinamide phosphoribosyltransferase	Mus musculus	40-45
32629939-11	2020	The Nampt/NAD axis may be a potent therapeutic target for AF.	NAD	10-13	nicotinamide phosphoribosyltransferase	Mus musculus	4-9
32591631-2	2020	We analyzed the mechanism of NADH-channeling from D-glyceraldehyde-3-phosphate dehydrogenase (GAPDH) to L-lactate Dehydrogenase (LDH) using enzymes from different cells.	NAD	29-33	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	94-99
32591631-3	2020	Enzyme kinetics studies showed that LDH activity with free NADH and GAPDH-NADH complex always take place in parallel.	NAD	74-78	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	68-73
32591631-4	2020	The channeling is observed only in assays that mimic cytosolic conditions where free NADH concentration is negligible and the GAPDH-NADH complex is dominant.	NAD	85-89	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	126-131
32591631-4	2020	The channeling is observed only in assays that mimic cytosolic conditions where free NADH concentration is negligible and the GAPDH-NADH complex is dominant.	NAD	132-136	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	126-131
32591631-5	2020	Molecular dynamics and protein-protein interaction studies showed that LDH and GAPDH can form a leaky channeling complex only at the limiting NADH concentrations.	NAD	142-146	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	79-84
32591631-6	2020	Surface calculations showed that positive electric field between the NAD(H) binding sites on LDH and GAPDH tetramers can merge in the LDH-GAPDH complex.	NAD	69-75	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	101-106
32591631-6	2020	Surface calculations showed that positive electric field between the NAD(H) binding sites on LDH and GAPDH tetramers can merge in the LDH-GAPDH complex.	NAD	69-75	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	138-143
32591631-7	2020	NAD(H)-channeling within the LDH-GAPDH complex can be an extension of NAD(H)-channeling within each tetramer.	NAD	0-6	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	33-38
32591631-7	2020	NAD(H)-channeling within the LDH-GAPDH complex can be an extension of NAD(H)-channeling within each tetramer.	NAD	70-76	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	33-38
32591631-8	2020	In the case of a transient LDH-(GAPDH-NADH) complex, the relative contribution from the channeled and the diffusive paths depends on the overlap between the off-rates for the LDH-(GAPDH-NADH) complex and the GAPDH-NADH complex.	NAD	38-42	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	32-37
32591631-8	2020	In the case of a transient LDH-(GAPDH-NADH) complex, the relative contribution from the channeled and the diffusive paths depends on the overlap between the off-rates for the LDH-(GAPDH-NADH) complex and the GAPDH-NADH complex.	NAD	38-42	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	180-185
32591631-8	2020	In the case of a transient LDH-(GAPDH-NADH) complex, the relative contribution from the channeled and the diffusive paths depends on the overlap between the off-rates for the LDH-(GAPDH-NADH) complex and the GAPDH-NADH complex.	NAD	38-42	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	180-185
32591631-8	2020	In the case of a transient LDH-(GAPDH-NADH) complex, the relative contribution from the channeled and the diffusive paths depends on the overlap between the off-rates for the LDH-(GAPDH-NADH) complex and the GAPDH-NADH complex.	NAD	186-190	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	32-37
32591631-8	2020	In the case of a transient LDH-(GAPDH-NADH) complex, the relative contribution from the channeled and the diffusive paths depends on the overlap between the off-rates for the LDH-(GAPDH-NADH) complex and the GAPDH-NADH complex.	NAD	186-190	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	180-185
32591631-8	2020	In the case of a transient LDH-(GAPDH-NADH) complex, the relative contribution from the channeled and the diffusive paths depends on the overlap between the off-rates for the LDH-(GAPDH-NADH) complex and the GAPDH-NADH complex.	NAD	186-190	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	180-185
32676581-3	2020	Here, we use the phasor-based approach to Fluorescence Lifetime IMaging (FLIM) microscopy to quantify the ratio between protein-bound and free Nicotinamide adenine dinucleotide (phosphate) species in their reduced form (NAD(P)H), and the Insulinoma cell line INS-1E as a beta-like cellular model.	NAD	143-176	amyloid beta precursor protein	Homo sapiens	269-275
32400970-3	2020	Here, we show that homologous recombination-defective (HRD) cancers rely on oxidative metabolism to supply NAD+ and ATP for poly(ADP-ribose) polymerase (PARP)-dependent DNA repair mechanisms.	NAD	107-111	poly(ADP-ribose) polymerase 1	Homo sapiens	124-151
32383848-3	2020	Superoxide dismutase (SOD) and catalase (CAT) were chosen as scavengers and covalently encapsulated into silica nanoreactors, together with glucose dehydrogenase (GDH) which simultaneously should produce the coenzyme nicotinamide adenine dinucleotide (NADH, reduced form).	NAD	217-250	catalase	Homo sapiens	41-44
32383848-3	2020	Superoxide dismutase (SOD) and catalase (CAT) were chosen as scavengers and covalently encapsulated into silica nanoreactors, together with glucose dehydrogenase (GDH) which simultaneously should produce the coenzyme nicotinamide adenine dinucleotide (NADH, reduced form).	NAD	252-256	catalase	Homo sapiens	41-44
32383848-4	2020	By the enzymatic reactions of SOD and CAT, the interior of silica nanoreactors becomes a "ROS safe zone" to protect the glucose-dependent NADH production of co-encapsulated GDH.	NAD	138-142	catalase	Homo sapiens	38-41
32400970-3	2020	Here, we show that homologous recombination-defective (HRD) cancers rely on oxidative metabolism to supply NAD+ and ATP for poly(ADP-ribose) polymerase (PARP)-dependent DNA repair mechanisms.	NAD	107-111	poly(ADP-ribose) polymerase 1	Homo sapiens	153-157
32278117-3	2020	This study aims to identify changes of specific components of NAD+/SIRTs system in white adipose tissue (WAT) and brown adipose tissue (BAT) of mice upon energy imbalance, focusing on key enzymes in NAD+ salvage (Nampt, Nmnat1, Nrk1), clearance (Nnmt, Aox1, Cyp2e1) and consumption pathways (Sirt1, Sirt2, Sirt3, Sirt6, Parp1).	NAD	62-66	nicotinamide phosphoribosyltransferase	Mus musculus	213-218
32502419-2	2020	(2020) now show that nicotinamide adenine dinucleotide (NAD+) can restore robust circadian gene expression and behavior in aged mice through SIRT1-dependent deacetylation of the core clock protein PER2.	NAD	21-54	period circadian clock 2	Mus musculus	197-201
32502419-2	2020	(2020) now show that nicotinamide adenine dinucleotide (NAD+) can restore robust circadian gene expression and behavior in aged mice through SIRT1-dependent deacetylation of the core clock protein PER2.	NAD	56-60	period circadian clock 2	Mus musculus	197-201
32278117-3	2020	This study aims to identify changes of specific components of NAD+/SIRTs system in white adipose tissue (WAT) and brown adipose tissue (BAT) of mice upon energy imbalance, focusing on key enzymes in NAD+ salvage (Nampt, Nmnat1, Nrk1), clearance (Nnmt, Aox1, Cyp2e1) and consumption pathways (Sirt1, Sirt2, Sirt3, Sirt6, Parp1).	NAD	199-203	sirtuin 6	Mus musculus	313-318
32278117-7	2020	NAD+ content negatively correlated with plasma cholesterol, TNF-alpha levels and calorie intake, while it positively correlated with plasma adiponectin level.	NAD	0-4	tumor necrosis factor	Mus musculus	60-69
32507768-0	2020	CD38 inhibition by apigenin ameliorates mitochondrial oxidative stress through restoration of the intracellular NAD+/NADH ratio and Sirt3 activity in renal tubular cells in diabetic rats.	NAD	112-116	CD38 molecule	Rattus norvegicus	0-4
32507768-0	2020	CD38 inhibition by apigenin ameliorates mitochondrial oxidative stress through restoration of the intracellular NAD+/NADH ratio and Sirt3 activity in renal tubular cells in diabetic rats.	NAD	117-121	CD38 molecule	Rattus norvegicus	0-4
32507768-6	2020	In vitro, inhibition of CD38 activity by apigenin or CD38 knockdown increased the NAD+/NADH ratio and Sirt3 activity in renal proximal tubular HK-2 cells cultured under high-glucose conditions.	NAD	82-86	CD38 molecule	Rattus norvegicus	24-28
32507768-6	2020	In vitro, inhibition of CD38 activity by apigenin or CD38 knockdown increased the NAD+/NADH ratio and Sirt3 activity in renal proximal tubular HK-2 cells cultured under high-glucose conditions.	NAD	82-86	CD38 molecule	Rattus norvegicus	53-57
32507768-6	2020	In vitro, inhibition of CD38 activity by apigenin or CD38 knockdown increased the NAD+/NADH ratio and Sirt3 activity in renal proximal tubular HK-2 cells cultured under high-glucose conditions.	NAD	87-91	CD38 molecule	Rattus norvegicus	24-28
32507768-6	2020	In vitro, inhibition of CD38 activity by apigenin or CD38 knockdown increased the NAD+/NADH ratio and Sirt3 activity in renal proximal tubular HK-2 cells cultured under high-glucose conditions.	NAD	87-91	CD38 molecule	Rattus norvegicus	53-57
32298659-3	2020	Nicotinamide (NAM) acts as a substrate of visfatin and Nicotinamide N-Methyltransferase (NNMT) leading to the generation of Nicotinamide Adenine Dinucleotide (NAD) and N1-Methylnicotinamide (MNAM), respectively.	NAD	124-157	nicotinamide N-methyltransferase	Rattus norvegicus	55-87
32298659-3	2020	Nicotinamide (NAM) acts as a substrate of visfatin and Nicotinamide N-Methyltransferase (NNMT) leading to the generation of Nicotinamide Adenine Dinucleotide (NAD) and N1-Methylnicotinamide (MNAM), respectively.	NAD	124-157	nicotinamide N-methyltransferase	Rattus norvegicus	89-93
32298659-3	2020	Nicotinamide (NAM) acts as a substrate of visfatin and Nicotinamide N-Methyltransferase (NNMT) leading to the generation of Nicotinamide Adenine Dinucleotide (NAD) and N1-Methylnicotinamide (MNAM), respectively.	NAD	159-162	nicotinamide N-methyltransferase	Rattus norvegicus	55-87
32298659-3	2020	Nicotinamide (NAM) acts as a substrate of visfatin and Nicotinamide N-Methyltransferase (NNMT) leading to the generation of Nicotinamide Adenine Dinucleotide (NAD) and N1-Methylnicotinamide (MNAM), respectively.	NAD	159-162	nicotinamide N-methyltransferase	Rattus norvegicus	89-93
32278117-3	2020	This study aims to identify changes of specific components of NAD+/SIRTs system in white adipose tissue (WAT) and brown adipose tissue (BAT) of mice upon energy imbalance, focusing on key enzymes in NAD+ salvage (Nampt, Nmnat1, Nrk1), clearance (Nnmt, Aox1, Cyp2e1) and consumption pathways (Sirt1, Sirt2, Sirt3, Sirt6, Parp1).	NAD	62-66	sirtuin 6	Mus musculus	313-318
32278117-3	2020	This study aims to identify changes of specific components of NAD+/SIRTs system in white adipose tissue (WAT) and brown adipose tissue (BAT) of mice upon energy imbalance, focusing on key enzymes in NAD+ salvage (Nampt, Nmnat1, Nrk1), clearance (Nnmt, Aox1, Cyp2e1) and consumption pathways (Sirt1, Sirt2, Sirt3, Sirt6, Parp1).	NAD	199-203	nicotinamide phosphoribosyltransferase	Mus musculus	213-218
31473978-0	2020	Ischemic Neuroprotectant PKCepsilon Restores Mitochondrial Glutamate Oxaloacetate Transaminase in the Neuronal NADH Shuttle after Ischemic Injury.	NAD	111-115	protein kinase C, epsilon	Rattus norvegicus	25-35
33071527-2	2020	Unfortunately, all marketed PARP1 inhibitors act by competing with the cofactor NAD+ and resistance is already developing to this anti-cancer mechanism.	NAD	80-84	poly(ADP-ribose) polymerase 1	Homo sapiens	28-33
31473978-2	2020	Previously, our laboratory demonstrated that protein kinase C epsilon (PKCepsilon) promotes the synthesis of mitochondrial nicotinamide adenine dinucleotide (NAD+).	NAD	123-156	protein kinase C, epsilon	Rattus norvegicus	45-69
31473978-2	2020	Previously, our laboratory demonstrated that protein kinase C epsilon (PKCepsilon) promotes the synthesis of mitochondrial nicotinamide adenine dinucleotide (NAD+).	NAD	123-156	protein kinase C, epsilon	Rattus norvegicus	71-81
32087266-6	2020	Meanwhile, NAD+ booster nicotinamide mononucleotide also counteracted the deleterious effects of ethanol by increasing SIRT1, suggesting the regulation of SIRT1-UCP2 axis may be associated with cellular NAD+/NADH ratio.	NAD	11-15	sirtuin 1	Rattus norvegicus	119-124
31473978-2	2020	Previously, our laboratory demonstrated that protein kinase C epsilon (PKCepsilon) promotes the synthesis of mitochondrial nicotinamide adenine dinucleotide (NAD+).	NAD	158-162	protein kinase C, epsilon	Rattus norvegicus	45-69
32087266-6	2020	Meanwhile, NAD+ booster nicotinamide mononucleotide also counteracted the deleterious effects of ethanol by increasing SIRT1, suggesting the regulation of SIRT1-UCP2 axis may be associated with cellular NAD+/NADH ratio.	NAD	11-15	sirtuin 1	Rattus norvegicus	155-160
31473978-2	2020	Previously, our laboratory demonstrated that protein kinase C epsilon (PKCepsilon) promotes the synthesis of mitochondrial nicotinamide adenine dinucleotide (NAD+).	NAD	158-162	protein kinase C, epsilon	Rattus norvegicus	71-81
32087266-6	2020	Meanwhile, NAD+ booster nicotinamide mononucleotide also counteracted the deleterious effects of ethanol by increasing SIRT1, suggesting the regulation of SIRT1-UCP2 axis may be associated with cellular NAD+/NADH ratio.	NAD	203-207	sirtuin 1	Rattus norvegicus	155-160
32087266-6	2020	Meanwhile, NAD+ booster nicotinamide mononucleotide also counteracted the deleterious effects of ethanol by increasing SIRT1, suggesting the regulation of SIRT1-UCP2 axis may be associated with cellular NAD+/NADH ratio.	NAD	208-212	sirtuin 1	Rattus norvegicus	119-124
32032607-6	2020	KKPA4026 was confirmed to induce the expression of the Nrf2-dependent antioxidant enzymes heme oxygenase-1, glutamate-cysteine ligase catalytic subunit, glutamate-cysteine ligase regulatory subunit, and NAD(P)H:quinone oxidoreductase 1 in BV-2 cells.	NAD	203-210	nuclear factor, erythroid derived 2, like 2	Mus musculus	55-59
32087266-6	2020	Meanwhile, NAD+ booster nicotinamide mononucleotide also counteracted the deleterious effects of ethanol by increasing SIRT1, suggesting the regulation of SIRT1-UCP2 axis may be associated with cellular NAD+/NADH ratio.	NAD	208-212	sirtuin 1	Rattus norvegicus	155-160
32766477-11	2020	NAD+ concentration was inversely related to serum bilirubin concentration (r 2 = -0.127; P = 0.04) and positively correlated with myeloperoxidase activity (r 2 = 0.31; P = 0.003).	NAD	0-4	myeloperoxidase	Homo sapiens	130-145
32222469-8	2020	Activation of NRF2 signaling leads to an increase in expression of NAD(P)H dehydrogenase [quinone] 1 (NQO1), nicotinamide adenine dinucleotide (NAD+) levels, sirtuin activity (nuclear and mitochondrial), and superoxide dismutase 2 (SOD2) expression/activity.	NAD	109-142	NFE2 like bZIP transcription factor 2	Homo sapiens	14-18
32222469-8	2020	Activation of NRF2 signaling leads to an increase in expression of NAD(P)H dehydrogenase [quinone] 1 (NQO1), nicotinamide adenine dinucleotide (NAD+) levels, sirtuin activity (nuclear and mitochondrial), and superoxide dismutase 2 (SOD2) expression/activity.	NAD	144-149	NFE2 like bZIP transcription factor 2	Homo sapiens	14-18
32392755-7	2020	Activation of the DNA damage sensor enzyme poly(ADP-ribose) polymerase 1 (PARP1), a major consumer of NAD+ in the nucleus, was fully blocked by NMNAT1 inactivation, leading to increased DNA damage (phospho-H2AX foci).	NAD	102-106	poly(ADP-ribose) polymerase 1	Homo sapiens	43-72
32392755-7	2020	Activation of the DNA damage sensor enzyme poly(ADP-ribose) polymerase 1 (PARP1), a major consumer of NAD+ in the nucleus, was fully blocked by NMNAT1 inactivation, leading to increased DNA damage (phospho-H2AX foci).	NAD	102-106	poly(ADP-ribose) polymerase 1	Homo sapiens	74-79
32371497-0	2020	p53 is regulated by aerobic glycolysis in cancer cells by the CtBP family of NADH-dependent transcriptional regulators.	NAD	77-81	tumor protein p53	Homo sapiens	0-3
32371497-2	2020	Maintenance of high glycolytic rates depends on the lactate dehydrogenase-catalyzed regeneration of NAD+ from GAPDH-generated NADH because an increased NADH:NAD+ ratio inhibits GAPDH.	NAD	100-104	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	110-115
32371497-2	2020	Maintenance of high glycolytic rates depends on the lactate dehydrogenase-catalyzed regeneration of NAD+ from GAPDH-generated NADH because an increased NADH:NAD+ ratio inhibits GAPDH.	NAD	100-104	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	177-182
32371497-2	2020	Maintenance of high glycolytic rates depends on the lactate dehydrogenase-catalyzed regeneration of NAD+ from GAPDH-generated NADH because an increased NADH:NAD+ ratio inhibits GAPDH.	NAD	126-130	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	110-115
32371497-2	2020	Maintenance of high glycolytic rates depends on the lactate dehydrogenase-catalyzed regeneration of NAD+ from GAPDH-generated NADH because an increased NADH:NAD+ ratio inhibits GAPDH.	NAD	126-130	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	177-182
32371497-2	2020	Maintenance of high glycolytic rates depends on the lactate dehydrogenase-catalyzed regeneration of NAD+ from GAPDH-generated NADH because an increased NADH:NAD+ ratio inhibits GAPDH.	NAD	152-156	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	110-115
31960754-7	2020	These results provide new pharmacological evidence that ALP facilitates neuroprotection via prevention of neuronal oxidative stress and promotion of cell survival signaling pathways.Abbreviations: ABTS: 2,2"-azino-bis-(3-ethylbenzothiazoline-6-sulfonicacid); AD: Alzheimer"s disease; ALP: polysaccharide extracts isolated from Annona muricata leaves; ARE: antioxidant response element; DPPH: 1,1-diphenyl-picrylhydrazyl; DCFH-DA: 2",7"-dichlorofluorescin diacetate; ECL: electrochemiluminescence; ERK: extracellular regulated kinase; FBS: Fetal bovine serum; FITC: fluorescein isothiocyanate; FRAP: ferric reducing antioxidant power; HO-1: Heme oxygenase-1; JNK: c-jun N-terminal kinase; MAPKs: mitogen-activated protein kinases; MDA: malondialdehyde; MMP: mitochondrial membrane potential; MTT: 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazoliumbromide; NQO1: NAD(P)H:quinine oxidoreductase 1, Nrf2: nuclear factor-E2-related factor 2; PD: parkinson"s disease; PI3K: phosphatidylinositol-3kinase; PVDF: polyvinylidene difluoride; ROS: reactive oxygen species; SOD: Superoxidedismutase; TPTZ: tripydyltriazine.	NAD	863-870	alopecia, recessive	Mus musculus	56-59
31775023-5	2020	A recent study suggested that the cytosolic enzyme NAD(P)H: quinone acceptor oxidoreductase (NQO1) is the major enzyme involved in the activation of idebenone, and the beneficial effects of idebenone are dependent on the expression of NQO1.	NAD	51-58	NAD(P)H quinone dehydrogenase 1	Homo sapiens	93-97
31775023-5	2020	A recent study suggested that the cytosolic enzyme NAD(P)H: quinone acceptor oxidoreductase (NQO1) is the major enzyme involved in the activation of idebenone, and the beneficial effects of idebenone are dependent on the expression of NQO1.	NAD	51-58	NAD(P)H quinone dehydrogenase 1	Homo sapiens	235-239
32402770-4	2021	However, because NAD+ is utilized by many enzymes other than PARP-1, NAD+ competitors tend to produce certain off-target effects.	NAD	69-73	poly(ADP-ribose) polymerase 1	Homo sapiens	61-67
32371497-2	2020	Maintenance of high glycolytic rates depends on the lactate dehydrogenase-catalyzed regeneration of NAD+ from GAPDH-generated NADH because an increased NADH:NAD+ ratio inhibits GAPDH.	NAD	152-156	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	177-182
32371497-2	2020	Maintenance of high glycolytic rates depends on the lactate dehydrogenase-catalyzed regeneration of NAD+ from GAPDH-generated NADH because an increased NADH:NAD+ ratio inhibits GAPDH.	NAD	157-161	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	110-115
32371497-2	2020	Maintenance of high glycolytic rates depends on the lactate dehydrogenase-catalyzed regeneration of NAD+ from GAPDH-generated NADH because an increased NADH:NAD+ ratio inhibits GAPDH.	NAD	157-161	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	177-182
32371497-3	2020	Here, using human breast cancer cell models, we identified a pathway in which changes in the extramitochondrial-free NADH:NAD+ ratio signaled through the CtBP family of NADH-sensitive transcriptional regulators to control the abundance and activity of p53.	NAD	117-121	tumor protein p53	Homo sapiens	252-255
32371497-3	2020	Here, using human breast cancer cell models, we identified a pathway in which changes in the extramitochondrial-free NADH:NAD+ ratio signaled through the CtBP family of NADH-sensitive transcriptional regulators to control the abundance and activity of p53.	NAD	122-126	tumor protein p53	Homo sapiens	252-255
32371497-3	2020	Here, using human breast cancer cell models, we identified a pathway in which changes in the extramitochondrial-free NADH:NAD+ ratio signaled through the CtBP family of NADH-sensitive transcriptional regulators to control the abundance and activity of p53.	NAD	169-173	tumor protein p53	Homo sapiens	252-255
32371497-4	2020	NADH-free forms of CtBPs cooperated with the p53-binding partner HDM2 to suppress p53 function, and loss of these forms in highly glycolytic cells resulted in p53 accumulation.	NAD	0-4	tumor protein p53	Homo sapiens	82-85
32371497-4	2020	NADH-free forms of CtBPs cooperated with the p53-binding partner HDM2 to suppress p53 function, and loss of these forms in highly glycolytic cells resulted in p53 accumulation.	NAD	0-4	tumor protein p53	Homo sapiens	82-85
32371497-5	2020	We propose that this pathway represents a "glycolytic stress response" in which the initiation of a protective p53 response by an increased NADH:NAD+ ratio enables cells to avoid cellular damage caused by mismatches between metabolic supply and demand.	NAD	140-144	tumor protein p53	Homo sapiens	111-114
32371497-5	2020	We propose that this pathway represents a "glycolytic stress response" in which the initiation of a protective p53 response by an increased NADH:NAD+ ratio enables cells to avoid cellular damage caused by mismatches between metabolic supply and demand.	NAD	145-149	tumor protein p53	Homo sapiens	111-114
32169417-2	2020	Recently, evidence has been obtained that AHR is involved in NAD+ and energy homeostasis in cooperation with NAD+-consuming enzymes including CD38, TiPARP and sirtuins.	NAD	109-113	TCDD inducible poly(ADP-ribose) polymerase	Homo sapiens	148-154
32072193-13	2020	Furthermore, immunoprecipitation and mass spectrometry analysis indicated that AKAP1 interacted with the NADH-ubiquinone oxidoreductase 75 kDa subunit (NDUFS1).	NAD	105-120	NADH:ubiquinone oxidoreductase core subunit S1	Mus musculus	152-158
31962129-3	2020	One of the enzymes that metabolizes NAD+ in axons is Sarm1 (Sterile Alpha and TIR Motif Containing 1), and its activity is thought to play a key role in axonal degeneration.	NAD	36-39	sterile alpha and HEAT/Armadillo motif containing 1	Mus musculus	53-58
31962129-3	2020	One of the enzymes that metabolizes NAD+ in axons is Sarm1 (Sterile Alpha and TIR Motif Containing 1), and its activity is thought to play a key role in axonal degeneration.	NAD	36-39	sterile alpha and HEAT/Armadillo motif containing 1	Mus musculus	60-100
31912134-9	2020	Cytoplasmic NAD(P)-dependent 10-formyl-tetrahydrofolate dehydrogenase (Aldh1/1) and mitochondrial NAD(P)-dependent 10-formyl-tetrahydrofolate dehydrogenase (Aldh1/2) , genes responsible for the catabolism of 10-formylTHF, were very weakly expressed in PP, low in livers of F and N, and reached the significantly higher adult levels in J.	NAD	12-18	aldehyde dehydrogenase 1 family, member L1	Rattus norvegicus	29-69
32358582-6	2020	Moreover, by examining dynamic structural changes of PARP1, we reveal changes in the secondary structure of PARP1 induced by NAD+ and PARP inhibitor binding.	NAD	125-129	poly(ADP-ribose) polymerase 1	Homo sapiens	53-58
32358582-6	2020	Moreover, by examining dynamic structural changes of PARP1, we reveal changes in the secondary structure of PARP1 induced by NAD+ and PARP inhibitor binding.	NAD	125-129	poly(ADP-ribose) polymerase 1	Homo sapiens	108-113
32358582-6	2020	Moreover, by examining dynamic structural changes of PARP1, we reveal changes in the secondary structure of PARP1 induced by NAD+ and PARP inhibitor binding.	NAD	125-129	poly(ADP-ribose) polymerase 1	Homo sapiens	53-57
32411727-8	2020	In this review, we describe the role of DNA damage-mediated metabolic remodeling in AF and other cardiovascular diseases, discuss novel druggable targets for AF and highlight future directions for clinical trials with drugs directed at PARP1-NAD+ pathway with the ultimate aim to preserve quality of life and to attenuate severe complications such as heart failure or stroke in patients with AF.	NAD	242-246	poly(ADP-ribose) polymerase 1	Homo sapiens	236-241
32301489-0	2020	NAD+ Attenuates Experimental Autoimmune Encephalomyelitis through Inducing of CD11b+ gr-1+ Myeloid-Derived Suppressor Cells.	NAD	0-4	integrin alpha M	Mus musculus	78-83
32301489-10	2020	Besides, NAD+ treatment up-regulated the expression of p-IkappaB and down-regulated the expression of p-NF-kappaB.	NAD	9-13	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	104-113
32301489-11	2020	In addition, NAD+ treatment could increase the numbers of CD11b+ gr-1+ MDSCs and the expression of Arginase-1.	NAD	13-17	integrin alpha M	Mus musculus	58-63
32301489-12	2020	Moreover, NAD+ treatment up-regulated the expressions of IL-13 and down-regulated the expression of IFN-gamma and IL-17.	NAD	10-14	interleukin 13	Mus musculus	57-62
32301489-12	2020	Moreover, NAD+ treatment up-regulated the expressions of IL-13 and down-regulated the expression of IFN-gamma and IL-17.	NAD	10-14	interferon gamma	Mus musculus	100-109
32301489-13	2020	CONCLUSIONS: The present study demonstrated that NAD+ treatment may induce the CD11b+ gr-1+ MDSCs to attenuate EAE via activating the phosphorylation of STAT6 expression.	NAD	49-53	integrin alpha M	Mus musculus	79-84
31274831-12	2020	In HPDE cells subjected to oxidative stress olaparib (1 muM) inhibited PARP activity, protected against the loss of cell viability and prevented the loss of cellular NAD levels.	NAD	166-169	latexin	Homo sapiens	56-59
32293172-0	2020	Specific Binding of snoRNAs to PARP-1 Promotes NAD+-Dependent Catalytic Activation.	NAD	47-51	poly(ADP-ribose) polymerase 1	Homo sapiens	31-37
32293172-1	2020	Poly(ADP-ribose) polymerase-1 (PARP-1) is an abundant and ubiquitous nuclear enzyme that catalyzes the transfer of ADP-ribose from donor NAD+ molecules to specific amino acids on substrate proteins.	NAD	137-141	poly(ADP-ribose) polymerase 1	Homo sapiens	0-29
32293172-1	2020	Poly(ADP-ribose) polymerase-1 (PARP-1) is an abundant and ubiquitous nuclear enzyme that catalyzes the transfer of ADP-ribose from donor NAD+ molecules to specific amino acids on substrate proteins.	NAD	137-141	poly(ADP-ribose) polymerase 1	Homo sapiens	31-37
32208631-5	2020	Under the function of active dsDNA, PARP-1 catalyzed to synthesize hyperbranched poly (ADP-ribose) polymer (PAR) by using nicotinamideadenine dinucleotide (NAD+) as substrates, forming Au50-dsDNA@PAR.	NAD	122-154	poly(ADP-ribose) polymerase 1	Homo sapiens	36-42
32208631-5	2020	Under the function of active dsDNA, PARP-1 catalyzed to synthesize hyperbranched poly (ADP-ribose) polymer (PAR) by using nicotinamideadenine dinucleotide (NAD+) as substrates, forming Au50-dsDNA@PAR.	NAD	156-160	poly(ADP-ribose) polymerase 1	Homo sapiens	36-42
32363189-3	2020	Mechanistic studies demonstrated that overexpression of CD38 specifically downregulated the expression of Rab7 and its adaptor protein pleckstrin homology domain-containing protein family member 1 (PLEKHM1) through nicotinamide adenine dinucleotide (NAD)-dependent and non-NAD-dependent pathways, respectively.	NAD	215-248	RAB7, member RAS oncogene family	Mus musculus	106-110
32259671-1	2020	Oxidation of formate to CO2 is catalyzed via the donation of electrons from formate dehydrogenase (FDH) to nicotinamide adenine dinucleotide (NAD+), and thus the charge transport characteristics of FDH become essential but remain unexplored.	NAD	107-140	aldehyde dehydrogenase 1 family member L1	Homo sapiens	76-97
32259671-1	2020	Oxidation of formate to CO2 is catalyzed via the donation of electrons from formate dehydrogenase (FDH) to nicotinamide adenine dinucleotide (NAD+), and thus the charge transport characteristics of FDH become essential but remain unexplored.	NAD	107-140	aldehyde dehydrogenase 1 family member L1	Homo sapiens	99-102
32259671-1	2020	Oxidation of formate to CO2 is catalyzed via the donation of electrons from formate dehydrogenase (FDH) to nicotinamide adenine dinucleotide (NAD+), and thus the charge transport characteristics of FDH become essential but remain unexplored.	NAD	107-140	aldehyde dehydrogenase 1 family member L1	Homo sapiens	198-201
32259671-1	2020	Oxidation of formate to CO2 is catalyzed via the donation of electrons from formate dehydrogenase (FDH) to nicotinamide adenine dinucleotide (NAD+), and thus the charge transport characteristics of FDH become essential but remain unexplored.	NAD	142-146	aldehyde dehydrogenase 1 family member L1	Homo sapiens	76-97
32259671-1	2020	Oxidation of formate to CO2 is catalyzed via the donation of electrons from formate dehydrogenase (FDH) to nicotinamide adenine dinucleotide (NAD+), and thus the charge transport characteristics of FDH become essential but remain unexplored.	NAD	142-146	aldehyde dehydrogenase 1 family member L1	Homo sapiens	99-102
32259671-1	2020	Oxidation of formate to CO2 is catalyzed via the donation of electrons from formate dehydrogenase (FDH) to nicotinamide adenine dinucleotide (NAD+), and thus the charge transport characteristics of FDH become essential but remain unexplored.	NAD	142-146	aldehyde dehydrogenase 1 family member L1	Homo sapiens	198-201
32259671-3	2020	We found that the coupling of NAD+ with FDH boosts the charge transport by ~2,100%, and the single-enzyme conductance highly correlates with the enzyme activity.	NAD	30-34	aldehyde dehydrogenase 1 family member L1	Homo sapiens	40-43
32259671-5	2020	Site-specific mutagenesis analysis demonstrated that FDH-NAD+ stably combined own higher bioactivity and boosts charge transport, and the coupling has been optimized via the natural selection.	NAD	57-61	aldehyde dehydrogenase 1 family member L1	Homo sapiens	53-56
32363189-3	2020	Mechanistic studies demonstrated that overexpression of CD38 specifically downregulated the expression of Rab7 and its adaptor protein pleckstrin homology domain-containing protein family member 1 (PLEKHM1) through nicotinamide adenine dinucleotide (NAD)-dependent and non-NAD-dependent pathways, respectively.	NAD	273-276	RAB7, member RAS oncogene family	Mus musculus	106-110
32312889-3	2020	SARM1 is known to mediate neuronal cell degeneration through depletion of essential metabolite NAD and induction of energy crisis.	NAD	95-98	sterile alpha and HEAT/Armadillo motif containing 1	Mus musculus	0-5
32312889-4	2020	Here, we demonstrate that SARM1 is expressed in photoreceptors, and using retinal tissue explant, we confirm that activation of SARM1 causes destruction of NAD pools in the photoreceptor layer.	NAD	156-159	sterile alpha and HEAT/Armadillo motif containing 1	Mus musculus	26-31
32312889-4	2020	Here, we demonstrate that SARM1 is expressed in photoreceptors, and using retinal tissue explant, we confirm that activation of SARM1 causes destruction of NAD pools in the photoreceptor layer.	NAD	156-159	sterile alpha and HEAT/Armadillo motif containing 1	Mus musculus	128-133
32312889-7	2020	Overall, our data indicate that endogenous SARM1 has the capacity to consume NAD in photoreceptor cells and identifies a previously unappreciated role for SARM1-dependent cell death in photoreceptor cell degeneration.	NAD	77-80	sterile alpha and HEAT/Armadillo motif containing 1	Mus musculus	43-48
32363189-3	2020	Mechanistic studies demonstrated that overexpression of CD38 specifically downregulated the expression of Rab7 and its adaptor protein pleckstrin homology domain-containing protein family member 1 (PLEKHM1) through nicotinamide adenine dinucleotide (NAD)-dependent and non-NAD-dependent pathways, respectively.	NAD	250-253	RAB7, member RAS oncogene family	Mus musculus	106-110
32187526-5	2020	Strikingly, when respiration is impaired, serine catabolism through methylene tetrahydrofolate dehydrogenase (MTHFD2) becomes a major NADH source.	NAD	134-138	methylenetetrahydrofolate dehydrogenase (NAD+ dependent), methenyltetrahydrofolate cyclohydrolase	Mus musculus	110-116
32059949-9	2020	Nudt3, Nudt16, and Nudt20 bound m7G capped RNA more tightly than RNA with NADH caps.	NAD	74-78	nudix hydrolase 3	Homo sapiens	0-5
32236231-1	2020	The nutraceutical Nicotinamide Riboside (NR), an efficacious biosynthetic precursor to NAD, is readily metabolized by the purine nucleoside phosphorylase (PNP).	NAD	87-90	purine nucleoside phosphorylase	Homo sapiens	122-153
32308644-8	2020	Sirtuins, a family of adenine dinucleotide (NAD+)-dependent histone deacetylases, have been demonstrated to regulate a series of physiological processes and affect diseases such as obesity, insulin resistance, type 2 diabetes (T2DM), heart disease, cancer, and aging.	NAD	44-47	insulin	Homo sapiens	190-197
32308774-8	2020	Results: We found that the concomitant activation of the NAD+-dependent deacetylase SIRT1 and the PI3K/AKT signaling pathway converge to increase the presence of deacetylated and phosphorylated FOXO3a, a transcription factor, in the nucleus.	NAD	57-60	AKT serine/threonine kinase 1	Rattus norvegicus	103-106
32244383-2	2020	ADP-ribose is covalently attached to target proteins by poly-ADP-ribose polymerases (PARPs), using nicotinamide adenine dinucleotide (NAD+) as a substrate.	NAD	99-132	poly(ADP-ribose) polymerase 1	Homo sapiens	85-90
31900990-2	2020	The role of the rate-limiting enzyme in the NAD+ salvage pathway, nicotinamide phosphoribosyltransferase (NAMPT), for regulation energy homeostasis by the hypothalamus has not been extensively studied.	NAD	44-47	nicotinamide phosphoribosyltransferase	Mus musculus	66-104
31900990-2	2020	The role of the rate-limiting enzyme in the NAD+ salvage pathway, nicotinamide phosphoribosyltransferase (NAMPT), for regulation energy homeostasis by the hypothalamus has not been extensively studied.	NAD	44-47	nicotinamide phosphoribosyltransferase	Mus musculus	106-111
31900990-8	2020	NAMPT inhibition in primary hypothalamic neurons significantly reduced levels of NAD+ , increased levels of ROS, and affected the expression of Agrp, Pomc, and genes related to mitochondrial function.	NAD	81-84	nicotinamide phosphoribosyltransferase	Mus musculus	0-5
32049549-5	2020	The results showed that UVB irradiation caused apparent corneal edema and cell apoptosis in mice, accompanied by reduced levels of NAD+ and its key biosynthesis enzyme, nicotinamide phosphoribosyltransferase (NAMPT), in the corneal endothelium.	NAD	131-135	nicotinamide phosphoribosyltransferase	Mus musculus	169-207
32049549-5	2020	The results showed that UVB irradiation caused apparent corneal edema and cell apoptosis in mice, accompanied by reduced levels of NAD+ and its key biosynthesis enzyme, nicotinamide phosphoribosyltransferase (NAMPT), in the corneal endothelium.	NAD	131-135	nicotinamide phosphoribosyltransferase	Mus musculus	209-214
32049549-10	2020	Therefore, we conclude that NAD+ precursors can effectively prevent the apoptosis of the corneal endothelium through reactivating AKT signaling; this represents a potential therapeutic approach for preventing UVB-induced corneal damage.	NAD	28-32	thymoma viral proto-oncogene 1	Mus musculus	130-133
31630478-8	2020	In addition to increasing cellular NAD+ /NADH ratio, B-LAP upregulated the cardiac levels of SIRT1, beclin-1, p-LKB1 and p-AMPK, and reduced the cardiac levels of p-mTOR, interleukin (IL)-1beta, TNF (tumour necrosis factor)-alpha and caspase-3.	NAD	35-38	eye lens aplasia	Mus musculus	55-58
31630478-8	2020	In addition to increasing cellular NAD+ /NADH ratio, B-LAP upregulated the cardiac levels of SIRT1, beclin-1, p-LKB1 and p-AMPK, and reduced the cardiac levels of p-mTOR, interleukin (IL)-1beta, TNF (tumour necrosis factor)-alpha and caspase-3.	NAD	41-45	eye lens aplasia	Mus musculus	55-58
31603249-4	2020	As an NAD+ -dependent deacetylase, sirtuin 6 (Sirt6) has been linked to different types of biological processes.	NAD	6-10	sirtuin 6	Mus musculus	35-44
31603249-4	2020	As an NAD+ -dependent deacetylase, sirtuin 6 (Sirt6) has been linked to different types of biological processes.	NAD	6-10	sirtuin 6	Mus musculus	46-51
32235505-2	2020	DHS catalyses the transfer of a 4-aminobutyl moiety of polyamine spermidine to a specific lysine of eukaryotic translation factor 5A (eIF5A) precursor in a nicotinamide adenine dinucleotide (NAD)-dependent manner.	NAD	156-189	deoxyhypusine synthase	Homo sapiens	0-3
32235505-2	2020	DHS catalyses the transfer of a 4-aminobutyl moiety of polyamine spermidine to a specific lysine of eukaryotic translation factor 5A (eIF5A) precursor in a nicotinamide adenine dinucleotide (NAD)-dependent manner.	NAD	191-194	deoxyhypusine synthase	Homo sapiens	0-3
32123312-4	2020	Treatment of neuroblastoma cells with the MCT1 inhibitor SR13800 increased intracellular lactate levels, disrupted the nicotinamide adenine dinucleotide (NADH/NAD+) ratio, and decreased intracellular glutathione levels.	NAD	119-152	solute carrier family 16 member 1	Homo sapiens	42-46
32123312-4	2020	Treatment of neuroblastoma cells with the MCT1 inhibitor SR13800 increased intracellular lactate levels, disrupted the nicotinamide adenine dinucleotide (NADH/NAD+) ratio, and decreased intracellular glutathione levels.	NAD	154-158	solute carrier family 16 member 1	Homo sapiens	42-46
32123312-4	2020	Treatment of neuroblastoma cells with the MCT1 inhibitor SR13800 increased intracellular lactate levels, disrupted the nicotinamide adenine dinucleotide (NADH/NAD+) ratio, and decreased intracellular glutathione levels.	NAD	159-163	solute carrier family 16 member 1	Homo sapiens	42-46
32244383-2	2020	ADP-ribose is covalently attached to target proteins by poly-ADP-ribose polymerases (PARPs), using nicotinamide adenine dinucleotide (NAD+) as a substrate.	NAD	134-138	poly(ADP-ribose) polymerase 1	Homo sapiens	85-90
32170186-7	2020	The changes in DL intensity and kinetics highlighted a possible effect of nanoparticle matrix on mitochondria, through the involvement of the NADH pool and ROS production that, in turn, activates ERK1/2 pathways.	NAD	142-146	mitogen-activated protein kinase 3	Homo sapiens	196-202
32142284-1	2020	Deoxyhypusine synthase (DHPS) utilizes spermidine and NAD as cofactors to incorporate a hypusine modification into the eukaryotic translation initiation factor 5A (eIF5A).	NAD	54-57	deoxyhypusine synthase	Homo sapiens	0-22
32142284-1	2020	Deoxyhypusine synthase (DHPS) utilizes spermidine and NAD as cofactors to incorporate a hypusine modification into the eukaryotic translation initiation factor 5A (eIF5A).	NAD	54-57	deoxyhypusine synthase	Homo sapiens	24-28
32245127-3	2020	It is shown that 7-MG competes with substrate NAD+ and its binding in the PARP-1 active site is mediated by hydrogen bonds and nonpolar interactions with the Gly863, Ala898, Ser904, and Tyr907 residues.	NAD	46-50	poly(ADP-ribose) polymerase 1	Homo sapiens	74-80
32245130-2	2020	Except for its role in the production of adenosine triphosphate (ATP), NAD+ acts as a substrate for several enzymes including sirtuin 1 (SIRT1) and poly ADP-ribose polymerase 1 (PARP1).	NAD	71-75	poly(ADP-ribose) polymerase 1	Homo sapiens	148-176
32245130-2	2020	Except for its role in the production of adenosine triphosphate (ATP), NAD+ acts as a substrate for several enzymes including sirtuin 1 (SIRT1) and poly ADP-ribose polymerase 1 (PARP1).	NAD	71-75	poly(ADP-ribose) polymerase 1	Homo sapiens	178-183
32257999-3	2020	Complexes could bind to bovine serum albumin (BSA) by means of static quenching mode, catalyze the oxidation of nicotinamide adenine dinucleotide (NADH) and increase the levels of reactive oxygen species (ROS).	NAD	112-145	albumin	Homo sapiens	31-44
32257999-3	2020	Complexes could bind to bovine serum albumin (BSA) by means of static quenching mode, catalyze the oxidation of nicotinamide adenine dinucleotide (NADH) and increase the levels of reactive oxygen species (ROS).	NAD	147-151	albumin	Homo sapiens	31-44
31988240-7	2020	These results indicate that by forming a complex with GAPDH, NAMPT can translocate to the nucleus and thereby sustain the stress-induced NMN/NAD+ salvage pathway.	NAD	141-144	nicotinamide phosphoribosyltransferase	Mus musculus	61-66
31859031-7	2020	NAD+ repletion via nicotinamide riboside ameliorated disease phenotypes in SCA7 mice and patient stem cell-derived neurons.	NAD	0-4	ataxin 7	Mus musculus	75-79
32028527-6	2020	In response to DNA damage and NAD+ binding site occupancy, the HPF1-PARP1/2 interaction is enhanced via allosteric networks operating within PARP1/2, providing an additional level of regulation in DNA repair induction.	NAD	30-33	histone PARylation factor 1	Homo sapiens	63-67
32028527-6	2020	In response to DNA damage and NAD+ binding site occupancy, the HPF1-PARP1/2 interaction is enhanced via allosteric networks operating within PARP1/2, providing an additional level of regulation in DNA repair induction.	NAD	30-33	poly(ADP-ribose) polymerase 1	Homo sapiens	68-73
32028527-6	2020	In response to DNA damage and NAD+ binding site occupancy, the HPF1-PARP1/2 interaction is enhanced via allosteric networks operating within PARP1/2, providing an additional level of regulation in DNA repair induction.	NAD	30-33	poly(ADP-ribose) polymerase 1	Homo sapiens	141-146
31855104-2	2020	There are 12 enzymatically active mono(ADP-ribose) polymerase (monoPARP) enzymes and 4 enzymatically active poly(ADP-ribose) polymerase (polyPARP) enzymes that use nicotinamide adenine dinucleotide (NAD+) as the ADP-ribose donating substrate to generate these modifications.	NAD	164-197	poly(ADP-ribose) polymerase 1	Homo sapiens	108-135
31855104-2	2020	There are 12 enzymatically active mono(ADP-ribose) polymerase (monoPARP) enzymes and 4 enzymatically active poly(ADP-ribose) polymerase (polyPARP) enzymes that use nicotinamide adenine dinucleotide (NAD+) as the ADP-ribose donating substrate to generate these modifications.	NAD	199-203	poly(ADP-ribose) polymerase 1	Homo sapiens	108-135
31899805-7	2020	The redox state represented by NADH also decreased in PSK1Delta compared with the wild type.	NAD	31-35	serine/threonine protein kinase PSK1	Saccharomyces cerevisiae S288C	54-63
31859031-4	2020	Transcription-factor binding-site analysis of downregulated genes yielded Sirt1 target sites, and we observed reduced Sirt1 activity in the SCA7 mouse cerebellum with NAD+ depletion.	NAD	167-171	ataxin 7	Mus musculus	140-144
31838391-9	2020	The data from AAV-sponge-mediated miR-34a-5p inhibition suggested that miR-34a-5p diminished NAD+ level by directly targeting NAMPT expression in BDE-47-treated mouse livers, which was confirmed by luciferase reporter assay.	NAD	93-96	microRNA 615	Mus musculus	34-37
31838391-9	2020	The data from AAV-sponge-mediated miR-34a-5p inhibition suggested that miR-34a-5p diminished NAD+ level by directly targeting NAMPT expression in BDE-47-treated mouse livers, which was confirmed by luciferase reporter assay.	NAD	93-96	microRNA 615	Mus musculus	71-74
31838391-9	2020	The data from AAV-sponge-mediated miR-34a-5p inhibition suggested that miR-34a-5p diminished NAD+ level by directly targeting NAMPT expression in BDE-47-treated mouse livers, which was confirmed by luciferase reporter assay.	NAD	93-96	nicotinamide phosphoribosyltransferase	Mus musculus	126-131
32061543-2	2020	Recently, Katsuyama et al., demonstrated that the CD38/NAD/Sirtuin1/EZH2 axis reduces cytolytic CD8+ T cell function and might be targeted to overcome incidence of infections.	NAD	55-58	enhancer of zeste 2 polycomb repressive complex 2 subunit	Homo sapiens	68-72
32103017-4	2020	We demonstrate that the NAD+-dependent deacylase SIRT2 removes the myristoyl group, and our evidence suggests that NMT prefers the GTP-bound while SIRT2 prefers the GDP-bound ARF6.	NAD	24-28	N-myristoyltransferase 1	Homo sapiens	115-118
31859031-8	2020	Sirt1 thus achieves neuroprotection by promoting calcium regulation, and NAD+ dysregulation underlies Sirt1 dysfunction in SCA7, indicating that cerebellar ataxias exhibit altered calcium homeostasis because of metabolic dysregulation, suggesting shared therapy targets.	NAD	73-77	ataxin 7	Homo sapiens	123-127
32015132-3	2020	Biallelic loss-of-function variants in HAAO or KYNU, two genes of the nicotinamide adenine dinucleotide (NAD) synthesis pathway, are causative of congenital malformation and miscarriage in humans and mice.	NAD	70-103	kynureninase	Homo sapiens	47-51
32015132-3	2020	Biallelic loss-of-function variants in HAAO or KYNU, two genes of the nicotinamide adenine dinucleotide (NAD) synthesis pathway, are causative of congenital malformation and miscarriage in humans and mice.	NAD	105-108	kynureninase	Homo sapiens	47-51
31782485-4	2020	Proteins from the poly(ADP-ribose) polymerase (PARP) family, such as PARP1 and PARP2, use NAD+ as a substrate to catalyse the synthesis of polymeric chains consisting of ADP-ribose units covalently attached to an acceptor molecule.	NAD	90-93	poly(ADP-ribose) polymerase 1	Homo sapiens	18-45
32093281-8	2020	Finally, we identified that TFAM knockdown increased the NAD+/NADH ratio in tumor cells.	NAD	57-61	transcription factor A, mitochondrial	Homo sapiens	28-32
32093281-8	2020	Finally, we identified that TFAM knockdown increased the NAD+/NADH ratio in tumor cells.	NAD	62-66	transcription factor A, mitochondrial	Homo sapiens	28-32
32093281-9	2020	This led to the upregulation of Sirtuin1 (SIRT1), a NAD-dependent protein deacetylase, to deacetylate p53 and attenuated its transcriptional activation on PISD.	NAD	52-55	tumor protein p53	Homo sapiens	102-105
32093281-9	2020	This led to the upregulation of Sirtuin1 (SIRT1), a NAD-dependent protein deacetylase, to deacetylate p53 and attenuated its transcriptional activation on PISD.	NAD	52-55	phosphatidylserine decarboxylase	Homo sapiens	155-159
31895696-3	2020	METHODS: Cell-free u-mtDNA, defined as copy number of mitochondrially-encoded NADH dehydrogenase-1 (MTND1) gene, was measured by real-time quantitative PCR and normalized to urine creatinine in cell-free urine samples from participants in the Subpopulations and Intermediate Outcome Measures in COPD Study (SPIROMICS) cohort.	NAD	78-82	mitochondrially encoded NADH dehydrogenase 1	Homo sapiens	100-105
31782485-4	2020	Proteins from the poly(ADP-ribose) polymerase (PARP) family, such as PARP1 and PARP2, use NAD+ as a substrate to catalyse the synthesis of polymeric chains consisting of ADP-ribose units covalently attached to an acceptor molecule.	NAD	90-93	poly(ADP-ribose) polymerase 1	Homo sapiens	47-51
31782485-4	2020	Proteins from the poly(ADP-ribose) polymerase (PARP) family, such as PARP1 and PARP2, use NAD+ as a substrate to catalyse the synthesis of polymeric chains consisting of ADP-ribose units covalently attached to an acceptor molecule.	NAD	90-93	poly(ADP-ribose) polymerase 1	Homo sapiens	69-74
31782485-4	2020	Proteins from the poly(ADP-ribose) polymerase (PARP) family, such as PARP1 and PARP2, use NAD+ as a substrate to catalyse the synthesis of polymeric chains consisting of ADP-ribose units covalently attached to an acceptor molecule.	NAD	90-93	poly(ADP-ribose) polymerase 2	Homo sapiens	79-84
32054506-4	2020	The associations between ERbeta and autophagy were detected in osteosarcoma U2-OS cells which were treated with E2, E2 + 2,3-Bis (4-hydroxyphenyl) propionitrile (DPN, ERbeta agonists), E2 + DPN + water, E2 + DPN + 3-Methyladenine (3-MA, autophagy inhibitor), respectively.	NAD	162-165	estrogen receptor 1	Homo sapiens	25-31
31816398-6	2020	Mitochondrial content and membrane potential were significantly reduced in response to H2O2 treatment, whereas activated NRF2-PPARalpha/AMPKalpha pathway by NAMPT overexpression rescued the mitochondrial membrane potential and content, suggesting that maintained mitochondrial content and integrity by NAMPT overexpression might be one of the key mechanisms to maintain mitochondrial NAD+ level and subsequently dictate cell survival under oxidative stress.	NAD	384-387	NFE2 like bZIP transcription factor 2	Homo sapiens	121-125
32054506-4	2020	The associations between ERbeta and autophagy were detected in osteosarcoma U2-OS cells which were treated with E2, E2 + 2,3-Bis (4-hydroxyphenyl) propionitrile (DPN, ERbeta agonists), E2 + DPN + water, E2 + DPN + 3-Methyladenine (3-MA, autophagy inhibitor), respectively.	NAD	190-193	estrogen receptor 1	Homo sapiens	25-31
32054506-4	2020	The associations between ERbeta and autophagy were detected in osteosarcoma U2-OS cells which were treated with E2, E2 + 2,3-Bis (4-hydroxyphenyl) propionitrile (DPN, ERbeta agonists), E2 + DPN + water, E2 + DPN + 3-Methyladenine (3-MA, autophagy inhibitor), respectively.	NAD	190-193	estrogen receptor 1	Homo sapiens	25-31
32054506-10	2020	In addition, DPN treatment upregulated the LC3II/I expression level and downregulated P62 and mTOR (mRNA level) and p-mTOR (protein level) expression levels.	NAD	13-16	mechanistic target of rapamycin kinase	Homo sapiens	94-98
32054506-10	2020	In addition, DPN treatment upregulated the LC3II/I expression level and downregulated P62 and mTOR (mRNA level) and p-mTOR (protein level) expression levels.	NAD	13-16	mechanistic target of rapamycin kinase	Homo sapiens	118-122
32042007-2	2020	Despite its role in DNA repair, AAG-initiated BER promotes cytotoxicity in a process dependent on poly (ADP-ribose) polymerase-1 (PARP-1); a NAD+-consuming enzyme activated by strand break intermediates of the AAG-initiated repair process.	NAD	141-144	poly(ADP-ribose) polymerase 1	Homo sapiens	98-128
32042007-2	2020	Despite its role in DNA repair, AAG-initiated BER promotes cytotoxicity in a process dependent on poly (ADP-ribose) polymerase-1 (PARP-1); a NAD+-consuming enzyme activated by strand break intermediates of the AAG-initiated repair process.	NAD	141-144	poly(ADP-ribose) polymerase 1	Homo sapiens	130-136
32046300-2	2020	PARP inhibitors, which inhibit PARylation through competitively binding to NAD+ binding site of PARP1 and PARP2, have improved clinical benefits for BRCA mutated tumors, leading to their accelerated clinical application.	NAD	75-78	poly(ADP-ribose) polymerase 1	Homo sapiens	0-4
32046300-2	2020	PARP inhibitors, which inhibit PARylation through competitively binding to NAD+ binding site of PARP1 and PARP2, have improved clinical benefits for BRCA mutated tumors, leading to their accelerated clinical application.	NAD	75-78	poly(ADP-ribose) polymerase 1	Homo sapiens	96-101
32046300-2	2020	PARP inhibitors, which inhibit PARylation through competitively binding to NAD+ binding site of PARP1 and PARP2, have improved clinical benefits for BRCA mutated tumors, leading to their accelerated clinical application.	NAD	75-78	poly(ADP-ribose) polymerase 2	Homo sapiens	106-111
31791580-2	2020	Nicotinamide phosphoribosyltransferase (NAMPT) catalyzes the rate-limiting step in the NAD+ biosynthesis pathway.	NAD	87-90	nicotinamide phosphoribosyltransferase	Mus musculus	0-38
31791580-2	2020	Nicotinamide phosphoribosyltransferase (NAMPT) catalyzes the rate-limiting step in the NAD+ biosynthesis pathway.	NAD	87-90	nicotinamide phosphoribosyltransferase	Mus musculus	40-45
32029763-6	2020	Furthermore, MID1 is associated with other trans-factors involved in NICOTINAMIDE ADENINE DINUCLEOTIDE HYDROGEN (NADH) DEHYDROGENASE SUBUNIT 2 (nad2) intron 1 splicing, and interacts directly with itself and MITOCHONDRIAL STABILITY FACTOR 1 (MTSF1).	NAD	69-89	NADH dehydrogenase subunit 2;hypothetical protein	Arabidopsis thaliana	144-148
31972266-1	2020	AIMS: Sirtuin 6 (Sirt6) is a NAD+-dependent deacetylase that plays a key role in DNA repair, inflammation and lipid regulation.	NAD	29-32	sirtuin 6	Mus musculus	6-15
31972266-1	2020	AIMS: Sirtuin 6 (Sirt6) is a NAD+-dependent deacetylase that plays a key role in DNA repair, inflammation and lipid regulation.	NAD	29-32	sirtuin 6	Mus musculus	17-22
31844879-8	2020	A homology model of C3larvinA with NADH and RhoA was built on the structure of the C3cer-NADH-RhoA complex which provided further evidence that C3larvinA is a C3-like toxin that shares an identical catalytic mechanism with C3cer from Bacillus cereus.	NAD	89-93	ras homolog family member A	Homo sapiens	94-98
31059816-4	2020	Nicotinamide phosphoribosyltransferase (NAMPT) is the most important NAD+ biosynthetic enzyme in mammalian cells and a direct target of the BRAF oncogenic signaling pathway.	NAD	69-73	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	140-144
31844879-8	2020	A homology model of C3larvinA with NADH and RhoA was built on the structure of the C3cer-NADH-RhoA complex which provided further evidence that C3larvinA is a C3-like toxin that shares an identical catalytic mechanism with C3cer from Bacillus cereus.	NAD	35-39	ras homolog family member A	Homo sapiens	94-98
31844879-8	2020	A homology model of C3larvinA with NADH and RhoA was built on the structure of the C3cer-NADH-RhoA complex which provided further evidence that C3larvinA is a C3-like toxin that shares an identical catalytic mechanism with C3cer from Bacillus cereus.	NAD	89-93	ras homolog family member A	Homo sapiens	44-48
31812668-6	2020	We also demonstrate that mutant p53 induces the expression of Sirtuin3 (SIRT3), a major mitochondrial NAD+-dependent deacetylase, stimulating MnSOD deacetylation and enzymatic activity.	NAD	102-105	tumor protein p53	Homo sapiens	32-35
31880924-4	2020	Catalysis of both NADH oxidation and lipophilic quinone reduction by membrane-bound NDH-2 followed the Michaelis-Menten model; however, the maximum turnover was only achieved when a high concentration of quinone (>3 mM) was present in the membrane, suggesting that quinone availability regulates NADH-coupled respiration activity.	NAD	18-22	DExH-box helicase 9	Homo sapiens	84-89
31880924-4	2020	Catalysis of both NADH oxidation and lipophilic quinone reduction by membrane-bound NDH-2 followed the Michaelis-Menten model; however, the maximum turnover was only achieved when a high concentration of quinone (>3 mM) was present in the membrane, suggesting that quinone availability regulates NADH-coupled respiration activity.	NAD	296-300	DExH-box helicase 9	Homo sapiens	84-89
31959836-0	2020	Extracellular NAD+ enhances PARP-dependent DNA repair capacity independently of CD73 activity.	NAD	14-17	poly(ADP-ribose) polymerase 1	Homo sapiens	28-32
31959836-2	2020	NAD+ levels also affect DNA repair capacity as NAD+ is a substrate for PARP-enzymes (mono/poly-ADP-ribosylation) and sirtuins (deacetylation).	NAD	0-3	poly(ADP-ribose) polymerase 1	Homo sapiens	71-75
31959836-2	2020	NAD+ levels also affect DNA repair capacity as NAD+ is a substrate for PARP-enzymes (mono/poly-ADP-ribosylation) and sirtuins (deacetylation).	NAD	47-50	poly(ADP-ribose) polymerase 1	Homo sapiens	71-75
31812668-6	2020	We also demonstrate that mutant p53 induces the expression of Sirtuin3 (SIRT3), a major mitochondrial NAD+-dependent deacetylase, stimulating MnSOD deacetylation and enzymatic activity.	NAD	102-105	sirtuin 3	Homo sapiens	62-70
31812668-6	2020	We also demonstrate that mutant p53 induces the expression of Sirtuin3 (SIRT3), a major mitochondrial NAD+-dependent deacetylase, stimulating MnSOD deacetylation and enzymatic activity.	NAD	102-105	sirtuin 3	Homo sapiens	72-77
32009904-10	2019	This effect was not observed in a control group (saline, N = 5) and was blocked when a 5-HT1 A antagonist (NAD-299) was administered with buspirone (N = 7).	NAD	107-110	5-hydroxytryptamine (serotonin) receptor 1A	Mus musculus	87-94
31761689-5	2020	More recently, SARM1 was found to execute degeneration by hydrolyzing NAD+.	NAD	70-73	sterile alpha and HEAT/Armadillo motif containing 1	Mus musculus	15-20
32009900-0	2019	Astrocytes and Microglia Are Resistant to NAD+-Mediated Cell Death Along the ARTC2/P2X7 Axis.	NAD	42-45	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	83-87
31947613-6	2020	Since Fbp2 oligomerization state and thus, its role is regulated by AMP and NAD+-crucial indicators of cellular metabolic conditions-we hypothesize that the Hif1alpha-dependent regulation of the metabolism in cancer is modulated through Fbp2, a sensor of the energy and redox state of a cell.	NAD	76-79	hypoxia inducible factor 1 subunit alpha	Homo sapiens	157-166
32009900-1	2019	ADP-ribosylation of the P2X7k splice variant on mouse T cells by Ecto-ADP-ribosyltransferase ARTC2.2 in response to its substrate extracellular nicotinamide adenine dinucleotide (NAD+) triggers cell death.	NAD	144-177	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	24-28
32009900-1	2019	ADP-ribosylation of the P2X7k splice variant on mouse T cells by Ecto-ADP-ribosyltransferase ARTC2.2 in response to its substrate extracellular nicotinamide adenine dinucleotide (NAD+) triggers cell death.	NAD	179-182	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	24-28
32009900-2	2019	Since NAD+ is released as a danger signal during tissue damage, this NAD+-induced cell death (NICD) may impact the survival of other cell populations co-expressing P2X7 and of one of the ARTC2 isoforms (ARTC2.1, ARTC2.2).	NAD	69-72	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	164-168
32079521-3	2020	In this work, a molecular dynamics model for the PARP-1 enzyme-substrate complex containing NAD+ molecule and the end of the poly(ADP-ribose) chain in the form of ADP molecule was obtained for the first time.	NAD	92-96	poly(ADP-ribose) polymerase 1	Homo sapiens	49-55
31879354-5	2020	Here, we show that NOC utilizes the dinucleotide NADP(H) as a substrate, removing the 2" phosphate to generate NAD(H), and is a direct regulator of oxidative stress response through its NADPH 2" phosphatase activity.	NAD	49-52	nocturnin	Homo sapiens	19-22
31914379-0	2020	The CD38/NAD/SIRTUIN1/EZH2 Axis Mitigates Cytotoxic CD8 T Cell Function and Identifies Patients with SLE Prone to Infections.	NAD	9-12	enhancer of zeste 2 polycomb repressive complex 2 subunit	Homo sapiens	22-26
31936501-5	2020	The activation of GPD1-mediated NAD+ regeneration in peroxisomes by GPD1 over-expression or activation of the malate-oxaloacetate NADH peroxisomal shuttle, by increasing flux in this NADH shuttle and over-expression of MDH3, resulted in lifespan extension of agc1Delta yeasts.	NAD	32-35	malate dehydrogenase MDH3	Saccharomyces cerevisiae S288C	219-223
31936501-5	2020	The activation of GPD1-mediated NAD+ regeneration in peroxisomes by GPD1 over-expression or activation of the malate-oxaloacetate NADH peroxisomal shuttle, by increasing flux in this NADH shuttle and over-expression of MDH3, resulted in lifespan extension of agc1Delta yeasts.	NAD	110-134	malate dehydrogenase MDH3	Saccharomyces cerevisiae S288C	219-223
31936501-5	2020	The activation of GPD1-mediated NAD+ regeneration in peroxisomes by GPD1 over-expression or activation of the malate-oxaloacetate NADH peroxisomal shuttle, by increasing flux in this NADH shuttle and over-expression of MDH3, resulted in lifespan extension of agc1Delta yeasts.	NAD	130-134	malate dehydrogenase MDH3	Saccharomyces cerevisiae S288C	219-223
31934345-8	2020	In this study, we report that NAD+ levels are reduced in the cochlea of CSB m/m mice and that short-term treatment (10 days) with the NAD+ precursor nicotinamide riboside (NR), prevents hearing loss, restores outer hair cell loss, and improves cochlear health in CSB m/m mice.	NAD	30-33	excision repair cross-complementing rodent repair deficiency, complementation group 6	Mus musculus	72-75
31934345-8	2020	In this study, we report that NAD+ levels are reduced in the cochlea of CSB m/m mice and that short-term treatment (10 days) with the NAD+ precursor nicotinamide riboside (NR), prevents hearing loss, restores outer hair cell loss, and improves cochlear health in CSB m/m mice.	NAD	134-137	excision repair cross-complementing rodent repair deficiency, complementation group 6	Mus musculus	263-266
31934345-13	2020	Intriguingly, NAD+ supplementation rescues reduced synaptic ribbon formation in both CSA -/- and CSB m/m mutant cochleae.	NAD	14-17	excision repair cross-complementing rodent repair deficiency, complementation group 6	Mus musculus	97-100
31936019-3	2020	Sirtuin 3 (SIRT3) is an NAD+-dependent deacetylase, which is important in regulating macroautophagy and lipid metabolism.	NAD	24-27	sirtuin 3	Homo sapiens	0-9
31936019-3	2020	Sirtuin 3 (SIRT3) is an NAD+-dependent deacetylase, which is important in regulating macroautophagy and lipid metabolism.	NAD	24-27	sirtuin 3	Homo sapiens	11-16
31625072-8	2020	In an FBA simulation, cells used respiratory terminal oxidases and two NADH dehydrogenases (NDH-1 and NDH-2) to balance the PSI and PSII excitations depending on the light conditions.	NAD	71-75	DExH-box helicase 9	Homo sapiens	102-107
32305562-3	2020	Sirtuin 6 (Sirt6), an NAD-dependent deacetylase, has been implicated in the fatty liver disease; however, the underlying molecular mechanisms in the NASH pathogenesis are elusive.	NAD	22-25	sirtuin 6	Mus musculus	0-9
32305562-3	2020	Sirtuin 6 (Sirt6), an NAD-dependent deacetylase, has been implicated in the fatty liver disease; however, the underlying molecular mechanisms in the NASH pathogenesis are elusive.	NAD	22-25	sirtuin 6	Mus musculus	11-16
31929756-7	2020	Thus, we hypothesized the aggregation of human SOD1 toxic protein and the fate of NSCs/NPCs in the ALS disease could be improved by the administration of nicotinamide riboside (NR), an NAD+ precursor.	NAD	185-189	superoxide dismutase 1	Homo sapiens	47-51
31676226-7	2020	We found that 8mg/kg DPN (ERbeta-specific agonist) replacement therapy (3 weeks) to the ovariectomized (OVX) mice significantly reduced ischemia injury and alleviated microglia and astrocyte activation, and markedly inhibited the expression of NF-kappaB and proinflammatory cytokines (TNF-alpha, IL-1beta, and IL-6).	NAD	21-24	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	244-253
31676226-7	2020	We found that 8mg/kg DPN (ERbeta-specific agonist) replacement therapy (3 weeks) to the ovariectomized (OVX) mice significantly reduced ischemia injury and alleviated microglia and astrocyte activation, and markedly inhibited the expression of NF-kappaB and proinflammatory cytokines (TNF-alpha, IL-1beta, and IL-6).	NAD	21-24	tumor necrosis factor	Mus musculus	285-294
31676226-7	2020	We found that 8mg/kg DPN (ERbeta-specific agonist) replacement therapy (3 weeks) to the ovariectomized (OVX) mice significantly reduced ischemia injury and alleviated microglia and astrocyte activation, and markedly inhibited the expression of NF-kappaB and proinflammatory cytokines (TNF-alpha, IL-1beta, and IL-6).	NAD	21-24	interleukin 1 beta	Mus musculus	296-304
31676226-7	2020	We found that 8mg/kg DPN (ERbeta-specific agonist) replacement therapy (3 weeks) to the ovariectomized (OVX) mice significantly reduced ischemia injury and alleviated microglia and astrocyte activation, and markedly inhibited the expression of NF-kappaB and proinflammatory cytokines (TNF-alpha, IL-1beta, and IL-6).	NAD	21-24	interleukin 6	Mus musculus	310-314
31676226-8	2020	Moreover, pretreatment (72 hours) with 10 nM DPN to the cell line of microglia (N9) or astrocyte (MA1800) significantly increased the cell viability and decreased the cell apoptosis and damage after OGD-R injury, and significantly inhibited the expression of NF-kappaB and proinflammatory cytokines.	NAD	45-48	nuclear factor kappa B subunit 1	Homo sapiens	259-268
31676226-9	2020	These results concluded that DPN replacement treatment alleviated the cerebral ischemia-reperfusion injury via inhibiting the activation of microglia and astrocyte and NF-kappaB mediated neruoinflammation.	NAD	29-32	nuclear factor kappa B subunit 1	Homo sapiens	168-177
32360040-2	2020	Collective evidence suggested that the activation of pulmonary nicotinamide adenine dinucleotide-dependent deacetylase sirtuin-1 (SIRT1) plays a critical role in inhibiting the production of reactive oxygen species (ROS) and tumor necrosis factor (TNF)-alpha, as well as the protection against ALI.	NAD	63-96	sirtuin 1	Rattus norvegicus	119-128
32360040-2	2020	Collective evidence suggested that the activation of pulmonary nicotinamide adenine dinucleotide-dependent deacetylase sirtuin-1 (SIRT1) plays a critical role in inhibiting the production of reactive oxygen species (ROS) and tumor necrosis factor (TNF)-alpha, as well as the protection against ALI.	NAD	63-96	sirtuin 1	Rattus norvegicus	130-135
32360040-2	2020	Collective evidence suggested that the activation of pulmonary nicotinamide adenine dinucleotide-dependent deacetylase sirtuin-1 (SIRT1) plays a critical role in inhibiting the production of reactive oxygen species (ROS) and tumor necrosis factor (TNF)-alpha, as well as the protection against ALI.	NAD	63-96	tumor necrosis factor	Rattus norvegicus	225-258
31892271-7	2019	The most active NAD+ analog against PARP-1 contained 5-iodouracil 2"-aminomethylmorpholino nucleoside with IC50 126 +- 6 muM, while in the case of PARP-2 it was adenine 2"-aminomethylmorpholino nucleoside (IC50 63 +- 10 muM).	NAD	16-20	poly(ADP-ribose) polymerase 1	Homo sapiens	36-42
31829559-4	2019	More recently, both PARP1 and PARP2 have been shown to bind to or be activated by RNA, a property that could interfere with the function of PARP1 and PARP2 in the response to DNA damage or lead to necrosis by depletion of cellular NAD+.	NAD	231-234	poly(ADP-ribose) polymerase 1	Homo sapiens	20-25
31829559-4	2019	More recently, both PARP1 and PARP2 have been shown to bind to or be activated by RNA, a property that could interfere with the function of PARP1 and PARP2 in the response to DNA damage or lead to necrosis by depletion of cellular NAD+.	NAD	231-234	poly(ADP-ribose) polymerase 2	Homo sapiens	30-35
31829559-4	2019	More recently, both PARP1 and PARP2 have been shown to bind to or be activated by RNA, a property that could interfere with the function of PARP1 and PARP2 in the response to DNA damage or lead to necrosis by depletion of cellular NAD+.	NAD	231-234	poly(ADP-ribose) polymerase 1	Homo sapiens	140-145
31829559-4	2019	More recently, both PARP1 and PARP2 have been shown to bind to or be activated by RNA, a property that could interfere with the function of PARP1 and PARP2 in the response to DNA damage or lead to necrosis by depletion of cellular NAD+.	NAD	231-234	poly(ADP-ribose) polymerase 2	Homo sapiens	150-155
31892271-9	2019	On the contrary, the adenine 2"-aminomethylmorpholino nucleoside-based NAD+ analogs were predicted to identify as PAR-analogs that target the acceptor binding site of PARP-2, representing a novel molecular mechanism for selective PARP inhibition.	NAD	71-75	poly(ADP-ribose) polymerase 2	Homo sapiens	167-173
31892271-7	2019	The most active NAD+ analog against PARP-1 contained 5-iodouracil 2"-aminomethylmorpholino nucleoside with IC50 126 +- 6 muM, while in the case of PARP-2 it was adenine 2"-aminomethylmorpholino nucleoside (IC50 63 +- 10 muM).	NAD	16-20	poly(ADP-ribose) polymerase 2	Homo sapiens	147-153
31892271-9	2019	On the contrary, the adenine 2"-aminomethylmorpholino nucleoside-based NAD+ analogs were predicted to identify as PAR-analogs that target the acceptor binding site of PARP-2, representing a novel molecular mechanism for selective PARP inhibition.	NAD	71-75	poly(ADP-ribose) polymerase 1	Homo sapiens	167-171
31599159-3	2019	Here, we report that ARH1, ARH3 and macrodomain proteins i.e. MacroD1, MacroD2, C6orf130 (TARG1), Af1521, hydrolyzed alpha-NAD+ but not beta-NAD+.	NAD	117-126	O-acyl-ADP-ribose deacylase 1	Homo sapiens	80-88
31599159-3	2019	Here, we report that ARH1, ARH3 and macrodomain proteins i.e. MacroD1, MacroD2, C6orf130 (TARG1), Af1521, hydrolyzed alpha-NAD+ but not beta-NAD+.	NAD	117-126	O-acyl-ADP-ribose deacylase 1	Homo sapiens	90-95
31599159-0	2019	The ARH and Macrodomain Families of alpha-ADP-ribose-acceptor Hydrolases Catalyze alpha-NAD+ Hydrolysis.	NAD	82-91	low density lipoprotein receptor adaptor protein 1	Homo sapiens	4-7
31920721-9	2019	In particular, higher production of reactive oxygen species deriving from a variety of enzymatic sources, including uncoupled endothelial nitric oxide synthase and the electron transport chain, causes DNA damage and activates the NAD+-consuming enzymes polyADP-ribose polymerase 1 (PARP1).	NAD	230-233	poly(ADP-ribose) polymerase 1	Homo sapiens	253-280
31920721-9	2019	In particular, higher production of reactive oxygen species deriving from a variety of enzymatic sources, including uncoupled endothelial nitric oxide synthase and the electron transport chain, causes DNA damage and activates the NAD+-consuming enzymes polyADP-ribose polymerase 1 (PARP1).	NAD	230-233	poly(ADP-ribose) polymerase 1	Homo sapiens	282-287
31920721-9	2019	In particular, higher production of reactive oxygen species deriving from a variety of enzymatic sources, including uncoupled endothelial nitric oxide synthase and the electron transport chain, causes DNA damage and activates the NAD+-consuming enzymes polyADP-ribose polymerase 1 (PARP1).	NAD	230-233	nitric oxide synthase 3	Homo sapiens	126-159
31808750-5	2019	Learning and memory, synaptic proteins, the NAD+/ NADH ratios, and ATP production were significantly lower in ApoE4 mice as well.	NAD	44-47	apolipoprotein E	Homo sapiens	110-115
31930280-1	2019	Post-translational modification of proteins by ADP-ribosylation, catalysed by poly (ADP-ribose) polymerases (PARPs) using NAD+ as a substrate, plays central roles in DNA damage signalling and repair, modulates a range of cellular signalling cascades and initiates programmed cell death by parthanatos.	NAD	122-125	poly(ADP-ribose) polymerase 1	Homo sapiens	109-114
31808750-5	2019	Learning and memory, synaptic proteins, the NAD+/ NADH ratios, and ATP production were significantly lower in ApoE4 mice as well.	NAD	50-54	apolipoprotein E	Homo sapiens	110-115
31141164-2	2019	Nicotinamide phosphoribosyltransferase (NAMPT) is an essential enzyme catalyzing nicotinamide adenine dinucleotide biosynthesis and is important for tumor metabolism.	NAD	81-114	nicotinamide phosphoribosyltransferase	Mus musculus	0-38
31796734-5	2019	Specifically, oxidative lesions promote direct binding of Banf1 to PARP1, a critical NAD+-dependent DNA repair protein, leading to inhibition of PARP1 auto-ADP-ribosylation and defective repair of oxidative lesions, in cells with increased Banf1.	NAD	85-88	BAF nuclear assembly factor 1	Homo sapiens	58-63
31796734-5	2019	Specifically, oxidative lesions promote direct binding of Banf1 to PARP1, a critical NAD+-dependent DNA repair protein, leading to inhibition of PARP1 auto-ADP-ribosylation and defective repair of oxidative lesions, in cells with increased Banf1.	NAD	85-88	poly(ADP-ribose) polymerase 1	Homo sapiens	67-72
31796734-5	2019	Specifically, oxidative lesions promote direct binding of Banf1 to PARP1, a critical NAD+-dependent DNA repair protein, leading to inhibition of PARP1 auto-ADP-ribosylation and defective repair of oxidative lesions, in cells with increased Banf1.	NAD	85-88	poly(ADP-ribose) polymerase 1	Homo sapiens	145-150
31796734-5	2019	Specifically, oxidative lesions promote direct binding of Banf1 to PARP1, a critical NAD+-dependent DNA repair protein, leading to inhibition of PARP1 auto-ADP-ribosylation and defective repair of oxidative lesions, in cells with increased Banf1.	NAD	85-88	BAF nuclear assembly factor 1	Homo sapiens	240-245
31141164-2	2019	Nicotinamide phosphoribosyltransferase (NAMPT) is an essential enzyme catalyzing nicotinamide adenine dinucleotide biosynthesis and is important for tumor metabolism.	NAD	81-114	nicotinamide phosphoribosyltransferase	Mus musculus	40-45
31702813-7	2019	Administration of NAD+ may also increase the expression of the key protein NAMPT and its related protein sirtuin 1 as well as the synthesis of NAD+.	NAD	18-22	nicotinamide phosphoribosyltransferase	Mus musculus	75-80
31674899-6	2019	Subsequently, in vivo and in vitro studies were used to show that PduT-C38S and PduT-C38A variants increased the diffusion of 1,2-propanediol, propionaldehyde, NAD+ and NADH across the shell of the MCP.	NAD	160-163	CD46 molecule	Homo sapiens	198-201
31674899-6	2019	Subsequently, in vivo and in vitro studies were used to show that PduT-C38S and PduT-C38A variants increased the diffusion of 1,2-propanediol, propionaldehyde, NAD+ and NADH across the shell of the MCP.	NAD	169-173	CD46 molecule	Homo sapiens	198-201
31674899-8	2019	Thus, genetic modification offers an approach to engineering the movement of larger molecules (such as NAD/H) across MCP shells, as well as a method for blocking transport through trimeric bacterial microcompartment (BMC) domain shell proteins.	NAD	103-106	CD46 molecule	Homo sapiens	117-120
31702813-5	2019	As a result of this treatment, the expression of NAMPT decreased, the synthesis of ATP and NAD+ became insufficient and the NAD+/NADH ratio was reduced.	NAD	124-128	nicotinamide phosphoribosyltransferase	Mus musculus	49-54
31702813-5	2019	As a result of this treatment, the expression of NAMPT decreased, the synthesis of ATP and NAD+ became insufficient and the NAD+/NADH ratio was reduced.	NAD	129-133	nicotinamide phosphoribosyltransferase	Mus musculus	49-54
31702813-8	2019	Therefore, increasing NAMPT expression levels may promote NAD+ production.	NAD	58-62	nicotinamide phosphoribosyltransferase	Mus musculus	22-27
31850237-0	2019	Group A Streptococcus NAD-Glycohydrolase Inhibits Caveolin 1-Mediated Internalization Into Human Epithelial Cells.	NAD	22-25	caveolin 1	Homo sapiens	50-60
31767171-8	2019	Despite the minor structural difference, we found that NRH uses different steps and enzymes to synthesize NAD+, thus revealing a new NRK1-independent pathway for NAD+ synthesis.	NAD	106-109	nicotinamide riboside kinase 1	Homo sapiens	133-137
31767171-8	2019	Despite the minor structural difference, we found that NRH uses different steps and enzymes to synthesize NAD+, thus revealing a new NRK1-independent pathway for NAD+ synthesis.	NAD	162-165	nicotinamide riboside kinase 1	Homo sapiens	133-137
31487495-2	2019	In oxidative genotoxic conditions, PARP1 activity is enhanced significantly, leading to excessive depletion of nicotinamide adenine dinucleotide (NAD+) and mitochondrial dysfunction.	NAD	111-144	poly(ADP-ribose) polymerase 1	Homo sapiens	35-40
31487495-2	2019	In oxidative genotoxic conditions, PARP1 activity is enhanced significantly, leading to excessive depletion of nicotinamide adenine dinucleotide (NAD+) and mitochondrial dysfunction.	NAD	146-150	poly(ADP-ribose) polymerase 1	Homo sapiens	35-40
31487495-3	2019	We hypothesized that PARP1-induced NAD+ depletion inhibits NAD+-dependent sirtuin deacetylase activity, thereby interfering with the mitochondrial regulator, peroxisome proliferator-activated receptor gamma coactivator-1alpha (PGC-1alpha).	NAD	35-39	poly(ADP-ribose) polymerase 1	Homo sapiens	21-26
31487495-3	2019	We hypothesized that PARP1-induced NAD+ depletion inhibits NAD+-dependent sirtuin deacetylase activity, thereby interfering with the mitochondrial regulator, peroxisome proliferator-activated receptor gamma coactivator-1alpha (PGC-1alpha).	NAD	35-39	PPARG coactivator 1 alpha	Homo sapiens	227-237
31487495-3	2019	We hypothesized that PARP1-induced NAD+ depletion inhibits NAD+-dependent sirtuin deacetylase activity, thereby interfering with the mitochondrial regulator, peroxisome proliferator-activated receptor gamma coactivator-1alpha (PGC-1alpha).	NAD	59-63	poly(ADP-ribose) polymerase 1	Homo sapiens	21-26
31487495-3	2019	We hypothesized that PARP1-induced NAD+ depletion inhibits NAD+-dependent sirtuin deacetylase activity, thereby interfering with the mitochondrial regulator, peroxisome proliferator-activated receptor gamma coactivator-1alpha (PGC-1alpha).	NAD	59-63	PPARG coactivator 1 alpha	Homo sapiens	227-237
31675930-9	2019	Functionally, miR-154 inhibited the NAD salvage pathway leading to a remarkable decrease in cell viability and increased rate of cell death.	NAD	36-39	microRNA 154	Homo sapiens	14-21
31399301-6	2019	It was found that sirtuin 6 (SIRT6), a nicotinamide adenine dinucleotide+ (NAD+)-dependent histone deacetylase, was down-regulated during ECs aging.	NAD	39-72	sirtuin 6	Mus musculus	18-27
31399301-6	2019	It was found that sirtuin 6 (SIRT6), a nicotinamide adenine dinucleotide+ (NAD+)-dependent histone deacetylase, was down-regulated during ECs aging.	NAD	39-72	sirtuin 6	Mus musculus	29-34
31589435-3	2019	We demonstrate that the chemical modification of protein with QPN, a ligand that could be reduced by tumor cell-specific NAD(P)H dehydrogenase [quinone] 1 (NQO1), is reversible in the presence of NQO1.	NAD	121-128	NAD(P)H quinone dehydrogenase 1	Homo sapiens	156-160
31589435-3	2019	We demonstrate that the chemical modification of protein with QPN, a ligand that could be reduced by tumor cell-specific NAD(P)H dehydrogenase [quinone] 1 (NQO1), is reversible in the presence of NQO1.	NAD	121-128	NAD(P)H quinone dehydrogenase 1	Homo sapiens	196-200
31694884-3	2019	Accordingly, we generated and analyzed adipocyte-specific nicotinamide phosphoribosyltransferase (Nampt) knockout (ANKO) and brown adipocyte-specific Nampt knockout (BANKO) mice because NAMPT is the rate-limiting NAD+ biosynthetic enzyme.	NAD	213-216	nicotinamide phosphoribosyltransferase	Mus musculus	186-191
31694884-5	2019	In addition, the absence of NAMPT in WAT markedly reduced adrenergic-mediated lipolytic activity, likely through inactivation of the NAD+-SIRT1-caveolin-1 axis, which limits an important fuel source fatty acid for BAT thermogenesis.	NAD	133-136	nicotinamide phosphoribosyltransferase	Mus musculus	28-33
31694884-6	2019	These metabolic abnormalities were rescued by treatment with nicotinamide mononucleotide (NMN), which bypasses the block in NAD+ synthesis induced by NAMPT deficiency.	NAD	124-127	nicotinamide phosphoribosyltransferase	Mus musculus	150-155
31694884-9	2019	These results demonstrate that adipose NAMPT-mediated NAD+ biosynthesis is essential for regulating adaptive thermogenesis, lipolysis, and whole-body energy metabolism.	NAD	54-57	nicotinamide phosphoribosyltransferase	Mus musculus	39-44
31675930-11	2019	CONCLUSIONS: It was concluded that the inhibition of NAD production by miR-154 might be introduced as an appropriate therapeutic approach in order to improve breast cancer outcome either alone or in combination with other conventional chemotherapeutic agents.	NAD	53-56	microRNA 154	Homo sapiens	71-78
31276316-2	2019	CPR shows a stringent preference for NADPH over the less expensive cofactor, NADH, economically limiting its use as a biocatalyst.	NAD	77-81	cytochrome p450 oxidoreductase	Homo sapiens	0-3
31276316-3	2019	The complexity of cofactor-linked CPR protein dynamics and the incomplete understanding of the interaction of CPR with both cofactors and electron acceptors present challenges for the successful rational engineering of a CPR with enhanced activity with NADH.	NAD	253-257	cytochrome p450 oxidoreductase	Homo sapiens	34-37
31276316-3	2019	The complexity of cofactor-linked CPR protein dynamics and the incomplete understanding of the interaction of CPR with both cofactors and electron acceptors present challenges for the successful rational engineering of a CPR with enhanced activity with NADH.	NAD	253-257	cytochrome p450 oxidoreductase	Homo sapiens	110-113
31276316-3	2019	The complexity of cofactor-linked CPR protein dynamics and the incomplete understanding of the interaction of CPR with both cofactors and electron acceptors present challenges for the successful rational engineering of a CPR with enhanced activity with NADH.	NAD	253-257	cytochrome p450 oxidoreductase	Homo sapiens	110-113
31276316-4	2019	Here, we report a rational evolution approach to enhance the activity of CPR with NADH, in which mutations were introduced into the NADPH-binding flavin adenine dinucleotide (FAD) domain.	NAD	82-86	cytochrome p450 oxidoreductase	Homo sapiens	73-76
31276316-5	2019	Multiple CPR mutants that used NADH more effectively than the wild-type CPR in the reduction of the surrogate electron acceptor, cytochrome c were found.	NAD	31-35	cytochrome p450 oxidoreductase	Homo sapiens	9-12
31276316-5	2019	Multiple CPR mutants that used NADH more effectively than the wild-type CPR in the reduction of the surrogate electron acceptor, cytochrome c were found.	NAD	31-35	cytochrome p450 oxidoreductase	Homo sapiens	72-75
31276316-5	2019	Multiple CPR mutants that used NADH more effectively than the wild-type CPR in the reduction of the surrogate electron acceptor, cytochrome c were found.	NAD	31-35	cytochrome c, somatic	Homo sapiens	129-141
31657440-4	2019	This was confirmed by the finding that recombinant mouse PNPO oxidized 6-NADH and 6-NADPH with catalytic efficiencies comparable to those observed with pyridoxine- and pyridoxamine-5"-phosphate.	NAD	71-77	pyridoxine 5'-phosphate oxidase	Mus musculus	57-61
31439642-6	2019	Moreover, Sarm1 gene deficiency attenuates intraepidermal nerve fiber loss in footpad skin; alleviates axon degeneration, the change of g-ratio in sciatic nerves, and NAD+ decrease; and relieves axonal outgrowth retardation of dorsal root ganglia from diabetic mice.	NAD	167-171	sterile alpha and HEAT/Armadillo motif containing 1	Mus musculus	10-15
31548671-5	2019	Moreover, complex 1 and NADH synergistically photoreduce cytochrome c under hypoxia.	NAD	24-28	cytochrome c, somatic	Homo sapiens	57-69
31539774-7	2019	In agreement with these observations, we found that PARP-1 was massively activated during ZIKV infection and the intracellular ATP and NAD+ concentrations rapidly declined.	NAD	135-139	poly(ADP-ribose) polymerase 1	Homo sapiens	52-58
31400709-1	2019	The enzyme nicotinamide phosphoribosyltransferase is both a key intracellular enzyme for NAD biosynthesis (iNAMPT) and an extracellular cytokine (eNAMPT).	NAD	89-92	nicotinamide phosphoribosyltransferase	Mus musculus	11-49
29728703-0	2019	NAD+ cellular redox and SIRT1 regulate the diurnal rhythms of tyrosine hydroxylase and conditioned cocaine reward.	NAD	0-4	tyrosine hydroxylase	Homo sapiens	62-82
31550162-4	2019	Treatment of (TrL)Co with a stoichiometric amount of 1-azidoadamantane (AdN3) furnished a three-coordinate, diamagnetic CoIII imide (TrL)Co(NAd) as confirmed by single-crystal X-ray diffraction, revealing a rare trigonal pyramidal geometry with an acute Co-Nimido-C angle 145.0(3) .	NAD	140-143	mitochondrially encoded cytochrome c oxidase III	Homo sapiens	120-125
31665043-7	2019	We further demonstrated that when expressed in human control fibroblasts, AtNDA2 shows an affinity for NADH oxidation similar to that of CI, thus competing with CI for the oxidation of NADH as opposed to our initial hypothesis.	NAD	103-107	alternative NAD(P)H dehydrogenase 2	Arabidopsis thaliana	74-80
31665043-7	2019	We further demonstrated that when expressed in human control fibroblasts, AtNDA2 shows an affinity for NADH oxidation similar to that of CI, thus competing with CI for the oxidation of NADH as opposed to our initial hypothesis.	NAD	185-189	alternative NAD(P)H dehydrogenase 2	Arabidopsis thaliana	74-80
31628378-2	2019	Transmembrane electron transfer via the Mtr pathway has been well characterized, however, the role of NADH dehydrogenases in feeding electrons to Mtr has been only minimally studied in S. oneidensis MR-1.	NAD	102-106	tryptophan permease	Shewanella oneidensis MR-1	146-149
31624074-3	2019	The level of NAD+ and Sir2 expression upregulate the transcriptional activity of PGC-1alpha.	NAD	13-16	spargel	Drosophila melanogaster	81-91
31624074-10	2019	Therefore, we declared that exercise training could improve lipotoxic cardiomyopathy induced by a HFD or cardiac dSir2 knockdown in old Drosophila The NAD+/dSIR2/PGC-1alpha pathway activation was an important molecular mechanism of exercise resistance against lipotoxic cardiomyopathy.	NAD	151-154	spargel	Drosophila melanogaster	162-172
31749697-3	2019	Electron transfer in POR occurs from NADH to FAD to FMN, and the flexible hinge region in POR is essential for domain movements to bring the FAD and FMN close together for electron transfer.	NAD	37-41	cytochrome p450 oxidoreductase	Homo sapiens	21-24
31749697-3	2019	Electron transfer in POR occurs from NADH to FAD to FMN, and the flexible hinge region in POR is essential for domain movements to bring the FAD and FMN close together for electron transfer.	NAD	37-41	cytochrome p450 oxidoreductase	Homo sapiens	90-93
31679124-12	2019	The cerebromicrovascular protective effects of pharmacological inhibition of PARP-1 highlight the preventive and therapeutic potential of treatments that restore NAD+ homeostasis as effective interventions in patients at risk for vascular cognitive impairment (VCI).	NAD	162-166	poly(ADP-ribose) polymerase 1	Homo sapiens	77-83
31681271-0	2019	Switch of NAD Salvage to de novo Biosynthesis Sustains SIRT1-RelB-Dependent Inflammatory Tolerance.	NAD	10-13	RELB proto-oncogene, NF-kB subunit	Homo sapiens	61-65
31681271-7	2019	Inhibition of IDO1 activity predominantly decreased nuclear NAD level, which promoted sequential dissociations of immunosuppressive SIRT1 and RelB from the promoter of pro-inflammatory TNF-alpha gene and broke endotoxin tolerance.	NAD	60-63	RELB proto-oncogene, NF-kB subunit	Homo sapiens	142-146
31681271-7	2019	Inhibition of IDO1 activity predominantly decreased nuclear NAD level, which promoted sequential dissociations of immunosuppressive SIRT1 and RelB from the promoter of pro-inflammatory TNF-alpha gene and broke endotoxin tolerance.	NAD	60-63	tumor necrosis factor	Homo sapiens	185-194
31347918-2	2019	Nicotinamide phosphoribosyl-transferase (Nampt) is a rate-limiting enzyme in the salvage pathway of NAD synthesis.	NAD	100-103	nicotinamide phosphoribosyltransferase	Mus musculus	0-39
31347918-2	2019	Nicotinamide phosphoribosyl-transferase (Nampt) is a rate-limiting enzyme in the salvage pathway of NAD synthesis.	NAD	100-103	nicotinamide phosphoribosyltransferase	Mus musculus	41-46
31347918-6	2019	The NAD level declined in Nampt+/- mice under PO (Wild: 377, Nampt+/-: 119 (pmol/mg tissue), p=0.028).	NAD	4-7	nicotinamide phosphoribosyltransferase	Mus musculus	26-31
31347918-6	2019	The NAD level declined in Nampt+/- mice under PO (Wild: 377, Nampt+/-: 119 (pmol/mg tissue), p=0.028).	NAD	4-7	nicotinamide phosphoribosyltransferase	Mus musculus	61-66
31347918-7	2019	In cultured cardiomyocytes, Nampt knockdown diminished mitochondrial NAD content and ATP production (relative ATP production: Wild:1, Nampt knockdown: 0.56, p=0.0068), suggesting that downregulation of Nampt induces mitochondrial dysfunction.	NAD	69-72	nicotinamide phosphoribosyltransferase	Mus musculus	28-33
31347918-8	2019	On the other hand, the NAD level was increased in Tg-Nampt mice at baseline but not during PO, possibly due to increased consumption of NAD by Sirt1.	NAD	23-26	nicotinamide phosphoribosyltransferase	Mus musculus	53-58
31347918-8	2019	On the other hand, the NAD level was increased in Tg-Nampt mice at baseline but not during PO, possibly due to increased consumption of NAD by Sirt1.	NAD	136-139	nicotinamide phosphoribosyltransferase	Mus musculus	53-58
30993413-5	2019	A recent study has uncovered a putative cross-regulation between the de novo NAD+ biosynthesis and copper homeostasis mediated by a copper-sensing transcription factor Mac1.	NAD	77-81	Mac1p	Saccharomyces cerevisiae S288C	168-172
30993413-6	2019	Mac1 appears to work with the Hst1-Sum1-Rfm1 complex to repress the expression of de novo NAD+ biosynthesis genes.	NAD	90-94	Mac1p	Saccharomyces cerevisiae S288C	0-4
31132363-1	2019	We identified a homozygous missense mutation in the gene encoding NAD synthesizing enzyme NMNAT2 in two siblings with childhood onset polyneuropathy with erythromelalgia.	NAD	66-69	nicotinamide nucleotide adenylyltransferase 2	Homo sapiens	90-96
31136762-13	2019	SIGNIFICANCE: Nicotinamide Mononucleotide Adenylyltransferase 2 (NMNAT2) both synthesizes the electron carrier Nicotinamide Adenine Dinucleotide (NAD+) and acts a protein chaperone.	NAD	111-144	nicotinamide nucleotide adenylyltransferase 2	Homo sapiens	14-63
31136762-13	2019	SIGNIFICANCE: Nicotinamide Mononucleotide Adenylyltransferase 2 (NMNAT2) both synthesizes the electron carrier Nicotinamide Adenine Dinucleotide (NAD+) and acts a protein chaperone.	NAD	111-144	nicotinamide nucleotide adenylyltransferase 2	Homo sapiens	65-71
31136762-13	2019	SIGNIFICANCE: Nicotinamide Mononucleotide Adenylyltransferase 2 (NMNAT2) both synthesizes the electron carrier Nicotinamide Adenine Dinucleotide (NAD+) and acts a protein chaperone.	NAD	146-150	nicotinamide nucleotide adenylyltransferase 2	Homo sapiens	14-63
31136762-13	2019	SIGNIFICANCE: Nicotinamide Mononucleotide Adenylyltransferase 2 (NMNAT2) both synthesizes the electron carrier Nicotinamide Adenine Dinucleotide (NAD+) and acts a protein chaperone.	NAD	146-150	nicotinamide nucleotide adenylyltransferase 2	Homo sapiens	65-71
31636635-2	2019	There, high extracellular levels of nucleotides, mainly NAD+ and ATP, are catabolized by different ectonucleotidases, which can be divided in two families according to substrate specificity: on one side those that metabolize NAD+, including CD38, CD157, and CD203a; on the other, those that convert ATP, namely CD39 (and other ENTPDases) and CD73.	NAD	56-60	bone marrow stromal cell antigen 1	Homo sapiens	247-252
31636635-2	2019	There, high extracellular levels of nucleotides, mainly NAD+ and ATP, are catabolized by different ectonucleotidases, which can be divided in two families according to substrate specificity: on one side those that metabolize NAD+, including CD38, CD157, and CD203a; on the other, those that convert ATP, namely CD39 (and other ENTPDases) and CD73.	NAD	225-229	bone marrow stromal cell antigen 1	Homo sapiens	247-252
31309731-1	2019	AIM: Nicotinamide Nucleotide Transhydrogenase (NNT) gene encodes a protein, which is an important antioxidative enzyme that converts NADH to NADPH.	NAD	133-137	nicotinamide nucleotide transhydrogenase	Homo sapiens	5-45
31309731-1	2019	AIM: Nicotinamide Nucleotide Transhydrogenase (NNT) gene encodes a protein, which is an important antioxidative enzyme that converts NADH to NADPH.	NAD	133-137	nicotinamide nucleotide transhydrogenase	Homo sapiens	47-50
31295065-3	2019	As quercetin activates PGC-1alpha through Sirtuin-1, an NAD+-dependent deacetylase, the depleted NAD+ in dystrophic skeletal muscle may limit quercetin efficacy, hence, supplementation with the NAD+ donor, nicotinamide riboside (NR), may facilitate quercetin efficacy.	NAD	56-59	PPARG coactivator 1 alpha	Homo sapiens	23-33
31401381-2	2019	Sirtuin6 (SIRT6), a NAD+-dependent class III histone deacetylase, participates in the regulation of cellular inflammation.	NAD	20-23	sirtuin 6	Mus musculus	0-8
31401381-2	2019	Sirtuin6 (SIRT6), a NAD+-dependent class III histone deacetylase, participates in the regulation of cellular inflammation.	NAD	20-23	sirtuin 6	Mus musculus	10-15
31295065-3	2019	As quercetin activates PGC-1alpha through Sirtuin-1, an NAD+-dependent deacetylase, the depleted NAD+ in dystrophic skeletal muscle may limit quercetin efficacy, hence, supplementation with the NAD+ donor, nicotinamide riboside (NR), may facilitate quercetin efficacy.	NAD	56-60	PPARG coactivator 1 alpha	Homo sapiens	23-33
31575956-7	2019	Antioxidant enzymes transcriptionally regulated by Nrf2 and involved in GSH, NADPH, and NADH generation were significantly lower including PRX1 and PRX3, GPX4, GSTP1, GCLC, and MTHFD2.	NAD	88-92	NFE2 like bZIP transcription factor 2	Homo sapiens	51-55
31337671-6	2019	Using our unique absolute quantitation, we found that P-AscH- mediated the overactivation of PARP1, which results in consumption of NAD+, and subsequently depletion of ATP leading to mitotic cell death.	NAD	132-136	poly(ADP-ribose) polymerase 1	Homo sapiens	93-98
31337671-10	2019	Genetic deletion and pharmacologic inhibition of PARP1 preserved both NAD+ and ATP; however, the toxicity of P-AscH- remained.	NAD	70-74	poly(ADP-ribose) polymerase 1	Homo sapiens	49-54
31292999-1	2019	Sirtuin-1 and -3 (SIRT1 and SIRT3) are important nicotinamide adenine dinucleotide (NAD+ )-dependent deacetylases known to regulate a variety of cellular functions.	NAD	49-82	sirtuin 3	Homo sapiens	28-33
31292999-1	2019	Sirtuin-1 and -3 (SIRT1 and SIRT3) are important nicotinamide adenine dinucleotide (NAD+ )-dependent deacetylases known to regulate a variety of cellular functions.	NAD	84-87	sirtuin 3	Homo sapiens	28-33
30661231-5	2019	Inhibition of NAD+ degrading enzymes, poly-ADP-ribose polymerase 1 (PARP1) and ectoenzyme CD38, following brain ischemic insult can provide neuroprotection.	NAD	14-18	poly(ADP-ribose) polymerase 1	Homo sapiens	38-66
30661231-5	2019	Inhibition of NAD+ degrading enzymes, poly-ADP-ribose polymerase 1 (PARP1) and ectoenzyme CD38, following brain ischemic insult can provide neuroprotection.	NAD	14-18	poly(ADP-ribose) polymerase 1	Homo sapiens	68-73
31065944-0	2019	PGC-1alpha, Sirtuins and PARPs in Huntington"s Disease and Other Neurodegenerative Conditions: NAD+ to Rule Them All.	NAD	95-99	PPARG coactivator 1 alpha	Homo sapiens	0-10
31575956-7	2019	Antioxidant enzymes transcriptionally regulated by Nrf2 and involved in GSH, NADPH, and NADH generation were significantly lower including PRX1 and PRX3, GPX4, GSTP1, GCLC, and MTHFD2.	NAD	88-92	paired related homeobox 1	Homo sapiens	139-143
31575956-10	2019	Cell viability, ROS, NADPH, NADH, and ATP levels were fully rescued by TRPM2 and partially by Nrf2.	NAD	28-32	NFE2 like bZIP transcription factor 2	Homo sapiens	94-98
31393480-5	2019	The complexes displayed a quasi-reversible Co(i)/Co(ii) redox couple at ~-1.1 V and an irreversible Co(ii)/Co(iii) couple at ~1.3 V vs. Ag/AgCl in DMF-0.1 M [Bun4N](ClO4).	NAD	43-48	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	49-55
31276581-2	2019	In CSB-deficient cells, poly (ADP ribose) polymerase (PARP) is persistently activated by unrepaired DNA damage and consumes and depletes cellular nicotinamide adenine dinucleotide, which leads to mitochondrial dysfunction.	NAD	146-179	ERCC excision repair 6, chromatin remodeling factor	Homo sapiens	3-6
31276581-2	2019	In CSB-deficient cells, poly (ADP ribose) polymerase (PARP) is persistently activated by unrepaired DNA damage and consumes and depletes cellular nicotinamide adenine dinucleotide, which leads to mitochondrial dysfunction.	NAD	146-179	poly(ADP-ribose) polymerase 1	Homo sapiens	24-52
31276581-2	2019	In CSB-deficient cells, poly (ADP ribose) polymerase (PARP) is persistently activated by unrepaired DNA damage and consumes and depletes cellular nicotinamide adenine dinucleotide, which leads to mitochondrial dysfunction.	NAD	146-179	poly(ADP-ribose) polymerase 1	Homo sapiens	54-58
31607329-9	2019	After treatment, the expressions of TLR2, TLR4, TLR6 and HMGB in CR and NAD groups was significantly lower than that before treatment (P<0.05), while the expressions levels of TLR2, TLR4, TLR6 and HMGB in AD and RD groups were no statistically significant different from those before treatment (P<0.05); the expressions levels of TLR2, TLR4, TLR6 and HMGB in dealth group all were higher than those in survival group (P<0.05).	NAD	72-75	toll like receptor 2	Homo sapiens	36-40
31607329-9	2019	After treatment, the expressions of TLR2, TLR4, TLR6 and HMGB in CR and NAD groups was significantly lower than that before treatment (P<0.05), while the expressions levels of TLR2, TLR4, TLR6 and HMGB in AD and RD groups were no statistically significant different from those before treatment (P<0.05); the expressions levels of TLR2, TLR4, TLR6 and HMGB in dealth group all were higher than those in survival group (P<0.05).	NAD	72-75	toll like receptor 6	Homo sapiens	48-52
31607329-9	2019	After treatment, the expressions of TLR2, TLR4, TLR6 and HMGB in CR and NAD groups was significantly lower than that before treatment (P<0.05), while the expressions levels of TLR2, TLR4, TLR6 and HMGB in AD and RD groups were no statistically significant different from those before treatment (P<0.05); the expressions levels of TLR2, TLR4, TLR6 and HMGB in dealth group all were higher than those in survival group (P<0.05).	NAD	72-75	toll like receptor 2	Homo sapiens	176-180
31607329-9	2019	After treatment, the expressions of TLR2, TLR4, TLR6 and HMGB in CR and NAD groups was significantly lower than that before treatment (P<0.05), while the expressions levels of TLR2, TLR4, TLR6 and HMGB in AD and RD groups were no statistically significant different from those before treatment (P<0.05); the expressions levels of TLR2, TLR4, TLR6 and HMGB in dealth group all were higher than those in survival group (P<0.05).	NAD	72-75	toll like receptor 6	Homo sapiens	188-192
31607329-9	2019	After treatment, the expressions of TLR2, TLR4, TLR6 and HMGB in CR and NAD groups was significantly lower than that before treatment (P<0.05), while the expressions levels of TLR2, TLR4, TLR6 and HMGB in AD and RD groups were no statistically significant different from those before treatment (P<0.05); the expressions levels of TLR2, TLR4, TLR6 and HMGB in dealth group all were higher than those in survival group (P<0.05).	NAD	72-75	toll like receptor 2	Homo sapiens	176-180
31607329-9	2019	After treatment, the expressions of TLR2, TLR4, TLR6 and HMGB in CR and NAD groups was significantly lower than that before treatment (P<0.05), while the expressions levels of TLR2, TLR4, TLR6 and HMGB in AD and RD groups were no statistically significant different from those before treatment (P<0.05); the expressions levels of TLR2, TLR4, TLR6 and HMGB in dealth group all were higher than those in survival group (P<0.05).	NAD	72-75	toll like receptor 6	Homo sapiens	188-192
30607371-9	2018	NAD + depletion reversibly inhibits cytosolic GAPDH activity, but retains mitochondrial oxidative metabolism, suggesting differential effects of this treatment on sub-cellular pyridine pools.	NAD	0-5	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	46-51
31390283-0	2019	NAD+ consumption by PARP1 in response to DNA damage triggers metabolic shift critical for damaged cell survival.	NAD	0-4	poly(ADP-ribose) polymerase 1	Homo sapiens	20-25
31390283-4	2019	Using the phasor approach to fluorescence lifetime imaging microscopy and fluorescence-based biosensors in combination with laser microirradiation, we found a rapid cell-wide increase of the bound NADH fraction in response to nuclear DNA damage, which is triggered by PARP-dependent NAD+ depletion.	NAD	197-201	poly(ADP-ribose) polymerase 1	Homo sapiens	268-272
31390283-4	2019	Using the phasor approach to fluorescence lifetime imaging microscopy and fluorescence-based biosensors in combination with laser microirradiation, we found a rapid cell-wide increase of the bound NADH fraction in response to nuclear DNA damage, which is triggered by PARP-dependent NAD+ depletion.	NAD	283-287	poly(ADP-ribose) polymerase 1	Homo sapiens	268-272
31320478-2	2019	Hepatocyte-specific knockout of the NAD+-synthesizing enzyme nicotinamide phosphoribosyltransferase (NAMPT) reduces liver NAD+ levels, but the metabolic phenotype of Nampt-deficient hepatocytes in mice is unknown.	NAD	36-40	nicotinamide phosphoribosyltransferase	Mus musculus	101-106
31583043-5	2019	Sirt1 is an NAD+-dependent deacetylase, and we showed that the expression of Sirt1 was decreased in NP tissues, while hyperglycaemia could suppress the expression and activity of Sirt1 in NP cells.	NAD	12-15	sirtuin 1	Rattus norvegicus	0-5
31583043-5	2019	Sirt1 is an NAD+-dependent deacetylase, and we showed that the expression of Sirt1 was decreased in NP tissues, while hyperglycaemia could suppress the expression and activity of Sirt1 in NP cells.	NAD	12-15	sirtuin 1	Rattus norvegicus	77-82
31583043-5	2019	Sirt1 is an NAD+-dependent deacetylase, and we showed that the expression of Sirt1 was decreased in NP tissues, while hyperglycaemia could suppress the expression and activity of Sirt1 in NP cells.	NAD	12-15	sirtuin 1	Rattus norvegicus	77-82
31320478-2	2019	Hepatocyte-specific knockout of the NAD+-synthesizing enzyme nicotinamide phosphoribosyltransferase (NAMPT) reduces liver NAD+ levels, but the metabolic phenotype of Nampt-deficient hepatocytes in mice is unknown.	NAD	36-40	nicotinamide phosphoribosyltransferase	Mus musculus	166-171
31320478-2	2019	Hepatocyte-specific knockout of the NAD+-synthesizing enzyme nicotinamide phosphoribosyltransferase (NAMPT) reduces liver NAD+ levels, but the metabolic phenotype of Nampt-deficient hepatocytes in mice is unknown.	NAD	122-126	nicotinamide phosphoribosyltransferase	Mus musculus	101-106
31320478-4	2019	Using the Cre-LoxP system, we generated hepatocyte-specific Nampt knockout (HNKO) mice, having a 50% reduction of liver NAD+ levels.	NAD	120-124	nicotinamide phosphoribosyltransferase	Mus musculus	60-65
31320478-10	2019	We conclude that NAMPT-deficient hepatocytes can maintain substantial NAD+ levels and that the Nampt knockout has only minor consequences for mitochondrial function in the mouse liver.	NAD	70-74	nicotinamide phosphoribosyltransferase	Mus musculus	17-22
31257855-5	2019	Once activated by the specific DNA, PARP-1 cleaves nicotinamideadenine dinucleotide (NAD+) into nicotinamide and ADP-ribose to synthesize a hyperbranched poly(ADP-ribose) polymer.	NAD	85-89	poly(ADP-ribose) polymerase 1	Homo sapiens	36-42
31422819-9	2019	GOT2, a member of the malate-aspartate shuttle, plays an essential role in the intracellular NAD(H) redox balance.	NAD	93-99	glutamatic-oxaloacetic transaminase 2, mitochondrial	Mus musculus	0-4
31257855-5	2019	Once activated by the specific DNA, PARP-1 cleaves nicotinamideadenine dinucleotide (NAD+) into nicotinamide and ADP-ribose to synthesize a hyperbranched poly(ADP-ribose) polymer.	NAD	51-83	poly(ADP-ribose) polymerase 1	Homo sapiens	36-42
31278893-0	2019	Exogenous nicotinamide adenine dinucleotide administration alleviates ischemia/reperfusion-induced oxidative injury in isolated rat hearts via Sirt5-SDH-succinate pathway.	NAD	10-43	sirtuin 5	Rattus norvegicus	143-148
31278893-3	2019	Silent information regulator 5 (Sirt5), a nicotinamide adenine dinucleotide (NAD)-dependent desuccinylase, desuccinylates and inactivates SDH thus exerting a protective effect on the myocardium.	NAD	42-75	sirtuin 5	Rattus norvegicus	0-30
31278893-3	2019	Silent information regulator 5 (Sirt5), a nicotinamide adenine dinucleotide (NAD)-dependent desuccinylase, desuccinylates and inactivates SDH thus exerting a protective effect on the myocardium.	NAD	42-75	sirtuin 5	Rattus norvegicus	32-37
31278893-3	2019	Silent information regulator 5 (Sirt5), a nicotinamide adenine dinucleotide (NAD)-dependent desuccinylase, desuccinylates and inactivates SDH thus exerting a protective effect on the myocardium.	NAD	77-80	sirtuin 5	Rattus norvegicus	0-30
31278893-3	2019	Silent information regulator 5 (Sirt5), a nicotinamide adenine dinucleotide (NAD)-dependent desuccinylase, desuccinylates and inactivates SDH thus exerting a protective effect on the myocardium.	NAD	77-80	sirtuin 5	Rattus norvegicus	32-37
31278893-4	2019	This research was designed to investigate whether exogenous NAD protects the myocardium from the ischemia-reperfusion-induced oxidative injury through regulating Sirt5-SDH pathway and succinate metabolism.	NAD	60-63	sirtuin 5	Rattus norvegicus	162-167
31278893-11	2019	Utilizing co-immunoprecipitation method, we found that NAD administration promoted the Sirt5 and SDH-a interaction and decreased the succinylation level of SDH-a.	NAD	55-58	sirtuin 5	Rattus norvegicus	87-92
31278893-12	2019	These results implied that exogenous NAD administration promoted Sirt5-mediated SDH-a desuccinylation and decreased the activity of SDH-a, which attenuated the succinate accumulation during ischemia and its depleting rate during reperfusion and finally alleviated reactive oxygen species generation.	NAD	37-40	sirtuin 5	Rattus norvegicus	65-70
30833708-1	2019	Nicotinamide phosphoribosyltransferase (Nampt) is the rate-limiting enzyme of nicotinamide adenine dinucleotide (NAD) salvage biosynthesis in mammals, and is involved in fundamental physiological processes and pathophysiology of many diseases.	NAD	78-111	nicotinamide phosphoribosyltransferase	Mus musculus	0-38
31551807-0	2019	CD38 Deficiency Alleviates D-Galactose-Induced Myocardial Cell Senescence Through NAD+/Sirt1 Signaling Pathway.	NAD	82-85	CD38 molecule	Rattus norvegicus	0-4
31551807-12	2019	Taken together, our results demonstrated that CD38 knockdown alleviated D-gal induced cell senescence and oxidative stress via NAD+/Sirt1 signaling pathway.	NAD	127-130	CD38 molecule	Rattus norvegicus	46-50
31551807-12	2019	Taken together, our results demonstrated that CD38 knockdown alleviated D-gal induced cell senescence and oxidative stress via NAD+/Sirt1 signaling pathway.	NAD	127-130	sirtuin 1	Rattus norvegicus	132-137
30833708-1	2019	Nicotinamide phosphoribosyltransferase (Nampt) is the rate-limiting enzyme of nicotinamide adenine dinucleotide (NAD) salvage biosynthesis in mammals, and is involved in fundamental physiological processes and pathophysiology of many diseases.	NAD	78-111	nicotinamide phosphoribosyltransferase	Mus musculus	40-45
30833708-1	2019	Nicotinamide phosphoribosyltransferase (Nampt) is the rate-limiting enzyme of nicotinamide adenine dinucleotide (NAD) salvage biosynthesis in mammals, and is involved in fundamental physiological processes and pathophysiology of many diseases.	NAD	113-116	nicotinamide phosphoribosyltransferase	Mus musculus	0-38
30833708-1	2019	Nicotinamide phosphoribosyltransferase (Nampt) is the rate-limiting enzyme of nicotinamide adenine dinucleotide (NAD) salvage biosynthesis in mammals, and is involved in fundamental physiological processes and pathophysiology of many diseases.	NAD	113-116	nicotinamide phosphoribosyltransferase	Mus musculus	40-45
30880062-0	2019	Non-NAD-like PARP-1 inhibitors in prostate cancer treatment.	NAD	4-7	poly(ADP-ribose) polymerase 1	Homo sapiens	13-19
30880062-2	2019	Because histone-dependent activation is unique to PARP-1, non-NAD-like PARP-1 inhibitors have the potential to bypass the off-target effects of classical NAD-dependent PARP-1 inhibitors, such as olaparib, veliparib, and rucaparib.	NAD	62-65	poly(ADP-ribose) polymerase 1	Homo sapiens	71-77
30936015-4	2019	The radioactivity of [32P]NAD+ was incorporated into human ADH1 by human poly(ADP-ribose) polymerase 1 in vitro, but was not incorporated when heat-inactivated PARP1 or a PARP inhibitor, 3-aminobenzamide, was used.	NAD	26-30	poly(ADP-ribose) polymerase 1	Homo sapiens	73-102
30880062-2	2019	Because histone-dependent activation is unique to PARP-1, non-NAD-like PARP-1 inhibitors have the potential to bypass the off-target effects of classical NAD-dependent PARP-1 inhibitors, such as olaparib, veliparib, and rucaparib.	NAD	62-65	poly(ADP-ribose) polymerase 1	Homo sapiens	71-77
30936015-4	2019	The radioactivity of [32P]NAD+ was incorporated into human ADH1 by human poly(ADP-ribose) polymerase 1 in vitro, but was not incorporated when heat-inactivated PARP1 or a PARP inhibitor, 3-aminobenzamide, was used.	NAD	26-30	poly(ADP-ribose) polymerase 1	Homo sapiens	160-164
30880062-2	2019	Because histone-dependent activation is unique to PARP-1, non-NAD-like PARP-1 inhibitors have the potential to bypass the off-target effects of classical NAD-dependent PARP-1 inhibitors, such as olaparib, veliparib, and rucaparib.	NAD	154-157	poly(ADP-ribose) polymerase 1	Homo sapiens	71-77
30880062-2	2019	Because histone-dependent activation is unique to PARP-1, non-NAD-like PARP-1 inhibitors have the potential to bypass the off-target effects of classical NAD-dependent PARP-1 inhibitors, such as olaparib, veliparib, and rucaparib.	NAD	154-157	poly(ADP-ribose) polymerase 1	Homo sapiens	71-77
30880062-5	2019	In contrast to NAD-like PARP-1 inhibitors, non-NAD-like PARP-1 inhibitors demonstrated efficacy against androgen-dependent and -independent routes of androgen receptor signaling activation.	NAD	47-50	poly(ADP-ribose) polymerase 1	Homo sapiens	56-62
30880062-5	2019	In contrast to NAD-like PARP-1 inhibitors, non-NAD-like PARP-1 inhibitors demonstrated efficacy against androgen-dependent and -independent routes of androgen receptor signaling activation.	NAD	47-50	androgen receptor	Homo sapiens	150-167
31366990-3	2019	Here, we demonstrate that NADH:ubiquinone oxidoreductase subunit AB1 (NDUFAB1), also known as mitochondrial acyl carrier protein, acts as a powerful cardio-protector by conferring greater capacity and efficiency of mitochondrial energy metabolism.	NAD	26-30	NADH:ubiquinone oxidoreductase subunit AB1	Mus musculus	70-77
31276434-3	2019	Meanwhile, poly (ADP-ribose) polymerase 1 (PARP1) utilizes nicotinamide adenine dinucleotide (NAD+) to repair DNA damage.	NAD	59-92	LOW QUALITY PROTEIN: poly [ADP-ribose] polymerase 1	Oryctolagus cuniculus	11-41
31276434-3	2019	Meanwhile, poly (ADP-ribose) polymerase 1 (PARP1) utilizes nicotinamide adenine dinucleotide (NAD+) to repair DNA damage.	NAD	59-92	LOW QUALITY PROTEIN: poly [ADP-ribose] polymerase 1	Oryctolagus cuniculus	43-48
31276434-3	2019	Meanwhile, poly (ADP-ribose) polymerase 1 (PARP1) utilizes nicotinamide adenine dinucleotide (NAD+) to repair DNA damage.	NAD	94-98	LOW QUALITY PROTEIN: poly [ADP-ribose] polymerase 1	Oryctolagus cuniculus	11-41
31276434-3	2019	Meanwhile, poly (ADP-ribose) polymerase 1 (PARP1) utilizes nicotinamide adenine dinucleotide (NAD+) to repair DNA damage.	NAD	94-98	LOW QUALITY PROTEIN: poly [ADP-ribose] polymerase 1	Oryctolagus cuniculus	43-48
31276434-4	2019	PARP1 overactivation results in excessive NAD+ consumption in the presence of pathological DNA damage.	NAD	42-46	LOW QUALITY PROTEIN: poly [ADP-ribose] polymerase 1	Oryctolagus cuniculus	0-5
31276434-5	2019	PJ34 is a PARP1 inhibitor that attenuates cellular NAD+ depletion and can prevent endothelial dysfunction.	NAD	51-55	LOW QUALITY PROTEIN: poly [ADP-ribose] polymerase 1	Oryctolagus cuniculus	10-15
31383716-6	2019	The role of mitochondrial ROS in lysosome dysfunction and M1 macrophage polarization is also demonstrated in mitochondrial complex I defective RAW 264.7 cells induced by silencing NADH:ubiquinone oxidoreductase subunit-S4 (Ndufs4).	NAD	180-184	NADH:ubiquinone oxidoreductase core subunit S4	Mus musculus	223-229
31462775-2	2019	NNT catalyses the transfer of a hydride between NADH and NADP+, coupled to the translocation of one proton across the membrane.	NAD	48-52	nicotinamide nucleotide transhydrogenase	Homo sapiens	0-3
31387164-6	2019	Structural comparisons between NAD+bound GAPDH and MMF-bound GAPDH revealed that the covalently linked MMF can block the binding of the NAD+ cosubstrate due to steric hindrance of the nicotinamide portion of the NAD+ molecule, illuminating the specific mechanism by which MMF inhibits GAPDH.	NAD	31-35	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	41-46
31387164-6	2019	Structural comparisons between NAD+bound GAPDH and MMF-bound GAPDH revealed that the covalently linked MMF can block the binding of the NAD+ cosubstrate due to steric hindrance of the nicotinamide portion of the NAD+ molecule, illuminating the specific mechanism by which MMF inhibits GAPDH.	NAD	136-140	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	41-46
31387164-6	2019	Structural comparisons between NAD+bound GAPDH and MMF-bound GAPDH revealed that the covalently linked MMF can block the binding of the NAD+ cosubstrate due to steric hindrance of the nicotinamide portion of the NAD+ molecule, illuminating the specific mechanism by which MMF inhibits GAPDH.	NAD	136-140	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	61-66
31387164-6	2019	Structural comparisons between NAD+bound GAPDH and MMF-bound GAPDH revealed that the covalently linked MMF can block the binding of the NAD+ cosubstrate due to steric hindrance of the nicotinamide portion of the NAD+ molecule, illuminating the specific mechanism by which MMF inhibits GAPDH.	NAD	136-140	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	61-66
31387164-6	2019	Structural comparisons between NAD+bound GAPDH and MMF-bound GAPDH revealed that the covalently linked MMF can block the binding of the NAD+ cosubstrate due to steric hindrance of the nicotinamide portion of the NAD+ molecule, illuminating the specific mechanism by which MMF inhibits GAPDH.	NAD	136-140	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	41-46
31387164-6	2019	Structural comparisons between NAD+bound GAPDH and MMF-bound GAPDH revealed that the covalently linked MMF can block the binding of the NAD+ cosubstrate due to steric hindrance of the nicotinamide portion of the NAD+ molecule, illuminating the specific mechanism by which MMF inhibits GAPDH.	NAD	136-140	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	61-66
31387164-6	2019	Structural comparisons between NAD+bound GAPDH and MMF-bound GAPDH revealed that the covalently linked MMF can block the binding of the NAD+ cosubstrate due to steric hindrance of the nicotinamide portion of the NAD+ molecule, illuminating the specific mechanism by which MMF inhibits GAPDH.	NAD	136-140	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	61-66
31378753-3	2019	It has been reported previously that the process of cell isolation from parotid glands triggers stress signaling mediated by Src and p38 mitogen-activated protein (MAP) kinase (p38), leading to dedifferentiation of acinar cells, and that an nicotinamide adenine dinucleotide phosphate (NADPH) oxidase inhibitor suppresses this activation of Src and p38, suggesting that reactive oxygen species initiate the dedifferentiation signal.	NAD	241-274	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	341-344
32055310-5	2019	This strategy is demonstrated using a PA probe designed for a tumor biomarker, human NAD(P)H: quinone oxidoreductase isozyme 1 (hNQO1), which affords high contrast and excellent sensitivity for PA detection and imaging of hNQO1 in living cells and animals.	NAD	85-92	NAD(P)H quinone dehydrogenase 1	Homo sapiens	128-133
32055310-5	2019	This strategy is demonstrated using a PA probe designed for a tumor biomarker, human NAD(P)H: quinone oxidoreductase isozyme 1 (hNQO1), which affords high contrast and excellent sensitivity for PA detection and imaging of hNQO1 in living cells and animals.	NAD	85-92	NAD(P)H quinone dehydrogenase 1	Homo sapiens	222-227
31374572-5	2019	Increased catalase activities, NADH/NAD+ ratio and contents of several metals, especially potassium, were observed by YCR102C overexpression under acetic acid stress.	NAD	31-35	uncharacterized protein	Saccharomyces cerevisiae S288C	118-125
31374572-5	2019	Increased catalase activities, NADH/NAD+ ratio and contents of several metals, especially potassium, were observed by YCR102C overexpression under acetic acid stress.	NAD	36-40	uncharacterized protein	Saccharomyces cerevisiae S288C	118-125
31248988-5	2019	A popular mouse model of mitochondrial disease that lacks NADH:ubiquinone oxidoreductase subunit S4 (NDUFS4), a subunit of mitochondrial complex I, phenocopies many traits of the human disease Leigh syndrome, including the development of optic atrophy.	NAD	58-62	NADH:ubiquinone oxidoreductase core subunit S4	Mus musculus	101-107
31680596-1	2019	Context: Sirtuin-3 (Sirt3), a NAD-dependent deacetylase, has been reported to be involved in many biological processes.Objective: The present study aimed to investigate the effect and mechanism of Sirt3 on diabetic mice and human umbilical vein endothelial cells (HUVECs) under high glucose (HG) condition.Materials and methods: HUVECs were cultured under HG and inflammation pathway was determined via qPCR, western blots, and immunofluorescence.Results: Sirt3 expression was reduced in the progression of diabetic nephropathy.	NAD	30-33	sirtuin 3	Homo sapiens	197-202
31415077-9	2019	The replenishment of NMN or NAD+ partially slowed down corneal nerve fiber degeneration, reduced the epithelial defect in denervated mice, and improved apoptosis induction in FK866-treated cells by restoring the activation levels of SIRT1, AKT, and CREB.	NAD	28-32	thymoma viral proto-oncogene 1	Mus musculus	240-243
31415077-9	2019	The replenishment of NMN or NAD+ partially slowed down corneal nerve fiber degeneration, reduced the epithelial defect in denervated mice, and improved apoptosis induction in FK866-treated cells by restoring the activation levels of SIRT1, AKT, and CREB.	NAD	28-32	cAMP responsive element binding protein 1	Mus musculus	249-253
31447696-1	2019	NAD+-dependent SIRT4 has been reported to be a key regulator of metabolic enzymes and antioxidant defense mechanisms in mitochondria.	NAD	0-4	sirtuin 4	Homo sapiens	15-20
31447857-7	2019	The P2Y11 receptor agonist ATPgammaS and NAD+ could independently stimulate the production of IL-8 in M2 macrophages, however, only the ATPgammaS-induced response was mediated by P2Y11 receptor.	NAD	41-45	C-X-C motif chemokine ligand 8	Homo sapiens	94-98
31204283-4	2019	Increasing circulating eNAMPT levels in aged mice by adipose-tissue-specific overexpression of NAMPT increases NAD+ levels in multiple tissues, thereby enhancing their functions and extending healthspan in female mice.	NAD	111-115	nicotinamide phosphoribosyltransferase	Mus musculus	24-29
31103013-5	2019	PARP-1 were activated under the function of activated dsDNA, as a result, branched polymers of ADP-ribose (PAR) with plentiful negative charge were formed in the presence of nicotinamide adenine dinucleotide (NAD+).	NAD	174-207	poly(ADP-ribose) polymerase 1	Homo sapiens	0-6
31103013-5	2019	PARP-1 were activated under the function of activated dsDNA, as a result, branched polymers of ADP-ribose (PAR) with plentiful negative charge were formed in the presence of nicotinamide adenine dinucleotide (NAD+).	NAD	209-213	poly(ADP-ribose) polymerase 1	Homo sapiens	0-6
31055111-2	2019	Silent information regulator 3 (Sirtuin3 or SIRT3) is a NAD-dependent deacetylase that regulates metabolic process.	NAD	56-59	sirtuin 3	Homo sapiens	32-40
31055111-2	2019	Silent information regulator 3 (Sirtuin3 or SIRT3) is a NAD-dependent deacetylase that regulates metabolic process.	NAD	56-59	sirtuin 3	Homo sapiens	44-49
30958623-2	2019	Sirtuin 3 (SIRT3), a mitochondrially localized member of NAD+ -dependent deacetylase has been shown to protect hepatocytes against the oxidative stress.	NAD	57-60	sirtuin 3	Homo sapiens	0-9
30958623-2	2019	Sirtuin 3 (SIRT3), a mitochondrially localized member of NAD+ -dependent deacetylase has been shown to protect hepatocytes against the oxidative stress.	NAD	57-60	sirtuin 3	Homo sapiens	11-16
31257865-0	2019	The Zebrafish Cytochrome b5/Cytochrome b5 Reductase/NADH System Efficiently Reduces Cytoglobins 1 and 2: Conserved Activity of Cytochrome b5/Cytochrome b5 Reductases during Vertebrate Evolution.	NAD	52-56	cytochrome b5 type A (microsomal)	Danio rerio	14-27
31324777-8	2019	Small molecule NAMPT activators such as SBI-797812 are a pioneering approach to raise intracellular NAD+ and realize its associated salutary effects.	NAD	100-104	nicotinamide phosphoribosyltransferase	Mus musculus	15-20
31257865-0	2019	The Zebrafish Cytochrome b5/Cytochrome b5 Reductase/NADH System Efficiently Reduces Cytoglobins 1 and 2: Conserved Activity of Cytochrome b5/Cytochrome b5 Reductases during Vertebrate Evolution.	NAD	52-56	cytochrome b5 type A (microsomal)	Danio rerio	28-41
31257865-0	2019	The Zebrafish Cytochrome b5/Cytochrome b5 Reductase/NADH System Efficiently Reduces Cytoglobins 1 and 2: Conserved Activity of Cytochrome b5/Cytochrome b5 Reductases during Vertebrate Evolution.	NAD	52-56	cytochrome b5 type A (microsomal)	Danio rerio	28-41
31257865-0	2019	The Zebrafish Cytochrome b5/Cytochrome b5 Reductase/NADH System Efficiently Reduces Cytoglobins 1 and 2: Conserved Activity of Cytochrome b5/Cytochrome b5 Reductases during Vertebrate Evolution.	NAD	52-56	cytochrome b5 type A (microsomal)	Danio rerio	28-41
31287140-5	2019	The ubiquitin-independent proteasome pathway regulates the stability of Polbeta in the cytosol via interaction between Polbeta and NAD(P)H quinone dehydrogenase 1 (NQO1) in an NADH-dependent manner.	NAD	176-180	NAD(P)H quinone dehydrogenase 1	Homo sapiens	131-162
31247812-4	2019	Electrochemical as well as spectroscopic investigations in CH3CN coupled to density functional theory (DFT) calculations point to decoordination of one of the amine upon reduction of Co(II) to the low-valent "Co(I)" form.	NAD	209-214	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	183-189
31129062-1	2019	Nuclear poly(ADP-ribose) polymerases 1 and 2 (PARP1 and PARP2) catalyze the synthesis of poly(ADP-ribose) (PAR) and use NAD+ as a substrate for the polymer synthesis.	NAD	120-124	poly(ADP-ribose) polymerase 1	Homo sapiens	8-44
31129062-1	2019	Nuclear poly(ADP-ribose) polymerases 1 and 2 (PARP1 and PARP2) catalyze the synthesis of poly(ADP-ribose) (PAR) and use NAD+ as a substrate for the polymer synthesis.	NAD	120-124	poly(ADP-ribose) polymerase 1	Homo sapiens	46-51
31129062-1	2019	Nuclear poly(ADP-ribose) polymerases 1 and 2 (PARP1 and PARP2) catalyze the synthesis of poly(ADP-ribose) (PAR) and use NAD+ as a substrate for the polymer synthesis.	NAD	120-124	poly(ADP-ribose) polymerase 2	Homo sapiens	56-61
33365629-3	2019	Excluding tRNA sequences, sequence divergence rate was lowest in rRNA genes and highest in genes encoding NADH (specifically ND1, ND2, ND3) and the control region.	NAD	106-110	mitochondrially encoded NADH dehydrogenase 1	Homo sapiens	125-128
31287140-5	2019	The ubiquitin-independent proteasome pathway regulates the stability of Polbeta in the cytosol via interaction between Polbeta and NAD(P)H quinone dehydrogenase 1 (NQO1) in an NADH-dependent manner.	NAD	176-180	NAD(P)H quinone dehydrogenase 1	Homo sapiens	164-168
31282472-8	2019	The structures also afford a structural explanation for the unusual ability of Ncb5or to utilize both NADH and NADPH, and represent the first examples of native, fully oxidized b5R family members in which the nicotinamide ring of NAD(P)+ resides in the active site.	NAD	102-106	cytochrome b5 reductase 4	Homo sapiens	79-85
29723660-2	2019	SIRT1, a NAD+-dependent protein deacetylase, deacetylates the p65 of NF-kappaB and shows protective effects in kidney disorders.	NAD	9-12	nuclear factor kappa B subunit 1	Homo sapiens	69-78
31073968-0	2019	Palmitic Acid-Induced NAD+ Depletion is Associated with the Reduced Function of SIRT1 and Increased Expression of BACE1 in Hippocampal Neurons.	NAD	22-26	beta-secretase 1	Homo sapiens	114-119
31053044-0	2019	NAD metabolites interfere with proliferation and functional properties of THP-1 cells.	NAD	0-3	GLI family zinc finger 2	Homo sapiens	74-79
31053044-8	2019	Our data show that the NAD metabolites interfere with early events associated with differentiation of THP-1 cells along the monocytic path and that they affect LPS-induced biological responses of the cell line.	NAD	23-26	GLI family zinc finger 2	Homo sapiens	102-107
30936458-3	2019	In this study, we report that lactate uptake alters the NAD+/NADH ratio in the cancer cells, which culminates with SIRT1-dependent PGC-1alpha activation and subsequent enhancement of mitochondrial mass and activity.	NAD	56-60	PPARG coactivator 1 alpha	Homo sapiens	131-141
30936458-3	2019	In this study, we report that lactate uptake alters the NAD+/NADH ratio in the cancer cells, which culminates with SIRT1-dependent PGC-1alpha activation and subsequent enhancement of mitochondrial mass and activity.	NAD	61-65	PPARG coactivator 1 alpha	Homo sapiens	131-141
31216043-1	2019	ADP-ribosylation is a reversible chemical modification catalysed by ADP-ribosyltransferases such as PARPs that utilize nicotinamide adenine dinucleotide (NAD+) as a cofactor to transfer monomer or polymers of ADP-ribose nucleotide onto macromolecular targets such as proteins and DNA.	NAD	119-152	poly(ADP-ribose) polymerase family member 10	Homo sapiens	100-105
31216043-1	2019	ADP-ribosylation is a reversible chemical modification catalysed by ADP-ribosyltransferases such as PARPs that utilize nicotinamide adenine dinucleotide (NAD+) as a cofactor to transfer monomer or polymers of ADP-ribose nucleotide onto macromolecular targets such as proteins and DNA.	NAD	154-158	poly(ADP-ribose) polymerase family member 10	Homo sapiens	100-105
30841754-4	2019	We now show that increasing total NAD+ content in astrocytes leads to the activation of the transcription factor nuclear factor, erythroid-derived 2, like 2 (Nfe2l2 or Nrf2) and up-regulation of the antioxidant proteins heme oxygenase 1 (HO-1) and sulfiredoxin 1 (SRXN1).	NAD	34-38	NFE2 like bZIP transcription factor 2	Homo sapiens	113-156
31175267-0	2019	Nicotinamide phosphoribosyltransferase postpones rat bone marrow mesenchymal stem cell senescence by mediating NAD+-Sirt1 signaling.	NAD	111-115	sirtuin 1	Rattus norvegicus	116-121
31175267-9	2019	Thus, Nampt suppresses MSC senescence via mediating NAD+-Sirt1 signaling.	NAD	52-56	sirtuin 1	Rattus norvegicus	57-62
30948509-8	2019	Studies to identify its biochemical mechanism of action showed that it does not inhibit NAD+ consumption, suggesting that it acts as a biochemical precursor to NAD+ Cell lysates possess an ATP-dependent kinase activity that efficiently converts NRH to the compound NMNH, but independent of Nrk1 or Nrk2.	NAD	160-164	nicotinamide riboside kinase 1	Homo sapiens	290-294
31134256-6	2019	PEG-HCCs accelerated the reduction of resazurin (a test indicator of mitochondrial viability) and cytochrome c by NADH and ascorbic acid in solution.	NAD	114-118	cytochrome c, somatic	Homo sapiens	98-110
31134256-8	2019	Electron paramagnetic resonance demonstrated NADH increased the magnitude of PEG-HCCs" intrinsic radical, which then reduced upon subsequent addition of cytochrome c or resazurin.	NAD	45-49	cytochrome c, somatic	Homo sapiens	153-165
31275331-0	2019	Calmodulin Is the Fundamental Regulator of NADK-Mediated NAD Signaling in Plants.	NAD	43-46	calmodulin 1	Homo sapiens	0-10
31275331-4	2019	In addition, the two respective derivatives from NAD+ (substrate of NADK) and NADP+ (product of NADK), cyclic ADP-ribose (cADPR) and nicotinic acid adenine dinucleotide phosphate (NAADP), have been considered to be the important messengers for intracellular Ca2+ homeostasis which could finally influence the combination between CaM and NADK, forming a feedback regulation mechanism.	NAD	49-53	calmodulin 1	Homo sapiens	329-332
31185608-2	2019	Interleukin-1beta (IL-1beta) has been shown to induce the upregulation of MMP-9 through nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX)-reactive oxygen species (ROS)-dependent signaling pathways.	NAD	88-121	interleukin 1 beta	Rattus norvegicus	0-17
31185608-2	2019	Interleukin-1beta (IL-1beta) has been shown to induce the upregulation of MMP-9 through nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX)-reactive oxygen species (ROS)-dependent signaling pathways.	NAD	88-121	interleukin 1 beta	Rattus norvegicus	19-27
30951610-3	2019	In the second basic protocol, experimental methods are detailed for the production of recombinant human NRK1 and NMNAT1 to catalyze conversion of S-NR to S-NAD+ .	NAD	156-160	nicotinamide riboside kinase 1	Homo sapiens	104-108
30841754-4	2019	We now show that increasing total NAD+ content in astrocytes leads to the activation of the transcription factor nuclear factor, erythroid-derived 2, like 2 (Nfe2l2 or Nrf2) and up-regulation of the antioxidant proteins heme oxygenase 1 (HO-1) and sulfiredoxin 1 (SRXN1).	NAD	34-38	NFE2 like bZIP transcription factor 2	Homo sapiens	158-164
30841754-4	2019	We now show that increasing total NAD+ content in astrocytes leads to the activation of the transcription factor nuclear factor, erythroid-derived 2, like 2 (Nfe2l2 or Nrf2) and up-regulation of the antioxidant proteins heme oxygenase 1 (HO-1) and sulfiredoxin 1 (SRXN1).	NAD	34-38	NFE2 like bZIP transcription factor 2	Homo sapiens	168-172
30879903-3	2019	Identified via complementary biochemical, organellar, and cellular approaches, we report that MDM2 negatively regulates NADH:ubiquinone oxidoreductase 75 kDa Fe-S protein 1 (NDUFS1), leading to decreased mitochondrial respiration, marked oxidative stress, and commitment to the mitochondrial pathway of apoptosis.	NAD	120-124	NADH:ubiquinone oxidoreductase core subunit S1	Mus musculus	174-180
31140365-4	2019	A recent report links these processes, such that decreased NAD+ levels associated with aging may attenuate the SASP potentially reducing its pathological effect.	NAD	59-63	aspartic peptidase retroviral like 1	Homo sapiens	111-115
31140365-10	2019	On the contrary, the lower NAD+ levels may attenuate SASP, decreasing the pathological influence of senescence.	NAD	27-31	aspartic peptidase retroviral like 1	Homo sapiens	53-57
30973715-4	2019	[18F]-SuPAR is a radiofluorinated nicotinamide adenine dinucleotide (NAD) analog that can be recognized by PARP-1/2 and incorporated into the long branched polymers of poly(ADP ribose) (PAR).	NAD	34-67	poly (ADP-ribose) polymerase family, member 12	Mus musculus	107-115
30973715-4	2019	[18F]-SuPAR is a radiofluorinated nicotinamide adenine dinucleotide (NAD) analog that can be recognized by PARP-1/2 and incorporated into the long branched polymers of poly(ADP ribose) (PAR).	NAD	69-72	poly (ADP-ribose) polymerase family, member 12	Mus musculus	107-115
31016551-4	2019	These cells co-express P2X7 and ADP-ribosyltransferase ARTC2, permitting gating of P2X7 by NAD+-dependent ADP-ribosylation without the need to add exogenous ATP.	NAD	91-95	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	23-27
31016551-4	2019	These cells co-express P2X7 and ADP-ribosyltransferase ARTC2, permitting gating of P2X7 by NAD+-dependent ADP-ribosylation without the need to add exogenous ATP.	NAD	91-95	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	83-87
31016551-5	2019	Yac-1 cells released ATP into the extracellular space within minutes after stimulation with NAD+.	NAD	92-96	ADP-ribosyltransferase 1	Mus musculus	0-5
31147539-4	2019	To identify the substrate of NOCT, we conducted a mass spectrometry screen and report that NOCT specifically and directly converts the dinucleotide NADP+ into NAD+ and NADPH into NADH.	NAD	159-163	nocturnin	Homo sapiens	29-33
31147539-4	2019	To identify the substrate of NOCT, we conducted a mass spectrometry screen and report that NOCT specifically and directly converts the dinucleotide NADP+ into NAD+ and NADPH into NADH.	NAD	159-163	nocturnin	Homo sapiens	91-95
31147539-4	2019	To identify the substrate of NOCT, we conducted a mass spectrometry screen and report that NOCT specifically and directly converts the dinucleotide NADP+ into NAD+ and NADPH into NADH.	NAD	179-183	nocturnin	Homo sapiens	29-33
31147539-4	2019	To identify the substrate of NOCT, we conducted a mass spectrometry screen and report that NOCT specifically and directly converts the dinucleotide NADP+ into NAD+ and NADPH into NADH.	NAD	179-183	nocturnin	Homo sapiens	91-95
31119097-5	2019	NAD+ feeds Poly-ADP polymerases (PARP) and NAD+-dependent deacetylases (SIRTUINS) contributing to GSC phenotype.	NAD	0-4	poly(ADP-ribose) polymerase 1	Homo sapiens	33-37
30826710-3	2019	The results evaluated by FMO highlight some key interactions between InhA and the derivatives, indicating that the most potent derivative has strong hydrogen bonds with the Met98 side chain of InhA and strong electrostatic interactions with the nicotinamide adenine dinucleotide cofactor.	NAD	245-278	inhibin subunit alpha	Homo sapiens	69-73
30993888-4	2019	An NAD-dependent deacetylase also known as Sirtuin-3 (SIRT3) has been shown to regulate cellular metabolism in various cancers dynamically.	NAD	3-6	sirtuin 3	Homo sapiens	43-52
30993888-4	2019	An NAD-dependent deacetylase also known as Sirtuin-3 (SIRT3) has been shown to regulate cellular metabolism in various cancers dynamically.	NAD	3-6	sirtuin 3	Homo sapiens	54-59
30050056-4	2019	p300 activity toward p53 is negatively regulated by the NAD-dependent deacetylase SIRT1, which deacetylates p53 preventing its transcriptional activation and the induction of p53-dependent apoptosis.	NAD	56-59	tumor protein p53	Homo sapiens	21-24
30050056-4	2019	p300 activity toward p53 is negatively regulated by the NAD-dependent deacetylase SIRT1, which deacetylates p53 preventing its transcriptional activation and the induction of p53-dependent apoptosis.	NAD	56-59	tumor protein p53	Homo sapiens	108-111
30050056-4	2019	p300 activity toward p53 is negatively regulated by the NAD-dependent deacetylase SIRT1, which deacetylates p53 preventing its transcriptional activation and the induction of p53-dependent apoptosis.	NAD	56-59	tumor protein p53	Homo sapiens	108-111
30216708-10	2019	DHA or EPA increased the messenger ribonucleic acid levels of Ho-1, nicotinamide adenine dinucleotide (phosphate) H quinone oxidoreductase 1 and catalase dose-dependently.	NAD	68-101	catalase	Mus musculus	116-153
30826710-3	2019	The results evaluated by FMO highlight some key interactions between InhA and the derivatives, indicating that the most potent derivative has strong hydrogen bonds with the Met98 side chain of InhA and strong electrostatic interactions with the nicotinamide adenine dinucleotide cofactor.	NAD	245-278	inhibin subunit alpha	Homo sapiens	193-197
30649099-2	2019	Our previous results demonstrated that sirtuin 1 (SIRT1), a nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase, alleviates neuropathic pain in type 2 diabetes mellitus rats.	NAD	60-93	sirtuin 1	Rattus norvegicus	39-48
30796690-13	2019	We also observed an additive increase in the activation of the NAD-dependent DNA repair enzyme poly (ADP-ribose) polymerase-1 (PARP-1) activity, which was accompanied by a decline in its essential substrate NAD+.	NAD	63-66	poly(ADP-ribose) polymerase 1	Homo sapiens	127-133
30796690-13	2019	We also observed an additive increase in the activation of the NAD-dependent DNA repair enzyme poly (ADP-ribose) polymerase-1 (PARP-1) activity, which was accompanied by a decline in its essential substrate NAD+.	NAD	207-211	poly(ADP-ribose) polymerase 1	Homo sapiens	127-133
31019297-8	2019	Dependence on another rate-limiting enzyme of the NAD synthesis pathway, NAMPT, as a result of enhancer remodelling is subject to resistance by NMRK1-dependent synthesis of NAD.	NAD	50-53	nicotinamide riboside kinase 1	Homo sapiens	144-149
31019297-8	2019	Dependence on another rate-limiting enzyme of the NAD synthesis pathway, NAMPT, as a result of enhancer remodelling is subject to resistance by NMRK1-dependent synthesis of NAD.	NAD	173-176	nicotinamide riboside kinase 1	Homo sapiens	144-149
30649099-2	2019	Our previous results demonstrated that sirtuin 1 (SIRT1), a nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase, alleviates neuropathic pain in type 2 diabetes mellitus rats.	NAD	60-93	sirtuin 1	Rattus norvegicus	50-55
31035592-3	2019	LDHA has a higher affinity for pyruvate, preferentially converting pyruvate to lactate, and NADH to NAD+ in anaerobic conditions, whereas LDHB possess a higher affinity for lactate, preferentially converting lactate to pyruvate, and NAD+ to NADH, when oxygen is abundant.	NAD	233-237	lactate dehydrogenase A	Homo sapiens	0-4
31035592-3	2019	LDHA has a higher affinity for pyruvate, preferentially converting pyruvate to lactate, and NADH to NAD+ in anaerobic conditions, whereas LDHB possess a higher affinity for lactate, preferentially converting lactate to pyruvate, and NAD+ to NADH, when oxygen is abundant.	NAD	241-245	lactate dehydrogenase A	Homo sapiens	0-4
31035592-3	2019	LDHA has a higher affinity for pyruvate, preferentially converting pyruvate to lactate, and NADH to NAD+ in anaerobic conditions, whereas LDHB possess a higher affinity for lactate, preferentially converting lactate to pyruvate, and NAD+ to NADH, when oxygen is abundant.	NAD	92-96	lactate dehydrogenase A	Homo sapiens	0-4
31035592-3	2019	LDHA has a higher affinity for pyruvate, preferentially converting pyruvate to lactate, and NADH to NAD+ in anaerobic conditions, whereas LDHB possess a higher affinity for lactate, preferentially converting lactate to pyruvate, and NAD+ to NADH, when oxygen is abundant.	NAD	100-104	lactate dehydrogenase A	Homo sapiens	0-4
31080405-0	2019	SIRT2, ERK and Nrf2 Mediate NAD+ Treatment-Induced Increase in the Antioxidant Capacity of PC12 Cells Under Basal Conditions.	NAD	28-32	Eph receptor B1	Rattus norvegicus	7-10
31080405-0	2019	SIRT2, ERK and Nrf2 Mediate NAD+ Treatment-Induced Increase in the Antioxidant Capacity of PC12 Cells Under Basal Conditions.	NAD	28-32	NFE2 like bZIP transcription factor 2	Rattus norvegicus	15-19
31080405-5	2019	NAD+ can also increase both the mRNA and protein level of gamma-glutamylcysteine ligase (gamma-GCL)-a key enzyme for glutathione synthesis, which appears to be mediated by the NAD+-induced increase in Nrf2 activity.	NAD	0-4	NFE2 like bZIP transcription factor 2	Rattus norvegicus	201-205
31080405-5	2019	NAD+ can also increase both the mRNA and protein level of gamma-glutamylcysteine ligase (gamma-GCL)-a key enzyme for glutathione synthesis, which appears to be mediated by the NAD+-induced increase in Nrf2 activity.	NAD	176-180	NFE2 like bZIP transcription factor 2	Rattus norvegicus	201-205
31080405-7	2019	The NAD+-induced changes can also be blocked by the ERK signaling inhibitor U0126.	NAD	4-8	Eph receptor B1	Rattus norvegicus	52-55
31080405-8	2019	Moreover, the NAD+-induced ERK activation can be blocked by both SIRT2 siRNA and AGK2.	NAD	14-18	Eph receptor B1	Rattus norvegicus	27-30
31080405-9	2019	Collectively, our study has provided the first evidence that NAD+ can enhance directly the antioxidant capacity of the cells under basal conditions, which is mediated by SIRT2, ERK, and Nrf2.	NAD	61-65	Eph receptor B1	Rattus norvegicus	177-180
30826252-3	2019	HSD3B2 is a two-substrate enzyme, which binds to cofactor NAD+ and a 3beta-steroid.	NAD	58-62	hydroxy-delta-5-steroid dehydrogenase, 3 beta- and steroid delta-isomerase 2	Homo sapiens	0-6
31080405-9	2019	Collectively, our study has provided the first evidence that NAD+ can enhance directly the antioxidant capacity of the cells under basal conditions, which is mediated by SIRT2, ERK, and Nrf2.	NAD	61-65	NFE2 like bZIP transcription factor 2	Rattus norvegicus	186-190
31118974-7	2019	Moreover, SAB increased HG- or PA-induced expression of Sirtuin 1 (Sirt1), a nicotinamide adenine dinucleotide- (NAD+-) dependent histone deacetylase.	NAD	77-110	SH3 domain binding protein 5	Homo sapiens	10-13
30921515-3	2019	We found that KARI from archaea Sulfolobus solfataricus (Sso-KARI) is unusual in being a dodecamer, bispecific to NADH and NADPH, and losing activity above pH 7.8.	NAD	114-118	hypothetical protein	Saccharolobus solfataricus	14-18
30921515-3	2019	We found that KARI from archaea Sulfolobus solfataricus (Sso-KARI) is unusual in being a dodecamer, bispecific to NADH and NADPH, and losing activity above pH 7.8.	NAD	114-118	hypothetical protein	Saccharolobus solfataricus	61-65
30921515-6	2019	We next solved cryo-EM structures of two Sso-KARI complexes, with NADH+inhibitor and NADPH+inhibitor at pH 7.5, which indicate that the bispecificity can be attributed to a unique asparagine at the cofactor binding loop.	NAD	66-70	hypothetical protein	Saccharolobus solfataricus	45-49
30986964-2	2019	Activated by the sensing of DNA strand breaks, poly(ADP-ribose)polymerase1 (PARP1) transfers ADP-ribose units onto itself and other target proteins using NAD+ as a substrate.	NAD	154-158	poly(ADP-ribose) polymerase 1	Homo sapiens	47-74
30695683-3	2019	Western blotting respectively assayed protein expression of LC3I, LC3II, Beclin-1, Autophagy-related protein 7 (Atg7), Autophagy-related protein 3 (Atg3), NAD-dependent deacetylase sirtuin-3 (SIRT3) and major histocompatibility complex class I chain-related gene A (MICA).	NAD	155-158	sirtuin 3	Homo sapiens	192-197
30777853-2	2019	We report that in tumor-bearing mice the macrophage colony-stimulating factor elevates the myeloid cell levels of nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme in the NAD salvage pathway, which acts as negative regulator of the CXCR4 retention axis of hematopoietic cells in the bone marrow.	NAD	194-197	nicotinamide phosphoribosyltransferase	Mus musculus	114-152
30777853-2	2019	We report that in tumor-bearing mice the macrophage colony-stimulating factor elevates the myeloid cell levels of nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme in the NAD salvage pathway, which acts as negative regulator of the CXCR4 retention axis of hematopoietic cells in the bone marrow.	NAD	194-197	nicotinamide phosphoribosyltransferase	Mus musculus	154-159
30777853-3	2019	NAMPT inhibits CXCR4 through a NAD/Sirtuin 1-mediated inactivation of HIF1alpha-driven CXCR4 gene transcription, leading to mobilization of immature myeloid-derived suppressor cells (MDSC) and enhancing their production of suppressive nitric oxide.	NAD	31-34	nicotinamide phosphoribosyltransferase	Mus musculus	0-5
30777853-3	2019	NAMPT inhibits CXCR4 through a NAD/Sirtuin 1-mediated inactivation of HIF1alpha-driven CXCR4 gene transcription, leading to mobilization of immature myeloid-derived suppressor cells (MDSC) and enhancing their production of suppressive nitric oxide.	NAD	31-34	hypoxia inducible factor 1 subunit alpha	Homo sapiens	70-79
30760525-0	2019	The copper-sensing transcription factor Mac1, the histone deacetylase Hst1, and nicotinic acid regulate de novo NAD+ biosynthesis in budding yeast.	NAD	112-116	Mac1p	Saccharomyces cerevisiae S288C	40-44
30760525-4	2019	We found that a mutant strain (mac1Delta) lacking Mac1, a copper-sensing transcription factor that activates copper transport genes during copper deprivation, exhibits increases in quinolinic acid (QA) production and NAD+ levels.	NAD	217-221	Mac1p	Saccharomyces cerevisiae S288C	50-54
30686744-5	2019	Consistent with this, a type 2 diabetes risk haplotype in SLC16A11 that reduces pyruvate transport (thus limiting lactate production) increases D5D/D6D activity in vitro and in humans, demonstrating a chronic effect of desaturase-mediated NAD+ recycling.	NAD	239-243	solute carrier family 16 member 11	Homo sapiens	58-66
30986964-2	2019	Activated by the sensing of DNA strand breaks, poly(ADP-ribose)polymerase1 (PARP1) transfers ADP-ribose units onto itself and other target proteins using NAD+ as a substrate.	NAD	154-158	poly(ADP-ribose) polymerase 1	Homo sapiens	76-81
29278652-5	2019	In this study, PARP1 protein expression, and the activity of mTOR and its three target substrates (p70 ribosomal S6 Kinase 1, eukaryotic initiation factor 4E--binding protein 1, and UNC-51-like kinase 1) were augmented; meanwhile, the nicotinamide adenine dinucleotide (NAD) content was significantly reduced in the process of cardiac fibrosis in vivo and in vitro.	NAD	235-268	poly(ADP-ribose) polymerase 1	Homo sapiens	15-20
30707625-1	2019	The nicotinamide adenine dinucleotide-dependent deacetylase, sirtuin (SIRT)1, in skeletal muscle is reduced in insulin-resistant states.	NAD	4-37	insulin	Homo sapiens	111-118
30556645-2	2019	The availability of free NAD+ can affect the activities of NAD+ -consuming enzymes such as sirtuin, PARP/ARTD, and cyclic ADPR-hydrolase family members.	NAD	25-29	poly(ADP-ribose) polymerase 1	Homo sapiens	100-104
30556645-2	2019	The availability of free NAD+ can affect the activities of NAD+ -consuming enzymes such as sirtuin, PARP/ARTD, and cyclic ADPR-hydrolase family members.	NAD	59-63	poly(ADP-ribose) polymerase 1	Homo sapiens	100-104
29278652-5	2019	In this study, PARP1 protein expression, and the activity of mTOR and its three target substrates (p70 ribosomal S6 Kinase 1, eukaryotic initiation factor 4E--binding protein 1, and UNC-51-like kinase 1) were augmented; meanwhile, the nicotinamide adenine dinucleotide (NAD) content was significantly reduced in the process of cardiac fibrosis in vivo and in vitro.	NAD	235-268	mechanistic target of rapamycin kinase	Homo sapiens	61-65
29278652-5	2019	In this study, PARP1 protein expression, and the activity of mTOR and its three target substrates (p70 ribosomal S6 Kinase 1, eukaryotic initiation factor 4E--binding protein 1, and UNC-51-like kinase 1) were augmented; meanwhile, the nicotinamide adenine dinucleotide (NAD) content was significantly reduced in the process of cardiac fibrosis in vivo and in vitro.	NAD	270-273	poly(ADP-ribose) polymerase 1	Homo sapiens	15-20
29278652-5	2019	In this study, PARP1 protein expression, and the activity of mTOR and its three target substrates (p70 ribosomal S6 Kinase 1, eukaryotic initiation factor 4E--binding protein 1, and UNC-51-like kinase 1) were augmented; meanwhile, the nicotinamide adenine dinucleotide (NAD) content was significantly reduced in the process of cardiac fibrosis in vivo and in vitro.	NAD	270-273	mechanistic target of rapamycin kinase	Homo sapiens	61-65
29278652-10	2019	PARP1 overexpression evoked cardiac fibrosis, which could be antagonized by mTOR inhibitors or NAD supplementation in CFs.	NAD	95-98	poly(ADP-ribose) polymerase 1	Homo sapiens	0-5
29278652-11	2019	These results provide novel and compelling evidence that PARP1 exacerbated cardiac fibrosis, which was partially attributed to NAD-dependent activation of mTOR.	NAD	127-130	poly(ADP-ribose) polymerase 1	Homo sapiens	57-62
29278652-11	2019	These results provide novel and compelling evidence that PARP1 exacerbated cardiac fibrosis, which was partially attributed to NAD-dependent activation of mTOR.	NAD	127-130	mechanistic target of rapamycin kinase	Homo sapiens	155-159
30277116-0	2019	Non-NAD-like PARP1 inhibitor enhanced synthetic lethal effect of NAD-like PARP inhibitors against BRCA1-deficient leukemia.	NAD	4-7	poly(ADP-ribose) polymerase 1	Homo sapiens	13-18
30777922-2	2019	High extracellular ATP concentrations or NAD-mediated P2RX7 ribosylation by the enzyme ARTC2.2 can induce P2RX7 pore formation and cell death.	NAD	41-44	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	54-59
30777922-2	2019	High extracellular ATP concentrations or NAD-mediated P2RX7 ribosylation by the enzyme ARTC2.2 can induce P2RX7 pore formation and cell death.	NAD	41-44	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	106-111
30782960-5	2019	NAD+ achieves these remarkable effects through sirtuin-mediated deacetylation of key transcriptional regulators, such as peroxisome proliferator-activated receptor gamma coactivator 1-alpha, LXR, and SREBPs, that control these cellular processes.	NAD	0-4	PPARG coactivator 1 alpha	Homo sapiens	121-189
30277116-0	2019	Non-NAD-like PARP1 inhibitor enhanced synthetic lethal effect of NAD-like PARP inhibitors against BRCA1-deficient leukemia.	NAD	4-7	poly(ADP-ribose) polymerase 1	Homo sapiens	13-17
30277116-0	2019	Non-NAD-like PARP1 inhibitor enhanced synthetic lethal effect of NAD-like PARP inhibitors against BRCA1-deficient leukemia.	NAD	65-68	poly(ADP-ribose) polymerase 1	Homo sapiens	13-18
30277116-0	2019	Non-NAD-like PARP1 inhibitor enhanced synthetic lethal effect of NAD-like PARP inhibitors against BRCA1-deficient leukemia.	NAD	65-68	poly(ADP-ribose) polymerase 1	Homo sapiens	13-17
30124109-2	2019	Quantification of NAD+:NADH and NADP+:NADPH ratios are pivotal to a wide variety of cellular processes, including intracellular secondary messenger signaling by CD38 glycohydrolases, DNA repair by poly(adenosine diphosphate ribose) polymerase (PARP), epigenetic regulation of gene expression by NAD-dependent histone deacetylase enzymes known as sirtuins, and regulation of the oxidative pentose phosphate pathway.	NAD	18-22	poly(ADP-ribose) polymerase 1	Homo sapiens	244-248
30858618-7	2019	In this setting, increased NAMPT expression allowed the maintenance of NAD+ pools sufficient for glyceraldehyde-3-phosphate dehydrogenase activity and Warburg metabolism.	NAD	71-75	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	97-137
30124109-2	2019	Quantification of NAD+:NADH and NADP+:NADPH ratios are pivotal to a wide variety of cellular processes, including intracellular secondary messenger signaling by CD38 glycohydrolases, DNA repair by poly(adenosine diphosphate ribose) polymerase (PARP), epigenetic regulation of gene expression by NAD-dependent histone deacetylase enzymes known as sirtuins, and regulation of the oxidative pentose phosphate pathway.	NAD	18-21	poly(ADP-ribose) polymerase 1	Homo sapiens	244-248
30799186-0	2019	ACMSD: A Novel Target for Modulating NAD+ Homeostasis.	NAD	37-41	aminocarboxymuconate semialdehyde decarboxylase	Homo sapiens	0-5
30799186-2	2019	A recent study (Palzer et al., Cell Rep. 2018, 25;1359-1370) demonstrated that alpha-amino-beta-carboxy-muconate-semialdehyde decarboxylase (ACMSD) is a key regulator of NAD+ metabolism and overexpression of human ACMSD leads to niacin dependency for NAD+ biosynthesis in mice, providing important insights into human diseases associated with niacin/NAD+ deficiency.	NAD	251-255	aminocarboxymuconate semialdehyde decarboxylase	Homo sapiens	79-139
30799186-2	2019	A recent study (Palzer et al., Cell Rep. 2018, 25;1359-1370) demonstrated that alpha-amino-beta-carboxy-muconate-semialdehyde decarboxylase (ACMSD) is a key regulator of NAD+ metabolism and overexpression of human ACMSD leads to niacin dependency for NAD+ biosynthesis in mice, providing important insights into human diseases associated with niacin/NAD+ deficiency.	NAD	170-174	aminocarboxymuconate semialdehyde decarboxylase	Homo sapiens	79-139
30799186-2	2019	A recent study (Palzer et al., Cell Rep. 2018, 25;1359-1370) demonstrated that alpha-amino-beta-carboxy-muconate-semialdehyde decarboxylase (ACMSD) is a key regulator of NAD+ metabolism and overexpression of human ACMSD leads to niacin dependency for NAD+ biosynthesis in mice, providing important insights into human diseases associated with niacin/NAD+ deficiency.	NAD	251-255	aminocarboxymuconate semialdehyde decarboxylase	Homo sapiens	141-146
30799186-2	2019	A recent study (Palzer et al., Cell Rep. 2018, 25;1359-1370) demonstrated that alpha-amino-beta-carboxy-muconate-semialdehyde decarboxylase (ACMSD) is a key regulator of NAD+ metabolism and overexpression of human ACMSD leads to niacin dependency for NAD+ biosynthesis in mice, providing important insights into human diseases associated with niacin/NAD+ deficiency.	NAD	251-255	aminocarboxymuconate semialdehyde decarboxylase	Homo sapiens	214-219
30799186-2	2019	A recent study (Palzer et al., Cell Rep. 2018, 25;1359-1370) demonstrated that alpha-amino-beta-carboxy-muconate-semialdehyde decarboxylase (ACMSD) is a key regulator of NAD+ metabolism and overexpression of human ACMSD leads to niacin dependency for NAD+ biosynthesis in mice, providing important insights into human diseases associated with niacin/NAD+ deficiency.	NAD	170-174	aminocarboxymuconate semialdehyde decarboxylase	Homo sapiens	141-146
30799186-2	2019	A recent study (Palzer et al., Cell Rep. 2018, 25;1359-1370) demonstrated that alpha-amino-beta-carboxy-muconate-semialdehyde decarboxylase (ACMSD) is a key regulator of NAD+ metabolism and overexpression of human ACMSD leads to niacin dependency for NAD+ biosynthesis in mice, providing important insights into human diseases associated with niacin/NAD+ deficiency.	NAD	170-174	aminocarboxymuconate semialdehyde decarboxylase	Homo sapiens	214-219
30799186-2	2019	A recent study (Palzer et al., Cell Rep. 2018, 25;1359-1370) demonstrated that alpha-amino-beta-carboxy-muconate-semialdehyde decarboxylase (ACMSD) is a key regulator of NAD+ metabolism and overexpression of human ACMSD leads to niacin dependency for NAD+ biosynthesis in mice, providing important insights into human diseases associated with niacin/NAD+ deficiency.	NAD	251-255	aminocarboxymuconate semialdehyde decarboxylase	Homo sapiens	79-139
30799186-2	2019	A recent study (Palzer et al., Cell Rep. 2018, 25;1359-1370) demonstrated that alpha-amino-beta-carboxy-muconate-semialdehyde decarboxylase (ACMSD) is a key regulator of NAD+ metabolism and overexpression of human ACMSD leads to niacin dependency for NAD+ biosynthesis in mice, providing important insights into human diseases associated with niacin/NAD+ deficiency.	NAD	251-255	aminocarboxymuconate semialdehyde decarboxylase	Homo sapiens	141-146
30799186-2	2019	A recent study (Palzer et al., Cell Rep. 2018, 25;1359-1370) demonstrated that alpha-amino-beta-carboxy-muconate-semialdehyde decarboxylase (ACMSD) is a key regulator of NAD+ metabolism and overexpression of human ACMSD leads to niacin dependency for NAD+ biosynthesis in mice, providing important insights into human diseases associated with niacin/NAD+ deficiency.	NAD	251-255	aminocarboxymuconate semialdehyde decarboxylase	Homo sapiens	214-219
30898999-0	2019	DNA damage-induced PARP1 activation confers cardiomyocyte dysfunction through NAD+ depletion in experimental atrial fibrillation.	NAD	78-82	poly(ADP-ribose) polymerase 1	Homo sapiens	19-24
30909652-9	2019	CETSA revealed that compounds 1 and 2 directly engaged with tNOX, leading to a decrease in the cellular NAD+/NADH ratio.	NAD	104-108	ecto-NOX disulfide-thiol exchanger 2	Homo sapiens	60-64
30909652-9	2019	CETSA revealed that compounds 1 and 2 directly engaged with tNOX, leading to a decrease in the cellular NAD+/NADH ratio.	NAD	109-113	ecto-NOX disulfide-thiol exchanger 2	Homo sapiens	60-64
30692220-8	2019	Notable among them is NICOTINAMIDASE 3 (NIC3) that encodes an enzyme that converts nicotinamide to nicotinic acid in the NAD+ salvage pathway.	NAD	121-125	nicotinamidase 3	Arabidopsis thaliana	22-38
30692220-8	2019	Notable among them is NICOTINAMIDASE 3 (NIC3) that encodes an enzyme that converts nicotinamide to nicotinic acid in the NAD+ salvage pathway.	NAD	121-125	nicotinamidase 3	Arabidopsis thaliana	40-44
30648291-1	2019	Apart from its vital function as a redox cofactor, nicotinamide adenine dinucleotide (NAD+ ) has emerged as a crucial substrate for NAD+ -consuming enzymes, including poly(ADP-ribosyl)transferase 1 (PARP1) and CD38/CD157.	NAD	51-84	poly(ADP-ribose) polymerase 1	Homo sapiens	199-204
30648291-1	2019	Apart from its vital function as a redox cofactor, nicotinamide adenine dinucleotide (NAD+ ) has emerged as a crucial substrate for NAD+ -consuming enzymes, including poly(ADP-ribosyl)transferase 1 (PARP1) and CD38/CD157.	NAD	51-84	bone marrow stromal cell antigen 1	Homo sapiens	215-220
30648291-1	2019	Apart from its vital function as a redox cofactor, nicotinamide adenine dinucleotide (NAD+ ) has emerged as a crucial substrate for NAD+ -consuming enzymes, including poly(ADP-ribosyl)transferase 1 (PARP1) and CD38/CD157.	NAD	86-90	poly(ADP-ribose) polymerase 1	Homo sapiens	199-204
30648291-1	2019	Apart from its vital function as a redox cofactor, nicotinamide adenine dinucleotide (NAD+ ) has emerged as a crucial substrate for NAD+ -consuming enzymes, including poly(ADP-ribosyl)transferase 1 (PARP1) and CD38/CD157.	NAD	86-90	bone marrow stromal cell antigen 1	Homo sapiens	215-220
30648291-1	2019	Apart from its vital function as a redox cofactor, nicotinamide adenine dinucleotide (NAD+ ) has emerged as a crucial substrate for NAD+ -consuming enzymes, including poly(ADP-ribosyl)transferase 1 (PARP1) and CD38/CD157.	NAD	132-136	poly(ADP-ribose) polymerase 1	Homo sapiens	199-204
30648291-1	2019	Apart from its vital function as a redox cofactor, nicotinamide adenine dinucleotide (NAD+ ) has emerged as a crucial substrate for NAD+ -consuming enzymes, including poly(ADP-ribosyl)transferase 1 (PARP1) and CD38/CD157.	NAD	132-136	bone marrow stromal cell antigen 1	Homo sapiens	215-220
30648291-10	2019	The distinct tolerance, displayed by diverse NAD+ producing and consuming enzymes, suggests unique biological recognition features and dependency on the purine N7 moiety, which is found to be of importance, if not essential, for PARP1-mediated reactions.	NAD	45-49	poly(ADP-ribose) polymerase 1	Homo sapiens	229-234
30898999-4	2019	PARP1-mediated synthesis of ADP-ribose chains in turn depletes nicotinamide adenine dinucleotide (NAD+), induces further DNA damage and contractile dysfunction.	NAD	63-96	poly(ADP-ribose) polymerase 1	Homo sapiens	0-5
30898999-4	2019	PARP1-mediated synthesis of ADP-ribose chains in turn depletes nicotinamide adenine dinucleotide (NAD+), induces further DNA damage and contractile dysfunction.	NAD	98-102	poly(ADP-ribose) polymerase 1	Homo sapiens	0-5
30633870-11	2019	It is thought that this activity of SARM is normally switched off by the axo-protective activities of NMNAT2 which maintain low levels of the NAD+ precursor NMN.	NAD	142-146	nicotinamide nucleotide adenylyltransferase 2	Homo sapiens	102-108
30846598-3	2019	Akt phosphorylates NAD kinase (NADK), the sole cytosolic enzyme that catalyzes the synthesis of NADP+ from NAD+ (the oxidized form of NADH), on three serine residues (Ser44, Ser46, and Ser48) within an amino-terminal domain.	NAD	107-111	AKT serine/threonine kinase 1	Homo sapiens	0-3
30846598-3	2019	Akt phosphorylates NAD kinase (NADK), the sole cytosolic enzyme that catalyzes the synthesis of NADP+ from NAD+ (the oxidized form of NADH), on three serine residues (Ser44, Ser46, and Ser48) within an amino-terminal domain.	NAD	134-138	AKT serine/threonine kinase 1	Homo sapiens	0-3
30833594-2	2019	Conversion of the ketone body acetoacetate (AcAc) to beta-hydroxybutyrate (beta-HB) by the mitochondrial enzyme beta-hydroxybutyrate dehydrogenase (BDH) depends upon NADH availability.	NAD	166-170	3-hydroxybutyrate dehydrogenase, type 1	Mus musculus	148-151
30875389-6	2019	Combined with the measurement of each cell"s volume, we determined absolute values (muM/h) of the rates of NAD+ synthesis (RS) and breakdown (RB) using a flux assay with a 2H (D)-labeled Nam, together with the absolute NAD+ concentrations in various mammalian cells including primary cultured cardiomyocytes under the physiological conditions and investigated the relations among total cellular Nampt activity, RS, RB, and the NAD+ concentration.	NAD	107-111	latexin	Homo sapiens	84-87
30875389-7	2019	NAD+ concentration was maintained within a narrow range (400-700 muM) in the cells.	NAD	0-4	latexin	Homo sapiens	65-68
30906265-12	2019	PDH regulated the rate of Glc and Palm consumption, consistent with its high sensitivity toward AcCoA, CoA, and NADH.	NAD	112-116	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	0-3
30833594-9	2019	These results were consistent with decreased BDH activity in tumors and associated with increased total cellular NAD+/NADH.	NAD	113-117	3-hydroxybutyrate dehydrogenase, type 1	Mus musculus	45-48
30833594-9	2019	These results were consistent with decreased BDH activity in tumors and associated with increased total cellular NAD+/NADH.	NAD	118-122	3-hydroxybutyrate dehydrogenase, type 1	Mus musculus	45-48
30625381-3	2019	SIRT1 is an NAD+ dependent protein deacetylase and increased availability of NAD+ has been shown to augment SIRT1 activity.	NAD	12-15	sirtuin 1	Rattus norvegicus	0-5
30625381-3	2019	SIRT1 is an NAD+ dependent protein deacetylase and increased availability of NAD+ has been shown to augment SIRT1 activity.	NAD	12-16	sirtuin 1	Rattus norvegicus	0-5
31037127-3	2019	Given the prominent role of nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase Sirtuin3 (SIRT3) in sustaining mitochondrial dynamics and homeostasis and that SIRT3 expression and activity can be influenced by oxidative stress-related signaling, we wondered whether SIRT3 could play an important role in vitiligo melanocyte degeneration by regulating mitochondrial dynamics.	NAD	28-61	sirtuin 3	Homo sapiens	91-99
30816177-3	2019	In Ndufs4-KO mice, a mouse model of Leigh syndrome, we found that Complex I deficiency led to declines in NAD+ levels and NAD+ redox imbalance.	NAD	106-110	NADH:ubiquinone oxidoreductase core subunit S4	Mus musculus	3-9
30816177-3	2019	In Ndufs4-KO mice, a mouse model of Leigh syndrome, we found that Complex I deficiency led to declines in NAD+ levels and NAD+ redox imbalance.	NAD	122-126	NADH:ubiquinone oxidoreductase core subunit S4	Mus musculus	3-9
30816177-4	2019	We tested the hypothesis that elevation of NAD+ levels would benefit Ndufs4-KO mice.	NAD	43-47	NADH:ubiquinone oxidoreductase core subunit S4	Mus musculus	69-75
30841449-7	2019	We further show that inhibition of 6PGD activates AMP-activated protein kinase (AMPK) and acetyl-coenzyme A carboxylase 1 (ACC1), and decreases level of NADPH/NAD + and NADH in HCC, leading to SIRT1 activity reduction and oxidative stress.	NAD	159-164	phosphogluconate dehydrogenase	Homo sapiens	35-39
30841449-7	2019	We further show that inhibition of 6PGD activates AMP-activated protein kinase (AMPK) and acetyl-coenzyme A carboxylase 1 (ACC1), and decreases level of NADPH/NAD + and NADH in HCC, leading to SIRT1 activity reduction and oxidative stress.	NAD	169-173	phosphogluconate dehydrogenase	Homo sapiens	35-39
30660702-5	2019	17beta-estradiol (E2), ERalpha-selective agonist PPT and ERbeta-selective agonist DPN induced a rapid increase on ERK1/2 phosphorylation.	NAD	82-85	estrogen receptor 1	Homo sapiens	57-63
30660702-5	2019	17beta-estradiol (E2), ERalpha-selective agonist PPT and ERbeta-selective agonist DPN induced a rapid increase on ERK1/2 phosphorylation.	NAD	82-85	mitogen-activated protein kinase 3	Homo sapiens	114-120
30778219-8	2019	HMGA proteins and NAMPT promote the proinflammatory SASP through NAD+-mediated suppression of AMPK kinase, which suppresses the p53-mediated inhibition of p38 MAPK to enhance NF-kappaB activity.	NAD	65-69	tumor protein p53	Homo sapiens	128-131
30778219-8	2019	HMGA proteins and NAMPT promote the proinflammatory SASP through NAD+-mediated suppression of AMPK kinase, which suppresses the p53-mediated inhibition of p38 MAPK to enhance NF-kappaB activity.	NAD	65-69	mitogen-activated protein kinase 14	Homo sapiens	155-158
30816177-5	2019	Administration of NAD+ precursor, nicotinamide mononucleotide (NMN) extended lifespan of Ndufs4-KO mice and attenuated lactic acidosis.	NAD	18-22	NADH:ubiquinone oxidoreductase core subunit S4	Mus musculus	89-95
31037127-3	2019	Given the prominent role of nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase Sirtuin3 (SIRT3) in sustaining mitochondrial dynamics and homeostasis and that SIRT3 expression and activity can be influenced by oxidative stress-related signaling, we wondered whether SIRT3 could play an important role in vitiligo melanocyte degeneration by regulating mitochondrial dynamics.	NAD	28-61	sirtuin 3	Homo sapiens	101-106
31037127-3	2019	Given the prominent role of nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase Sirtuin3 (SIRT3) in sustaining mitochondrial dynamics and homeostasis and that SIRT3 expression and activity can be influenced by oxidative stress-related signaling, we wondered whether SIRT3 could play an important role in vitiligo melanocyte degeneration by regulating mitochondrial dynamics.	NAD	63-66	sirtuin 3	Homo sapiens	91-99
31037127-3	2019	Given the prominent role of nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase Sirtuin3 (SIRT3) in sustaining mitochondrial dynamics and homeostasis and that SIRT3 expression and activity can be influenced by oxidative stress-related signaling, we wondered whether SIRT3 could play an important role in vitiligo melanocyte degeneration by regulating mitochondrial dynamics.	NAD	63-66	sirtuin 3	Homo sapiens	101-106
30582911-8	2019	The results showed an increase in the expression of UCP2, coinciding with an increase in the level of apoptosis, NAD+/NADH ratio, SIRT3 activity, LDH release and a decrease in the level of ATP and antioxidant-related molecules after 1 h of ischemia and 24 h of reperfusion.	NAD	113-117	uncoupling protein 2 (mitochondrial, proton carrier)	Mus musculus	52-56
29295624-4	2019	NAD+ produces its beneficial effects by targeting at multiple pathological pathways, including attenuating mitochondrial alterations, DNA damage, and oxidative stress, by modulating such enzymes as sirtuins, glyceraldehyde-3-phosphate dehydrogenase, and AP endonuclease.	NAD	0-4	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	208-248
29295624-7	2019	The NAD+ deficiency in the diseases and aging results from not only poly(ADP-ribose) polymerase-1 (PARP-1) activation but also decreased nicotinamide phosphoribosyltransferase (Nampt) activity and increased CD38 activity.	NAD	4-8	poly(ADP-ribose) polymerase 1	Homo sapiens	68-97
29295624-7	2019	The NAD+ deficiency in the diseases and aging results from not only poly(ADP-ribose) polymerase-1 (PARP-1) activation but also decreased nicotinamide phosphoribosyltransferase (Nampt) activity and increased CD38 activity.	NAD	4-8	poly(ADP-ribose) polymerase 1	Homo sapiens	99-105
30710058-1	2019	ADP-ribosylation is an ancient and reversible post-translational modification (PTM) of proteins, in which the ADP-ribose moiety is transferred from NAD+ to target proteins by members of poly-ADP-ribosyl polymerase (PARP) family.	NAD	148-152	poly(ADP-ribose) polymerase 1	Homo sapiens	186-213
30710058-1	2019	ADP-ribosylation is an ancient and reversible post-translational modification (PTM) of proteins, in which the ADP-ribose moiety is transferred from NAD+ to target proteins by members of poly-ADP-ribosyl polymerase (PARP) family.	NAD	148-152	poly(ADP-ribose) polymerase 1	Homo sapiens	215-219
30582911-8	2019	The results showed an increase in the expression of UCP2, coinciding with an increase in the level of apoptosis, NAD+/NADH ratio, SIRT3 activity, LDH release and a decrease in the level of ATP and antioxidant-related molecules after 1 h of ischemia and 24 h of reperfusion.	NAD	118-122	uncoupling protein 2 (mitochondrial, proton carrier)	Mus musculus	52-56
30698872-11	2019	In addition, VB6 increased levels of intracellular NADH/NADPH and glutathione through the activation of nuclear factor E2-related factor 2 (Nrf2) signalling.	NAD	51-55	NFE2 like bZIP transcription factor 2	Homo sapiens	140-144
30741937-1	2019	ADP-ribosylation is a unique posttranslational modification catalyzed by poly(ADP-ribose) polymerases (PARPs) using NAD+ as ADP-ribose donor.	NAD	116-120	poly(ADP-ribose) polymerase 1	Homo sapiens	103-108
30741937-5	2019	Here, we show that ovarian cancer cells with higher level of NADP+, an NAD+ derivative, are more sensitive to PARP inhibitors.	NAD	71-75	poly(ADP-ribose) polymerase 1	Homo sapiens	110-114
30881593-1	2019	Pyruvate dehydrogenase (PDH) complex, a multienzyme complex at the nexus of glycolytic and Krebs cycles, provides acetyl-CoA to the Krebs cycle and NADH to complex I thus supporting a critical role in mitochondrial energy production and cellular survival.	NAD	148-152	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	0-22
30881593-1	2019	Pyruvate dehydrogenase (PDH) complex, a multienzyme complex at the nexus of glycolytic and Krebs cycles, provides acetyl-CoA to the Krebs cycle and NADH to complex I thus supporting a critical role in mitochondrial energy production and cellular survival.	NAD	148-152	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	24-27
30496822-7	2019	The extracts reduced the oxidative effect of H2O2 on over-activation of poly (ADP-ribose) polymerase (PARP1), therefore preventing the cell death by restoring the NAD+ levels.	NAD	163-167	poly(ADP-ribose) polymerase 1	Homo sapiens	72-100
30496822-7	2019	The extracts reduced the oxidative effect of H2O2 on over-activation of poly (ADP-ribose) polymerase (PARP1), therefore preventing the cell death by restoring the NAD+ levels.	NAD	163-167	poly(ADP-ribose) polymerase 1	Homo sapiens	102-107
30774990-1	2019	Nicotinamide phosphoribosyltransferase (NAMPT) functions in NAD synthesis, apoptosis, and inflammation.	NAD	60-63	nicotinamide phosphoribosyltransferase	Mus musculus	40-45
30745932-2	2019	SIRT4 is a mitochondrial NAD+-dependent adenosine diphsophate-ribosyltransferase.	NAD	25-28	sirtuin 4	Homo sapiens	0-5
30502458-9	2019	In BMDMs, LPS-induced PARP1 suppression lead to prevention of NAD+ depletion.	NAD	62-66	poly(ADP-ribose) polymerase 1	Homo sapiens	22-27
30458637-1	2019	As a nicotinamide adenine dinucleotide (NAD)+-dependent protein deacetylase, SIRT3 is highly expressed in tissues with high metabolic turnover and mitochondrial content.	NAD	5-38	sirtuin 3	Homo sapiens	77-82
30530497-1	2019	Sirt6 is an NADH (NAD+)-dependent deacetylase with a critical role in hepatic lipid metabolism.	NAD	12-16	sirtuin 6	Mus musculus	0-5
30670978-1	2018	The present study examined whether angiotensin II (Ang II) mediates the pressor effect through nicotinamide adenine dinucleotide phosphate (NADPH) oxidase-derived reactive oxygen species (ROS)-mitogen-activated protein kinase (MAPK) signaling in the glutamatergic neurons of the rostral ventrolateral medulla (RVLM) in stress-induced hypertensive rats (SIHR).	NAD	95-128	angiotensinogen	Rattus norvegicus	35-49
30267267-7	2019	Some extracts prevented cell death by reducing the activation of poly (ADP-ribose) polymerase (PARP1) by QUIN, therefore by maintaining NAD+ levels.	NAD	136-140	poly(ADP-ribose) polymerase 1	Homo sapiens	65-93
30267267-7	2019	Some extracts prevented cell death by reducing the activation of poly (ADP-ribose) polymerase (PARP1) by QUIN, therefore by maintaining NAD+ levels.	NAD	136-140	poly(ADP-ribose) polymerase 1	Homo sapiens	95-100
30699348-5	2019	We developed stem cell models from patients and created stem cell knockout rescue systems, documenting mitochondrial morphology defects, impaired oxidative metabolism, and reduced expression of nicotinamide adenine dinucleotide (NAD+) production enzymes in SCA7 models.	NAD	194-227	ataxin 7	Homo sapiens	257-261
30699348-5	2019	We developed stem cell models from patients and created stem cell knockout rescue systems, documenting mitochondrial morphology defects, impaired oxidative metabolism, and reduced expression of nicotinamide adenine dinucleotide (NAD+) production enzymes in SCA7 models.	NAD	229-233	ataxin 7	Homo sapiens	257-261
30699348-6	2019	We observed NAD+ reductions in mitochondria of SCA7 patient NPCs using ratiometric fluorescent sensors and documented alterations in tryptophan-kynurenine metabolism in patients.	NAD	12-16	ataxin 7	Homo sapiens	47-51
30699348-7	2019	Our results indicate that mitochondrial dysfunction, stemming from decreased NAD+, is a defining feature of SCA7.	NAD	77-81	ataxin 7	Homo sapiens	108-112
29634344-2	2019	NAD+ depletion may occur in response to either excessive DNA damage due to free radical or ultraviolet attack, resulting in significant poly(ADP-ribose) polymerase (PARP) activation and a high turnover and subsequent depletion of NAD+, and/or chronic immune activation and inflammatory cytokine production resulting in accelerated CD38 activity and decline in NAD+ levels.	NAD	0-4	poly(ADP-ribose) polymerase 1	Homo sapiens	136-163
29634344-2	2019	NAD+ depletion may occur in response to either excessive DNA damage due to free radical or ultraviolet attack, resulting in significant poly(ADP-ribose) polymerase (PARP) activation and a high turnover and subsequent depletion of NAD+, and/or chronic immune activation and inflammatory cytokine production resulting in accelerated CD38 activity and decline in NAD+ levels.	NAD	0-4	poly(ADP-ribose) polymerase 1	Homo sapiens	165-169
30670969-3	2018	The present study identified SIRT6, an important subtype of NAD+ dependent class III histone deacetylase, to be a negative regulator of NFATc4 in cardiomyocyte hypertrophy.	NAD	60-64	nuclear factor of activated T cells 4	Homo sapiens	136-142
30670978-1	2018	The present study examined whether angiotensin II (Ang II) mediates the pressor effect through nicotinamide adenine dinucleotide phosphate (NADPH) oxidase-derived reactive oxygen species (ROS)-mitogen-activated protein kinase (MAPK) signaling in the glutamatergic neurons of the rostral ventrolateral medulla (RVLM) in stress-induced hypertensive rats (SIHR).	NAD	95-128	angiotensinogen	Rattus norvegicus	51-57
29936181-1	2019	CD157/BST1 glycosylphosphatidylinositol-anchored glycoprotein is an evolutionary conserved dual-function receptor and beta-NAD+-metabolizing ectoenzyme of the ADP-ribosyl cyclases gene family.	NAD	118-127	bone marrow stromal cell antigen 1	Homo sapiens	0-5
31682209-5	2019	Decreased sirtuins, poly-ADP ribose polymerase-driven decreases in nicotinamide adenine dinucleotide (NAD+), hyperserotonemia, decreased monoamine oxidase, alterations in 14-3-3 proteins, microRNA alterations, dysregulated aryl hydrocarbon receptor activity, suboptimal mitochondria functioning, and decreases in the melatonergic pathways are intimately linked to this.	NAD	67-100	poly(ADP-ribose) polymerase 1	Homo sapiens	20-46
31682209-5	2019	Decreased sirtuins, poly-ADP ribose polymerase-driven decreases in nicotinamide adenine dinucleotide (NAD+), hyperserotonemia, decreased monoamine oxidase, alterations in 14-3-3 proteins, microRNA alterations, dysregulated aryl hydrocarbon receptor activity, suboptimal mitochondria functioning, and decreases in the melatonergic pathways are intimately linked to this.	NAD	102-106	poly(ADP-ribose) polymerase 1	Homo sapiens	20-46
30455381-8	2019	Specifically, CFZ treatment reduced the expression of nicotinamide phosphoribosyltransferase (NAMPT), thus limiting IDH2 activation through the NAD+-dependent deacetylase SIRT3.	NAD	144-148	isocitrate dehydrogenase (NADP(+)) 2	Homo sapiens	116-120
30455381-8	2019	Specifically, CFZ treatment reduced the expression of nicotinamide phosphoribosyltransferase (NAMPT), thus limiting IDH2 activation through the NAD+-dependent deacetylase SIRT3.	NAD	144-148	sirtuin 3	Homo sapiens	171-176
29936181-1	2019	CD157/BST1 glycosylphosphatidylinositol-anchored glycoprotein is an evolutionary conserved dual-function receptor and beta-NAD+-metabolizing ectoenzyme of the ADP-ribosyl cyclases gene family.	NAD	118-127	bone marrow stromal cell antigen 1	Homo sapiens	6-10
29958894-3	2019	Among the host responses to the release of ATP, NAD+ and related small molecules is their breakdown on behalf of a panel of leukocyte ectonucleotidases - CD38, CD39, CD73, CD157, CD203a and CD203c -, whose activities are concatenated to form two nucleotide-catabolizing channels defined as the canonical and non-canonical adenosinergic pathways.	NAD	48-52	bone marrow stromal cell antigen 1	Homo sapiens	172-177
31208524-0	2019	Role of mitochondria in diabetic peripheral neuropathy: Influencing the NAD+-dependent SIRT1-PGC-1alpha-TFAM pathway.	NAD	72-75	PPARG coactivator 1 alpha	Homo sapiens	93-103
31208524-5	2019	One of the key pathways that is impaired in diabetic peripheral neuropathy (DPN) is the energy sensing pathway comprising the nicotinamide-adenine dinucleotide (NAD+)-dependent Sirtuin 1 (SIRT1)/peroxisome proliferator-activated receptor-gamma coactivator alpha (PGC-1alpha)/Mt transcription factor A (TFAM or mtTFA) signaling pathway.	NAD	126-159	transcription factor A, mitochondrial	Homo sapiens	302-306
31208524-0	2019	Role of mitochondria in diabetic peripheral neuropathy: Influencing the NAD+-dependent SIRT1-PGC-1alpha-TFAM pathway.	NAD	72-75	transcription factor A, mitochondrial	Homo sapiens	104-108
31208524-5	2019	One of the key pathways that is impaired in diabetic peripheral neuropathy (DPN) is the energy sensing pathway comprising the nicotinamide-adenine dinucleotide (NAD+)-dependent Sirtuin 1 (SIRT1)/peroxisome proliferator-activated receptor-gamma coactivator alpha (PGC-1alpha)/Mt transcription factor A (TFAM or mtTFA) signaling pathway.	NAD	126-159	transcription factor A, mitochondrial	Homo sapiens	310-315
31208524-5	2019	One of the key pathways that is impaired in diabetic peripheral neuropathy (DPN) is the energy sensing pathway comprising the nicotinamide-adenine dinucleotide (NAD+)-dependent Sirtuin 1 (SIRT1)/peroxisome proliferator-activated receptor-gamma coactivator alpha (PGC-1alpha)/Mt transcription factor A (TFAM or mtTFA) signaling pathway.	NAD	126-159	PPARG coactivator 1 alpha	Homo sapiens	263-273
31208524-5	2019	One of the key pathways that is impaired in diabetic peripheral neuropathy (DPN) is the energy sensing pathway comprising the nicotinamide-adenine dinucleotide (NAD+)-dependent Sirtuin 1 (SIRT1)/peroxisome proliferator-activated receptor-gamma coactivator alpha (PGC-1alpha)/Mt transcription factor A (TFAM or mtTFA) signaling pathway.	NAD	161-165	PPARG coactivator 1 alpha	Homo sapiens	263-273
31208524-5	2019	One of the key pathways that is impaired in diabetic peripheral neuropathy (DPN) is the energy sensing pathway comprising the nicotinamide-adenine dinucleotide (NAD+)-dependent Sirtuin 1 (SIRT1)/peroxisome proliferator-activated receptor-gamma coactivator alpha (PGC-1alpha)/Mt transcription factor A (TFAM or mtTFA) signaling pathway.	NAD	161-165	transcription factor A, mitochondrial	Homo sapiens	302-306
30540938-0	2018	Dual Inhibition of the Lactate Transporters MCT1 and MCT4 Is Synthetic Lethal with Metformin due to NAD+ Depletion in Cancer Cells.	NAD	100-104	solute carrier family 16 member 1	Homo sapiens	44-48
31208524-5	2019	One of the key pathways that is impaired in diabetic peripheral neuropathy (DPN) is the energy sensing pathway comprising the nicotinamide-adenine dinucleotide (NAD+)-dependent Sirtuin 1 (SIRT1)/peroxisome proliferator-activated receptor-gamma coactivator alpha (PGC-1alpha)/Mt transcription factor A (TFAM or mtTFA) signaling pathway.	NAD	161-165	transcription factor A, mitochondrial	Homo sapiens	310-315
30218374-10	2019	Nicotinamide phosphoribosyltransferase (Nampt) generates a key NAD+ intermediate, nicotinamide mononucleotide, from nicotinamide and 5-phosphoribosyl 1-pyrophosphate.	NAD	63-67	nicotinamide phosphoribosyltransferase	Mus musculus	0-38
30576653-2	2018	(2018) describe a mechanism by which insulin signaling represses the NAD+-dependent SIRT1 deacetylase by promoting PACS-2 binding and provide structural clues to understanding how SIRT1 activating compounds (STACs) work.	NAD	69-73	insulin	Homo sapiens	37-44
30576653-2	2018	(2018) describe a mechanism by which insulin signaling represses the NAD+-dependent SIRT1 deacetylase by promoting PACS-2 binding and provide structural clues to understanding how SIRT1 activating compounds (STACs) work.	NAD	69-73	phosphofurin acidic cluster sorting protein 2	Homo sapiens	115-121
30828537-6	2019	Furthermore, the released beta-lapachone is capable of producing ROS under the catalysis of nicotinamide adenine dinucleotide (NAD)(P)H:quinone oxidoreductase-1 (NQO1), which induces the self-amplifiable disassembly of the micelles and drug release to consume adenosine triphosphate (ATP) and downregulate P-glycoprotein (P-gp), eventually overcoming MDR.	NAD	92-125	NAD(P)H quinone dehydrogenase 1	Homo sapiens	127-160
30828537-6	2019	Furthermore, the released beta-lapachone is capable of producing ROS under the catalysis of nicotinamide adenine dinucleotide (NAD)(P)H:quinone oxidoreductase-1 (NQO1), which induces the self-amplifiable disassembly of the micelles and drug release to consume adenosine triphosphate (ATP) and downregulate P-glycoprotein (P-gp), eventually overcoming MDR.	NAD	92-125	NAD(P)H quinone dehydrogenase 1	Homo sapiens	162-166
30828537-6	2019	Furthermore, the released beta-lapachone is capable of producing ROS under the catalysis of nicotinamide adenine dinucleotide (NAD)(P)H:quinone oxidoreductase-1 (NQO1), which induces the self-amplifiable disassembly of the micelles and drug release to consume adenosine triphosphate (ATP) and downregulate P-glycoprotein (P-gp), eventually overcoming MDR.	NAD	92-125	ATP binding cassette subfamily B member 1	Homo sapiens	306-320
30828537-6	2019	Furthermore, the released beta-lapachone is capable of producing ROS under the catalysis of nicotinamide adenine dinucleotide (NAD)(P)H:quinone oxidoreductase-1 (NQO1), which induces the self-amplifiable disassembly of the micelles and drug release to consume adenosine triphosphate (ATP) and downregulate P-glycoprotein (P-gp), eventually overcoming MDR.	NAD	92-125	ATP binding cassette subfamily B member 1	Homo sapiens	322-326
30414145-5	2019	Importantly, several of the cofactors that are known to regulate FOXO transcriptional activity are also sensitive to changes in the cellular redox status, in particular the deacetylase SirT1 is activated in response to reduced levels of reducing equivalents (increased NAD+/NADH+ ratio) and the coactivator PGC-1alpha is induced in response to increased cellular oxidative stress.	NAD	269-273	PPARG coactivator 1 alpha	Homo sapiens	307-317
31055583-0	2019	Metabolic Stress Resistance in Acute Kidney Injury: Evidence for a PPAR-Gamma-Coactivator-1 Alpha-Nicotinamide Adenine Dinucleotide Pathway.	NAD	98-131	PPARG coactivator 1 alpha	Homo sapiens	67-97
30420415-1	2018	The poly(ADP-ribose) polymerase (PARP) superfamily of enzymes catalyses the ADP-ribosylation (ADPr) of target proteins by using nicotinamide adenine dinucleotide (NAD+) as a donor.	NAD	128-161	poly(ADP-ribose) polymerase 1	Homo sapiens	4-31
30420415-1	2018	The poly(ADP-ribose) polymerase (PARP) superfamily of enzymes catalyses the ADP-ribosylation (ADPr) of target proteins by using nicotinamide adenine dinucleotide (NAD+) as a donor.	NAD	128-161	poly(ADP-ribose) polymerase 1	Homo sapiens	33-37
30420415-1	2018	The poly(ADP-ribose) polymerase (PARP) superfamily of enzymes catalyses the ADP-ribosylation (ADPr) of target proteins by using nicotinamide adenine dinucleotide (NAD+) as a donor.	NAD	163-167	poly(ADP-ribose) polymerase 1	Homo sapiens	4-31
30420415-1	2018	The poly(ADP-ribose) polymerase (PARP) superfamily of enzymes catalyses the ADP-ribosylation (ADPr) of target proteins by using nicotinamide adenine dinucleotide (NAD+) as a donor.	NAD	163-167	poly(ADP-ribose) polymerase 1	Homo sapiens	33-37
30552101-4	2018	RNA profiling revealed that TRM from liver and small intestine express P2RX7, a damage/danger-associated molecular pattern (DAMP) receptor that is triggered by extracellular nucleotides (ATP, NAD+).	NAD	192-196	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	71-76
30552101-6	2018	Tissue damage induced during routine isolation of liver lymphocytes led to P2RX7 activation and resulted in selective cell death of TRM P2RX7 activation in vivo by exogenous NAD+ led to a specific depletion of TRM while retaining TCIRC The effect was absent in P2RX7-deficient mice and after P2RX7 blockade.	NAD	174-178	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	136-141
30552101-6	2018	Tissue damage induced during routine isolation of liver lymphocytes led to P2RX7 activation and resulted in selective cell death of TRM P2RX7 activation in vivo by exogenous NAD+ led to a specific depletion of TRM while retaining TCIRC The effect was absent in P2RX7-deficient mice and after P2RX7 blockade.	NAD	174-178	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	136-141
30552101-6	2018	Tissue damage induced during routine isolation of liver lymphocytes led to P2RX7 activation and resulted in selective cell death of TRM P2RX7 activation in vivo by exogenous NAD+ led to a specific depletion of TRM while retaining TCIRC The effect was absent in P2RX7-deficient mice and after P2RX7 blockade.	NAD	174-178	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	136-141
30514854-5	2018	ApoE4 expression has been shown to decrease the level of the NAD-dependent deacetylase and major longevity determinant SirT1 in brain tissue and serum of AD patients as compared to normal controls.	NAD	61-64	apolipoprotein E	Homo sapiens	0-5
30333228-0	2018	c-Jun N-terminal kinase (JNK)-mediated phosphorylation of SARM1 regulates NAD+ cleavage activity to inhibit mitochondrial respiration.	NAD	74-78	mitogen-activated protein kinase 8	Homo sapiens	0-23
30333228-0	2018	c-Jun N-terminal kinase (JNK)-mediated phosphorylation of SARM1 regulates NAD+ cleavage activity to inhibit mitochondrial respiration.	NAD	74-78	mitogen-activated protein kinase 8	Homo sapiens	25-28
30333228-5	2018	The phosphorylation of SARM1 was mediated by c-jun N-terminal kinase (JNK) under oxidative stress conditions, resulting in inhibition of mitochondrial respiration concomitant with enhanced activity of NAD+ cleavage.	NAD	201-205	mitogen-activated protein kinase 8	Homo sapiens	45-68
30333228-5	2018	The phosphorylation of SARM1 was mediated by c-jun N-terminal kinase (JNK) under oxidative stress conditions, resulting in inhibition of mitochondrial respiration concomitant with enhanced activity of NAD+ cleavage.	NAD	201-205	mitogen-activated protein kinase 8	Homo sapiens	70-73
30631755-8	2018	NAD also serves as a substrate for poly(ADP-ribose) polymerase (PARP), sirtuin, and NAD gylycohydrolase (CD38 and CD157); thus, NAD regulates DNA repair, gene expression, and stress response through these enzymes.	NAD	0-3	poly(ADP-ribose) polymerase 1	Homo sapiens	35-62
30631755-8	2018	NAD also serves as a substrate for poly(ADP-ribose) polymerase (PARP), sirtuin, and NAD gylycohydrolase (CD38 and CD157); thus, NAD regulates DNA repair, gene expression, and stress response through these enzymes.	NAD	0-3	poly(ADP-ribose) polymerase 1	Homo sapiens	64-68
29968072-4	2018	Extensive DNA breakage in cells results in excessive activation of PARP with resultant depletion of the cellular stores of nicotinamide adenine dinucleotide (NAD+) which slows the rate of glycolysis, mitochondrial electron transport, and ultimately ATP formation in these cells.	NAD	123-156	poly(ADP-ribose) polymerase 1	Homo sapiens	67-71
30077773-0	2018	GAPDH with NAD+-binding site mutation competitively inhibits the wild-type and affects glucose metabolism in cancer.	NAD	11-15	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	0-5
30077773-4	2018	METHODS: Using site-directed mutagenesis, the human GAPDH clone was mutated at one of the NAD+-binding sites, (i.e.) arginine (R13) and isoleucine (I14) to glutamine (Q13) and phenylalanine (F14), respectively.	NAD	90-94	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	52-57
30077773-9	2018	Mechanistically, structural analysis by bioinformatics revealed that the mutations at the NAD+-binding site altered the solvent-accessibility that perhaps affected the functionality of mutant-GAPDH.	NAD	90-94	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	192-197
30077773-11	2018	GENERAL SIGNIFICANCE: Our findings demonstrate that a minimal mutation at the NAD+-binding site is sufficient to generate a competitive but dysfunctional GAPDH, and its ectopic expression inhibits the wild-type to disrupt glycolysis.	NAD	78-82	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	154-159
29968072-2	2018	Upon detection of a DNA strand break, PARP1 binds to the DNA, cleaves nicotinamide adenine dinucleotide between nicotinamide and ribose and then modifies the DNA nuclear acceptor proteins by formation of a bond between the protein and the ADP-ribose residue.	NAD	70-103	poly(ADP-ribose) polymerase 1	Homo sapiens	38-43
29968072-4	2018	Extensive DNA breakage in cells results in excessive activation of PARP with resultant depletion of the cellular stores of nicotinamide adenine dinucleotide (NAD+) which slows the rate of glycolysis, mitochondrial electron transport, and ultimately ATP formation in these cells.	NAD	158-162	poly(ADP-ribose) polymerase 1	Homo sapiens	67-71
29968072-13	2018	Inhibition of PARP attenuates neutrophil infiltration and inflammatory cytokine expression in the reperfused myocardium and preserves myocardial NAD+ and ATP.	NAD	145-149	poly(ADP-ribose) polymerase 1	Homo sapiens	14-18
29968072-17	2018	In this manner, PARP inhibition partially restores the myocardial concentrations of NAD+, limits ventricular remodeling and fibrosis, and prevents significant decreases in myocardial contractility.	NAD	84-88	poly(ADP-ribose) polymerase 1	Homo sapiens	16-20
29470999-5	2018	Furthermore, NAD+-mediated CD4+ T-cell differentiation was investigated in vivo by using wild-type C57BL/6, MC-/-, MHC class II-/-, Wiskott-Aldrich syndrome protein (WASP)-/-, 5C.C7 recombination-activating gene 2 (Rag2)-/-, and CD11b-DTR transgenic mice.	NAD	13-17	recombination activating gene 2	Mus musculus	215-219
29470999-5	2018	Furthermore, NAD+-mediated CD4+ T-cell differentiation was investigated in vivo by using wild-type C57BL/6, MC-/-, MHC class II-/-, Wiskott-Aldrich syndrome protein (WASP)-/-, 5C.C7 recombination-activating gene 2 (Rag2)-/-, and CD11b-DTR transgenic mice.	NAD	13-17	integrin alpha M	Mus musculus	229-234
29470999-9	2018	More importantly, although treatment with NAD+ resulted in decreased MHC II expression on CD11c+ cells, MC-mediated CD4+ T-cell differentiation rendered mice resistant to administration of lethal doses of L monocytogenes.	NAD	42-46	histocompatibility-2, MHC	Mus musculus	69-75
30173009-6	2018	The PEDOT CMs electrodes detected NADH over the range of 20-240 muM, with a sensitivity of 0.0156 muA/muM and a limit of detection of 5.3 muM.	NAD	34-38	latexin	Homo sapiens	64-67
30281804-1	2018	Among mitochondrial NADP-reducing enzymes, nicotinamide nucleotide transhydrogenase (NNT) establishes an elevated matrix NADPH/NADP+ by catalyzing the reduction of NADP+ at the expense of NADH oxidation coupled to inward proton translocation across the inner mitochondrial membrane.	NAD	188-192	nicotinamide nucleotide transhydrogenase	Mus musculus	85-88
30173009-6	2018	The PEDOT CMs electrodes detected NADH over the range of 20-240 muM, with a sensitivity of 0.0156 muA/muM and a limit of detection of 5.3 muM.	NAD	34-38	latexin	Homo sapiens	102-105
30173009-6	2018	The PEDOT CMs electrodes detected NADH over the range of 20-240 muM, with a sensitivity of 0.0156 muA/muM and a limit of detection of 5.3 muM.	NAD	34-38	latexin	Homo sapiens	102-105
30346689-4	2018	Through enzymological and biochemical studies, we demonstrate that a rapamycin-upregulated enolase isozyme (ENO1) favors gluconeogenesis and a rapamycin-upregulated alcohol dehydrogenase isozyme (ALD4) promotes the reduction of NAD+ to NADH (instead of NADP+ to NADPH).	NAD	228-232	phosphopyruvate hydratase ENO1	Saccharomyces cerevisiae S288C	108-112
29897845-6	2018	Additionally, expression of the NAD-degrading enzyme, CD38, was increased, and the NAD+/NADH (reduced NAD) ratio was reduced in the renal cortex of ZDFRs.	NAD	32-35	CD38 molecule	Rattus norvegicus	54-58
29897845-9	2018	CD38 overexpression may be related to a reduction in the NAD+/NADH ratio in the diabetic kidney.	NAD	57-61	CD38 molecule	Rattus norvegicus	0-4
29897845-9	2018	CD38 overexpression may be related to a reduction in the NAD+/NADH ratio in the diabetic kidney.	NAD	62-66	CD38 molecule	Rattus norvegicus	0-4
30461420-3	2018	We identify an unexpected role of the nicotinamide adenine dinucleotide (NAD+) synthesizing enzyme, NMAT-2/NMNAT, in axon regeneration.	NAD	38-71	Nicotinamide/nicotinic acid mononucleotide adenylyltransferase 2	Caenorhabditis elegans	100-106
30461420-3	2018	We identify an unexpected role of the nicotinamide adenine dinucleotide (NAD+) synthesizing enzyme, NMAT-2/NMNAT, in axon regeneration.	NAD	73-77	Nicotinamide/nicotinic acid mononucleotide adenylyltransferase 2	Caenorhabditis elegans	100-106
30496306-2	2018	Glycolysis relies upon NAD+ to accept electrons in the glyceraldehyde-3-phosphate dehydrogenase (GAPDH) reaction, linking the redox state of the cytosolic NAD+ pool to glycolytic rate.	NAD	23-27	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	55-95
30496306-2	2018	Glycolysis relies upon NAD+ to accept electrons in the glyceraldehyde-3-phosphate dehydrogenase (GAPDH) reaction, linking the redox state of the cytosolic NAD+ pool to glycolytic rate.	NAD	23-27	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	97-102
30496306-2	2018	Glycolysis relies upon NAD+ to accept electrons in the glyceraldehyde-3-phosphate dehydrogenase (GAPDH) reaction, linking the redox state of the cytosolic NAD+ pool to glycolytic rate.	NAD	155-159	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	55-95
30496306-2	2018	Glycolysis relies upon NAD+ to accept electrons in the glyceraldehyde-3-phosphate dehydrogenase (GAPDH) reaction, linking the redox state of the cytosolic NAD+ pool to glycolytic rate.	NAD	155-159	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	97-102
30429362-1	2018	Mono-ADP-ribosylation of an (arginine) protein catalyzed by ADP-ribosyltransferase 1 (ART1) - i.e., transfer of ADP-ribose from NAD to arginine - is reversed by ADP-ribosylarginine hydrolase 1 (ARH1) cleavage of the ADP-ribose-arginine bond.	NAD	128-131	ADP-ribosyltransferase 1	Mus musculus	60-84
30448921-8	2018	Determination of the MM/PBSA free energy indicated that the binding of DHP-8 to SIRT1 significantly increased the binding affinity of SIRT1 to its substrate p53-W as well as to NAD+.	NAD	177-181	dihydropyrimidinase	Homo sapiens	71-74
30053027-5	2018	We showed here that NAD+ salvage pathway was altered in the heart of mouse and human carrying LMNA mutation, leading to an alteration of one of NAD+ co-substrate enzymes, PARP-1.	NAD	20-24	poly(ADP-ribose) polymerase 1	Homo sapiens	171-177
30053027-5	2018	We showed here that NAD+ salvage pathway was altered in the heart of mouse and human carrying LMNA mutation, leading to an alteration of one of NAD+ co-substrate enzymes, PARP-1.	NAD	144-148	poly(ADP-ribose) polymerase 1	Homo sapiens	171-177
30429362-1	2018	Mono-ADP-ribosylation of an (arginine) protein catalyzed by ADP-ribosyltransferase 1 (ART1) - i.e., transfer of ADP-ribose from NAD to arginine - is reversed by ADP-ribosylarginine hydrolase 1 (ARH1) cleavage of the ADP-ribose-arginine bond.	NAD	128-131	ADP-ribosyltransferase 1	Mus musculus	86-90
30429362-1	2018	Mono-ADP-ribosylation of an (arginine) protein catalyzed by ADP-ribosyltransferase 1 (ART1) - i.e., transfer of ADP-ribose from NAD to arginine - is reversed by ADP-ribosylarginine hydrolase 1 (ARH1) cleavage of the ADP-ribose-arginine bond.	NAD	128-131	ADP-ribosylarginine hydrolase	Mus musculus	161-192
30429362-1	2018	Mono-ADP-ribosylation of an (arginine) protein catalyzed by ADP-ribosyltransferase 1 (ART1) - i.e., transfer of ADP-ribose from NAD to arginine - is reversed by ADP-ribosylarginine hydrolase 1 (ARH1) cleavage of the ADP-ribose-arginine bond.	NAD	128-131	ADP-ribosylarginine hydrolase	Mus musculus	194-198
28753256-1	2018	Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) is an energy metabolism-related enzyme, which generates NADH in glycolysis.	NAD	105-109	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	0-40
30404003-4	2018	Nicotinamide adenine dinucleotide (NAD) was found to improve mitochondrial function in DGUOK-deficient hepatocyte-like cells by activating the peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC1alpha).	NAD	0-33	PPARG coactivator 1 alpha	Homo sapiens	143-211
30404003-4	2018	Nicotinamide adenine dinucleotide (NAD) was found to improve mitochondrial function in DGUOK-deficient hepatocyte-like cells by activating the peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC1alpha).	NAD	0-33	PPARG coactivator 1 alpha	Homo sapiens	213-222
30404003-4	2018	Nicotinamide adenine dinucleotide (NAD) was found to improve mitochondrial function in DGUOK-deficient hepatocyte-like cells by activating the peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC1alpha).	NAD	35-38	PPARG coactivator 1 alpha	Homo sapiens	143-211
30404003-4	2018	Nicotinamide adenine dinucleotide (NAD) was found to improve mitochondrial function in DGUOK-deficient hepatocyte-like cells by activating the peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC1alpha).	NAD	35-38	PPARG coactivator 1 alpha	Homo sapiens	213-222
30519106-1	2018	Background: SIRT4 is a member of the sirtuin family of nicotinamide adenine dinucleotide-dependent enzymes located in the mitochondria, and is involved in regulating energy metabolism, stress response, and cellular lifespan in mammalian cells.	NAD	55-88	sirtuin 4	Homo sapiens	12-17
30585266-0	2018	The intracellular NADH level regulates atrophic nonunion pathogenesis through the CtBP2-p300-Runx2 transcriptional complex.	NAD	18-22	C-terminal binding protein 2	Homo sapiens	82-87
30585266-0	2018	The intracellular NADH level regulates atrophic nonunion pathogenesis through the CtBP2-p300-Runx2 transcriptional complex.	NAD	18-22	RUNX family transcription factor 2	Homo sapiens	93-98
30585266-5	2018	The lower NADH level in atrophic nonunion tissues disrupted CtBP2 dimerization and enhanced the blockage of the accessibility of the p300-Runx2 complex to the promoters of a series of bone-related target genes, such as OSC, ALPL, COL1A1, IBSP, SPP1 and MMP13.	NAD	10-14	C-terminal binding protein 2	Homo sapiens	60-65
30585266-5	2018	The lower NADH level in atrophic nonunion tissues disrupted CtBP2 dimerization and enhanced the blockage of the accessibility of the p300-Runx2 complex to the promoters of a series of bone-related target genes, such as OSC, ALPL, COL1A1, IBSP, SPP1 and MMP13.	NAD	10-14	RUNX family transcription factor 2	Homo sapiens	138-143
30585266-5	2018	The lower NADH level in atrophic nonunion tissues disrupted CtBP2 dimerization and enhanced the blockage of the accessibility of the p300-Runx2 complex to the promoters of a series of bone-related target genes, such as OSC, ALPL, COL1A1, IBSP, SPP1 and MMP13.	NAD	10-14	integrin binding sialoprotein	Homo sapiens	238-242
30585266-5	2018	The lower NADH level in atrophic nonunion tissues disrupted CtBP2 dimerization and enhanced the blockage of the accessibility of the p300-Runx2 complex to the promoters of a series of bone-related target genes, such as OSC, ALPL, COL1A1, IBSP, SPP1 and MMP13.	NAD	10-14	matrix metallopeptidase 13	Homo sapiens	253-258
30585266-7	2018	In conclusion, our study revealed that NADH levels determine the expression of bone formation and development of related genes through affecting the dissociation or binding of CtBP2 to the p300-Runx2 complex.	NAD	39-43	C-terminal binding protein 2	Homo sapiens	176-181
30585266-7	2018	In conclusion, our study revealed that NADH levels determine the expression of bone formation and development of related genes through affecting the dissociation or binding of CtBP2 to the p300-Runx2 complex.	NAD	39-43	RUNX family transcription factor 2	Homo sapiens	194-199
30585266-8	2018	These results represent a conserved mechanism, by which CtBP2 serves as a NADH-dependent repressor of the p300-Runx2 transcriptional complex and thus affects bone formation.	NAD	74-78	C-terminal binding protein 2	Homo sapiens	56-61
30585266-8	2018	These results represent a conserved mechanism, by which CtBP2 serves as a NADH-dependent repressor of the p300-Runx2 transcriptional complex and thus affects bone formation.	NAD	74-78	RUNX family transcription factor 2	Homo sapiens	111-116
28753256-1	2018	Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) is an energy metabolism-related enzyme, which generates NADH in glycolysis.	NAD	105-109	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	42-47
28753256-7	2018	Correspondingly, NADH significantly inhibited TNF-alpha and enhanced IL-10 production with elevation of both M1/M2 macrophage markers.	NAD	17-21	tumor necrosis factor	Homo sapiens	46-55
28753256-8	2018	These data suggest that extracellular GAPDH induces intermediate M1/M2 macrophages for termination of inflammation, partly through its enzyme activity for generation of NADH.	NAD	169-173	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	38-43
30078073-4	2018	We present evidence for C4-specific paralogs of NAD-malic enzyme 2, MPC1 and MPC2 (mitochondrial pyruvate carriers) via increased transcript abundance and associated rates of evolution, implicating them as genes recruited to perform C4 photosynthesis within NAD-ME and PEPCK subtypes.	NAD	48-51	malic enzyme 2	Homo sapiens	258-264
30179604-0	2018	Exogenous nicotinamide adenine dinucleotide regulates energy metabolism via hypothalamic connexin 43.	NAD	10-43	gap junction protein, alpha 1	Mus musculus	89-100
30179604-6	2018	Extracellular NAD was imported into N1 hypothalamic neuronal cells in a connexin 43-dependent and CD73-independent manner.	NAD	14-17	gap junction protein, alpha 1	Mus musculus	72-83
30179604-7	2018	Consistent with the in vitro data, inhibition of hypothalamic connexin 43 blocked hypothalamic NAD uptake and NAD-induced anorexia.	NAD	95-98	gap junction protein, alpha 1	Mus musculus	62-73
30179604-7	2018	Consistent with the in vitro data, inhibition of hypothalamic connexin 43 blocked hypothalamic NAD uptake and NAD-induced anorexia.	NAD	110-113	gap junction protein, alpha 1	Mus musculus	62-73
30179604-8	2018	Exogenous NAD suppressed NPY and AgRP transcriptional activity, which was mediated by SIRT1 and FOXO1.	NAD	10-13	agouti related neuropeptide	Mus musculus	33-37
30179604-9	2018	CONCLUSIONS: Exogenous NAD is effectively transported to the hypothalamus via a connexin 43-dependent mechanism and increases hypothalamic NAD content.	NAD	23-26	gap junction protein, alpha 1	Mus musculus	80-91
30380424-0	2018	Alpha-Amino-Beta-Carboxy-Muconate-Semialdehyde Decarboxylase Controls Dietary Niacin Requirements for NAD+ Synthesis.	NAD	102-106	aminocarboxymuconate semialdehyde decarboxylase	Homo sapiens	0-60
30380424-7	2018	This study shows that ACMSD is a key regulator of mammalian dietary niacin requirements and NAD+ metabolism and that the ANDY mouse represents a versatile platform for investigating pathologies linked to low NAD+ levels in aging and neurodegenerative diseases.	NAD	92-96	aminocarboxymuconate semialdehyde decarboxylase	Homo sapiens	22-27
30247868-1	2018	Poly(ADP-ribose) polymerase 14 (PARP14) is a member of the PARP family of enzymes that transfer ADP-ribose from NAD+ to nucleophilic amino acids on target proteins, a process known as mono-ADP-ribosylation (MARylation).	NAD	112-116	poly(ADP-ribose) polymerase 1	Homo sapiens	32-36
30359294-0	2018	Correction to: PARP1 inhibitor (PJ34) improves the function of aging-induced endothelial progenitor cells by preserving intracellular NAD+ levels and increasing SIRT1 activity.	NAD	134-138	poly(ADP-ribose) polymerase 1	Homo sapiens	15-20
30195617-8	2018	KEY FINDINGS: Transcriptomic analysis revealed that genes involved in NAD+ synthesis (Nampt and Nmnat1) in the BAT were negatively correlated with body weight and fat mass.	NAD	70-74	nicotinamide phosphoribosyltransferase	Mus musculus	86-91
30209241-2	2018	Lactate dehydrogenase A (LDHA) has a key role in aerobic glycolysis (the Warburg effect) through regeneration of the electron acceptor NAD+ and is widely regarded as a desirable target for cancer therapeutics.	NAD	135-139	lactate dehydrogenase A	Homo sapiens	0-23
30209241-2	2018	Lactate dehydrogenase A (LDHA) has a key role in aerobic glycolysis (the Warburg effect) through regeneration of the electron acceptor NAD+ and is widely regarded as a desirable target for cancer therapeutics.	NAD	135-139	lactate dehydrogenase A	Homo sapiens	25-29
30405351-0	2018	Extracellular Degradation Into Adenosine and the Activities of Adenosine Kinase and AMPK Mediate Extracellular NAD+-Produced Increases in the Adenylate Pool of BV2 Microglia Under Basal Conditions.	NAD	111-115	adenosine kinase	Homo sapiens	63-79
30405351-8	2018	Collectively, our study has suggested a novel mechanism underlying the protective effects of NAD+ administration, which is mediated by extracellular NAD+ degradation into adenosine as well as the activities of adenosine kinase and AMPK.	NAD	93-97	adenosine kinase	Homo sapiens	210-226
30405740-10	2018	MAN induced declines of both HMGB1/TLR4/p-p65 and TNF-alpha were substantially reversed by cotreatment with nicotinamide mononucleotide or NAD.	NAD	139-142	tumor necrosis factor	Homo sapiens	50-59
30405740-11	2018	These results suggest that downregulation of NAMPT/NAD by MAN treatments contributes to the alleviation of TLR4/NF-kappaB-mediated inflammations in macrophage, which is essential for amelioration of ALI in rats.	NAD	51-54	nuclear factor kappa B subunit 1	Homo sapiens	112-121
29886033-12	2018	Targeting of NAMPT-mediated NAD salvage pathway by miR-206 might provide a new insight in the possible molecular mechanism of breast cancer cell growth regulation.	NAD	28-31	microRNA 206	Homo sapiens	51-58
30055263-6	2018	We further uncovered that the transfer of [14C]MeNA from the root to leaf was significantly increased in both MES2 knockdown and NaMT1-overexpressing lines, suggesting that both NaMT1 and MES2 fine-tune the long-distance transport of MeNA, which is ultimately utilized for NAD production.	NAD	273-276	acetone-cyanohydrin lyase	Arabidopsis thaliana	110-114
30055263-6	2018	We further uncovered that the transfer of [14C]MeNA from the root to leaf was significantly increased in both MES2 knockdown and NaMT1-overexpressing lines, suggesting that both NaMT1 and MES2 fine-tune the long-distance transport of MeNA, which is ultimately utilized for NAD production.	NAD	273-276	S-adenosyl-L-methionine-dependent methyltransferases superfamily protein	Arabidopsis thaliana	129-134
30055263-6	2018	We further uncovered that the transfer of [14C]MeNA from the root to leaf was significantly increased in both MES2 knockdown and NaMT1-overexpressing lines, suggesting that both NaMT1 and MES2 fine-tune the long-distance transport of MeNA, which is ultimately utilized for NAD production.	NAD	273-276	S-adenosyl-L-methionine-dependent methyltransferases superfamily protein	Arabidopsis thaliana	178-183
30055263-6	2018	We further uncovered that the transfer of [14C]MeNA from the root to leaf was significantly increased in both MES2 knockdown and NaMT1-overexpressing lines, suggesting that both NaMT1 and MES2 fine-tune the long-distance transport of MeNA, which is ultimately utilized for NAD production.	NAD	273-276	acetone-cyanohydrin lyase	Arabidopsis thaliana	188-192
29886033-11	2018	miR-206 reduced NAMPT expression at the protein level, leading to a significant decrease in the intracellular NAD level and subsequent decline in cell survival and induction of apoptosis.	NAD	110-113	microRNA 206	Homo sapiens	0-7
30114477-3	2018	In this study, we provide evidence that NAD(P)H:quinone oxidoreductase 1 (NQO1) interacts with and activates SIRT2 in an NAD-dependent manner.	NAD	40-43	NAD(P)H quinone dehydrogenase 1	Homo sapiens	74-78
30279312-4	2018	MDH3 is a glyoxysomal enzyme that is involved in the reoxidation of NADH, which is produced during fatty-acid beta-oxidation.	NAD	68-72	malate dehydrogenase MDH3	Saccharomyces cerevisiae S288C	0-4
29980616-0	2018	Decreased NAD Activates STAT3 and Integrin Pathways to Drive Epithelial-Mesenchymal Transition.	NAD	10-13	signal transducer and activator of transcription 3	Homo sapiens	24-29
28877980-8	2018	FK866 potently inhibited NAMPT activity as demonstrated by reduced mucosal NAD, resulting in reduced abundances and activities of NAD-dependent enzymes including PARP1, Sirt6 and CD38, reduced nuclear factor kappa B activation, and decreased cellular infiltration by inflammatory monocytes, macrophages and activated T cells.	NAD	130-133	poly(ADP-ribose) polymerase 1	Homo sapiens	162-167
29980616-8	2018	Secretomic analysis also showed that decreased NAD triggered interleukin-6 and transforming growth factor beta (TGFbeta) secretion, which activated integrin-beta-catenin, TGFbeta-MAPK, and inflammation signaling pathways to sustain the signaling required for EMT.	NAD	47-50	interleukin 6	Homo sapiens	61-74
29980616-8	2018	Secretomic analysis also showed that decreased NAD triggered interleukin-6 and transforming growth factor beta (TGFbeta) secretion, which activated integrin-beta-catenin, TGFbeta-MAPK, and inflammation signaling pathways to sustain the signaling required for EMT.	NAD	47-50	transforming growth factor beta 1	Homo sapiens	79-110
29980616-8	2018	Secretomic analysis also showed that decreased NAD triggered interleukin-6 and transforming growth factor beta (TGFbeta) secretion, which activated integrin-beta-catenin, TGFbeta-MAPK, and inflammation signaling pathways to sustain the signaling required for EMT.	NAD	47-50	transforming growth factor beta 1	Homo sapiens	112-119
29980616-8	2018	Secretomic analysis also showed that decreased NAD triggered interleukin-6 and transforming growth factor beta (TGFbeta) secretion, which activated integrin-beta-catenin, TGFbeta-MAPK, and inflammation signaling pathways to sustain the signaling required for EMT.	NAD	47-50	transforming growth factor beta 1	Homo sapiens	171-178
29980616-9	2018	We further revealed that decreased NAD inactivated sirtuin 1, resulting in increased signal transducer and activator of transcription 3 (STAT3) acetylation and phosphorylation, and STAT3 activation.	NAD	35-38	signal transducer and activator of transcription 3	Homo sapiens	85-135
29980616-9	2018	We further revealed that decreased NAD inactivated sirtuin 1, resulting in increased signal transducer and activator of transcription 3 (STAT3) acetylation and phosphorylation, and STAT3 activation.	NAD	35-38	signal transducer and activator of transcription 3	Homo sapiens	137-142
29980616-9	2018	We further revealed that decreased NAD inactivated sirtuin 1, resulting in increased signal transducer and activator of transcription 3 (STAT3) acetylation and phosphorylation, and STAT3 activation.	NAD	35-38	signal transducer and activator of transcription 3	Homo sapiens	181-186
30095923-1	2018	SIRT3 is a NAD+-dependent mitochondrial protein deacetylase implicated in the regulation of central metabolism and mitochondrial proteostasis.	NAD	11-14	sirtuin 3	Homo sapiens	0-5
30283350-2	2018	Among the metabolic disorders involved in this syndrome, NAD metabolism was shown to be altered in skeletalmuscle, with an important role for the NAMPT enzyme recycling the nicotinamide precursor.	NAD	57-60	nicotinamide phosphoribosyltransferase	Mus musculus	146-151
29408602-2	2018	In the liver, NAD+ is primarily generated by nicotinamide phosphoribosyltransferase (NAMPT), and hepatic levels of NAMPT and NAD+ have been reported to be dependent on age and body composition.	NAD	14-18	nicotinamide phosphoribosyltransferase	Mus musculus	45-83
29408602-2	2018	In the liver, NAD+ is primarily generated by nicotinamide phosphoribosyltransferase (NAMPT), and hepatic levels of NAMPT and NAD+ have been reported to be dependent on age and body composition.	NAD	14-18	nicotinamide phosphoribosyltransferase	Mus musculus	85-90
30250252-2	2018	TRPM2 is polymodal and can be activated by a wide range of stimuli1-7, including temperature, oxidative stress and NAD+-related metabolites such as ADP-ribose (ADPR).	NAD	115-119	transient receptor potential cation channel, subfamily M, member 2	Danio rerio	0-5
30190133-1	2018	The human nucleoside-diphosphate linked moiety-X (NUDIX) hydrolases that utilize ADP-ribose and NADH/NAD+ are overexpressed in cancer cells, but their roles in hypoxia inducible factor-1alpha (HIF-1alpha) regulation have not yet been revealed.	NAD	96-100	hypoxia inducible factor 1 subunit alpha	Homo sapiens	160-191
30190133-1	2018	The human nucleoside-diphosphate linked moiety-X (NUDIX) hydrolases that utilize ADP-ribose and NADH/NAD+ are overexpressed in cancer cells, but their roles in hypoxia inducible factor-1alpha (HIF-1alpha) regulation have not yet been revealed.	NAD	96-100	hypoxia inducible factor 1 subunit alpha	Homo sapiens	193-203
30190133-1	2018	The human nucleoside-diphosphate linked moiety-X (NUDIX) hydrolases that utilize ADP-ribose and NADH/NAD+ are overexpressed in cancer cells, but their roles in hypoxia inducible factor-1alpha (HIF-1alpha) regulation have not yet been revealed.	NAD	101-105	hypoxia inducible factor 1 subunit alpha	Homo sapiens	160-191
30190133-1	2018	The human nucleoside-diphosphate linked moiety-X (NUDIX) hydrolases that utilize ADP-ribose and NADH/NAD+ are overexpressed in cancer cells, but their roles in hypoxia inducible factor-1alpha (HIF-1alpha) regulation have not yet been revealed.	NAD	101-105	hypoxia inducible factor 1 subunit alpha	Homo sapiens	193-203
29527628-14	2018	Values of serum alanine aminotransferase (ALAT), aspartate aminotransferase (ASAT), urea, and creatinine increased significantly in the DPN and diabetic rats without peripheral neuropathy (PN) compared with control group.	NAD	136-139	glutamic-oxaloacetic transaminase 2	Rattus norvegicus	49-75
29527628-14	2018	Values of serum alanine aminotransferase (ALAT), aspartate aminotransferase (ASAT), urea, and creatinine increased significantly in the DPN and diabetic rats without peripheral neuropathy (PN) compared with control group.	NAD	136-139	glutamic-oxaloacetic transaminase 2	Rattus norvegicus	77-81
29775755-5	2018	EGP1 had a mutation in the NADH gene of the mitochondrial genome ND4 (m.11778 G &gt; A) that causes Leber"s hereditary optic neuropathy.	NAD	27-31	tumor associated calcium signal transducer 2	Homo sapiens	0-4
29753648-1	2018	Nicotinamide phosphoribosyltransferase (NAMPT), a rate-limiting enzyme in nicotinamide adenine dinucleotide (NAD) biosynthesis in mammals, converts nicotinamide into nicotinamide mononucleotide (NMN).	NAD	74-107	nicotinamide phosphoribosyltransferase	Mus musculus	0-38
29753648-1	2018	Nicotinamide phosphoribosyltransferase (NAMPT), a rate-limiting enzyme in nicotinamide adenine dinucleotide (NAD) biosynthesis in mammals, converts nicotinamide into nicotinamide mononucleotide (NMN).	NAD	74-107	nicotinamide phosphoribosyltransferase	Mus musculus	40-45
29753648-1	2018	Nicotinamide phosphoribosyltransferase (NAMPT), a rate-limiting enzyme in nicotinamide adenine dinucleotide (NAD) biosynthesis in mammals, converts nicotinamide into nicotinamide mononucleotide (NMN).	NAD	109-112	nicotinamide phosphoribosyltransferase	Mus musculus	0-38
29753648-1	2018	Nicotinamide phosphoribosyltransferase (NAMPT), a rate-limiting enzyme in nicotinamide adenine dinucleotide (NAD) biosynthesis in mammals, converts nicotinamide into nicotinamide mononucleotide (NMN).	NAD	109-112	nicotinamide phosphoribosyltransferase	Mus musculus	40-45
29753648-9	2018	Our results suggest that NAMPT-mediated NAD biosynthesis may modify cocaine behavioral effects through SIRT1.	NAD	40-43	nicotinamide phosphoribosyltransferase	Mus musculus	25-30
30127395-3	2018	Here we show that a bottleneck enzyme in de novo biosynthesis, quinolinate phosphoribosyltransferase (QPRT), defends renal NAD+ and mediates resistance to acute kidney injury (AKI).	NAD	123-127	quinolinate phosphoribosyltransferase	Homo sapiens	63-100
30127395-3	2018	Here we show that a bottleneck enzyme in de novo biosynthesis, quinolinate phosphoribosyltransferase (QPRT), defends renal NAD+ and mediates resistance to acute kidney injury (AKI).	NAD	123-127	quinolinate phosphoribosyltransferase	Homo sapiens	102-106
30096284-3	2018	We found that ERalpha and/or ERbeta activation using their agonists (0.5 mg/kg E2, PPT or DPN) ameliorate memory impairment in the Morris water maze (MWM) and Y-maze tests and suppress apoptosis as evidenced by decreased caspase-3 activity and increased ratio of Bcl-2/Bax.	NAD	90-93	B cell leukemia/lymphoma 2	Mus musculus	263-268
30059901-3	2018	The NNT is considered a key antioxidative enzyme based on its ability to regenerate NADPH from NADH.	NAD	95-99	nicotinamide nucleotide transhydrogenase	Homo sapiens	4-7
29976663-5	2018	PARP1, or poly(ADP-ribose) polymerase 1, catalyzes the transfer of a poly(ADP-ribose) (PAR) moiety from NAD+ onto acceptor proteins, including itself, histone proteins, and CTCF.	NAD	104-108	poly(ADP-ribose) polymerase 1	Homo sapiens	0-5
29976663-5	2018	PARP1, or poly(ADP-ribose) polymerase 1, catalyzes the transfer of a poly(ADP-ribose) (PAR) moiety from NAD+ onto acceptor proteins, including itself, histone proteins, and CTCF.	NAD	104-108	poly(ADP-ribose) polymerase 1	Homo sapiens	10-39
30139380-0	2018	PARP1 inhibitor (PJ34) improves the function of aging-induced endothelial progenitor cells by preserving intracellular NAD+ levels and increasing SIRT1 activity.	NAD	119-123	poly(ADP-ribose) polymerase 1	Homo sapiens	0-5
30139380-2	2018	Poly (ADP-ribose) polymerase 1 (PARP1) and sirtuin 1 (SIRT1) affect cellular NAD+ levels and play essential roles in regulating metabolism.	NAD	77-81	poly(ADP-ribose) polymerase 1	Homo sapiens	0-30
30139380-2	2018	Poly (ADP-ribose) polymerase 1 (PARP1) and sirtuin 1 (SIRT1) affect cellular NAD+ levels and play essential roles in regulating metabolism.	NAD	77-81	poly(ADP-ribose) polymerase 1	Homo sapiens	32-37
30126181-8	2018	SIRT3 is an NAD+-dependent deacetylase which regulates, among many functions, the redox state of the mitochondria.	NAD	12-15	sirtuin 3	Homo sapiens	0-5
29438734-6	2018	Furthermore, the level of PARP-1 protein and PARP activity decreased and the levels of the PARP substrate nicotinamide adenine dinucleotide (NAD+) and of adenosine triphosphate (ATP), necessary to replenish NAD+ pools, were lowered by isoproterenol treatment.	NAD	207-211	poly(ADP-ribose) polymerase 1	Homo sapiens	26-32
29754052-4	2018	PARP-1 lead to the synthesis of hyperbranched poly (ADP-ribose) polymers (PAR) using nicotinamide adenine dinucleotide (NAD+) as substrate during DNA damage repairing.	NAD	85-118	poly(ADP-ribose) polymerase 1	Homo sapiens	0-6
29754052-4	2018	PARP-1 lead to the synthesis of hyperbranched poly (ADP-ribose) polymers (PAR) using nicotinamide adenine dinucleotide (NAD+) as substrate during DNA damage repairing.	NAD	120-124	poly(ADP-ribose) polymerase 1	Homo sapiens	0-6
30116283-3	2018	The small-molecule NAD+ mimetics, olaparib, niraparib, rucaparib, veliparib, and talazoparib, inhibit the catalytic activity of PARP-1 and PARP-2 and are currently being studied in later-stage clinical trials.	NAD	19-23	poly(ADP-ribose) polymerase 1	Homo sapiens	128-134
30116283-3	2018	The small-molecule NAD+ mimetics, olaparib, niraparib, rucaparib, veliparib, and talazoparib, inhibit the catalytic activity of PARP-1 and PARP-2 and are currently being studied in later-stage clinical trials.	NAD	19-23	poly(ADP-ribose) polymerase 2	Homo sapiens	139-145
29604362-10	2018	Further, diabetic KHK-A KO mice contained decreased renal NAD+ level with the increase of renal hypoxia-inducible factor 1-alpha expression despite having increased renal nicotinamide (NAM) level.	NAD	58-62	ketohexokinase	Mus musculus	18-21
30099653-3	2018	When employed for detection of NADH, it exhibits electrooxidation at a low potential of 150 mV (vs. Ag/AgCl) with high sensitivity of 0.0814 microA microM-1 cm2 over a wide linear range (1-280 muM), good selectivity, and a low limit of detection (1 muM).	NAD	31-35	latexin	Homo sapiens	193-196
30099653-3	2018	When employed for detection of NADH, it exhibits electrooxidation at a low potential of 150 mV (vs. Ag/AgCl) with high sensitivity of 0.0814 microA microM-1 cm2 over a wide linear range (1-280 muM), good selectivity, and a low limit of detection (1 muM).	NAD	31-35	latexin	Homo sapiens	249-252
29935245-6	2018	The expression of NAD+-synthesis enzymes, NaPRT1, nicotinamide riboside kinase1 (NRK1) and nicotinamide mononucleotide adenylyltransferase1 (Nmnat1) was significantly increased at both the mRNA and protein levels in OXY-treated LS 174T cells.	NAD	18-22	nicotinamide riboside kinase 1	Homo sapiens	50-79
29935245-8	2018	In conclusion, OXY increases NAD+ levels, resulting in the stimulation of MUC2 expression in LS 174T cells.	NAD	29-33	mucin 2, oligomeric mucus/gel-forming	Homo sapiens	74-78
29935245-9	2018	These findings present a novel role for NAD+ in stimulation of MUC2 expression.	NAD	40-44	mucin 2, oligomeric mucus/gel-forming	Homo sapiens	63-67
30038627-6	2018	Injection of the ARTC2.2-blocking nanobody s+16a 30 min prior to organ harvesting effectively prevented ADP-ribosylation of P2X7 during cell preparation and thereby prevented NAD-induced cell death of the isolated Trm upon subsequent incubation at 37 C. Consequently, preserving Trm vitality by s+16a injection enabled a highly sensitive in vitro cytokine expression profile analyses of FACS sorted liver Trm.	NAD	175-178	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	124-128
30030453-1	2018	SIRT6 is a NAD-dependent histone 3 deacetylase.	NAD	11-14	sirtuin 6	Mus musculus	0-5
29921717-4	2018	Here, we investigated the roles of NAD+ metabolism in SC functions in vivo by mutating NAMPT, the rate-limiting enzyme of NAD+ biosynthesis, specifically in SCs.	NAD	122-126	nicotinamide phosphoribosyltransferase	Mus musculus	87-92
29921717-6	2018	JUN, a master regulator of SC dedifferentiation, is elevated in NAMPT SCKO SCs, suggesting that decreased NAD+ levels cause them to arrest at an immature stage.	NAD	106-110	nicotinamide phosphoribosyltransferase	Mus musculus	64-69
29921717-10	2018	Aberrant regulation of NAD+ biosynthesis via NAMPT deletion results in a blockade of Schwann cell maturation during development and severe peripheral neuropathy without significant axon loss.	NAD	23-27	nicotinamide phosphoribosyltransferase	Mus musculus	45-50
30026729-4	2018	KL1333 is an orally available, small organic molecule that reacts with NAD(P)H:quinone oxidoreductase 1 (NQO1) as a substrate, resulting in increases in intracellular NAD+ levels via NADH oxidation.	NAD	167-171	NAD(P)H quinone dehydrogenase 1	Homo sapiens	71-103
30026729-4	2018	KL1333 is an orally available, small organic molecule that reacts with NAD(P)H:quinone oxidoreductase 1 (NQO1) as a substrate, resulting in increases in intracellular NAD+ levels via NADH oxidation.	NAD	167-171	NAD(P)H quinone dehydrogenase 1	Homo sapiens	105-109
30026729-4	2018	KL1333 is an orally available, small organic molecule that reacts with NAD(P)H:quinone oxidoreductase 1 (NQO1) as a substrate, resulting in increases in intracellular NAD+ levels via NADH oxidation.	NAD	183-187	NAD(P)H quinone dehydrogenase 1	Homo sapiens	71-103
30026729-4	2018	KL1333 is an orally available, small organic molecule that reacts with NAD(P)H:quinone oxidoreductase 1 (NQO1) as a substrate, resulting in increases in intracellular NAD+ levels via NADH oxidation.	NAD	183-187	NAD(P)H quinone dehydrogenase 1	Homo sapiens	105-109
30038627-1	2018	On murine T cells, GPI-anchored ADP-ribosyltransferase 2.2 (ARTC2.2) ADP-ribosylates the P2X7 ion channel at arginine 125 in response to nicotinamide adenine dinucleotide (NAD+) released during cell preparation.	NAD	137-170	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	89-93
30038627-1	2018	On murine T cells, GPI-anchored ADP-ribosyltransferase 2.2 (ARTC2.2) ADP-ribosylates the P2X7 ion channel at arginine 125 in response to nicotinamide adenine dinucleotide (NAD+) released during cell preparation.	NAD	172-176	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	89-93
29774488-1	2018	Sirtuin 3 is a nicotinamide adenine dinucleotide dependent mitochondrial deacetylase that governs mitochondrial metabolism and oxidative defense.	NAD	15-48	sirtuin 3	Homo sapiens	0-9
29887397-4	2018	We show that responsiveness to hypoxia progressively disappears after inducible deletion of the Ndufs2 gene, which encodes the 49 kDa subunit forming the coenzyme Q binding site in MCI, even in the presence of MCII substrates and chemical NAD+ regeneration.	NAD	239-243	NADH:ubiquinone oxidoreductase core subunit S2	Homo sapiens	96-102
29444200-1	2018	Aims: Sirtuin 3 (Sirt3) is a mitochondrial, nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase that reduces oxidative stress by activation of superoxide dismutase 2 (SOD2).	NAD	44-77	superoxide dismutase 2, mitochondrial	Mus musculus	154-176
29444200-1	2018	Aims: Sirtuin 3 (Sirt3) is a mitochondrial, nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase that reduces oxidative stress by activation of superoxide dismutase 2 (SOD2).	NAD	44-77	superoxide dismutase 2, mitochondrial	Mus musculus	178-182
29444200-1	2018	Aims: Sirtuin 3 (Sirt3) is a mitochondrial, nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase that reduces oxidative stress by activation of superoxide dismutase 2 (SOD2).	NAD	79-82	superoxide dismutase 2, mitochondrial	Mus musculus	154-176
29444200-1	2018	Aims: Sirtuin 3 (Sirt3) is a mitochondrial, nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase that reduces oxidative stress by activation of superoxide dismutase 2 (SOD2).	NAD	79-82	superoxide dismutase 2, mitochondrial	Mus musculus	178-182
30018712-0	2018	NADH protect against radiation enteritis by enhancing autophagy and inhibiting inflammation through PI3K/AKT pathway.	NAD	0-4	AKT serine/threonine kinase 1	Rattus norvegicus	105-108
30018712-9	2018	Western blot data indicated that NADH promoted the microtubule associated protein 1A/1B-light chain 3(LC3)-I to LC3II and the expression of IL-1beta and TNFalpha decreased in a dose dependent manner.	NAD	33-37	interleukin 1 beta	Rattus norvegicus	140-148
30018712-9	2018	Western blot data indicated that NADH promoted the microtubule associated protein 1A/1B-light chain 3(LC3)-I to LC3II and the expression of IL-1beta and TNFalpha decreased in a dose dependent manner.	NAD	33-37	tumor necrosis factor	Rattus norvegicus	153-161
30018712-11	2018	In the animal experiment, after 12 Gy radiation, there were less TNFalpha and more LC3II in the RT+NADH group than that of RT group.	NAD	99-103	tumor necrosis factor	Rattus norvegicus	65-73
30018712-13	2018	Thus, our study provides the evidence that NADH may protect against radiation enteritis by suppressing inflammation and enhancing autophagy through PI3K/AKT pathway in normal intestinal cells.	NAD	43-47	AKT serine/threonine kinase 1	Rattus norvegicus	153-156
29477240-3	2018	SIRT1 encodes an NAD-dependent deacetylase that modifies the activity of key transcriptional regulators affected in diabetic kidneys, including NF-kappaB, STAT3, p53, FOXO4, and PGC1-alpha.	NAD	17-20	signal transducer and activator of transcription 3	Mus musculus	155-160
29905535-0	2018	Loss of NAMPT in aging retinal pigment epithelium reduces NAD+ availability and promotes cellular senescence.	NAD	58-62	nicotinamide phosphoribosyltransferase	Mus musculus	8-13
29905535-4	2018	NAD+ levels declined with age and correlated directly with decreased nicotinamide phosphoribosyltransferase (NAMPT) expression, increased expression of senescence markers (p16INK4a, p21Waf/Cip1, ApoJ, CTGF and beta-galactosidase) and significant reductions in SIRT1 expression and activity.	NAD	0-4	nicotinamide phosphoribosyltransferase	Mus musculus	69-107
29905535-4	2018	NAD+ levels declined with age and correlated directly with decreased nicotinamide phosphoribosyltransferase (NAMPT) expression, increased expression of senescence markers (p16INK4a, p21Waf/Cip1, ApoJ, CTGF and beta-galactosidase) and significant reductions in SIRT1 expression and activity.	NAD	0-4	nicotinamide phosphoribosyltransferase	Mus musculus	109-114
29905535-4	2018	NAD+ levels declined with age and correlated directly with decreased nicotinamide phosphoribosyltransferase (NAMPT) expression, increased expression of senescence markers (p16INK4a, p21Waf/Cip1, ApoJ, CTGF and beta-galactosidase) and significant reductions in SIRT1 expression and activity.	NAD	0-4	cyclin dependent kinase inhibitor 2A	Mus musculus	172-180
29905535-5	2018	We simulated in vitro the age-dependent decline in NAD+ and the related increase in RPE senescence in human (ARPE-19) and mouse primary RPE using the NAMPT inhibitor FK866 and demonstrated the positive impact of NAD+-enhancing therapies on RPE cell viability.	NAD	51-55	nicotinamide phosphoribosyltransferase	Mus musculus	150-155
29905535-5	2018	We simulated in vitro the age-dependent decline in NAD+ and the related increase in RPE senescence in human (ARPE-19) and mouse primary RPE using the NAMPT inhibitor FK866 and demonstrated the positive impact of NAD+-enhancing therapies on RPE cell viability.	NAD	212-216	nicotinamide phosphoribosyltransferase	Mus musculus	150-155
29645357-2	2018	The complexes showed excellent bovine serum albumin (BSA) and DNA binding properties and were able to oxidize NADH to NAD+ (NAD=nicotinamide adenine dinucleotide) efficiently.	NAD	110-114	albumin	Homo sapiens	38-51
29645357-2	2018	The complexes showed excellent bovine serum albumin (BSA) and DNA binding properties and were able to oxidize NADH to NAD+ (NAD=nicotinamide adenine dinucleotide) efficiently.	NAD	118-122	albumin	Homo sapiens	38-51
29645357-2	2018	The complexes showed excellent bovine serum albumin (BSA) and DNA binding properties and were able to oxidize NADH to NAD+ (NAD=nicotinamide adenine dinucleotide) efficiently.	NAD	110-113	albumin	Homo sapiens	38-51
29645357-2	2018	The complexes showed excellent bovine serum albumin (BSA) and DNA binding properties and were able to oxidize NADH to NAD+ (NAD=nicotinamide adenine dinucleotide) efficiently.	NAD	128-161	albumin	Homo sapiens	38-51
29571013-5	2018	We here constructed structural models of Sirt4 by homology modeling and threading, and docked nicotinamide adenine dinucleotide+ (NAD+) to Sirt4.	NAD	94-127	sirtuin 4	Homo sapiens	41-46
29571013-5	2018	We here constructed structural models of Sirt4 by homology modeling and threading, and docked nicotinamide adenine dinucleotide+ (NAD+) to Sirt4.	NAD	94-127	sirtuin 4	Homo sapiens	139-144
29571013-5	2018	We here constructed structural models of Sirt4 by homology modeling and threading, and docked nicotinamide adenine dinucleotide+ (NAD+) to Sirt4.	NAD	130-134	sirtuin 4	Homo sapiens	41-46
29571013-5	2018	We here constructed structural models of Sirt4 by homology modeling and threading, and docked nicotinamide adenine dinucleotide+ (NAD+) to Sirt4.	NAD	130-134	sirtuin 4	Homo sapiens	139-144
29571013-6	2018	In addition, a partial GDH structure was docked to the Sirt4-NAD+ complex model.	NAD	61-65	sirtuin 4	Homo sapiens	55-60
29508376-2	2018	Depending on several parameters like extracellular NAD+ , P2X7 can be ADP-ribosylated rapidly by adjacent ARTC2.2 resulting in susceptibilities to apoptosis to a varying extent.	NAD	51-55	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	58-62
28548540-5	2018	CRITICAL ISSUES: Three distinct families of enzymes consume NAD+ as substrate: poly(ADP-ribose) polymerases (PARPs), ADP-ribosyl cyclases (CD38/CD157) and sirtuins.	NAD	60-64	bone marrow stromal cell antigen 1	Homo sapiens	144-149
29700119-4	2018	Here, multi-angle light scattering (MALS) data established the NAD+- and NADH-dependent assembly of CtBP1 and CtBP2 into tetramers.	NAD	63-67	C-terminal binding protein 2	Homo sapiens	110-115
29700119-4	2018	Here, multi-angle light scattering (MALS) data established the NAD+- and NADH-dependent assembly of CtBP1 and CtBP2 into tetramers.	NAD	73-77	C-terminal binding protein 2	Homo sapiens	110-115
29700119-5	2018	An examination of subunit interactions within CtBP1 and CtBP2 crystal lattices revealed that both share a very similar tetrameric arrangement resulting from assembly of two dimeric pairs, with specific interactions probably being sensitive to NAD(H) binding.	NAD	243-249	C-terminal binding protein 2	Homo sapiens	56-61
29874584-6	2018	Human neurons require nicotinamide phosphoribosyltransferase (NAMPT) to maintain the NAD+ pool and utilize NRK1 to synthesize NAD+ from NAD+ precursors.	NAD	126-130	nicotinamide riboside kinase 1	Homo sapiens	107-111
29874584-6	2018	Human neurons require nicotinamide phosphoribosyltransferase (NAMPT) to maintain the NAD+ pool and utilize NRK1 to synthesize NAD+ from NAD+ precursors.	NAD	126-130	nicotinamide riboside kinase 1	Homo sapiens	107-111
29627626-1	2018	Poly (ADP-ribose) polymerase 1 (PARP1) is a DNA damage sensor that catalyzes the poly (ADP-ribose) (PAR) onto a variety of target proteins, such as histones, DSB repair factors and PARP1 itself under consumption of NAD+.	NAD	215-219	poly(ADP-ribose) polymerase 1	Homo sapiens	0-30
28840449-4	2018	MB can reroute electrons in the mitochondrial electron transfer chain directly from NADH to cytochrome c, increasing the activity of complex IV and effectively promoting mitochondrial activity while mitigating oxidative stress.	NAD	84-88	cytochrome c, somatic	Homo sapiens	92-104
29627626-1	2018	Poly (ADP-ribose) polymerase 1 (PARP1) is a DNA damage sensor that catalyzes the poly (ADP-ribose) (PAR) onto a variety of target proteins, such as histones, DSB repair factors and PARP1 itself under consumption of NAD+.	NAD	215-219	poly(ADP-ribose) polymerase 1	Homo sapiens	32-37
29627626-1	2018	Poly (ADP-ribose) polymerase 1 (PARP1) is a DNA damage sensor that catalyzes the poly (ADP-ribose) (PAR) onto a variety of target proteins, such as histones, DSB repair factors and PARP1 itself under consumption of NAD+.	NAD	215-219	poly(ADP-ribose) polymerase 1	Homo sapiens	181-186
29664094-4	2018	PARP, activated by dsDNA, catalyzed its substrate nicotinamide adenine dinucleotide (NAD+) to polymerize as a poly(ADP-ribose) polymer (PAR).	NAD	50-83	poly(ADP-ribose) polymerase 1	Homo sapiens	0-4
29977153-8	2018	However, re-expression of CD38 in the knockdown clones reversed the effect on Sirt1/NF-kappaB/TLR2 signaling, which is NAD-dependent.	NAD	119-122	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	84-93
29664094-4	2018	PARP, activated by dsDNA, catalyzed its substrate nicotinamide adenine dinucleotide (NAD+) to polymerize as a poly(ADP-ribose) polymer (PAR).	NAD	85-89	poly(ADP-ribose) polymerase 1	Homo sapiens	0-4
29795234-7	2018	Finally, the inhibition study carried out after a high-throughput in silico screening and an in vitro testing with hPARP1 and bacterial PARPs identified a different inhibitory profile, a new highly inhibitory compound never before described for hPARP1, and a specificity of bacterial PARPs for a compound that mimics NAD+ (EB-47).	NAD	317-321	poly(ADP-ribose) polymerase 1	Homo sapiens	136-141
29795984-0	2018	Reexamining IFN-gamma Stimulation of De Novo NAD+ in Monocyte-Derived Macrophages.	NAD	45-49	interferon gamma	Homo sapiens	12-21
29217642-8	2018	We show that the Nmrk2 gene is an AMP-activated protein kinase and peroxisome proliferator-activated receptor alpha responsive gene that is activated by energy stress and NAD+ depletion in isolated rat cardiomyocytes.	NAD	171-175	nicotinamide riboside kinase 2	Rattus norvegicus	17-22
29740774-4	2018	SIRT1 is a NAD+-dependent deacetylase that can deacetylate and activate peroxisome proliferator-activated receptor-gamma coactivator 1alpha (PGC-1alpha), a master regulator of mitochondrial integrity, biogenesis, and function.	NAD	11-14	PPARG coactivator 1 alpha	Homo sapiens	72-139
29748257-4	2018	Adipogenic signaling rapidly induces cytoplasmic NMNAT-2, which competes with nuclear NMNAT-1 for the common substrate, nicotinamide mononucleotide, leading to a precipitous reduction in nuclear NAD+ levels.	NAD	195-199	nicotinamide nucleotide adenylyltransferase 2	Homo sapiens	49-56
29748257-5	2018	This inhibits the catalytic activity of poly[adenosine diphosphate (ADP)-ribose] polymerase-1 (PARP-1), a NAD+-dependent enzyme that represses adipogenic transcription by ADP-ribosylating the adipogenic transcription factor C/EBPbeta.	NAD	106-110	poly(ADP-ribose) polymerase 1	Homo sapiens	95-101
29748257-6	2018	Reversal of PARP-1-mediated repression by NMNAT-2-mediated nuclear NAD+ depletion in response to adipogenic signals drives adipogenesis.	NAD	67-71	poly(ADP-ribose) polymerase 1	Homo sapiens	12-18
29748257-6	2018	Reversal of PARP-1-mediated repression by NMNAT-2-mediated nuclear NAD+ depletion in response to adipogenic signals drives adipogenesis.	NAD	67-71	nicotinamide nucleotide adenylyltransferase 2	Homo sapiens	42-49
29740774-4	2018	SIRT1 is a NAD+-dependent deacetylase that can deacetylate and activate peroxisome proliferator-activated receptor-gamma coactivator 1alpha (PGC-1alpha), a master regulator of mitochondrial integrity, biogenesis, and function.	NAD	11-14	PPARG coactivator 1 alpha	Homo sapiens	141-151
29717994-7	2018	At the S-loop, the bound trehalose in the GAPDH structure induces a 2.4  rotation compared with the NAD+-free ecGAPDH structure and a 3.1  rotation compared with the NAD+-bound ecGAPDH structure.	NAD	100-104	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	42-47
29717994-7	2018	At the S-loop, the bound trehalose in the GAPDH structure induces a 2.4  rotation compared with the NAD+-free ecGAPDH structure and a 3.1  rotation compared with the NAD+-bound ecGAPDH structure.	NAD	166-170	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	42-47
29551635-0	2018	NAMPT-mediated NAD+ biosynthesis is indispensable for adipose tissue plasticity and development of obesity.	NAD	15-19	nicotinamide phosphoribosyltransferase	Mus musculus	0-5
29537672-9	2018	Interestingly, the NADH-stimulated oxygen consumption and ATP synthesis increased in the presence of the physiological platelets agonists, thrombin or collagen.	NAD	19-23	coagulation factor II, thrombin	Homo sapiens	139-147
29398136-8	2018	Third, experiments in which nicotinamide and a specific Nampt inhibitor (FK866) were administered in the active and rest phases revealed that the Nampt/NAD+ system is involved in renal inorganic phosphate excretion.	NAD	152-156	nicotinamide phosphoribosyltransferase	Mus musculus	56-61
29398136-8	2018	Third, experiments in which nicotinamide and a specific Nampt inhibitor (FK866) were administered in the active and rest phases revealed that the Nampt/NAD+ system is involved in renal inorganic phosphate excretion.	NAD	152-156	nicotinamide phosphoribosyltransferase	Mus musculus	146-151
29398136-10	2018	In systemic Nampt+/- mice, NAD levels were significantly reduced in the liver, kidney, and intestine, and the daily oscillation (active and rest phases) of the plasma phosphate concentration was attenuated.	NAD	27-30	nicotinamide phosphoribosyltransferase	Mus musculus	12-17
29398136-11	2018	Thus, the Nampt/NAD+ system for Npt2 regulation and cellular shifts to tissues such as the liver play an important role in generating daily oscillation of plasma inorganic phosphate levels.	NAD	16-20	nicotinamide phosphoribosyltransferase	Mus musculus	10-15
29476819-2	2018	SIRT1 deacetylates p53 in a NAD+-dependent manner to inhibit transcription activity of p53, in turn modulate pathways that are implicated in regulation of tissue homoeostasis and many disease states.	NAD	28-32	tumor protein p53	Homo sapiens	19-22
29476819-2	2018	SIRT1 deacetylates p53 in a NAD+-dependent manner to inhibit transcription activity of p53, in turn modulate pathways that are implicated in regulation of tissue homoeostasis and many disease states.	NAD	28-32	tumor protein p53	Homo sapiens	87-90
29752474-5	2018	Mechanistically, the interaction between CHES1 and ERalpha enhanced the recruitment of nicotinamide adenine dinucleotide (NAD+) deacetylase Sirtuin 1 (SIRT1), and it further induced SIRT1-mediated ERalpha deacetylation and repression on the promoter-binding enrichment of ERalpha.	NAD	87-120	estrogen receptor 1	Homo sapiens	51-58
29752474-5	2018	Mechanistically, the interaction between CHES1 and ERalpha enhanced the recruitment of nicotinamide adenine dinucleotide (NAD+) deacetylase Sirtuin 1 (SIRT1), and it further induced SIRT1-mediated ERalpha deacetylation and repression on the promoter-binding enrichment of ERalpha.	NAD	87-120	estrogen receptor 1	Homo sapiens	197-204
29752474-5	2018	Mechanistically, the interaction between CHES1 and ERalpha enhanced the recruitment of nicotinamide adenine dinucleotide (NAD+) deacetylase Sirtuin 1 (SIRT1), and it further induced SIRT1-mediated ERalpha deacetylation and repression on the promoter-binding enrichment of ERalpha.	NAD	87-120	estrogen receptor 1	Homo sapiens	197-204
31938369-2	2018	The aim of this study was to determine whether sirtuin type 1 (SIRT1), an NAD+ dependent deacetylase, affected allodynia and hyperalgesia in neuropathic pain.	NAD	74-77	sirtuin 1	Rattus norvegicus	47-61
31938369-2	2018	The aim of this study was to determine whether sirtuin type 1 (SIRT1), an NAD+ dependent deacetylase, affected allodynia and hyperalgesia in neuropathic pain.	NAD	74-77	sirtuin 1	Rattus norvegicus	63-68
29638231-5	2018	The trapped single leukemia cells, e.g., THP-1, Jurkat and K562 cells, are distinguished from WBCs in the phasor-FLIM lifetime map, as they exhibit significant shift towards shorter fluorescence lifetime and a higher ratio of free/bound NADH compared to WBCs, because of their glycolysis-dominant metabolism for rapid proliferation.	NAD	237-241	GLI family zinc finger 2	Homo sapiens	41-46
29551635-6	2018	Here we investigated how the NAD+ biosynthetic enzyme nicotinamide phosphoribosyltransferase (NAMPT) supports adipose plasticity and the pathological progression to obesity.	NAD	29-33	nicotinamide phosphoribosyltransferase	Mus musculus	54-92
29551635-6	2018	Here we investigated how the NAD+ biosynthetic enzyme nicotinamide phosphoribosyltransferase (NAMPT) supports adipose plasticity and the pathological progression to obesity.	NAD	29-33	nicotinamide phosphoribosyltransferase	Mus musculus	94-99
29534964-7	2018	Of note, we observed the decreased level of NADPH, NADH and enzymatic activity of sirtuin-1 in response to 6PGD inhibition in doxorubicin-resistant ATC cells.	NAD	51-55	phosphogluconate dehydrogenase	Homo sapiens	107-111
29710809-3	2018	B-Hydroxybutyrate, the most studied ketone body, has been shown to reduce the production of reactive oxygen species (ROS), improving mitochondrial respiration: it stimulates the cellular endogenous antioxidant system with the activation of nuclear factor erythroid-derived 2-related factor 2 (Nrf2), it modulates the ratio between the oxidized and reduced forms of nicotinamide adenine dinucleotide (NAD+/NADH) and it increases the efficiency of electron transport chain through the expression of uncoupling proteins.	NAD	365-398	NFE2 like bZIP transcription factor 2	Homo sapiens	240-291
29710809-3	2018	B-Hydroxybutyrate, the most studied ketone body, has been shown to reduce the production of reactive oxygen species (ROS), improving mitochondrial respiration: it stimulates the cellular endogenous antioxidant system with the activation of nuclear factor erythroid-derived 2-related factor 2 (Nrf2), it modulates the ratio between the oxidized and reduced forms of nicotinamide adenine dinucleotide (NAD+/NADH) and it increases the efficiency of electron transport chain through the expression of uncoupling proteins.	NAD	400-404	NFE2 like bZIP transcription factor 2	Homo sapiens	240-291
29710809-3	2018	B-Hydroxybutyrate, the most studied ketone body, has been shown to reduce the production of reactive oxygen species (ROS), improving mitochondrial respiration: it stimulates the cellular endogenous antioxidant system with the activation of nuclear factor erythroid-derived 2-related factor 2 (Nrf2), it modulates the ratio between the oxidized and reduced forms of nicotinamide adenine dinucleotide (NAD+/NADH) and it increases the efficiency of electron transport chain through the expression of uncoupling proteins.	NAD	405-409	NFE2 like bZIP transcription factor 2	Homo sapiens	240-291
29478906-4	2018	Here, we report the identification of Vacor as a substrate metabolized by the consecutive action of NAMPT and NMNAT2 into the NAD analog Vacor adenine dinucleotide (VAD).	NAD	126-129	nicotinamide nucleotide adenylyltransferase 2	Homo sapiens	110-116
29478906-5	2018	This leads to inhibition of both enzymes, as well as NAD-dependent dehydrogenases, thereby causing unprecedented rapid NAD depletion, glycolytic block, energy failure, and necrotic death of NMNAT2-proficient cancer cells.	NAD	53-56	nicotinamide nucleotide adenylyltransferase 2	Homo sapiens	190-196
29642888-3	2018	RESULTS: A new metabolic module was established here, in which, permease Gap1p for L-phenylalanine transportation, catalytic enzymes Aro8p, Aro10p and Adh2p in Ehrlich pathway respectively responsible for transamination, decarboxylation and reduction were assembled, besides, glutamate dehydrogenase Gdh2p was harbored for re-supplying another substrate 2-oxoglutarate, relieving product glutamate repression and regenerating cofactor NADH.	NAD	435-439	amino acid permease GAP1	Saccharomyces cerevisiae S288C	73-78
29208611-1	2018	Nicotinamide adenine dinucleotide (NAD+) can be synthesized by nicotinamide phosphoribosyltransferase (NAMPT).	NAD	0-33	nicotinamide phosphoribosyltransferase	Mus musculus	63-101
29642561-0	2018	beta-Nicotinamide Adenine Dinucleotide (beta-NAD) Inhibits ATP-Dependent IL-1beta Release from Human Monocytic Cells.	NAD	0-38	interleukin 1 beta	Homo sapiens	73-81
29642561-0	2018	beta-Nicotinamide Adenine Dinucleotide (beta-NAD) Inhibits ATP-Dependent IL-1beta Release from Human Monocytic Cells.	NAD	40-48	interleukin 1 beta	Homo sapiens	73-81
29642561-2	2018	ATP, a stimulus of IL-1beta maturation, is released from damaged cells along with beta-nicotinamide adenine dinucleotide (beta-NAD).	NAD	82-120	interleukin 1 beta	Homo sapiens	19-27
29642561-2	2018	ATP, a stimulus of IL-1beta maturation, is released from damaged cells along with beta-nicotinamide adenine dinucleotide (beta-NAD).	NAD	122-130	interleukin 1 beta	Homo sapiens	19-27
29642561-3	2018	Here, we tested the hypothesis that beta-NAD controls ATP-signaling and, hence, IL-1beta release.	NAD	36-44	interleukin 1 beta	Homo sapiens	80-88
29642561-7	2018	Exogenous beta-NAD signaled via P2Y receptors and dose-dependently (IC50 = 15 microM) suppressed the BzATP-induced IL-1beta release.	NAD	10-18	interleukin 1 beta	Homo sapiens	115-123
29642561-10	2018	In conclusion, we describe a novel triple membrane-passing signaling cascade triggered by extracellular beta-NAD that suppresses ATP-induced release of IL-1beta by monocytic cells.	NAD	104-112	interleukin 1 beta	Homo sapiens	152-160
29351413-7	2018	NADH:ubiquinone oxidotreductase subunit-A9 (NDUFA9) protein abundance was lower in soleus muscle of 28- and 70-day mdx mice and EDL muscle of 70-day mdx mice compared with same muscles in WT (C57/BL10ScSn) animals.	NAD	0-4	NADH:ubiquinone oxidoreductase subunit A9	Mus musculus	44-50
29208611-1	2018	Nicotinamide adenine dinucleotide (NAD+) can be synthesized by nicotinamide phosphoribosyltransferase (NAMPT).	NAD	0-33	nicotinamide phosphoribosyltransferase	Mus musculus	103-108
29208611-1	2018	Nicotinamide adenine dinucleotide (NAD+) can be synthesized by nicotinamide phosphoribosyltransferase (NAMPT).	NAD	35-39	nicotinamide phosphoribosyltransferase	Mus musculus	63-101
29208611-1	2018	Nicotinamide adenine dinucleotide (NAD+) can be synthesized by nicotinamide phosphoribosyltransferase (NAMPT).	NAD	35-39	nicotinamide phosphoribosyltransferase	Mus musculus	103-108
29208611-2	2018	We aimed to determine the role of NAMPT in maintaining NAD+ levels, mitochondrial function, and metabolic homeostasis in skeletal muscle cells.	NAD	55-59	nicotinamide phosphoribosyltransferase	Mus musculus	34-39
29208611-5	2018	In sh Nampt KD C2C12 myoblasts, Nampt and NAD+ levels were reduced by 70% and 50%, respectively, and maximal respiratory capacity was reduced by 25%.	NAD	42-46	nicotinamide phosphoribosyltransferase	Mus musculus	6-11
29208611-7	2018	Treatment with the NAD+ precursor nicotinamide riboside restored NAD+ levels in sh Nampt cells and increased maximal respiratory capacity by 18% and 32% in control and sh Nampt KD cells, respectively.	NAD	19-23	nicotinamide phosphoribosyltransferase	Mus musculus	83-88
29208611-7	2018	Treatment with the NAD+ precursor nicotinamide riboside restored NAD+ levels in sh Nampt cells and increased maximal respiratory capacity by 18% and 32% in control and sh Nampt KD cells, respectively.	NAD	19-23	nicotinamide phosphoribosyltransferase	Mus musculus	171-176
29208611-7	2018	Treatment with the NAD+ precursor nicotinamide riboside restored NAD+ levels in sh Nampt cells and increased maximal respiratory capacity by 18% and 32% in control and sh Nampt KD cells, respectively.	NAD	65-69	nicotinamide phosphoribosyltransferase	Mus musculus	83-88
29208611-8	2018	Expression of Cre recombinase in muscle of floxed Nampt mice reduced NAMPT and NAD+ levels by 38% and 43%, respectively.	NAD	79-83	nicotinamide phosphoribosyltransferase	Mus musculus	50-55
29208611-12	2018	Our findings suggest that NAMPT plays a key role for maintaining NAD+ levels in skeletal muscle and that NAMPT deficiency compromises oxidative phosphorylation capacity and alters energy homeostasis in this tissue.	NAD	65-69	nicotinamide phosphoribosyltransferase	Mus musculus	26-31
29408361-3	2018	Molecular dynamic simulations predicted the binding of alpha-synuclein to the positively charged groove comprising NAD+-binding pocket of GAPDH.	NAD	115-119	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	138-143
29413602-4	2018	Rebinding after template removal was evaluated by quantifying the suppression of the diffusive permeability of the signal for ferricyanide and by the NADH-dependent reduction of cytochrome c by the reductase domain (BMR).	NAD	150-154	cytochrome c, somatic	Homo sapiens	178-190
29543820-2	2018	The structure is broadly commensurate with Hst2/SIRT2 proteins of yeast and human origin, reproducing many of the structural features common to these sirtuin deacetylases, including the characteristic small zinc-binding domain, and the larger Rossmann-fold domain involved in NAD+-binding interactions.	NAD	276-280	histone deacetylase HST2	Saccharomyces cerevisiae S288C	43-47
29520010-1	2018	Most members of the poly(ADP-ribose)polymerase family, PARP family, have a catalytic activity that involves the transfer of ADP-ribose from a beta-NAD+-molecule to protein acceptors.	NAD	142-151	poly(ADP-ribose) polymerase 1	Homo sapiens	55-59
29541451-5	2018	In addition, resistant CCRF-CEM cells, which exhibit high quinolinate phosphoribosyltransferase (QPRT) activity, also exploited amino acid catabolism as an alternative source for NAD+ production, becoming addicted to tryptophan and glutamine and sensitive to treatment with the amino acid transport inhibitor JPH203 and with l-asparaginase, which affects glutamine exploitation.	NAD	179-183	quinolinate phosphoribosyltransferase	Homo sapiens	58-95
29541451-5	2018	In addition, resistant CCRF-CEM cells, which exhibit high quinolinate phosphoribosyltransferase (QPRT) activity, also exploited amino acid catabolism as an alternative source for NAD+ production, becoming addicted to tryptophan and glutamine and sensitive to treatment with the amino acid transport inhibitor JPH203 and with l-asparaginase, which affects glutamine exploitation.	NAD	179-183	quinolinate phosphoribosyltransferase	Homo sapiens	97-101
29514063-3	2018	Three protein deacylases, SIRT3, SIRT4, and SIRT5, reside in the mitochondria and remove these modifications from targeted proteins in an NAD+-dependent manner.	NAD	138-142	sirtuin 3	Homo sapiens	26-31
29518970-6	2018	We also defined a mutation threshold for the m.3571insC truncative mutation in mitochondrially encoded NADH:ubiquinone oxidoreductase core subunit 1 (MT-ND1), below which CI and its supramolecular organization is recovered, strengthening the notion that a certain amount of human ND1 is required for CI and supercomplexes biogenesis.	NAD	103-107	mitochondrially encoded NADH dehydrogenase 1	Homo sapiens	150-156
29518970-6	2018	We also defined a mutation threshold for the m.3571insC truncative mutation in mitochondrially encoded NADH:ubiquinone oxidoreductase core subunit 1 (MT-ND1), below which CI and its supramolecular organization is recovered, strengthening the notion that a certain amount of human ND1 is required for CI and supercomplexes biogenesis.	NAD	103-107	mitochondrially encoded NADH dehydrogenase 1	Homo sapiens	153-156
29514063-3	2018	Three protein deacylases, SIRT3, SIRT4, and SIRT5, reside in the mitochondria and remove these modifications from targeted proteins in an NAD+-dependent manner.	NAD	138-142	sirtuin 4	Homo sapiens	33-38
29558042-2	2018	Class I HDACs are zinc-dependent and NAD+-independent enzymes, and include 4 isoforms closely related to yeast RPD3: HDAC1, 2, 3, and 8.	NAD	37-41	histone deacetylase RPD3	Saccharomyces cerevisiae S288C	111-115
29511198-0	2018	Author Correction: Rev1 contributes to proper mitochondrial function via the PARP-NAD+-SIRT1-PGC1alpha axis.	NAD	82-86	REV1 DNA directed polymerase	Homo sapiens	19-23
29511198-0	2018	Author Correction: Rev1 contributes to proper mitochondrial function via the PARP-NAD+-SIRT1-PGC1alpha axis.	NAD	82-86	PPARG coactivator 1 alpha	Homo sapiens	93-102
29196784-6	2018	On one hand, PARP1 ablation rescued BPDE-induced NAD+ depletion and protected cells from BPDE-induced short-term toxicity.	NAD	49-53	poly(ADP-ribose) polymerase 1	Homo sapiens	13-18
29277324-3	2018	Sirtuin 3 (SIRT3), an NAD-dependent deacetylase, is sensitive to the metabolic status and mediates adaptation responses.	NAD	22-25	sirtuin 3	Homo sapiens	0-9
29277324-3	2018	Sirtuin 3 (SIRT3), an NAD-dependent deacetylase, is sensitive to the metabolic status and mediates adaptation responses.	NAD	22-25	sirtuin 3	Homo sapiens	11-16
29863179-3	2018	AR reduces glucose to sorbitol at the expense of NADPH, while sorbitol dehydrogenase converts sorbitol to fructose at the expense of NAD+, leading to NADH production.	NAD	150-154	aldo-keto reductase family 1 member B	Homo sapiens	0-2
29341930-9	2018	In DU-145 cells, the activation of ERbeta1 by DPN increased the expression of E-cadherin.	NAD	46-49	cadherin 1	Homo sapiens	78-88
29487285-0	2018	NAD+ analog reveals PARP-1 substrate-blocking mechanism and allosteric communication from catalytic center to DNA-binding domains.	NAD	0-4	poly(ADP-ribose) polymerase 1	Homo sapiens	20-26
29487285-1	2018	PARP-1 cleaves NAD+ and transfers the resulting ADP-ribose moiety onto target proteins and onto subsequent polymers of ADP-ribose.	NAD	15-19	poly(ADP-ribose) polymerase 1	Homo sapiens	0-6
29487285-3	2018	Here, we show using the non-hydrolyzable NAD+ analog benzamide adenine dinucleotide (BAD) that PARP-1 autoinhibition results from a selective block on NAD+ binding.	NAD	41-45	poly(ADP-ribose) polymerase 1	Homo sapiens	95-101
29535637-1	2018	Sirt6 is one of the sirtuin family members, a kind of NAD+-dependent histone deacetylase and ADP-ribose transferase enzyme.	NAD	54-58	sirtuin 6	Mus musculus	0-5
29487285-3	2018	Here, we show using the non-hydrolyzable NAD+ analog benzamide adenine dinucleotide (BAD) that PARP-1 autoinhibition results from a selective block on NAD+ binding.	NAD	151-155	poly(ADP-ribose) polymerase 1	Homo sapiens	95-101
29487285-5	2018	Our findings reveal a two-step mechanism to activate and to then stabilize PARP-1 on a DNA break, indicate that PARP-1 allostery influences persistence on DNA damage, and have important implications for PARP inhibitors that engage the NAD+ binding site.	NAD	235-239	poly(ADP-ribose) polymerase 1	Homo sapiens	75-81
29487285-5	2018	Our findings reveal a two-step mechanism to activate and to then stabilize PARP-1 on a DNA break, indicate that PARP-1 allostery influences persistence on DNA damage, and have important implications for PARP inhibitors that engage the NAD+ binding site.	NAD	235-239	poly(ADP-ribose) polymerase 1	Homo sapiens	112-118
29487285-5	2018	Our findings reveal a two-step mechanism to activate and to then stabilize PARP-1 on a DNA break, indicate that PARP-1 allostery influences persistence on DNA damage, and have important implications for PARP inhibitors that engage the NAD+ binding site.	NAD	235-239	poly(ADP-ribose) polymerase 1	Homo sapiens	75-79
29466723-1	2018	Sirtuin 3 (SIRT3) is a NAD+-dependent deacetylase downregulated in aging and age-associated diseases such as cancer and neurodegeneration and in high-fat diet (HFD)-induced metabolic disorders.	NAD	23-26	sirtuin 3	Homo sapiens	0-9
29466723-1	2018	Sirtuin 3 (SIRT3) is a NAD+-dependent deacetylase downregulated in aging and age-associated diseases such as cancer and neurodegeneration and in high-fat diet (HFD)-induced metabolic disorders.	NAD	23-26	sirtuin 3	Homo sapiens	11-16
29449813-4	2018	Solid data show that NAD+ covalently modifies the P2X7R of mouse T lymphocytes, thus lowering the ATP threshold for activation.	NAD	21-25	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	50-55
29643974-2	2018	Recent studies suggest that sirtuin 3 (SIRT3), the mitochondrial NAD+-dependent deacetylase, may regulate mitochondrial function and biosynthetic pathways such as glucose and fatty acid metabolism and the tricarboxylic acid (TCA) cycle, oxidative stress, and apoptosis by reversible protein lysine deacetylation.	NAD	65-68	sirtuin 3	Homo sapiens	28-37
29643974-2	2018	Recent studies suggest that sirtuin 3 (SIRT3), the mitochondrial NAD+-dependent deacetylase, may regulate mitochondrial function and biosynthetic pathways such as glucose and fatty acid metabolism and the tricarboxylic acid (TCA) cycle, oxidative stress, and apoptosis by reversible protein lysine deacetylation.	NAD	65-68	sirtuin 3	Homo sapiens	39-44
29194006-5	2018	Kinetic characterization of the fusion GST-hLDHA protein toward GSH and NADH, suggested retention of functional activities of GST and hLDHA in fused protein as indicated by the kinetic parameters km and kcat/km.	NAD	72-76	lactate dehydrogenase A	Homo sapiens	43-48
29194006-5	2018	Kinetic characterization of the fusion GST-hLDHA protein toward GSH and NADH, suggested retention of functional activities of GST and hLDHA in fused protein as indicated by the kinetic parameters km and kcat/km.	NAD	72-76	lactate dehydrogenase A	Homo sapiens	134-139
29345930-0	2018	alpha-Amino-beta-carboxymuconate-epsilon-semialdehyde Decarboxylase (ACMSD) Inhibitors as Novel Modulators of De Novo Nicotinamide Adenine Dinucleotide (NAD+) Biosynthesis.	NAD	118-151	aminocarboxymuconate semialdehyde decarboxylase	Homo sapiens	0-67
29345930-0	2018	alpha-Amino-beta-carboxymuconate-epsilon-semialdehyde Decarboxylase (ACMSD) Inhibitors as Novel Modulators of De Novo Nicotinamide Adenine Dinucleotide (NAD+) Biosynthesis.	NAD	118-151	aminocarboxymuconate semialdehyde decarboxylase	Homo sapiens	69-74
29345930-0	2018	alpha-Amino-beta-carboxymuconate-epsilon-semialdehyde Decarboxylase (ACMSD) Inhibitors as Novel Modulators of De Novo Nicotinamide Adenine Dinucleotide (NAD+) Biosynthesis.	NAD	153-157	aminocarboxymuconate semialdehyde decarboxylase	Homo sapiens	0-67
29345930-0	2018	alpha-Amino-beta-carboxymuconate-epsilon-semialdehyde Decarboxylase (ACMSD) Inhibitors as Novel Modulators of De Novo Nicotinamide Adenine Dinucleotide (NAD+) Biosynthesis.	NAD	153-157	aminocarboxymuconate semialdehyde decarboxylase	Homo sapiens	69-74
29345930-4	2018	Herein we report the discovery of 3-[[[5-cyano-1,6-dihydro-6-oxo-4-(2-thienyl)-2-pyrimidinyl]thio]methyl]phenylacetic acid (TES-1025, 22), the first potent and selective inhibitor of human ACMSD (IC50 = 0.013 muM) that increases NAD+ levels in cellular systems.	NAD	229-233	aminocarboxymuconate semialdehyde decarboxylase	Homo sapiens	189-194
29345930-4	2018	Herein we report the discovery of 3-[[[5-cyano-1,6-dihydro-6-oxo-4-(2-thienyl)-2-pyrimidinyl]thio]methyl]phenylacetic acid (TES-1025, 22), the first potent and selective inhibitor of human ACMSD (IC50 = 0.013 muM) that increases NAD+ levels in cellular systems.	NAD	229-233	latexin	Homo sapiens	209-212
29345930-5	2018	The results of physicochemical-property, ADME, and safety profiling, coupled with in vivo target-engagement studies, support the hypothesis that ACMSD inhibition increases de novo NAD+ biosynthesis and position 22 as a first-class molecule for the evaluation of the therapeutic potential of ACMSD inhibition in treating disorders with perturbed NAD+ supply or homeostasis.	NAD	180-184	aminocarboxymuconate semialdehyde decarboxylase	Homo sapiens	145-150
29345930-5	2018	The results of physicochemical-property, ADME, and safety profiling, coupled with in vivo target-engagement studies, support the hypothesis that ACMSD inhibition increases de novo NAD+ biosynthesis and position 22 as a first-class molecule for the evaluation of the therapeutic potential of ACMSD inhibition in treating disorders with perturbed NAD+ supply or homeostasis.	NAD	345-349	aminocarboxymuconate semialdehyde decarboxylase	Homo sapiens	145-150
28500758-4	2018	Further co-culture of UCB MSCs have shown to induce anti-inflammatory cytokines like IL-4, IL-10 and TGF-beta and anti-apoptotic Bclxl/Bcl2 expression in the DPN sera stressed cells.	NAD	158-161	BCL2 like 1	Homo sapiens	129-134
28500758-4	2018	Further co-culture of UCB MSCs have shown to induce anti-inflammatory cytokines like IL-4, IL-10 and TGF-beta and anti-apoptotic Bclxl/Bcl2 expression in the DPN sera stressed cells.	NAD	158-161	BCL2 apoptosis regulator	Homo sapiens	135-139
28500758-5	2018	Amelioration of elevated [Ca2+ ]i and cROS, the portent behind the NFkappaB/Caspase-3 mediated inflammation in DPN rescued the cells from apoptosis.	NAD	111-114	nuclear factor kappa B subunit 1	Homo sapiens	67-75
28500758-5	2018	Amelioration of elevated [Ca2+ ]i and cROS, the portent behind the NFkappaB/Caspase-3 mediated inflammation in DPN rescued the cells from apoptosis.	NAD	111-114	caspase 3	Homo sapiens	76-85
29307819-4	2018	In this study, the fluorescence lifetime of the metabolic coenzyme NADH reveals that the absence of REV3L can promote the p53-mediated upregulation of oxidative phosphorylation in cisplatin-treated H1299 lung carcinoma cells and increases cancer cell sensitivity to this platinum-based chemotherapy.	NAD	67-71	REV3 like, DNA directed polymerase zeta catalytic subunit	Homo sapiens	100-105
29266439-8	2018	In S. lividans, an NAD+ -dependent sirtuin deacetylase from Streptomyces, SrtA (a homologue of the human SIRT4 protein) was needed to maintain SlAcs function in vivo.	NAD	19-23	sirtuin 4	Homo sapiens	105-110
28847709-4	2018	Recently, some flavonoids were shown to inhibit poly (ADP-ribose) polymerases (PARPs) and cyclic ADP-ribose (cADP) synthases (CD38 and CD157), elevate intracellular nicotinamide adenine dinucleotide+ (NAD+) levels and activate NAD+ dependent sirtuin -mediated signaling pathways.	NAD	165-199	bone marrow stromal cell antigen 1	Homo sapiens	135-140
28847709-4	2018	Recently, some flavonoids were shown to inhibit poly (ADP-ribose) polymerases (PARPs) and cyclic ADP-ribose (cADP) synthases (CD38 and CD157), elevate intracellular nicotinamide adenine dinucleotide+ (NAD+) levels and activate NAD+ dependent sirtuin -mediated signaling pathways.	NAD	201-205	bone marrow stromal cell antigen 1	Homo sapiens	135-140
28847709-4	2018	Recently, some flavonoids were shown to inhibit poly (ADP-ribose) polymerases (PARPs) and cyclic ADP-ribose (cADP) synthases (CD38 and CD157), elevate intracellular nicotinamide adenine dinucleotide+ (NAD+) levels and activate NAD+ dependent sirtuin -mediated signaling pathways.	NAD	227-231	bone marrow stromal cell antigen 1	Homo sapiens	135-140
29307819-4	2018	In this study, the fluorescence lifetime of the metabolic coenzyme NADH reveals that the absence of REV3L can promote the p53-mediated upregulation of oxidative phosphorylation in cisplatin-treated H1299 lung carcinoma cells and increases cancer cell sensitivity to this platinum-based chemotherapy.	NAD	67-71	tumor protein p53	Homo sapiens	122-125
29339820-9	2018	We further pinpointed that the function of macroH2A1.1 in EMT suppression is dependent on its ability to bind the NAD+ metabolite PAR, in agreement with the inability to suppress EMT by macroH2A1.2, which lacks the PAR binding domain.	NAD	114-118	macroH2A.1 histone	Homo sapiens	43-54
30146805-8	2018	The mRNA expression of E-cadherin and vimentin, and the activated ERK1/2 were significantly increased after 1.0 nmol/L FK866 treatment for 72 h. The pretreatment with nicotinamide adenine dinucleotide (NAD) precursor nicotinamide mononucleotide(1.0 mmol/L) or ERK1/2 inhibitor U0126 (10.0 mumol/L) reversed the up-regulation of E-cadherin and vimentin expression induced by FK866.	NAD	167-200	cadherin 1	Homo sapiens	23-33
30146805-8	2018	The mRNA expression of E-cadherin and vimentin, and the activated ERK1/2 were significantly increased after 1.0 nmol/L FK866 treatment for 72 h. The pretreatment with nicotinamide adenine dinucleotide (NAD) precursor nicotinamide mononucleotide(1.0 mmol/L) or ERK1/2 inhibitor U0126 (10.0 mumol/L) reversed the up-regulation of E-cadherin and vimentin expression induced by FK866.	NAD	167-200	mitogen-activated protein kinase 3	Homo sapiens	66-72
30146805-8	2018	The mRNA expression of E-cadherin and vimentin, and the activated ERK1/2 were significantly increased after 1.0 nmol/L FK866 treatment for 72 h. The pretreatment with nicotinamide adenine dinucleotide (NAD) precursor nicotinamide mononucleotide(1.0 mmol/L) or ERK1/2 inhibitor U0126 (10.0 mumol/L) reversed the up-regulation of E-cadherin and vimentin expression induced by FK866.	NAD	167-200	mitogen-activated protein kinase 3	Homo sapiens	260-266
30146805-8	2018	The mRNA expression of E-cadherin and vimentin, and the activated ERK1/2 were significantly increased after 1.0 nmol/L FK866 treatment for 72 h. The pretreatment with nicotinamide adenine dinucleotide (NAD) precursor nicotinamide mononucleotide(1.0 mmol/L) or ERK1/2 inhibitor U0126 (10.0 mumol/L) reversed the up-regulation of E-cadherin and vimentin expression induced by FK866.	NAD	167-200	cadherin 1	Homo sapiens	328-338
29342113-12	2018	In the case of extensive DNA damage, PARP-1 becomes overactivated and rapidly depletes the intracellular NAD+ and ATP pools.	NAD	105-109	poly(ADP-ribose) polymerase 1	Homo sapiens	37-43
29189472-0	2018	SIRT2 and Akt mediate NAD+-induced and NADH-induced increases in the intracellular ATP levels of BV2 microglia under basal conditions.	NAD	22-26	thymoma viral proto-oncogene 1	Mus musculus	10-13
29189472-0	2018	SIRT2 and Akt mediate NAD+-induced and NADH-induced increases in the intracellular ATP levels of BV2 microglia under basal conditions.	NAD	39-43	thymoma viral proto-oncogene 1	Mus musculus	10-13
29189472-4	2018	We found that both NAD and NADH significantly increased the intracellular ATP levels of BV2 microglia, which were attenuated by SIRT2 siRNA, the SIRT2 inhibitor AGK2, and the phosphatidylinositol 3-kinase/Akt inhibitor LY294002.	NAD	19-22	thymoma viral proto-oncogene 1	Mus musculus	205-208
29189472-4	2018	We found that both NAD and NADH significantly increased the intracellular ATP levels of BV2 microglia, which were attenuated by SIRT2 siRNA, the SIRT2 inhibitor AGK2, and the phosphatidylinositol 3-kinase/Akt inhibitor LY294002.	NAD	27-31	thymoma viral proto-oncogene 1	Mus musculus	205-208
29189472-5	2018	Our study has also suggested that SIRT2 mediates the NAD-induced and NADH-induced increase in Akt phosphorylation in BV2 microglia.	NAD	69-73	thymoma viral proto-oncogene 1	Mus musculus	94-97
29189472-6	2018	Collectively, our study has suggested that SIRT2 mediates both NAD-induced and NADH-induced increases in the intracellular ATP levels of BV2 microglia by modulating Akt phosphorylation.	NAD	79-83	thymoma viral proto-oncogene 1	Mus musculus	165-168
29253500-5	2018	Importantly, the suppression of COL1A2 transcription following CA treatment depended on the reduction of Smad3 acetylation via the activation of Sirtuin 1 (SIRT1), a nicotinamide adenine dinucleotide+ (NAD+)-dependent deacetylase.	NAD	166-199	sirtuin 1	Rattus norvegicus	145-154
29253500-5	2018	Importantly, the suppression of COL1A2 transcription following CA treatment depended on the reduction of Smad3 acetylation via the activation of Sirtuin 1 (SIRT1), a nicotinamide adenine dinucleotide+ (NAD+)-dependent deacetylase.	NAD	166-199	sirtuin 1	Rattus norvegicus	156-161
29253500-5	2018	Importantly, the suppression of COL1A2 transcription following CA treatment depended on the reduction of Smad3 acetylation via the activation of Sirtuin 1 (SIRT1), a nicotinamide adenine dinucleotide+ (NAD+)-dependent deacetylase.	NAD	166-199	collagen type I alpha 2 chain	Rattus norvegicus	32-38
29320709-3	2018	(2018) demonstrate that intratumoral CD4+ T cell functions and memory can be improved by targeting a CD38-NAD+-Sirt1-Foxo1 metabolic circuit.	NAD	106-110	forkhead box O1	Homo sapiens	117-122
29253500-5	2018	Importantly, the suppression of COL1A2 transcription following CA treatment depended on the reduction of Smad3 acetylation via the activation of Sirtuin 1 (SIRT1), a nicotinamide adenine dinucleotide+ (NAD+)-dependent deacetylase.	NAD	166-199	SMAD family member 3	Rattus norvegicus	105-110
29343967-0	2018	Indoleamine 2,3-Dioxygenase Activity Increases NAD+ Production in IFN-gamma-Stimulated Human Primary Mononuclear Cells.	NAD	47-51	interferon gamma	Homo sapiens	66-75
29343967-5	2018	IFN-gamma activation of macrophages resulted in the highest induction of IDO but decreased intracellular NAD+ concentrations at both 24 and 48 hours.	NAD	105-109	interferon gamma	Homo sapiens	0-9
29343967-6	2018	However, IFN-gamma activation of both day 6 and day 10 macrophages in the presence of a PARP inhibitor resulted in significantly higher intracellular NAD+ levels at 24 hours.	NAD	150-154	interferon gamma	Homo sapiens	9-18
29343967-6	2018	However, IFN-gamma activation of both day 6 and day 10 macrophages in the presence of a PARP inhibitor resulted in significantly higher intracellular NAD+ levels at 24 hours.	NAD	150-154	poly(ADP-ribose) polymerase 1	Homo sapiens	88-92
29191657-5	2018	Furthermore, we showed that miR-761 putatively targeted three proteins, thyroid hormone receptor interactor 6 (TRIP6), lamin A/C (LMNA), and NAD-dependent protein deacetylase sirtuin-3 (SIRT3).	NAD	141-144	sirtuin 3	Homo sapiens	186-191
29721988-3	2018	Moreover, we found that this NAD+-dependent retinal homeostasis relies, in part, on maintenance of optimal activity of the mitochondrial sirtuins and of SIRT3 in particular.	NAD	29-33	sirtuin 3	Homo sapiens	153-158
29025729-8	2018	Ethanol causes a robust dose-dependent increase in cytosolic NADH/NAD+ ratio, and this increase is mitigated by the presence of NAD+-generating substrates of LDH or SDH.	NAD	61-65	sorbitol dehydrogenase	Homo sapiens	165-168
29025729-8	2018	Ethanol causes a robust dose-dependent increase in cytosolic NADH/NAD+ ratio, and this increase is mitigated by the presence of NAD+-generating substrates of LDH or SDH.	NAD	66-70	sorbitol dehydrogenase	Homo sapiens	165-168
29025729-8	2018	Ethanol causes a robust dose-dependent increase in cytosolic NADH/NAD+ ratio, and this increase is mitigated by the presence of NAD+-generating substrates of LDH or SDH.	NAD	128-132	sorbitol dehydrogenase	Homo sapiens	165-168
28473297-0	2018	NADH reduction of nitroaromatics as a probe for residual ferric form high-spin in a cytochrome P450.	NAD	0-4	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	84-99
29298345-7	2018	In untreated human cells, regions with high intensity immunostaining for NQO1 co-localize with acetyl alpha-tubulin and the NAD+-dependent deacetylase Sirt2 on the centrosome(s), the mitotic spindle and midbody during cell division.	NAD	124-128	NAD(P)H quinone dehydrogenase 1	Homo sapiens	73-77
29298345-8	2018	These data provide evidence that during the centriole duplication cycle NQO1 may provide NAD+ for Sirt2-mediated deacetylation of microtubules.	NAD	89-93	NAD(P)H quinone dehydrogenase 1	Homo sapiens	72-76
28719017-1	2018	Both sirtuin and poly(ADP-ribose)polymerase (PARP) family of enzymes utilize NAD+ as co-substrate.	NAD	77-81	poly(ADP-ribose) polymerase 1	Homo sapiens	17-43
30261504-4	2018	Nicotinamide phosphoribosyltransferase (Nampt) catalyzes the first step in the biosynthesis of nicotinamide adenine dinucleotide (NAD) and is known to be induced by IL-1beta.	NAD	95-128	interleukin 1 beta	Homo sapiens	165-173
30261504-4	2018	Nicotinamide phosphoribosyltransferase (Nampt) catalyzes the first step in the biosynthesis of nicotinamide adenine dinucleotide (NAD) and is known to be induced by IL-1beta.	NAD	130-133	interleukin 1 beta	Homo sapiens	165-173
28719017-1	2018	Both sirtuin and poly(ADP-ribose)polymerase (PARP) family of enzymes utilize NAD+ as co-substrate.	NAD	77-81	poly(ADP-ribose) polymerase 1	Homo sapiens	45-49
29356095-1	2018	BACKGROUND: In veterinary medicine, congenital methemoglobinemia associated with nicotinamide adenine dinucleotide (NADH)-cytochrome b5 reductase (b5R) deficiency is rare.	NAD	81-114	cytochrome b5 reductase 3	Canis lupus familiaris	133-145
30787047-4	2018	Functional studies of the SARM1 gene product have revealed the presence of an enzymatic activity directed toward the hydrolysis of NAD+ Finally, an unbiased drug screen performed in living mice led to the discovery of a neuroprotective chemical designated P7C3.	NAD	131-135	sterile alpha and HEAT/Armadillo motif containing 1	Mus musculus	26-31
30787047-5	2018	Biochemical studies of the P7C3 chemical show that it can enhance recovery of NAD+ from nicotinamide by activating NAMPT, the first enzyme in the salvage pathway.	NAD	78-82	nicotinamide phosphoribosyltransferase	Mus musculus	115-120
29049850-4	2018	SIRT6, a NAD-dependent sirtuin deacylase, modulates aging, energy metabolism, and neurodegeneration.	NAD	9-12	sirtuin 6	Mus musculus	0-5
29356095-1	2018	BACKGROUND: In veterinary medicine, congenital methemoglobinemia associated with nicotinamide adenine dinucleotide (NADH)-cytochrome b5 reductase (b5R) deficiency is rare.	NAD	81-114	cytochrome b5 reductase 3	Canis lupus familiaris	147-150
30518708-1	2018	SIRT1, an NAD+-dependent deacetylase, causes deacetylation and down-regulation of its target p53.	NAD	10-13	tumor protein p53	Homo sapiens	93-96
29356095-1	2018	BACKGROUND: In veterinary medicine, congenital methemoglobinemia associated with nicotinamide adenine dinucleotide (NADH)-cytochrome b5 reductase (b5R) deficiency is rare.	NAD	116-120	cytochrome b5 reductase 3	Canis lupus familiaris	133-145
29356095-1	2018	BACKGROUND: In veterinary medicine, congenital methemoglobinemia associated with nicotinamide adenine dinucleotide (NADH)-cytochrome b5 reductase (b5R) deficiency is rare.	NAD	116-120	cytochrome b5 reductase 3	Canis lupus familiaris	147-150
30097861-1	2018	The poly(ADP-ribose) polymerase (PARP) family of proteins utilize NAD+ as the substrate to modify protein acceptors with either mono(ADP-ribose) (MAR) or poly(ADP-ribose) (PAR).	NAD	66-70	poly(ADP-ribose) polymerase 1	Homo sapiens	4-31
30097861-1	2018	The poly(ADP-ribose) polymerase (PARP) family of proteins utilize NAD+ as the substrate to modify protein acceptors with either mono(ADP-ribose) (MAR) or poly(ADP-ribose) (PAR).	NAD	66-70	poly(ADP-ribose) polymerase 1	Homo sapiens	33-37
30097868-2	2018	ARH1 hydrolyzes mono(ADP-ribosyl)ated arginine, which results from actions of cholera toxin and other nicotinamide adenine dinucleotide (NAD+):arginine ADP-ribosyl-transferases, while ARH3 hydrolyzes poly(ADP-ribose) and O-acetyl-ADP-ribose, resulting from the action of poly(ADP-ribose) polymerases and sirtuins, respectively.	NAD	137-141	low density lipoprotein receptor adaptor protein 1	Homo sapiens	0-4
30097863-6	2018	Second, the purified recombinant PARPs are incubated individually in the presence of different concentrations of NAD+ (as a donor of ADPR groups) and sheared DNA (to activate their catalytic activities) resulting in various forms of auto-ADP-ribosylation.	NAD	113-117	poly(ADP-ribose) polymerase 1	Homo sapiens	33-38
30097881-1	2018	Nuclear poly(ADP-ribose) polymerases (PARPs), including PARPs 1, 2, and 3 and the Tankyrases, belong to a family of enzymes that can bind to chromatin and covalently modify histone- and chromatin-associated proteins with ADP-ribose derived from nuclear NAD+.	NAD	253-257	poly(ADP-ribose) polymerase 1	Homo sapiens	38-43
30097881-1	2018	Nuclear poly(ADP-ribose) polymerases (PARPs), including PARPs 1, 2, and 3 and the Tankyrases, belong to a family of enzymes that can bind to chromatin and covalently modify histone- and chromatin-associated proteins with ADP-ribose derived from nuclear NAD+.	NAD	253-257	poly(ADP-ribose) polymerase 1	Homo sapiens	56-73
30097868-2	2018	ARH1 hydrolyzes mono(ADP-ribosyl)ated arginine, which results from actions of cholera toxin and other nicotinamide adenine dinucleotide (NAD+):arginine ADP-ribosyl-transferases, while ARH3 hydrolyzes poly(ADP-ribose) and O-acetyl-ADP-ribose, resulting from the action of poly(ADP-ribose) polymerases and sirtuins, respectively.	NAD	102-135	low density lipoprotein receptor adaptor protein 1	Homo sapiens	0-4
29146412-1	2018	OBJECTIVE: Nicotinamide phosphoribosyl transferase (NAMPT) is the rate-limiting enzyme in the salvage pathway that produces nicotinamide adenine dinucleotide (NAD+), an essential co-substrate regulating a myriad of signaling pathways.	NAD	124-157	nicotinamide phosphoribosyltransferase	Mus musculus	11-50
29807573-2	2018	Indeed, upon genotoxic stress, CCAR2, phosphorylated by the apical DDR kinases ATM and ATR, increases its binding to the NAD+-dependent histone deacetylase SIRT1 and inhibits SIRT1 activity.	NAD	121-125	ATR serine/threonine kinase	Homo sapiens	87-90
29146412-1	2018	OBJECTIVE: Nicotinamide phosphoribosyl transferase (NAMPT) is the rate-limiting enzyme in the salvage pathway that produces nicotinamide adenine dinucleotide (NAD+), an essential co-substrate regulating a myriad of signaling pathways.	NAD	124-157	nicotinamide phosphoribosyltransferase	Mus musculus	52-57
29146412-1	2018	OBJECTIVE: Nicotinamide phosphoribosyl transferase (NAMPT) is the rate-limiting enzyme in the salvage pathway that produces nicotinamide adenine dinucleotide (NAD+), an essential co-substrate regulating a myriad of signaling pathways.	NAD	159-163	nicotinamide phosphoribosyltransferase	Mus musculus	52-57
29146412-1	2018	OBJECTIVE: Nicotinamide phosphoribosyl transferase (NAMPT) is the rate-limiting enzyme in the salvage pathway that produces nicotinamide adenine dinucleotide (NAD+), an essential co-substrate regulating a myriad of signaling pathways.	NAD	159-163	nicotinamide phosphoribosyltransferase	Mus musculus	11-50
30069770-2	2018	It is rationally designed to act as a competitive inhibitor of NAD+ at the catalytic site of PARP1 and PARP2, both members of the PARP family of enzymes that are central to the repair of DNA single-strand breaks (SSBs) mediated via the base excision repair (BER) pathway.	NAD	63-67	poly(ADP-ribose) polymerase 1	Homo sapiens	93-98
30069770-2	2018	It is rationally designed to act as a competitive inhibitor of NAD+ at the catalytic site of PARP1 and PARP2, both members of the PARP family of enzymes that are central to the repair of DNA single-strand breaks (SSBs) mediated via the base excision repair (BER) pathway.	NAD	63-67	poly(ADP-ribose) polymerase 2	Homo sapiens	103-108
30069770-2	2018	It is rationally designed to act as a competitive inhibitor of NAD+ at the catalytic site of PARP1 and PARP2, both members of the PARP family of enzymes that are central to the repair of DNA single-strand breaks (SSBs) mediated via the base excision repair (BER) pathway.	NAD	63-67	poly(ADP-ribose) polymerase 1	Homo sapiens	93-97
29138502-9	2017	Using these results, we further establish efficient Sirt4 activity assays, an unusual Sirt4 regulation by NADH, and Sirt4 effects of pharmacological modulators.	NAD	106-110	sirtuin 4	Homo sapiens	86-91
29236713-6	2017	Here, we demonstrated that Sirt3, a nicotinamide adenine dinucleotide (NAD+)-dependent protein deacetylase, an enzyme linked to human longevity, was expressed in mouse neutrophils and platelets.	NAD	36-69	sirtuin 3	Homo sapiens	27-32
29236713-6	2017	Here, we demonstrated that Sirt3, a nicotinamide adenine dinucleotide (NAD+)-dependent protein deacetylase, an enzyme linked to human longevity, was expressed in mouse neutrophils and platelets.	NAD	71-74	sirtuin 3	Homo sapiens	27-32
29242353-3	2017	METHODS AND RESULTS: Microarray data analysis and mitochondrial isobaric tags for relative and absolute quantification proteomics revealed that the expression of D-beta-hydroxybutyrate dehydrogenase I (Bdh1), an enzyme that catalyzes the NAD+/NADH coupled interconversion of acetoacetate and beta-hydroxybutyrate, was increased 2.5- and 2.8-fold, respectively, in the heart after transverse aortic constriction.	NAD	238-242	3-hydroxybutyrate dehydrogenase, type 1	Mus musculus	202-206
29242353-3	2017	METHODS AND RESULTS: Microarray data analysis and mitochondrial isobaric tags for relative and absolute quantification proteomics revealed that the expression of D-beta-hydroxybutyrate dehydrogenase I (Bdh1), an enzyme that catalyzes the NAD+/NADH coupled interconversion of acetoacetate and beta-hydroxybutyrate, was increased 2.5- and 2.8-fold, respectively, in the heart after transverse aortic constriction.	NAD	243-247	3-hydroxybutyrate dehydrogenase, type 1	Mus musculus	202-206
29464059-7	2018	Finally, we perform analysis of SDHC synthetic lethality with lactate dehydrogenase A (LDHA) and pyruvate carboxylase (PCX), which are important for regeneration of NAD+ and aspartate biosynthesis, respectively.	NAD	165-169	succinate dehydrogenase complex, subunit C, integral membrane protein	Mus musculus	32-36
29129681-4	2017	LRRK2 G2019S iPSC-derived dopaminergic neuron cultures displayed unique abnormalities in mitochondrial distribution and trafficking, which corresponded to reduced sirtuin deacetylase activity and nicotinamide adenine dinucleotide levels despite increased sirtuin levels.	NAD	196-229	leucine rich repeat kinase 2	Homo sapiens	0-5
29178516-6	2017	Furthermore, we showed that constitutive Nampt over-expression increases cellular NAD+ content and delays cellular senescence of MEF cells in vitro.	NAD	82-86	nicotinamide phosphoribosyltransferase	Mus musculus	41-46
29162908-1	2017	CD157/Bst1 is a dual-function receptor and beta-NAD+-metabolizing ectoenzyme of the ADP-ribosyl cyclase family.	NAD	43-52	bone marrow stromal cell antigen 1	Homo sapiens	0-5
29162908-1	2017	CD157/Bst1 is a dual-function receptor and beta-NAD+-metabolizing ectoenzyme of the ADP-ribosyl cyclase family.	NAD	43-52	bone marrow stromal cell antigen 1	Homo sapiens	6-10
29138502-9	2017	Using these results, we further establish efficient Sirt4 activity assays, an unusual Sirt4 regulation by NADH, and Sirt4 effects of pharmacological modulators.	NAD	106-110	sirtuin 4	Homo sapiens	86-91
28973648-0	2017	The NAD+-dependent deacetylase SIRT2 attenuates oxidative stress and mitochondrial dysfunction and improves insulin sensitivity in hepatocytes.	NAD	4-8	insulin	Homo sapiens	108-115
28950656-1	2017	Several human cancers including the breast display elevated expression of Lactate dehydrogenase-A (LDH-A), the enzyme that converts pyruvate to lactate and oxidizes NADH to NAD+.	NAD	165-169	lactate dehydrogenase A	Homo sapiens	74-97
28950656-1	2017	Several human cancers including the breast display elevated expression of Lactate dehydrogenase-A (LDH-A), the enzyme that converts pyruvate to lactate and oxidizes NADH to NAD+.	NAD	165-169	lactate dehydrogenase A	Homo sapiens	99-104
28950656-1	2017	Several human cancers including the breast display elevated expression of Lactate dehydrogenase-A (LDH-A), the enzyme that converts pyruvate to lactate and oxidizes NADH to NAD+.	NAD	173-177	lactate dehydrogenase A	Homo sapiens	74-97
28950656-1	2017	Several human cancers including the breast display elevated expression of Lactate dehydrogenase-A (LDH-A), the enzyme that converts pyruvate to lactate and oxidizes NADH to NAD+.	NAD	173-177	lactate dehydrogenase A	Homo sapiens	99-104
28711502-2	2017	A variety of small molecules have been developed to target deacetylases, but extremely few of these molecules are capable of activating the mitochondrial NAD-dependent deacetylase sirtuin-3 (SIRT3) (Gertz and Steegborn, 2016; Scholz et al., 2015) [3,4].	NAD	154-157	sirtuin 3	Homo sapiens	191-196
28916726-4	2017	beta-Lapachone"s therapeutic efficacy partially stems from the drug"s induction of a futile NQO1-mediated redox cycle that causes high levels of superoxide and then peroxide formation, which damages DNA and causes hyperactivation of poly(ADP-ribose) polymerase, resulting in extensive NAD+/ATP depletion.	NAD	285-289	NAD(P)H quinone dehydrogenase 1	Homo sapiens	92-96
28916726-4	2017	beta-Lapachone"s therapeutic efficacy partially stems from the drug"s induction of a futile NQO1-mediated redox cycle that causes high levels of superoxide and then peroxide formation, which damages DNA and causes hyperactivation of poly(ADP-ribose) polymerase, resulting in extensive NAD+/ATP depletion.	NAD	285-289	poly(ADP-ribose) polymerase 1	Homo sapiens	233-260
28916726-7	2017	In this study, a multimodal analysis, including metabolic imaging using hyperpolarized pyruvate, points to reduced oxidative flux due to NAD+ depletion after beta-lapachone treatment of NQO1+ human pancreatic cancer cells.	NAD	137-141	NAD(P)H quinone dehydrogenase 1	Homo sapiens	186-190
28688179-6	2017	CONCLUSION: Resveratrol exhibits benefits against ethanol-induced insulin resistance via improving the ratio of NAD+ /NADH to regulate SIRT1, which is associated with the modulation of ethanol metabolism enzymes.	NAD	112-116	sirtuin 1	Rattus norvegicus	135-140
28688179-1	2017	SCOPE: Resveratrol has been shown to improve insulin resistance via activating the NAD+ -dependent deacetylase SIRT1, but the effects of resveratrol on ethanol-induced insulin resistance remain unclear.	NAD	83-86	sirtuin 1	Rattus norvegicus	111-116
28688179-6	2017	CONCLUSION: Resveratrol exhibits benefits against ethanol-induced insulin resistance via improving the ratio of NAD+ /NADH to regulate SIRT1, which is associated with the modulation of ethanol metabolism enzymes.	NAD	118-122	sirtuin 1	Rattus norvegicus	135-140
28650465-4	2017	Upregulation of MCU clearly enhanced the Ca2+ uptake into mitochondria, which significantly promoted ROS production by downregulating nicotinamide adenine dinucleotide+ (NAD+)/reduced form of nicotinamide adenine dinucleotid (NADH) ratio and the NAD+-dependent deacetylase activity of sirtuin 3 to inhibit superoxide dismutase 2 (SOD2) activity.	NAD	170-173	mitochondrial calcium uniporter	Homo sapiens	16-19
29081403-1	2017	The stress-responsive mitochondrial sirtuin SIRT4 controls cellular energy metabolism in a NAD+-dependent manner and is implicated in cellular senescence and aging.	NAD	91-95	sirtuin 4	Homo sapiens	44-49
29073231-4	2017	Pharmacological treatment with specific PARP-1 (the major NAD+ consuming poly(ADP-ribose)polymerases) and PARP-1/PARP-2 inhibitors after the oxidant insult recovered normal mitochondrial morphology and, hence, increased the viability of human hepatic cells.	NAD	58-62	poly(ADP-ribose) polymerase 1	Homo sapiens	40-46
28650465-0	2017	MCU-dependent mitochondrial Ca2+ inhibits NAD+/SIRT3/SOD2 pathway to promote ROS production and metastasis of HCC cells.	NAD	42-46	mitochondrial calcium uniporter	Homo sapiens	0-3
28650465-0	2017	MCU-dependent mitochondrial Ca2+ inhibits NAD+/SIRT3/SOD2 pathway to promote ROS production and metastasis of HCC cells.	NAD	42-46	sirtuin 3	Homo sapiens	47-52
28882480-3	2017	Using a cardiac specific KLF4 deficient mouse line that is sensitive to stress, we found mitochondrial protein hyperacetylation coupled with reduced Sirt3 and NAD+ levels in the heart before stress, suggesting that the KLF4-deficient heart is predisposed to NAD+-associated defects.	NAD	159-163	Kruppel-like factor 4 (gut)	Mus musculus	219-223
28882480-3	2017	Using a cardiac specific KLF4 deficient mouse line that is sensitive to stress, we found mitochondrial protein hyperacetylation coupled with reduced Sirt3 and NAD+ levels in the heart before stress, suggesting that the KLF4-deficient heart is predisposed to NAD+-associated defects.	NAD	258-262	Kruppel-like factor 4 (gut)	Mus musculus	219-223
28991266-0	2017	MacroH2A1.1 regulates mitochondrial respiration by limiting nuclear NAD+ consumption.	NAD	68-72	macroH2A.1 histone	Homo sapiens	0-11
28991266-2	2017	The histone variant macroH2A1.1 contains a macrodomain capable of binding NAD+-derived metabolites.	NAD	74-78	macroH2A.1 histone	Homo sapiens	20-31
28991266-5	2017	Through direct binding, macroH2A1.1 inhibits basal poly-ADP ribose polymerase 1 (PARP-1) activity and thus reduces nuclear NAD+ consumption.	NAD	123-127	macroH2A.1 histone	Homo sapiens	24-35
28991266-5	2017	Through direct binding, macroH2A1.1 inhibits basal poly-ADP ribose polymerase 1 (PARP-1) activity and thus reduces nuclear NAD+ consumption.	NAD	123-127	poly(ADP-ribose) polymerase 1	Homo sapiens	51-79
28991266-5	2017	Through direct binding, macroH2A1.1 inhibits basal poly-ADP ribose polymerase 1 (PARP-1) activity and thus reduces nuclear NAD+ consumption.	NAD	123-127	poly(ADP-ribose) polymerase 1	Homo sapiens	81-87
28991266-7	2017	Our data indicate that macroH2A1.1-containing chromatin regulates mitochondrial respiration by limiting nuclear NAD+ consumption and establishing a buffer of NAD+ precursors in differentiated cells.	NAD	112-116	macroH2A.1 histone	Homo sapiens	23-34
28991266-7	2017	Our data indicate that macroH2A1.1-containing chromatin regulates mitochondrial respiration by limiting nuclear NAD+ consumption and establishing a buffer of NAD+ precursors in differentiated cells.	NAD	158-162	macroH2A.1 histone	Homo sapiens	23-34
28650465-4	2017	Upregulation of MCU clearly enhanced the Ca2+ uptake into mitochondria, which significantly promoted ROS production by downregulating nicotinamide adenine dinucleotide+ (NAD+)/reduced form of nicotinamide adenine dinucleotid (NADH) ratio and the NAD+-dependent deacetylase activity of sirtuin 3 to inhibit superoxide dismutase 2 (SOD2) activity.	NAD	134-167	mitochondrial calcium uniporter	Homo sapiens	16-19
28650465-4	2017	Upregulation of MCU clearly enhanced the Ca2+ uptake into mitochondria, which significantly promoted ROS production by downregulating nicotinamide adenine dinucleotide+ (NAD+)/reduced form of nicotinamide adenine dinucleotid (NADH) ratio and the NAD+-dependent deacetylase activity of sirtuin 3 to inhibit superoxide dismutase 2 (SOD2) activity.	NAD	226-230	mitochondrial calcium uniporter	Homo sapiens	16-19
28847921-0	2017	A Bacterial Multidomain NAD-Independent d-Lactate Dehydrogenase Utilizes Flavin Adenine Dinucleotide and Fe-S Clusters as Cofactors and Quinone as an Electron Acceptor for d-Lactate Oxidization.	NAD	24-27	FAD-binding oxidoreductase	Pseudomonas putida KT2440	40-63
28847921-1	2017	Bacterial membrane-associated NAD-independent d-lactate dehydrogenase (Fe-S d-iLDH) oxidizes d-lactate into pyruvate.	NAD	30-33	FAD-binding oxidoreductase	Pseudomonas putida KT2440	46-69
28847921-13	2017	In recent years, novel bacterial lactate-oxidizing enzymes have been continually reported, including the unique NAD-independent d-lactate dehydrogenase that contains an Fe-S oxidoreductase domain besides the typical flavin-containing domain (Fe-S d-iLDH).	NAD	112-115	FAD-binding oxidoreductase	Pseudomonas putida KT2440	128-151
28830811-4	2017	METHODS: GAPDH activity was measured via reduction of NAD+ cofactor (340 nm).	NAD	54-58	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	9-14
29029745-3	2017	In presence of NADH at aerobic conditions, SHL catalyzed the decarboxylative hydroxylation of SAF and released a redox reporter amino ferrocene (AF 6).	NAD	15-19	FAS antisense RNA 1	Homo sapiens	94-97
28753212-3	2017	Mice lacking Ndufs4, encoding NADH: ubiquinone oxidoreductase iron-sulfur protein 4 (NDUFS4) recapitulates the main findings of complex I (cI)-related LS, including severe multisystemic cI deficiency and progressive neurodegeneration.	NAD	30-34	NADH:ubiquinone oxidoreductase core subunit S4	Mus musculus	13-19
28978450-2	2017	It funnels electrons coming from NADH and ubiquinol to cytochrome c, but it is also capable of producing significant amounts of the free radical superoxide.	NAD	33-37	cytochrome c, somatic	Homo sapiens	55-67
27990620-8	2017	PARP-1, an isoform of PARP, is a DNA nick-sensing enzyme that becomes activated upon sensing DNA breakage and triggers the cleavage of NAD+ into nicotinamide and ADP-ribose and polymerizes the latter on nuclear acceptor proteins.	NAD	135-139	poly(ADP-ribose) polymerase 1	Homo sapiens	0-6
27990620-8	2017	PARP-1, an isoform of PARP, is a DNA nick-sensing enzyme that becomes activated upon sensing DNA breakage and triggers the cleavage of NAD+ into nicotinamide and ADP-ribose and polymerizes the latter on nuclear acceptor proteins.	NAD	135-139	poly(ADP-ribose) polymerase 1	Homo sapiens	0-4
29037129-1	2017	Cystathionine beta-synthase (CBS) domains discovered 20 years ago can bind different adenosine derivatives (AMP, ADP, ATP, S-adenosylmethionine, NAD, diadenosine polyphosphates) and thus regulate the activities of numerous proteins.	NAD	145-148	cystathionine beta-synthase	Homo sapiens	0-27
27990620-9	2017	Peroxynitrite-induced hyperactivation of PARP causes depletion of NAD+ and ATP culminating cell dysfunction, necrosis or apoptosis.	NAD	66-70	poly(ADP-ribose) polymerase 1	Homo sapiens	41-45
28753212-3	2017	Mice lacking Ndufs4, encoding NADH: ubiquinone oxidoreductase iron-sulfur protein 4 (NDUFS4) recapitulates the main findings of complex I (cI)-related LS, including severe multisystemic cI deficiency and progressive neurodegeneration.	NAD	30-34	NADH:ubiquinone oxidoreductase core subunit S4	Mus musculus	85-91
28935892-6	2017	Changes in the NADH:NAD+ ratio regulate CtBP binding to the acetyltransferase p300, and regulate binding of p300 and the transcription factor NF-kappaB to pro-inflammatory gene promoters.	NAD	20-24	nuclear factor kappa B subunit 1	Homo sapiens	142-151
29042923-8	2017	Inversely, ERalpha-knocked down osteoblasts were treated with ERbeta agonist 2,3-bis(4-hydroxyphenyl)-propionitrile (DPN) to activate ERbeta.	NAD	117-120	estrogen receptor 1	Homo sapiens	11-18
29042923-11	2017	Treatment with ERbeta agonist DPN significantly rescued the effects of downregulation of ERalpha on cell viability (P&lt;0.01).	NAD	30-33	estrogen receptor 1	Homo sapiens	89-96
28302504-6	2017	Poly (ADP-ribose) polymerase 1 (PARP1) is activated after DNA damage, which depletes NAD+ pools and results in the PARylation of nuclear and mitochondrial proteins.	NAD	85-89	poly(ADP-ribose) polymerase 1	Homo sapiens	0-30
28302504-6	2017	Poly (ADP-ribose) polymerase 1 (PARP1) is activated after DNA damage, which depletes NAD+ pools and results in the PARylation of nuclear and mitochondrial proteins.	NAD	85-89	poly(ADP-ribose) polymerase 1	Homo sapiens	32-37
28751004-3	2017	The energy homeostasis is regulated by a network consisting of "fuel gauze" called AMP-activated protein kinase (AMPK), the NAD+ dependent type III deacetylase (SIRT1) and peroxisome proliferator-activated receptor-gamma coactivator-1alpha (PGC-1alpha) which is disrupted in T2D.	NAD	124-128	sirtuin 1	Rattus norvegicus	161-166
28751004-3	2017	The energy homeostasis is regulated by a network consisting of "fuel gauze" called AMP-activated protein kinase (AMPK), the NAD+ dependent type III deacetylase (SIRT1) and peroxisome proliferator-activated receptor-gamma coactivator-1alpha (PGC-1alpha) which is disrupted in T2D.	NAD	124-128	PPARG coactivator 1 alpha	Rattus norvegicus	241-251
26603930-5	2017	Current research indicates that methylene blue, a century old drug, can receive electron from NADH in the presence of complex I and donates it to cytochrome c, providing an alternative electron transfer pathway.	NAD	94-98	cytochrome c, somatic	Homo sapiens	146-158
28756225-5	2017	We uncovered novel and unexpected mechanisms of resistance including significantly increased expression of quinolinate phosphoribosyl transferase (QPRT), a key enzyme in the de novo NAD+ synthesis pathway.	NAD	182-186	quinolinate phosphoribosyltransferase	Homo sapiens	107-145
28756225-5	2017	We uncovered novel and unexpected mechanisms of resistance including significantly increased expression of quinolinate phosphoribosyl transferase (QPRT), a key enzyme in the de novo NAD+ synthesis pathway.	NAD	182-186	quinolinate phosphoribosyltransferase	Homo sapiens	147-151
28756225-7	2017	The combination of upregulation of the NAD+ de novo synthesis pathway through QPRT over-expression and NAMPT mutation confers resistance to GMX1778, but the cells are only partially resistant to next-generation NAMPT inhibitors.	NAD	39-43	quinolinate phosphoribosyltransferase	Homo sapiens	78-82
28935892-3	2017	Here, we show that glucose metabolism regulates pro-inflammatory NF-kappaB transcriptional activity through effects on the cytosolic NADH:NAD+ ratio and the NAD(H) sensitive transcriptional co-repressor CtBP.	NAD	133-137	nuclear factor kappa B subunit 1	Homo sapiens	65-74
28935892-3	2017	Here, we show that glucose metabolism regulates pro-inflammatory NF-kappaB transcriptional activity through effects on the cytosolic NADH:NAD+ ratio and the NAD(H) sensitive transcriptional co-repressor CtBP.	NAD	138-142	nuclear factor kappa B subunit 1	Homo sapiens	65-74
28935892-3	2017	Here, we show that glucose metabolism regulates pro-inflammatory NF-kappaB transcriptional activity through effects on the cytosolic NADH:NAD+ ratio and the NAD(H) sensitive transcriptional co-repressor CtBP.	NAD	157-163	nuclear factor kappa B subunit 1	Homo sapiens	65-74
28935892-6	2017	Changes in the NADH:NAD+ ratio regulate CtBP binding to the acetyltransferase p300, and regulate binding of p300 and the transcription factor NF-kappaB to pro-inflammatory gene promoters.	NAD	15-19	nuclear factor kappa B subunit 1	Homo sapiens	142-151
28928432-3	2017	When cells are grown on oleate medium, peroxisomal NADH is reoxidised to NAD+ by malate dehydrogenase (Mdh3p) and reduction equivalents are transferred to the cytosol by the malate/oxaloacetate shuttle.	NAD	51-55	malate dehydrogenase MDH3	Saccharomyces cerevisiae S288C	103-108
28928432-3	2017	When cells are grown on oleate medium, peroxisomal NADH is reoxidised to NAD+ by malate dehydrogenase (Mdh3p) and reduction equivalents are transferred to the cytosol by the malate/oxaloacetate shuttle.	NAD	73-77	malate dehydrogenase MDH3	Saccharomyces cerevisiae S288C	103-108
28912546-4	2017	Increasing NAD+ or oxidising cytoplasmic NADH was able to rescue the growth of PEPCK depleted tumors, suggesting a problem in clearing cytoplasmic NADH.	NAD	11-15	Phosphoenolpyruvate carboxykinase 1	Drosophila melanogaster	79-84
28912546-4	2017	Increasing NAD+ or oxidising cytoplasmic NADH was able to rescue the growth of PEPCK depleted tumors, suggesting a problem in clearing cytoplasmic NADH.	NAD	41-45	Phosphoenolpyruvate carboxykinase 1	Drosophila melanogaster	79-84
28912546-4	2017	Increasing NAD+ or oxidising cytoplasmic NADH was able to rescue the growth of PEPCK depleted tumors, suggesting a problem in clearing cytoplasmic NADH.	NAD	147-151	Phosphoenolpyruvate carboxykinase 1	Drosophila melanogaster	79-84
27670385-5	2017	Spectral fitting provided an NAD+ concentration of 107 +- 28 muM for 1 H-MRS and 367 +- 78 muM and 312 +- 65 muM for 31 P-MRS when uridine diphosphate glucose (UDPG) was excluded and included, respectively, as an overlapping signal.	NAD	29-33	UDP-glucose pyrophosphorylase 2	Homo sapiens	160-164
27670385-7	2017	NAD+ detection by 31 P-MRS has near-complete NMR visibility, but it is complicated by spectral overlap with NADH and UDPG.	NAD	0-4	UDP-glucose pyrophosphorylase 2	Homo sapiens	117-121
28714002-13	2017	Stochastic perturbation analysis revealed that NADH:ubiquinone oxidoreductase subunit B2 (NDUFB2), NDUFB8 and ubiquinol-cytochrome c reductase hinge protein (UQCRH) were associated with cellular respiration in Gram-negative samples, whereas large tumor suppressor kinase 2 (LATS2) was associated with G1/S transition of the mitotic cell cycle in Gram-positive samples.	NAD	47-51	NADH:ubiquinone oxidoreductase subunit B2	Homo sapiens	90-96
28525621-2	2017	Under robust oxidative DNA damage, PARP-1 is hyperactivated, resulting in the depletion of NAD+ and ATP with accompanying elevations in intracellular calcium concentrations (iCa2+), and ultimately necrotic cell death.	NAD	91-95	poly(ADP-ribose) polymerase 1	Homo sapiens	35-41
28625912-4	2017	The specific activity of the freshly purified hGAPDH constitutes 117 +- 5 mumol NADH/min per mg protein (pH 9.0, 22  C), which is close to the specific activity of rabbit muscle glyceraldehyde-3-phosphate dehydrogenase determined under the same conditions and several times exceeds the specific activity of his-tagged GAPDH preparations.	NAD	80-84	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	46-52
28819322-11	2017	Furthermore, in vivo inhibition of the NAMPT-NAD+-SIRT axis by NIC injection in mice ameliorated the periodontal inflammation and alveolar bone erosion caused by intragingival injection of Ad-Nampt.	NAD	45-49	nicotinamide phosphoribosyltransferase	Mus musculus	39-44
28819322-11	2017	Furthermore, in vivo inhibition of the NAMPT-NAD+-SIRT axis by NIC injection in mice ameliorated the periodontal inflammation and alveolar bone erosion caused by intragingival injection of Ad-Nampt.	NAD	45-49	nicotinamide phosphoribosyltransferase	Mus musculus	189-197
28756945-3	2017	Here, we report that the nicotinamide adenine dinucleotide (NAD)-dependent deacetylase SIRT1 acts as an energy sensor and negatively regulates poly(A)RNA transport via deacetylating a poly(A)-binding protein, PABP1.	NAD	25-58	poly(A) binding protein cytoplasmic 1 pseudogene 1	Homo sapiens	209-214
28756945-3	2017	Here, we report that the nicotinamide adenine dinucleotide (NAD)-dependent deacetylase SIRT1 acts as an energy sensor and negatively regulates poly(A)RNA transport via deacetylating a poly(A)-binding protein, PABP1.	NAD	60-63	poly(A) binding protein cytoplasmic 1 pseudogene 1	Homo sapiens	209-214
28625978-2	2017	It is known that PARP activation consumes NAD+ during base excision repair (BER) of chemotherapy-induced DNA damage.	NAD	42-46	poly(ADP-ribose) polymerase 1	Homo sapiens	17-21
28625978-5	2017	The acute time period (&lt;3 hours) after temozolomide treatment displayed a burst of NAD+ consumption driven by PARP activation.	NAD	86-90	poly(ADP-ribose) polymerase 1	Homo sapiens	113-117
28845527-0	2017	Extracellular NAMPT/visfatin causes p53 deacetylation via NAD production and SIRT1 activation in breast cancer cells.	NAD	58-61	tumor protein p53	Homo sapiens	36-39
28845527-10	2017	In conclusion, the results show that extracellular visfatin produces NAD that causes upregulation of SIRT1 activity and p53 deacetylation.	NAD	69-72	tumor protein p53	Homo sapiens	120-123
28669870-5	2017	The recombinant protein was purified by immobilized metal ion affinity chromatography yielding above 17 mg of purified 17beta-HSD1 protein per liter of cell culture, with a specific activity of 8.54 mumoL/min/mg of protein for conversion of estradiol into estrone, with NAD+ as cofactor at pH 9.2.	NAD	270-274	hydroxysteroid 17-beta dehydrogenase 1	Homo sapiens	119-130
28883796-6	2017	Emerging roles of NQO1 include its function as an efficient intracellular generator of NAD+ for enzymes including PARP and sirtuins which has gained particular attention with respect to metabolic syndrome.	NAD	87-91	NAD(P)H quinone dehydrogenase 1	Homo sapiens	18-22
29029387-0	2017	The beta-NAD+ salvage pathway and PKC-mediated signaling influence localized PARP-1 activity and CTCF Poly(ADP)ribosylation.	NAD	4-13	poly(ADP-ribose) polymerase 1	Homo sapiens	77-83
29029387-3	2017	We investigated the metabolic and mechanistic processes that regulate PARP-1-mediated CTCF PARylation in human cancer cell lines and discovered a key role for the expression and activity of beta-NAD+ salvage enzymes, NAMPT and NMNAT-1.	NAD	190-199	poly(ADP-ribose) polymerase 1	Homo sapiens	70-76
29029387-9	2017	Our findings suggest that CTCF PARylation is underpinned by a cellular metabolic context engendered by regulation of the beta-NAD+ salvage pathway in which NMNAT-1 acts as a rheostat to control localized beta-NAD+ synthesis at CTCF/PARP-1 complexes.	NAD	121-130	poly(ADP-ribose) polymerase 1	Homo sapiens	232-238
29029387-9	2017	Our findings suggest that CTCF PARylation is underpinned by a cellular metabolic context engendered by regulation of the beta-NAD+ salvage pathway in which NMNAT-1 acts as a rheostat to control localized beta-NAD+ synthesis at CTCF/PARP-1 complexes.	NAD	204-213	poly(ADP-ribose) polymerase 1	Homo sapiens	232-238
28527616-1	2017	Hepatic ethanol oxidation increases according to its concentration and is raised to near-saturation levels of alcohol dehydrogenase (ADH); therefore, re-oxidation of NADH becomes rate limiting in ethanol metabolism by the liver.	NAD	166-170	aldo-keto reductase family 1 member A1	Rattus norvegicus	110-131
28527616-1	2017	Hepatic ethanol oxidation increases according to its concentration and is raised to near-saturation levels of alcohol dehydrogenase (ADH); therefore, re-oxidation of NADH becomes rate limiting in ethanol metabolism by the liver.	NAD	166-170	aldo-keto reductase family 1 member A1	Rattus norvegicus	133-136
28478381-2	2017	NNT knockdown cells show limited abilities to maintain NAD+ and NADPH levels and have reduced proliferation and tumorigenicity.	NAD	55-59	nicotinamide nucleotide transhydrogenase	Homo sapiens	0-3
28478381-7	2017	These findings suggest that NNT is essential to homeostasis of NADH and NADPH pools, anomalies of which affect HIF-1alpha- and HDAC1-dependent pathways, and hence retrograde response of mitochondria.	NAD	63-67	nicotinamide nucleotide transhydrogenase	Homo sapiens	28-31
28478381-7	2017	These findings suggest that NNT is essential to homeostasis of NADH and NADPH pools, anomalies of which affect HIF-1alpha- and HDAC1-dependent pathways, and hence retrograde response of mitochondria.	NAD	63-67	hypoxia inducible factor 1 subunit alpha	Homo sapiens	111-121
28478381-7	2017	These findings suggest that NNT is essential to homeostasis of NADH and NADPH pools, anomalies of which affect HIF-1alpha- and HDAC1-dependent pathways, and hence retrograde response of mitochondria.	NAD	63-67	histone deacetylase 1	Homo sapiens	127-132
27215901-3	2017	Modification of the sulfhydryl groups of the enzyme inhibits the enzymatic activity of GAPDH, resulting in slowdown of glycolysis, and may lead to the dissociation of the cofactor NAD from the active site of the enzyme.	NAD	180-183	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	87-92
28679650-1	2017	Our study aimed at exploring the effects of miR-211 on the proliferation and apoptosis of lens epithelial cells in diabetic cataract mice by targetting NAD+-dependent histone deacetylase sirtulin 1 (SIRT1).	NAD	152-156	microRNA 211	Mus musculus	44-51
28525376-10	2017	Addition of NAD+ re-stabilized LDHA and reversed riluzole induced cell death.	NAD	12-16	lactate dehydrogenase A	Homo sapiens	31-35
28724915-2	2017	In hepatocytes, quinolinate phosphoribosyl transferase (QPRT) catabolizes quinolinic acid (QA) to nicotinic acid mononucleotide (NAMN) for de novo NAD synthesis.	NAD	147-150	quinolinate phosphoribosyltransferase	Homo sapiens	16-54
28724915-2	2017	In hepatocytes, quinolinate phosphoribosyl transferase (QPRT) catabolizes quinolinic acid (QA) to nicotinic acid mononucleotide (NAMN) for de novo NAD synthesis.	NAD	147-150	quinolinate phosphoribosyltransferase	Homo sapiens	56-60
28724915-7	2017	Activation of QPRT with clofibrate (CLO) or addition of QPRT catabolite NAD both inhibited HCV replication in cells, probably through NAD+-dependent Sirt1 inhibition of cellular lipogenesis.	NAD	72-75	quinolinate phosphoribosyltransferase	Homo sapiens	56-60
28724915-7	2017	Activation of QPRT with clofibrate (CLO) or addition of QPRT catabolite NAD both inhibited HCV replication in cells, probably through NAD+-dependent Sirt1 inhibition of cellular lipogenesis.	NAD	134-138	quinolinate phosphoribosyltransferase	Homo sapiens	14-18
28724915-7	2017	Activation of QPRT with clofibrate (CLO) or addition of QPRT catabolite NAD both inhibited HCV replication in cells, probably through NAD+-dependent Sirt1 inhibition of cellular lipogenesis.	NAD	134-138	quinolinate phosphoribosyltransferase	Homo sapiens	56-60
28704930-6	2017	PARP-1 inhibition using N-(6-Oxo-5,6-dihydro-phenanthridin-2-yl)- N,N-dimethylacetamide (PJ-34) in vivo administration was associated with preserved NAD+ levels and NAD+-dependent mitochondrial respiration, and improved CA1 neuronal survival.	NAD	149-153	poly(ADP-ribose) polymerase 1	Homo sapiens	0-6
28704930-6	2017	PARP-1 inhibition using N-(6-Oxo-5,6-dihydro-phenanthridin-2-yl)- N,N-dimethylacetamide (PJ-34) in vivo administration was associated with preserved NAD+ levels and NAD+-dependent mitochondrial respiration, and improved CA1 neuronal survival.	NAD	165-169	poly(ADP-ribose) polymerase 1	Homo sapiens	0-6
28704930-8	2017	The deleterious effects of PARP-1 hyperactivation on mitochondrial respiration are in part mediated through intracellular NAD+ depletion.	NAD	122-126	poly(ADP-ribose) polymerase 1	Homo sapiens	27-33
28506746-0	2017	The NAD+-dependent deacetylase, Bifidobacterium longum Sir2 in response to oxidative stress by deacetylating SigH (sigmaH) and FOXO3a in Bifidobacterium longum and HEK293T cell respectively.	NAD	4-7	forkhead box O3	Homo sapiens	127-133
28485916-6	2017	Our mechanism assessment elucidated extremely high pseudo-CAT and pseudo-SOD activities of NADH with coexistence of HbO2, and reactivity of NADH with NO.	NAD	91-95	catalase	Rattus norvegicus	58-61
28723574-1	2017	Tankyrase 1 (TNKS) and tankyrase 2 (TNKS2) belong to the poly(ADP-ribose) polymerase family of proteins, which use nicotinamide adenine dinucleotide to modify substrate proteins with ADP-ribose modifications.	NAD	115-148	tankyrase	Homo sapiens	0-11
28723574-1	2017	Tankyrase 1 (TNKS) and tankyrase 2 (TNKS2) belong to the poly(ADP-ribose) polymerase family of proteins, which use nicotinamide adenine dinucleotide to modify substrate proteins with ADP-ribose modifications.	NAD	115-148	tankyrase	Homo sapiens	13-17
28263970-3	2017	Regeneration of the NAD required to support enhanced glycolysis has been attributed to the terminal glycolytic enzyme, lactate dehydrogenase (LDH).	NAD	20-23	hexokinase 1	Homo sapiens	100-117
27215901-4	2017	The resulting apo-GAPDH (without NAD) is less stable and prone to dissociation, denaturation, and subsequent aggregation.	NAD	33-36	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	18-23
28051090-2	2017	In this issue of Mucosal Immunology, Hashimoto-Hill et al.1 show that retinoic acid (RA) transcriptionally upregulates P2X7 primarily in effector T cells of the intestine sensitizing them to NAD-induced cell death (NICD); thus, demonstrating a previously unrecognized role of RA in effector T-cell contraction.	NAD	191-194	purinergic receptor P2X 7	Homo sapiens	119-123
28263025-4	2017	PARP catalyzes poly(ADP-ribosyl)ation of proteins by repeatedly adding ADP-ribose units onto proteins using nicotinamide adenine dinucleotide (NAD+ ) as the donor.	NAD	108-141	poly(ADP-ribose) polymerase 1	Homo sapiens	0-4
28263025-4	2017	PARP catalyzes poly(ADP-ribosyl)ation of proteins by repeatedly adding ADP-ribose units onto proteins using nicotinamide adenine dinucleotide (NAD+ ) as the donor.	NAD	143-147	poly(ADP-ribose) polymerase 1	Homo sapiens	0-4
28346693-4	2017	DNA damage created by ARQ761 in pancreatic cancer cells "hyperactivates" PARP1, causing metabolic catastrophe and NAD +- keresis cell death.	NAD	114-119	poly(ADP-ribose) polymerase 1	Homo sapiens	73-78
28375741-2	2017	The three IDH isoforms (nicotinamide adenine dinucleotide phosphate-dependent IDH1 and IDH2, and nicotinamide adenine dinucleotide-dependent IDH3) contribute to regulating the circuitry of central metabolism.	NAD	24-57	isocitrate dehydrogenase (NADP(+)) 2	Homo sapiens	87-91
28978059-5	2017	Further, inhibition of 6PGD activity reduced NADH levels and enzymatic activity of the oxidized NADH-dependent sirtuin-1.	NAD	45-49	phosphogluconate dehydrogenase	Homo sapiens	23-27
28978059-5	2017	Further, inhibition of 6PGD activity reduced NADH levels and enzymatic activity of the oxidized NADH-dependent sirtuin-1.	NAD	96-100	phosphogluconate dehydrogenase	Homo sapiens	23-27
28659816-1	2017	SIRT6, a member of the NAD (+)-dependent class III deacetylase sirtuin family, plays important roles in the maintenance of cardiovascular homeostasis.	NAD	23-30	sirtuin 6	Mus musculus	0-5
28604662-0	2017	Upregulation of mitochondrial NAD+ levels impairs the clonogenicity of SSEA1+ glioblastoma tumor-initiating cells.	NAD	30-34	fucosyltransferase 4	Homo sapiens	71-76
28356339-8	2017	SMC-Nampt knockout mice were viable but with mildly dilated aortas that had a 43% reduction in NAD+ in the media.	NAD	95-99	nicotinamide phosphoribosyltransferase	Mus musculus	4-9
28604662-3	2017	In this study, we provide evidence that the mitochondrial NAD+ levels affect the characteristics of glioma-driven SSEA1+ TICs, including clonogenic growth potential.	NAD	58-62	fucosyltransferase 4	Homo sapiens	114-119
28752046-5	2017	RESULTS: Skeletal muscle cells primarily rely on nicotinamide phosphoribosyltransferase (NAMPT), NRK1, and NRK2 for salvage biosynthesis of NAD+.	NAD	140-144	nicotinamide phosphoribosyltransferase	Mus musculus	49-87
28295574-10	2017	Finally, increased levels of NAD+ , caused by CD38 deficiency, are likely to be responsible for the suppression of astrocytic Cx43 expression and OL differentiation.	NAD	29-33	gap junction protein, alpha 1	Mus musculus	126-130
27922186-8	2017	In this study, we demonstrate that pretreatment of colorectal cancer cells with IL-1beta diminished butyrate oxidation and NADH levels.	NAD	123-127	interleukin 1 beta	Homo sapiens	80-88
28537485-6	2017	DBC1-PARP1 complexes in old mice can be broken by increasing NAD+ levels through treatment with NMN, reducing DNA damage and restoring PARP activity to youthful levels.	NAD	61-65	cell cycle activator and apoptosis regulator 2	Mus musculus	0-4
28537485-8	2017	There is a correlation of PARP activity with mammalian life span that suggests that NAD+/SIRT1/PARP1 may be more significant than the modest effects on life span observed for NR supplementation in old mice.	NAD	84-88	poly(ADP-ribose) polymerase 1	Homo sapiens	26-30
28537485-8	2017	There is a correlation of PARP activity with mammalian life span that suggests that NAD+/SIRT1/PARP1 may be more significant than the modest effects on life span observed for NR supplementation in old mice.	NAD	84-88	poly(ADP-ribose) polymerase 1	Homo sapiens	95-100
28592850-6	2017	Moreover, we confirmed that the increase of cellular NAD+ by NQO1 enzymatic action using the substrate beta-Lapachone suppressed caerulein-induced AP with down-regulating TLR4-mediated inflammasome signalling, and thereby reducing the inflammatory responses and pancreatic cell death.	NAD	53-57	NAD(P)H quinone dehydrogenase 1	Homo sapiens	61-65
28915567-6	2017	Melatonin reduced the IL-1beta-increased nicotinamide phosphoribosyltransferase (NAMPT) expression and the NAD+ level in chondrocytes in a Sirt1-dependent manner.	NAD	107-111	interleukin 1 beta	Homo sapiens	22-30
28537485-4	2017	Decreased NAD+ levels cause NAD+-binding protein DBC1 to form a complex with PARP1, inhibiting poly(adenosine diphosphate-ribose) polymerase (PARP) catalytic activity.	NAD	10-14	cell cycle activator and apoptosis regulator 2	Mus musculus	49-53
28537485-4	2017	Decreased NAD+ levels cause NAD+-binding protein DBC1 to form a complex with PARP1, inhibiting poly(adenosine diphosphate-ribose) polymerase (PARP) catalytic activity.	NAD	28-32	cell cycle activator and apoptosis regulator 2	Mus musculus	49-53
28603486-5	2017	Mammalian sirtuins, especially the mitochondrial NAD+ dependent sirtuin 3 (SIRT3), regulate mitochondrial function and aging processes.	NAD	49-53	sirtuin 3	Homo sapiens	64-73
28603486-5	2017	Mammalian sirtuins, especially the mitochondrial NAD+ dependent sirtuin 3 (SIRT3), regulate mitochondrial function and aging processes.	NAD	49-53	sirtuin 3	Homo sapiens	75-80
28752046-5	2017	RESULTS: Skeletal muscle cells primarily rely on nicotinamide phosphoribosyltransferase (NAMPT), NRK1, and NRK2 for salvage biosynthesis of NAD+.	NAD	140-144	nicotinamide phosphoribosyltransferase	Mus musculus	89-94
28752046-6	2017	NAMPT inhibition depletes muscle NAD+ availability and can be rescued by NR and NMN as the preferred precursors for elevating muscle cell NAD+ in a pathway that depends on NRK1 and NRK2.	NAD	33-37	nicotinamide phosphoribosyltransferase	Mus musculus	0-5
28752046-6	2017	NAMPT inhibition depletes muscle NAD+ availability and can be rescued by NR and NMN as the preferred precursors for elevating muscle cell NAD+ in a pathway that depends on NRK1 and NRK2.	NAD	138-142	nicotinamide phosphoribosyltransferase	Mus musculus	0-5
28752046-10	2017	CONCLUSIONS: These results identify skeletal muscle cells as requiring NAMPT to maintain NAD+ availability and reveal that NRK1 and 2 display overlapping function in salvage of exogenous NR and NMN to augment intracellular NAD+ availability.	NAD	89-93	nicotinamide phosphoribosyltransferase	Mus musculus	71-76
28427145-6	2017	These results indicated that COP rats have an increased capacity to maintain NAD+-dependent SIRT1 activity under genotoxic stress.	NAD	77-81	sirtuin 1	Rattus norvegicus	92-97
28536482-6	2017	Our findings additionally support a role for decreased NAD+ dependent Sirt6 activity in mediating dioxin toxicity following PARP activation.	NAD	55-59	sirtuin 6	Gallus gallus	70-75
28546856-3	2017	Here we reported the key role of nicotinamide phosphoribosyltransferase (Nampt), which is the rate-limiting enzyme in the salvage pathway of NAD biosynthesis from nicotinamide, in the osteogenic differentiation of bone marrow stromal cells.	NAD	141-144	nicotinamide phosphoribosyltransferase	Mus musculus	33-71
28546856-3	2017	Here we reported the key role of nicotinamide phosphoribosyltransferase (Nampt), which is the rate-limiting enzyme in the salvage pathway of NAD biosynthesis from nicotinamide, in the osteogenic differentiation of bone marrow stromal cells.	NAD	141-144	nicotinamide phosphoribosyltransferase	Mus musculus	73-78
28977855-2	2017	Q3STCy is a newly synthesized, NIR light-emitting probe that is activated by an enzyme commonly overexpressed in tumor cells, human nicotinamide adenine dinucleotide (phosphate): quinone oxidoreductase isozyme 1, known as hNQO1 or DT-diaphorase.	NAD	132-165	NAD(P)H quinone dehydrogenase 1	Homo sapiens	222-227
28977855-2	2017	Q3STCy is a newly synthesized, NIR light-emitting probe that is activated by an enzyme commonly overexpressed in tumor cells, human nicotinamide adenine dinucleotide (phosphate): quinone oxidoreductase isozyme 1, known as hNQO1 or DT-diaphorase.	NAD	132-165	NAD(P)H quinone dehydrogenase 1	Homo sapiens	231-244
28131761-1	2017	AIMS: Sirtuin 3 (SIRT3) is a mitochondria-specific protein required for the deacetylation of metabolic enzymes and the action of oxidative phosphorylation by acting as a nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase.	NAD	170-203	sirtuin 3	Homo sapiens	6-15
28131761-1	2017	AIMS: Sirtuin 3 (SIRT3) is a mitochondria-specific protein required for the deacetylation of metabolic enzymes and the action of oxidative phosphorylation by acting as a nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase.	NAD	170-203	sirtuin 3	Homo sapiens	17-22
28131761-1	2017	AIMS: Sirtuin 3 (SIRT3) is a mitochondria-specific protein required for the deacetylation of metabolic enzymes and the action of oxidative phosphorylation by acting as a nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase.	NAD	205-209	sirtuin 3	Homo sapiens	6-15
28131761-1	2017	AIMS: Sirtuin 3 (SIRT3) is a mitochondria-specific protein required for the deacetylation of metabolic enzymes and the action of oxidative phosphorylation by acting as a nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase.	NAD	205-209	sirtuin 3	Homo sapiens	17-22
28448551-1	2017	The NAD+-dependent SIRT6 deacetylase was shown to be a major regulator of lifespan and healthspan.	NAD	4-8	sirtuin 6	Mus musculus	19-24
28416276-3	2017	Here we show that two enzymes committed to NAD biosynthesis, nicotinamide phosphoribosyltransferase (NAMPT) and nicotinate phosphoribosyltransferase (NAPT), can both catalyze the synthesis and degradation of Ap4 through their facultative ATPase activity.	NAD	43-46	nicotinamide phosphoribosyltransferase	Mus musculus	61-99
28416276-3	2017	Here we show that two enzymes committed to NAD biosynthesis, nicotinamide phosphoribosyltransferase (NAMPT) and nicotinate phosphoribosyltransferase (NAPT), can both catalyze the synthesis and degradation of Ap4 through their facultative ATPase activity.	NAD	43-46	nicotinamide phosphoribosyltransferase	Mus musculus	101-106
28250020-1	2017	Sirt6 is an NAD+-dependent deacetylase that is involved in the control of energy metabolism.	NAD	12-15	sirtuin 6	Mus musculus	0-5
28449683-2	2017	Nicotinamide phosphoribosyltransferase (NAMPT) has been recently identified as an enzyme involved in nicotinamide adenine dinucleotide (NAD+) biosynthesis and plays an important role in cellular metabolism in variety of organs in mammals.	NAD	101-134	nicotinamide phosphoribosyltransferase	Mus musculus	0-38
28449683-2	2017	Nicotinamide phosphoribosyltransferase (NAMPT) has been recently identified as an enzyme involved in nicotinamide adenine dinucleotide (NAD+) biosynthesis and plays an important role in cellular metabolism in variety of organs in mammals.	NAD	101-134	nicotinamide phosphoribosyltransferase	Mus musculus	40-45
28449683-2	2017	Nicotinamide phosphoribosyltransferase (NAMPT) has been recently identified as an enzyme involved in nicotinamide adenine dinucleotide (NAD+) biosynthesis and plays an important role in cellular metabolism in variety of organs in mammals.	NAD	136-140	nicotinamide phosphoribosyltransferase	Mus musculus	0-38
28449683-2	2017	Nicotinamide phosphoribosyltransferase (NAMPT) has been recently identified as an enzyme involved in nicotinamide adenine dinucleotide (NAD+) biosynthesis and plays an important role in cellular metabolism in variety of organs in mammals.	NAD	136-140	nicotinamide phosphoribosyltransferase	Mus musculus	40-45
28449683-14	2017	On the one hand, the inhibition of NAMPT reduced the production of NAD+ through inhibiting the NAD+ salvage pathway, resulting in the decrease of Sirt1 activity, and then attenuated the deacetylation of SREBP1 in which the inhibition of SREBP1 activity promoted the expressions of FASN and ACC.	NAD	67-71	nicotinamide phosphoribosyltransferase	Mus musculus	35-40
28449683-14	2017	On the one hand, the inhibition of NAMPT reduced the production of NAD+ through inhibiting the NAD+ salvage pathway, resulting in the decrease of Sirt1 activity, and then attenuated the deacetylation of SREBP1 in which the inhibition of SREBP1 activity promoted the expressions of FASN and ACC.	NAD	67-71	fatty acid synthase	Mus musculus	281-285
28449683-14	2017	On the one hand, the inhibition of NAMPT reduced the production of NAD+ through inhibiting the NAD+ salvage pathway, resulting in the decrease of Sirt1 activity, and then attenuated the deacetylation of SREBP1 in which the inhibition of SREBP1 activity promoted the expressions of FASN and ACC.	NAD	95-99	nicotinamide phosphoribosyltransferase	Mus musculus	35-40
28490746-7	2017	Pharmacological activation of transcription factor Nrf2 increased mitochondrial NADH levels and restored mitochondrial membrane potential in p62-deficient cells.	NAD	80-84	NFE2 like bZIP transcription factor 2	Homo sapiens	51-55
28279754-11	2017	DPN reduced OT and increased AVP levels, regardless hemorrhage.	NAD	0-3	arginine vasopressin	Rattus norvegicus	29-32
28079261-5	2017	A PARP-1 inhibitor (PJ-34) was used to confirm the relationship between PARP-1 activation and NAD+ depletion.	NAD	94-98	poly(ADP-ribose) polymerase 1	Homo sapiens	72-78
28079261-8	2017	PARP-1 activation led to NAD+ depletion (P&lt;.05).	NAD	25-29	poly(ADP-ribose) polymerase 1	Homo sapiens	0-6
28079261-11	2017	Parthanatos (PARP-1-dependent cell death) was definitely involved in ropivacaine-induced neuronal injury, and exogenous NAD+ may be a novel therapeutic method for parthanatos-dependent neuronal injury.	NAD	120-124	poly(ADP-ribose) polymerase 1	Homo sapiens	13-19
27519885-3	2017	Similar to dietary restriction, mice overexpressing the NAD+ dependent protein deacylase SIRT6 (MOSES) live longer and have reduced IGF-1 levels.	NAD	56-59	sirtuin 6	Mus musculus	89-94
28580284-2	2017	Nicotinamide nucleotide transhydrogenase (NNT) typically produces NADPH at the expense of NADH and DeltapH in energized mitochondria.	NAD	90-94	nicotinamide nucleotide transhydrogenase	Mus musculus	0-40
28330719-3	2017	Nicotinamide mononucleotide (NMN), the important precursor of NAD+, is produced during the reaction of nicotinamide phosphoribosyl transferase (Nampt).	NAD	62-66	nicotinamide phosphoribosyltransferase	Mus musculus	103-142
28330719-3	2017	Nicotinamide mononucleotide (NMN), the important precursor of NAD+, is produced during the reaction of nicotinamide phosphoribosyl transferase (Nampt).	NAD	62-66	nicotinamide phosphoribosyltransferase	Mus musculus	144-149
28396387-8	2017	Consequently, because PIK3CA mutant cells exhibit a profound reliance on glucose metabolism, malate-aspartate shuttle deregulation leads to a specific proliferative block due to the inability to maintain NAD+/NADH homeostasis.	NAD	204-208	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	22-28
28396387-8	2017	Consequently, because PIK3CA mutant cells exhibit a profound reliance on glucose metabolism, malate-aspartate shuttle deregulation leads to a specific proliferative block due to the inability to maintain NAD+/NADH homeostasis.	NAD	209-213	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	22-28
28580284-2	2017	Nicotinamide nucleotide transhydrogenase (NNT) typically produces NADPH at the expense of NADH and DeltapH in energized mitochondria.	NAD	90-94	nicotinamide nucleotide transhydrogenase	Mus musculus	42-45
28387379-7	2017	Under this protocol, MTT reduction was coupled with catalysis of GAPDH and was promoted by electron transfer from NADH.	NAD	114-118	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	65-70
27888691-7	2017	We also measured the protein content of NAD+ dependent enzymes such as sirtuin3 (sirt3) and NAD(P)H: quinone oxidoreductase 1 (NQO1).	NAD	40-44	NAD(P)H quinone dehydrogenase 1	Rattus norvegicus	92-125
27866308-2	2017	Combining with formate dehydrogenase (FDH) for regenerating the expensive coenzyme NADH, leucine dehydrogenase (LeuDH) is continually used for synthesizing L-Tle from alpha-keto acid.	NAD	83-87	aldehyde dehydrogenase 1 family member L1	Homo sapiens	15-36
27866308-2	2017	Combining with formate dehydrogenase (FDH) for regenerating the expensive coenzyme NADH, leucine dehydrogenase (LeuDH) is continually used for synthesizing L-Tle from alpha-keto acid.	NAD	83-87	aldehyde dehydrogenase 1 family member L1	Homo sapiens	38-41
28032259-7	2017	In vitro NADH-dependent O 2 - production at the plasma membrane in the presence of NQR was reduced upon addition of AIR12.	NAD	9-13	plasma membrane ascorbate-reducible b-type cytochrome family protein	Glycine max	116-121
28088384-4	2017	RTC-1-induced inhibition of NADH:ubiquinone oxidoreductase was found to promote glucose uptake in C2C12 myotubes in vitro, through the activation of the Akt substrate of 160kDa (AS160), in response to the increased activity of Akt and AMP-activated protein kinase (AMPK).	NAD	28-32	thymoma viral proto-oncogene 1	Mus musculus	153-156
28202508-5	2017	The PARP1-associated DNA repair pathway was extensively compromised in mutant cells due to decreased NAD+ availability.	NAD	101-105	poly(ADP-ribose) polymerase 1	Homo sapiens	4-9
27888691-7	2017	We also measured the protein content of NAD+ dependent enzymes such as sirtuin3 (sirt3) and NAD(P)H: quinone oxidoreductase 1 (NQO1).	NAD	40-44	NAD(P)H quinone dehydrogenase 1	Rattus norvegicus	127-131
28351995-2	2017	Sirtuin (Sirt) 6, a nicotinamide adenine dinucleotide (NAD)-dependent histone deacetylase, has been shown to protect against multiple age-associated phenotypes; however it is unknown whether Sirt6 has a direct pathophysiologic role in the kidney.	NAD	20-53	sirtuin 6	Mus musculus	9-16
28361886-2	2017	In cellular preparations and isolated mitochondria suspensions, enzyme-dependent fluorescence recovery after photobleaching (ED-FRAP) of NADH has been shown to be an effective approach for measuring the rate of NADH production to assess dehydrogenase enzyme activity.	NAD	137-141	mechanistic target of rapamycin kinase	Homo sapiens	128-132
28361886-2	2017	In cellular preparations and isolated mitochondria suspensions, enzyme-dependent fluorescence recovery after photobleaching (ED-FRAP) of NADH has been shown to be an effective approach for measuring the rate of NADH production to assess dehydrogenase enzyme activity.	NAD	211-215	mechanistic target of rapamycin kinase	Homo sapiens	128-132
28361886-6	2017	NADH ED-FRAP parameters were optimized to deliver 23.8 mJ of photobleaching light energy at a pulse width of 6 msec and a duty cycle of 50%.	NAD	0-4	mechanistic target of rapamycin kinase	Homo sapiens	8-12
28361886-10	2017	Overall, our results indicate that myocardial NADH ED-FRAP is a useful optical non-destructive approach for assessing dehydrogenase activity.	NAD	46-50	mechanistic target of rapamycin kinase	Homo sapiens	54-58
28351995-2	2017	Sirtuin (Sirt) 6, a nicotinamide adenine dinucleotide (NAD)-dependent histone deacetylase, has been shown to protect against multiple age-associated phenotypes; however it is unknown whether Sirt6 has a direct pathophysiologic role in the kidney.	NAD	55-58	sirtuin 6	Mus musculus	9-16
28336669-4	2017	The binding of NAD+ to the NHD domain of DBC1 (deleted in breast cancer 1) prevents it from inhibiting PARP1 [poly(adenosine diphosphate-ribose) polymerase], a critical DNA repair protein.	NAD	15-19	cell cycle activator and apoptosis regulator 2	Mus musculus	41-45
28188256-4	2017	Moreover, we showed for the first time that NADH can, like NADPH, form active complexes with Pchlide and POR, however, at much higher concentrations.	NAD	44-48	cytochrome p450 oxidoreductase	Homo sapiens	105-108
28333140-5	2017	In Nampt-/- mice versus Nampt+/+ mice, biochemical assays indicated that liver and intestinal tissue NAD levels were decreased significantly; histological examination showed that mouse intestinal villi were atrophic and disrupted, and visceral fat was depleted; mass spectrometry detected unusual higher serum polyunsaturated fatty acid containing triglycerides.	NAD	101-104	nicotinamide phosphoribosyltransferase	Mus musculus	3-8
28336669-4	2017	The binding of NAD+ to the NHD domain of DBC1 (deleted in breast cancer 1) prevents it from inhibiting PARP1 [poly(adenosine diphosphate-ribose) polymerase], a critical DNA repair protein.	NAD	15-19	cell cycle activator and apoptosis regulator 2	Mus musculus	47-73
28336669-5	2017	As mice age and NAD+ concentrations decline, DBC1 is increasingly bound to PARP1, causing DNA damage to accumulate, a process rapidly reversed by restoring the abundance of NAD+ Thus, NAD+ directly regulates protein-protein interactions, the modulation of which may protect against cancer, radiation, and aging.	NAD	16-20	cell cycle activator and apoptosis regulator 2	Mus musculus	45-49
28336669-5	2017	As mice age and NAD+ concentrations decline, DBC1 is increasingly bound to PARP1, causing DNA damage to accumulate, a process rapidly reversed by restoring the abundance of NAD+ Thus, NAD+ directly regulates protein-protein interactions, the modulation of which may protect against cancer, radiation, and aging.	NAD	173-177	cell cycle activator and apoptosis regulator 2	Mus musculus	45-49
28336669-5	2017	As mice age and NAD+ concentrations decline, DBC1 is increasingly bound to PARP1, causing DNA damage to accumulate, a process rapidly reversed by restoring the abundance of NAD+ Thus, NAD+ directly regulates protein-protein interactions, the modulation of which may protect against cancer, radiation, and aging.	NAD	173-177	cell cycle activator and apoptosis regulator 2	Mus musculus	45-49
28424540-6	2017	MC4 also exerted more potent effects than FK866, at concentrations as low as 0.3 nM, to attenuate TNFalpha-mediated intracellular cytokine expression, nicotinamide adenine dinucleotide (NAD+) and its reduced form NADH levels, and nuclear factor kappa B p65 phosphorylation and nuclear translocation in A549 cells.	NAD	151-184	tumor necrosis factor	Mus musculus	98-106
28165742-1	2017	Nicotinamide phosphoribosyltransferase (NAMPT) is a key enzyme involved in the recycling of nicotinamide to maintain adequate NAD levels inside the cells.	NAD	126-129	nicotinamide phosphoribosyltransferase	Mus musculus	0-38
28165742-1	2017	Nicotinamide phosphoribosyltransferase (NAMPT) is a key enzyme involved in the recycling of nicotinamide to maintain adequate NAD levels inside the cells.	NAD	126-129	nicotinamide phosphoribosyltransferase	Mus musculus	40-45
28202712-0	2017	RIBEYE(B)-domain binds to lipid components of synaptic vesicles in an NAD(H)-dependent, redox-sensitive manner.	NAD	70-76	C-terminal binding protein 2	Homo sapiens	0-6
28202712-3	2017	RIBEYE consists of a unique A-domain and a carboxyterminal B-domain, which binds NAD(H).	NAD	81-87	C-terminal binding protein 2	Homo sapiens	0-6
28202712-8	2017	Interestingly, binding of liposomes to RIBEYE(B) depends on NAD(H) in a redox-sensitive manner.	NAD	60-66	C-terminal binding protein 2	Homo sapiens	39-45
28382184-5	2017	Herein, we compare the substrate scope and applicability of different NAD+ analogues for the investigation of the polymer-synthesising enzymes ARTD1, ARTD2, ARTD5 and ARTD6.	NAD	70-74	poly(ADP-ribose) polymerase 1	Homo sapiens	143-148
28382184-5	2017	Herein, we compare the substrate scope and applicability of different NAD+ analogues for the investigation of the polymer-synthesising enzymes ARTD1, ARTD2, ARTD5 and ARTD6.	NAD	70-74	poly(ADP-ribose) polymerase 2	Homo sapiens	150-155
28382184-5	2017	Herein, we compare the substrate scope and applicability of different NAD+ analogues for the investigation of the polymer-synthesising enzymes ARTD1, ARTD2, ARTD5 and ARTD6.	NAD	70-74	tankyrase	Homo sapiens	157-162
28424540-6	2017	MC4 also exerted more potent effects than FK866, at concentrations as low as 0.3 nM, to attenuate TNFalpha-mediated intracellular cytokine expression, nicotinamide adenine dinucleotide (NAD+) and its reduced form NADH levels, and nuclear factor kappa B p65 phosphorylation and nuclear translocation in A549 cells.	NAD	213-217	tumor necrosis factor	Mus musculus	98-106
27989687-12	2017	CONCLUSION: NADH activated PKCdelta by enhancing PLD activity.	NAD	12-16	glycosylphosphatidylinositol specific phospholipase D1	Homo sapiens	49-52
28159473-2	2017	In a previous study, we found that osteogenic differentiation of the multipotent and omnipotent preosteoblasts are accompanied by the alterations of intracellular NAD metabolism in which nicotinamide phosphoribosyltransferase (Nampt) plays a regulatory role.	NAD	163-166	nicotinamide phosphoribosyltransferase	Mus musculus	187-225
28159473-2	2017	In a previous study, we found that osteogenic differentiation of the multipotent and omnipotent preosteoblasts are accompanied by the alterations of intracellular NAD metabolism in which nicotinamide phosphoribosyltransferase (Nampt) plays a regulatory role.	NAD	163-166	nicotinamide phosphoribosyltransferase	Mus musculus	227-232
28159473-3	2017	The increased Nampt during osteoblast differentiation, the enzyme catalyzing NAD resynthesis from nicotinamide was noted.	NAD	77-80	nicotinamide phosphoribosyltransferase	Mus musculus	14-19
28159473-8	2017	In addition, declined osteoblastogenesis by Nampt deficiency or addition of FK866 was related to lower intracellular NAD concentration and decreased Sirt1 activity.	NAD	117-120	nicotinamide phosphoribosyltransferase	Mus musculus	44-49
28159473-9	2017	The present findings demonstrate that osteogenic differentiation in MSCs can be modulated by intracellular NAD metabolism, in which Nampt may serve as an applicable marker for the osteoblast determination.	NAD	107-110	nicotinamide phosphoribosyltransferase	Mus musculus	132-137
27989687-7	2017	RESULTS: NADH enhanced PLD activity (1.6- +- 0.1-fold, P &lt;.01) and activated PKCdelta.	NAD	9-13	glycosylphosphatidylinositol specific phospholipase D1	Homo sapiens	23-26
27135296-5	2017	The difference in GAPDS activity in DFS and normal spermatozoa was statistically significant (0.19 +- 0.11 and 0.75 +- 0.11 mumol NADH per min per mg protein respectively).	NAD	130-134	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	18-23
27929719-5	2017	In C. elegans, NAD+ repletion can clear accumulated dysfunctional mitochondria through restoration of compromised mitophagy via upregulation of DCT-1.	NAD	15-19	NIP3 homolog	Caenorhabditis elegans	144-149
27836583-1	2017	SIRT6, a member of the Sirtuin family of NAD+-dependent enzymes, has established roles in chromatin signaling and genome maintenance.	NAD	41-45	sirtuin 6	Mus musculus	0-5
28122359-5	2017	In AGS cells, we found that the oxaliplatin-inhibited tNOX effectively attenuated the NAD+/NADH ratio and reduced the deacetylase activity of an NAD+-dependent sirtuin 1, thereby enhancing p53 acetylation and apoptosis.	NAD	86-90	ecto-NOX disulfide-thiol exchanger 2	Homo sapiens	54-58
28122359-5	2017	In AGS cells, we found that the oxaliplatin-inhibited tNOX effectively attenuated the NAD+/NADH ratio and reduced the deacetylase activity of an NAD+-dependent sirtuin 1, thereby enhancing p53 acetylation and apoptosis.	NAD	91-95	ecto-NOX disulfide-thiol exchanger 2	Homo sapiens	54-58
28122359-5	2017	In AGS cells, we found that the oxaliplatin-inhibited tNOX effectively attenuated the NAD+/NADH ratio and reduced the deacetylase activity of an NAD+-dependent sirtuin 1, thereby enhancing p53 acetylation and apoptosis.	NAD	86-89	ecto-NOX disulfide-thiol exchanger 2	Homo sapiens	54-58
28232723-6	2017	Furthermore, we show that elevated NOX4 activity accelerates oxidation of NADH and supports increased glycolysis by generating NAD+, a substrate for GAPDH-mediated glycolytic reaction, promoting PDAC cell growth.	NAD	127-131	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	149-154
28017962-4	2017	Silent information regulator family protein 1 (SIRT1), a member of the NAD+-dependent protein deacetylases, has been shown to exhibit neuroprotective activities in animal models of various pathologies, including ischemic brain injury, subarachnoid hemorrhage and several neurodegenerative diseases.	NAD	71-74	sirtuin 1	Rattus norvegicus	0-45
28017962-4	2017	Silent information regulator family protein 1 (SIRT1), a member of the NAD+-dependent protein deacetylases, has been shown to exhibit neuroprotective activities in animal models of various pathologies, including ischemic brain injury, subarachnoid hemorrhage and several neurodegenerative diseases.	NAD	71-74	sirtuin 1	Rattus norvegicus	47-52
27929731-4	2017	In this report, using both human and murine models of CSCs, we demonstrate that basal levels of autophagy are required to maintain the pluripotency of CSCs, and that this process is differentially regulated by the rate-limiting enzyme in the NAD+ synthesis pathway NAMPT (nicotinamide phosphoribosyltransferase) and the transcription factor POU5F1/OCT4 (POU class 5 homeobox 1).	NAD	242-246	nicotinamide phosphoribosyltransferase	Mus musculus	265-270
27929731-4	2017	In this report, using both human and murine models of CSCs, we demonstrate that basal levels of autophagy are required to maintain the pluripotency of CSCs, and that this process is differentially regulated by the rate-limiting enzyme in the NAD+ synthesis pathway NAMPT (nicotinamide phosphoribosyltransferase) and the transcription factor POU5F1/OCT4 (POU class 5 homeobox 1).	NAD	242-246	nicotinamide phosphoribosyltransferase	Mus musculus	272-310
28147277-0	2017	Regulation of Serine-Threonine Kinase Akt Activation by NAD+-Dependent Deacetylase SIRT7.	NAD	56-59	thymoma viral proto-oncogene 1	Mus musculus	38-41
27302189-7	2017	Activity of SIRT-1 and PAR modification of VEGF in turn, was found to be correlated to the cellular NAD+ levels.	NAD	100-104	vascular endothelial growth factor A	Homo sapiens	43-47
27889632-4	2017	Compounds 5b and 5d showed H-bonding interactions with Tyr158, Thr196 and co-factor NAD+ that fitted well within the binding pocket of InhA.	NAD	84-88	inhibin subunit alpha	Homo sapiens	135-139
27889611-2	2017	When investigating possible gene expression network partners of WT1 in a large acute myeloid leukemia (AML) patient cohort, one of the genes with the highest correlation to WT1 was quinolinate phosphoribosyltransferase (QPRT), a key enzyme in the de novo nicotinamide adenine dinucleotide (NAD+) synthesis pathway.	NAD	255-288	WT1 transcription factor	Homo sapiens	64-67
28122227-5	2017	Reduced p53 activity in HFD-fed Mdm2C305F/C305F mice resulted in higher levels of p53 downregulated targets GLUT4 and SIRT1, leading to increased biosynthesis of NAD+, and increased energy expenditure.	NAD	162-166	solute carrier family 2 (facilitated glucose transporter), member 4	Mus musculus	108-113
27913299-1	2017	beta-lapachone (beta-L) is a substrate of reduced nicotinamide adenine dinucleotide (NADH): quinone oxidoreductase 1 (NQO1).	NAD	50-83	NAD(P)H quinone dehydrogenase 1	Homo sapiens	118-122
27913299-1	2017	beta-lapachone (beta-L) is a substrate of reduced nicotinamide adenine dinucleotide (NADH): quinone oxidoreductase 1 (NQO1).	NAD	85-89	NAD(P)H quinone dehydrogenase 1	Homo sapiens	118-122
27913299-2	2017	NQO1 reduces quinones to hydroquinones using NADH as an electron donor and consequently increases the intracellular NAD+/NADH ratio.	NAD	45-49	NAD(P)H quinone dehydrogenase 1	Homo sapiens	0-4
27889611-2	2017	When investigating possible gene expression network partners of WT1 in a large acute myeloid leukemia (AML) patient cohort, one of the genes with the highest correlation to WT1 was quinolinate phosphoribosyltransferase (QPRT), a key enzyme in the de novo nicotinamide adenine dinucleotide (NAD+) synthesis pathway.	NAD	255-288	WT1 transcription factor	Homo sapiens	173-176
27913299-2	2017	NQO1 reduces quinones to hydroquinones using NADH as an electron donor and consequently increases the intracellular NAD+/NADH ratio.	NAD	116-120	NAD(P)H quinone dehydrogenase 1	Homo sapiens	0-4
27913299-2	2017	NQO1 reduces quinones to hydroquinones using NADH as an electron donor and consequently increases the intracellular NAD+/NADH ratio.	NAD	121-125	NAD(P)H quinone dehydrogenase 1	Homo sapiens	0-4
27889611-2	2017	When investigating possible gene expression network partners of WT1 in a large acute myeloid leukemia (AML) patient cohort, one of the genes with the highest correlation to WT1 was quinolinate phosphoribosyltransferase (QPRT), a key enzyme in the de novo nicotinamide adenine dinucleotide (NAD+) synthesis pathway.	NAD	255-288	quinolinate phosphoribosyltransferase	Homo sapiens	181-218
27889611-2	2017	When investigating possible gene expression network partners of WT1 in a large acute myeloid leukemia (AML) patient cohort, one of the genes with the highest correlation to WT1 was quinolinate phosphoribosyltransferase (QPRT), a key enzyme in the de novo nicotinamide adenine dinucleotide (NAD+) synthesis pathway.	NAD	255-288	quinolinate phosphoribosyltransferase	Homo sapiens	220-224
27889611-2	2017	When investigating possible gene expression network partners of WT1 in a large acute myeloid leukemia (AML) patient cohort, one of the genes with the highest correlation to WT1 was quinolinate phosphoribosyltransferase (QPRT), a key enzyme in the de novo nicotinamide adenine dinucleotide (NAD+) synthesis pathway.	NAD	290-294	WT1 transcription factor	Homo sapiens	64-67
27889611-2	2017	When investigating possible gene expression network partners of WT1 in a large acute myeloid leukemia (AML) patient cohort, one of the genes with the highest correlation to WT1 was quinolinate phosphoribosyltransferase (QPRT), a key enzyme in the de novo nicotinamide adenine dinucleotide (NAD+) synthesis pathway.	NAD	290-294	WT1 transcription factor	Homo sapiens	173-176
27889611-2	2017	When investigating possible gene expression network partners of WT1 in a large acute myeloid leukemia (AML) patient cohort, one of the genes with the highest correlation to WT1 was quinolinate phosphoribosyltransferase (QPRT), a key enzyme in the de novo nicotinamide adenine dinucleotide (NAD+) synthesis pathway.	NAD	290-294	quinolinate phosphoribosyltransferase	Homo sapiens	181-218
27889611-2	2017	When investigating possible gene expression network partners of WT1 in a large acute myeloid leukemia (AML) patient cohort, one of the genes with the highest correlation to WT1 was quinolinate phosphoribosyltransferase (QPRT), a key enzyme in the de novo nicotinamide adenine dinucleotide (NAD+) synthesis pathway.	NAD	290-294	quinolinate phosphoribosyltransferase	Homo sapiens	220-224
27889611-7	2017	Interestingly, the rescue effect of QPRT overexpression was not correlated to increased NAD + levels, suggesting NAD + independent mechanisms.	NAD	113-118	quinolinate phosphoribosyltransferase	Homo sapiens	36-40
28253987-14	2017	SIRT3 deacetylates and activates key metabolic enzymes and transcriptional regulators, utilizing NAD+ in the process.	NAD	97-101	sirtuin 3	Homo sapiens	0-5
29103054-3	2017	ACMSD is part of the kynurenine pathway, responsible for the catalytic breakdown of tryptophan into NAD+, generating several neuroactive metabolites in the process.	NAD	100-104	aminocarboxymuconate semialdehyde decarboxylase	Homo sapiens	0-5
29104319-5	2017	Using HPLC analysis we detected up to five ellipticine metabolites, which were formed by human hepatic microsomes and human CYP3A4 in the presence of NADPH or NADH.	NAD	159-163	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	124-130
29104319-8	2017	Using the 32P-postlabeling method two ellipticine-derived DNA adducts were generated by microsomes and the CYP3A4-Supersome system, both in the presence of NADPH and NADH.	NAD	166-170	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	107-113
29104319-10	2017	In the presence of NADPH or NADH, cytochrome b5 stimulated the CYP3A4-mediated oxidation of ellipticine, but the stimulation effect differed for individual ellipticine metabolites.	NAD	28-32	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	63-69
29104319-12	2017	The results demonstrate that cytochrome b5 plays a dual role in the CYP3A4-catalyzed oxidation of ellipticine: (1) cytochrome b5 mediates CYP3A4 catalytic activities by donating the first and second electron to this enzyme in its catalytic cycle, indicating that NADH:cytochrome b5 reductase can substitute NADPH-dependent POR in this enzymatic reaction and (2) cytochrome b5 can act as an allosteric modifier of the CYP3A4 oxygenase.	NAD	263-267	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	68-74
29104319-12	2017	The results demonstrate that cytochrome b5 plays a dual role in the CYP3A4-catalyzed oxidation of ellipticine: (1) cytochrome b5 mediates CYP3A4 catalytic activities by donating the first and second electron to this enzyme in its catalytic cycle, indicating that NADH:cytochrome b5 reductase can substitute NADPH-dependent POR in this enzymatic reaction and (2) cytochrome b5 can act as an allosteric modifier of the CYP3A4 oxygenase.	NAD	263-267	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	138-144
29104319-12	2017	The results demonstrate that cytochrome b5 plays a dual role in the CYP3A4-catalyzed oxidation of ellipticine: (1) cytochrome b5 mediates CYP3A4 catalytic activities by donating the first and second electron to this enzyme in its catalytic cycle, indicating that NADH:cytochrome b5 reductase can substitute NADPH-dependent POR in this enzymatic reaction and (2) cytochrome b5 can act as an allosteric modifier of the CYP3A4 oxygenase.	NAD	263-267	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	138-144
28591759-6	2017	Recent work proposes that renal PGC1alpha directly increases levels of nicotinamide adenine dinucleotide (NAD+), an essential co-factor for energy metabolism that has lately been proposed as an anti-aging factor.	NAD	71-104	PPARG coactivator 1 alpha	Homo sapiens	32-41
28591759-6	2017	Recent work proposes that renal PGC1alpha directly increases levels of nicotinamide adenine dinucleotide (NAD+), an essential co-factor for energy metabolism that has lately been proposed as an anti-aging factor.	NAD	106-110	PPARG coactivator 1 alpha	Homo sapiens	32-41
28095293-1	2017	Injury-induced (Wallerian) axonal degeneration is regulated via the opposing actions of pro-degenerative factors such as SARM1 and a MAPK signal and pro-survival factors, the most important of which is the NAD+ biosynthetic enzyme NMNAT2 that inhibits activation of the SARM1 pathway.	NAD	206-210	nicotinamide nucleotide adenylyltransferase 2	Homo sapiens	231-237
27993241-2	2017	With the recent understanding that TGF-beta"s canonical signaling pathway may be modified by acetylation as well as phosphorylation, we explored the role of the NAD+-dependent lysine deacetylase, sirtuin 1 (SIRT1) in fibrogenesis in the cell culture, animal model, and human settings.	NAD	161-165	transforming growth factor beta 1	Homo sapiens	35-43
27689878-6	2017	PARP inhibitor restores cellular NAD+ content and redox index and ATP pool, suggesting that PARP overactivation is cause of decreased complex I-driven respiration.	NAD	33-37	poly(ADP-ribose) polymerase 1	Homo sapiens	0-4
27689878-6	2017	PARP inhibitor restores cellular NAD+ content and redox index and ATP pool, suggesting that PARP overactivation is cause of decreased complex I-driven respiration.	NAD	33-37	poly(ADP-ribose) polymerase 1	Homo sapiens	92-96
28695500-1	2017	Poly(ADP-ribosyl)ation of proteins is a posttranslational modification mediated by poly(ADP-ribose) polymerases (PARPs) that use NAD+ as substrate to form the negatively charged polymer of poly(ADP-ribose) (PAR).	NAD	129-133	poly(ADP-ribose) polymerase 1	Homo sapiens	113-118
28695501-3	2017	Overactivation of PARP, as reflected by increased poly-ADP-ribosylation, accumulation of pADPr-modified proteins or free pADPr, contributes to depletion of NAD+ and mitochondrial dysfunction, potentially leading to cell death.	NAD	156-160	poly(ADP-ribose) polymerase 1	Homo sapiens	18-22
28695502-2	2017	The detection and relative quantification of these individual pools is difficult because of the methods usually applied, which require cell disruption and fractionation.Here, we describe an immunochemical method to visualize and relatively quantify subcellular NAD+ pools, which relies on the NAD+-consuming activity of poly-ADP-ribose polymerase 1 (PARP1).	NAD	261-265	poly(ADP-ribose) polymerase 1	Homo sapiens	320-348
28695502-2	2017	The detection and relative quantification of these individual pools is difficult because of the methods usually applied, which require cell disruption and fractionation.Here, we describe an immunochemical method to visualize and relatively quantify subcellular NAD+ pools, which relies on the NAD+-consuming activity of poly-ADP-ribose polymerase 1 (PARP1).	NAD	261-265	poly(ADP-ribose) polymerase 1	Homo sapiens	350-355
28695502-2	2017	The detection and relative quantification of these individual pools is difficult because of the methods usually applied, which require cell disruption and fractionation.Here, we describe an immunochemical method to visualize and relatively quantify subcellular NAD+ pools, which relies on the NAD+-consuming activity of poly-ADP-ribose polymerase 1 (PARP1).	NAD	293-297	poly(ADP-ribose) polymerase 1	Homo sapiens	320-348
28695502-2	2017	The detection and relative quantification of these individual pools is difficult because of the methods usually applied, which require cell disruption and fractionation.Here, we describe an immunochemical method to visualize and relatively quantify subcellular NAD+ pools, which relies on the NAD+-consuming activity of poly-ADP-ribose polymerase 1 (PARP1).	NAD	293-297	poly(ADP-ribose) polymerase 1	Homo sapiens	350-355
28695507-0	2017	Identification of Protein Substrates of Specific PARP Enzymes Using Analog-Sensitive PARP Mutants and a "Clickable" NAD+ Analog.	NAD	116-120	poly(ADP-ribose) polymerase 1	Homo sapiens	49-53
28695507-1	2017	The PARP family of ADP-ribosyl transferases contains 17 members in human cells, most of which catalyze the transfer of the ADP-ribose moiety of NAD+ onto their target proteins.	NAD	144-148	poly(ADP-ribose) polymerase 1	Homo sapiens	4-8
28695507-4	2017	Recently, we developed a robust NAD+ analog-sensitive approach for PARPs, which allows PARP-specific ADP-ribosylation of substrates that is suitable for subsequent copper-catalyzed azide-alkyne cycloaddition ("click chemistry") reactions.	NAD	32-36	poly(ADP-ribose) polymerase 1	Homo sapiens	67-72
28695507-4	2017	Recently, we developed a robust NAD+ analog-sensitive approach for PARPs, which allows PARP-specific ADP-ribosylation of substrates that is suitable for subsequent copper-catalyzed azide-alkyne cycloaddition ("click chemistry") reactions.	NAD	32-36	poly(ADP-ribose) polymerase 1	Homo sapiens	67-71
28695511-1	2017	The impact of poly(ADP-ribose) polymerase (PARP) enzymes on cellular NAD+ has been established for almost 30 years now and its sequel, the metabolic collapse of cells upon PARP overactivation is a nearly 20-year-old observation.	NAD	69-73	poly(ADP-ribose) polymerase 1	Homo sapiens	14-41
28695511-1	2017	The impact of poly(ADP-ribose) polymerase (PARP) enzymes on cellular NAD+ has been established for almost 30 years now and its sequel, the metabolic collapse of cells upon PARP overactivation is a nearly 20-year-old observation.	NAD	69-73	poly(ADP-ribose) polymerase 1	Homo sapiens	43-47
28695511-1	2017	The impact of poly(ADP-ribose) polymerase (PARP) enzymes on cellular NAD+ has been established for almost 30 years now and its sequel, the metabolic collapse of cells upon PARP overactivation is a nearly 20-year-old observation.	NAD	69-73	poly(ADP-ribose) polymerase 1	Homo sapiens	172-176
28695517-3	2017	Most of them were designed competitors with NAD for a binding site on PARP-1 molecule.	NAD	44-47	poly(ADP-ribose) polymerase 1	Homo sapiens	70-76
28695517-4	2017	This strategy resulted in a discovery of mainly nucleotide-like PARP-1 inhibitors, which may target not only PARP-1 but also other pathways involving NAD and other nucleotides.	NAD	150-153	poly(ADP-ribose) polymerase 1	Homo sapiens	64-70
28695517-5	2017	Many cancer types demonstrate rapid development of resistance to NAD-like PARP-1 inhibitors.	NAD	65-68	poly(ADP-ribose) polymerase 1	Homo sapiens	74-80
28695520-4	2017	Poly(ADP-ribose) polymerase 1 (PARP-1) also utilizes NAD+ as a substrate to synthesize poly(ADP-ribose).	NAD	53-57	poly(ADP-ribose) polymerase 1	Homo sapiens	0-29
28695520-4	2017	Poly(ADP-ribose) polymerase 1 (PARP-1) also utilizes NAD+ as a substrate to synthesize poly(ADP-ribose).	NAD	53-57	poly(ADP-ribose) polymerase 1	Homo sapiens	31-37
28695520-6	2017	However, most PARP-1 inhibitors, including olaparib, were developed as NAD+ analogs.	NAD	71-75	poly(ADP-ribose) polymerase 1	Homo sapiens	14-20
28695520-9	2017	We use this method to analyze the effects of olaparib and non-NAD+-like PARP-1 inhibitor (5F02) on IMPDH activity.	NAD	62-66	poly(ADP-ribose) polymerase 1	Homo sapiens	72-78
28250737-5	2017	NAD+ also serves as a substrate for the DNA "nick sensor" and putative nuclear repair enzyme, poly(ADP-ribose) polymerase (PARP).	NAD	0-4	poly(ADP-ribose) polymerase 1	Homo sapiens	94-121
28250737-5	2017	NAD+ also serves as a substrate for the DNA "nick sensor" and putative nuclear repair enzyme, poly(ADP-ribose) polymerase (PARP).	NAD	0-4	poly(ADP-ribose) polymerase 1	Homo sapiens	123-127
28482792-6	2017	CONCLUSION: The action mode of PARP1 inhibitors developed so far is competing with NAD+ for the catalytic site of PARP1.	NAD	83-87	poly(ADP-ribose) polymerase 1	Homo sapiens	31-36
28482792-6	2017	CONCLUSION: The action mode of PARP1 inhibitors developed so far is competing with NAD+ for the catalytic site of PARP1.	NAD	83-87	poly(ADP-ribose) polymerase 1	Homo sapiens	114-119
28637419-5	2017	We first discuss the biological principles of NAD+ metabolism in normal and malignant cells, with a focus on the feasibility of selectively targeting cancer cells by pharmacological inhibition of nicotinamide phosphoribosyltransferase (NAMPT) and indoleamine/tryptophan 2,3-dioxygenases (IDO/TDO), the rate-limiting salvage and de novo NAD+ biosynthetic enzymes, respectively.	NAD	336-340	nicotinamide phosphoribosyltransferase	Mus musculus	236-241
27912063-7	2016	The structure suggests a possible mechanism by which electrons are transferred from NADH to cytochrome c and provides a platform for future functional dissection of respiration.	NAD	84-88	cytochrome c, somatic	Homo sapiens	92-104
27614022-4	2016	Because of its dependence on NAD+, Sirt1 also functions as a nutrient/redox sensor, and new novel data show a function of this enzyme in the maturation of hypothalamic peptide hormones controlling energy balance either through regulation of specific nuclear transcription factors or by regulating specific pro-hormone convertases (PCs) involved in the post-translational processing of pro-hormones.	NAD	29-33	sirtuin 1	Rattus norvegicus	35-40
27880725-1	2016	Sirt3, a mitochondrial NAD+-dependent histone deacetylase, is the only member proven to promote longevity in mammalian Sirtuin family.	NAD	23-26	sirtuin 3	Homo sapiens	0-5
28073422-1	2016	The deacetylase Sirtuin 3 (SIRT3) is a member of the Sirtuins mainly located in the mitochondrial matrix, and as a nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase, it can regulate cellular energy metabolism and oxidative stress-related pathways.	NAD	115-148	sirtuin 3	Homo sapiens	16-25
28073422-1	2016	The deacetylase Sirtuin 3 (SIRT3) is a member of the Sirtuins mainly located in the mitochondrial matrix, and as a nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase, it can regulate cellular energy metabolism and oxidative stress-related pathways.	NAD	115-148	sirtuin 3	Homo sapiens	27-32
28073422-1	2016	The deacetylase Sirtuin 3 (SIRT3) is a member of the Sirtuins mainly located in the mitochondrial matrix, and as a nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase, it can regulate cellular energy metabolism and oxidative stress-related pathways.	NAD	150-154	sirtuin 3	Homo sapiens	16-25
28073422-1	2016	The deacetylase Sirtuin 3 (SIRT3) is a member of the Sirtuins mainly located in the mitochondrial matrix, and as a nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase, it can regulate cellular energy metabolism and oxidative stress-related pathways.	NAD	150-154	sirtuin 3	Homo sapiens	27-32
27840909-1	2016	The NAD-dependent protein deacetylase sirtuin 3 (SIRT3) is an enzyme localized primarily in the mitochondrion, where it modulates cellular functions such as nutrient metabolism, ATP balance, antioxidant machinery, and other mechanisms fundamental to mitochondria.	NAD	4-7	sirtuin 3	Homo sapiens	49-54
27105286-1	2016	Type II NADH:quinone oxidoreductases (NDH-2s) are membrane proteins, crucial for the catabolic metabolism, because they contribute to the maintenance of the NADH/NAD+ balance.	NAD	8-12	DExH-box helicase 9	Homo sapiens	38-43
27105286-1	2016	Type II NADH:quinone oxidoreductases (NDH-2s) are membrane proteins, crucial for the catabolic metabolism, because they contribute to the maintenance of the NADH/NAD+ balance.	NAD	157-161	DExH-box helicase 9	Homo sapiens	38-43
27105286-1	2016	Type II NADH:quinone oxidoreductases (NDH-2s) are membrane proteins, crucial for the catabolic metabolism, because they contribute to the maintenance of the NADH/NAD+ balance.	NAD	162-166	DExH-box helicase 9	Homo sapiens	38-43
27105286-2	2016	In several pathogenic bacteria and protists, NDH-2s are the only enzymes performing respiratory NADH:quinone oxidoreductase activity.	NAD	96-100	DExH-box helicase 9	Homo sapiens	45-50
27105286-7	2016	The data obtained and the already available information allowed systematizing several properties of NDH-2s: (i) the existence of additional sequence motifs with putative regulatory functions, (ii) specificity towards NADH or NADPH and (iii) the type of quinone binding motif.	NAD	217-221	DExH-box helicase 9	Homo sapiens	100-105
27465020-5	2016	NAD(+) is utilized by various proteins including sirtuins, poly ADP-ribose polymerases (PARPs) and cyclic ADP-ribose synthases.	NAD	0-6	poly(ADP-ribose) polymerase 1	Homo sapiens	88-93
27465020-7	2016	Raising cellular NAD(+) content by inducing its biosynthesis or inhibiting the activity of PARP and cADP-ribose synthases via genetic or pharmacological means lead to sirtuins activation.	NAD	17-23	poly(ADP-ribose) polymerase 1	Homo sapiens	91-95
28043598-3	2016	Resistance to INH among MDR-TB patients may cause ETH to be ineffective, as both target nicotinamide adenine dinucleotide-dependent enoyl-acyl carrier protein reductase inhA protein and mutations within inhA gene may lead to their cross-resistance.	NAD	88-121	inhibin subunit alpha	Homo sapiens	169-173
27724820-4	2016	In this study, we investigated the role of CD38, a TNFalpha-inducible NADH+ cyclase and hydrolase.	NAD	70-74	CD38 molecule	Rattus norvegicus	43-47
27816507-5	2016	Additionally, depletion of NAD+ causes sensitization of cancer cells to oxidative damage by disruption of the anti-oxidant defense system, decreased cell proliferation, and initiation of cell death through manipulation of cell signaling pathways (e.g., SIRT1 and p53).	NAD	27-31	tumor protein p53	Homo sapiens	263-266
27587602-11	2016	Besides, significantly increased protein levels of transforming growth factor beta1 (TGF-beta1), gene expression of TGF-beta1, connective tissue growth factor (CTGF), p22 phox and gp91 phox subunits of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, as well as increased media thickness and aortic media area/lumen area (AM/LA) in the untreated hypertensive rats were significantly reduced (p &lt; 0.05) to control levels by all treatments.	NAD	202-235	transforming growth factor, beta 1	Rattus norvegicus	51-83
27587602-11	2016	Besides, significantly increased protein levels of transforming growth factor beta1 (TGF-beta1), gene expression of TGF-beta1, connective tissue growth factor (CTGF), p22 phox and gp91 phox subunits of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, as well as increased media thickness and aortic media area/lumen area (AM/LA) in the untreated hypertensive rats were significantly reduced (p &lt; 0.05) to control levels by all treatments.	NAD	202-235	transforming growth factor, beta 1	Rattus norvegicus	116-125
27773814-3	2016	Sirtuin3(Sirt3), a kind of mitochondria-localized nicotinamide adenine dinucleotide(NAD+)-dependent protein deacetylase, has been reported to regulate the generation of ROS in mitochondria through regulating acetylation level and activity of several key mitochondrial enzymes.	NAD	50-83	sirtuin 3	Homo sapiens	0-8
27773814-3	2016	Sirtuin3(Sirt3), a kind of mitochondria-localized nicotinamide adenine dinucleotide(NAD+)-dependent protein deacetylase, has been reported to regulate the generation of ROS in mitochondria through regulating acetylation level and activity of several key mitochondrial enzymes.	NAD	50-83	sirtuin 3	Homo sapiens	9-14
27773814-3	2016	Sirtuin3(Sirt3), a kind of mitochondria-localized nicotinamide adenine dinucleotide(NAD+)-dependent protein deacetylase, has been reported to regulate the generation of ROS in mitochondria through regulating acetylation level and activity of several key mitochondrial enzymes.	NAD	84-87	sirtuin 3	Homo sapiens	0-8
27773814-3	2016	Sirtuin3(Sirt3), a kind of mitochondria-localized nicotinamide adenine dinucleotide(NAD+)-dependent protein deacetylase, has been reported to regulate the generation of ROS in mitochondria through regulating acetylation level and activity of several key mitochondrial enzymes.	NAD	84-87	sirtuin 3	Homo sapiens	9-14
27558805-8	2016	NQO1 and CYP450OR exhibited a reciprocal preference for reducing equivalents in beta-cells: while CYP450OR preferentially utilized NADPH, NQO1 primarily utilized NADH.	NAD	162-166	NAD(P)H quinone dehydrogenase 1	Homo sapiens	0-4
27558805-8	2016	NQO1 and CYP450OR exhibited a reciprocal preference for reducing equivalents in beta-cells: while CYP450OR preferentially utilized NADPH, NQO1 primarily utilized NADH.	NAD	162-166	cytochrome p450 oxidoreductase	Homo sapiens	9-17
27558805-8	2016	NQO1 and CYP450OR exhibited a reciprocal preference for reducing equivalents in beta-cells: while CYP450OR preferentially utilized NADPH, NQO1 primarily utilized NADH.	NAD	162-166	NAD(P)H quinone dehydrogenase 1	Homo sapiens	138-142
27452907-5	2016	The NAD+-dependent histone deacetylase sirtuin (SIRT)1 amplified the pro-apoptotic effect by deacetylating FOXO3a, which induced EGR1 binding to the Bim promoter and activated Bim expression.	NAD	4-8	forkhead box O3	Homo sapiens	107-113
27428041-4	2016	Enzymes, such as nicotinamide nucleotide transhydrogenase (NNT) and nicotinamide mononucleotide adenylyltransferase 3 (NMNAT3), that control mitochondrial NAD+ levels appear to be susceptible to aging.	NAD	155-159	nicotinamide nucleotide transhydrogenase	Homo sapiens	17-57
27428041-4	2016	Enzymes, such as nicotinamide nucleotide transhydrogenase (NNT) and nicotinamide mononucleotide adenylyltransferase 3 (NMNAT3), that control mitochondrial NAD+ levels appear to be susceptible to aging.	NAD	155-159	nicotinamide nucleotide transhydrogenase	Homo sapiens	59-62
27428041-7	2016	Importantly, restoring mitochondrial NAD+ levels by overexpressing NNT and NMNAT3 enhanced reprogramming efficiency of aged somatic cells and extended the lifespan of human mesenchymal stem cells by delaying replicative senescence.	NAD	37-41	nicotinamide nucleotide transhydrogenase	Homo sapiens	67-70
27179565-2	2016	In the present study, tunneling of enzyme activity was achieved using redox cofactors namely oxidized cytochrome-c (Cyt-c) and Co-enzyme-Q (Co-Q) immobilized on Quantum dots (QDs) which acted as a bio-probe for NAD(+) dependent dehydrogenase catalyzed reaction.	NAD	211-217	cytochrome c, somatic	Homo sapiens	102-114
27179565-2	2016	In the present study, tunneling of enzyme activity was achieved using redox cofactors namely oxidized cytochrome-c (Cyt-c) and Co-enzyme-Q (Co-Q) immobilized on Quantum dots (QDs) which acted as a bio-probe for NAD(+) dependent dehydrogenase catalyzed reaction.	NAD	211-217	cytochrome c, somatic	Homo sapiens	116-121
27819261-4	2016	In this study, we provide evidence that the NAD+-dependent class III protein deacetylase SIRT1 deacetylates Nkx2.5 in cardiomyocytes and represses the transcriptional activity of Nkx2.5.	NAD	44-48	NK2 homeobox 5	Homo sapiens	108-114
27819261-4	2016	In this study, we provide evidence that the NAD+-dependent class III protein deacetylase SIRT1 deacetylates Nkx2.5 in cardiomyocytes and represses the transcriptional activity of Nkx2.5.	NAD	44-48	NK2 homeobox 5	Homo sapiens	179-185
27727003-5	2016	NAD is utilized by many enzymes other than PARP-1, resulting in a trade-off trap between their specificity and efficacy.	NAD	0-3	poly(ADP-ribose) polymerase 1	Homo sapiens	43-49
27727003-8	2016	In addition to compounds that show structural similarity to NAD or known PARP-1 inhibitors, the screen identified structurally new non-NAD-like inhibitors that block PARP-1 activity in cancer cells with greater efficacy and potency than classical PARP-1 inhibitors currently used in clinic.	NAD	135-138	poly(ADP-ribose) polymerase 1	Homo sapiens	166-172
27727003-8	2016	In addition to compounds that show structural similarity to NAD or known PARP-1 inhibitors, the screen identified structurally new non-NAD-like inhibitors that block PARP-1 activity in cancer cells with greater efficacy and potency than classical PARP-1 inhibitors currently used in clinic.	NAD	135-138	poly(ADP-ribose) polymerase 1	Homo sapiens	166-172
27727003-9	2016	These non-NAD-like PARP-1 inhibitors are effective against several types of human cancer xenografts, including kidney, prostate, and breast tumors in vivo.	NAD	10-13	poly(ADP-ribose) polymerase 1	Homo sapiens	19-25
27724820-4	2016	In this study, we investigated the role of CD38, a TNFalpha-inducible NADH+ cyclase and hydrolase.	NAD	70-74	tumor necrosis factor	Rattus norvegicus	51-59
27732853-4	2016	We demonstrate that Skp1a regulates the protein level of the nicotinamide adenine dinucleotide (NAD)+ synthesizing enzyme nicotinamide mononucleotide adenylyltransferase 2 (Nmnat2) in axons.	NAD	61-94	nicotinamide nucleotide adenylyltransferase 2	Homo sapiens	122-171
27552971-2	2016	Mice engineered to express additional copies of SIRT1 or SIRT6, or treated with sirtuin-activating compounds (STACs) such as resveratrol and SRT2104 or with NAD+ precursors, have improved organ function, physical endurance, disease resistance and longevity.	NAD	157-161	sirtuin 6	Mus musculus	57-62
27790619-3	2016	Recent evidence demonstrated that the mitochondrial NAD+-dependent deacetylase sirtuin 3 (SIRT3) may regulate these mitochondrial functions by reversible protein lysine deacetylation.	NAD	52-56	sirtuin 3	Homo sapiens	90-95
27790619-5	2016	Gain of function studies and treatment approaches increasing mitochondrial NAD+ availability that ameliorate these cardiac pathologies have led to the proposal that activation of SIRT3 may represent a promising therapeutic strategy to improve mitochondrial derangements in various cardiac pathologies.	NAD	75-79	sirtuin 3	Homo sapiens	179-184
27798264-3	2016	Furthermore, the skeletal muscle transcriptomes of patients with Duchene"s muscular dystrophy (DMD) and other muscle diseases were enriched for various poly[adenosine 5"-diphosphate (ADP)-ribose] polymerases (PARPs) and for nicotinamide N-methyltransferase (NNMT), enzymes that are major consumers of NAD+ and are involved in pleiotropic events, including inflammation.	NAD	301-305	poly(ADP-ribose) polymerase 1	Homo sapiens	209-214
27798264-4	2016	In the mdx mouse model of DMD, we observed significant reductions in muscle NAD+ levels, concurrent increases in PARP activity, and reduced expression of nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme for NAD+ biosynthesis.	NAD	231-235	nicotinamide phosphoribosyltransferase	Mus musculus	154-192
27798264-4	2016	In the mdx mouse model of DMD, we observed significant reductions in muscle NAD+ levels, concurrent increases in PARP activity, and reduced expression of nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme for NAD+ biosynthesis.	NAD	231-235	nicotinamide phosphoribosyltransferase	Mus musculus	194-199
27798264-6	2016	The effects of NAD+ repletion in mdx mice relied on the improvement in mitochondrial function and structural protein expression (alpha-dystrobrevin and delta-sarcoglycan) and on the reductions in general poly(ADP)-ribosylation, inflammation, and fibrosis.	NAD	15-19	dystrobrevin alpha	Mus musculus	129-147
27798264-7	2016	In combination, these studies suggest that the replenishment of NAD+ may benefit patients with muscular dystrophies or other neuromuscular degenerative conditions characterized by the PARP/NNMT gene expression signatures.	NAD	64-68	poly(ADP-ribose) polymerase 1	Homo sapiens	184-188
27735788-0	2016	NMNAT1 inhibits axon degeneration via blockade of SARM1-mediated NAD+ depletion.	NAD	65-69	sterile alpha and HEAT/Armadillo motif containing 1	Mus musculus	50-55
27731314-6	2016	Our results in combination with the role of NAM in NAD+ metabolism suggest an intriguing link between metabolic regulation and TRPV channel activity.	NAD	51-55	nanchung	Drosophila melanogaster	127-131
27732853-4	2016	We demonstrate that Skp1a regulates the protein level of the nicotinamide adenine dinucleotide (NAD)+ synthesizing enzyme nicotinamide mononucleotide adenylyltransferase 2 (Nmnat2) in axons.	NAD	61-94	nicotinamide nucleotide adenylyltransferase 2	Homo sapiens	173-179
27732853-4	2016	We demonstrate that Skp1a regulates the protein level of the nicotinamide adenine dinucleotide (NAD)+ synthesizing enzyme nicotinamide mononucleotide adenylyltransferase 2 (Nmnat2) in axons.	NAD	96-99	nicotinamide nucleotide adenylyltransferase 2	Homo sapiens	122-171
27732853-4	2016	We demonstrate that Skp1a regulates the protein level of the nicotinamide adenine dinucleotide (NAD)+ synthesizing enzyme nicotinamide mononucleotide adenylyltransferase 2 (Nmnat2) in axons.	NAD	96-99	nicotinamide nucleotide adenylyltransferase 2	Homo sapiens	173-179
27448710-3	2016	Both the CG9940 and exercise are closely relative to NAD(+) level, and NAD(+) plays important roles not only in energy metabolism and mitochondrial functions but also in aging.	NAD	53-59	NAD synthetase	Drosophila melanogaster	9-15
27562971-8	2016	Decreasing NADH pharmacologically with MTOB or genetically blocking CtBP1 with siRNA upregulated the cyclin-dependent genes (p15 and p21) and proapoptotic regulators (NOXA and PERP), attenuated proliferation, corrected the glycolytic reprogramming phenotype of PH-Fibs, and augmented transcription of the anti-inflammatory gene HMOX1.	NAD	11-15	cyclin dependent kinase inhibitor 2B	Homo sapiens	125-128
27562971-8	2016	Decreasing NADH pharmacologically with MTOB or genetically blocking CtBP1 with siRNA upregulated the cyclin-dependent genes (p15 and p21) and proapoptotic regulators (NOXA and PERP), attenuated proliferation, corrected the glycolytic reprogramming phenotype of PH-Fibs, and augmented transcription of the anti-inflammatory gene HMOX1.	NAD	11-15	cyclin dependent kinase inhibitor 1A	Homo sapiens	133-136
27264531-3	2016	The P. putida KT2440 genome contains an NAD-dependent d-lactate dehydrogenase encoding gene, but mutation of this gene does not play a role in d-lactate utilization.	NAD	40-43	FAD-binding oxidoreductase	Pseudomonas putida KT2440	54-77
27725675-3	2016	Here we show that nicotinamide riboside kinase 1 (NRK1) is necessary and rate-limiting for the use of exogenous NR and NMN for NAD+ synthesis.	NAD	127-131	nicotinamide riboside kinase 1	Homo sapiens	18-48
27725675-3	2016	Here we show that nicotinamide riboside kinase 1 (NRK1) is necessary and rate-limiting for the use of exogenous NR and NMN for NAD+ synthesis.	NAD	127-131	nicotinamide riboside kinase 1	Homo sapiens	50-54
27725675-4	2016	Using genetic gain- and loss-of-function models, we further demonstrate that the role of NRK1 in driving NAD+ synthesis from other NAD+ precursors, such as nicotinamide or nicotinic acid, is dispensable.	NAD	105-109	nicotinamide riboside kinase 1	Homo sapiens	89-93
27725675-4	2016	Using genetic gain- and loss-of-function models, we further demonstrate that the role of NRK1 in driving NAD+ synthesis from other NAD+ precursors, such as nicotinamide or nicotinic acid, is dispensable.	NAD	131-135	nicotinamide riboside kinase 1	Homo sapiens	89-93
27500459-0	2016	Treatment with NAD(+) inhibited experimental autoimmune encephalomyelitis by activating AMPK/SIRT1 signaling pathway and modulating Th1/Th17 immune responses in mice.	NAD	15-21	negative elongation factor complex member C/D, Th1l	Mus musculus	132-135
27459240-6	2016	Structure-based analysis allowed the identification of H-NNT residues forming the NAD binding site, the proton canal and the large interaction site on the H-NNT dimer.	NAD	82-85	nicotinamide nucleotide transhydrogenase	Homo sapiens	57-60
27459240-6	2016	Structure-based analysis allowed the identification of H-NNT residues forming the NAD binding site, the proton canal and the large interaction site on the H-NNT dimer.	NAD	82-85	nicotinamide nucleotide transhydrogenase	Homo sapiens	157-160
27233476-0	2016	Regulation of the Nampt-mediated NAD salvage pathway and its therapeutic implications in pancreatic cancer.	NAD	33-36	nicotinamide phosphoribosyltransferase	Mus musculus	18-23
27566573-0	2016	De-novo NAD+ synthesis regulates SIRT1-FOXO1 apoptotic pathway in response to NQO1 substrates in lung cancer cells.	NAD	8-12	forkhead box O1	Homo sapiens	39-44
27566573-0	2016	De-novo NAD+ synthesis regulates SIRT1-FOXO1 apoptotic pathway in response to NQO1 substrates in lung cancer cells.	NAD	8-12	NAD(P)H quinone dehydrogenase 1	Homo sapiens	78-82
27566573-3	2016	Here, we establish a mechanistic link from L-type amino acid transporter 1 (LAT1) mediated transport of tryptophan and the subsequent de-novo NAD+ synthesis to SIRT1-FOXO1 regulated apoptotic signaling in A549 cells in response to NQO1 activation.	NAD	142-146	forkhead box O1	Homo sapiens	166-171
27566573-3	2016	Here, we establish a mechanistic link from L-type amino acid transporter 1 (LAT1) mediated transport of tryptophan and the subsequent de-novo NAD+ synthesis to SIRT1-FOXO1 regulated apoptotic signaling in A549 cells in response to NQO1 activation.	NAD	142-146	NAD(P)H quinone dehydrogenase 1	Homo sapiens	231-235
27566573-5	2016	Decreased uptake of tryptophan due to the downregulation of LAT1 coordinates with PARP-1 hyperactivation to induce rapid depletion of NAD+ pool.	NAD	134-138	poly(ADP-ribose) polymerase 1	Homo sapiens	82-88
27566573-7	2016	Because NQO1 activation is characterized with oxidative challenge induced DNA damage, these results suggest that LAT1 and de-novo NAD+ synthesis in NSCLC cells may play essential roles in sensing excessive oxidative stress.	NAD	130-134	NAD(P)H quinone dehydrogenase 1	Homo sapiens	8-12
27681422-0	2016	NAMPT-Mediated NAD(+) Biosynthesis Is Essential for Vision In Mice.	NAD	15-21	nicotinamide phosphoribosyltransferase	Mus musculus	0-5
27681422-3	2016	We found that rod or cone photoreceptor-specific deletion of nicotinamide phosphoribosyltransferase (Nampt), the rate-limiting enzyme in the major NAD(+) biosynthetic pathway beginning with nicotinamide, caused retinal degeneration.	NAD	147-153	nicotinamide phosphoribosyltransferase	Mus musculus	61-99
27681422-3	2016	We found that rod or cone photoreceptor-specific deletion of nicotinamide phosphoribosyltransferase (Nampt), the rate-limiting enzyme in the major NAD(+) biosynthetic pathway beginning with nicotinamide, caused retinal degeneration.	NAD	147-153	nicotinamide phosphoribosyltransferase	Mus musculus	101-106
27324704-17	2016	PARP activation is a potential mechanisms linking OSA to DPN and endothelial dysfunction in patients with type 2 diabetes.	NAD	57-60	poly(ADP-ribose) polymerase 1	Homo sapiens	0-4
27233476-4	2016	This study showed that the expression of Nampt, the rate-limiting enzyme of the NAD salvage pathway, was significantly increased in PDAC cells and PDAC tissues.	NAD	80-83	nicotinamide phosphoribosyltransferase	Mus musculus	41-46
27233476-5	2016	Additionally, inhibition of Nampt impaired tumor growth in vitro and tumorigenesis in vivo, which was accompanied by a decreased cellular NAD level and glycolytic activity.	NAD	138-141	nicotinamide phosphoribosyltransferase	Mus musculus	28-33
27233476-8	2016	In conclusion, the present study revealed a novel regulatory mechanism for Nampt in PDAC and suggested that Nampt inhibition may override gemcitabine resistance by decreasing the NAD level and suppressing glycolytic activity, warranting further clinical investigation for pancreatic cancer treatment.	NAD	179-182	nicotinamide phosphoribosyltransferase	Mus musculus	108-113
27508874-4	2016	We examined this question in murine skeletal muscle by specifically depleting Nampt, an essential enzyme in the NAD salvage pathway.	NAD	112-115	nicotinamide phosphoribosyltransferase	Mus musculus	78-83
27404282-8	2016	When P450 1A1 was reconstituted with CBR and cytochrome b5 plus NADH, BaP-3-ol was the predominant metabolite too, and an adduct 2 was also generated.	NAD	64-68	BAI1 associated protein 3	Homo sapiens	70-75
27498863-0	2016	NAMPT-Mediated NAD(+) Biosynthesis in Adipocytes Regulates Adipose Tissue Function and Multi-organ Insulin Sensitivity in Mice.	NAD	15-21	nicotinamide phosphoribosyltransferase	Mus musculus	0-5
27498863-3	2016	Here, we characterized mice with adipocyte-specific deletion of nicotinamide phosphoribosyltransferase (NAMPT), a rate-limiting NAD(+) biosynthetic enzyme known to decrease in adipose tissue of obese and aged rodents and people.	NAD	128-134	nicotinamide phosphoribosyltransferase	Mus musculus	64-102
27498863-3	2016	Here, we characterized mice with adipocyte-specific deletion of nicotinamide phosphoribosyltransferase (NAMPT), a rate-limiting NAD(+) biosynthetic enzyme known to decrease in adipose tissue of obese and aged rodents and people.	NAD	128-134	nicotinamide phosphoribosyltransferase	Mus musculus	104-109
27508874-7	2016	Additionally, lifelong overexpression of Nampt preserved muscle NAD levels and exercise capacity in aged mice, supporting a critical role for tissue-autonomous NAD homeostasis in maintaining muscle mass and function.	NAD	64-67	nicotinamide phosphoribosyltransferase	Mus musculus	41-46
27508874-7	2016	Additionally, lifelong overexpression of Nampt preserved muscle NAD levels and exercise capacity in aged mice, supporting a critical role for tissue-autonomous NAD homeostasis in maintaining muscle mass and function.	NAD	160-163	nicotinamide phosphoribosyltransferase	Mus musculus	41-46
27174364-3	2016	EXPERIMENTAL APPROACH: Hepatic concentrations of NAD(+) , protein levels of nicotinamide phosphoribosyltransferase (NAMPT) and several other critical enzymes regulating NAD(+) biosynthesis, were compared in middle-aged and aged mice or patients.	NAD	169-175	nicotinamide phosphoribosyltransferase	Mus musculus	116-121
27337687-6	2016	Moreover, a decrease in the NAD(+):NADH ratio and increase in intracellular ROS content after treatment with palmitic acid in combination with lipopolysaccharide were more pronounced in Mphis from Atg7 cKO mice, suggesting that mitochondrial dysfunction in autophagy-deficient Mphis leads to an increase in lipid-induced inflammasome and metabolic deterioration in Atg7 cKO-ob/ob mice.	NAD	35-39	autophagy related 7	Mus musculus	197-201
27384481-2	2016	Based on the basic mechanism of ALDH converting aldehyde to carboxylic acid with by-product NADH, we suggested that ALDH1L1 may contribute to ATP production using NADH through oxidative phosphorylation.	NAD	92-96	aldehyde dehydrogenase 1 family member L1	Homo sapiens	116-123
27384481-2	2016	Based on the basic mechanism of ALDH converting aldehyde to carboxylic acid with by-product NADH, we suggested that ALDH1L1 may contribute to ATP production using NADH through oxidative phosphorylation.	NAD	163-167	aldehyde dehydrogenase 1 family member L1	Homo sapiens	116-123
27384481-3	2016	ALDH1L1 knockdown reduced ATP production by up to 60% concomitantly with decrease of NADH in NSCLC.	NAD	85-89	aldehyde dehydrogenase 1 family member L1	Homo sapiens	0-7
27163581-5	2016	The NAD(+)-binding site contains a hydrophobic cavity which accommodates the 2-aryl group; in TNKS-2, this has a tunnel to the exterior but the cavity is closed in PARP-1.	NAD	4-10	poly(ADP-ribose) polymerase 1	Homo sapiens	164-170
27339462-0	2016	alpha7 Nicotinic Acetylcholine Receptor Relieves Angiotensin II-Induced Senescence in Vascular Smooth Muscle Cells by Raising Nicotinamide Adenine Dinucleotide-Dependent SIRT1 Activity.	NAD	126-159	angiotensinogen (serpin peptidase inhibitor, clade A, member 8)	Mus musculus	49-63
27339462-11	2016	CONCLUSIONS: Our results demonstrate that activation of alpha7nAChR alleviates Ang II-induced VSMC senescence through promoting NAD(+)-SIRT1 pathway, suggesting that alpha7nAChR may be a potential therapeutic target for the treatment of Ang II-associated vascular aging disorders.	NAD	128-134	angiotensinogen (serpin peptidase inhibitor, clade A, member 8)	Mus musculus	79-85
27174364-6	2016	NAMPT-controlled NAD(+) salvage, but not de novo biosynthesis pathway, was compromised in liver of elderly mice and humans.	NAD	17-23	nicotinamide phosphoribosyltransferase	Mus musculus	0-5
27174364-7	2016	Given normal chow, middle-age DN-NAMPT mice displayed systemic NAD(+) reduction and had moderate NAFLD phenotypes, including lipid accumulation, enhanced oxidative stress, triggered inflammation and impaired insulin sensitivity in liver.	NAD	63-69	nicotinamide phosphoribosyltransferase	Mus musculus	33-38
27357440-1	2016	Sirt1 is a highly conserved nicotinamide adenine dinucleotide (NAD(+)) dependent histone deacetylase which plays an important role in heart diseases.	NAD	28-61	sirtuin 1	Rattus norvegicus	0-5
27608947-1	2016	Nicotinamide phosphoribosyltransferase (NAMPT) catalyzes the first rate-limiting step in converting nicotinamide to NAD(+), essential for a number of enzymes and regulatory proteins involved in a variety of cellular processes, including deacetylation enzyme SIRT1 which modulates several tumor suppressors such as p53 and FOXO.	NAD	116-122	tumor protein p53	Homo sapiens	314-317
27608947-2	2016	Herein we report that NQO1 substrates Tanshione IIA (TSA) and beta-lapachone (beta-lap) induced a rapid depletion of NAD(+) pool but adaptively a significant upregulation of NAMPT.	NAD	117-123	NAD(P)H quinone dehydrogenase 1	Homo sapiens	22-26
27311481-1	2016	Deacetylation of alpha-tubulin at lysine 40 is catalyzed by two enzymes, the NAD-dependent deacetylase SIRT2 and the NAD-independent deacetylase HDAC6, in apparently redundant reactions.	NAD	77-80	histone deacetylase 6	Homo sapiens	145-150
27311481-1	2016	Deacetylation of alpha-tubulin at lysine 40 is catalyzed by two enzymes, the NAD-dependent deacetylase SIRT2 and the NAD-independent deacetylase HDAC6, in apparently redundant reactions.	NAD	117-120	histone deacetylase 6	Homo sapiens	145-150
27357440-1	2016	Sirt1 is a highly conserved nicotinamide adenine dinucleotide (NAD(+)) dependent histone deacetylase which plays an important role in heart diseases.	NAD	63-69	sirtuin 1	Rattus norvegicus	0-5
32263401-9	2016	The electrode is highly sensitive towards NADH and it could detect as low as 0.4 muM NADH at the potential of 40 mV at neutral pH without any interference from co-existing bioanalytes.	NAD	42-46	latexin	Homo sapiens	81-84
27107935-2	2016	17beta-estradiol and the ERbeta-selective agonist DPN, but not the ERalpha-selective agonist PPT, increased the incorporation of [methyl-(3)H]thymidine and the expression of Cyclin D2, suggesting that ERbeta mediates the proliferative effect of estrogen on PC-3 cells.	NAD	50-53	cyclin D2	Homo sapiens	174-183
27107935-3	2016	In addition, upregulation of Cyclin D2 and incorporation of [methyl-(3)H]thymidine induced by 17beta-estradiol and DPN were blocked by the ERbeta-selective antagonist PHTPP in PC-3 cells.	NAD	115-118	cyclin D2	Homo sapiens	29-38
27107935-4	2016	Upregulation of Cyclin D2 and incorporation of [methyl-(3)H]thymidine induced by DPN were also blocked by PKF118-310, a compound that disrupts beta-catenin-TCF (T-cell-specific transcription factor) complex, suggesting the involvement of beta-catenin in the estradiol effects in PC-3 cells.	NAD	81-84	cyclin D2	Homo sapiens	16-25
32263401-9	2016	The electrode is highly sensitive towards NADH and it could detect as low as 0.4 muM NADH at the potential of 40 mV at neutral pH without any interference from co-existing bioanalytes.	NAD	85-89	latexin	Homo sapiens	81-84
27216459-2	2016	Sirtuin-3 (SIRT3), a member of the NAD(+)-dependent Class III histone deacetylases, may function as different role depending on the cell-type and tumor-type.	NAD	35-41	sirtuin 3	Homo sapiens	0-9
27166188-7	2016	ME2 has two cofactors, NAD+ or NADP+, which are used to produce NADH and NADPH for ATP production and ROS clearance, respectively.	NAD	23-27	malic enzyme 2	Homo sapiens	0-3
27166188-7	2016	ME2 has two cofactors, NAD+ or NADP+, which are used to produce NADH and NADPH for ATP production and ROS clearance, respectively.	NAD	64-68	malic enzyme 2	Homo sapiens	0-3
27300721-5	2016	A bridge-protonated Co(I) species was ruled out as a catalytic intermediate for Co(II)(dmgBF2)2(CH3CN)2 from voltammograms recorded at 1000 psi of H2.	NAD	20-25	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	80-86
27216459-2	2016	Sirtuin-3 (SIRT3), a member of the NAD(+)-dependent Class III histone deacetylases, may function as different role depending on the cell-type and tumor-type.	NAD	35-41	sirtuin 3	Homo sapiens	11-16
27126960-8	2016	This regulation involves SIRT3, a mitochondrial NAD(+)-dependent deacetylase and is critically dependent on NAD(+) levels.	NAD	48-54	sirtuin 3	Homo sapiens	25-30
27068062-4	2016	In the presence of inhibitor, both malate and glutamate were required to generate a high enough NADH/NAD(+) ratio to support ROS production through the coordinated activity of malate dehydrogenase (MDH) and aspartate aminotransferase (AST).	NAD	96-100	solute carrier family 17 member 5	Homo sapiens	207-233
27068062-4	2016	In the presence of inhibitor, both malate and glutamate were required to generate a high enough NADH/NAD(+) ratio to support ROS production through the coordinated activity of malate dehydrogenase (MDH) and aspartate aminotransferase (AST).	NAD	96-100	solute carrier family 17 member 5	Homo sapiens	235-238
27068062-4	2016	In the presence of inhibitor, both malate and glutamate were required to generate a high enough NADH/NAD(+) ratio to support ROS production through the coordinated activity of malate dehydrogenase (MDH) and aspartate aminotransferase (AST).	NAD	101-107	solute carrier family 17 member 5	Homo sapiens	207-233
27282776-0	2016	Enhancement by GOSPEL protein of GAPDH aggregation induced by nitric oxide donor and its inhibition by NAD(.).	NAD	103-109	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	33-38
27068062-4	2016	In the presence of inhibitor, both malate and glutamate were required to generate a high enough NADH/NAD(+) ratio to support ROS production through the coordinated activity of malate dehydrogenase (MDH) and aspartate aminotransferase (AST).	NAD	101-107	solute carrier family 17 member 5	Homo sapiens	235-238
27068062-7	2016	alpha-ketoglutarate (KG) as well as AST inhibition also reversed NADH generation and inhibited ROS production.	NAD	65-69	solute carrier family 17 member 5	Homo sapiens	36-39
27264719-0	2016	SIRT2 mediates NADH-induced increases in Nrf2, GCL, and glutathione by modulating Akt phosphorylation in PC12 cells.	NAD	15-19	NFE2 like bZIP transcription factor 2	Rattus norvegicus	41-45
27264719-3	2016	By studying NADH-treated differentiated PC12 cells, we found that NADH induced a significant increase in the nuclear Nrf2, which was prevented by both SIRT2 siRNA and SIRT2 inhibitor, AGK2.	NAD	12-16	NFE2 like bZIP transcription factor 2	Rattus norvegicus	117-121
27264719-3	2016	By studying NADH-treated differentiated PC12 cells, we found that NADH induced a significant increase in the nuclear Nrf2, which was prevented by both SIRT2 siRNA and SIRT2 inhibitor, AGK2.	NAD	66-70	NFE2 like bZIP transcription factor 2	Rattus norvegicus	117-121
27282776-5	2016	NAD(+) inhibited both GAPDH aggregation and co-aggregation with GOSPEL, a hitherto undescribed effect of the coenzyme against the consequences of oxidative stress.	NAD	0-6	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	22-27
27264719-5	2016	Moreover, SIRT2 siRNA and AGK2 blocked NADH-induced Akt phosphorylation, and inhibition of Akt phosphorylation prevented NADH-induced increases in the nuclear Nrf2 and glutathione.	NAD	121-125	NFE2 like bZIP transcription factor 2	Rattus norvegicus	159-163
27129925-2	2016	We present data on the extra-mitochondrial NADH oxidation catalysed by exogenous (cytosolic) cyto-c, as a possible answer to the paradox of apoptosis being an energy-dependent program but characterized by the impairment of the respiratory chain.	NAD	43-47	cytochrome c, somatic	Homo sapiens	93-99
26878683-8	2016	This effect was was mimicked by ERalpha agonist 4",4"",4"""-(4-propyl-[1H]-pyrazole-1,3,5-triyl) trisphenol (PPT), but not ERbeta agonist 2,3-bis-(4-hydroxyphenyl)-propionitrile (DPN), indicating that ERalpha is involved in this action.	NAD	179-182	estrogen receptor 1	Homo sapiens	32-39
27129925-3	2016	The reduction of molecular oxygen induced by the cytosolic NADH/cyto-c pathway is coupled to the generation of an electrochemical proton gradient available for ATP synthesis.	NAD	59-63	cytochrome c, somatic	Homo sapiens	64-70
27129925-4	2016	Original findings show that SH reagents inhibit the NADH/cyto-c system with a conformational change mechanism.	NAD	52-56	cytochrome c, somatic	Homo sapiens	57-63
27129925-6	2016	Valinomycin at 2nM stimulates both the energy-dependent reversible mitochondrial swelling and the NADH/cyto-c oxidation pathway.	NAD	98-102	cytochrome c, somatic	Homo sapiens	103-109
27129925-7	2016	The pro-apoptotic activity of valinomycin, as well as to the dissipation of membrane potential, can be also ascribed to the increased activity of the NADH/cyto-c oxidation pathway useful as an additional source of energy for apoptosis.	NAD	150-154	cytochrome c, somatic	Homo sapiens	155-161
27129925-8	2016	It can be speculated that the activation of the NADH/cyto-c system coupled to valinomycin-induced mitochondrial osmotic swelling may represent a strategy to activate apoptosis in confined solid tumours.	NAD	48-52	cytochrome c, somatic	Homo sapiens	53-59
27173464-2	2016	Here, we investigated the relationship between the nicotinamide phosphoribosyltransferase (NAMPT)-controlled nicotinamide adenine dinucleotide (NAD) metabolism and the impaired mobilization of BM-derived EPCs in diabetic condition.	NAD	109-142	nicotinamide phosphoribosyltransferase	Mus musculus	51-89
27668604-2	2016	When bound to damaged DNA, some members of the PARP family are activated and use NAD^(+) as a source of ADP to catalyze synthesis of poly(ADP-ribose) (PAR) covalently attached to a target protein.	NAD	81-88	poly(ADP-ribose) polymerase 1	Homo sapiens	47-51
27256882-1	2016	Poly[adenosine diphosphate (ADP)-ribose] polymerases (PARPs) are a family of enzymes that modulate diverse biological processes through covalent transfer of ADP-ribose from the oxidized form of nicotinamide adenine dinucleotide (NAD(+)) onto substrate proteins.	NAD	194-227	poly(ADP-ribose) polymerase 1	Homo sapiens	54-59
27256882-1	2016	Poly[adenosine diphosphate (ADP)-ribose] polymerases (PARPs) are a family of enzymes that modulate diverse biological processes through covalent transfer of ADP-ribose from the oxidized form of nicotinamide adenine dinucleotide (NAD(+)) onto substrate proteins.	NAD	229-235	poly(ADP-ribose) polymerase 1	Homo sapiens	54-59
27256882-2	2016	Here we report a robust NAD(+) analog-sensitive approach for PARPs, which allows PARP-specific ADP-ribosylation of substrates that is suitable for subsequent copper-catalyzed azide-alkyne cycloaddition reactions.	NAD	24-30	poly(ADP-ribose) polymerase 1	Homo sapiens	61-66
27256882-2	2016	Here we report a robust NAD(+) analog-sensitive approach for PARPs, which allows PARP-specific ADP-ribosylation of substrates that is suitable for subsequent copper-catalyzed azide-alkyne cycloaddition reactions.	NAD	24-30	poly(ADP-ribose) polymerase 1	Homo sapiens	61-65
27367673-0	2016	The NAD-Dependent Deacetylase Sirtuin-1 Regulates the Expression of Osteogenic Transcriptional Activator Runt-Related Transcription Factor 2 (Runx2) and Production of Matrix Metalloproteinase (MMP)-13 in Chondrocytes in Osteoarthritis.	NAD	4-7	RUNX family transcription factor 2	Homo sapiens	142-147
27061137-2	2016	SIRT1, one of the NAD+-dependent class III histone deacetylases, controls cellular processes and is regulated by hypoxia and inflammatory cytokines in a cell-type-dependent manner.	NAD	18-22	sirtuin 1	Rattus norvegicus	0-5
27154340-1	2016	In the present study, we analyze the interactions of NAD+-dependent deacetylase (Sir2 homolog yeast Hst2) with carba-nicotinamide-adenine-dinucleotide (ADP-HPD).	NAD	53-56	histone deacetylase HST2	Saccharomyces cerevisiae S288C	100-104
27181414-1	2016	Recent research in nutritional control of aging suggests that cytosolic increases in the reduced form of nicotinamide adenine dinucleotide and decreasing nicotinamide adenine dinucleotide metabolism plays a central role in controlling the longevity gene products sirtuin 1 (SIRT1), adenosine monophosphate-activated protein kinase (AMPK) and forkhead box O3 (FOXO3).	NAD	105-138	forkhead box O3	Homo sapiens	342-357
27181414-1	2016	Recent research in nutritional control of aging suggests that cytosolic increases in the reduced form of nicotinamide adenine dinucleotide and decreasing nicotinamide adenine dinucleotide metabolism plays a central role in controlling the longevity gene products sirtuin 1 (SIRT1), adenosine monophosphate-activated protein kinase (AMPK) and forkhead box O3 (FOXO3).	NAD	105-138	forkhead box O3	Homo sapiens	359-364
27181414-1	2016	Recent research in nutritional control of aging suggests that cytosolic increases in the reduced form of nicotinamide adenine dinucleotide and decreasing nicotinamide adenine dinucleotide metabolism plays a central role in controlling the longevity gene products sirtuin 1 (SIRT1), adenosine monophosphate-activated protein kinase (AMPK) and forkhead box O3 (FOXO3).	NAD	154-187	forkhead box O3	Homo sapiens	342-357
27181414-1	2016	Recent research in nutritional control of aging suggests that cytosolic increases in the reduced form of nicotinamide adenine dinucleotide and decreasing nicotinamide adenine dinucleotide metabolism plays a central role in controlling the longevity gene products sirtuin 1 (SIRT1), adenosine monophosphate-activated protein kinase (AMPK) and forkhead box O3 (FOXO3).	NAD	154-187	forkhead box O3	Homo sapiens	359-364
27053302-1	2016	SIRT3 is a member of Sirtuins family, which belongs to NAD(+) dependent class III histone deacetylases.	NAD	55-61	sirtuin 3	Homo sapiens	0-5
27304511-0	2016	CD38 Dictates Age-Related NAD Decline and Mitochondrial Dysfunction through an SIRT3-Dependent Mechanism.	NAD	26-29	sirtuin 3	Homo sapiens	79-84
27304511-3	2016	Here we demonstrate that expression and activity of the NADase CD38 increase with aging and that CD38 is required for the age-related NAD decline and mitochondrial dysfunction via a pathway mediated at least in part by regulation of SIRT3 activity.	NAD	56-59	sirtuin 3	Homo sapiens	233-238
27173464-2	2016	Here, we investigated the relationship between the nicotinamide phosphoribosyltransferase (NAMPT)-controlled nicotinamide adenine dinucleotide (NAD) metabolism and the impaired mobilization of BM-derived EPCs in diabetic condition.	NAD	109-142	nicotinamide phosphoribosyltransferase	Mus musculus	91-96
27173464-2	2016	Here, we investigated the relationship between the nicotinamide phosphoribosyltransferase (NAMPT)-controlled nicotinamide adenine dinucleotide (NAD) metabolism and the impaired mobilization of BM-derived EPCs in diabetic condition.	NAD	144-147	nicotinamide phosphoribosyltransferase	Mus musculus	51-89
27173464-2	2016	Here, we investigated the relationship between the nicotinamide phosphoribosyltransferase (NAMPT)-controlled nicotinamide adenine dinucleotide (NAD) metabolism and the impaired mobilization of BM-derived EPCs in diabetic condition.	NAD	144-147	nicotinamide phosphoribosyltransferase	Mus musculus	91-96
27002158-0	2016	Enhancing NAD+ Salvage Pathway Reverts the Toxicity of Primary Astrocytes Expressing Amyotrophic Lateral Sclerosis-linked Mutant Superoxide Dismutase 1 (SOD1).	NAD	10-14	superoxide dismutase 1	Homo sapiens	129-151
27058624-0	2016	Gene silencing of indoleamine 2,3-dioxygenase 2 in melanoma cells induces apoptosis through the suppression of NAD+ and inhibits in vivo tumor growth.	NAD	111-115	indoleamine 2,3-dioxygenase 2	Mus musculus	18-47
27058624-6	2016	Knockdown of IDO2 decreased the generation of nicotinamide adenine dinucleotide (NAD+) while increasing the generation of reactive oxygen species (ROS).	NAD	46-79	indoleamine 2,3-dioxygenase 2	Mus musculus	13-17
27058624-6	2016	Knockdown of IDO2 decreased the generation of nicotinamide adenine dinucleotide (NAD+) while increasing the generation of reactive oxygen species (ROS).	NAD	81-85	indoleamine 2,3-dioxygenase 2	Mus musculus	13-17
27058624-7	2016	We further demonstrate that cell apoptosis, induced by IDO2 downregulation, can be weakened by addition of exogenous NAD+, suggesting a novel mechanism by which IDO2 promotes tumor growth through its metabolite product NAD+.	NAD	117-121	indoleamine 2,3-dioxygenase 2	Mus musculus	55-59
27058624-7	2016	We further demonstrate that cell apoptosis, induced by IDO2 downregulation, can be weakened by addition of exogenous NAD+, suggesting a novel mechanism by which IDO2 promotes tumor growth through its metabolite product NAD+.	NAD	117-121	indoleamine 2,3-dioxygenase 2	Mus musculus	161-165
27058624-7	2016	We further demonstrate that cell apoptosis, induced by IDO2 downregulation, can be weakened by addition of exogenous NAD+, suggesting a novel mechanism by which IDO2 promotes tumor growth through its metabolite product NAD+.	NAD	219-223	indoleamine 2,3-dioxygenase 2	Mus musculus	55-59
27058624-7	2016	We further demonstrate that cell apoptosis, induced by IDO2 downregulation, can be weakened by addition of exogenous NAD+, suggesting a novel mechanism by which IDO2 promotes tumor growth through its metabolite product NAD+.	NAD	219-223	indoleamine 2,3-dioxygenase 2	Mus musculus	161-165
27095738-0	2016	Modulation of NADH Levels by Arabidopsis Nudix Hydrolases, AtNUDX6 and 7, and the Respective Proteins Themselves Play Distinct Roles in the Regulation of Various Cellular Responses Involved in Biotic/Abiotic Stresses.	NAD	14-18	nudix hydrolase homolog 6	Arabidopsis thaliana	59-66
27095738-1	2016	Arabidopsis Nudix hydrolases, AtNUDX6 and 7, exhibit pyrophosphohydrolase activities toward NADH and contribute to the modulation of various defense responses, such as the poly(ADP-ribosyl)ation (PAR) reaction and salicylic acid (SA)-induced Nonexpresser of Pathogenesis-Related genes 1 (NPR1)-dependent defense pathway, against biotic and abiotic stresses.	NAD	92-96	nudix hydrolase homolog 6	Arabidopsis thaliana	30-43
27095738-4	2016	The transient expression of active AtNUDX6 and 7 proteins suppressed NADH levels and induced PAR activity, whereas that of their inactive forms did not, indicating the involvement of NADH metabolism in the regulation of the PAR reaction.	NAD	69-73	nudix hydrolase homolog 6	Arabidopsis thaliana	35-42
27095738-4	2016	The transient expression of active AtNUDX6 and 7 proteins suppressed NADH levels and induced PAR activity, whereas that of their inactive forms did not, indicating the involvement of NADH metabolism in the regulation of the PAR reaction.	NAD	183-187	nudix hydrolase homolog 6	Arabidopsis thaliana	35-42
27095738-5	2016	A transcriptome analysis using KO-nudx6, KO-nudx7 and double KO-nudx6/7 plants, in which intracellular NADH levels increased, identified genes (NADH-responsive genes, NRGs) whose expression levels positively and negatively correlated with NADH levels.	NAD	103-107	nudix hydrolase homolog 6	Arabidopsis thaliana	64-69
27095738-5	2016	A transcriptome analysis using KO-nudx6, KO-nudx7 and double KO-nudx6/7 plants, in which intracellular NADH levels increased, identified genes (NADH-responsive genes, NRGs) whose expression levels positively and negatively correlated with NADH levels.	NAD	144-148	nudix hydrolase homolog 6	Arabidopsis thaliana	34-39
27095738-5	2016	A transcriptome analysis using KO-nudx6, KO-nudx7 and double KO-nudx6/7 plants, in which intracellular NADH levels increased, identified genes (NADH-responsive genes, NRGs) whose expression levels positively and negatively correlated with NADH levels.	NAD	144-148	nudix hydrolase homolog 6	Arabidopsis thaliana	64-69
27095738-5	2016	A transcriptome analysis using KO-nudx6, KO-nudx7 and double KO-nudx6/7 plants, in which intracellular NADH levels increased, identified genes (NADH-responsive genes, NRGs) whose expression levels positively and negatively correlated with NADH levels.	NAD	144-148	nudix hydrolase homolog 6	Arabidopsis thaliana	34-39
27095738-5	2016	A transcriptome analysis using KO-nudx6, KO-nudx7 and double KO-nudx6/7 plants, in which intracellular NADH levels increased, identified genes (NADH-responsive genes, NRGs) whose expression levels positively and negatively correlated with NADH levels.	NAD	144-148	nudix hydrolase homolog 6	Arabidopsis thaliana	64-69
27240523-5	2016	In addition, NAD(+) administration to H2O2-treated RPE cells inhibited the activation of PARP-1 and protected the RPE cells against necrotic death.	NAD	13-19	poly(ADP-ribose) polymerase 1	Homo sapiens	89-95
27240523-9	2016	Taken together, our findings indicate that that exogenous NAD(+) administration suppresses H2O2-induced oxidative stress and protects RPE cells against PARP-1 mediated necrotic death through the up-regulation of autophagy.	NAD	58-64	poly(ADP-ribose) polymerase 1	Homo sapiens	152-158
27135737-3	2016	Enzyme-triggered theranostic prodrug 1 selectively targets cancer cells and is subsequently activated in the presence of NAD(P)H: quinone oxidoreductase-1 (NQO1), a cytosolic flavoprotein that catalyzes the two-electron reduction of quinone moieties with the concomitant consumption of NADH or NADPH as electron donors.	NAD	286-290	NAD(P)H quinone dehydrogenase 1	Homo sapiens	121-154
27135737-3	2016	Enzyme-triggered theranostic prodrug 1 selectively targets cancer cells and is subsequently activated in the presence of NAD(P)H: quinone oxidoreductase-1 (NQO1), a cytosolic flavoprotein that catalyzes the two-electron reduction of quinone moieties with the concomitant consumption of NADH or NADPH as electron donors.	NAD	286-290	NAD(P)H quinone dehydrogenase 1	Homo sapiens	156-160
27002158-0	2016	Enhancing NAD+ Salvage Pathway Reverts the Toxicity of Primary Astrocytes Expressing Amyotrophic Lateral Sclerosis-linked Mutant Superoxide Dismutase 1 (SOD1).	NAD	10-14	superoxide dismutase 1	Homo sapiens	153-157
27002158-4	2016	Three distinct families of enzymes consume NAD(+) as substrate: poly(ADP-ribose) polymerases, ADP-ribosyl cyclases (CD38 and CD157), and sirtuins (SIRT1-7).	NAD	43-49	bone marrow stromal cell antigen 1	Homo sapiens	125-130
26912215-3	2016	Aadh1p has 64% identity with Saccharomyces cerevisiae Adh1p, is localized in the cytoplasm and uses NAD(+) as cofactor.	NAD	100-106	alcohol dehydrogenase ADH1	Saccharomyces cerevisiae S288C	54-59
27274295-4	2016	On the other hand, NAD(+) can be diminished or depleted by overactivation of poly ADP ribose polymerase that uses NAD(+) as its substrate.	NAD	19-25	poly(ADP-ribose) polymerase 1	Homo sapiens	77-103
27274295-4	2016	On the other hand, NAD(+) can be diminished or depleted by overactivation of poly ADP ribose polymerase that uses NAD(+) as its substrate.	NAD	114-120	poly(ADP-ribose) polymerase 1	Homo sapiens	77-103
27052539-0	2016	Nicotinamide Riboside Is a Major NAD+ Precursor Vitamin in Cow Milk.	NAD	33-37	Weaning weight-maternal milk	Bos taurus	63-67
27052539-3	2016	OBJECTIVE: We aimed to determine NAD(+) precursor vitamin concentration in raw samples of milk from individual cows and from commercially available cow milk.	NAD	33-39	Weaning weight-maternal milk	Bos taurus	90-94
27052539-6	2016	RESULTS: Cow milk typically contained ~12 mumol NAD(+) precursor vitamins/L, of which 60% was present as nicotinamide and 40% was present as NR.	NAD	48-54	Weaning weight-maternal milk	Bos taurus	13-17
27052539-10	2016	CONCLUSIONS: NR is a major NAD(+) precursor vitamin in cow milk.	NAD	27-33	Weaning weight-maternal milk	Bos taurus	59-63
27052539-11	2016	Control of S. aureus may be important to preserve the NAD(+) precursor vitamin concentration of milk.	NAD	54-60	Weaning weight-maternal milk	Bos taurus	96-100
26926998-7	2016	Furthermore, mutations in genes encoding the other five Arabidopsis Elongator subunits (ELO2/AtELP1, AtELP2, ELO1/AtELP4, AtELP5, and AtELP6) also compromise exogenous NAD(+)-induced PR gene expression and resistance to P. syringae pv.	NAD	168-174	IKI3 family protein	Arabidopsis thaliana	88-92
26952442-3	2016	A fast, linear and highly sensitive response was observed for NADH in the concentration range between 0.1 and 200 muM with a detection limit (S/N=3) of 32 nM.	NAD	62-66	latexin	Homo sapiens	114-117
26926998-7	2016	Furthermore, mutations in genes encoding the other five Arabidopsis Elongator subunits (ELO2/AtELP1, AtELP2, ELO1/AtELP4, AtELP5, and AtELP6) also compromise exogenous NAD(+)-induced PR gene expression and resistance to P. syringae pv.	NAD	168-174	IKI3 family protein	Arabidopsis thaliana	93-99
26926998-7	2016	Furthermore, mutations in genes encoding the other five Arabidopsis Elongator subunits (ELO2/AtELP1, AtELP2, ELO1/AtELP4, AtELP5, and AtELP6) also compromise exogenous NAD(+)-induced PR gene expression and resistance to P. syringae pv.	NAD	168-174	elongator protein 6	Arabidopsis thaliana	134-140
27102823-6	2016	The increase in both the NAD(+) availability and Sirt1 mRNA levels, in turn, resulted in the hepatic activation of SIRT1, which was significantly associated with improved protection against hepatic triglyceride accumulation.	NAD	25-31	sirtuin 1	Rattus norvegicus	115-120
27035562-2	2016	Nicotinamide phosphoribosyltransferase (NAMPT) catalyzes the first rate-limiting step in the nicotinamide adenine dinucleotide (NAD+) biosynthetic pathway in mammals, is a substrate for NAD+-dependent enzymes, such as sirtuin 1 (SIRT1), and contributes to cell fate decisions.	NAD	93-126	sirtuin 1	Rattus norvegicus	218-227
27035562-2	2016	Nicotinamide phosphoribosyltransferase (NAMPT) catalyzes the first rate-limiting step in the nicotinamide adenine dinucleotide (NAD+) biosynthetic pathway in mammals, is a substrate for NAD+-dependent enzymes, such as sirtuin 1 (SIRT1), and contributes to cell fate decisions.	NAD	93-126	sirtuin 1	Rattus norvegicus	229-234
27035562-2	2016	Nicotinamide phosphoribosyltransferase (NAMPT) catalyzes the first rate-limiting step in the nicotinamide adenine dinucleotide (NAD+) biosynthetic pathway in mammals, is a substrate for NAD+-dependent enzymes, such as sirtuin 1 (SIRT1), and contributes to cell fate decisions.	NAD	128-132	sirtuin 1	Rattus norvegicus	218-227
27035562-2	2016	Nicotinamide phosphoribosyltransferase (NAMPT) catalyzes the first rate-limiting step in the nicotinamide adenine dinucleotide (NAD+) biosynthetic pathway in mammals, is a substrate for NAD+-dependent enzymes, such as sirtuin 1 (SIRT1), and contributes to cell fate decisions.	NAD	128-132	sirtuin 1	Rattus norvegicus	229-234
27035562-2	2016	Nicotinamide phosphoribosyltransferase (NAMPT) catalyzes the first rate-limiting step in the nicotinamide adenine dinucleotide (NAD+) biosynthetic pathway in mammals, is a substrate for NAD+-dependent enzymes, such as sirtuin 1 (SIRT1), and contributes to cell fate decisions.	NAD	186-190	sirtuin 1	Rattus norvegicus	218-227
27035562-2	2016	Nicotinamide phosphoribosyltransferase (NAMPT) catalyzes the first rate-limiting step in the nicotinamide adenine dinucleotide (NAD+) biosynthetic pathway in mammals, is a substrate for NAD+-dependent enzymes, such as sirtuin 1 (SIRT1), and contributes to cell fate decisions.	NAD	186-190	sirtuin 1	Rattus norvegicus	229-234
27080463-7	2016	Further study revealed that the expression of SIRT1 and phosphorylated Akt1 (p-Akt1) was up-regulated when NAD was added into the culturing medium.	NAD	107-110	AKT serine/threonine kinase 1	Homo sapiens	71-75
27080463-7	2016	Further study revealed that the expression of SIRT1 and phosphorylated Akt1 (p-Akt1) was up-regulated when NAD was added into the culturing medium.	NAD	107-110	AKT serine/threonine kinase 1	Homo sapiens	79-83
27080463-8	2016	Taking together, our results demonstrated that NAD might delay the axonal degeneration through SIRT1/Akt1 pathways.	NAD	47-50	AKT serine/threonine kinase 1	Homo sapiens	101-105
27102823-7	2016	Our data clearly indicates that PAC consumption could be a valid tool to enhance hepatic SIRT1 activity through the modulation of NAD(+) levels.	NAD	130-136	sirtuin 1	Rattus norvegicus	89-94
26867495-0	2016	Metabolism of isoniazid by neutrophil myeloperoxidase leads to isoniazid-NAD(+) adduct formation: A comparison of the reactivity of isoniazid with its known human metabolites.	NAD	73-79	myeloperoxidase	Homo sapiens	38-53
26867495-3	2016	The role of neutrophil myeloperoxidase (MPO) in INH-NAD(+) adduct formation has never been explored; this is important, as neutrophils are recruited at the site of tuberculosis infection (granuloma) through infected macrophages" cell death signals.	NAD	52-58	myeloperoxidase	Homo sapiens	40-43
26774271-8	2016	We also provide evidence that Ser3 and Ser33, which are primarily known for oxidizing 3-phosphoglycerate in the main serine biosynthesis pathway, in addition reduce alpha-ketoglutarate to D-2HG using NADH and represent major intracellular sources of D-2HG in yeast.	NAD	200-204	phosphoglycerate dehydrogenase SER3	Saccharomyces cerevisiae S288C	30-34
26867495-5	2016	MPO or activated human neutrophils (by phorbol myristate acetate) catalyzed the oxidation of INH and formed several free radical intermediates; the inclusion of superoxide dismutase revealed a carbon-centered radical which is considered to be the reactive metabolite that binds with NAD(+).	NAD	283-289	myeloperoxidase	Homo sapiens	0-3
26867495-8	2016	Furthermore, only INH oxidation by MPO led to a new product (lambdamax=326nm) in the presence of NAD(+).	NAD	97-103	myeloperoxidase	Homo sapiens	35-38
26748095-1	2016	The Saccharomyces cerevisiae genome encodes five sirtuins (Sir2 and Hst1-4), which constitute a conserved family of NAD-dependent histone deacetylases.	NAD	116-119	histone deacetylase HST2	Saccharomyces cerevisiae S288C	68-74
26975537-8	2016	We focus on the regulation of NAD(+)/NADH homeostasis and the effects of NAD(+) consumption by poly(ADP-ribose) (PAR) polymerase-1 (PARP-1), NAD(+)-dependent deacetylation by sirtuins and NAD(+) metabolites on autophagy processes and the underlying mechanisms.	NAD	73-79	poly(ADP-ribose) polymerase 1	Homo sapiens	132-138
26975537-8	2016	We focus on the regulation of NAD(+)/NADH homeostasis and the effects of NAD(+) consumption by poly(ADP-ribose) (PAR) polymerase-1 (PARP-1), NAD(+)-dependent deacetylation by sirtuins and NAD(+) metabolites on autophagy processes and the underlying mechanisms.	NAD	73-79	poly(ADP-ribose) polymerase 1	Homo sapiens	132-138
26975537-8	2016	We focus on the regulation of NAD(+)/NADH homeostasis and the effects of NAD(+) consumption by poly(ADP-ribose) (PAR) polymerase-1 (PARP-1), NAD(+)-dependent deacetylation by sirtuins and NAD(+) metabolites on autophagy processes and the underlying mechanisms.	NAD	73-79	poly(ADP-ribose) polymerase 1	Homo sapiens	132-138
27031963-1	2016	The co-enzyme nicotinamide adenine dinucleotide (NAD(+)) is an essential co-factor for cellular energy generation in mitochondria as well as for DNA repair mechanisms in the cell nucleus involving NAD(+)-consuming poly (ADP-ribose) polymerases (PARPs).	NAD	14-47	poly(ADP-ribose) polymerase 1	Homo sapiens	245-250
27031963-1	2016	The co-enzyme nicotinamide adenine dinucleotide (NAD(+)) is an essential co-factor for cellular energy generation in mitochondria as well as for DNA repair mechanisms in the cell nucleus involving NAD(+)-consuming poly (ADP-ribose) polymerases (PARPs).	NAD	49-55	poly(ADP-ribose) polymerase 1	Homo sapiens	245-250
27031963-1	2016	The co-enzyme nicotinamide adenine dinucleotide (NAD(+)) is an essential co-factor for cellular energy generation in mitochondria as well as for DNA repair mechanisms in the cell nucleus involving NAD(+)-consuming poly (ADP-ribose) polymerases (PARPs).	NAD	49-53	poly(ADP-ribose) polymerase 1	Homo sapiens	245-250
27031963-5	2016	Further, by mutating Parp in parkin mutants, we show that this increases levels of NAD(+) and its salvage metabolites.	NAD	83-89	poly(ADP-ribose) polymerase 1	Homo sapiens	21-25
27031963-7	2016	We conclude that strategies to enhance NAD(+) levels by administration of dietary precursors or the inhibition of NAD(+)-dependent enzymes, such as PARP, that compete with mitochondria for NAD(+) could be used to delay neuronal death associated with mitochondrial dysfunction.	NAD	39-45	poly(ADP-ribose) polymerase 1	Homo sapiens	148-152
27031963-7	2016	We conclude that strategies to enhance NAD(+) levels by administration of dietary precursors or the inhibition of NAD(+)-dependent enzymes, such as PARP, that compete with mitochondria for NAD(+) could be used to delay neuronal death associated with mitochondrial dysfunction.	NAD	114-120	poly(ADP-ribose) polymerase 1	Homo sapiens	148-152
27031963-7	2016	We conclude that strategies to enhance NAD(+) levels by administration of dietary precursors or the inhibition of NAD(+)-dependent enzymes, such as PARP, that compete with mitochondria for NAD(+) could be used to delay neuronal death associated with mitochondrial dysfunction.	NAD	114-120	poly(ADP-ribose) polymerase 1	Homo sapiens	148-152
27020835-0	2016	Blocking NAD(+)/CD38/cADPR/Ca(2+) pathway in sepsis prevents organ damage.	NAD	9-15	CD38 molecule	Rattus norvegicus	16-20
27020835-1	2016	BACKGROUND: Although the nicotinamide adenine dinucleotide (NAD(+))/CD38/cyclic ADP ribose (cADPR)/Ca(2+) signaling pathway has been shown to regulate intracellular calcium homeostasis and functions in multiple inflammatory processes, its role in sepsis remains unknown.	NAD	25-58	CD38 molecule	Rattus norvegicus	68-72
27020835-1	2016	BACKGROUND: Although the nicotinamide adenine dinucleotide (NAD(+))/CD38/cyclic ADP ribose (cADPR)/Ca(2+) signaling pathway has been shown to regulate intracellular calcium homeostasis and functions in multiple inflammatory processes, its role in sepsis remains unknown.	NAD	60-67	CD38 molecule	Rattus norvegicus	68-72
27020835-2	2016	The aim of this study was to determine whether the NAD(+)/CD38/cADPR/Ca(2+) signaling pathway is activated during sepsis and whether an inhibitor of this pathway, 8-Br-cADPR, protects the organs from sepsis-induced damage.	NAD	51-57	CD38 molecule	Rattus norvegicus	58-62
27020835-8	2016	CONCLUSIONS: The NAD(+)/CD38/cADPR/Ca(2+) signaling pathway was activated during sepsis in the CLP rat model.	NAD	17-23	CD38 molecule	Rattus norvegicus	24-28
30868093-1	2017	PLA2G6-associated neurodegeneration comprises a heterogeneous spectrum of age-related phenotypes, with three forms classically recognized, including infantile neuroaxonal dystrophy (INAD) with onset in infancy, atypical neuroaxonal dystrophy (atypical NAD) with onset in childhood, and dystonia-parkinsonism (PARK14) with onset in early adulthood.	NAD	183-186	phospholipase A2 group VI	Homo sapiens	0-6
26792859-8	2016	Under HG ambience, MIOX overexpression accentuated redox imbalance, perturbed NAD(+)/NADH ratios, increased ROS generation, depleted reduced glutathione, reduced GSH/GSSG ratio, and enhanced adaptive changes in the profile of the antioxidant defense system.	NAD	78-84	inositol oxygenase	Sus scrofa	19-23
26973386-4	2016	One member of a family of growth-related nicotinamide adenine dinucleotide (NADH or hydroquinone) oxidases is tumor-associated NADH oxidase (tNOX; ENOX2).	NAD	41-74	ecto-NOX disulfide-thiol exchanger 2	Homo sapiens	110-139
26973386-4	2016	One member of a family of growth-related nicotinamide adenine dinucleotide (NADH or hydroquinone) oxidases is tumor-associated NADH oxidase (tNOX; ENOX2).	NAD	41-74	ecto-NOX disulfide-thiol exchanger 2	Homo sapiens	141-145
26973386-4	2016	One member of a family of growth-related nicotinamide adenine dinucleotide (NADH or hydroquinone) oxidases is tumor-associated NADH oxidase (tNOX; ENOX2).	NAD	41-74	ecto-NOX disulfide-thiol exchanger 2	Homo sapiens	147-152
26973386-4	2016	One member of a family of growth-related nicotinamide adenine dinucleotide (NADH or hydroquinone) oxidases is tumor-associated NADH oxidase (tNOX; ENOX2).	NAD	76-80	ecto-NOX disulfide-thiol exchanger 2	Homo sapiens	110-139
26919468-10	2016	Our recent biochemical studies showed that the archael Thi4 orthologs use nicotinamide adenine dinucleotide, glycine, and free sulfide to form the thiamin thiazole in an iron-dependent reaction [Eser, B., Zhang, X., Chanani, P. K., Begley, T. P., and Ealick, S. E. (2016) J.	NAD	74-107	thiamine thiazole synthase	Saccharomyces cerevisiae S288C	55-59
26792859-8	2016	Under HG ambience, MIOX overexpression accentuated redox imbalance, perturbed NAD(+)/NADH ratios, increased ROS generation, depleted reduced glutathione, reduced GSH/GSSG ratio, and enhanced adaptive changes in the profile of the antioxidant defense system.	NAD	85-89	inositol oxygenase	Sus scrofa	19-23
26973386-4	2016	One member of a family of growth-related nicotinamide adenine dinucleotide (NADH or hydroquinone) oxidases is tumor-associated NADH oxidase (tNOX; ENOX2).	NAD	76-80	ecto-NOX disulfide-thiol exchanger 2	Homo sapiens	141-145
26973386-4	2016	One member of a family of growth-related nicotinamide adenine dinucleotide (NADH or hydroquinone) oxidases is tumor-associated NADH oxidase (tNOX; ENOX2).	NAD	76-80	ecto-NOX disulfide-thiol exchanger 2	Homo sapiens	147-152
26681113-4	2016	The origin of NF-kappaB activation was related to the age-dependent Bmal1/Clock/RORalpha/Rev-Erbalpha loop disruption, which lowers NAD(+) levels, reducing the SIRT1 deacetylase ability to inactivate NF-kappaB.	NAD	132-138	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	14-23
26939608-7	2016	We employed a push/pull strategy to shunt citrate towards ACL by deletion of the mitochondrial NAD(+)-dependent isocitrate dehydrogenase (IDH1) and engineering higher flux through the upper mevalonate pathway.	NAD	95-101	isocitrate dehydrogenase (NAD(+)) IDH1	Saccharomyces cerevisiae S288C	138-142
26707577-3	2016	Nicotinamide adenine dinucleotide (NAD(+)/NADH) is a major coenzyme for oxidoreduction reactions in energy metabolism; it has recently emerged as a signalling molecule with a broad range of activities, ranging from calcium (Ca(2+)) signalling (CD38 ectoenzyme) to the epigenetic regulation of gene expression involved in the oxidative stress response, catabolic metabolism and mitochondrial biogenesis (sirtuins, poly[adenosine diphosphate-ribose] polymerases [PARPs]).	NAD	42-46	poly(ADP-ribose) polymerase 1	Homo sapiens	461-466
26786260-1	2016	SIRT6, a member of the NAD(+)-dependent class III deacetylase sirtuin family, has been revealed to play important roles in promoting cellular resistance against oxidative stress.	NAD	23-29	sirtuin 6	Mus musculus	0-5
26518726-1	2016	PARP-family ADP-ribosyltransferases (PARPs) and sirtuin deacetylases all use NAD(+) as cosubstrate for ADP-ribosyl transfer.	NAD	77-83	poly(ADP-ribose) polymerase 1	Homo sapiens	0-4
26518726-1	2016	PARP-family ADP-ribosyltransferases (PARPs) and sirtuin deacetylases all use NAD(+) as cosubstrate for ADP-ribosyl transfer.	NAD	77-83	poly(ADP-ribose) polymerase 1	Homo sapiens	37-42
26518726-3	2016	With the exception of a few tankyrase inhibitors, all current PARP inhibitors mimic the nicotinamide moiety in NAD(+) and block the nicotinamide binding pocket.	NAD	111-117	poly(ADP-ribose) polymerase 1	Homo sapiens	62-66
26518726-6	2016	In conclusion, a simple commercially available assay can be used to rule out interference of novel PARP inhibitors with sirtuin NAD(+) binding.	NAD	128-134	poly(ADP-ribose) polymerase 1	Homo sapiens	99-103
26709612-1	2016	3-Hydroxybenzoate 6-hydroxylase (3HB6H) from Rhodococcus jostii RHA1 is an NADH-specific flavoprotein monooxygenase that contains FAD as a redox-active cofactor.	NAD	75-79	3-hydroxybenzoate 6-hydroxylase	Rhodococcus jostii RHA1	0-38
26565538-1	2016	Here, we describe three cases of loss-of-function mutations in the nicotinamide adenine dinucleotide phosphate (NADPH)-oxidase (NOX) domain of dual oxidase 2 (DUOX2) occurring along with concurrent missense mutations in thyroid peroxidase (TPO), leading to transient congenital hypothyroidism (CH).	NAD	67-100	dual oxidase 2	Homo sapiens	143-157
26565538-1	2016	Here, we describe three cases of loss-of-function mutations in the nicotinamide adenine dinucleotide phosphate (NADPH)-oxidase (NOX) domain of dual oxidase 2 (DUOX2) occurring along with concurrent missense mutations in thyroid peroxidase (TPO), leading to transient congenital hypothyroidism (CH).	NAD	67-100	dual oxidase 2	Homo sapiens	159-164
26707577-3	2016	Nicotinamide adenine dinucleotide (NAD(+)/NADH) is a major coenzyme for oxidoreduction reactions in energy metabolism; it has recently emerged as a signalling molecule with a broad range of activities, ranging from calcium (Ca(2+)) signalling (CD38 ectoenzyme) to the epigenetic regulation of gene expression involved in the oxidative stress response, catabolic metabolism and mitochondrial biogenesis (sirtuins, poly[adenosine diphosphate-ribose] polymerases [PARPs]).	NAD	0-33	poly(ADP-ribose) polymerase 1	Homo sapiens	461-466
26707577-3	2016	Nicotinamide adenine dinucleotide (NAD(+)/NADH) is a major coenzyme for oxidoreduction reactions in energy metabolism; it has recently emerged as a signalling molecule with a broad range of activities, ranging from calcium (Ca(2+)) signalling (CD38 ectoenzyme) to the epigenetic regulation of gene expression involved in the oxidative stress response, catabolic metabolism and mitochondrial biogenesis (sirtuins, poly[adenosine diphosphate-ribose] polymerases [PARPs]).	NAD	35-41	poly(ADP-ribose) polymerase 1	Homo sapiens	461-466
26341473-7	2016	Furthermore, we show that the induction of cellular NAD(+) levels using dunnione, which targets intracellular NQO1, prevents the toxic effects of cisplatin through the regulation of PARP-1 and SIRT1 activity.	NAD	52-58	NAD(P)H quinone dehydrogenase 1	Homo sapiens	110-114
26341473-7	2016	Furthermore, we show that the induction of cellular NAD(+) levels using dunnione, which targets intracellular NQO1, prevents the toxic effects of cisplatin through the regulation of PARP-1 and SIRT1 activity.	NAD	52-58	poly(ADP-ribose) polymerase 1	Homo sapiens	182-188
26760174-1	2016	CONTEXT: Sirtuins (SIRTs) and poly(ADP-ribose) polymerases (PARPs) are 2 important nicotinamide adenine dinucleotide (NAD)(+)-dependent enzyme families with opposing metabolic effects.	NAD	83-116	poly(ADP-ribose) polymerase 1	Homo sapiens	60-65
26760174-1	2016	CONTEXT: Sirtuins (SIRTs) and poly(ADP-ribose) polymerases (PARPs) are 2 important nicotinamide adenine dinucleotide (NAD)(+)-dependent enzyme families with opposing metabolic effects.	NAD	118-125	poly(ADP-ribose) polymerase 1	Homo sapiens	60-65
26760174-6	2016	MAIN OUTCOME MEASURES: SAT mRNA expressions of SIRTs 1-7 and the rate-limiting gene in NAD(+) biosynthesis, nicotinamide phosphoribosyltransferase (NAMPT) were measured by Affymetrix, and total PARP activity by ELISA kit.	NAD	87-93	poly(ADP-ribose) polymerase 1	Homo sapiens	194-198
26928119-0	2016	NAD(+) regulates Treg cell fate and promotes allograft survival via a systemic IL-10 production that is CD4(+) CD25(+) Foxp3(+) T cells independent.	NAD	0-6	CD4 molecule	Homo sapiens	104-107
26928119-4	2016	Here, we investigated the impact of NAD(+) on the fate of CD4(+) CD25(+) Foxp3(+) Tregs in-depth, dissected their transcriptional signature profile and explored mechanisms underlying their conversion into IL-17A producing cells.	NAD	36-42	CD4 molecule	Homo sapiens	58-61
26928119-6	2016	Despite the reduced number of Tregs, known to promote homeostasis, and an increased number of pro-inflammatory Th17 cells, NAD(+) was able to promote an impressive allograft survival through a robust systemic IL-10 production that was CD4(+) CD25(+) Foxp3(+) independent.	NAD	123-129	CD4 molecule	Homo sapiens	235-238
26729717-4	2016	We have also developed a new variant of the delitto perfetto methodology to place BDH1 under the control of the GAL1 promoter, resulting in a yeast strain that overexpresses butanediol dehydrogenase and formate dehydrogenase activities in the presence of galactose and regenerates NADH in the presence of formate.	NAD	281-285	(R,R)-butanediol dehydrogenase	Saccharomyces cerevisiae S288C	82-86
26899247-4	2016	At later time points, Akt delivered the NAD(+)-dependent protein deacetylase Sirtuin 2 (Sirt 2) to the vicinity of phosphorylated H2A in response to irreversible DNA damage, thereby inducing H2A deacetylation and subsequently leading to apoptotic death.	NAD	40-46	AKT serine/threonine kinase 1	Rattus norvegicus	22-25
26452612-3	2016	More important, the dual-emission intensity ratio (I395/I550), fitting by a single-exponential decay function, can efficiently detect various NAD(+) levels from 100 to 4000 muM, as well as label NAD(+)/NADH (reduced form of NAD) ratios in the range of 1-50.	NAD	142-148	latexin	Homo sapiens	173-176
26452612-3	2016	More important, the dual-emission intensity ratio (I395/I550), fitting by a single-exponential decay function, can efficiently detect various NAD(+) levels from 100 to 4000 muM, as well as label NAD(+)/NADH (reduced form of NAD) ratios in the range of 1-50.	NAD	202-206	latexin	Homo sapiens	173-176
26452612-3	2016	More important, the dual-emission intensity ratio (I395/I550), fitting by a single-exponential decay function, can efficiently detect various NAD(+) levels from 100 to 4000 muM, as well as label NAD(+)/NADH (reduced form of NAD) ratios in the range of 1-50.	NAD	224-228	latexin	Homo sapiens	173-176
26805589-0	2016	Structural Insights into the Quaternary Catalytic Mechanism of Hexameric Human Quinolinate Phosphoribosyltransferase, a Key Enzyme in de novo NAD Biosynthesis.	NAD	142-145	quinolinate phosphoribosyltransferase	Homo sapiens	79-116
26805589-1	2016	Quinolinate phosphoribosyltransferase (QPRT) catalyses the production of nicotinic acid mononucleotide, a precursor of de novo biosynthesis of the ubiquitous coenzyme nicotinamide adenine dinucleotide.	NAD	167-200	quinolinate phosphoribosyltransferase	Homo sapiens	0-37
26805589-1	2016	Quinolinate phosphoribosyltransferase (QPRT) catalyses the production of nicotinic acid mononucleotide, a precursor of de novo biosynthesis of the ubiquitous coenzyme nicotinamide adenine dinucleotide.	NAD	167-200	quinolinate phosphoribosyltransferase	Homo sapiens	39-43
26742628-5	2016	Furthermore, the ERalpha-selective agonist PPT selectively increased the expression of ERbeta and the ERbeta-selective agonist DPN increased ERalpha levels.	NAD	127-130	estrogen receptor 1	Homo sapiens	141-148
26383629-4	2016	Upon induction of specific forms of genotoxic stimuli, several poly(ADP-ribose) polymerases (PARPs) synthesize the nucleic acid-like biopolymer poly(ADP-ribose) (PAR) by using NAD(+) as a substrate.	NAD	176-182	poly(ADP-ribose) polymerase 1	Homo sapiens	93-98
26844829-2	2016	Active degeneration requires SARM1 and MAP kinases, including DLK, while the NAD+ synthetic enzyme NMNAT2 prevents degeneration.	NAD	77-81	nicotinamide nucleotide adenylyltransferase 2	Homo sapiens	99-105
26774478-1	2016	ADP-ribosyltransferases (ARTD1-16) have emerged as major downstream effectors of NAD(+) signaling in the cell.	NAD	81-87	poly(ADP-ribose) polymerase 1	Homo sapiens	25-30
26774478-2	2016	Most ARTDs (ARTD7 and 8, 10-12, and 14-17) catalyze the transfer of a single unit of ADP-ribose from NAD(+) to target proteins, a process known as mono-ADP-ribosylation (MARylation).	NAD	101-107	poly(ADP-ribose) polymerase family member 15	Homo sapiens	12-17
26712469-2	2016	The current study aimed to decode the impact of acetylation/deacetylation of non-histone targets i.e. FoxO1/3a and p53 of sirtuins (NAD(+) dependent enzymes with lysine deacetylase activity) in berberine treated human hepatoma cells.	NAD	132-138	forkhead box O1	Homo sapiens	102-107
26712469-2	2016	The current study aimed to decode the impact of acetylation/deacetylation of non-histone targets i.e. FoxO1/3a and p53 of sirtuins (NAD(+) dependent enzymes with lysine deacetylase activity) in berberine treated human hepatoma cells.	NAD	132-138	tumor protein p53	Homo sapiens	115-118
26764408-0	2016	Intracellular NAD+ levels are associated with LPS-induced TNF-alpha release in pro-inflammatory macrophages.	NAD	14-18	tumor necrosis factor	Homo sapiens	58-67
26764408-2	2016	NAD(+) has previously been shown to regulate tumour necrosis factor-alpha (TNF-alpha) synthesis and TNF-alpha has been shown to regulate NAD(+) homoeostasis providing a link between a pro-inflammatory response and redox status.	NAD	0-6	tumor necrosis factor	Homo sapiens	75-84
26764408-2	2016	NAD(+) has previously been shown to regulate tumour necrosis factor-alpha (TNF-alpha) synthesis and TNF-alpha has been shown to regulate NAD(+) homoeostasis providing a link between a pro-inflammatory response and redox status.	NAD	137-143	tumor necrosis factor	Homo sapiens	100-109
26764408-5	2016	Challenge with bacterial lipopolysaccharide, a pro-inflammatory stimulus for macrophages, caused a large, biphasic and transient increase in NAD(+) levels in pro- but not anti-inflammatory macrophages that were correlated with TNF-alpha release and inhibition of certain NAD(+) synthesis pathways blocked TNF-alpha release.	NAD	141-147	tumor necrosis factor	Homo sapiens	227-236
26764408-5	2016	Challenge with bacterial lipopolysaccharide, a pro-inflammatory stimulus for macrophages, caused a large, biphasic and transient increase in NAD(+) levels in pro- but not anti-inflammatory macrophages that were correlated with TNF-alpha release and inhibition of certain NAD(+) synthesis pathways blocked TNF-alpha release.	NAD	141-147	tumor necrosis factor	Homo sapiens	305-314
27817742-1	2016	Poly(ADP-ribose) polymerases (PARPs) family proteins catalyze poly(ADP-ribosylation) (PARylation) by conjugating ADP-ribose residues repeatedly on amino acid residues using nicotinamide adenine dinucleotide as a substrate.	NAD	173-206	poly(ADP-ribose) polymerase 1	Homo sapiens	30-35
26929388-9	2016	Nonetheless AKT inhibition in the context of loss of NAD-dependent SIRT1 deacetylase modulates FOXO3 localization in HSPCs.	NAD	53-56	AKT serine/threonine kinase 1	Homo sapiens	12-15
26929388-9	2016	Nonetheless AKT inhibition in the context of loss of NAD-dependent SIRT1 deacetylase modulates FOXO3 localization in HSPCs.	NAD	53-56	forkhead box O3	Homo sapiens	95-100
26001219-0	2016	Intracellular nicotinamide adenine dinucleotide promotes TNF-induced necroptosis in a sirtuin-dependent manner.	NAD	14-47	tumor necrosis factor	Mus musculus	57-60
26001219-6	2016	Using a panel of pharmacological and genetic approaches, we show that intracellular NAD(+) promotes necroptosis of the L929 cell line in response to TNF.	NAD	84-90	tumor necrosis factor	Mus musculus	149-152
26709902-2	2016	Upon sensing DNA breaks, PARP-1 gets activated and cleaves NAD into nicotinamide and ADP-ribose and polymerizes the latter onto nuclear acceptor proteins including histones, transcription factors, and PARP-1 itself.	NAD	59-62	poly(ADP-ribose) polymerase 1	Homo sapiens	25-31
26709902-2	2016	Upon sensing DNA breaks, PARP-1 gets activated and cleaves NAD into nicotinamide and ADP-ribose and polymerizes the latter onto nuclear acceptor proteins including histones, transcription factors, and PARP-1 itself.	NAD	59-62	poly(ADP-ribose) polymerase 1	Homo sapiens	201-207
26709902-4	2016	However, oxidative stress-induced over-activation of PARP-1 consumes excess of NAD and consequently ATP, culminating into cell necrosis.	NAD	79-82	poly(ADP-ribose) polymerase 1	Homo sapiens	53-59
26709902-8	2016	Conventionally, there are many studies which employed the concept of direct inhibition of PARP-1 by competing with NAD.	NAD	115-118	poly(ADP-ribose) polymerase 1	Homo sapiens	90-96
26307000-5	2016	Furthermore, NAD can activate the P2X7 receptor via ADP-ribosyltransferase (ART) enzymes and cause cell depletion in murine models.	NAD	13-16	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	34-47
26307000-13	2016	In conclusion, our results suggest that the altered function and expression of P2X7 and ART1 in the human CD39+ Treg or CD39- Treg cells could participate in the resistance against cell death induced by ATP or NAD.	NAD	210-213	purinergic receptor P2X 7	Homo sapiens	79-83
26307000-13	2016	In conclusion, our results suggest that the altered function and expression of P2X7 and ART1 in the human CD39+ Treg or CD39- Treg cells could participate in the resistance against cell death induced by ATP or NAD.	NAD	210-213	ADP-ribosyltransferase 1	Homo sapiens	88-92
27110038-8	2016	The results demonstrate that NADH can act as a sole electron donor for both the first and the second reduction of CYP1A1 during its reaction cycle catalyzing oxidation of BaP, and suggest that the NADH:cytochrome b5 reductase as the NADH-dependent reductase might substitute POR in this enzymatic system.	NAD	29-33	cytochrome p450 oxidoreductase	Homo sapiens	275-278
26574954-5	2016	RESULTS: SIRT1, SIRT3, SIRT5, NAMPT, NMNAT2, NMNAT3, and NRK1 expressions were significantly down-regulated and the activity of main cellular NAD(+) consumers, PARPs, trended to be higher in the SAT of heavier co-twins of body mass index-discordant pairs.	NAD	142-148	sirtuin 3	Homo sapiens	16-21
26574954-5	2016	RESULTS: SIRT1, SIRT3, SIRT5, NAMPT, NMNAT2, NMNAT3, and NRK1 expressions were significantly down-regulated and the activity of main cellular NAD(+) consumers, PARPs, trended to be higher in the SAT of heavier co-twins of body mass index-discordant pairs.	NAD	142-148	nicotinamide nucleotide adenylyltransferase 2	Homo sapiens	37-43
26574954-5	2016	RESULTS: SIRT1, SIRT3, SIRT5, NAMPT, NMNAT2, NMNAT3, and NRK1 expressions were significantly down-regulated and the activity of main cellular NAD(+) consumers, PARPs, trended to be higher in the SAT of heavier co-twins of body mass index-discordant pairs.	NAD	142-148	nicotinamide riboside kinase 1	Homo sapiens	57-61
26574954-5	2016	RESULTS: SIRT1, SIRT3, SIRT5, NAMPT, NMNAT2, NMNAT3, and NRK1 expressions were significantly down-regulated and the activity of main cellular NAD(+) consumers, PARPs, trended to be higher in the SAT of heavier co-twins of body mass index-discordant pairs.	NAD	142-148	poly(ADP-ribose) polymerase 1	Homo sapiens	160-165
26574954-8	2016	CONCLUSIONS: Our data highlight a strong relationship of reduced NAD(+)/SIRT pathway expression with acquired obesity, inflammation, insulin resistance, and impaired mitochondrial protein homeostasis in SAT.	NAD	65-71	insulin	Homo sapiens	133-140
28217402-12	2016	After 24 h, Torin-2 significantly decreased glycolysis intermediates (fructose 1,6-bisphosphate (FBP), and 2-phosphoglycerate/3-phosphoglycerate), TCA intermediate metabolites (citrate/isocitrate, and malate), as well as Nicotinamide Adenine Dinucleotide (NAD+) and Flavin Adenine Dinucleotide (FAD), and ATP levels.	NAD	221-254	peroxiredoxin 2	Homo sapiens	12-17
28217402-12	2016	After 24 h, Torin-2 significantly decreased glycolysis intermediates (fructose 1,6-bisphosphate (FBP), and 2-phosphoglycerate/3-phosphoglycerate), TCA intermediate metabolites (citrate/isocitrate, and malate), as well as Nicotinamide Adenine Dinucleotide (NAD+) and Flavin Adenine Dinucleotide (FAD), and ATP levels.	NAD	256-260	peroxiredoxin 2	Homo sapiens	12-17
28217402-13	2016	When HPAF-II cells were incubated with both Torin-2 and metformin, there was a significant reduction in NAD+ and FAD, suggesting decreased levels of the energy equivalents that are available to the electron transport chain.	NAD	104-108	peroxiredoxin 2	Homo sapiens	44-49
28217402-14	2016	Targeted metabolomics data indicate that mTOR complexes inhibition by Torin 2 reduced glycolytic intermediates and TCA metabolites in HPAF- II and may synergize with metformin to decrease the electron acceptors NAD+ and FAD which may lead to reduced energy production.	NAD	211-215	mechanistic target of rapamycin kinase	Homo sapiens	41-45
28217402-14	2016	Targeted metabolomics data indicate that mTOR complexes inhibition by Torin 2 reduced glycolytic intermediates and TCA metabolites in HPAF- II and may synergize with metformin to decrease the electron acceptors NAD+ and FAD which may lead to reduced energy production.	NAD	211-215	peroxiredoxin 2	Homo sapiens	70-75
27110038-8	2016	The results demonstrate that NADH can act as a sole electron donor for both the first and the second reduction of CYP1A1 during its reaction cycle catalyzing oxidation of BaP, and suggest that the NADH:cytochrome b5 reductase as the NADH-dependent reductase might substitute POR in this enzymatic system.	NAD	197-201	cytochrome p450 oxidoreductase	Homo sapiens	275-278
26862571-1	2016	The energy-generating membrane protein NADH dehydrogenase (NDH-2), a proposed antibacterial drug target (see "Inhibitors of type II NADH:menaquinone oxidoreductase represent a class of antitubercular drugs" Weinstein et al.	NAD	39-43	DExH-box helicase 9	Homo sapiens	59-64
26633734-0	2015	Synthesis and Characterization of 4,11-Diaminoanthra[2,3-b]furan-5,10-diones: Tumor Cell Apoptosis through tNOX-Modulated NAD(+)/NADH Ratio and SIRT1.	NAD	122-128	ecto-NOX disulfide-thiol exchanger 2	Homo sapiens	107-111
26633734-0	2015	Synthesis and Characterization of 4,11-Diaminoanthra[2,3-b]furan-5,10-diones: Tumor Cell Apoptosis through tNOX-Modulated NAD(+)/NADH Ratio and SIRT1.	NAD	129-133	ecto-NOX disulfide-thiol exchanger 2	Homo sapiens	107-111
26686637-1	2015	Axon injury leads to rapid depletion of NAD-biosynthetic enzyme NMNAT2 and high levels of its substrate, NMN.	NAD	40-43	nicotinamide nucleotide adenylyltransferase 2	Homo sapiens	64-70
26159182-10	2016	Treatment with DPN increased phosphorylation of ERK and TrkB, but it did not alter that of Akt.	NAD	15-18	Eph receptor B1	Rattus norvegicus	48-51
26159182-10	2016	Treatment with DPN increased phosphorylation of ERK and TrkB, but it did not alter that of Akt.	NAD	15-18	neurotrophic receptor tyrosine kinase 2	Rattus norvegicus	56-60
27477457-1	2016	Poly(ADP-ribose), identified in 1966 independently by three groups Strassbourg, Kyoto and Tokyo, is synthesized by poly(ADP-ribose) polymerases (PARP) from NAD(+) as a substrate in the presence of Mg(2+).	NAD	156-162	poly(ADP-ribose) polymerase 1	Homo sapiens	115-143
27477457-1	2016	Poly(ADP-ribose), identified in 1966 independently by three groups Strassbourg, Kyoto and Tokyo, is synthesized by poly(ADP-ribose) polymerases (PARP) from NAD(+) as a substrate in the presence of Mg(2+).	NAD	156-162	poly(ADP-ribose) polymerase 1	Homo sapiens	145-149
26544624-8	2015	Together with our previous findings, these results suggest that enhancement of NAD+-dependent SIRT1 activity contributes to the chemopreventive efficacy of MSC by restoring epigenetic regulation of circadian gene expression at early stages of mammary tumorigenesis.	NAD	79-83	sirtuin 1	Rattus norvegicus	94-99
26544624-0	2015	Enhancement of NAD+-dependent SIRT1 deacetylase activity by methylselenocysteine resets the circadian clock in carcinogen-treated mammary epithelial cells.	NAD	15-19	sirtuin 1	Rattus norvegicus	30-35
26641458-5	2015	Furthermore, we demonstrated that loss of NDUFB9 promotes MDA-MB-231 cells proliferation, migration, and invasion because of elevated levels of mtROS, disturbance of the NAD+/NADH balance, and depletion of mtDNA.	NAD	170-174	NADH:ubiquinone oxidoreductase subunit B9	Homo sapiens	42-48
26544624-4	2015	Moreover, NMU inhibited intracellular NAD+/NADH ratio and reduced NAD+-dependent SIRT1 activity in a dose-dependent manner, while MSC restored NAD+/NADH and SIRT1 activity in the NMU-treated cells, indicating that the NAD+-SIRT1 pathway was targeted by NMU and MSC.	NAD	66-70	sirtuin 1	Rattus norvegicus	81-86
26544624-4	2015	Moreover, NMU inhibited intracellular NAD+/NADH ratio and reduced NAD+-dependent SIRT1 activity in a dose-dependent manner, while MSC restored NAD+/NADH and SIRT1 activity in the NMU-treated cells, indicating that the NAD+-SIRT1 pathway was targeted by NMU and MSC.	NAD	66-70	sirtuin 1	Rattus norvegicus	81-86
26544624-4	2015	Moreover, NMU inhibited intracellular NAD+/NADH ratio and reduced NAD+-dependent SIRT1 activity in a dose-dependent manner, while MSC restored NAD+/NADH and SIRT1 activity in the NMU-treated cells, indicating that the NAD+-SIRT1 pathway was targeted by NMU and MSC.	NAD	66-70	sirtuin 1	Rattus norvegicus	81-86
26518650-4	2015	In this study, we conducted thermodynamic and nuclear magnetic resonance (NMR) analyses, and demonstrated that L-PGDS binds to nicotinamide coenzymes, including NADPH, NADP(+), and NADH.	NAD	181-185	prostaglandin D2 synthase	Homo sapiens	111-117
26626480-1	2015	Poly(ADP-ribose) polymerase-1 (PARP-1) creates the posttranslational modification PAR from substrate NAD(+) to regulate multiple cellular processes.	NAD	101-107	poly(ADP-ribose) polymerase 1	Homo sapiens	0-29
26626480-1	2015	Poly(ADP-ribose) polymerase-1 (PARP-1) creates the posttranslational modification PAR from substrate NAD(+) to regulate multiple cellular processes.	NAD	101-107	poly(ADP-ribose) polymerase 1	Homo sapiens	31-37
26878573-8	2015	As distinct from the somatic isoenzyme, GAPDS exhibits positive cooperativity in binding of the coenzyme NAD+.	NAD	105-109	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	40-45
26641458-5	2015	Furthermore, we demonstrated that loss of NDUFB9 promotes MDA-MB-231 cells proliferation, migration, and invasion because of elevated levels of mtROS, disturbance of the NAD+/NADH balance, and depletion of mtDNA.	NAD	175-179	NADH:ubiquinone oxidoreductase subunit B9	Homo sapiens	42-48
26478723-8	2015	PARP activation led to a significant depletion of NAD+.	NAD	50-54	poly(ADP-ribose) polymerase 1	Homo sapiens	0-4
26478723-9	2015	PARP inhibition using veliparib (ABT-888) was able to successfully restore the NAD+ levels in MMS-treated cells.	NAD	79-83	poly(ADP-ribose) polymerase 1	Homo sapiens	0-4
26697174-5	2015	We also report that mTOR inhibition attenuated or reversed the majority of the PAH-specific abnormalities in lipogenesis, glycosylation, glutathione, and NAD metabolism without affecting altered polyunsaturated fatty acid metabolism.	NAD	154-157	mechanistic target of rapamycin kinase	Homo sapiens	20-24
26209889-0	2015	Reciprocal regulation by hypoxia-inducible factor-2alpha and the NAMPT-NAD(+)-SIRT axis in articular chondrocytes is involved in osteoarthritis.	NAD	71-77	nicotinamide phosphoribosyltransferase	Mus musculus	65-70
26209889-7	2015	RESULTS: HIF-2alpha activated the NAMPT-NAD(+)-SIRT axis in chondrocytes by upregulating NAMPT, which stimulated NAD(+) synthesis and thereby activated SIRT family members.	NAD	40-46	nicotinamide phosphoribosyltransferase	Mus musculus	34-39
26209889-7	2015	RESULTS: HIF-2alpha activated the NAMPT-NAD(+)-SIRT axis in chondrocytes by upregulating NAMPT, which stimulated NAD(+) synthesis and thereby activated SIRT family members.	NAD	40-46	nicotinamide phosphoribosyltransferase	Mus musculus	89-94
26209889-7	2015	RESULTS: HIF-2alpha activated the NAMPT-NAD(+)-SIRT axis in chondrocytes by upregulating NAMPT, which stimulated NAD(+) synthesis and thereby activated SIRT family members.	NAD	113-119	nicotinamide phosphoribosyltransferase	Mus musculus	34-39
26209889-7	2015	RESULTS: HIF-2alpha activated the NAMPT-NAD(+)-SIRT axis in chondrocytes by upregulating NAMPT, which stimulated NAD(+) synthesis and thereby activated SIRT family members.	NAD	113-119	nicotinamide phosphoribosyltransferase	Mus musculus	89-94
26209889-11	2015	CONCLUSION: The reciprocal regulation of HIF-2alpha and the NAMPT-NAD(+)-SIRT axis in articular chondrocytes is involved in OA cartilage destruction caused by HIF-2alpha or NAMPT.	NAD	66-72	nicotinamide phosphoribosyltransferase	Mus musculus	60-65
26209889-11	2015	CONCLUSION: The reciprocal regulation of HIF-2alpha and the NAMPT-NAD(+)-SIRT axis in articular chondrocytes is involved in OA cartilage destruction caused by HIF-2alpha or NAMPT.	NAD	66-72	nicotinamide phosphoribosyltransferase	Mus musculus	173-178
26512921-7	2015	Pyruvic acid and NAD+/NADH levels also changed when miR-29b expression was suppressed; this effect could be blocked by specific AKT inhibitors, suggesting the miR-29b-AKT axis regulates the Warburg effect in ovarian cancer.	NAD	17-21	thymoma viral proto-oncogene 1	Mus musculus	128-131
26512921-7	2015	Pyruvic acid and NAD+/NADH levels also changed when miR-29b expression was suppressed; this effect could be blocked by specific AKT inhibitors, suggesting the miR-29b-AKT axis regulates the Warburg effect in ovarian cancer.	NAD	17-21	thymoma viral proto-oncogene 1	Mus musculus	167-170
26512921-7	2015	Pyruvic acid and NAD+/NADH levels also changed when miR-29b expression was suppressed; this effect could be blocked by specific AKT inhibitors, suggesting the miR-29b-AKT axis regulates the Warburg effect in ovarian cancer.	NAD	22-26	thymoma viral proto-oncogene 1	Mus musculus	128-131
26512921-7	2015	Pyruvic acid and NAD+/NADH levels also changed when miR-29b expression was suppressed; this effect could be blocked by specific AKT inhibitors, suggesting the miR-29b-AKT axis regulates the Warburg effect in ovarian cancer.	NAD	22-26	thymoma viral proto-oncogene 1	Mus musculus	167-170
26498527-4	2015	In the present study, we demonstrated that the hyper-activation of poly(ADP-ribose) polymerase-1 (PARP-1) is closely associated with the depletion of NAD(+) in the small intestine after cisplatin treatment, which results in downregulation of sirtuin1 (SIRT1) activity.	NAD	150-156	poly(ADP-ribose) polymerase 1	Homo sapiens	67-96
26618989-0	2015	Nmnat1-Rbp7 Is a Conserved Fusion-Protein That Combines NAD+ Catalysis of Nmnat1 with Subcellular Localization of Rbp7.	NAD	56-60	retinol binding protein 7a, cellular	Danio rerio	7-11
26618989-0	2015	Nmnat1-Rbp7 Is a Conserved Fusion-Protein That Combines NAD+ Catalysis of Nmnat1 with Subcellular Localization of Rbp7.	NAD	56-60	retinol binding protein 7a, cellular	Danio rerio	114-118
26618989-6	2015	Further, we describe a novel nmnat1-rbp7 transcript encoding a fusion of Rbp7 and the NAD+ (Nicotinamide adenine dinucleotide) synthesizing enzyme Nmnat1.	NAD	86-90	retinol binding protein 7a, cellular	Danio rerio	36-40
26618989-6	2015	Further, we describe a novel nmnat1-rbp7 transcript encoding a fusion of Rbp7 and the NAD+ (Nicotinamide adenine dinucleotide) synthesizing enzyme Nmnat1.	NAD	86-90	retinol binding protein 7a, cellular	Danio rerio	73-77
26618989-6	2015	Further, we describe a novel nmnat1-rbp7 transcript encoding a fusion of Rbp7 and the NAD+ (Nicotinamide adenine dinucleotide) synthesizing enzyme Nmnat1.	NAD	92-125	retinol binding protein 7a, cellular	Danio rerio	36-40
26618989-6	2015	Further, we describe a novel nmnat1-rbp7 transcript encoding a fusion of Rbp7 and the NAD+ (Nicotinamide adenine dinucleotide) synthesizing enzyme Nmnat1.	NAD	92-125	retinol binding protein 7a, cellular	Danio rerio	73-77
26618989-8	2015	Injection experiments in zebrafish further revealed that Nmnat1-Rbp7a and Nmnat1 have similar NAD+ catalyzing activities but a different subcellular localization.	NAD	94-98	retinol binding protein 7a, cellular	Danio rerio	64-69
26618989-9	2015	HPLC measurements and protein localization analysis highlight Nmnat1-Rbp7a as the only known cytoplasmic and presumably endoplasmic reticulum (ER) specific NAD+ catalyzing enzyme.	NAD	156-160	retinol binding protein 7a, cellular	Danio rerio	69-74
26618989-10	2015	These studies, taken together with previously documented NAD+ dependent interaction of RBPs with ER-associated enzymes of retinal catalysis, implicate functions of this newly described NMNAT1-Rbp7 fusion protein in retinol oxidation.	NAD	57-61	retinol binding protein 7a, cellular	Danio rerio	192-196
26498527-4	2015	In the present study, we demonstrated that the hyper-activation of poly(ADP-ribose) polymerase-1 (PARP-1) is closely associated with the depletion of NAD(+) in the small intestine after cisplatin treatment, which results in downregulation of sirtuin1 (SIRT1) activity.	NAD	150-156	poly(ADP-ribose) polymerase 1	Homo sapiens	98-104
26498527-6	2015	However, use of dunnione as a strong substrate for the NADH:quinone oxidoreductase 1 (NQO1) enzyme led to an increase in intracellular NAD(+) levels and prevented the cisplatin-induced small intestinal damage correlating with the modulation of PARP-1, SIRT1, and NF-kappaB.	NAD	135-141	NAD(P)H quinone dehydrogenase 1	Homo sapiens	55-84
26498527-6	2015	However, use of dunnione as a strong substrate for the NADH:quinone oxidoreductase 1 (NQO1) enzyme led to an increase in intracellular NAD(+) levels and prevented the cisplatin-induced small intestinal damage correlating with the modulation of PARP-1, SIRT1, and NF-kappaB.	NAD	135-141	NAD(P)H quinone dehydrogenase 1	Homo sapiens	86-90
26498527-7	2015	These results suggest that direct modulation of cellular NAD(+) levels by pharmacological NQO1 substrates could be a promising therapeutic approach for protecting against cisplatin-induced small intestinal damage.	NAD	57-63	NAD(P)H quinone dehydrogenase 1	Homo sapiens	90-94
26629320-0	2015	Disruption of NAD(+) binding site in glyceraldehyde 3-phosphate dehydrogenase affects its intranuclear interactions.	NAD	14-20	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	37-77
26466337-2	2015	However, alternative electron donors may exist such as cytochrome b5 reductase and cytochrome b5 (CBR and CYB5, respectively) via, which is NADH-dependent and are also anchored to the endoplasmic reticulum.	NAD	140-144	Cyb5p	Saccharomyces cerevisiae S288C	106-110
26629320-7	2015	RESULTS: Using MALDI-TOF analysis, we identified novel phosphorylation sites within the NAD(+) binding center of GAPDH at Y94, S98, and T99.	NAD	88-94	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	113-118
26629320-10	2015	Site-mutagenesis at positions S98 and T99 in the NAD(+) binding center reduced enzymatic activity of GAPDH due to decreased affinity to NAD(+) (Km = 741 +- 257 mumol/L in T99I vs 57 +- 11.1 micromol/L in wild type GAPDH.	NAD	49-55	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	101-106
26629320-10	2015	Site-mutagenesis at positions S98 and T99 in the NAD(+) binding center reduced enzymatic activity of GAPDH due to decreased affinity to NAD(+) (Km = 741 +- 257 mumol/L in T99I vs 57 +- 11.1 micromol/L in wild type GAPDH.	NAD	49-55	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	214-219
26629320-10	2015	Site-mutagenesis at positions S98 and T99 in the NAD(+) binding center reduced enzymatic activity of GAPDH due to decreased affinity to NAD(+) (Km = 741 +- 257 mumol/L in T99I vs 57 +- 11.1 micromol/L in wild type GAPDH.	NAD	136-142	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	101-106
26629320-10	2015	Site-mutagenesis at positions S98 and T99 in the NAD(+) binding center reduced enzymatic activity of GAPDH due to decreased affinity to NAD(+) (Km = 741 +- 257 mumol/L in T99I vs 57 +- 11.1 micromol/L in wild type GAPDH.	NAD	136-142	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	214-219
26629320-11	2015	Molecular modeling experiments revealed the effect of mutations on NAD(+) binding with GAPDH.	NAD	67-73	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	87-92
26629320-12	2015	FRAP (fluorescence recovery after photo bleaching) analysis showed that mutations in NAD(+) binding center of GAPDH abrogated its intranuclear interactions.	NAD	85-91	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	110-115
26629320-13	2015	CONCLUSION: Our results suggest an important functional role of phosphorylated amino acids in the NAD(+) binding center in GAPDH interactions with its intranuclear partners.	NAD	98-104	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	123-128
26702395-6	2015	Additionally, we obtained data suggesting that the reaction catalyzed by the 6-phosphogluconate dehydrogenase is active during growth on glucose, and it also produces NADH.	NAD	167-171	decarboxylating 6-phosphogluconate dehydrogenase	Pseudomonas putida KT2440	77-109
26522369-1	2015	Nicotinamide phosphoribosyltransferase (Nampt) catalyzes the rate-limiting step in the salvage pathway for nicotinamide adenine dinucleotide (NAD(+)) biosynthesis, and thereby regulates the deacetylase activity of sirtuins.	NAD	107-140	nicotinamide phosphoribosyltransferase	Mus musculus	0-38
26522369-1	2015	Nicotinamide phosphoribosyltransferase (Nampt) catalyzes the rate-limiting step in the salvage pathway for nicotinamide adenine dinucleotide (NAD(+)) biosynthesis, and thereby regulates the deacetylase activity of sirtuins.	NAD	142-148	nicotinamide phosphoribosyltransferase	Mus musculus	0-38
25975984-3	2015	Under homeostatic conditions, Nrf2 affects the mitochondrial membrane potential, fatty acid oxidation, availability of substrates (NADH and FADH2/succinate) for respiration, and ATP synthesis.	NAD	131-135	NFE2 like bZIP transcription factor 2	Homo sapiens	30-34
26002966-2	2015	AKR1C34 and AKR1C35 similarly oxidized various xenobiotic alicyclic alcohols using NAD(+), but differed in their substrate specificity for hydroxysteroids and inhibitor sensitivity.	NAD	83-89	aldo-keto reductase family 1 member C13	Mesocricetus auratus	0-7
26124049-1	2015	BACKGROUND: The energy status of the cell is regulated by the energy sensing network constituted by AMP-activated protein kinase (AMPK), the NAD+-dependent type III deacetylase silence information regulator T1 (SIRT1) and peroxisome proliferator-activated receptor-gamma coactivator-1alpha (PGC-1alpha).	NAD	141-145	sirtuin 1	Rattus norvegicus	177-209
26124049-1	2015	BACKGROUND: The energy status of the cell is regulated by the energy sensing network constituted by AMP-activated protein kinase (AMPK), the NAD+-dependent type III deacetylase silence information regulator T1 (SIRT1) and peroxisome proliferator-activated receptor-gamma coactivator-1alpha (PGC-1alpha).	NAD	141-145	sirtuin 1	Rattus norvegicus	211-216
26124049-1	2015	BACKGROUND: The energy status of the cell is regulated by the energy sensing network constituted by AMP-activated protein kinase (AMPK), the NAD+-dependent type III deacetylase silence information regulator T1 (SIRT1) and peroxisome proliferator-activated receptor-gamma coactivator-1alpha (PGC-1alpha).	NAD	141-145	PPARG coactivator 1 alpha	Rattus norvegicus	222-289
26124049-1	2015	BACKGROUND: The energy status of the cell is regulated by the energy sensing network constituted by AMP-activated protein kinase (AMPK), the NAD+-dependent type III deacetylase silence information regulator T1 (SIRT1) and peroxisome proliferator-activated receptor-gamma coactivator-1alpha (PGC-1alpha).	NAD	141-145	PPARG coactivator 1 alpha	Rattus norvegicus	291-301
26058697-4	2015	In this study, we investigated whether mitochondrial NAD(+)-dependent Sirtuin 3 (SIRT3) could mediate the neuroprotective effects of ketone bodies after ischemic stroke.	NAD	53-59	sirtuin 3	Homo sapiens	70-79
26058697-4	2015	In this study, we investigated whether mitochondrial NAD(+)-dependent Sirtuin 3 (SIRT3) could mediate the neuroprotective effects of ketone bodies after ischemic stroke.	NAD	53-59	sirtuin 3	Homo sapiens	81-86
26058697-8	2015	We further showed that ketones" effects were achieved by upregulating NAD(+)-dependent SIRT3 and its downstream substrates forkhead box O3a (FoxO3a) and superoxide dismutase 2 (SOD2) in the penumbra region since knocking down SIRT3 in vitro diminished ketones" beneficial effects.	NAD	70-76	sirtuin 3	Homo sapiens	87-92
26058697-8	2015	We further showed that ketones" effects were achieved by upregulating NAD(+)-dependent SIRT3 and its downstream substrates forkhead box O3a (FoxO3a) and superoxide dismutase 2 (SOD2) in the penumbra region since knocking down SIRT3 in vitro diminished ketones" beneficial effects.	NAD	70-76	forkhead box O3	Homo sapiens	141-147
26058697-8	2015	We further showed that ketones" effects were achieved by upregulating NAD(+)-dependent SIRT3 and its downstream substrates forkhead box O3a (FoxO3a) and superoxide dismutase 2 (SOD2) in the penumbra region since knocking down SIRT3 in vitro diminished ketones" beneficial effects.	NAD	70-76	sirtuin 3	Homo sapiens	226-231
26300330-2	2015	Sirtuin1 (SIRT1), a NAD(+)-dependent class III histone deacetylase, participates in the regulation of cellular inflammation.	NAD	20-26	NAD-dependent protein deacetylase sirtuin-1	Oryctolagus cuniculus	0-8
26300330-2	2015	Sirtuin1 (SIRT1), a NAD(+)-dependent class III histone deacetylase, participates in the regulation of cellular inflammation.	NAD	20-26	NAD-dependent protein deacetylase sirtuin-1	Oryctolagus cuniculus	10-15
26311173-3	2015	Essential to this utilization is the NAD+-dependent dehydrogenase BdhA that converts (R)-3-HB into acetoacetate, a molecule that readily enters central metabolism.	NAD	37-40	3-hydroxybutyrate dehydrogenase	Pseudomonas aeruginosa PAO1	66-70
25896882-0	2015	Secondary NAD+ deficiency in the inherited defect of glutamine synthetase.	NAD	10-14	glutamate-ammonia ligase	Homo sapiens	53-73
26404723-6	2015	Inversion recovery measurements indicate that UDPG, like its diphosphate analogue NAD, has apparent T1 shorter than that of monophosphates (Pi, PMEs, and PDEs) but longer than that of triphosphate ATP, highlighting the significance of the (31)P-(31)P dipolar mechanism in T1 relaxation of polyphosphates.	NAD	82-85	UDP-glucose pyrophosphorylase 2	Homo sapiens	46-50
26393338-3	2015	The mechanistic investigations suggest the involvement of a Co(ii)-Co(i) cycle in the catalysis.	NAD	67-72	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	60-66
26528183-4	2015	These protumoral activities of lactate depend on lactate uptake, a process primarily facilitated by the inward, passive lactate-proton symporter monocarboxylate transporter 1 (MCT1); the conversion of lactate and NAD(+) to pyruvate, NADH and H(+) by lactate dehydrogenase-1 (LDH-1); and a competition between pyruvate and alpha-ketoglutarate that inhibits prolylhydroxylases (PHDs).	NAD	213-219	solute carrier family 16 member 1	Homo sapiens	176-180
26528183-4	2015	These protumoral activities of lactate depend on lactate uptake, a process primarily facilitated by the inward, passive lactate-proton symporter monocarboxylate transporter 1 (MCT1); the conversion of lactate and NAD(+) to pyruvate, NADH and H(+) by lactate dehydrogenase-1 (LDH-1); and a competition between pyruvate and alpha-ketoglutarate that inhibits prolylhydroxylases (PHDs).	NAD	233-237	solute carrier family 16 member 1	Homo sapiens	145-174
26528183-4	2015	These protumoral activities of lactate depend on lactate uptake, a process primarily facilitated by the inward, passive lactate-proton symporter monocarboxylate transporter 1 (MCT1); the conversion of lactate and NAD(+) to pyruvate, NADH and H(+) by lactate dehydrogenase-1 (LDH-1); and a competition between pyruvate and alpha-ketoglutarate that inhibits prolylhydroxylases (PHDs).	NAD	233-237	solute carrier family 16 member 1	Homo sapiens	176-180
26528183-6	2015	In addition to HIF-1, lactate can indeed activate transcription factor nuclear factor-kappaB (NF-kappaB) in these cells, through a mechanism not only depending on PHD inhibition but also on NADH alimenting NAD(P)H oxidases to generate reactive oxygen species (ROS).	NAD	190-194	nuclear factor kappa B subunit 1	Homo sapiens	71-92
26528183-6	2015	In addition to HIF-1, lactate can indeed activate transcription factor nuclear factor-kappaB (NF-kappaB) in these cells, through a mechanism not only depending on PHD inhibition but also on NADH alimenting NAD(P)H oxidases to generate reactive oxygen species (ROS).	NAD	190-194	nuclear factor kappa B subunit 1	Homo sapiens	94-103
26462257-5	2015	ss-Lap is an NADPH:quinone oxidoreductase (NQO1)-bioactivatable drug that leads to NADPH depletion through high levels of reactive oxygen species (ROS) from the futile redox cycling of the drug and subsequently nicotinamide adenine dinucleotide (NAD)+ depletion through poly(ADP ribose) polymerase (PARP) hyperactivation.	NAD	211-244	NAD(P)H quinone dehydrogenase 1	Rattus norvegicus	43-47
26462257-5	2015	ss-Lap is an NADPH:quinone oxidoreductase (NQO1)-bioactivatable drug that leads to NADPH depletion through high levels of reactive oxygen species (ROS) from the futile redox cycling of the drug and subsequently nicotinamide adenine dinucleotide (NAD)+ depletion through poly(ADP ribose) polymerase (PARP) hyperactivation.	NAD	13-16	NAD(P)H quinone dehydrogenase 1	Rattus norvegicus	43-47
26462257-7	2015	As such, ss-lap treatment concurrent with inhibition of glutamine metabolism in mutant KRAS, NQO1 overexpressing PDA leads to massive redox imbalance, extensive DNA damage, rapid PARP-mediated NAD+ consumption, and PDA cell death-features not observed in NQO1-low, wild-type KRAS expressing cells.	NAD	193-197	NAD(P)H quinone dehydrogenase 1	Rattus norvegicus	93-97
26334453-1	2015	The ubiquitary Co(I) complex CoCl(PPh3)3 was found to be a convenient catalyst for the [2 + 2 + 2] cycloaddition of functionalized triynes under mild reaction conditions and devoid of any additional additive, yielding the substituted arene compounds.	NAD	15-20	caveolin 1	Homo sapiens	34-38
26426055-4	2015	Intracellular adenosine diphosphate (ADP)-ribosylation refers to the nicotinamide adenine dinucleotide (NAD+)-dependent modification of proteins with ADP-ribose and is catalyzed by enzymes of the ARTD (ADP-ribosyltransferase diphtheria toxin like, also known as PARP) family as well as some members of the Sirtuin family.	NAD	69-102	poly(ADP-ribose) polymerase 1	Homo sapiens	262-266
25761756-8	2015	While the expression and activity of the NAD(+) dependent deacetylase sirtuin 1, a ChREBP-negative target, were down-regulated in the liver of alcohol-fed mice, they were restored to control levels upon ChREBP silencing.	NAD	41-47	MLX interacting protein-like	Mus musculus	83-89
25761756-8	2015	While the expression and activity of the NAD(+) dependent deacetylase sirtuin 1, a ChREBP-negative target, were down-regulated in the liver of alcohol-fed mice, they were restored to control levels upon ChREBP silencing.	NAD	41-47	MLX interacting protein-like	Mus musculus	203-209
25288139-6	2015	Specifically, deacetylation of histone 3 at lysine 9 (H3K9), through the coordinated action of the NAD+-dependent protein deacetylase sirtuin-6 (SIRT6) and nuclear factor kappa B (NFkappaB), sequesters GR expression leading to disinhibition of CRF.	NAD	99-103	nuclear factor kappa B subunit 1	Homo sapiens	156-178
25288139-6	2015	Specifically, deacetylation of histone 3 at lysine 9 (H3K9), through the coordinated action of the NAD+-dependent protein deacetylase sirtuin-6 (SIRT6) and nuclear factor kappa B (NFkappaB), sequesters GR expression leading to disinhibition of CRF.	NAD	99-103	nuclear factor kappa B subunit 1	Homo sapiens	180-188
26481044-7	2015	These results support a novel, important role for Nampt-mediated NAD(+) biosynthesis in LTD and in the function of GluN2B-containing NMDARs.	NAD	65-71	nicotinamide phosphoribosyltransferase	Mus musculus	50-55
26010430-3	2015	However, the role of sirtuin 6 (SIRT6), a NAD+-dependent nuclear deacetylase, in wound healing specifically under diabetic condition remains unclear.	NAD	42-45	sirtuin 6	Mus musculus	21-30
26010430-3	2015	However, the role of sirtuin 6 (SIRT6), a NAD+-dependent nuclear deacetylase, in wound healing specifically under diabetic condition remains unclear.	NAD	42-45	sirtuin 6	Mus musculus	32-37
26788021-7	2015	A DNA nick sensing enzyme, poly(ADP-ribose) polymerase-1 (PARP-1) becomes activated upon detecting DNA breakage and it cleaves NAD(+) into nicotinamide and ADP-ribose and polymerizes the latter on nuclear acceptor proteins.	NAD	127-133	poly(ADP-ribose) polymerase 1	Homo sapiens	27-56
26788021-7	2015	A DNA nick sensing enzyme, poly(ADP-ribose) polymerase-1 (PARP-1) becomes activated upon detecting DNA breakage and it cleaves NAD(+) into nicotinamide and ADP-ribose and polymerizes the latter on nuclear acceptor proteins.	NAD	127-133	poly(ADP-ribose) polymerase 1	Homo sapiens	58-64
26788021-8	2015	Over-activation of PARP induced by peroxynitrite consumes NAD(+) and consequently ATP decreases, culminating in cell dysfunction, apoptosis or necrosis.	NAD	58-64	poly(ADP-ribose) polymerase 1	Homo sapiens	19-23
26426055-4	2015	Intracellular adenosine diphosphate (ADP)-ribosylation refers to the nicotinamide adenine dinucleotide (NAD+)-dependent modification of proteins with ADP-ribose and is catalyzed by enzymes of the ARTD (ADP-ribosyltransferase diphtheria toxin like, also known as PARP) family as well as some members of the Sirtuin family.	NAD	104-108	poly(ADP-ribose) polymerase 1	Homo sapiens	262-266
26170451-6	2015	Using (32)P-labeled NAD(+) and immunoblotting, we also demonstrate that both subunits of the XPC-RAD23B are poly(ADP-ribosyl)ated by PARP1.	NAD	20-26	poly(ADP-ribose) polymerase 1	Homo sapiens	133-138
26033245-1	2015	Nicotinamide phosphoribosyltransferase (Nampt) is the rate-limiting enzyme for NAD salvage and the abundance of Nampt has been shown to be altered in non-alcoholic fatty liver disease.	NAD	79-82	nicotinamide phosphoribosyltransferase	Mus musculus	40-45
26033245-5	2015	Enhanced NAD levels were associated with deacetylation of p53 and Nfkappab indicating increased activation of Sirt1.	NAD	9-12	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	66-74
25964294-7	2015	Combining Pgp inhibitors with APO866 led to increased intracellular APO866 levels, compounded NAD(+) and ATP shortage, and induced DeltaPsi(m) dissipation.	NAD	94-100	ATP binding cassette subfamily B member 1	Homo sapiens	10-13
26189030-2	2015	Using NAD(+) as a substrate, they poly(ADP-ribosyl)ate TRF1 (regulating lengths of telomeres), NuMA (facilitating mitosis) and axin (in wnt/beta-catenin signalling).	NAD	6-12	telomeric repeat binding factor 1	Homo sapiens	55-59
26189030-2	2015	Using NAD(+) as a substrate, they poly(ADP-ribosyl)ate TRF1 (regulating lengths of telomeres), NuMA (facilitating mitosis) and axin (in wnt/beta-catenin signalling).	NAD	6-12	nuclear mitotic apparatus protein 1	Homo sapiens	95-99
26256392-3	2015	The nicotinamide nucleotide transhydrogenase (Nnt) is considered a key antioxidative enzyme based on its ability to regenerate NADPH from NADH.	NAD	138-142	nicotinamide nucleotide transhydrogenase	Homo sapiens	4-44
26256392-3	2015	The nicotinamide nucleotide transhydrogenase (Nnt) is considered a key antioxidative enzyme based on its ability to regenerate NADPH from NADH.	NAD	138-142	nicotinamide nucleotide transhydrogenase	Homo sapiens	46-49
26256392-4	2015	Here, we show that pathological metabolic demand reverses the direction of the Nnt, consuming NADPH to support NADH and ATP production, but at the cost of NADPH-linked antioxidative capacity.	NAD	111-115	nicotinamide nucleotide transhydrogenase	Homo sapiens	79-82
26209623-2	2015	In response to NAD(+) released from damaged cells during inflammation, ARTC2.2 ADP-ribosylates and thereby gates the P2X7 ion channel.	NAD	15-21	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	117-121
26124278-8	2015	Interestingly, we also observed that gaba mutants display a general disruption in bioenergetics as measured by altered levels of tricarboxylic acid cycle intermediates, NAD(+)/NADH, and ATP levels.	NAD	169-175	Resistant to dieldrin	Drosophila melanogaster	37-41
26114812-7	2015	In Raji cells exposed to compound 1 we evidenced the occurrence of effects usually observed in cancer cells after LDH-A inhibition: reduced lactate production and NAD/NADH ratio, apoptosis.	NAD	163-166	lactate dehydrogenase A	Homo sapiens	114-119
26114812-7	2015	In Raji cells exposed to compound 1 we evidenced the occurrence of effects usually observed in cancer cells after LDH-A inhibition: reduced lactate production and NAD/NADH ratio, apoptosis.	NAD	167-171	lactate dehydrogenase A	Homo sapiens	114-119
26063804-12	2015	We propose that AIF and AMID are previously unidentified mammalian NDH-2 enzymes, whose bioenergetic function could be supplemental NADH oxidation in cells.	NAD	132-136	DExH-box helicase 9	Homo sapiens	67-72
26275361-1	2015	Sirtuin (Sirt) 1 and Sirt 3 are nicotinamide adenine dinucleotide ((+))-dependent protein deacetylases that are important to a number of mitochondrial-related functions; thus, identification of sirtuin activators is important.	NAD	32-65	sirtuin 3	Homo sapiens	21-27
26124278-8	2015	Interestingly, we also observed that gaba mutants display a general disruption in bioenergetics as measured by altered levels of tricarboxylic acid cycle intermediates, NAD(+)/NADH, and ATP levels.	NAD	176-180	Resistant to dieldrin	Drosophila melanogaster	37-41
26152715-0	2015	Metformin Inhibits the Production of Reactive Oxygen Species from NADH:Ubiquinone Oxidoreductase to Limit Induction of Interleukin-1beta (IL-1beta) and Boosts Interleukin-10 (IL-10) in Lipopolysaccharide (LPS)-activated Macrophages.	NAD	66-70	interleukin 1 beta	Homo sapiens	119-136
26152715-0	2015	Metformin Inhibits the Production of Reactive Oxygen Species from NADH:Ubiquinone Oxidoreductase to Limit Induction of Interleukin-1beta (IL-1beta) and Boosts Interleukin-10 (IL-10) in Lipopolysaccharide (LPS)-activated Macrophages.	NAD	66-70	interleukin 1 beta	Homo sapiens	138-146
25964165-5	2015	We now report that DPN treatment in primary hippocampal neurons attenuates soluble Abeta-oligomer induced dendritic mitochondrial fission and reduced mobility.	NAD	19-22	amyloid beta precursor protein	Homo sapiens	83-88
25964165-6	2015	Additionally, Abeta treatment reduced the respiratory reserve capacity of hippocampal neuron and inhibited phosphorylation of Drp1 at its PKA site, which induces excessive mitochondrial fission, and DPN treatment ameliorates these inhibitions.	NAD	199-202	amyloid beta precursor protein	Homo sapiens	14-19
28324552-8	2015	The phosphorylated PK exhibited 40 % reduced activity (PK = 0.2 +- 0.015 muM NADH/min/ml to P-PK = 0.12 +- 0.01 muM NADH/min/ml).	NAD	77-81	AT695_RS09030	Staphylococcus aureus	19-21
28324552-8	2015	The phosphorylated PK exhibited 40 % reduced activity (PK = 0.2 +- 0.015 muM NADH/min/ml to P-PK = 0.12 +- 0.01 muM NADH/min/ml).	NAD	77-81	AT695_RS09030	Staphylococcus aureus	55-57
28324552-8	2015	The phosphorylated PK exhibited 40 % reduced activity (PK = 0.2 +- 0.015 muM NADH/min/ml to P-PK = 0.12 +- 0.01 muM NADH/min/ml).	NAD	116-120	AT695_RS09030	Staphylococcus aureus	19-21
27683589-12	2015	Indeed, cross-regulation of PHO, PKA, TOR and Sch9 pathways was reported to potentially affect NAD+ metabolism; though detailed mechanisms remain unclear.	NAD	95-99	serine/threonine protein kinase SCH9	Saccharomyces cerevisiae S288C	46-50
25881497-1	2015	Clostridium perfringens, a strictly anaerobic microorganism and inhabitant of the human intestine, has been shown to produce an azoreductase enzyme (AzoC), an NADH-dependent flavin oxidoreductase.	NAD	159-163	NAD(P)H quinone dehydrogenase 1	Homo sapiens	128-140
25936797-0	2015	Structural basis for the NAD binding cooperativity and catalytic characteristics of sperm-specific glyceraldehyde-3-phosphate dehydrogenase.	NAD	25-28	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	99-139
25936797-2	2015	We exploited mammalian glyceraldehyde-3-phosphate dehydrogenase as a model protein and examined the structural basis of the NAD(+) cooperative binding exhibited by its homologous isoenzymes: the somatic enzyme (GAPD) and the recombinant sperm-specific enzyme (dN-GAPDS).	NAD	124-130	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	23-63
25936797-2	2015	We exploited mammalian glyceraldehyde-3-phosphate dehydrogenase as a model protein and examined the structural basis of the NAD(+) cooperative binding exhibited by its homologous isoenzymes: the somatic enzyme (GAPD) and the recombinant sperm-specific enzyme (dN-GAPDS).	NAD	124-130	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	211-215
26551700-7	2015	One way by which Nrf2 influences mitochondrial activity is through increasing the availability of substrates (NADH and FADH2) for respiration.	NAD	110-114	NFE2 like bZIP transcription factor 2	Homo sapiens	17-21
25908444-3	2015	SOD2 is activated by sirtuin 3 (SIRT3) through NAD(+)-dependent deacetylation.	NAD	47-53	sirtuin 3	Homo sapiens	21-30
25908444-3	2015	SOD2 is activated by sirtuin 3 (SIRT3) through NAD(+)-dependent deacetylation.	NAD	47-53	sirtuin 3	Homo sapiens	32-37
25940138-0	2015	Acyl-CoA-binding domain containing 3 modulates NAD+ metabolism through activating poly(ADP-ribose) polymerase 1.	NAD	47-51	poly(ADP-ribose) polymerase 1	Homo sapiens	82-111
26200012-6	2015	Further, ERRalpha was required for the regulation of NF-kappaB signaling by controlling p65 acetylation via maintenance of NAD(+) levels and sirtuin 1 activation.	NAD	123-129	estrogen related receptor, alpha	Mus musculus	9-17
26086877-1	2015	BACKGROUND: SIRT4, which is localised in the mitochondria, is one of the least characterised members of the sirtuin family of nicotinamide adenine dinucleotide-dependent enzymes that play key roles in multiple cellular processes such as metabolism, stress response and longevity.	NAD	126-159	sirtuin 4	Homo sapiens	12-17
25940138-4	2015	In the present study, we showed that overexpressed acyl-CoA-binding domain containing 3 (ACBD3), a Golgi-bound protein, significantly reduced cellular NAD(+) content via enhancing PARP1"s polymerase activity and enhancing auto-modification of the enzyme in a DNA damage-independent manner.	NAD	151-157	poly(ADP-ribose) polymerase 1	Homo sapiens	180-185
25940138-7	2015	Taken together, these findings suggest that ACBD3 has prominent impacts on cellular NAD(+) metabolism via regulating PARP1 activation-dependent auto-modification and thus cell metabolism and function.	NAD	84-90	poly(ADP-ribose) polymerase 1	Homo sapiens	117-122
25965594-2	2015	Sirtuin 1 (SIRT1), a nicotinamide adenine dinucleotide NAD(+)-dependent deacetylase, is known to play a role in diabetes-related complications as well as ER-stress.	NAD	21-54	sirtuin 1	Rattus norvegicus	0-9
25965594-2	2015	Sirtuin 1 (SIRT1), a nicotinamide adenine dinucleotide NAD(+)-dependent deacetylase, is known to play a role in diabetes-related complications as well as ER-stress.	NAD	21-54	sirtuin 1	Rattus norvegicus	11-16
26196026-1	2015	BACKGROUND: Phospholipase-associated neurodegeneration (PLAN) caused by PLA2G6 mutations is a recessively inherited disorder with three known phenotypes: the typical infantile onset neuroaxonal dystrophy (INAD); an atypical later onset form (atypical NAD); and the more recently recognized young-onset dystonia-parkinsonism (PLAN-DP).	NAD	206-209	phospholipase A2 group VI	Homo sapiens	72-78
26185373-10	2015	This was concomitant with increased levels of NAD(+) (0.87 +- 0.22 vs 1.195 +- 0.144, P &lt; 0.05) the co-factor necessary for SIRT1 activity, as well as with decreases in ac-FoxO1 expression.	NAD	46-52	sirtuin 1	Rattus norvegicus	127-132
25536389-4	2015	Furthermore, treatment with PJ34 reversed the oleic acid-induced decrease in intracellular NAD concentration, while exogenous NAD protected cells against oleic acid-induced insulin insensitivity.	NAD	126-129	insulin	Homo sapiens	173-180
25536389-0	2015	Effect of NAD on PARP-mediated insulin sensitivity in oleic acid treated hepatocytes.	NAD	10-13	poly(ADP-ribose) polymerase 1	Homo sapiens	17-21
25536389-0	2015	Effect of NAD on PARP-mediated insulin sensitivity in oleic acid treated hepatocytes.	NAD	10-13	insulin	Homo sapiens	31-38
25536389-7	2015	Taken together, these data suggest that NAD depletion by PARP1 activation is essential for the modulation of insulin sensitivity in oleic acid-induced lipotoxicity.	NAD	40-43	poly(ADP-ribose) polymerase 1	Homo sapiens	57-62
25536389-7	2015	Taken together, these data suggest that NAD depletion by PARP1 activation is essential for the modulation of insulin sensitivity in oleic acid-induced lipotoxicity.	NAD	40-43	insulin	Homo sapiens	109-116
25840449-8	2015	The protein expression levels of two nicotinamide adenine dinucleotide (NAD+)-dependent deacetylases, sirtuin 1 and sirtuin 3, were significantly but transiently upregulated 4 but not 24 h after irradiation.	NAD	37-70	sirtuin 3	Homo sapiens	116-125
25840449-8	2015	The protein expression levels of two nicotinamide adenine dinucleotide (NAD+)-dependent deacetylases, sirtuin 1 and sirtuin 3, were significantly but transiently upregulated 4 but not 24 h after irradiation.	NAD	72-75	sirtuin 3	Homo sapiens	116-125
26121691-1	2015	SIRT3 is a key NAD+-dependent protein deacetylase in the mitochondria of mammalian cells, functioning to prevent cell aging and transformation via regulation of mitochondrial metabolic homeostasis.	NAD	15-18	sirtuin 3	Homo sapiens	0-5
26942084-5	2016	PARP enzymes catalytically cleave beta-NAD+ and transfer the ADP-ribose moiety to acceptor proteins, modifying their function.	NAD	34-43	poly(ADP-ribose) polymerase 1	Homo sapiens	0-4
26060246-3	2015	In this study, we investigated the role of Nampt-NAD cascade in brain regeneration after ischemic stroke.	NAD	49-52	nicotinamide phosphoribosyltransferase	Mus musculus	43-48
26060246-10	2015	Knockdown of NAD-dependent deacetylase sirtuin 1 (SIRT1) and SIRT2 inhibited the progrowth action of Nampt-NAD axis, whereas knockdown of SIRT1, SIRT2, and SIRT6 compromised the prodifferentiation effect of Nampt-NAD axis.	NAD	13-16	nicotinamide phosphoribosyltransferase	Mus musculus	101-106
26060246-10	2015	Knockdown of NAD-dependent deacetylase sirtuin 1 (SIRT1) and SIRT2 inhibited the progrowth action of Nampt-NAD axis, whereas knockdown of SIRT1, SIRT2, and SIRT6 compromised the prodifferentiation effect of Nampt-NAD axis.	NAD	13-16	sirtuin 6	Mus musculus	156-161
26060246-10	2015	Knockdown of NAD-dependent deacetylase sirtuin 1 (SIRT1) and SIRT2 inhibited the progrowth action of Nampt-NAD axis, whereas knockdown of SIRT1, SIRT2, and SIRT6 compromised the prodifferentiation effect of Nampt-NAD axis.	NAD	13-16	nicotinamide phosphoribosyltransferase	Mus musculus	207-212
26060246-10	2015	Knockdown of NAD-dependent deacetylase sirtuin 1 (SIRT1) and SIRT2 inhibited the progrowth action of Nampt-NAD axis, whereas knockdown of SIRT1, SIRT2, and SIRT6 compromised the prodifferentiation effect of Nampt-NAD axis.	NAD	107-110	nicotinamide phosphoribosyltransferase	Mus musculus	101-106
26060246-10	2015	Knockdown of NAD-dependent deacetylase sirtuin 1 (SIRT1) and SIRT2 inhibited the progrowth action of Nampt-NAD axis, whereas knockdown of SIRT1, SIRT2, and SIRT6 compromised the prodifferentiation effect of Nampt-NAD axis.	NAD	107-110	sirtuin 6	Mus musculus	156-161
26060246-10	2015	Knockdown of NAD-dependent deacetylase sirtuin 1 (SIRT1) and SIRT2 inhibited the progrowth action of Nampt-NAD axis, whereas knockdown of SIRT1, SIRT2, and SIRT6 compromised the prodifferentiation effect of Nampt-NAD axis.	NAD	107-110	nicotinamide phosphoribosyltransferase	Mus musculus	207-212
26060246-10	2015	Knockdown of NAD-dependent deacetylase sirtuin 1 (SIRT1) and SIRT2 inhibited the progrowth action of Nampt-NAD axis, whereas knockdown of SIRT1, SIRT2, and SIRT6 compromised the prodifferentiation effect of Nampt-NAD axis.	NAD	107-110	nicotinamide phosphoribosyltransferase	Mus musculus	101-106
26060246-10	2015	Knockdown of NAD-dependent deacetylase sirtuin 1 (SIRT1) and SIRT2 inhibited the progrowth action of Nampt-NAD axis, whereas knockdown of SIRT1, SIRT2, and SIRT6 compromised the prodifferentiation effect of Nampt-NAD axis.	NAD	107-110	sirtuin 6	Mus musculus	156-161
26060246-10	2015	Knockdown of NAD-dependent deacetylase sirtuin 1 (SIRT1) and SIRT2 inhibited the progrowth action of Nampt-NAD axis, whereas knockdown of SIRT1, SIRT2, and SIRT6 compromised the prodifferentiation effect of Nampt-NAD axis.	NAD	107-110	nicotinamide phosphoribosyltransferase	Mus musculus	207-212
26060246-11	2015	CONCLUSIONS: Our data demonstrate that the Nampt-NAD cascade may act as a centralizing switch in postischemic regeneration through controlling different sirtuins and therefore represent a promising therapeutic target for long-term recovery of ischemic stroke.	NAD	49-52	nicotinamide phosphoribosyltransferase	Mus musculus	43-48
26125921-4	2015	GAPDH transcript levels were quantified by real-time polymerase chain reaction amplification, and GAPDH activity (assessed by levels of NADH oxidation) was measured by spectrophotometry.	NAD	136-140	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	98-103
25895450-2	2015	Elimination of alcohol dehydrogenase E (adhE), acetate kinase A-phosphotransacetylase (ackA-pta), and lactate dehydrogenase A (ldhA) enzymes allowed BDO production as a primary pathway for NADH re-oxidation, and significantly reduced by-products.	NAD	189-193	alcohol dehydrogenase	Klebsiella oxytoca	15-36
25709099-2	2015	NAD is generated de novo from tryptophan or recycled from NAM through the NAMPT-dependent salvage pathway.	NAD	0-3	SH3 and cysteine rich domain 3	Homo sapiens	58-61
25863291-0	2015	NAD(+)-dependent SIRT1 deactivation has a key role on ischemia-reperfusion-induced apoptosis.	NAD	0-6	sirtuin 1	Rattus norvegicus	17-22
25716654-4	2015	Analysis of downstream targets of the mutations in these two genes showed that the HNRNPA0 mutation affected expression patterns in the PI3 kinase and ERK/MAPK signaling pathways, while the WIF1 variant influenced expression of genes that play a role in NAD biosynthesis.	NAD	254-257	mitogen-activated protein kinase 1	Homo sapiens	151-154
25725292-6	2015	Inhibition of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX) by a pan-NOX inhibitor (VAS-2870) and a specific inhibitor of Rac1 (NSC23766) significantly reduced TNF-alpha/CHX-induced total ROS and cell death levels.	NAD	14-47	tumor necrosis factor	Mus musculus	180-189
26344237-0	2015	Identifying Direct Protein Targets of Poly-ADP-Ribose Polymerases (PARPs) Using Engineered PARP Variants-Orthogonal Nicotinamide Adenine Dinucleotide (NAD+) Analog Pairs.	NAD	116-149	poly(ADP-ribose) polymerase 1	Homo sapiens	67-71
26344237-0	2015	Identifying Direct Protein Targets of Poly-ADP-Ribose Polymerases (PARPs) Using Engineered PARP Variants-Orthogonal Nicotinamide Adenine Dinucleotide (NAD+) Analog Pairs.	NAD	151-155	poly(ADP-ribose) polymerase 1	Homo sapiens	67-71
26344237-5	2015	To address this challenge, we have engineered a PARP variant that efficiently uses an orthogonal NAD+ analog, an analog that endogenous PARPs cannot use, as a substrate for ADP-ribosylation.	NAD	97-101	poly(ADP-ribose) polymerase 1	Homo sapiens	48-52
26344237-6	2015	The protocols in this unit describe a general procedure for using engineered PARP variants-orthogonal NAD+ analog pairs for labeling and identifying the direct targets of the poly-subfamily of PARPs (PARPs 1-3, 5, and 6).	NAD	102-106	poly(ADP-ribose) polymerase 1	Homo sapiens	77-81
26181362-4	2015	PARP1 stimulates TDP1; the stimulation effect was abolished in the presence of NAD(+).	NAD	79-85	poly(ADP-ribose) polymerase 1	Homo sapiens	0-5
25716654-4	2015	Analysis of downstream targets of the mutations in these two genes showed that the HNRNPA0 mutation affected expression patterns in the PI3 kinase and ERK/MAPK signaling pathways, while the WIF1 variant influenced expression of genes that play a role in NAD biosynthesis.	NAD	254-257	mitogen-activated protein kinase 1	Homo sapiens	155-159
25639585-3	2015	The aim of this study was two fold: (1) to establish if the administration of the proinflammatory cytokine interferon-gamma (IFN-gamma) and/or UVB radiation elicits differential KP expression patterns in human fibroblast and keratinocytes; and (2) to evaluate the effect of KP metabolites on intracellular nicotinamide adenine dinucleotide (NAD(+) ) levels, and cell viability.	NAD	306-339	interferon gamma	Homo sapiens	107-123
25639585-3	2015	The aim of this study was two fold: (1) to establish if the administration of the proinflammatory cytokine interferon-gamma (IFN-gamma) and/or UVB radiation elicits differential KP expression patterns in human fibroblast and keratinocytes; and (2) to evaluate the effect of KP metabolites on intracellular nicotinamide adenine dinucleotide (NAD(+) ) levels, and cell viability.	NAD	306-339	interferon gamma	Homo sapiens	125-134
25639585-3	2015	The aim of this study was two fold: (1) to establish if the administration of the proinflammatory cytokine interferon-gamma (IFN-gamma) and/or UVB radiation elicits differential KP expression patterns in human fibroblast and keratinocytes; and (2) to evaluate the effect of KP metabolites on intracellular nicotinamide adenine dinucleotide (NAD(+) ) levels, and cell viability.	NAD	341-349	interferon gamma	Homo sapiens	107-123
25639585-3	2015	The aim of this study was two fold: (1) to establish if the administration of the proinflammatory cytokine interferon-gamma (IFN-gamma) and/or UVB radiation elicits differential KP expression patterns in human fibroblast and keratinocytes; and (2) to evaluate the effect of KP metabolites on intracellular nicotinamide adenine dinucleotide (NAD(+) ) levels, and cell viability.	NAD	341-349	interferon gamma	Homo sapiens	125-134
25788480-7	2015	At variance with prior work in mice, however, NR supplementation, but not PARP-1 inhibition, increased intracellular NAD content in NDUFS1 mutant human fibroblasts.	NAD	117-120	NADH:ubiquinone oxidoreductase core subunit S1	Mus musculus	132-138
25788480-10	2015	Overall, data provide the first evidence that in human cells harboring a mitochondrial respiratory defect exposure to NR or PARP-1, inhibitors activate different signaling pathways that are not invariantly prompted by NAD increases, but equally able to improve energetic derangement.	NAD	218-221	poly(ADP-ribose) polymerase 1	Homo sapiens	124-130
25902503-0	2015	Accessory NUMM (NDUFS6) subunit harbors a Zn-binding site and is essential for biogenesis of mitochondrial complex I. Mitochondrial proton-pumping NADH:ubiquinone oxidoreductase (respiratory complex I) comprises more than 40 polypeptides and contains eight canonical FeS clusters.	NAD	147-151	NADH:ubiquinone oxidoreductase subunit S6	Homo sapiens	16-22
26521446-1	2015	Poly(ADP-ribose)polymerase-1 (PARP-1) plays a significant role in the DNA repair process by catalyzing the transfer of ADP-ribose from NAD+ to its receptors.	NAD	135-139	poly(ADP-ribose) polymerase 1	Homo sapiens	0-28
26521446-1	2015	Poly(ADP-ribose)polymerase-1 (PARP-1) plays a significant role in the DNA repair process by catalyzing the transfer of ADP-ribose from NAD+ to its receptors.	NAD	135-139	poly(ADP-ribose) polymerase 1	Homo sapiens	30-36
26042119-4	2015	Murine T cells express a sensitive splice variant of P2X7 that can be activated either by non-covalent binding of ATP or, in the presence of nicotinamide adenine dinucleotide, by its covalent ADP-ribosylation catalyzed by the ecto-ADP-ribosyltransferase ARTC2.2.	NAD	141-174	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	53-57
25921090-1	2015	Nicotinamide phosphoribosyltransferase (NAMPT), the key NAD(+) biosynthetic enzyme, has two different forms, intra- and extracellular (iNAMPT and eNAMPT), in mammals.	NAD	56-62	nicotinamide phosphoribosyltransferase	Mus musculus	40-45
25921090-5	2015	Adipose tissue-specific Nampt knockout and knockin (ANKO and ANKI) mice show reciprocal changes in circulating eNAMPT, affecting hypothalamic NAD(+)/SIRT1 signaling and physical activity accordingly.	NAD	142-148	nicotinamide phosphoribosyltransferase	Mus musculus	24-29
25921090-7	2015	Furthermore, administration of a NAMPT-neutralizing antibody decreases hypothalamic NAD(+) production, and treating ex vivo hypothalamic explants with purified eNAMPT enhances NAD(+), SIRT1 activity, and neural activation.	NAD	84-90	nicotinamide phosphoribosyltransferase	Mus musculus	33-38
26020938-5	2015	The proposed model involves two DNA damage response proteins, SIRT1 and PARP1, that are each consumers of nicotinamide adenine dinucleotide (NAD), a metabolite involved in oxidation-reduction reactions and in ATP synthesis.	NAD	106-139	poly(ADP-ribose) polymerase 1	Homo sapiens	72-77
26020938-5	2015	The proposed model involves two DNA damage response proteins, SIRT1 and PARP1, that are each consumers of nicotinamide adenine dinucleotide (NAD), a metabolite involved in oxidation-reduction reactions and in ATP synthesis.	NAD	141-144	poly(ADP-ribose) polymerase 1	Homo sapiens	72-77
26020938-6	2015	This model builds on two key findings: 1) that SIRT1 (a protein deacetylase) is involved in both the positive (i.e. transcriptional activation) and negative (i.e. transcriptional repression) arms of the circadian regulation and 2) that PARP1 is a major consumer of NAD during the DNA damage response.	NAD	265-268	poly(ADP-ribose) polymerase 1	Homo sapiens	236-241
26020938-7	2015	In our simulations, we observe that increased PARP1 activity may be able to trigger SIRT1-induced circadian phase advancements by decreasing SIRT1 activity through competition for NAD supplies.	NAD	180-183	poly(ADP-ribose) polymerase 1	Homo sapiens	46-51
26221253-2	2015	SIRT1 (Sir2) is a NAD-dependent deacetylase and is reported to regulate a wide variety of cellular processes including inflammation, aging and lifespan extension.	NAD	18-21	sirtuin 1	Rattus norvegicus	0-5
26221253-2	2015	SIRT1 (Sir2) is a NAD-dependent deacetylase and is reported to regulate a wide variety of cellular processes including inflammation, aging and lifespan extension.	NAD	18-21	sirtuin 1	Rattus norvegicus	7-11
25767076-10	2015	Oxaliplatin treatment resulted in poly(ADP-ribose) polymerase-1 (PARP-1) overactivation, as indicated by the increase of poly(ADP-ribose) (PAR), which led to NAD(+) and ATP depletion.	NAD	158-164	poly(ADP-ribose) polymerase 1	Homo sapiens	65-71
25684751-1	2015	Nicotinamide phosphoribosyltransferase (NAMPT) is the key enzyme in the biosynthesis of nicotinamide adenine dinucleotide (NAD).	NAD	88-121	nicotinamide phosphoribosyltransferase	Mus musculus	40-45
25870284-6	2015	Biochemical assays using mutant forms of GAPDH with either reduced activity or reduced affinity to SRR revealed that GAPDH suppresses SRR activity by direct binding to GAPDH and through NADH, a product of GAPDH.	NAD	186-190	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	41-46
25870284-6	2015	Biochemical assays using mutant forms of GAPDH with either reduced activity or reduced affinity to SRR revealed that GAPDH suppresses SRR activity by direct binding to GAPDH and through NADH, a product of GAPDH.	NAD	186-190	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	117-122
25870284-6	2015	Biochemical assays using mutant forms of GAPDH with either reduced activity or reduced affinity to SRR revealed that GAPDH suppresses SRR activity by direct binding to GAPDH and through NADH, a product of GAPDH.	NAD	186-190	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	117-122
25870284-6	2015	Biochemical assays using mutant forms of GAPDH with either reduced activity or reduced affinity to SRR revealed that GAPDH suppresses SRR activity by direct binding to GAPDH and through NADH, a product of GAPDH.	NAD	186-190	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	117-122
25323584-2	2015	Axons depend on the activity of the central enzyme in NAD biosynthesis, nicotinamide mononucleotide adenylyltransferase 2 (NMNAT2), for their maintenance and degenerate rapidly when this activity is lost.	NAD	54-57	nicotinamide nucleotide adenylyltransferase 2	Homo sapiens	72-121
25323584-2	2015	Axons depend on the activity of the central enzyme in NAD biosynthesis, nicotinamide mononucleotide adenylyltransferase 2 (NMNAT2), for their maintenance and degenerate rapidly when this activity is lost.	NAD	54-57	nicotinamide nucleotide adenylyltransferase 2	Homo sapiens	123-129
25660995-3	2015	Poly(ADP-ribosyl)ation (PARylation), a NAD-dependent protein modification carried out by poly(ADP-ribose) polymerase (PARP) enzymes recently emerged as a new regulatory mechanism fine-tuning osteoblast differentiation and mineralization.	NAD	39-42	poly(ADP-ribose) polymerase 1	Homo sapiens	89-116
25660995-3	2015	Poly(ADP-ribosyl)ation (PARylation), a NAD-dependent protein modification carried out by poly(ADP-ribose) polymerase (PARP) enzymes recently emerged as a new regulatory mechanism fine-tuning osteoblast differentiation and mineralization.	NAD	39-42	poly(ADP-ribose) polymerase 1	Homo sapiens	118-122
25849131-2	2015	One process that is considered a key feature of resveratrol action is the activation of the nicotinamide adenine dinucleotide (NAD(+))-dependent deacetylase sirtuin 1 (SIRT1) in various tissues.	NAD	92-125	sirtuin 1	Rattus norvegicus	168-173
25849131-2	2015	One process that is considered a key feature of resveratrol action is the activation of the nicotinamide adenine dinucleotide (NAD(+))-dependent deacetylase sirtuin 1 (SIRT1) in various tissues.	NAD	127-134	sirtuin 1	Rattus norvegicus	168-173
25908823-0	2015	SARM1 activation triggers axon degeneration locally via NAD+ destruction.	NAD	56-60	sterile alpha and HEAT/Armadillo motif containing 1	Mus musculus	0-5
25908823-3	2015	We report that SARM1 initiates a local destruction program involving rapid breakdown of nicotinamide adenine dinucleotide (NAD(+)) after injury.	NAD	88-121	sterile alpha and HEAT/Armadillo motif containing 1	Mus musculus	15-20
25908823-3	2015	We report that SARM1 initiates a local destruction program involving rapid breakdown of nicotinamide adenine dinucleotide (NAD(+)) after injury.	NAD	123-129	sterile alpha and HEAT/Armadillo motif containing 1	Mus musculus	15-20
25908823-6	2015	Formation of the SARM1 TIR dimer triggered rapid breakdown of NAD(+), whereas SARM1-induced axon destruction could be counteracted by increased NAD(+) synthesis.	NAD	62-68	sterile alpha and HEAT/Armadillo motif containing 1	Mus musculus	17-22
25908823-6	2015	Formation of the SARM1 TIR dimer triggered rapid breakdown of NAD(+), whereas SARM1-induced axon destruction could be counteracted by increased NAD(+) synthesis.	NAD	144-150	sterile alpha and HEAT/Armadillo motif containing 1	Mus musculus	78-83
25908823-7	2015	SARM1-induced depletion of NAD(+) may explain the potent axon protection in Wallerian degeneration slow (Wld(s)) mutant mice.	NAD	27-33	sterile alpha and HEAT/Armadillo motif containing 1	Mus musculus	0-5
25684751-1	2015	Nicotinamide phosphoribosyltransferase (NAMPT) is the key enzyme in the biosynthesis of nicotinamide adenine dinucleotide (NAD).	NAD	123-126	nicotinamide phosphoribosyltransferase	Mus musculus	40-45
25755250-0	2015	SIRT3-dependent GOT2 acetylation status affects the malate-aspartate NADH shuttle activity and pancreatic tumor growth.	NAD	69-73	sirtuin 3	Homo sapiens	0-5
25925963-7	2015	Moreover, we found that OSC-related decrease in NAD(+) amounts among middle-aged rats is associated to increased NADPH levels and SIRT1 activity.	NAD	48-54	sirtuin 1	Rattus norvegicus	130-135
26131100-1	2015	SIRT3 is a member of the NAD+-dependent class III deacetylase sirtuin family and plays pivotal roles in regulating cellular functions.	NAD	25-29	sirtuin 3	Homo sapiens	0-5
25925963-8	2015	In contrast, we associated OSC-related decrease in NAD(+) amounts among young rats to decreased NADPH levels and increased SIRT1 activity.	NAD	51-57	sirtuin 1	Rattus norvegicus	123-128
25712525-6	2015	We focused on heat shock protein 70 (HSP70) because NAD(+)/ATP depletion does not directly cause apoptosis, and HSP70 can inhibit the activation of caspase-9 or caspase-3 by preventing apoptosome formation or cytochrome C release.	NAD	52-58	heat shock protein 1B	Mus musculus	14-35
25876076-0	2015	Nutritional energy stimulates NAD+ production to promote tankyrase-mediated PARsylation in insulinoma cells.	NAD	30-34	tankyrase	Homo sapiens	57-66
25876076-2	2015	This TNKS activity uses NAD+ as a co-substrate to post-translationally modify various acceptor proteins including TNKS itself.	NAD	24-28	tankyrase	Homo sapiens	5-9
25876076-2	2015	This TNKS activity uses NAD+ as a co-substrate to post-translationally modify various acceptor proteins including TNKS itself.	NAD	24-28	tankyrase	Homo sapiens	114-118
25876076-4	2015	Whether this TNKS activity is regulated by physiological changes in NAD+ levels or, more broadly, in cellular energy charge has not been investigated.	NAD	68-72	tankyrase	Homo sapiens	13-17
25876076-5	2015	Because the NAD+ biosynthetic enzyme nicotinamide phosphoribosyltransferase (NAMPT) in vitro is robustly potentiated by ATP, we hypothesized that nutritional energy might stimulate cellular NAMPT to produce NAD+ and thereby augment TNKS catalysis.	NAD	12-16	tankyrase	Homo sapiens	232-236
32262409-2	2015	In the presence of nicotinamide adenine dinucleotide as a cofactor, oxaloacetic acid is converted by malate dehydrogenase into l-malic acid.	NAD	19-52	malic enzyme 2	Homo sapiens	101-121
25876076-7	2015	This glucose effect on TNKS is mediated primarily by NAD+ since it is mirrored by the NAD+ precursor nicotinamide mononucleotide (NMN), and is blunted by the NAMPT inhibitor FK866.	NAD	53-57	tankyrase	Homo sapiens	23-27
25876076-7	2015	This glucose effect on TNKS is mediated primarily by NAD+ since it is mirrored by the NAD+ precursor nicotinamide mononucleotide (NMN), and is blunted by the NAMPT inhibitor FK866.	NAD	86-90	tankyrase	Homo sapiens	23-27
25876076-10	2015	Collectively our data uncover a metabolic pathway whereby nutritional energy augments NAD+ production to drive the PARsylating activity of TNKS, leading to autoPARsylation-dependent degradation of the TNKS protein.	NAD	86-90	tankyrase	Homo sapiens	139-143
25876076-10	2015	Collectively our data uncover a metabolic pathway whereby nutritional energy augments NAD+ production to drive the PARsylating activity of TNKS, leading to autoPARsylation-dependent degradation of the TNKS protein.	NAD	86-90	tankyrase	Homo sapiens	201-205
25722455-3	2015	METHODS AND RESULTS: In cultured primary human endothelial cells, genetic targeting of CypD using siRNA or shRNA resulted in a constitutive increase in mitochondrial matrix Ca(2+) and reduced nicotinamide adenine dinucleotide (NADH).	NAD	192-225	peptidylprolyl isomerase F	Homo sapiens	87-91
25722455-3	2015	METHODS AND RESULTS: In cultured primary human endothelial cells, genetic targeting of CypD using siRNA or shRNA resulted in a constitutive increase in mitochondrial matrix Ca(2+) and reduced nicotinamide adenine dinucleotide (NADH).	NAD	227-231	peptidylprolyl isomerase F	Homo sapiens	87-91
25722455-8	2015	The NAD(+) precursor nicotinamide mononucleotide restored the cellular NAD(+)/NADH ratio and normalized the CypD-deficient phenotype.	NAD	4-10	peptidylprolyl isomerase F (cyclophilin F)	Mus musculus	108-112
25712525-6	2015	We focused on heat shock protein 70 (HSP70) because NAD(+)/ATP depletion does not directly cause apoptosis, and HSP70 can inhibit the activation of caspase-9 or caspase-3 by preventing apoptosome formation or cytochrome C release.	NAD	52-58	heat shock protein 1B	Mus musculus	37-42
26085945-2	2015	Full-atom models of lactate dehydrogenase A (in complex with NADH and in the apo form) have been generated to enable structure-based design of novel inhibitors competing with pyruvate and NADH.	NAD	61-65	lactate dehydrogenase A	Homo sapiens	20-43
26085945-2	2015	Full-atom models of lactate dehydrogenase A (in complex with NADH and in the apo form) have been generated to enable structure-based design of novel inhibitors competing with pyruvate and NADH.	NAD	188-192	lactate dehydrogenase A	Homo sapiens	20-43
25533949-4	2015	Resveratrol nullifies the catalytic activity and redirects TyrRS to a nuclear function, stimulating NAD(+)-dependent auto-poly-ADP-ribosylation of poly(ADP-ribose) polymerase 1 (PARP1).	NAD	100-106	poly(ADP-ribose) polymerase 1	Homo sapiens	147-176
25128692-0	2015	NAD-dependent ADP-ribosylation of the human antimicrobial and immune-modulatory peptide LL-37 by ADP-ribosyltransferase-1.	NAD	0-3	cathelicidin antimicrobial peptide	Homo sapiens	88-93
25128692-0	2015	NAD-dependent ADP-ribosylation of the human antimicrobial and immune-modulatory peptide LL-37 by ADP-ribosyltransferase-1.	NAD	0-3	ADP-ribosyltransferase 1	Homo sapiens	97-121
25128692-2	2015	Here we show that the mammalian mono-ADP-ribosyltransferase-1 (ART1), which selectively transfers the ADP-ribose moiety from NAD to arginine residues, ADP-ribosylates LL-37 in vitro.	NAD	125-128	ADP-ribosyltransferase 1	Homo sapiens	32-61
25128692-2	2015	Here we show that the mammalian mono-ADP-ribosyltransferase-1 (ART1), which selectively transfers the ADP-ribose moiety from NAD to arginine residues, ADP-ribosylates LL-37 in vitro.	NAD	125-128	ADP-ribosyltransferase 1	Homo sapiens	63-67
25128692-2	2015	Here we show that the mammalian mono-ADP-ribosyltransferase-1 (ART1), which selectively transfers the ADP-ribose moiety from NAD to arginine residues, ADP-ribosylates LL-37 in vitro.	NAD	125-128	cathelicidin antimicrobial peptide	Homo sapiens	167-172
25128692-4	2015	Mass-spectrometry showed that up to four of the five arginine residues present in LL-37 could be ADP-ribosylated on the same peptide when incubated at a high NAD concentration in the presence of ART1.	NAD	158-161	cathelicidin antimicrobial peptide	Homo sapiens	82-87
25128692-4	2015	Mass-spectrometry showed that up to four of the five arginine residues present in LL-37 could be ADP-ribosylated on the same peptide when incubated at a high NAD concentration in the presence of ART1.	NAD	158-161	ADP-ribosyltransferase 1	Homo sapiens	195-199
25798922-1	2015	SIRT1 is a NAD+-dependent deacetylase thought to regulate cellular metabolic pathways in response to alterations in nutrient flux.	NAD	11-15	sirtuin 1	Rattus norvegicus	0-5
25635049-6	2015	The crystal structure of the PARP homology domain of PARP13 shows obstruction of the canonical active site, precluding NAD(+) binding.	NAD	119-125	poly(ADP-ribose) polymerase 1	Homo sapiens	29-33
25533949-4	2015	Resveratrol nullifies the catalytic activity and redirects TyrRS to a nuclear function, stimulating NAD(+)-dependent auto-poly-ADP-ribosylation of poly(ADP-ribose) polymerase 1 (PARP1).	NAD	100-106	poly(ADP-ribose) polymerase 1	Homo sapiens	178-183
25533949-5	2015	Downstream activation of key stress signalling pathways are causally connected to TyrRS-PARP1-NAD(+) collaboration.	NAD	94-100	poly(ADP-ribose) polymerase 1	Homo sapiens	88-93
25595186-5	2015	The encoded protein domains of WWOX are conserved through evolution (between humans and Drosophila melanogaster) and include WW domains, an NAD -binding site, short-chain dehydrogenase/reductase enzyme and nuclear compartmentalization signals.	NAD	140-143	WW domain containing oxidoreductase	Homo sapiens	31-35
24681946-8	2015	Moreover, a pharmacological agent that increased the intracellular NAD(+)/NADH ratio led to the degradation of HIF-1alpha by increasing SIRT2-mediated deacetylation and subsequent hydroxylation.	NAD	67-73	hypoxia inducible factor 1 subunit alpha	Homo sapiens	111-121
24681946-8	2015	Moreover, a pharmacological agent that increased the intracellular NAD(+)/NADH ratio led to the degradation of HIF-1alpha by increasing SIRT2-mediated deacetylation and subsequent hydroxylation.	NAD	74-78	hypoxia inducible factor 1 subunit alpha	Homo sapiens	111-121
25596911-6	2015	The rate of synthesis of NAD and niacin from tryptophan oxidation depends on the induction of the enzyme indoleamine 2,3-dioxygenase (IDO) by pro-inflammatory cytokines such as interferon-gamma.	NAD	25-28	interferon gamma	Homo sapiens	177-193
25534702-9	2015	This study identifies nicotinamide adenine dinucleotide phosphate oxidase-4-dependent upregulation of Nrf2 as an important endogenous protective pathway that limits mitochondrial damage and apoptosis-inducing factor-related cell death in the heart under hemodynamic overload.	NAD	22-55	nuclear factor, erythroid derived 2, like 2	Mus musculus	102-106
25425164-4	2015	In the presence of NADH, mARC proteins exert N-reductive activity together with the two electron transport proteins cytochrome b5 type B and NADH cytochrome b5 reductase.	NAD	19-23	cytochrome b5 type B	Homo sapiens	116-136
25411384-8	2015	Sirt-1 activity could be reestablished by treatment with NAD(+), silencing NOX4, and poly (ADP-ribose) polymerase-1 (PARP-1) blockade, or with theobromine.	NAD	57-63	sirtuin 1	Rattus norvegicus	0-6
25881554-2	2015	Under oxidative stress conditions PARP-1 activity increases, leading to an accumulation of ADP-ribose polymers and NAD(+) depletion, that induces energy crisis and finally cell death.	NAD	115-121	poly(ADP-ribose) polymerase 1	Homo sapiens	34-40
25549802-1	2015	Poly(ADP-ribose) polymerase 1 (PARP-1) is a key eukaryotic enzyme,catalyzing the NAD+ dependent poly(ADP-ribosyl)ation of protein substrates, crucial for major DNA repair pathways, and involved in other fundamental cellular processes, such as transcription, cell cycle control, and apoptosis.	NAD	81-85	poly(ADP-ribose) polymerase 1	Homo sapiens	0-29
25549802-1	2015	Poly(ADP-ribose) polymerase 1 (PARP-1) is a key eukaryotic enzyme,catalyzing the NAD+ dependent poly(ADP-ribosyl)ation of protein substrates, crucial for major DNA repair pathways, and involved in other fundamental cellular processes, such as transcription, cell cycle control, and apoptosis.	NAD	81-85	poly(ADP-ribose) polymerase 1	Homo sapiens	31-37
25684941-11	2015	The elevated SIRT1 activity in presence of TMZ can be attributed to the enhanced NAMPT protein and NAD(+)/NADH levels.	NAD	99-105	sirtuin 1	Rattus norvegicus	13-18
25684941-11	2015	The elevated SIRT1 activity in presence of TMZ can be attributed to the enhanced NAMPT protein and NAD(+)/NADH levels.	NAD	106-110	sirtuin 1	Rattus norvegicus	13-18
24681949-0	2015	Regulation of the mitogen-activated protein kinase kinase (MEK)-1 by NAD(+)-dependent deacetylases.	NAD	69-75	mitogen-activated protein kinase kinase 7	Homo sapiens	18-57
24681949-0	2015	Regulation of the mitogen-activated protein kinase kinase (MEK)-1 by NAD(+)-dependent deacetylases.	NAD	69-75	mitogen-activated protein kinase kinase 7	Homo sapiens	59-62
25411384-12	2015	These results suggest that in diabetes mellitus, Sirt-1 activity is reduced by PARP-1 activation and NAD(+) depletion due to low AMPK, which increases NOX4 expression, leading to ECM accumulation mediated by transforming growth factor (TGF)-beta1 signaling.	NAD	101-107	sirtuin 1	Rattus norvegicus	49-55
25411384-12	2015	These results suggest that in diabetes mellitus, Sirt-1 activity is reduced by PARP-1 activation and NAD(+) depletion due to low AMPK, which increases NOX4 expression, leading to ECM accumulation mediated by transforming growth factor (TGF)-beta1 signaling.	NAD	101-107	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	129-133
25834895-0	2010	Discovery of two small molecule inhibitors, ML387 and ML388, of human NAD(+)-dependent 15-hydroxyprostaglandin dehydrogenase The central role of hydroxyprostaglandin dehydrogenase(HPGD) is to inactivate prostaglandins such as prostaglandin E2 (PGE2) or prostaglandin D2 (PGD2).	NAD	70-76	prostaglandin D2 synthase	Homo sapiens	253-269
25664730-1	2015	Lactate dehydrogenase (LDH) is an essential metabolic enzyme that catalyzes the interconversion of pyruvate and lactate using NADH/NAD(+) as a co-substrate.	NAD	126-130	lactate dehydrogenase A	Homo sapiens	23-26
25664730-1	2015	Lactate dehydrogenase (LDH) is an essential metabolic enzyme that catalyzes the interconversion of pyruvate and lactate using NADH/NAD(+) as a co-substrate.	NAD	131-137	lactate dehydrogenase A	Homo sapiens	23-26
25664730-4	2015	The X-ray crystal structures of LDHA in complex with each inhibitor were determined; both inhibitors bind to a site overlapping with the NADH-binding site.	NAD	137-141	lactate dehydrogenase A	Homo sapiens	32-36
25664730-5	2015	Further, an apo LDHA crystal structure solved in a new space group is reported, as well as a complex with both NADH and the substrate analogue oxalate bound in seven of the eight molecules and an oxalate only bound in the eighth molecule in the asymmetric unit.	NAD	111-115	lactate dehydrogenase A	Homo sapiens	16-20
25590809-3	2015	beta-Lap is bioactivated by NADPH:quinone oxidoreductase 1 (NQO1) in a futile redox cycle that consumes oxygen and generates high levels of reactive oxygen species (ROS) that cause extensive DNA damage and rapid PARP1-mediated NAD(+) consumption.	NAD	227-233	NAD(P)H quinone dehydrogenase 1	Homo sapiens	28-58
25694965-5	2015	RESULTS: We observed a 47% and 26% decrease in the NADH redox in Bcl-2 deficient lungs, Bcl-2 -/- and Bcl-2 VE-cad, respectively.	NAD	51-55	B cell leukemia/lymphoma 2	Mus musculus	65-70
25694965-5	2015	RESULTS: We observed a 47% and 26% decrease in the NADH redox in Bcl-2 deficient lungs, Bcl-2 -/- and Bcl-2 VE-cad, respectively.	NAD	51-55	B cell leukemia/lymphoma 2	Mus musculus	88-93
25694965-5	2015	RESULTS: We observed a 47% and 26% decrease in the NADH redox in Bcl-2 deficient lungs, Bcl-2 -/- and Bcl-2 VE-cad, respectively.	NAD	51-55	B cell leukemia/lymphoma 2	Mus musculus	88-93
25694965-5	2015	RESULTS: We observed a 47% and 26% decrease in the NADH redox in Bcl-2 deficient lungs, Bcl-2 -/- and Bcl-2 VE-cad, respectively.	NAD	51-55	cadherin 5	Mus musculus	108-114
26246802-1	2015	Lactate dehydrogenase A (LDHA) is the enzyme that converts pyruvate to lactate and oxidizes the reduced form of nicotinamide adenine dinucleotide (NADH) to NAD+.	NAD	112-145	lactate dehydrogenase A	Homo sapiens	0-23
26246802-1	2015	Lactate dehydrogenase A (LDHA) is the enzyme that converts pyruvate to lactate and oxidizes the reduced form of nicotinamide adenine dinucleotide (NADH) to NAD+.	NAD	112-145	lactate dehydrogenase A	Homo sapiens	25-29
26246802-1	2015	Lactate dehydrogenase A (LDHA) is the enzyme that converts pyruvate to lactate and oxidizes the reduced form of nicotinamide adenine dinucleotide (NADH) to NAD+.	NAD	147-151	lactate dehydrogenase A	Homo sapiens	0-23
26246802-1	2015	Lactate dehydrogenase A (LDHA) is the enzyme that converts pyruvate to lactate and oxidizes the reduced form of nicotinamide adenine dinucleotide (NADH) to NAD+.	NAD	147-151	lactate dehydrogenase A	Homo sapiens	25-29
26246802-1	2015	Lactate dehydrogenase A (LDHA) is the enzyme that converts pyruvate to lactate and oxidizes the reduced form of nicotinamide adenine dinucleotide (NADH) to NAD+.	NAD	156-160	lactate dehydrogenase A	Homo sapiens	0-23
26246802-1	2015	Lactate dehydrogenase A (LDHA) is the enzyme that converts pyruvate to lactate and oxidizes the reduced form of nicotinamide adenine dinucleotide (NADH) to NAD+.	NAD	156-160	lactate dehydrogenase A	Homo sapiens	25-29
24469059-4	2015	Using a focused RNA interference library for genes involved in epigenetic regulation, we identify sirtuin2 (SIRT2), an NAD(+)-dependent deacetylase, as a modulator of the response to EGFR inhibitors in colon and lung cancer.	NAD	119-125	epidermal growth factor receptor	Homo sapiens	183-187
25590809-2	2015	Reducing NAD(+) pools by inhibiting NAMPT primed pancreatic ductal adenocarcinoma (PDA) cells for poly(ADP ribose) polymerase (PARP1)-dependent cell death induced by the targeted cancer therapeutic, beta-lapachone (beta-lap, ARQ761), independent of poly(ADP ribose) (PAR) accumulation.	NAD	9-15	poly(ADP-ribose) polymerase 1	Homo sapiens	98-125
25590809-2	2015	Reducing NAD(+) pools by inhibiting NAMPT primed pancreatic ductal adenocarcinoma (PDA) cells for poly(ADP ribose) polymerase (PARP1)-dependent cell death induced by the targeted cancer therapeutic, beta-lapachone (beta-lap, ARQ761), independent of poly(ADP ribose) (PAR) accumulation.	NAD	9-15	poly(ADP-ribose) polymerase 1	Homo sapiens	127-132
25590809-3	2015	beta-Lap is bioactivated by NADPH:quinone oxidoreductase 1 (NQO1) in a futile redox cycle that consumes oxygen and generates high levels of reactive oxygen species (ROS) that cause extensive DNA damage and rapid PARP1-mediated NAD(+) consumption.	NAD	227-233	NAD(P)H quinone dehydrogenase 1	Homo sapiens	60-64
25590809-9	2015	The concept of reducing NAD(+) pools in cancer cells to sensitize them to ROS-mediated cell death by beta-lap is a novel strategy with potential application for pancreatic and other types of NQO1+ solid tumors.	NAD	24-30	NAD(P)H quinone dehydrogenase 1	Homo sapiens	191-195
25568071-5	2015	Biophysical studies revealed that 4-hydroxy-2-pyridones bound specifically to InhA in an NADH (reduced form of nicotinamide adenine dinucleotide)-dependent manner and blocked the enoyl substrate-binding pocket.	NAD	89-93	inhibin alpha	Mus musculus	78-82
25568071-5	2015	Biophysical studies revealed that 4-hydroxy-2-pyridones bound specifically to InhA in an NADH (reduced form of nicotinamide adenine dinucleotide)-dependent manner and blocked the enoyl substrate-binding pocket.	NAD	111-144	inhibin alpha	Mus musculus	78-82
26584302-1	2015	BACKGROUND/AIMS: Adenosine diphosphate ribose (ADPR), a product of beta-NAD+ metabolism generated by the multifunctional enzyme CD38, is recognized as a novel signaling molecule.	NAD	67-76	CD38 molecule	Rattus norvegicus	128-132
25404738-1	2015	We reported that NAD(+)-dependent SIRT1, RELB, and SIRT6 nuclear proteins in monocytes regulate a switch from the glycolysis-dependent acute inflammatory response to fatty acid oxidation-dependent sepsis adaptation.	NAD	17-23	RELB proto-oncogene, NF-kB subunit	Homo sapiens	41-45
25048519-6	2015	Our working hypothesis, to be discussed and partially tested herein, is that CD38, and likely BST1/CD157--both NAD(+) -consuming enzymes, are active in the myeloma niche and lead a discontinuous chain of ectoenzymes whose final products are exploited by the neoplastic plasma cell as part of its local survival strategy.	NAD	111-117	bone marrow stromal cell antigen 1	Homo sapiens	94-98
25048519-6	2015	Our working hypothesis, to be discussed and partially tested herein, is that CD38, and likely BST1/CD157--both NAD(+) -consuming enzymes, are active in the myeloma niche and lead a discontinuous chain of ectoenzymes whose final products are exploited by the neoplastic plasma cell as part of its local survival strategy.	NAD	111-117	bone marrow stromal cell antigen 1	Homo sapiens	99-104
26558285-5	2015	Finally, low sirtuin-1 and sirtuin-3 gene expressions due to higher NADH/NAD in Cmah-null mice decreased Foxo-1 and MnSOD gene expression, suggesting that oxidative stress may result in mitochondrial dysfunction in Cmah-null mouse.	NAD	68-72	superoxide dismutase 2, mitochondrial	Mus musculus	116-121
26558285-5	2015	Finally, low sirtuin-1 and sirtuin-3 gene expressions due to higher NADH/NAD in Cmah-null mice decreased Foxo-1 and MnSOD gene expression, suggesting that oxidative stress may result in mitochondrial dysfunction in Cmah-null mouse.	NAD	68-71	superoxide dismutase 2, mitochondrial	Mus musculus	116-121
24951727-3	2015	beta-Lapachone (betaL) increases the cellular NAD(+)/NADH ratio by activating NAD(P)H: quinone oxidoreductase 1 (NQO1).	NAD	46-52	NAD(P)H quinone dehydrogenase 1	Rattus norvegicus	78-111
24951727-3	2015	beta-Lapachone (betaL) increases the cellular NAD(+)/NADH ratio by activating NAD(P)H: quinone oxidoreductase 1 (NQO1).	NAD	46-52	NAD(P)H quinone dehydrogenase 1	Rattus norvegicus	113-117
24951727-3	2015	beta-Lapachone (betaL) increases the cellular NAD(+)/NADH ratio by activating NAD(P)H: quinone oxidoreductase 1 (NQO1).	NAD	53-57	NAD(P)H quinone dehydrogenase 1	Rattus norvegicus	78-111
24951727-3	2015	beta-Lapachone (betaL) increases the cellular NAD(+)/NADH ratio by activating NAD(P)H: quinone oxidoreductase 1 (NQO1).	NAD	53-57	NAD(P)H quinone dehydrogenase 1	Rattus norvegicus	113-117
25766524-1	2015	BACKGROUND: SIRT1, which belongs to the Sirtuin family of NAD-dependent enzymes, plays diverse roles in aging, metabolism, and disease biology.	NAD	58-61	sirtuin 1	Rattus norvegicus	12-17
25048544-5	2015	ADP-ribosylation of P2X7 in the presence of low micromolar extracellular NAD(+) induces long-lasting P2X7 activation and triggers cell death.	NAD	73-79	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	20-24
26080611-2	2015	PARP-1 usually uses NAD+ as a donor of ADP-ribose units to regulate the synthesis of poly(ADP-ribose).	NAD	20-24	poly(ADP-ribose) polymerase 1	Homo sapiens	0-6
25048544-8	2015	This review will highlight the recent discoveries on the in vivo role of the ARTC2.2/P2X7 pathway triggered by the endogenous release of extracellular NAD(+), the relative sensitivity of lymphocytes subsets to this regulatory pathway and its pharmacological manipulation using camelid-derived ARTC2.2-blocking nanobodies.	NAD	151-157	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	85-89
25048544-5	2015	ADP-ribosylation of P2X7 in the presence of low micromolar extracellular NAD(+) induces long-lasting P2X7 activation and triggers cell death.	NAD	73-79	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	101-105
26180598-2	2015	Hyperglycemia decreases NAD(+) levels by activation of the polyol pathway and by overactivation of poly(ADP-ribose)-polymerase (PARP).	NAD	24-30	poly(ADP-ribose) polymerase 1	Homo sapiens	99-126
25918543-5	2015	Theoretical molecular docking studies of hLDH-A indicate that PGG acts through competitive binding at the NADH cofactor site, effects confirmed by functional enzyme studies where the IC50 = 27.32 nM was reversed with increasing concentration of NADH.	NAD	106-110	lactate dehydrogenase A	Homo sapiens	41-47
25918543-5	2015	Theoretical molecular docking studies of hLDH-A indicate that PGG acts through competitive binding at the NADH cofactor site, effects confirmed by functional enzyme studies where the IC50 = 27.32 nM was reversed with increasing concentration of NADH.	NAD	245-249	lactate dehydrogenase A	Homo sapiens	41-47
25971446-9	2015	CAP metabolites preferentially caused double base lesion, the G and C of the ACG sequence complementary to codon 273 of the p53 gene, in the presence of NADH and Cu(II).	NAD	153-157	tumor protein p53	Homo sapiens	124-127
25774718-1	2015	To test the hypothesis that a fall in cellular ATP following stimulation of endothelial cells with thrombin is secondary to a decrease in NAD levels caused by poly(ADP-Ribose)polymerase (PARP), we measured the levels of NAD and ATP in endothelial cells after treatment with thrombin, the Ca(++)-ionophore A23187, or hydrogen peroxide (H2O2), and compared the effects of inhibitors of PARP, NAD synthesis, and ADP-ribose breakdown on these responses.	NAD	220-223	coagulation factor II, thrombin	Homo sapiens	99-107
25774718-1	2015	To test the hypothesis that a fall in cellular ATP following stimulation of endothelial cells with thrombin is secondary to a decrease in NAD levels caused by poly(ADP-Ribose)polymerase (PARP), we measured the levels of NAD and ATP in endothelial cells after treatment with thrombin, the Ca(++)-ionophore A23187, or hydrogen peroxide (H2O2), and compared the effects of inhibitors of PARP, NAD synthesis, and ADP-ribose breakdown on these responses.	NAD	220-223	poly(ADP-ribose) polymerase 1	Homo sapiens	187-191
26075038-7	2015	NAD(H) depletion in primary astrocytes was prevented by pretreatment with 1 muM of lycopene for 3.5 hours.	NAD	0-6	latexin	Homo sapiens	76-79
26075038-8	2015	Unexpectedly, in U251 cells lycopene treatment at concentrations &gt;= 5 muM resulted in significant reductions in [NAD(H)].	NAD	116-122	latexin	Homo sapiens	73-76
26568959-2	2015	While pyruvate and NADH metabolic pathways are known to be involved in regulating insulin secretion in response to glucose stimulation, the roles of many other components along the metabolic pathways remain poorly understood.	NAD	19-23	insulin	Homo sapiens	82-89
25774718-1	2015	To test the hypothesis that a fall in cellular ATP following stimulation of endothelial cells with thrombin is secondary to a decrease in NAD levels caused by poly(ADP-Ribose)polymerase (PARP), we measured the levels of NAD and ATP in endothelial cells after treatment with thrombin, the Ca(++)-ionophore A23187, or hydrogen peroxide (H2O2), and compared the effects of inhibitors of PARP, NAD synthesis, and ADP-ribose breakdown on these responses.	NAD	138-141	coagulation factor II, thrombin	Homo sapiens	99-107
25774718-1	2015	To test the hypothesis that a fall in cellular ATP following stimulation of endothelial cells with thrombin is secondary to a decrease in NAD levels caused by poly(ADP-Ribose)polymerase (PARP), we measured the levels of NAD and ATP in endothelial cells after treatment with thrombin, the Ca(++)-ionophore A23187, or hydrogen peroxide (H2O2), and compared the effects of inhibitors of PARP, NAD synthesis, and ADP-ribose breakdown on these responses.	NAD	138-141	poly(ADP-ribose) polymerase 1	Homo sapiens	159-185
25774718-1	2015	To test the hypothesis that a fall in cellular ATP following stimulation of endothelial cells with thrombin is secondary to a decrease in NAD levels caused by poly(ADP-Ribose)polymerase (PARP), we measured the levels of NAD and ATP in endothelial cells after treatment with thrombin, the Ca(++)-ionophore A23187, or hydrogen peroxide (H2O2), and compared the effects of inhibitors of PARP, NAD synthesis, and ADP-ribose breakdown on these responses.	NAD	138-141	poly(ADP-ribose) polymerase 1	Homo sapiens	187-191
25774718-1	2015	To test the hypothesis that a fall in cellular ATP following stimulation of endothelial cells with thrombin is secondary to a decrease in NAD levels caused by poly(ADP-Ribose)polymerase (PARP), we measured the levels of NAD and ATP in endothelial cells after treatment with thrombin, the Ca(++)-ionophore A23187, or hydrogen peroxide (H2O2), and compared the effects of inhibitors of PARP, NAD synthesis, and ADP-ribose breakdown on these responses.	NAD	220-223	coagulation factor II, thrombin	Homo sapiens	99-107
25774718-1	2015	To test the hypothesis that a fall in cellular ATP following stimulation of endothelial cells with thrombin is secondary to a decrease in NAD levels caused by poly(ADP-Ribose)polymerase (PARP), we measured the levels of NAD and ATP in endothelial cells after treatment with thrombin, the Ca(++)-ionophore A23187, or hydrogen peroxide (H2O2), and compared the effects of inhibitors of PARP, NAD synthesis, and ADP-ribose breakdown on these responses.	NAD	220-223	poly(ADP-ribose) polymerase 1	Homo sapiens	187-191
26180598-2	2015	Hyperglycemia decreases NAD(+) levels by activation of the polyol pathway and by overactivation of poly(ADP-ribose)-polymerase (PARP).	NAD	24-30	poly(ADP-ribose) polymerase 1	Homo sapiens	128-132
26180598-8	2015	We conclude that this protective effect of flavonoids on NAD(+) levels is a combination of the flavonoids ability to inhibit both PARP activation and aldose reductase enzyme activity.	NAD	57-63	poly(ADP-ribose) polymerase 1	Homo sapiens	130-134
26180598-8	2015	We conclude that this protective effect of flavonoids on NAD(+) levels is a combination of the flavonoids ability to inhibit both PARP activation and aldose reductase enzyme activity.	NAD	57-63	aldo-keto reductase family 1 member B	Homo sapiens	150-166
25485873-7	2014	In particular, here we show that p26 interacts with PARP1 after irradiation, and this interaction exerts an inhibitory effect on PARP1 activity as measured by NAD+ levels.	NAD	159-163	poly(ADP-ribose) polymerase 1	Homo sapiens	129-134
25517164-4	2014	Regulation of PDH via regulation of the E3 component by the NAD(+)/NADH ratio represents one of the important physiological control mechanisms of PDH activity.	NAD	60-66	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	14-17
25517164-4	2014	Regulation of PDH via regulation of the E3 component by the NAD(+)/NADH ratio represents one of the important physiological control mechanisms of PDH activity.	NAD	60-66	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	146-149
25517164-4	2014	Regulation of PDH via regulation of the E3 component by the NAD(+)/NADH ratio represents one of the important physiological control mechanisms of PDH activity.	NAD	67-71	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	14-17
25517164-4	2014	Regulation of PDH via regulation of the E3 component by the NAD(+)/NADH ratio represents one of the important physiological control mechanisms of PDH activity.	NAD	67-71	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	146-149
25453901-3	2014	URI inhibits aryl hydrocarbon (AhR)- and estrogen receptor (ER)-mediated transcription of enzymes implicated in L-tryptophan/kynurenine/nicotinamide adenine dinucleotide (NAD(+)) metabolism, thereby causing DNA damage at early stages of tumorigenesis.	NAD	136-169	estrogen receptor 1	Homo sapiens	41-58
25453901-3	2014	URI inhibits aryl hydrocarbon (AhR)- and estrogen receptor (ER)-mediated transcription of enzymes implicated in L-tryptophan/kynurenine/nicotinamide adenine dinucleotide (NAD(+)) metabolism, thereby causing DNA damage at early stages of tumorigenesis.	NAD	136-169	estrogen receptor 1	Homo sapiens	60-62
25453901-3	2014	URI inhibits aryl hydrocarbon (AhR)- and estrogen receptor (ER)-mediated transcription of enzymes implicated in L-tryptophan/kynurenine/nicotinamide adenine dinucleotide (NAD(+)) metabolism, thereby causing DNA damage at early stages of tumorigenesis.	NAD	171-177	estrogen receptor 1	Homo sapiens	41-58
25453901-3	2014	URI inhibits aryl hydrocarbon (AhR)- and estrogen receptor (ER)-mediated transcription of enzymes implicated in L-tryptophan/kynurenine/nicotinamide adenine dinucleotide (NAD(+)) metabolism, thereby causing DNA damage at early stages of tumorigenesis.	NAD	171-177	estrogen receptor 1	Homo sapiens	60-62
25392945-1	2015	Human alpha-amino-beta-carboxymuconate-epsilon-semialdehyde decarboxylase determines the fate of tryptophan metabolites in the kynurenine pathway by controlling the quinolinate levels for de novo nicotinamide adenine dinucleotide biosynthesis.	NAD	196-229	aminocarboxymuconate semialdehyde decarboxylase	Homo sapiens	6-73
25250980-10	2014	This comparison identified several residues in hCD157 (F108 and F173) that can potentially hinder the binding of dinucleotide substrates (NAD+).	NAD	138-142	bone marrow stromal cell antigen 1	Homo sapiens	47-53
25429601-3	2014	CtBP1 and CtBP2 are closely related and act as transcriptional corepressors when activated by nicotinamide adenine dinucleotide binding to their dehydrogenase domains.	NAD	94-127	C-terminal binding protein 2	Homo sapiens	10-15
25392530-2	2014	Airway epithelial cells express arginine-specific ADP ribosyltransferase (ART)-1, a GPI-anchored ART that transfers ADP-ribose from NAD to arginines 14 and 24 of HNP-1.	NAD	132-135	ADP-ribosyltransferase 1	Homo sapiens	50-80
25441760-4	2014	PARP inhibitors that compete with NAD(+) at the enzyme"s activity site can be used in BRCA-deficient cells as single agent therapies acting through the principle of synthetic lethality exploiting these cells deficient DNA double-strand break repair.	NAD	34-40	poly(ADP-ribose) polymerase 1	Homo sapiens	0-4
25341895-1	2014	AIMS: Intracellular nicotinamide phosphoribosyltransferase (NAMPT) is the rate-limiting enzyme for nicotinamide adenine dinucleotide (NAD(+)) biosynthesis.	NAD	99-132	nicotinamide phosphoribosyltransferase	Mus musculus	20-58
25341895-1	2014	AIMS: Intracellular nicotinamide phosphoribosyltransferase (NAMPT) is the rate-limiting enzyme for nicotinamide adenine dinucleotide (NAD(+)) biosynthesis.	NAD	99-132	nicotinamide phosphoribosyltransferase	Mus musculus	60-65
25341895-0	2014	Intracellular NAMPT-NAD+-SIRT1 cascade improves post-ischaemic vascular repair by modulating Notch signalling in endothelial progenitors.	NAD	20-24	nicotinamide phosphoribosyltransferase	Mus musculus	14-19
25341895-1	2014	AIMS: Intracellular nicotinamide phosphoribosyltransferase (NAMPT) is the rate-limiting enzyme for nicotinamide adenine dinucleotide (NAD(+)) biosynthesis.	NAD	134-141	nicotinamide phosphoribosyltransferase	Mus musculus	20-58
25341895-1	2014	AIMS: Intracellular nicotinamide phosphoribosyltransferase (NAMPT) is the rate-limiting enzyme for nicotinamide adenine dinucleotide (NAD(+)) biosynthesis.	NAD	134-141	nicotinamide phosphoribosyltransferase	Mus musculus	60-65
25341895-2	2014	This study investigated the role of NAMPT-mediated NAD(+) signalling in post-ischaemic vascular repair.	NAD	51-57	nicotinamide phosphoribosyltransferase	Mus musculus	36-41
25341895-11	2014	CONCLUSIONS: These results demonstrate that intracellular NAMPT-NAD(+)-SIRT1 cascade improves post-ischaemic neovascularization.	NAD	64-70	nicotinamide phosphoribosyltransferase	Mus musculus	58-63
25491822-0	2014	Application of CdO nanoparticle ionic liquid modified carbon paste electrode as a high sensitive biosensor for square wave voltammetric determination of NADH.	NAD	153-157	cell adhesion associated, oncogene regulated	Homo sapiens	15-18
25598664-0	2014	Scant Extracellular NAD Cleaving Activity of Human Neutrophils is Down-Regulated by fMLP via FPRL1.	NAD	20-23	formyl peptide receptor 1	Homo sapiens	84-88
25491822-1	2014	In this paper we report the synthesis and application of CdO nanoparticle (CdO/NPs) and 1,3-dipropylimidazolium bromide as high sensitive sensors for voltammetric determination of nicotinamide adenine dinucleotide (NADH) using carbon paste electrode.	NAD	180-213	cell adhesion associated, oncogene regulated	Homo sapiens	57-60
25491822-1	2014	In this paper we report the synthesis and application of CdO nanoparticle (CdO/NPs) and 1,3-dipropylimidazolium bromide as high sensitive sensors for voltammetric determination of nicotinamide adenine dinucleotide (NADH) using carbon paste electrode.	NAD	180-213	cell adhesion associated, oncogene regulated	Homo sapiens	75-78
25491822-1	2014	In this paper we report the synthesis and application of CdO nanoparticle (CdO/NPs) and 1,3-dipropylimidazolium bromide as high sensitive sensors for voltammetric determination of nicotinamide adenine dinucleotide (NADH) using carbon paste electrode.	NAD	215-219	cell adhesion associated, oncogene regulated	Homo sapiens	57-60
25491822-1	2014	In this paper we report the synthesis and application of CdO nanoparticle (CdO/NPs) and 1,3-dipropylimidazolium bromide as high sensitive sensors for voltammetric determination of nicotinamide adenine dinucleotide (NADH) using carbon paste electrode.	NAD	215-219	cell adhesion associated, oncogene regulated	Homo sapiens	75-78
25491822-3	2014	Compared to common carbon paste electrode, the electrochemical response was greatly improved for NADH electrooxidation at a surface of CdO/NP modified ionic liquid carbon paste electrode (IL/CdO/NP/CPE).	NAD	97-101	cell adhesion associated, oncogene regulated	Homo sapiens	135-138
25491822-3	2014	Compared to common carbon paste electrode, the electrochemical response was greatly improved for NADH electrooxidation at a surface of CdO/NP modified ionic liquid carbon paste electrode (IL/CdO/NP/CPE).	NAD	97-101	cell adhesion associated, oncogene regulated	Homo sapiens	191-194
25387075-6	2014	Using different approaches including confocal imaging, mitochondrial DNA measurement and Western blot analysis of PGC-1 and NRF-1, we also found that NAD+ could significantly attenuate glutamate-induced mitochondrial fragmentation and the impairment of mitochondrial biogenesis.	NAD	150-154	PPARG coactivator 1 alpha	Homo sapiens	114-119
25477764-2	2014	Neuron death in acute bacterial meningitis involves the excessive activation of NMDA receptors and p53-mediated apoptosis, and the latter is triggered by the depletion of NAD + and ATP cellular stores by the DNA repair enzyme poly(ADP-ribose) polymerase.	NAD	171-176	poly(ADP-ribose) polymerase 1	Homo sapiens	226-253
25398022-9	2014	Immunoreactivity of the catalytic subunit of nicotinamide-adenine dinucleotide phosphate (NADPH) oxidase, Nox2, and superoxide were elevated in ApoE-/- mice that were fed the low n-3 PUFA diet, and this was also significantly attenuated in mice that were fed the high n-3 PUFA diet.	NAD	45-78	apolipoprotein E	Mus musculus	144-148
25237129-1	2014	Formate dehydrogenase (FDH; EC 1.2.1.2) is an NAD-dependent enzyme that catalyzes the oxidation of formate to carbon dioxide.	NAD	46-49	formate dehydrogenase	Arabidopsis thaliana	0-21
25440052-3	2014	(2014) demonstrate that increasing NAD(+) levels may reverse the inactivation of Sirt1 and mitochondrial defects in Cockayne Syndrome B that stem from nuclear NAD(+) depletion by the DNA repair protein PARP.	NAD	35-41	poly(ADP-ribose) polymerase 1	Homo sapiens	202-206
25440052-3	2014	(2014) demonstrate that increasing NAD(+) levels may reverse the inactivation of Sirt1 and mitochondrial defects in Cockayne Syndrome B that stem from nuclear NAD(+) depletion by the DNA repair protein PARP.	NAD	159-165	poly(ADP-ribose) polymerase 1	Homo sapiens	202-206
25145669-5	2014	Pemetrexed is known to activate PARPs, thereby accelerating NAD consumption.	NAD	60-63	poly(ADP-ribose) polymerase 1	Homo sapiens	32-37
25078118-7	2014	Metabolic collapse appears to be central in the hydrogen peroxide-PARP1-p38 pathway as silencing PARP1 or inhibition of p38 prevented differentiation-associated loss of cellular NAD, inhibition of mitochondrial respiration, and glycolytic activity.	NAD	178-181	poly(ADP-ribose) polymerase 1	Homo sapiens	66-71
25078118-7	2014	Metabolic collapse appears to be central in the hydrogen peroxide-PARP1-p38 pathway as silencing PARP1 or inhibition of p38 prevented differentiation-associated loss of cellular NAD, inhibition of mitochondrial respiration, and glycolytic activity.	NAD	178-181	mitogen-activated protein kinase 1	Homo sapiens	72-75
25078118-7	2014	Metabolic collapse appears to be central in the hydrogen peroxide-PARP1-p38 pathway as silencing PARP1 or inhibition of p38 prevented differentiation-associated loss of cellular NAD, inhibition of mitochondrial respiration, and glycolytic activity.	NAD	178-181	poly(ADP-ribose) polymerase 1	Homo sapiens	97-102
25078118-7	2014	Metabolic collapse appears to be central in the hydrogen peroxide-PARP1-p38 pathway as silencing PARP1 or inhibition of p38 prevented differentiation-associated loss of cellular NAD, inhibition of mitochondrial respiration, and glycolytic activity.	NAD	178-181	mitogen-activated protein kinase 1	Homo sapiens	120-123
24814981-2	2014	The acetylation reaction is catalyzed by alpha-tubulin N-acetyltransferase and the modification can be reversed by either the NAD-independent class II histone deacetylase HDAC6 or the NAD-dependent deacetylase SIRT2.	NAD	126-129	histone deacetylase 6	Homo sapiens	171-176
25223558-3	2014	Distinct metabolic routes, starting from various precursors, are known to support NAD(+) biosynthesis with tissue/cell-specific efficiencies, probably reflecting differential expression of the corresponding rate-limiting enzymes, i.e. nicotinamide phosphoribosyltransferase, quinolinate phosphoribosyltransferase, nicotinate phosphoribosyltransferase and nicotinamide riboside kinase.	NAD	82-88	quinolinate phosphoribosyltransferase	Homo sapiens	275-312
25223558-7	2014	The screening enabled us to gather novel findings, including (a) the presence of quinolinate phosphoribosyltransferase and nicotinamide riboside kinase in all examined tissues/cell lines, indicating that quinolinate and nicotinamide riboside are relevant NAD(+) precursors, and (b) the unexpected occurrence of nicotinate phosphoribosyltransferase in human plasma.	NAD	255-261	quinolinate phosphoribosyltransferase	Homo sapiens	81-118
25237129-1	2014	Formate dehydrogenase (FDH; EC 1.2.1.2) is an NAD-dependent enzyme that catalyzes the oxidation of formate to carbon dioxide.	NAD	46-49	formate dehydrogenase	Arabidopsis thaliana	23-26
25350109-6	2014	The effects by ET-1, Ang-T, NADH, diazoxide, and 3-NPA were opposed by blocking intraluminal O2- (SOD) and XO, and were mimicked by XO activation (hypoxanthine).	NAD	28-32	superoxide dismutase [Mn], mitochondrial	Cavia porcellus	98-101
25290058-3	2014	We show that NAD(+) regulates CD4(+) T-cell differentiation through tryptophan hydroxylase-1 (Tph1), independently of well-established transcription factors.	NAD	13-19	tryptophan hydroxylase 1	Mus musculus	68-92
25314136-4	2014	Resveratrol increases intracellular Ca2+ (Cai) and AMP kinase (AMPK) and NAD-dependent deacetylase sirtuin1 (SIRT1) activities, all of which could activate NO production.	NAD	73-76	sirtuin 1	Rattus norvegicus	99-107
25314136-4	2014	Resveratrol increases intracellular Ca2+ (Cai) and AMP kinase (AMPK) and NAD-dependent deacetylase sirtuin1 (SIRT1) activities, all of which could activate NO production.	NAD	73-76	sirtuin 1	Rattus norvegicus	109-114
25290058-3	2014	We show that NAD(+) regulates CD4(+) T-cell differentiation through tryptophan hydroxylase-1 (Tph1), independently of well-established transcription factors.	NAD	13-19	tryptophan hydroxylase 1	Mus musculus	94-98
25620190-1	2014	Poly(ADP-ribose) polymerase (PARP) is a 116kDa enzyme catalysing the synthesis of ADP-ribose polymers from NAD+.	NAD	107-111	poly(ADP-ribose) polymerase 1	Homo sapiens	0-27
25280219-3	2014	Here, we show that the NAD-dependent SIRT1 deacetylase is selectively overexpressed in primary human FLT3-ITD AML LSCs.	NAD	23-26	fms related receptor tyrosine kinase 3	Homo sapiens	101-105
25051436-7	2014	SLIT3 mRNA concentrations were increased in DPN-treated human endometrial endothelial cells and in 4,4",4""-(4-propyl-(1H)-pyrazole-1,3,5-tryl) trisphenol-treated (EC50 200) rat dorsal root ganglia neurons.	NAD	44-47	slit guidance ligand 3	Homo sapiens	0-5
25620190-1	2014	Poly(ADP-ribose) polymerase (PARP) is a 116kDa enzyme catalysing the synthesis of ADP-ribose polymers from NAD+.	NAD	107-111	poly(ADP-ribose) polymerase 1	Homo sapiens	29-33
25215490-3	2014	This derivative was found to bind nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme involved in the conversion of nicotinamide into nicotinamide adenine dinucleotide (NAD).	NAD	190-193	nicotinamide phosphoribosyltransferase	Mus musculus	34-72
24799340-5	2014	The Au-SH-OC-DPCs showed a good voltammetric performance in the electrochemical detection of NADH with a low detection limit (1.0 nM), high sensitivity (4.934 muA/muM), and wide linear concentration range (5.0 nM-10 microM).	NAD	93-97	latexin	Homo sapiens	163-166
25221980-5	2014	Through experimental kinetic studies, we demonstrate that NAM inhibition of SIRT3 involves apparent competition between the inhibitor and the enzyme cofactor NAD+, contrary to the traditional characterization of base exchange as noncompetitive inhibition.	NAD	158-162	sirtuin 3	Homo sapiens	76-81
25221980-6	2014	We report a model for base exchange inhibition that relates such kinetic properties to physicochemical properties, including the free energies of enzyme-ligand binding, and estimate the latter through the first reported computational binding affinity calculations for SIRT3:NAD+, SIRT3:NAM, and analogous complexes for Sir2.	NAD	274-278	sirtuin 3	Homo sapiens	268-273
25215490-3	2014	This derivative was found to bind nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme involved in the conversion of nicotinamide into nicotinamide adenine dinucleotide (NAD).	NAD	155-188	nicotinamide phosphoribosyltransferase	Mus musculus	34-72
25215490-3	2014	This derivative was found to bind nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme involved in the conversion of nicotinamide into nicotinamide adenine dinucleotide (NAD).	NAD	155-188	nicotinamide phosphoribosyltransferase	Mus musculus	74-79
24934242-8	2014	There was also a fall in nicotinamide adenine dinucleotide (NAD(+)) indicating cardiomyocyte death which was confirmed by early release of cTnT and CK-MB during CPB.	NAD	25-58	troponin T2, cardiac type	Homo sapiens	139-143
24934242-8	2014	There was also a fall in nicotinamide adenine dinucleotide (NAD(+)) indicating cardiomyocyte death which was confirmed by early release of cTnT and CK-MB during CPB.	NAD	60-66	troponin T2, cardiac type	Homo sapiens	139-143
25339333-7	2014	CONCLUSION: High dose of Vitamin B3 may play an important role in increasing absolute neutrophil count in healthy rat under steady state, and the mechanism may be dependent on NAMPT-NAD+-SIRT1 signaling pathways.	NAD	182-186	sirtuin 1	Rattus norvegicus	187-192
25220464-0	2014	ARTD1/PARP1 negatively regulates glycolysis by inhibiting hexokinase 1 independent of NAD+ depletion.	NAD	86-90	poly(ADP-ribose) polymerase 1	Homo sapiens	0-5
25220464-0	2014	ARTD1/PARP1 negatively regulates glycolysis by inhibiting hexokinase 1 independent of NAD+ depletion.	NAD	86-90	poly(ADP-ribose) polymerase 1	Homo sapiens	6-11
25220464-2	2014	ARTD1-induced cell death is associated with NAD(+) depletion and ATP loss; however, the molecular mechanism of ARTD1-mediated energy collapse remains elusive.	NAD	44-50	poly(ADP-ribose) polymerase 1	Homo sapiens	0-5
25253021-4	2014	We observed that Abeta application to the somato-dendritic compartment triggers a "dying-back" process, involving caspase and NAD(+) signalling pathways, whereas exposure of the axonal/distal compartment to Abeta deposits did not induce axonal degeneration.	NAD	126-132	histocompatibility 2, class II antigen A, beta 1	Mus musculus	17-22
25215490-3	2014	This derivative was found to bind nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme involved in the conversion of nicotinamide into nicotinamide adenine dinucleotide (NAD).	NAD	190-193	nicotinamide phosphoribosyltransferase	Mus musculus	74-79
25215490-5	2014	Active P7C3 variants likewise enhanced the activity of the purified NAMPT enzyme, providing further evidence that they act by increasing NAD levels through its NAMPT-mediated salvage.	NAD	137-140	nicotinamide phosphoribosyltransferase	Mus musculus	68-73
25215490-5	2014	Active P7C3 variants likewise enhanced the activity of the purified NAMPT enzyme, providing further evidence that they act by increasing NAD levels through its NAMPT-mediated salvage.	NAD	137-140	nicotinamide phosphoribosyltransferase	Mus musculus	160-165
25059721-3	2014	Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, a major source of reactive oxygen species (ROS), is also activated by TNF-alpha and plays a crucial role in redox-sensitive signaling pathways.	NAD	0-33	tumor necrosis factor	Homo sapiens	131-140
24953559-8	2014	Erythropoietin also reversed increased nicotinamide adenine dinucleotide by hypoxia via increased AMP-activated protein kinase.	NAD	39-72	erythropoietin	Homo sapiens	0-14
25566462-0	2014	NAMPT regulates mitochondria biogenesis via NAD metabolism and calcium binding proteins during skeletal muscle contraction.	NAD	44-47	nicotinamide phosphoribosyltransferase	Mus musculus	0-5
25566462-1	2014	PURPOSE: The purpose of this study was to investigate the effect that muscle contraction induced NAD metabolism via NAMPT has on mitochondrial biogenesis.	NAD	97-100	nicotinamide phosphoribosyltransferase	Mus musculus	116-121
25566462-11	2014	CONCLUSION: In conclusion, the results indicate that NAMPT plays an important role in NAD metabolism and mitochondrial biogenesis.	NAD	86-89	nicotinamide phosphoribosyltransferase	Mus musculus	53-58
25026599-5	2014	Troxerutin largely suppressed oxidative stress-mediated NAD(+)-depletion by increasing nicotinamide phosphoribosyltransferase (NAMPT) protein expression and decreasing poly (ADP-ribose) polymerase-1 (PARP1) protein expression and activity in HFD-treated mouse livers.	NAD	56-62	nicotinamide phosphoribosyltransferase	Mus musculus	87-125
25026599-5	2014	Troxerutin largely suppressed oxidative stress-mediated NAD(+)-depletion by increasing nicotinamide phosphoribosyltransferase (NAMPT) protein expression and decreasing poly (ADP-ribose) polymerase-1 (PARP1) protein expression and activity in HFD-treated mouse livers.	NAD	56-62	nicotinamide phosphoribosyltransferase	Mus musculus	127-132
24953559-5	2014	Erythropoietin increased cellular nicotinamide adenine dinucleotide via increased AMP-activated protein kinase activity, possibly leading to Sirtuin1 activation.	NAD	34-67	erythropoietin	Homo sapiens	0-14
25037916-2	2014	Biochemical and surface plasmon resonance experiments performed with a screening hit (LDHA IC50=1.7 muM) indicated that the compound specifically associated with human LDHA in a manner that required simultaneous binding of the NADH co-factor.	NAD	227-231	lactate dehydrogenase A	Homo sapiens	86-90
25037916-2	2014	Biochemical and surface plasmon resonance experiments performed with a screening hit (LDHA IC50=1.7 muM) indicated that the compound specifically associated with human LDHA in a manner that required simultaneous binding of the NADH co-factor.	NAD	227-231	lactate dehydrogenase A	Homo sapiens	168-172
25287956-1	2014	BACKGROUND: A previously discovered mutant of Saccharomyces cerevisiae alcohol dehydrogenase 1 (Adh1p) was shown to enable a unique NADH-dependent reduction of 5-hydroxymethylfurfural (HMF), a well-known inhibitor of yeast fermentation.	NAD	132-136	alcohol dehydrogenase ADH1	Saccharomyces cerevisiae S288C	96-101
25038521-7	2014	In this regard, the GHRH-GH-IGF-1/Insulin, TOR-S6K1,NAD(+)-Sirtuin, P53, Klotho and APOE pathways have been linked to processes associated with age-related diseases, including cancer, cardiovascular disease, diabetes, osteoporosis, and neurodegenerative diseases, all of which directly influence health in aging, and represent key targets in anti-aging therapy.	NAD	52-58	growth hormone releasing hormone	Homo sapiens	20-24
24866129-2	2014	Using hexahistidine tagged, recombinant Lot6p, we determined the steady-state enzyme kinetic parameters with both NADH and NADPH as electron donors; no cooperativity was observed with these substrates.	NAD	114-118	flavin-dependent quinone reductase	Saccharomyces cerevisiae S288C	40-45
24991831-4	2014	Using in silico, in vitro, and in vivo studies, we discovered defective mitophagy in XPA due to PARP1 hyperactivation and NAD(+) (and thus, SIRT1) depletion.	NAD	122-128	XPA, DNA damage recognition and repair factor	Homo sapiens	85-88
24835770-5	2014	RNA interference analysis and activity inhibition assay indicate that life-span extension was mediated by the upregulation of Sir-2.1, a NAD-dependent histone deacetylase ortholog of mammalian SIRT1.	NAD	137-140	Deacetylase sirtuin-type domain-containing protein;NAD-dependent protein deacetylase sir-2.1	Caenorhabditis elegans	126-133
24916104-1	2014	Poly (ADP-ribose) polymerase-1 (PARP1) is an abundant, ubiquitously expressed NAD(+)-dependent nuclear enzyme that has prognostic value for a multitude of human cancers.	NAD	78-84	poly(ADP-ribose) polymerase 1	Homo sapiens	0-30
24916104-1	2014	Poly (ADP-ribose) polymerase-1 (PARP1) is an abundant, ubiquitously expressed NAD(+)-dependent nuclear enzyme that has prognostic value for a multitude of human cancers.	NAD	78-84	poly(ADP-ribose) polymerase 1	Homo sapiens	32-37
25083875-2	2014	Specifically, the NAD(+)-dependent deacetylase SIRT1, the founding member of the sirtuin family, contributes to clock function.	NAD	18-24	circadian locomotor output cycles kaput	Mus musculus	112-117
25033286-1	2014	Up-regulated sirtuin 1 (SIRT1), an NAD+-dependent class III histone deacetylase, deacetylates p53 and inhibits its transcriptional activity, leading to cell survival.	NAD	35-39	tumor protein p53	Homo sapiens	94-97
25009184-4	2014	Further mechanistic studies show that p53 directly activates expression of the NAD(+)-dependent histone deacetylase sirtuin 6 (SIRT6), whose interaction with FoxO1 leads to FoxO1 deacetylation and export to the cytoplasm.	NAD	79-85	sirtuin 6	Mus musculus	116-125
25009184-4	2014	Further mechanistic studies show that p53 directly activates expression of the NAD(+)-dependent histone deacetylase sirtuin 6 (SIRT6), whose interaction with FoxO1 leads to FoxO1 deacetylation and export to the cytoplasm.	NAD	79-85	sirtuin 6	Mus musculus	127-132
25043379-1	2014	The poly(adenosine diphosphate (ADP)-ribose) polymerase (PARP) protein family generates ADP-ribose (ADPr) modifications onto target proteins using NAD(+) as substrate.	NAD	147-153	poly(ADP-ribose) polymerase 1	Homo sapiens	57-61
25043379-2	2014	Based on the composition of three NAD(+) coordinating amino acids, the H-Y-E motif, each PARP is predicted to generate either poly(ADPr) (PAR) or mono(ADPr) (MAR).	NAD	34-40	poly(ADP-ribose) polymerase 1	Homo sapiens	89-93
25051362-6	2014	Furthermore, adiponectin can increase AMP-activated protein kinase (AMPK) phosphorylation and NAD-dependent deacetylase sirtuin-1 (Sirt1) of PC cells.	NAD	94-97	adiponectin, C1Q and collagen domain containing	Homo sapiens	13-24
24898058-1	2014	Poly(ADP-ribose) polymerases (PARPs) modify target proteins post-translationally with poly(ADP-ribose) (PAR) or mono(ADP-ribose) (MAR) using NAD(+) as substrate.	NAD	141-147	poly(ADP-ribose) polymerase 1	Homo sapiens	30-35
24859603-1	2014	Poly(ADP-ribose) polymerase-1 (PARP-1) enzyme, as a sensor of DNA damage, could convert nicotinamide adenine dinucleotide (NAD) into long poly(ADP-ribose) chains and regulate many cellular processes, including DNA repair, gene transcription, cell survival and chromatin remodeling.	NAD	88-121	poly(ADP-ribose) polymerase 1	Homo sapiens	0-29
24859603-1	2014	Poly(ADP-ribose) polymerase-1 (PARP-1) enzyme, as a sensor of DNA damage, could convert nicotinamide adenine dinucleotide (NAD) into long poly(ADP-ribose) chains and regulate many cellular processes, including DNA repair, gene transcription, cell survival and chromatin remodeling.	NAD	88-121	poly(ADP-ribose) polymerase 1	Homo sapiens	31-37
24859603-1	2014	Poly(ADP-ribose) polymerase-1 (PARP-1) enzyme, as a sensor of DNA damage, could convert nicotinamide adenine dinucleotide (NAD) into long poly(ADP-ribose) chains and regulate many cellular processes, including DNA repair, gene transcription, cell survival and chromatin remodeling.	NAD	123-126	poly(ADP-ribose) polymerase 1	Homo sapiens	0-29
24859603-1	2014	Poly(ADP-ribose) polymerase-1 (PARP-1) enzyme, as a sensor of DNA damage, could convert nicotinamide adenine dinucleotide (NAD) into long poly(ADP-ribose) chains and regulate many cellular processes, including DNA repair, gene transcription, cell survival and chromatin remodeling.	NAD	123-126	poly(ADP-ribose) polymerase 1	Homo sapiens	31-37
24859603-2	2014	However, excessive activation of PARP-1 depletes its substrate NAD and leads to cell death.	NAD	63-66	poly(ADP-ribose) polymerase 1	Homo sapiens	33-39
25068084-6	2014	Indeed, after TNFalpha treatment in 3T3-L1 cells, visfatin was downregulated, leading to decreased nicotinamide adenine dinucleotide (NAD(+)) concentrations in cells.	NAD	99-132	nicotinamide phosphoribosyltransferase	Mus musculus	50-58
25068084-6	2014	Indeed, after TNFalpha treatment in 3T3-L1 cells, visfatin was downregulated, leading to decreased nicotinamide adenine dinucleotide (NAD(+)) concentrations in cells.	NAD	134-141	tumor necrosis factor	Mus musculus	14-22
25068084-6	2014	Indeed, after TNFalpha treatment in 3T3-L1 cells, visfatin was downregulated, leading to decreased nicotinamide adenine dinucleotide (NAD(+)) concentrations in cells.	NAD	134-141	nicotinamide phosphoribosyltransferase	Mus musculus	50-58
25068084-9	2014	Here, we demonstrated a complete pathway involving visfatin, NAD(+), Sirt1, and PTP1B that led to the perturbation of insulin signaling by TNFalpha in 3T3-L1 adipocytes.	NAD	61-67	tumor necrosis factor	Mus musculus	139-147
24825348-5	2014	Here, we show that the loss of BubR1 levels with age is due to a decline in NAD(+) and the ability of SIRT2 to maintain lysine-668 of BubR1 in a deacetylated state, which is counteracted by the acetyltransferase CBP.	NAD	76-82	BUB1B, mitotic checkpoint serine/threonine kinase	Mus musculus	31-36
24825348-6	2014	Overexpression of SIRT2 or treatment of mice with the NAD(+) precursor nicotinamide mononucleotide (NMN) increases BubR1 abundance in vivo.	NAD	54-60	BUB1B, mitotic checkpoint serine/threonine kinase	Mus musculus	115-120
24987120-2	2014	Accompanying the formation of PAR are the reduction of cellular NAD(+) and energetic collapse, which have been thought to be caused by the consumption of cellular NAD(+) by PARP-1.	NAD	163-169	poly(ADP-ribose) polymerase 1	Homo sapiens	173-179
24987120-4	2014	Instead PARP-1 activation initiates glycolytic defects via PAR-dependent inhibition of hexokinase, which precedes the NAD(+) depletion in N-methyl-N-nitroso-N-nitroguanidine (MNNG)-treated cortical neurons.	NAD	118-124	poly(ADP-ribose) polymerase 1	Homo sapiens	8-14
24987120-4	2014	Instead PARP-1 activation initiates glycolytic defects via PAR-dependent inhibition of hexokinase, which precedes the NAD(+) depletion in N-methyl-N-nitroso-N-nitroguanidine (MNNG)-treated cortical neurons.	NAD	118-124	hexokinase 1	Homo sapiens	87-97
25068084-0	2014	Visfatin is involved in TNFalpha-mediated insulin resistance via an NAD(+)/Sirt1/PTP1B pathway in 3T3-L1 adipocytes.	NAD	68-74	nicotinamide phosphoribosyltransferase	Mus musculus	0-8
25068084-6	2014	Indeed, after TNFalpha treatment in 3T3-L1 cells, visfatin was downregulated, leading to decreased nicotinamide adenine dinucleotide (NAD(+)) concentrations in cells.	NAD	99-132	tumor necrosis factor	Mus musculus	14-22
24968225-1	2014	BACKGROUND: NAD(H) kinase (NADK) is the key enzyme that catalyzes de novo synthesis of NADP(H) from NAD(H) for NADP(H)-based metabolic pathways.	NAD	12-18	NAD(H) kinase 3	Arabidopsis thaliana	27-31
24752504-5	2014	Thus, inhibition of PARP-1 with PJ34 completely blocked TGHQ-mediated accumulation of poly(ADP-ribose) polymers and NAD consumption, and delayed HK-2 cell death.	NAD	116-119	poly(ADP-ribose) polymerase 1	Homo sapiens	20-26
24957098-1	2014	Mitochondrial malic enzyme 2 (ME2) catalyzes the oxidative decarboxylation of malate to yield CO2 and pyruvate, with concomitant reduction of dinucleotide cofactor NAD(+) or NADP(+).	NAD	164-170	malic enzyme 2	Homo sapiens	14-28
24957098-1	2014	Mitochondrial malic enzyme 2 (ME2) catalyzes the oxidative decarboxylation of malate to yield CO2 and pyruvate, with concomitant reduction of dinucleotide cofactor NAD(+) or NADP(+).	NAD	164-170	malic enzyme 2	Homo sapiens	30-33
24796879-3	2014	Our most recent study found that DPN, an estrogen receptor (ER) beta-specific agonist, activated the Ndrg2 promoter and elevated endogenous NDRG2 protein expression in MCF7, HSG and T-47D cells.	NAD	33-36	estrogen receptor 1	Homo sapiens	41-58
24889606-5	2014	We find that these effects of NAD(+) are mediated by the activation of the mitochondrial sirtuin sirtuin-3 (SIRT3).	NAD	30-36	sirtuin 3	Homo sapiens	108-113
24889606-6	2014	Overexpression of SIRT3 prevents microtubule disassembly and apoptosis elicited by antimicrotubule agents and knockdown of SIRT3 prevents the protective effects of NAD(+) on microtubule polymers.	NAD	164-170	sirtuin 3	Homo sapiens	18-23
24889606-6	2014	Overexpression of SIRT3 prevents microtubule disassembly and apoptosis elicited by antimicrotubule agents and knockdown of SIRT3 prevents the protective effects of NAD(+) on microtubule polymers.	NAD	164-170	sirtuin 3	Homo sapiens	123-128
24796879-3	2014	Our most recent study found that DPN, an estrogen receptor (ER) beta-specific agonist, activated the Ndrg2 promoter and elevated endogenous NDRG2 protein expression in MCF7, HSG and T-47D cells.	NAD	33-36	estrogen receptor 1	Homo sapiens	60-62
24650937-1	2014	We recently showed that poly(ADP-ribose) polymerase (PARP) inhibitors exert their cytotoxicity primarily by trapping PARP-DNA complexes in addition to their NAD(+)-competitive catalytic inhibitory mechanism.	NAD	157-163	poly(ADP-ribose) polymerase 1	Homo sapiens	24-51
24922076-7	2014	Moreover, we show that the induction of cellular NAD(+) levels using beta-lapachone (beta-Lap), whose intracellular target is NQO1, prevents the toxic effects of cisplatin through the regulation of PARP-1 and SIRT1 activity.	NAD	49-55	NAD(P)H quinone dehydrogenase 1	Homo sapiens	126-130
24922076-7	2014	Moreover, we show that the induction of cellular NAD(+) levels using beta-lapachone (beta-Lap), whose intracellular target is NQO1, prevents the toxic effects of cisplatin through the regulation of PARP-1 and SIRT1 activity.	NAD	49-55	poly(ADP-ribose) polymerase 1	Homo sapiens	198-204
24905194-1	2014	Nicotinamide phosphoribosyltransferase (Nampt), the rate-limiting enzyme for nicotinamide adenine dinucleotide (NAD+) synthesis, and Sirt1, an NAD+-dependent histone deacetylase, protect the heart against ischemia/reperfusion (I/R).	NAD	77-110	nicotinamide phosphoribosyltransferase	Mus musculus	40-45
24905194-1	2014	Nicotinamide phosphoribosyltransferase (Nampt), the rate-limiting enzyme for nicotinamide adenine dinucleotide (NAD+) synthesis, and Sirt1, an NAD+-dependent histone deacetylase, protect the heart against ischemia/reperfusion (I/R).	NAD	112-116	nicotinamide phosphoribosyltransferase	Mus musculus	40-45
24905194-1	2014	Nicotinamide phosphoribosyltransferase (Nampt), the rate-limiting enzyme for nicotinamide adenine dinucleotide (NAD+) synthesis, and Sirt1, an NAD+-dependent histone deacetylase, protect the heart against ischemia/reperfusion (I/R).	NAD	112-115	nicotinamide phosphoribosyltransferase	Mus musculus	40-45
24905194-2	2014	It remains unknown whether Nampt mediates the protective effect of ischemic preconditioning (IPC), whether nicotinamide mononucleotide (NMN, 500 mg/kg), a product of Nampt in the NAD+ salvage pathway, mimics the effect of IPC, or whether caloric restriction (CR) upregulates Nampt and protects the heart through a Sirt1-dependent mechanism.	NAD	179-183	nicotinamide phosphoribosyltransferase	Mus musculus	166-171
24905194-2	2014	It remains unknown whether Nampt mediates the protective effect of ischemic preconditioning (IPC), whether nicotinamide mononucleotide (NMN, 500 mg/kg), a product of Nampt in the NAD+ salvage pathway, mimics the effect of IPC, or whether caloric restriction (CR) upregulates Nampt and protects the heart through a Sirt1-dependent mechanism.	NAD	179-183	nicotinamide phosphoribosyltransferase	Mus musculus	166-171
24922076-0	2014	Augmentation of NAD(+) by NQO1 attenuates cisplatin-mediated hearing impairment.	NAD	16-22	NAD(P)H quinone dehydrogenase 1	Homo sapiens	26-30
24750959-2	2014	The intracellular form of visfatin is proved to be nicotinamide phosphoribosyltransferase (NAMPT) and exhibits neuroprotection through maintaining intracellular NAD(+) pool.	NAD	161-167	nicotinamide phosphoribosyltransferase	Mus musculus	26-34
24650937-1	2014	We recently showed that poly(ADP-ribose) polymerase (PARP) inhibitors exert their cytotoxicity primarily by trapping PARP-DNA complexes in addition to their NAD(+)-competitive catalytic inhibitory mechanism.	NAD	157-163	poly(ADP-ribose) polymerase 1	Homo sapiens	53-57
24722990-4	2014	We hypothesized that nicotinamide nucleotide transhydrogenase (Nnt), which utilizes the proton gradient to generate NADPH from NADH and NADP(+), provides the link between mitochondrial respiration and H2O2 detoxification through the thioredoxin/peroxiredoxin system.	NAD	127-131	nicotinamide nucleotide transhydrogenase	Homo sapiens	63-66
24667915-0	2014	Protein kinase C epsilon regulates mitochondrial pools of Nampt and NAD following resveratrol and ischemic preconditioning in the rat cortex.	NAD	68-71	protein kinase C, epsilon	Rattus norvegicus	0-24
24667915-3	2014	In this study, we investigated the roles of protein kinase C epsilon (PKCe) and AMP-activated protein kinase (AMPK) in regulating mitochondrial pools of Nampt and NAD after resveratrol or ischemic preconditioning (IPC) in the cortex and in primary neuronal-glial cortical cultures.	NAD	163-166	protein kinase C, epsilon	Rattus norvegicus	44-68
24667915-3	2014	In this study, we investigated the roles of protein kinase C epsilon (PKCe) and AMP-activated protein kinase (AMPK) in regulating mitochondrial pools of Nampt and NAD after resveratrol or ischemic preconditioning (IPC) in the cortex and in primary neuronal-glial cortical cultures.	NAD	163-166	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	110-114
24667915-6	2014	Analysis of intrinsic NAD autofluorescence using two-photon microscopy revealed that PKCe modulated NAD in the mitochondrial fraction.	NAD	22-25	protein kinase C, epsilon	Rattus norvegicus	85-89
24667915-6	2014	Analysis of intrinsic NAD autofluorescence using two-photon microscopy revealed that PKCe modulated NAD in the mitochondrial fraction.	NAD	100-103	protein kinase C, epsilon	Rattus norvegicus	85-89
24667915-7	2014	Further assessments of mitochondrial NAD concentrations showed that PKCe has a key role in regulating the mitochondrial NAD(+)/nicotinamide adenine dinucleotide reduced (NADH) ratio after IPC and resveratrol treatment in an AMPK- and Nampt-dependent manner.	NAD	37-40	protein kinase C, epsilon	Rattus norvegicus	68-72
24667915-7	2014	Further assessments of mitochondrial NAD concentrations showed that PKCe has a key role in regulating the mitochondrial NAD(+)/nicotinamide adenine dinucleotide reduced (NADH) ratio after IPC and resveratrol treatment in an AMPK- and Nampt-dependent manner.	NAD	120-126	protein kinase C, epsilon	Rattus norvegicus	68-72
24667915-7	2014	Further assessments of mitochondrial NAD concentrations showed that PKCe has a key role in regulating the mitochondrial NAD(+)/nicotinamide adenine dinucleotide reduced (NADH) ratio after IPC and resveratrol treatment in an AMPK- and Nampt-dependent manner.	NAD	120-126	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	224-228
24667915-7	2014	Further assessments of mitochondrial NAD concentrations showed that PKCe has a key role in regulating the mitochondrial NAD(+)/nicotinamide adenine dinucleotide reduced (NADH) ratio after IPC and resveratrol treatment in an AMPK- and Nampt-dependent manner.	NAD	127-160	protein kinase C, epsilon	Rattus norvegicus	68-72
24667915-7	2014	Further assessments of mitochondrial NAD concentrations showed that PKCe has a key role in regulating the mitochondrial NAD(+)/nicotinamide adenine dinucleotide reduced (NADH) ratio after IPC and resveratrol treatment in an AMPK- and Nampt-dependent manner.	NAD	170-175	protein kinase C, epsilon	Rattus norvegicus	68-72
24667915-7	2014	Further assessments of mitochondrial NAD concentrations showed that PKCe has a key role in regulating the mitochondrial NAD(+)/nicotinamide adenine dinucleotide reduced (NADH) ratio after IPC and resveratrol treatment in an AMPK- and Nampt-dependent manner.	NAD	170-175	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	224-228
24667915-8	2014	These findings indicate that PKCe is critical to increase or maintain mitochondrial Nampt and NAD after pathways of ischemic neuroprotection in the brain.	NAD	94-97	protein kinase C, epsilon	Rattus norvegicus	29-33
24819061-0	2014	Identification of LDH-A as a therapeutic target for cancer cell killing via (i) p53/NAD(H)-dependent and (ii) p53-independent pathways.	NAD	84-90	lactate dehydrogenase A	Homo sapiens	18-23
24875183-5	2014	Sirtuin family member SIRT1 was found to interact with and deacetylate FOXA2, the latter process being dependent on the NAD+-binding catalytic site of SIRT1.	NAD	120-124	forkhead box A2	Mus musculus	71-76
24819061-2	2014	The enzyme lactate dehydrogenase-A (LDH-A) is key to cancer"s glycolytic phenotype, catalysing the regeneration of nicotinamide adenine dinucleotide (NAD(+)) from reduced nicotinamide adenine dinucleotide (NADH) necessary to sustain glycolysis.	NAD	115-148	lactate dehydrogenase A	Homo sapiens	11-34
24819061-2	2014	The enzyme lactate dehydrogenase-A (LDH-A) is key to cancer"s glycolytic phenotype, catalysing the regeneration of nicotinamide adenine dinucleotide (NAD(+)) from reduced nicotinamide adenine dinucleotide (NADH) necessary to sustain glycolysis.	NAD	115-148	lactate dehydrogenase A	Homo sapiens	36-41
24622975-7	2014	Furthermore, Akt2 knockout displayed upregulated apoptotic protein markers (Bax, caspase-3, caspase-9, and caspace-12) and mitochondrial damage (reduced aconitase activity and NAD(+), elevated cytochrome-c release from mitochondria) along with reduced phosphorylation of PTEN, Akt, and GSK3beta in the absence of changes in pan protein expression, the effects of which were abolished or significantly ameliorated by H2S treatment.	NAD	176-182	thymoma viral proto-oncogene 1	Mus musculus	13-16
24819599-10	2014	In addition, we found that phospho-AKT expressions in SKOV3 cells were reduced by 80% after treatment with MPP and DPN, indicating that the AKT pathway was involved.	NAD	115-118	AKT serine/threonine kinase 1	Homo sapiens	35-38
24819599-10	2014	In addition, we found that phospho-AKT expressions in SKOV3 cells were reduced by 80% after treatment with MPP and DPN, indicating that the AKT pathway was involved.	NAD	115-118	AKT serine/threonine kinase 1	Homo sapiens	140-143
24819061-2	2014	The enzyme lactate dehydrogenase-A (LDH-A) is key to cancer"s glycolytic phenotype, catalysing the regeneration of nicotinamide adenine dinucleotide (NAD(+)) from reduced nicotinamide adenine dinucleotide (NADH) necessary to sustain glycolysis.	NAD	150-156	lactate dehydrogenase A	Homo sapiens	11-34
24816116-1	2014	Lactate dehydrogenase A (LDH-A) is a key enzyme in anaerobic respiration that is predominantly found in skeletal muscle and catalyses the reversible conversion of pyruvate to lactate in the presence of NADH.	NAD	202-206	lactate dehydrogenase A	Homo sapiens	0-23
24819061-2	2014	The enzyme lactate dehydrogenase-A (LDH-A) is key to cancer"s glycolytic phenotype, catalysing the regeneration of nicotinamide adenine dinucleotide (NAD(+)) from reduced nicotinamide adenine dinucleotide (NADH) necessary to sustain glycolysis.	NAD	150-156	lactate dehydrogenase A	Homo sapiens	36-41
24819061-2	2014	The enzyme lactate dehydrogenase-A (LDH-A) is key to cancer"s glycolytic phenotype, catalysing the regeneration of nicotinamide adenine dinucleotide (NAD(+)) from reduced nicotinamide adenine dinucleotide (NADH) necessary to sustain glycolysis.	NAD	171-204	lactate dehydrogenase A	Homo sapiens	11-34
24819061-2	2014	The enzyme lactate dehydrogenase-A (LDH-A) is key to cancer"s glycolytic phenotype, catalysing the regeneration of nicotinamide adenine dinucleotide (NAD(+)) from reduced nicotinamide adenine dinucleotide (NADH) necessary to sustain glycolysis.	NAD	171-204	lactate dehydrogenase A	Homo sapiens	36-41
24819061-2	2014	The enzyme lactate dehydrogenase-A (LDH-A) is key to cancer"s glycolytic phenotype, catalysing the regeneration of nicotinamide adenine dinucleotide (NAD(+)) from reduced nicotinamide adenine dinucleotide (NADH) necessary to sustain glycolysis.	NAD	206-210	lactate dehydrogenase A	Homo sapiens	11-34
24819061-2	2014	The enzyme lactate dehydrogenase-A (LDH-A) is key to cancer"s glycolytic phenotype, catalysing the regeneration of nicotinamide adenine dinucleotide (NAD(+)) from reduced nicotinamide adenine dinucleotide (NADH) necessary to sustain glycolysis.	NAD	206-210	lactate dehydrogenase A	Homo sapiens	36-41
24819061-6	2014	Unexpectedly, however, we uncovered a novel role for p53 in the regulation of cancer cell NAD(+) and its reduced form NADH.	NAD	90-96	tumor protein p53	Homo sapiens	53-56
24819061-6	2014	Unexpectedly, however, we uncovered a novel role for p53 in the regulation of cancer cell NAD(+) and its reduced form NADH.	NAD	118-122	tumor protein p53	Homo sapiens	53-56
24819061-7	2014	Thus, LDH-A silencing by RNAi, or its inhibition using a small-molecule inhibitor, resulted in a p53-dependent increase in the cancer cell ratio of NADH:NAD(+).	NAD	148-152	lactate dehydrogenase A	Homo sapiens	6-11
24819061-7	2014	Thus, LDH-A silencing by RNAi, or its inhibition using a small-molecule inhibitor, resulted in a p53-dependent increase in the cancer cell ratio of NADH:NAD(+).	NAD	148-152	tumor protein p53	Homo sapiens	97-100
24819061-7	2014	Thus, LDH-A silencing by RNAi, or its inhibition using a small-molecule inhibitor, resulted in a p53-dependent increase in the cancer cell ratio of NADH:NAD(+).	NAD	153-159	lactate dehydrogenase A	Homo sapiens	6-11
24819061-7	2014	Thus, LDH-A silencing by RNAi, or its inhibition using a small-molecule inhibitor, resulted in a p53-dependent increase in the cancer cell ratio of NADH:NAD(+).	NAD	153-159	tumor protein p53	Homo sapiens	97-100
24819061-8	2014	This effect was specific for p53(+/+) cancer cells and correlated with (i) reduced activity of NAD(+)-dependent deacetylase sirtuin 1 (SIRT1) and (ii) an increase in acetylated p53, a known target of SIRT1 deacetylation activity.	NAD	95-101	tumor protein p53	Homo sapiens	29-32
24819061-11	2014	Our results identify a unique strategy by which the NADH/NAD(+) cellular redox status can be modulated in a cancer-specific, p53-dependent manner and we show that this can impact upon the activity of important NAD(H)-dependent enzymes.	NAD	52-56	tumor protein p53	Homo sapiens	125-128
24819061-11	2014	Our results identify a unique strategy by which the NADH/NAD(+) cellular redox status can be modulated in a cancer-specific, p53-dependent manner and we show that this can impact upon the activity of important NAD(H)-dependent enzymes.	NAD	57-63	tumor protein p53	Homo sapiens	125-128
24819061-11	2014	Our results identify a unique strategy by which the NADH/NAD(+) cellular redox status can be modulated in a cancer-specific, p53-dependent manner and we show that this can impact upon the activity of important NAD(H)-dependent enzymes.	NAD	210-216	tumor protein p53	Homo sapiens	125-128
24819061-12	2014	To summarise, this work indicates two distinct mechanisms by which suppressing LDH-A could potentially be used to kill cancer cells selectively, (i) through induction of apoptosis, irrespective of cancer cell p53 status and (ii) as a part of a combinatorial approach with redox-sensitive anticancer drugs via a novel p53/NAD(H)-dependent mechanism.	NAD	321-327	lactate dehydrogenase A	Homo sapiens	79-84
24813611-0	2014	Defective mitophagy in XPA via PARP-1 hyperactivation and NAD(+)/SIRT1 reduction.	NAD	58-64	XPA, DNA damage recognition and repair factor	Homo sapiens	23-26
24813611-4	2014	The mitochondrial abnormalities appear to be caused by decreased activation of the NAD(+)-SIRT1-PGC-1alpha axis triggered by hyperactivation of the DNA damage sensor PARP-1.	NAD	83-89	PPARG coactivator 1 alpha	Homo sapiens	96-106
24813611-4	2014	The mitochondrial abnormalities appear to be caused by decreased activation of the NAD(+)-SIRT1-PGC-1alpha axis triggered by hyperactivation of the DNA damage sensor PARP-1.	NAD	83-89	poly(ADP-ribose) polymerase 1	Homo sapiens	166-172
24813611-5	2014	This phenotype is rescued by PARP-1 inhibition or by supplementation with NAD(+) precursors that also rescue the lifespan defect in xpa-1 nematodes.	NAD	74-80	XPA, DNA damage recognition and repair factor	Homo sapiens	132-135
24681895-13	2014	CONCLUSION: NPD389 is a potent ME2 inhibitor that binds to the enzyme in a fast-binding mode, acting as an uncompetitive inhibitor with respect to the substrate NAD(+) and a mixed-type inhibitor with respect to the substrate L-malate.	NAD	161-167	malic enzyme 2	Homo sapiens	31-34
24816116-1	2014	Lactate dehydrogenase A (LDH-A) is a key enzyme in anaerobic respiration that is predominantly found in skeletal muscle and catalyses the reversible conversion of pyruvate to lactate in the presence of NADH.	NAD	202-206	lactate dehydrogenase A	Homo sapiens	25-30
24586040-6	2014	With NAD-linked substrates, and using rotenone to deenergize, iPLA2 activation can be reversed by adding succinate to reestablish a membrane potential.	NAD	5-8	phospholipase A2 group VI	Homo sapiens	62-67
24548601-1	2014	BACKGROUND: Together with p53, the NAD-dependent lysine deacetylase SIRT1 and the microRNA miR-34a form a feedback loop which self-regulates SIRT1 expression and modulates p53-dependent responses.	NAD	35-38	tumor protein p53	Homo sapiens	26-29
24548601-1	2014	BACKGROUND: Together with p53, the NAD-dependent lysine deacetylase SIRT1 and the microRNA miR-34a form a feedback loop which self-regulates SIRT1 expression and modulates p53-dependent responses.	NAD	35-38	tumor protein p53	Homo sapiens	172-175
24657618-3	2014	Crystal structures of human CtBP1 and CtBP2 in complex with MTOB and NAD(+) revealed two key features: a conserved tryptophan that likely contributes to substrate specificity and a hydrophilic cavity that links MTOB with an NAD(+) phosphate.	NAD	69-75	C-terminal binding protein 2	Homo sapiens	38-43
24755153-7	2014	Ang II effects were nicotinamide adenine dinucleotide phosphate (NADPH) oxidase dependent because preincubation with gp 91ds-tat, an inhibitor of NADPH oxidase, abolished the increase in eNOS glutathionylation and loss of eNOS activity.	NAD	20-53	angiotensinogen	Homo sapiens	0-6
24760840-4	2014	The rate-limiting step in the NAD(+) biosynthetic pathway from nicotinamide is performed by nicotinamide phosphoribosyltransferase (Nampt).	NAD	30-36	nicotinamide phosphoribosyltransferase	Mus musculus	92-130
24760840-4	2014	The rate-limiting step in the NAD(+) biosynthetic pathway from nicotinamide is performed by nicotinamide phosphoribosyltransferase (Nampt).	NAD	30-36	nicotinamide phosphoribosyltransferase	Mus musculus	132-137
24760840-5	2014	Here, we tested the hypothesis that neurons use intracellular Nampt-mediated NAD(+) biosynthesis by generating and evaluating mice lacking Nampt in forebrain excitatory neurons (CaMKIIalphaNampt(-/-) mice).	NAD	77-83	nicotinamide phosphoribosyltransferase	Mus musculus	62-67
24760840-8	2014	These results clearly demonstrate that forebrain excitatory neurons mainly use intracellular Nampt-mediated NAD(+) biosynthesis to mediate their survival and function.	NAD	108-114	nicotinamide phosphoribosyltransferase	Mus musculus	93-98
24356876-8	2014	In contrast, 17beta-estradiol or DPN relaxed placental arteries (maximum relaxation to 42 +- 1.1 or 47.6 +- 6.53% of preconstriction, respectively) to a lesser extent than myometrial arteries (to 0.03 +- 0.03 or 8.0 +- 1.0%) and in an endothelial-independent manner whereas PPT was without effect.	NAD	33-36	tachykinin precursor 1	Homo sapiens	274-277
24755287-2	2014	In this study, we show that the mating circuits" functional durability depends on the metabolic regulator SIR-2.1, a NAD(+)-dependent histone deacetylase.	NAD	117-123	Deacetylase sirtuin-type domain-containing protein;NAD-dependent protein deacetylase sir-2.1	Caenorhabditis elegans	106-113
24596095-4	2014	Five of the 19S proteasome complex subunits contain a putative NADH binding motif (GxGxxG) including the AAA-ATPase subunit, Psmc1 (Rpt2).	NAD	63-67	proteasome 26S subunit, ATPase 1	Homo sapiens	125-130
24760190-2	2014	Hydroxyprostaglandin dehydrogenase 15-(nicotinamide adenine dinucleotide) (15-PGDH, HPGD) is down-regulated in colorectal cancers and functions as a metabolic antagonist of PTGS2.	NAD	39-72	prostaglandin-endoperoxide synthase 2	Homo sapiens	173-178
24596095-5	2014	We demonstrate that recombinant Psmc1 binds NADH via the GxGxxG motif.	NAD	44-48	proteasome 26S subunit, ATPase 1	Homo sapiens	32-37
24504254-0	2014	Edc3 function in yeast and mammals is modulated by interaction with NAD-related compounds.	NAD	68-71	Edc3p	Saccharomyces cerevisiae S288C	0-4
24504254-6	2014	We also show that human and yeast Edc3 chemically modify NAD in vitro.	NAD	57-60	Edc3p	Saccharomyces cerevisiae S288C	34-38
24596095-6	2014	Introducing the DeltaGxGxxG Psmc1 mutant into cells results in reduced NADH-stabilized 26S proteasomes and decreased viability following redox stress induced by the mitochondrial inhibitor rotenone.	NAD	71-75	proteasome 26S subunit, ATPase 1	Homo sapiens	28-33
24700712-1	2014	In this issue of Blood, Zhang et al show that mice lacking the stromal-interacting molecule 1 (STIM1) gene in bone marrow cells are more susceptible to bacterial infection but are resistant to ischemia/reperfusion injury because of defective activation of phagocyte nicotinamide adenine dinucleotide phosphate (NADPH) oxidase.	NAD	266-299	stromal interaction molecule 1	Mus musculus	63-93
24641686-5	2014	Guided by initial inhibitor studies with nicotinamide analogues containing substituents at the C-5 position, we synthesized an orthogonal NAD(+) variant and found that it is used as a substrate for several engineered ARTDs (ARTD1, -2, and -6) but not their wild-type counterparts.	NAD	138-144	poly(ADP-ribose) polymerase 1	Homo sapiens	224-229
24700712-1	2014	In this issue of Blood, Zhang et al show that mice lacking the stromal-interacting molecule 1 (STIM1) gene in bone marrow cells are more susceptible to bacterial infection but are resistant to ischemia/reperfusion injury because of defective activation of phagocyte nicotinamide adenine dinucleotide phosphate (NADPH) oxidase.	NAD	266-299	stromal interaction molecule 1	Mus musculus	95-100
23384296-0	2014	Exogenous NAD(+) supplementation protects H9c2 cardiac myoblasts against hypoxia/reoxygenation injury via Sirt1-p53 pathway.	NAD	10-16	sirtuin 1	Rattus norvegicus	106-111
24337988-2	2014	NAD(+) has emerged as a major signalling molecule that serves as the sole substrate for several enzymatic reactions including the DNA repair enzyme, poly(ADP-ribose) polymerase (PARP), NAD-dependent protein deacetylases or CD38, and transcriptional factors by a new class of histone deacetylases known as sirtuins.	NAD	0-6	CD38 molecule	Rattus norvegicus	223-227
24337988-8	2014	Among the multiple physiological pathways associated with NAD(+) catabolism, our discovery of CD38 as the major regulator of cellular NAD(+) levels in rat neurons indicates that CD38 is a promising therapeutic target for the treatment of age-related neurodegenerative diseases.	NAD	58-64	CD38 molecule	Rattus norvegicus	178-182
24337988-8	2014	Among the multiple physiological pathways associated with NAD(+) catabolism, our discovery of CD38 as the major regulator of cellular NAD(+) levels in rat neurons indicates that CD38 is a promising therapeutic target for the treatment of age-related neurodegenerative diseases.	NAD	134-140	CD38 molecule	Rattus norvegicus	94-98
24337988-8	2014	Among the multiple physiological pathways associated with NAD(+) catabolism, our discovery of CD38 as the major regulator of cellular NAD(+) levels in rat neurons indicates that CD38 is a promising therapeutic target for the treatment of age-related neurodegenerative diseases.	NAD	134-140	CD38 molecule	Rattus norvegicus	178-182
24292505-3	2014	The present study demonstrates that extracellular NAD(+) at concentrations found in the inflamed tissues profoundly delays spontaneous apoptosis of human neutrophils as was evidenced by inhibition of phosphatidylserine (PS) exposure, DNA fragmentation and caspase-3 activation.	NAD	50-56	caspase 3	Homo sapiens	256-265
24292505-7	2014	Extracellular NAD(+) inhibited proteasome-dependent degradation of Mcl-1 upstream of caspase activation and, furthermore, suppressed Bax translocation to the mitochondria and attenuated both dissipation of mitochondrial transmembrane potential (DeltaPsim) and cytochrome c release from the mitochondria into the cytosol.	NAD	14-20	BCL2 associated X, apoptosis regulator	Homo sapiens	133-136
24292505-7	2014	Extracellular NAD(+) inhibited proteasome-dependent degradation of Mcl-1 upstream of caspase activation and, furthermore, suppressed Bax translocation to the mitochondria and attenuated both dissipation of mitochondrial transmembrane potential (DeltaPsim) and cytochrome c release from the mitochondria into the cytosol.	NAD	14-20	cytochrome c, somatic	Homo sapiens	260-272
24292505-9	2014	Together, these results demonstrate that extracellular NAD(+) inhibits neutrophil apoptosis via P2Y11 receptor and cAMP/PKA pathway by regulating Mcl-1 level, Bax targeting to the mitochondria and mitochondrial apoptotic pathway.	NAD	55-61	BCL2 associated X, apoptosis regulator	Homo sapiens	159-162
24147777-5	2014	The NAD+-dependent deacetylase SIRT1 (silent information regulator T1) was found to be up-regulated after AICAR treatment but, conversely, was down-regulated after IL-1beta treatment.	NAD	4-8	interleukin 1 beta	Homo sapiens	164-172
23384296-1	2014	Nicotinamide adenine dinucleotide (NAD(+) ) not only transfers electrons in mitochondrial respiration, but also acts as an indispensable cosubstrate for Sirt1, the class III histone/nonhistone deacetylase.	NAD	0-33	sirtuin 1	Rattus norvegicus	153-158
23384296-1	2014	Nicotinamide adenine dinucleotide (NAD(+) ) not only transfers electrons in mitochondrial respiration, but also acts as an indispensable cosubstrate for Sirt1, the class III histone/nonhistone deacetylase.	NAD	35-41	sirtuin 1	Rattus norvegicus	153-158
23384296-9	2014	NAD(+) replenishment restored Sirt1 activity, reduced the acetylation level of p53 (Lys373 &amp; 382), and attenuated cell apoptosis in HR-stressed H9c2 cells, whereas inhibition of Sirt1 activity alleviated the effects of NAD(+) replenishment.	NAD	0-6	sirtuin 1	Rattus norvegicus	30-35
23384296-9	2014	NAD(+) replenishment restored Sirt1 activity, reduced the acetylation level of p53 (Lys373 &amp; 382), and attenuated cell apoptosis in HR-stressed H9c2 cells, whereas inhibition of Sirt1 activity alleviated the effects of NAD(+) replenishment.	NAD	0-6	sirtuin 1	Rattus norvegicus	182-187
23384296-10	2014	These results indicated that exogenous NAD(+) supplementation attenuated HR-induced cell apoptosis, which was at least partly mediated by restoring Sirt1 activity and subsequently inhibiting p53 activity via deacetylating p53 at lysine 373 and 382.	NAD	39-45	sirtuin 1	Rattus norvegicus	148-153
24588584-2	2014	PARP-1 catalyzes the polymerization of nicotinamide adenine dinucleotide on itself and other acceptor proteins, forming long branched poly(ADP-ribose) polymers.	NAD	39-72	poly(ADP-ribose) polymerase 1	Homo sapiens	0-6
24607900-5	2014	We find that SIRT6, one of the NAD(+)-dependent class III deacetylase SIRTUINs, is down-regulated in human glioma tissues and that the level of SIRT6 is negatively correlated with PCBP2 level while H3K9ac enrichment on the promoter of PCBP2 is positively correlated with PCBP2 expression.	NAD	31-37	poly(rC) binding protein 2	Homo sapiens	180-185
24607900-5	2014	We find that SIRT6, one of the NAD(+)-dependent class III deacetylase SIRTUINs, is down-regulated in human glioma tissues and that the level of SIRT6 is negatively correlated with PCBP2 level while H3K9ac enrichment on the promoter of PCBP2 is positively correlated with PCBP2 expression.	NAD	31-37	poly(rC) binding protein 2	Homo sapiens	235-240
24607900-5	2014	We find that SIRT6, one of the NAD(+)-dependent class III deacetylase SIRTUINs, is down-regulated in human glioma tissues and that the level of SIRT6 is negatively correlated with PCBP2 level while H3K9ac enrichment on the promoter of PCBP2 is positively correlated with PCBP2 expression.	NAD	31-37	poly(rC) binding protein 2	Homo sapiens	235-240
24474689-8	2014	The study also reports the effect of Notch signaling on mitochondrial function and status of high energy intermediates ATP, NADH, and NADPH.	NAD	124-128	notch receptor 1	Homo sapiens	37-42
24382396-7	2014	The results suggest that the HTS assays for PARP2 inhibitors using chemical quantification of NAD(+), biotin-based quantification of PAR, and ELISA quantification of PAR are sensitive, robust, and cost effective.	NAD	94-100	poly(ADP-ribose) polymerase 2	Homo sapiens	44-49
24515115-7	2014	Depending on the substrates present, the dominant sites of superoxide/H2O2 production at the level of NADH may be the OGDH and PDH complexes, but these activities may often be misattributed to complex I.	NAD	102-106	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	127-130
24038671-1	2014	Quinolinic acid (QA), a biologically potent but neurodestructive metabolite is catabolized by quinolinic acid phosphoribosyltransferase (QPRT) in the first step of the de novo NAD(+) biosynthesis pathway.	NAD	176-182	quinolinate phosphoribosyltransferase	Homo sapiens	137-141
23864032-7	2014	Finally, ACOT9 activity is strongly regulated by NADH and CoA, suggesting that mitochondrial metabolic state regulates the function of ACOT9.	NAD	49-53	acyl-CoA thioesterase 9	Mus musculus	9-14
23864032-7	2014	Finally, ACOT9 activity is strongly regulated by NADH and CoA, suggesting that mitochondrial metabolic state regulates the function of ACOT9.	NAD	49-53	acyl-CoA thioesterase 9	Mus musculus	135-140
24502590-1	2014	The proline catabolic enzyme Delta(1)-pyrroline-5-carboxylate dehydrogenase (ALDH4A1) catalyzes the NAD(+)-dependent oxidation of gamma-glutamate semialdehyde to l-glutamate.	NAD	100-106	aldehyde dehydrogenase 4 family member A1	Homo sapiens	77-84
24726141-1	2014	Poly(ADP-ribose) polymerase-1 (PARP1) catalyzes the poly(ADP-ribosyl)ation of protein acceptors using NAD(+) as the substrate is now considered as an important target for development of anticancer therapy.	NAD	102-108	poly(ADP-ribose) polymerase 1	Homo sapiens	0-29
24726141-1	2014	Poly(ADP-ribose) polymerase-1 (PARP1) catalyzes the poly(ADP-ribosyl)ation of protein acceptors using NAD(+) as the substrate is now considered as an important target for development of anticancer therapy.	NAD	102-108	poly(ADP-ribose) polymerase 1	Homo sapiens	31-36
24038671-2	2014	This puts QPRT at the junction of two different pathways, that is, de novo NAD(+) biosynthesis and the kynurenine pathway of tryptophan degradation.	NAD	75-81	quinolinate phosphoribosyltransferase	Homo sapiens	10-14
24425865-5	2014	We show that acetylation of AceCS1 is cyclic and that its rhythmicity requires a functional circadian clock and the NAD(+)-dependent deacetylase SIRT1.	NAD	116-122	acyl-CoA synthetase short chain family member 1	Homo sapiens	28-34
24586272-1	2014	Poly(ADP-ribose)polymerase and sirtuin 1 are both NAD(+)-dependent enzymes.	NAD	50-56	sirtuin 1	Rattus norvegicus	31-40
24413890-1	2014	Nicotinamidase (Pnc1) is a member of Zn-dependent amidohydrolases that hydrolyzes nicotinamide (NAM) to nicotinic acid (NA), which is a key step in the salvage pathway of NAD(+) biosynthesis.	NAD	171-177	solute carrier family 25 member 33	Homo sapiens	16-20
24447297-1	2014	Type II NADH-quinone oxidoreductase (NDH-2) catalyzes the transfer electrons from NADH to the quinone pool and plays an essential role in the oxidative phosphorylation system of Mycobacterium tuberculosis (Mtb).	NAD	8-12	DExH-box helicase 9	Homo sapiens	37-42
24447297-3	2014	To fully establish the kinetic properties of this enzyme, we studied the interaction of Mtb NDH-2 with substrates, NADH, and various quinone analogues and their products in both membrane and soluble environments.	NAD	115-119	DExH-box helicase 9	Homo sapiens	92-97
24447297-4	2014	These studies, and comparative analyses of the kinetics with thio-NAD(+) and quinone electron acceptors, provided evidence that Mtb NDH-2 catalyzes the transfer electrons from NADH to quinone substrates by a nonclassical, two-site ping-pong kinetic mechanism whereby substrate quinones bind to a site that is distinct from the NADH-binding site.	NAD	176-180	DExH-box helicase 9	Homo sapiens	132-137
24447297-4	2014	These studies, and comparative analyses of the kinetics with thio-NAD(+) and quinone electron acceptors, provided evidence that Mtb NDH-2 catalyzes the transfer electrons from NADH to quinone substrates by a nonclassical, two-site ping-pong kinetic mechanism whereby substrate quinones bind to a site that is distinct from the NADH-binding site.	NAD	327-331	DExH-box helicase 9	Homo sapiens	132-137
24287278-7	2014	The inflammatory cytokine TNFalpha increased NAMPT mRNA, protein and NAD production in cultured kidney human tubular cells.	NAD	69-72	tumor necrosis factor	Homo sapiens	26-34
24462865-6	2014	In addition, SalB reversed the depletion of cellular NAD(+) induced by AngII.	NAD	53-59	angiotensinogen	Rattus norvegicus	71-76
24120939-5	2014	The CTR forms a beta hairpin structure that complements the beta sheet of the NAD(+)-binding domain, covering an essentially invariant hydrophobic surface.	NAD	78-84	calcitonin receptor	Homo sapiens	4-7
24120939-5	2014	The CTR forms a beta hairpin structure that complements the beta sheet of the NAD(+)-binding domain, covering an essentially invariant hydrophobic surface.	NAD	78-84	amyloid beta precursor protein	Homo sapiens	14-20
24296261-1	2014	Sirtuin1 (SIRT1) is a nicotinamide adenine dinucleotide (NAD(+))-dependent deacetylase functioning in the regulation of metabolism, cell survival and organismal lifespan.	NAD	22-55	sirtuin 1	Rattus norvegicus	0-8
24296261-1	2014	Sirtuin1 (SIRT1) is a nicotinamide adenine dinucleotide (NAD(+))-dependent deacetylase functioning in the regulation of metabolism, cell survival and organismal lifespan.	NAD	22-55	sirtuin 1	Rattus norvegicus	10-15
24296261-1	2014	Sirtuin1 (SIRT1) is a nicotinamide adenine dinucleotide (NAD(+))-dependent deacetylase functioning in the regulation of metabolism, cell survival and organismal lifespan.	NAD	57-64	sirtuin 1	Rattus norvegicus	0-8
24296261-1	2014	Sirtuin1 (SIRT1) is a nicotinamide adenine dinucleotide (NAD(+))-dependent deacetylase functioning in the regulation of metabolism, cell survival and organismal lifespan.	NAD	57-64	sirtuin 1	Rattus norvegicus	10-15
24275857-4	2014	Here we show that the NAMPT inhibitor FK866 induces NAD depletion in various mouse organs but selectively causes dramatic atrophy of the spleen red pulp.	NAD	52-55	nicotinamide phosphoribosyltransferase	Mus musculus	22-27
24275857-11	2014	Data demonstrate a unique sensitivity of resting lymphocytes to NAD-depleting agents, providing new hints of relevance to lymphocyte biology and therapeutic interventions with NAMPT inhibitors.	NAD	64-67	nicotinamide phosphoribosyltransferase	Mus musculus	176-181
24241058-2	2014	Adenosine 5"-monophosphate-activated protein kinase (AMPK) is crucial for GTPCH-1 preservation, and tumor suppressor kinase liver kinase B1 (LKB1), an upstream kinase of AMPK, is activated by NAD-dependent class III histone deacetylase sirtuin 1 (SIRT1)-mediated deacetylation.	NAD	192-195	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	0-51
23873758-2	2014	COL2A1 gene expression is positively regulated by the NAD-dependent protein deacetylase Sirtuin 1 (SirT1), through its ability to bind chromatin regions of the COL2A1 promoter and enhancer.	NAD	54-57	collagen type II alpha 1 chain	Homo sapiens	0-6
23873758-2	2014	COL2A1 gene expression is positively regulated by the NAD-dependent protein deacetylase Sirtuin 1 (SirT1), through its ability to bind chromatin regions of the COL2A1 promoter and enhancer.	NAD	54-57	collagen type II alpha 1 chain	Homo sapiens	160-166
24241058-3	2014	beta-Lapachone has been shown to increase cellular NAD/NADH ratio via NAD(P)H: quinone oxidoreductase 1 (NQO1) activation.	NAD	51-54	NAD(P)H quinone dehydrogenase 1	Rattus norvegicus	70-103
24241058-3	2014	beta-Lapachone has been shown to increase cellular NAD/NADH ratio via NAD(P)H: quinone oxidoreductase 1 (NQO1) activation.	NAD	51-54	NAD(P)H quinone dehydrogenase 1	Rattus norvegicus	105-109
24241058-2	2014	Adenosine 5"-monophosphate-activated protein kinase (AMPK) is crucial for GTPCH-1 preservation, and tumor suppressor kinase liver kinase B1 (LKB1), an upstream kinase of AMPK, is activated by NAD-dependent class III histone deacetylase sirtuin 1 (SIRT1)-mediated deacetylation.	NAD	192-195	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	170-174
24241058-3	2014	beta-Lapachone has been shown to increase cellular NAD/NADH ratio via NAD(P)H: quinone oxidoreductase 1 (NQO1) activation.	NAD	55-59	NAD(P)H quinone dehydrogenase 1	Rattus norvegicus	70-103
24241058-3	2014	beta-Lapachone has been shown to increase cellular NAD/NADH ratio via NAD(P)H: quinone oxidoreductase 1 (NQO1) activation.	NAD	55-59	NAD(P)H quinone dehydrogenase 1	Rattus norvegicus	105-109
24241058-2	2014	Adenosine 5"-monophosphate-activated protein kinase (AMPK) is crucial for GTPCH-1 preservation, and tumor suppressor kinase liver kinase B1 (LKB1), an upstream kinase of AMPK, is activated by NAD-dependent class III histone deacetylase sirtuin 1 (SIRT1)-mediated deacetylation.	NAD	192-195	sirtuin 1	Rattus norvegicus	236-245
24241058-2	2014	Adenosine 5"-monophosphate-activated protein kinase (AMPK) is crucial for GTPCH-1 preservation, and tumor suppressor kinase liver kinase B1 (LKB1), an upstream kinase of AMPK, is activated by NAD-dependent class III histone deacetylase sirtuin 1 (SIRT1)-mediated deacetylation.	NAD	192-195	sirtuin 1	Rattus norvegicus	247-252
24323707-7	2014	PARP-1 consumes cytosolic NAD(+), thereby blocking both glycolytic ATP production and delivery of glucose carbon to mitochondria for oxidative metabolism.	NAD	26-32	poly(ADP-ribose) polymerase 1	Homo sapiens	0-6
23990142-5	2014	An increased expression of nuclear-encoded stress-responsive genes, as well as mitochondrial-encoded NAD genes of complex I and genes of the alternative respiratory pathway, was observed in slo2 mutants, further enhanced by ABA treatment.	NAD	101-104	Pentatricopeptide repeat (PPR) superfamily protein	Arabidopsis thaliana	190-194
24292073-0	2014	Pyridomycin bridges the NADH- and substrate-binding pockets of the enoyl reductase InhA.	NAD	24-28	inhibin subunit alpha	Homo sapiens	83-87
24292073-2	2014	Here, we unveil the co-crystal structure and unique ability of pyridomycin to block both the NADH cofactor- and lipid substrate-binding pockets of InhA.	NAD	93-97	inhibin subunit alpha	Homo sapiens	147-151
24184921-2	2014	We test whether the addition of nicotinamide (to enhance NAD(+) levels) or PARP-1 inhibition (to prevent consumption of NAD(+)) can be effective in improving either loss of neuronal function or hyperoxidation following severe hypoxic injury in hippocampal slices.	NAD	120-126	poly(ADP-ribose) polymerase 1	Homo sapiens	75-81
24293653-4	2014	We discovered that poly(ADP-ribose) synthesis catalysed by PARP1 at the sites of unrepaired SBs activates ARF transcription through a protein signalling cascade, including the NAD(+)-dependent deacetylase SIRT1 and the transcription factor E2F1.	NAD	176-182	poly(ADP-ribose) polymerase 1	Homo sapiens	59-64
23761196-5	2014	Whereas SHR VSMCs exposure to angiotensin II overexpressed AT1R and Nox4 nicotinamide-adenine dinucleotide phosphate (NADPH) oxidase and slightly downregulated caveolin-1 expression, losartan decreased AT1R protein levels and increased caveolin-1 and Hsp70 expression in SHR VSMC membranes.	NAD	73-106	angiotensinogen	Rattus norvegicus	30-44
24056172-3	2014	E2 and the ESR2-selective agonist DPN, but not PPT, increased, in a PI3K and CREB-dependent manner, the expression of CDKN1B and the transcription factors GATA-1 and DMRT1.	NAD	34-37	GATA binding protein 1	Rattus norvegicus	155-161
24056172-3	2014	E2 and the ESR2-selective agonist DPN, but not PPT, increased, in a PI3K and CREB-dependent manner, the expression of CDKN1B and the transcription factors GATA-1 and DMRT1.	NAD	34-37	doublesex and mab-3 related transcription factor 1	Rattus norvegicus	166-171
24165824-4	2014	These surface captured ALP enzymes catalyze the conversion of p-aminophenylphosphate to p-aminophenol, which generates amplified catalytic current responses due to the redox-recycling process during the potential sweep in the presence of the co-reactant NADH.	NAD	254-258	alkaline phosphatase, placental	Homo sapiens	23-26
24287180-1	2014	SIRT3 is a NAD(+)-dependent histone deacetylaseand and plays a critical role in various human carcinomas.	NAD	11-15	sirtuin 3	Homo sapiens	0-5
25932355-6	2014	The activation of PGC-1alpha by FGF21 occurred via the NAD(+)-dependent deacetylase Sirtuin-1 (SIRT1) subsequent to an increase in the enzyme, nicotinamide phosphoribosyltransferase (Nampt).	NAD	55-61	PPARG coactivator 1 alpha	Homo sapiens	18-28
25932355-6	2014	The activation of PGC-1alpha by FGF21 occurred via the NAD(+)-dependent deacetylase Sirtuin-1 (SIRT1) subsequent to an increase in the enzyme, nicotinamide phosphoribosyltransferase (Nampt).	NAD	55-61	fibroblast growth factor 21	Homo sapiens	32-37
25485588-5	2014	Interestingly, the high efficiency of PARP1 triggered by BRCA1 inactivation may further inhibit BRCA1 transcription by NAD depletion.	NAD	119-122	poly(ADP-ribose) polymerase 1	Homo sapiens	38-43
24552824-0	2014	The NAD+ synthesizing enzyme nicotinamide mononucleotide adenylyltransferase 2 (NMNAT-2) is a p53 downstream target.	NAD	4-7	nicotinamide nucleotide adenylyltransferase 2	Homo sapiens	29-78
24552824-0	2014	The NAD+ synthesizing enzyme nicotinamide mononucleotide adenylyltransferase 2 (NMNAT-2) is a p53 downstream target.	NAD	4-7	nicotinamide nucleotide adenylyltransferase 2	Homo sapiens	80-87
24552824-0	2014	The NAD+ synthesizing enzyme nicotinamide mononucleotide adenylyltransferase 2 (NMNAT-2) is a p53 downstream target.	NAD	4-7	tumor protein p53	Homo sapiens	94-97
24552824-4	2014	This notion led us to examine whether p53 can regulate NAD(+) biosynthesis in the cell.	NAD	55-61	tumor protein p53	Homo sapiens	38-41
24552824-8	2014	Furthermore, knockdown of NMNAT-2 significantly reduces cellular NAD(+) levels and protects cells from p53-dependent cell death upon DNA damage, suggesting an important functional role of NMNAT-2 in p53-mediated signaling.	NAD	65-71	nicotinamide nucleotide adenylyltransferase 2	Homo sapiens	26-33
24552824-8	2014	Furthermore, knockdown of NMNAT-2 significantly reduces cellular NAD(+) levels and protects cells from p53-dependent cell death upon DNA damage, suggesting an important functional role of NMNAT-2 in p53-mediated signaling.	NAD	65-71	tumor protein p53	Homo sapiens	199-202
24552824-9	2014	Our demonstration that p53 modulates cellular NAD(+) synthesis is congruent with p53"s emerging role as a key regulator of metabolism and related cell fate.	NAD	46-52	tumor protein p53	Homo sapiens	23-26
24552824-9	2014	Our demonstration that p53 modulates cellular NAD(+) synthesis is congruent with p53"s emerging role as a key regulator of metabolism and related cell fate.	NAD	46-52	tumor protein p53	Homo sapiens	81-84
24498074-7	2014	The SCN concentration of nicotinamide adenine dinucleotide (NAD(+)), a CLOCK regulator, was assessed by liquid chromatography-mass spectrometry.	NAD	25-58	circadian locomotor output cycles kaput	Mus musculus	71-76
24498074-7	2014	The SCN concentration of nicotinamide adenine dinucleotide (NAD(+)), a CLOCK regulator, was assessed by liquid chromatography-mass spectrometry.	NAD	60-66	circadian locomotor output cycles kaput	Mus musculus	71-76
24504413-2	2014	PARP-1 is activated by interaction with NAD+, DNA, and core histones.	NAD	40-44	poly(ADP-ribose) polymerase 1	Homo sapiens	0-6
24504413-9	2014	We also demonstrate synergistic inhibition of PARP-1, combining MGBLs with conventional NAD+-dependent inhibitors in human cancer cells.	NAD	88-92	poly(ADP-ribose) polymerase 1	Homo sapiens	46-52
25483087-5	2014	CSCs demonstrated significant upregulation of CtBP1 and CtBP2 levels (mRNA and protein) and activity partly due to increased NADH/NAD ratio, as well as increased TCF/LEF transcriptional activity, compared to respective controls.	NAD	125-129	C-terminal binding protein 2	Homo sapiens	56-61
25483087-5	2014	CSCs demonstrated significant upregulation of CtBP1 and CtBP2 levels (mRNA and protein) and activity partly due to increased NADH/NAD ratio, as well as increased TCF/LEF transcriptional activity, compared to respective controls.	NAD	125-128	C-terminal binding protein 2	Homo sapiens	56-61
24343700-1	2014	Silent information regulator type-1 (SIRT1) is the best-studied member of the Sirtuin (Sir2) family of nicotinamide dinucleotide (NAD)-dependent class III histone deacetylases (HDACs), but has not yet been explored in cutaneous T-cell lymphoma (CTCL).	NAD	103-128	TSPY like 2	Homo sapiens	245-249
24343700-1	2014	Silent information regulator type-1 (SIRT1) is the best-studied member of the Sirtuin (Sir2) family of nicotinamide dinucleotide (NAD)-dependent class III histone deacetylases (HDACs), but has not yet been explored in cutaneous T-cell lymphoma (CTCL).	NAD	130-133	TSPY like 2	Homo sapiens	245-249
24579667-6	2014	The hyperactivation of PARP has also been shown to result in a specific programmed cell death pathway involving NAD+/ATP depletion, mu-calpain activation, loss of mitochondrial membrane potential, and the release of apoptosis inducing factor.	NAD	112-116	poly(ADP-ribose) polymerase 1	Homo sapiens	23-27
24292509-3	2014	NADPH was a much better electron donor than NADH with various electron acceptors, such as oxygen, hydrogen peroxide, DCPIP, cytochrome c, and dithiobisnitrobenzoate.	NAD	44-48	cytochrome c, somatic	Homo sapiens	124-136
25262803-1	2014	Tankyrase 1 and 2 belonging to the family of poly(ADP-ribosyl)ases play an important role in PARsylation by utilizing NAD+ as a substrate in order to generate ADP-ribose polymers.	NAD	118-122	tankyrase	Homo sapiens	0-17
25289390-0	2014	Regulation of rat hepatic alpha-amino-beta-carboxymuconate-epsilon-semialdehyde decarboxylase, a key enzyme in the tryptophan- NAD pathway, by dietary cholesterol and sterol regulatory element-binding protein-2.	NAD	127-130	aminocarboxymuconate semialdehyde decarboxylase	Rattus norvegicus	26-93
25289390-3	2014	In mammals, alpha-amino-beta-carboxymuconate-epsilon-semialdehyde decarboxylase (ACMSD) plays a key role in NAD biosynthesis from tryptophan.	NAD	108-111	aminocarboxymuconate semialdehyde decarboxylase	Rattus norvegicus	12-79
25289390-3	2014	In mammals, alpha-amino-beta-carboxymuconate-epsilon-semialdehyde decarboxylase (ACMSD) plays a key role in NAD biosynthesis from tryptophan.	NAD	108-111	aminocarboxymuconate semialdehyde decarboxylase	Rattus norvegicus	81-86
24194524-1	2013	Massive poly(ADP-ribose) formation by poly(ADP-ribose) polymerase-1 (PARP-1) triggers NAD depletion and cell death.	NAD	86-89	poly(ADP-ribose) polymerase 1	Homo sapiens	38-67
24389190-1	2014	CD157 is a member of the ADP-ribosyl cyclase gene family that is involved in the metabolism of NAD.	NAD	95-98	bone marrow stromal cell antigen 1	Homo sapiens	0-5
25019091-5	2014	The elevated levels of both NADH and ROS can inhibit and inactivate glyceraldehyde 3-phosphate dehydrogenase (GAPDH), respectively, resulting in blockage of the glycolytic pathway and accumulation of glycerol 3-phospate and its prior metabolites along the pathway.	NAD	28-32	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	68-108
25019091-5	2014	The elevated levels of both NADH and ROS can inhibit and inactivate glyceraldehyde 3-phosphate dehydrogenase (GAPDH), respectively, resulting in blockage of the glycolytic pathway and accumulation of glycerol 3-phospate and its prior metabolites along the pathway.	NAD	28-32	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	110-115
24178296-7	2013	This higher NAD(+) level initiates a SIRT3-dependent increase in the mitochondrial substrate supply pathways (i.e. the tricarboxylic acid cycle and fatty acid oxidation).	NAD	12-18	sirtuin 3	Homo sapiens	37-42
24178296-9	2013	We conclude that the increase in NADH oxidation by complex I is a crucial event for SIRT3 activation by RSV.	NAD	33-37	sirtuin 3	Homo sapiens	84-89
24239904-1	2014	The NAD(+) depending enzyme SIRT1 regulates the mitochondrial biogenesis, fat and glucose metabolism through catalyzing the deacetylation of several metabolism-related protein-substrates.	NAD	4-10	sirtuin 1	Rattus norvegicus	28-33
24284820-6	2014	E2, PPT, and DPN stimulated expression of the pituitary transcription factor Pou1f1 and increased its binding to the GH promoter.	NAD	13-16	POU domain, class 1, transcription factor 1	Mus musculus	77-83
24360018-2	2013	Both SIRT1 and PARP1 share a common co-factor nicotinamide adenine dinucleotide (NAD+) and several common substrates, including regulators of DNA damage response and circadian rhythms.	NAD	46-79	poly(ADP-ribose) polymerase 1	Homo sapiens	15-20
24360018-2	2013	Both SIRT1 and PARP1 share a common co-factor nicotinamide adenine dinucleotide (NAD+) and several common substrates, including regulators of DNA damage response and circadian rhythms.	NAD	81-85	poly(ADP-ribose) polymerase 1	Homo sapiens	15-20
24194524-1	2013	Massive poly(ADP-ribose) formation by poly(ADP-ribose) polymerase-1 (PARP-1) triggers NAD depletion and cell death.	NAD	86-89	poly(ADP-ribose) polymerase 1	Homo sapiens	69-75
24194524-5	2013	Here, we challenge this scenario by showing that PARP-1 hyperactivation in cells cultured in the absence of glucose (Glu(-) cells) is followed by NAD depletion and an unexpected PARP-1 activity-dependent ATP increase.	NAD	146-149	poly(ADP-ribose) polymerase 1	Homo sapiens	49-55
23850783-2	2013	Herein, the AuNCs prepared by using polyamidoamine dendrimer as template were constructed not only as nanocarriers for anchoring the large amounts of secondary thrombin aptamers but also as nanocatalysts to catalyze the oxidation of NADH efficiently.	NAD	233-237	coagulation factor II, thrombin	Homo sapiens	160-168
24183892-2	2013	Recent evidence suggests that the NAD(+)-dependent histone deacetylase sirtuin 1 (SIRT1) plays a prominent role in linking changes in nutritional availability with cellular fate regulation.	NAD	34-40	sirtuin 1	Rattus norvegicus	71-80
24183892-2	2013	Recent evidence suggests that the NAD(+)-dependent histone deacetylase sirtuin 1 (SIRT1) plays a prominent role in linking changes in nutritional availability with cellular fate regulation.	NAD	34-40	sirtuin 1	Rattus norvegicus	82-87
24277839-6	2013	We were able to show that formation of a functional vascular system requires glutaredoxin 2-dependent reversible S-glutathionylation of the NAD(+)-dependent protein deacetylase sirtuin 1.	NAD	140-146	glutaredoxin 2	Danio rerio	77-91
23975935-0	2013	NAD+ acts on mitochondrial SirT3 to prevent axonal caspase activation and axonal degeneration.	NAD	0-4	sirtuin 3	Homo sapiens	27-32
24129570-1	2013	3-Hydroxybenzoate 6-hydroxylase (3HB6H) from Rhodococcus jostii RHA1 is an NADH-specific flavoprotein monooxygenase that catalyzes the para-hydroxylation of 3-hydroxybenzoate (3HB) to form 2,5-dihydroxybenzoate (2,5-DHB).	NAD	75-79	3-hydroxybenzoate 6-hydroxylase	Rhodococcus jostii RHA1	0-38
23834033-0	2013	Elevated microRNA-34a in obesity reduces NAD+ levels and SIRT1 activity by directly targeting NAMPT.	NAD	41-45	microRNA 34a	Mus musculus	9-21
23834033-5	2013	Here, we further show that miR-34a reduces NAD(+) levels and SIRT1 activity by targeting NAMPT, the rate-limiting enzyme for NAD(+) biosynthesis.	NAD	43-49	microRNA 34a	Mus musculus	27-34
23834033-5	2013	Here, we further show that miR-34a reduces NAD(+) levels and SIRT1 activity by targeting NAMPT, the rate-limiting enzyme for NAD(+) biosynthesis.	NAD	43-49	nicotinamide phosphoribosyltransferase	Mus musculus	89-94
23834033-5	2013	Here, we further show that miR-34a reduces NAD(+) levels and SIRT1 activity by targeting NAMPT, the rate-limiting enzyme for NAD(+) biosynthesis.	NAD	125-131	microRNA 34a	Mus musculus	27-34
23834033-5	2013	Here, we further show that miR-34a reduces NAD(+) levels and SIRT1 activity by targeting NAMPT, the rate-limiting enzyme for NAD(+) biosynthesis.	NAD	125-131	nicotinamide phosphoribosyltransferase	Mus musculus	89-94
23834033-7	2013	Hepatic overexpression of miR-34a reduced NAMPT/NAD(+) levels, increased acetylation of the SIRT1 target transcriptional regulators, PGC-1alpha, SREBP-1c, FXR, and NF-kappaB, and resulted in obesity-mimetic outcomes.	NAD	48-54	microRNA 34a	Mus musculus	26-33
23834033-9	2013	Further, the miR-34a-mediated decreases were reversed by treatment with the NAD(+) intermediate, nicotinamide mononucleotide.	NAD	76-82	microRNA 34a	Mus musculus	13-20
23834033-10	2013	Conversely, antagonism of miR-34a in diet-induced obese mice restored NAMPT/NAD(+) levels and alleviated steatosis, inflammation, and glucose intolerance.	NAD	76-82	microRNA 34a	Mus musculus	26-33
23834033-11	2013	Anti-miR-34a-mediated increases in NAD(+) levels were attenuated when NAMPT was downregulated.	NAD	35-41	microRNA 34a	Mus musculus	5-12
23834033-11	2013	Anti-miR-34a-mediated increases in NAD(+) levels were attenuated when NAMPT was downregulated.	NAD	35-41	nicotinamide phosphoribosyltransferase	Mus musculus	70-75
23954443-0	2013	Knock-down of glutaminase 2 expression decreases glutathione, NADH, and sensitizes cervical cancer to ionizing radiation.	NAD	62-66	glutaminase 2	Homo sapiens	14-27
23954443-15	2013	At the molecular level, knock-down of GLS2 increased the intracellular ROS levels of HeLaR exposed to irradiation by decreasing the productions of antioxidant GSH, NADH and NADPH.	NAD	164-168	glutaminase 2	Homo sapiens	38-42
23975935-8	2013	Using complementary pharmacological and genetic approaches, we further demonstrate that NAD(+) and grape wine polyphenols prevent axonal apoptosis and act via mitochondrial SirT3 activation in axons.	NAD	88-94	sirtuin 3	Homo sapiens	173-178
23290998-2	2013	PARPs use NAD(+) as substrate and upon cleaving off nicotinamide they transfer the ADP-ribosyl moiety covalently to suitable acceptor proteins and elongate the chain by adding further ADP-ribose units to create a branched polymer, termed poly(ADP-ribose) (PAR), which is rapidly degraded by poly(ADP-ribose) glycohydrolase (PARG) and ADP-ribosylhydrolase 3 (ARH3).	NAD	10-16	poly(ADP-ribose) polymerase 1	Homo sapiens	0-5
24299267-4	2013	CPR from A. annua shows a 3.5-fold increase in uncoupled NADPH oxidation compared to human CPR and a strong preference (85 100-fold) for NADPH over NADH.	NAD	148-152	cytochrome p450 oxidoreductase	Homo sapiens	0-3
23990359-7	2013	PPARalpha also cooperates with Sirt1 activated by EPO through modulating the NAD+ level to regulate metabolic activity.	NAD	77-81	peroxisome proliferator activated receptor alpha	Mus musculus	0-9
23290998-2	2013	PARPs use NAD(+) as substrate and upon cleaving off nicotinamide they transfer the ADP-ribosyl moiety covalently to suitable acceptor proteins and elongate the chain by adding further ADP-ribose units to create a branched polymer, termed poly(ADP-ribose) (PAR), which is rapidly degraded by poly(ADP-ribose) glycohydrolase (PARG) and ADP-ribosylhydrolase 3 (ARH3).	NAD	10-16	poly(ADP-ribose) glycohydrolase	Homo sapiens	291-322
23290998-2	2013	PARPs use NAD(+) as substrate and upon cleaving off nicotinamide they transfer the ADP-ribosyl moiety covalently to suitable acceptor proteins and elongate the chain by adding further ADP-ribose units to create a branched polymer, termed poly(ADP-ribose) (PAR), which is rapidly degraded by poly(ADP-ribose) glycohydrolase (PARG) and ADP-ribosylhydrolase 3 (ARH3).	NAD	10-16	poly(ADP-ribose) glycohydrolase	Homo sapiens	324-328
23357755-2	2013	PARP-1 possesses an intrinsic enzymatic activity that catalyzes the transfer of ADP-ribose (ADPR) units from nicotinamide adenine dinucleotide (NAD(+)) onto target gene regulatory proteins, thereby modulating their activities.	NAD	109-142	poly(ADP-ribose) polymerase 1	Homo sapiens	0-6
23357755-2	2013	PARP-1 possesses an intrinsic enzymatic activity that catalyzes the transfer of ADP-ribose (ADPR) units from nicotinamide adenine dinucleotide (NAD(+)) onto target gene regulatory proteins, thereby modulating their activities.	NAD	144-151	poly(ADP-ribose) polymerase 1	Homo sapiens	0-6
23357756-1	2013	Poly(ADP-ribose) polymerases (PARPs) are NAD(+) dependent enzymes that were identified as DNA repair proteins, however, today it seems clear that PARPs are responsible for a plethora of biological functions.	NAD	41-47	poly(ADP-ribose) polymerase 1	Homo sapiens	30-35
23357756-1	2013	Poly(ADP-ribose) polymerases (PARPs) are NAD(+) dependent enzymes that were identified as DNA repair proteins, however, today it seems clear that PARPs are responsible for a plethora of biological functions.	NAD	41-47	poly(ADP-ribose) polymerase 1	Homo sapiens	146-151
23357756-3	2013	Hereby we review the current understanding of the SIRT-PARP interplay in regard to the biochemical nature of the interaction (competition for the common NAD(+) substrate, mutual posttranslational modifications and direct transcriptional effects) and the physiological or pathophysiological consequences of the interactions (metabolic events, oxidative stress response, genomic stability and aging).	NAD	153-159	poly(ADP-ribose) polymerase 1	Homo sapiens	55-59
23416893-6	2013	Currently, three major pathways have been made responsible for PARP-mediated necroptotic cell death: (1) compromised cellular energetics mainly due to depletion of NAD, the substrate of PARPs; (2) PAR mediated translocation of apoptosis inducing factor (AIF) from mitochondria to nucleus (parthanatos) and (3) a mostly elusive crosstalk between PARylation and cell death/survival kinases and phosphatases.	NAD	164-167	poly(ADP-ribose) polymerase 1	Homo sapiens	63-67
23416893-6	2013	Currently, three major pathways have been made responsible for PARP-mediated necroptotic cell death: (1) compromised cellular energetics mainly due to depletion of NAD, the substrate of PARPs; (2) PAR mediated translocation of apoptosis inducing factor (AIF) from mitochondria to nucleus (parthanatos) and (3) a mostly elusive crosstalk between PARylation and cell death/survival kinases and phosphatases.	NAD	164-167	poly(ADP-ribose) polymerase 1	Homo sapiens	186-191
23999614-2	2013	We found that the two Co(I) species were oxidized by these sulfur-containing compounds to Co(II) forms: oxidation by excess thiosulfate leads to penta-coordinate complexes and oxidation by excess sulfite or dithionite leads to hexa-coordinate Co(II)-SO2(-) complexes.	NAD	22-27	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	90-96
24064205-3	2013	In assays containing dithiothreitol (DTT) and NAD(+), the GTN reductase activity of purified GAPDH produces nitrite and 1,2-GDN as the major products.	NAD	46-52	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	93-98
24350055-1	2013	Poly(ADP-ribose) polymerases (PARPs) are DNA-dependent nuclear enzymes that transfer negatively charged ADP-ribose moieties from cellular nicotinamide-adenine-dinucleotide (NAD(+)) to a variety of protein substrates, altering protein-protein and protein-DNA interactions.	NAD	138-171	poly(ADP-ribose) polymerase 1	Homo sapiens	30-35
24350055-1	2013	Poly(ADP-ribose) polymerases (PARPs) are DNA-dependent nuclear enzymes that transfer negatively charged ADP-ribose moieties from cellular nicotinamide-adenine-dinucleotide (NAD(+)) to a variety of protein substrates, altering protein-protein and protein-DNA interactions.	NAD	173-179	poly(ADP-ribose) polymerase 1	Homo sapiens	30-35
23999614-2	2013	We found that the two Co(I) species were oxidized by these sulfur-containing compounds to Co(II) forms: oxidation by excess thiosulfate leads to penta-coordinate complexes and oxidation by excess sulfite or dithionite leads to hexa-coordinate Co(II)-SO2(-) complexes.	NAD	22-27	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	243-249
24260155-9	2013	In addition, DPN treatment (an ERbeta agonist) induced the ARE-luciferase reporter gene, promoting Nrf2 nuclear translocation.	NAD	13-16	NFE2 like bZIP transcription factor 2	Homo sapiens	99-103
24105795-2	2013	In this study, DFT calculations were used to investigate their catalytic mechanism, to demonstrate that the initial active state was a Co(I) complex and that H2 was evolved in a heterolytic manner through the protonation of a Co(II)-hydride intermediate.	NAD	135-140	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	226-231
23994215-6	2013	These data demonstrated that cellular NAD depletion and decline of SIRT1 activity play critical roles in PARP-1-mediated epileptic neuronal death in the HNC model of acute AE.	NAD	38-41	poly(ADP-ribose) polymerase 1	Homo sapiens	105-111
24013482-5	2013	For example, the activities of NAD(P)-dependent enzymes such as glyceraldehyde-3-phosphate dehydrogenase (G3PDH) in chloroplasts and isocitrate dehydrogenase (ICDH) in mitochondria were elevated, along with levels of pyridine nucleotides (nicotinamide coenzymes) [NAD(H) and NADP(H)] and activity of NAD kinase (NADP forming enzyme).	NAD	264-270	cytosolic isocitrate dehydrogenase	Cucumis sativus	133-157
24013482-5	2013	For example, the activities of NAD(P)-dependent enzymes such as glyceraldehyde-3-phosphate dehydrogenase (G3PDH) in chloroplasts and isocitrate dehydrogenase (ICDH) in mitochondria were elevated, along with levels of pyridine nucleotides (nicotinamide coenzymes) [NAD(H) and NADP(H)] and activity of NAD kinase (NADP forming enzyme).	NAD	264-270	cytosolic isocitrate dehydrogenase	Cucumis sativus	159-163
23860243-7	2013	Analysis of recombinant peroxisomal NADH-dependent HPR1 activity from Arabidopsis in the presence of H2O2, NO, GSH and peroxynitrite showed that the ONOO(-) molecule caused the highest inhibition of activity (51% at 5mM SIN-1), with 5mM H2O2 having no inhibitory effect.	NAD	36-40	nuclear matrix protein-like protein	Arabidopsis thaliana	51-55
23803694-3	2013	Various lines of evidence indicate that nicotinamide adenine dinucleotide(P)H quinone oxidoreductase 1 (NQO1) plays an important role in cancer prevention, but the molecular mechanisms underlying this effect have not yet been fully elucidated.	NAD	40-73	NAD(P)H quinone dehydrogenase 1	Homo sapiens	104-108
24042441-9	2013	Downregulation of SIRT3 inhibited acetylation of NMNAT2 and NAD+ synthesis activity of the enzyme.	NAD	60-64	sirtuin 3	Homo sapiens	18-23
23922380-9	2013	Finally, RelB also couples with bioenergy NAD(+) sensor SIRT1 to integrate acute inflammation with changes in metabolism and mitochondrial bioenergetics.	NAD	42-48	RELB proto-oncogene, NF-kB subunit	Homo sapiens	9-13
23994215-0	2013	Cellular NAD depletion and decline of SIRT1 activity play critical roles in PARP-1-mediated acute epileptic neuronal death in vitro.	NAD	9-12	poly(ADP-ribose) polymerase 1	Homo sapiens	76-82
23994215-4	2013	The results showed that PARP-1 over-activation caused by Mg2+-free stimuli led to cellular NAD depletion which could block AIF translocation from mitochondria to nucleus and attenuate neuronal death.	NAD	91-94	poly(ADP-ribose) polymerase 1	Homo sapiens	24-30
24555099-4	2013	RcFAH12 requires an electron supply from NADH:cytochrome b5 reductase (CBR1) and cytochrome b5 (Cb5) to synthesize ricinoleic acid.	NAD	41-45	NADH:cytochrome B5 reductase 1	Arabidopsis thaliana	71-75
23900421-4	2013	The level of tricarboxylic acid cycle intermediates, including malate and oxaloacetate, and the NADH-to-NAD(+) ratio are perturbed in the liver of Gcn2 KO mice either in the fed or fasted state, which may directly impinge upon GNG.	NAD	96-100	eukaryotic translation initiation factor 2 alpha kinase 4	Mus musculus	147-151
23900421-4	2013	The level of tricarboxylic acid cycle intermediates, including malate and oxaloacetate, and the NADH-to-NAD(+) ratio are perturbed in the liver of Gcn2 KO mice either in the fed or fasted state, which may directly impinge upon GNG.	NAD	104-110	eukaryotic translation initiation factor 2 alpha kinase 4	Mus musculus	147-151
23918774-2	2013	Nicotinamide phosphoribosyl transferase (Nampt) is the rate-limiting enzyme in the NAD salvage pathway responsible for converting NAM to NAD to maintain cellular redox state.	NAD	83-86	nicotinamide phosphoribosyltransferase	Mus musculus	0-39
23918774-2	2013	Nicotinamide phosphoribosyl transferase (Nampt) is the rate-limiting enzyme in the NAD salvage pathway responsible for converting NAM to NAD to maintain cellular redox state.	NAD	83-86	nicotinamide phosphoribosyltransferase	Mus musculus	41-46
23918774-2	2013	Nicotinamide phosphoribosyl transferase (Nampt) is the rate-limiting enzyme in the NAD salvage pathway responsible for converting NAM to NAD to maintain cellular redox state.	NAD	137-140	nicotinamide phosphoribosyltransferase	Mus musculus	0-39
23918774-2	2013	Nicotinamide phosphoribosyl transferase (Nampt) is the rate-limiting enzyme in the NAD salvage pathway responsible for converting NAM to NAD to maintain cellular redox state.	NAD	137-140	nicotinamide phosphoribosyltransferase	Mus musculus	41-46
24048848-5	2013	Dorsal hippocampal (DH) infusion of ERalpha (PPT) or ERbeta (DPN) agonists enhanced novel object recognition and object placement memory in ovariectomized female mice in an ERK-dependent manner, suggesting that these receptors influence memory by rapidly activating hippocampal cell signaling.	NAD	61-64	mitogen-activated protein kinase 1	Mus musculus	173-176
24035395-4	2013	Ifh1p is acetylated at numerous sites in its N-terminal region by Gcn5p and deacetylated by NAD(+)-dependent deacetylases of the sirtuin family.	NAD	92-98	Ifh1p	Saccharomyces cerevisiae S288C	0-5
23813101-0	2013	Insulin resistance and dysregulation of tryptophan-kynurenine and kynurenine-nicotinamide adenine dinucleotide metabolic pathways.	NAD	77-110	insulin	Homo sapiens	0-7
23749777-3	2013	beta-lapachone (betaL) has been shown to increase cellular NAD(+)/NADH ratio via activation of NAD(P)H:quinone oxidoreductase 1 (NQO1).	NAD	59-65	NAD(P)H quinone dehydrogenase 1	Rattus norvegicus	129-133
23864660-1	2013	3-Hydroxybenzoate 6-hydroxylase (3HB6H) from Rhodococcus jostii RHA1 is a dimeric flavoprotein that catalyzes the NADH- and oxygen-dependent para-hydroxylation of 3-hydroxybenzoate to 2,5-dihydroxybenzoate.	NAD	114-118	3-hydroxybenzoate 6-hydroxylase	Rhodococcus jostii RHA1	0-38
24012758-1	2013	The NAD(+)-dependent protein deacetylase SIRT6 regulates genome stability, cancer, and lifespan.	NAD	4-10	sirtuin 6	Mus musculus	41-46
24280423-8	2013	RESULTS: 3-((3-carbamoyl-7-(3,5-dimethylisoxazol-4-yl)-6-methoxyquinolin-4-yl) amino) benzoic acid was identified as an NADH-competitive LDHA inhibitor.	NAD	120-124	lactate dehydrogenase A	Homo sapiens	137-141
23749777-3	2013	beta-lapachone (betaL) has been shown to increase cellular NAD(+)/NADH ratio via activation of NAD(P)H:quinone oxidoreductase 1 (NQO1).	NAD	66-70	NAD(P)H quinone dehydrogenase 1	Rattus norvegicus	129-133
23764826-6	2013	The calculated redox tuning of Co(I)H interactions on the reduction potential of Co(II)/Co(I) couple (60-800 mV vs standard hydrogen electrode (SHE)), irrespective of the beta-axial ligand considered, is significantly higher than the biological redox gap between the reduction potential of Co(II)/Co(I) couple and that of the biological reducing agents (50 mV vs SHE).	NAD	31-36	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	81-87
24167412-5	2013	We have now developed a number of multi target drugs which possess neuroprotective, and neurorestorative activity as well as being able to active PGC-1alpha (peroxisome proliferator-activated receptor gamma coactivator-1alpha), SIRT1 (NAD-dependent deacetylase protein) and NTF (mitochondrial transcription factor) that are intimately associated with mitochondrial biogenesis.	NAD	235-238	PPARG coactivator 1 alpha	Homo sapiens	158-225
23764826-6	2013	The calculated redox tuning of Co(I)H interactions on the reduction potential of Co(II)/Co(I) couple (60-800 mV vs standard hydrogen electrode (SHE)), irrespective of the beta-axial ligand considered, is significantly higher than the biological redox gap between the reduction potential of Co(II)/Co(I) couple and that of the biological reducing agents (50 mV vs SHE).	NAD	31-36	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	290-296
23798679-5	2013	There is also evidence that metabolites such as NAD(+) (acting via deacetylases such as SIRT1 and SIRT2) and succinate (which regulates hypoxia-inducible factor 1alpha) are signals that regulate innate immunity.	NAD	48-54	hypoxia inducible factor 1 subunit alpha	Homo sapiens	136-167
23842789-1	2013	Sirt3, a member of the mammalian sirtuin family protein that is localized to mitochondria, is a NAD+-dependent deacetylase and plays an important role in the control of metabolic activity.	NAD	96-99	sirtuin 3	Homo sapiens	0-5
23597856-5	2013	Poly(ADP-ribose)-1 (PARP-1) is an abundant nuclear enzyme that consumes NAD(+) in the process of forming (ADP-ribose)polymers on target proteins, and extensive PARP-1 activation can reduce intracellular NAD(+) concentrations.	NAD	72-78	poly(ADP-ribose) polymerase 1	Homo sapiens	20-26
23897466-5	2013	A crystal structure of Sirt3 in complex with SRT1720 and an NAD(+) analogue reveals that the compound partially occupies the acetyl-Lys binding site, thus explaining the reported competition with the peptide substrate.	NAD	60-66	sirtuin 3	Homo sapiens	23-28
23597856-0	2013	Poly(ADP-ribose) polymerase-1-induced NAD(+) depletion promotes nuclear factor-kappaB transcriptional activity by preventing p65 de-acetylation.	NAD	38-44	poly(ADP-ribose) polymerase 1	Homo sapiens	0-29
23597856-5	2013	Poly(ADP-ribose)-1 (PARP-1) is an abundant nuclear enzyme that consumes NAD(+) in the process of forming (ADP-ribose)polymers on target proteins, and extensive PARP-1 activation can reduce intracellular NAD(+) concentrations.	NAD	72-78	poly(ADP-ribose) polymerase 1	Homo sapiens	160-166
23597856-5	2013	Poly(ADP-ribose)-1 (PARP-1) is an abundant nuclear enzyme that consumes NAD(+) in the process of forming (ADP-ribose)polymers on target proteins, and extensive PARP-1 activation can reduce intracellular NAD(+) concentrations.	NAD	203-209	poly(ADP-ribose) polymerase 1	Homo sapiens	20-26
23597856-5	2013	Poly(ADP-ribose)-1 (PARP-1) is an abundant nuclear enzyme that consumes NAD(+) in the process of forming (ADP-ribose)polymers on target proteins, and extensive PARP-1 activation can reduce intracellular NAD(+) concentrations.	NAD	203-209	poly(ADP-ribose) polymerase 1	Homo sapiens	160-166
23597856-6	2013	Here we tested the idea that PARP-1 activation can regulate NF-kappaB transcriptional activity by reducing NAD(+) concentrations and thereby inhibiting de-acetylation of p65.	NAD	107-113	poly(ADP-ribose) polymerase 1	Homo sapiens	29-35
23597856-10	2013	The effects of PARP-1 activation were replicated by a SIRT1 inhibitor, EX-527, and were reversed by exogenous NAD(+).	NAD	110-116	poly(ADP-ribose) polymerase 1	Homo sapiens	15-21
23597856-11	2013	These findings demonstrate that PARP-1-induced changes in NAD(+) levels can modulate NF-kappaB transcriptional activity through effects on p65 acetylation.	NAD	58-64	poly(ADP-ribose) polymerase 1	Homo sapiens	32-38
23583951-6	2013	Knockdown of the NAD(+)-dependent protein deacetylase sirtuin 1 (SIRT1) by siRNA prevented the upregulation of eNOS mRNA and protein by resveratrol.	NAD	17-23	nitric oxide synthase 3	Homo sapiens	111-115
24009628-1	2013	BACKGROUND: Silent mating type information regulation 2 homolog 1 (SIRT1), an NAD+-dependent deacetylase, might act as a tumor promoter by inhibiting p53, but may also as a tumor suppressor by inhibiting several oncogenes such as beta-catenin and survivin.	NAD	78-81	tumor protein p53	Homo sapiens	150-153
23603111-6	2013	DPN treatment of EAE animals resulted in phosphorylated ERbeta and activated the phosphatidylinositol 3-kinase (PI3K)/serine-threonine-specific protein kinase (Akt)/mammalian target of rapamycin (mTOR) signaling pathway, a pathway required for oligodendrocyte survival and axon myelination.	NAD	0-3	AKT serine/threonine kinase 1	Homo sapiens	160-163
23603111-6	2013	DPN treatment of EAE animals resulted in phosphorylated ERbeta and activated the phosphatidylinositol 3-kinase (PI3K)/serine-threonine-specific protein kinase (Akt)/mammalian target of rapamycin (mTOR) signaling pathway, a pathway required for oligodendrocyte survival and axon myelination.	NAD	0-3	mechanistic target of rapamycin kinase	Homo sapiens	165-194
23603111-6	2013	DPN treatment of EAE animals resulted in phosphorylated ERbeta and activated the phosphatidylinositol 3-kinase (PI3K)/serine-threonine-specific protein kinase (Akt)/mammalian target of rapamycin (mTOR) signaling pathway, a pathway required for oligodendrocyte survival and axon myelination.	NAD	0-3	mechanistic target of rapamycin kinase	Homo sapiens	196-200
23542362-3	2013	SIRT1 is regulated by a NAD(+)-dependent DNA repair enzyme, poly(ADP-ribose) polymerase-1 (PARP1), and subsequent NAD(+) depletion by oxidative stress may have consequent effects on inflammatory and stress responses as well as cellular senescence.	NAD	24-30	poly(ADP-ribose) polymerase 1	Homo sapiens	60-89
23542362-3	2013	SIRT1 is regulated by a NAD(+)-dependent DNA repair enzyme, poly(ADP-ribose) polymerase-1 (PARP1), and subsequent NAD(+) depletion by oxidative stress may have consequent effects on inflammatory and stress responses as well as cellular senescence.	NAD	24-30	poly(ADP-ribose) polymerase 1	Homo sapiens	91-96
23770670-4	2013	We recently identified a pathway by which the AHR target gene TiPARP (TCDD-inducible poly(ADP-ribose) polymerase) contributes to TCDD suppression of transcription of phosphoenolpyruvate carboxykinase (PEPCK), a key regulator of gluconeogenesis, by consuming NAD(+) and decreasing Sirtuin 1 activation of the peroxisome proliferator-activated receptor gamma coactivator 1alpha (PGC1alpha), a transcriptional activator of PEPCK.	NAD	258-264	TCDD inducible poly(ADP-ribose) polymerase	Homo sapiens	62-68
23770670-4	2013	We recently identified a pathway by which the AHR target gene TiPARP (TCDD-inducible poly(ADP-ribose) polymerase) contributes to TCDD suppression of transcription of phosphoenolpyruvate carboxykinase (PEPCK), a key regulator of gluconeogenesis, by consuming NAD(+) and decreasing Sirtuin 1 activation of the peroxisome proliferator-activated receptor gamma coactivator 1alpha (PGC1alpha), a transcriptional activator of PEPCK.	NAD	258-264	TCDD inducible poly(ADP-ribose) polymerase	Homo sapiens	70-112
23770670-4	2013	We recently identified a pathway by which the AHR target gene TiPARP (TCDD-inducible poly(ADP-ribose) polymerase) contributes to TCDD suppression of transcription of phosphoenolpyruvate carboxykinase (PEPCK), a key regulator of gluconeogenesis, by consuming NAD(+) and decreasing Sirtuin 1 activation of the peroxisome proliferator-activated receptor gamma coactivator 1alpha (PGC1alpha), a transcriptional activator of PEPCK.	NAD	258-264	PPARG coactivator 1 alpha	Homo sapiens	308-375
23770670-4	2013	We recently identified a pathway by which the AHR target gene TiPARP (TCDD-inducible poly(ADP-ribose) polymerase) contributes to TCDD suppression of transcription of phosphoenolpyruvate carboxykinase (PEPCK), a key regulator of gluconeogenesis, by consuming NAD(+) and decreasing Sirtuin 1 activation of the peroxisome proliferator-activated receptor gamma coactivator 1alpha (PGC1alpha), a transcriptional activator of PEPCK.	NAD	258-264	PPARG coactivator 1 alpha	Homo sapiens	377-386
23744286-12	2013	Thus, it was concluded that the overexpression of GRE2 together with ADH1 restores glycolaldehyde tolerance by augmenting the NADPH-dependent reduction pathway in addition to NADH-dependent reduction pathway.	NAD	175-179	alcohol dehydrogenase ADH1	Saccharomyces cerevisiae S288C	69-73
23744286-4	2013	Glycolaldehyde-reducing activity of the ADH1-overexpressing strain was NADH-dependent but not NADPH-dependent.	NAD	71-75	alcohol dehydrogenase ADH1	Saccharomyces cerevisiae S288C	40-44
23742622-5	2013	Indeed, supplying excess precursors, or blocking its utilization by poly(ADP-ribose) polymerase (PARP) enzymes or CD38/CD157, boosts NAD+ levels, activates sirtuins and promotes healthy aging.	NAD	133-137	poly(ADP-ribose) polymerase 1	Homo sapiens	68-95
23786618-3	2013	In one of the adult fibroblast strains evaluated, these changes in procollagen-1 and NAD(+)/NADH in response to the complex of bioactives were in parallel with increased expression of mRNA biomarkers related primarily to dermal matrix and basement membrane structure, including COL1A1, COL3A1, COL5A1, COL14A1, ELN and LOXL2, in addition to SOD2, NAMPT and TGFBR3; MMP1 was decreased in expression.	NAD	85-91	collagen type V alpha 1 chain	Homo sapiens	294-300
23786618-3	2013	In one of the adult fibroblast strains evaluated, these changes in procollagen-1 and NAD(+)/NADH in response to the complex of bioactives were in parallel with increased expression of mRNA biomarkers related primarily to dermal matrix and basement membrane structure, including COL1A1, COL3A1, COL5A1, COL14A1, ELN and LOXL2, in addition to SOD2, NAMPT and TGFBR3; MMP1 was decreased in expression.	NAD	85-91	lysyl oxidase like 2	Homo sapiens	319-324
23786618-3	2013	In one of the adult fibroblast strains evaluated, these changes in procollagen-1 and NAD(+)/NADH in response to the complex of bioactives were in parallel with increased expression of mRNA biomarkers related primarily to dermal matrix and basement membrane structure, including COL1A1, COL3A1, COL5A1, COL14A1, ELN and LOXL2, in addition to SOD2, NAMPT and TGFBR3; MMP1 was decreased in expression.	NAD	92-96	collagen type V alpha 1 chain	Homo sapiens	294-300
23786618-3	2013	In one of the adult fibroblast strains evaluated, these changes in procollagen-1 and NAD(+)/NADH in response to the complex of bioactives were in parallel with increased expression of mRNA biomarkers related primarily to dermal matrix and basement membrane structure, including COL1A1, COL3A1, COL5A1, COL14A1, ELN and LOXL2, in addition to SOD2, NAMPT and TGFBR3; MMP1 was decreased in expression.	NAD	92-96	lysyl oxidase like 2	Homo sapiens	319-324
23742622-5	2013	Indeed, supplying excess precursors, or blocking its utilization by poly(ADP-ribose) polymerase (PARP) enzymes or CD38/CD157, boosts NAD+ levels, activates sirtuins and promotes healthy aging.	NAD	133-137	poly(ADP-ribose) polymerase 1	Homo sapiens	97-101
23648480-5	2013	NQO1 binds and protects PGC-1alpha from degradation in an NADH-dependent manner.	NAD	58-62	NAD(P)H quinone dehydrogenase 1	Homo sapiens	0-4
23648480-5	2013	NQO1 binds and protects PGC-1alpha from degradation in an NADH-dependent manner.	NAD	58-62	PPARG coactivator 1 alpha	Homo sapiens	24-34
23548271-1	2013	Quinolinic acid is a product of tryptophan degradation and may serve as a precursor for NAD(+), an important enzymatic cofactor for enzymes such as the DNA repair protein PARP.	NAD	88-94	poly(ADP-ribose) polymerase 1	Homo sapiens	171-175
23951401-6	2013	In addition, the rate of regeneration of NADH after inhibition of respiration is much slower in Nrf2-knockout cells than in their wild-type counterparts.	NAD	41-45	nuclear factor, erythroid derived 2, like 2	Mus musculus	96-100
23675962-7	2013	The addition of NADH to an aqueous solution of the met-Hb2-(HSA-LF)3 cluster reduced the inactive ferric Hb center to the functional ferrous Hb.	NAD	16-20	albumin	Homo sapiens	60-63
24195366-6	2013	The expression of hPARPI was visualized by SDS-PAGE and Western blotting; the activity of expressed and purified hPARP1 was confirmed by the reaction of consumption of NAD+ by hPARP1 in vitro.	NAD	168-172	poly(ADP-ribose) polymerase 1	Homo sapiens	113-119
24195366-6	2013	The expression of hPARPI was visualized by SDS-PAGE and Western blotting; the activity of expressed and purified hPARP1 was confirmed by the reaction of consumption of NAD+ by hPARP1 in vitro.	NAD	168-172	poly(ADP-ribose) polymerase 1	Homo sapiens	176-182
23518685-10	2013	Moreover, PAG treatment significantly attenuated the increase in NADH fluorescence following ET-1 exposure during endotoxemia (61 grayscale units LPS vs. 21 units in PAG/LPS, P &lt; 0.05), suggesting an improvement in hepatic oxygen availability.	NAD	65-69	endothelin 1	Rattus norvegicus	93-97
23628333-2	2013	Biochemical, surface plasmon resonance, and saturation transfer difference NMR experiments indicated that the compound specifically associated with human LDHA in a manner that required simultaneous binding of the NADH co-factor.	NAD	213-217	lactate dehydrogenase A	Homo sapiens	154-158
23548271-6	2013	Human malignant glioma cells, but not nonneoplastic astrocytes, expressed quinolinic acid phosphoribosyltransferase (QPRT) to use quinolinic acid for NAD(+) synthesis and prevent apoptosis when de novo NAD(+) synthesis was blocked.	NAD	150-156	quinolinate phosphoribosyltransferase	Homo sapiens	74-115
23548271-6	2013	Human malignant glioma cells, but not nonneoplastic astrocytes, expressed quinolinic acid phosphoribosyltransferase (QPRT) to use quinolinic acid for NAD(+) synthesis and prevent apoptosis when de novo NAD(+) synthesis was blocked.	NAD	150-156	quinolinate phosphoribosyltransferase	Homo sapiens	117-121
23548271-6	2013	Human malignant glioma cells, but not nonneoplastic astrocytes, expressed quinolinic acid phosphoribosyltransferase (QPRT) to use quinolinic acid for NAD(+) synthesis and prevent apoptosis when de novo NAD(+) synthesis was blocked.	NAD	202-208	quinolinate phosphoribosyltransferase	Homo sapiens	74-115
23548271-6	2013	Human malignant glioma cells, but not nonneoplastic astrocytes, expressed quinolinic acid phosphoribosyltransferase (QPRT) to use quinolinic acid for NAD(+) synthesis and prevent apoptosis when de novo NAD(+) synthesis was blocked.	NAD	202-208	quinolinate phosphoribosyltransferase	Homo sapiens	117-121
23548271-10	2013	Our data indicate that neoplastic transformation in astrocytes is associated with a QPRT-mediated switch in NAD(+) metabolism by exploiting microglia-derived quinolinic acid as an alternative source of replenishing intracellular NAD(+) pools.	NAD	108-114	quinolinate phosphoribosyltransferase	Homo sapiens	84-88
23307072-6	2013	The addition of lactic acid rescued and knockdown of LDH-A replicated the effects of [NAD(H)] on motility.	NAD	86-92	lactate dehydrogenase A	Homo sapiens	53-58
23548271-10	2013	Our data indicate that neoplastic transformation in astrocytes is associated with a QPRT-mediated switch in NAD(+) metabolism by exploiting microglia-derived quinolinic acid as an alternative source of replenishing intracellular NAD(+) pools.	NAD	229-235	quinolinate phosphoribosyltransferase	Homo sapiens	84-88
23054211-6	2013	Herein, we mechanistically link ENOX1-mediated regulation of cellular NADH concentrations with proteomics profiling of endothelial cell protein expression following exposure to VJ115.	NAD	70-74	ecto-NOX disulfide-thiol exchanger 1	Homo sapiens	32-37
23435312-3	2013	The coenzyme nicotinamide adenine dinucleotide (NAD(+)) is not only essential for cellular metabolism; it also affects activity of NAD-dependent enzymes, such as PARP-1 and SIRT-1.	NAD	13-46	poly(ADP-ribose) polymerase 1	Homo sapiens	162-168
23435312-3	2013	The coenzyme nicotinamide adenine dinucleotide (NAD(+)) is not only essential for cellular metabolism; it also affects activity of NAD-dependent enzymes, such as PARP-1 and SIRT-1.	NAD	48-55	poly(ADP-ribose) polymerase 1	Homo sapiens	162-168
23435312-3	2013	The coenzyme nicotinamide adenine dinucleotide (NAD(+)) is not only essential for cellular metabolism; it also affects activity of NAD-dependent enzymes, such as PARP-1 and SIRT-1.	NAD	48-51	poly(ADP-ribose) polymerase 1	Homo sapiens	162-168
23435312-9	2013	PBEF1 activity and NAD(+) content were reduced in MM cells by APO866, resulting in lower activity of PARP-1 and SIRT-1.	NAD	19-25	poly(ADP-ribose) polymerase 1	Homo sapiens	101-107
23054211-10	2013	These data support the hypothesis that VJ115 inhibition of ENOX1 can impact expression of proteins involved in cytoskeletal reorganization and support a hypothesis in which ENOX1 activity links elevated cellular NADH concentrations with cytoskeletal reorganization and angiogenesis.	NAD	212-216	ecto-NOX disulfide-thiol exchanger 1	Homo sapiens	173-178
23798621-7	2013	DACH1 binding to p53 was inhibited by NAD-dependent deacetylation via DACH1 K628.	NAD	38-41	tumor protein p53	Homo sapiens	17-20
23225495-4	2013	In this work, we show that dynamic MRSI of hyperpolarized [1-(13) C]pyruvate and its conversion to [1-(13) C]lactate can provide an indirect in vivo measurement of ALDH2 activity via the concentration of NADH (nicotinamide adenine dinucleotide, reduced form), a co-factor common to both the reduction of pyruvate to lactate and the oxidation of acetaldehyde to acetate.	NAD	204-208	aldehyde dehydrogenase 1 family, member A1	Rattus norvegicus	164-169
23225495-4	2013	In this work, we show that dynamic MRSI of hyperpolarized [1-(13) C]pyruvate and its conversion to [1-(13) C]lactate can provide an indirect in vivo measurement of ALDH2 activity via the concentration of NADH (nicotinamide adenine dinucleotide, reduced form), a co-factor common to both the reduction of pyruvate to lactate and the oxidation of acetaldehyde to acetate.	NAD	210-243	aldehyde dehydrogenase 1 family, member A1	Rattus norvegicus	164-169
23318931-5	2013	Our data show that TPI(sugarkill) animals exhibit higher levels of the oxidized forms of NAD(+), NADP(+) and glutathione in an age-dependent manner.	NAD	89-95	triosephosphate isomerase 1	Homo sapiens	19-22
23422569-2	2013	Previous studies demonstrate that the activity of the evolutionarily conserved NAD(+)-dependent deacetylase SIRT1 declines with age and that pharmacological activators of SIRT1 confer significant anti-aging cardiovascular effects.	NAD	79-85	sirtuin 1	Rattus norvegicus	108-113
23504317-4	2013	Nicotinamide nucleotide transhydrogenase (NNT) is a mitochondrial enzyme that transfers reducing equivalents from NADH to NADPH.	NAD	114-118	nicotinamide nucleotide transhydrogenase	Homo sapiens	0-40
23504317-4	2013	Nicotinamide nucleotide transhydrogenase (NNT) is a mitochondrial enzyme that transfers reducing equivalents from NADH to NADPH.	NAD	114-118	nicotinamide nucleotide transhydrogenase	Homo sapiens	42-45
23666923-2	2013	In one form of programmed necrotic cell death, induced by cytotoxic alkylating agents, hyperactivation of poly-ADP-ribose polymerase (PARP) leads to cellular NAD and ATP depletion, mitochondrial dysfunction, reactive oxygen species formation, and ensuing cell death.	NAD	158-161	poly(ADP-ribose) polymerase 1	Homo sapiens	106-132
23666923-2	2013	In one form of programmed necrotic cell death, induced by cytotoxic alkylating agents, hyperactivation of poly-ADP-ribose polymerase (PARP) leads to cellular NAD and ATP depletion, mitochondrial dysfunction, reactive oxygen species formation, and ensuing cell death.	NAD	158-161	poly(ADP-ribose) polymerase 1	Homo sapiens	134-138
23666923-5	2013	Like wild-type cells, ALKBH7-depleted cells undergo PARP hyperactivation and NAD depletion after severe DNA damage but, unlike wild-type cells, exhibit rapid recovery of intracellular NAD and ATP levels.	NAD	77-80	alkB homolog 7	Homo sapiens	22-28
23666923-5	2013	Like wild-type cells, ALKBH7-depleted cells undergo PARP hyperactivation and NAD depletion after severe DNA damage but, unlike wild-type cells, exhibit rapid recovery of intracellular NAD and ATP levels.	NAD	184-187	alkB homolog 7	Homo sapiens	22-28
23597945-4	2013	In addition, we demonstrated that the Myc/HIF-1-targeted glyceraldehyde-3-phosphate dehydrogenase (GAPDH) catalyzing a key step producing the NADH cofactor, activates the Akt pathway, thereby upregulating expression of the anti-apoptotic Bcl-xL.	NAD	142-146	hypoxia inducible factor 1 subunit alpha	Homo sapiens	42-47
23597945-4	2013	In addition, we demonstrated that the Myc/HIF-1-targeted glyceraldehyde-3-phosphate dehydrogenase (GAPDH) catalyzing a key step producing the NADH cofactor, activates the Akt pathway, thereby upregulating expression of the anti-apoptotic Bcl-xL.	NAD	142-146	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	57-97
23597945-4	2013	In addition, we demonstrated that the Myc/HIF-1-targeted glyceraldehyde-3-phosphate dehydrogenase (GAPDH) catalyzing a key step producing the NADH cofactor, activates the Akt pathway, thereby upregulating expression of the anti-apoptotic Bcl-xL.	NAD	142-146	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	99-104
23597945-4	2013	In addition, we demonstrated that the Myc/HIF-1-targeted glyceraldehyde-3-phosphate dehydrogenase (GAPDH) catalyzing a key step producing the NADH cofactor, activates the Akt pathway, thereby upregulating expression of the anti-apoptotic Bcl-xL.	NAD	142-146	AKT serine/threonine kinase 1	Homo sapiens	171-174
23597945-4	2013	In addition, we demonstrated that the Myc/HIF-1-targeted glyceraldehyde-3-phosphate dehydrogenase (GAPDH) catalyzing a key step producing the NADH cofactor, activates the Akt pathway, thereby upregulating expression of the anti-apoptotic Bcl-xL.	NAD	142-146	BCL2 like 1	Homo sapiens	238-244
23422569-2	2013	Previous studies demonstrate that the activity of the evolutionarily conserved NAD(+)-dependent deacetylase SIRT1 declines with age and that pharmacological activators of SIRT1 confer significant anti-aging cardiovascular effects.	NAD	79-85	sirtuin 1	Rattus norvegicus	171-176
23502856-4	2013	Inducers of the NLRP3 inflammasome caused aberrant mitochondrial homeostasis to diminish the concentration of the coenzyme NAD(+), which in turn inactivated the NAD(+)-dependent alpha-tubulin deacetylase sirtuin 2; this resulted in the accumulation of acetylated alpha-tubulin.	NAD	123-129	NLR family pyrin domain containing 3	Homo sapiens	16-21
23349504-3	2013	LKB1 MKO mice also show decreased muscle SIK3 activity, increased histone deacetylase 4 expression, decreased NAD+ concentration and SIRT1 activity, and decreased expression of genes involved in FA oxidation.	NAD	110-114	serine/threonine kinase 11	Mus musculus	0-4
23089953-3	2013	The azoreductase had highest specific activity (153.16 U/mg) at pH 6.5, which showed a preference for nicotinamide adenine dinucleotide (NADH) as electron donor.	NAD	102-135	NAD(P)H quinone dehydrogenase 1	Homo sapiens	4-16
23089953-3	2013	The azoreductase had highest specific activity (153.16 U/mg) at pH 6.5, which showed a preference for nicotinamide adenine dinucleotide (NADH) as electron donor.	NAD	137-141	NAD(P)H quinone dehydrogenase 1	Homo sapiens	4-16
23089953-4	2013	The phylogenetic tree analysis indicated that the azoreductase had preference for NADH and dependence for flavin mononucleotide (FMN).	NAD	82-86	NAD(P)H quinone dehydrogenase 1	Homo sapiens	50-62
23398717-4	2013	Replacement of XYL1 with GRE3 has been regarded as an undesirable approach because NADPH-specific aldose reductase (GRE3) would aggravate redox balance with xylitol dehydrogenase (XYL2) using NAD(+) exclusively.	NAD	192-198	trifunctional aldehyde reductase/xylose reductase/glucose 1-dehydrogenase (NADP(+))	Saccharomyces cerevisiae S288C	25-29
23398717-4	2013	Replacement of XYL1 with GRE3 has been regarded as an undesirable approach because NADPH-specific aldose reductase (GRE3) would aggravate redox balance with xylitol dehydrogenase (XYL2) using NAD(+) exclusively.	NAD	192-198	trifunctional aldehyde reductase/xylose reductase/glucose 1-dehydrogenase (NADP(+))	Saccharomyces cerevisiae S288C	116-120
23296366-5	2013	Other examples are the epimerase and the ATP-dependent dehydratase that repair hydrated forms of NADH and NADPH; ethylmalonyl-CoA decarboxylase, which eliminates an abnormal metabolite formed by acetyl-CoA carboxylase, an enzyme of fatty acid synthesis; L-pipecolate oxidase, which repairs a metabolite formed by a side activity of an enzyme of L-proline biosynthesis.	NAD	97-101	pipecolic acid and sarcosine oxidase	Homo sapiens	254-274
23508103-6	2013	Activation of AhR induced tetrachlorodibenzo-p-dioxin (TCDD)-inducible poly(ADP-ribose) polymerase (TiPARP) gene expression, depleted NAD(+), deactivated the mitochondrial sirtuin deacetylase 3 (Sirt3), increased SOD2 acetylation, and thereby decreased SOD2 activity.	NAD	134-140	aryl-hydrocarbon receptor	Mus musculus	14-17
23502856-4	2013	Inducers of the NLRP3 inflammasome caused aberrant mitochondrial homeostasis to diminish the concentration of the coenzyme NAD(+), which in turn inactivated the NAD(+)-dependent alpha-tubulin deacetylase sirtuin 2; this resulted in the accumulation of acetylated alpha-tubulin.	NAD	161-167	NLR family pyrin domain containing 3	Homo sapiens	16-21
23905384-1	2013	OBJECTIVE: To explore effects of exercise combined Danzhi Jiangtang Capsule (DJC) on the protein expression of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase p22phox in pancreatic tissues of diabetic rats.	NAD	111-144	cytochrome b-245 alpha chain	Rattus norvegicus	171-178
23454167-5	2013	KEY FINDINGS: NAD(+), but not adenosine and nicotinamide, could restore the cellular NAD(+) levels decreased by PARP activation.	NAD	85-91	poly(ADP-ribose) polymerase 1	Homo sapiens	112-116
23537654-4	2013	In the present study, we investigated the expression pattern of Nampt, the rate-limiting enzyme in NAD salvaging pathway, during osteogenic differentiation of the multipotent mouse fibroblast C3H10T1/2 and the omnipotent preosteoblast MC3T3-E1 cells.	NAD	99-102	nicotinamide phosphoribosyltransferase	Mus musculus	64-69
23537654-6	2013	The increase of Nampt was associated with higher NAD concentration and Sirt1 activity.	NAD	49-52	nicotinamide phosphoribosyltransferase	Mus musculus	16-21
23537654-7	2013	Knockdown of Nampt or addition of its specific inhibitor FK866 leads to lower intracellular NAD concentration and decline in osteogenesis.	NAD	92-95	nicotinamide phosphoribosyltransferase	Mus musculus	13-18
23537654-8	2013	These findings indicate that osteogenic differentiation correlates with intracellular NAD metabolism in which Nampt plays a regulatory role.	NAD	86-89	nicotinamide phosphoribosyltransferase	Mus musculus	110-115
23454167-0	2013	NAD(+) influx through connexin hemichannels prevents poly(ADP-ribose) polymerase-mediated astrocyte death.	NAD	0-6	poly(ADP-ribose) polymerase 1	Homo sapiens	53-80
23454167-1	2013	AIM: Cell death induced by excessive activation of poly(ADP-ribose) polymerase (PARP) is inhibited by administration of NAD(+) extracellularly, but its preventive mechanism remains unclear.	NAD	120-126	poly(ADP-ribose) polymerase 1	Homo sapiens	51-78
23454167-1	2013	AIM: Cell death induced by excessive activation of poly(ADP-ribose) polymerase (PARP) is inhibited by administration of NAD(+) extracellularly, but its preventive mechanism remains unclear.	NAD	120-126	poly(ADP-ribose) polymerase 1	Homo sapiens	80-84
23454167-2	2013	Here we investigated the involvement of NAD(+) and/or its metabolites, adenosine and nicotinamide, in the rescue of PARP-mediated astrocyte death by NAD(+) and explored the pathway through which intact NAD(+) could enter cells.	NAD	40-46	poly(ADP-ribose) polymerase 1	Homo sapiens	116-120
23454167-2	2013	Here we investigated the involvement of NAD(+) and/or its metabolites, adenosine and nicotinamide, in the rescue of PARP-mediated astrocyte death by NAD(+) and explored the pathway through which intact NAD(+) could enter cells.	NAD	149-155	poly(ADP-ribose) polymerase 1	Homo sapiens	116-120
23454167-2	2013	Here we investigated the involvement of NAD(+) and/or its metabolites, adenosine and nicotinamide, in the rescue of PARP-mediated astrocyte death by NAD(+) and explored the pathway through which intact NAD(+) could enter cells.	NAD	149-155	poly(ADP-ribose) polymerase 1	Homo sapiens	116-120
23454167-7	2013	The increase in the cellular NAD(+) level caused by NAD(+) administration to PARP-activated cells was significantly inhibited by a connexin hemichannel blocker, carbenoxolone, but not by P2X7 receptor inhibition with selective antagonists and siRNA, or pannexin-selective blockers.	NAD	29-35	poly(ADP-ribose) polymerase 1	Homo sapiens	77-81
23454167-5	2013	KEY FINDINGS: NAD(+), but not adenosine and nicotinamide, could restore the cellular NAD(+) levels decreased by PARP activation.	NAD	14-20	poly(ADP-ribose) polymerase 1	Homo sapiens	112-116
23454167-7	2013	The increase in the cellular NAD(+) level caused by NAD(+) administration to PARP-activated cells was significantly inhibited by a connexin hemichannel blocker, carbenoxolone, but not by P2X7 receptor inhibition with selective antagonists and siRNA, or pannexin-selective blockers.	NAD	52-58	poly(ADP-ribose) polymerase 1	Homo sapiens	77-81
23454167-8	2013	Finally, pharmacological blockade of connexin hemichannels with 18beta-glycyrrhetinic acid, octanol and carbenoxolone inhibited the NAD(+)-mediated cell rescue of PARP-triggered cell death.	NAD	132-138	poly(ADP-ribose) polymerase 1	Homo sapiens	163-167
23454167-9	2013	SIGNIFICANCE: These findings suggested that intact NAD(+) could get into astrocytes through connexin hemichannels, and that this process should play a key role in NAD(+)-mediated prevention of PARP-triggered astrocyte death.	NAD	51-57	poly(ADP-ribose) polymerase 1	Homo sapiens	193-197
23454167-9	2013	SIGNIFICANCE: These findings suggested that intact NAD(+) could get into astrocytes through connexin hemichannels, and that this process should play a key role in NAD(+)-mediated prevention of PARP-triggered astrocyte death.	NAD	163-169	poly(ADP-ribose) polymerase 1	Homo sapiens	193-197
23517006-5	2013	Electrochemical studies of ((tBu)N4)M complexes suggest that (tBu)N4 is suitable to stabilize Co(I), Ni(I), Co(III), Fe(III) solvato-complexes, while the electrochemical oxidation of ((tBu)N4)NiCl2 complex leads to formation of a Ni(III) species, supporting the ability of the (tBu)N4 ligand to stabilize first row transition metal complexes in various oxidation states.	NAD	94-99	mitochondrially encoded cytochrome c oxidase III	Homo sapiens	111-114
23598272-7	2013	Genetic deletion of cyclophilin D (CypD(-/-)) prevented loss of total NAD(+) and PARP activity, and mPTP-mediated loss of mitochondrial function.	NAD	70-76	peptidylprolyl isomerase F (cyclophilin F)	Mus musculus	20-33
23598272-7	2013	Genetic deletion of cyclophilin D (CypD(-/-)) prevented loss of total NAD(+) and PARP activity, and mPTP-mediated loss of mitochondrial function.	NAD	70-76	peptidylprolyl isomerase F (cyclophilin F)	Mus musculus	35-39
23517006-5	2013	Electrochemical studies of ((tBu)N4)M complexes suggest that (tBu)N4 is suitable to stabilize Co(I), Ni(I), Co(III), Fe(III) solvato-complexes, while the electrochemical oxidation of ((tBu)N4)NiCl2 complex leads to formation of a Ni(III) species, supporting the ability of the (tBu)N4 ligand to stabilize first row transition metal complexes in various oxidation states.	NAD	94-99	mitochondrially encoded cytochrome c oxidase III	Homo sapiens	120-123
23001007-0	2013	Reduction of furan derivatives by overexpressing NADH-dependent Adh1 improves ethanol fermentation using xylose as sole carbon source with Saccharomyces cerevisiae harboring XR-XDH pathway.	NAD	49-53	alcohol dehydrogenase ADH1	Saccharomyces cerevisiae S288C	64-68
23001007-4	2013	We showed that overexpression of mutant NADH-dependent ADH1 derived from TMB3000 strain in the recombinant Saccharomyces cerevisiae, into which xylose reductase (XR) and xylitol dehydrogenase (XDH) pathway of Pichia stipitis has been introduced, improved ethanol production from xylose as a sole carbon source in the presence of 5-HMF.	NAD	40-44	alcohol dehydrogenase ADH1	Saccharomyces cerevisiae S288C	55-59
23331011-7	2013	Mechanistically, MBD1 is associated with Twist and NAD-dependent deacetylase sirtuin-1 (SIRT1), thereby forming the Twist-MBD1-SIRT1 complex on the CDH1 promoter, which resulted in reduced E-cadherin transcription activity and increased cell EMT ability.	NAD	51-54	methyl-CpG binding domain protein 1	Homo sapiens	17-21
23246565-1	2013	Poly(ADP-ribosyl)ation (PARylation) is a NAD(+)-dependent protein modification carried out by PARP [poly(ADP-ribose) polymerase] enzymes.	NAD	41-47	poly(ADP-ribose) polymerase 1	Homo sapiens	94-98
23246565-1	2013	Poly(ADP-ribosyl)ation (PARylation) is a NAD(+)-dependent protein modification carried out by PARP [poly(ADP-ribose) polymerase] enzymes.	NAD	41-47	poly(ADP-ribose) polymerase 1	Homo sapiens	100-127
23313413-1	2013	At optimal NADH concentration (50muM), the complex I-mediated process results in a formation of two superoxide anions and H(2)O(2) as the reaction products in approximately 0.7 ratio.	NAD	11-15	latexin	Homo sapiens	33-36
23331011-7	2013	Mechanistically, MBD1 is associated with Twist and NAD-dependent deacetylase sirtuin-1 (SIRT1), thereby forming the Twist-MBD1-SIRT1 complex on the CDH1 promoter, which resulted in reduced E-cadherin transcription activity and increased cell EMT ability.	NAD	51-54	methyl-CpG binding domain protein 1	Homo sapiens	122-126
23331011-7	2013	Mechanistically, MBD1 is associated with Twist and NAD-dependent deacetylase sirtuin-1 (SIRT1), thereby forming the Twist-MBD1-SIRT1 complex on the CDH1 promoter, which resulted in reduced E-cadherin transcription activity and increased cell EMT ability.	NAD	51-54	cadherin 1	Homo sapiens	148-152
23331011-7	2013	Mechanistically, MBD1 is associated with Twist and NAD-dependent deacetylase sirtuin-1 (SIRT1), thereby forming the Twist-MBD1-SIRT1 complex on the CDH1 promoter, which resulted in reduced E-cadherin transcription activity and increased cell EMT ability.	NAD	51-54	cadherin 1	Homo sapiens	189-199
22452634-1	2013	AIMS: Nicotinamide phosphoribosyltransferase (Nampt) is a key enzyme for nicotinamide adenine dinucleotide (NAD(+)) biosynthesis, and recent evidence indicates its role in inflammatory processes.	NAD	73-106	nicotinamide phosphoribosyltransferase	Mus musculus	6-44
23274584-8	2013	Similarly, ZnT3-KO and RPE65-KO mice showed less Zn(2+) staining, NAD(+) loss, and RPE or photoreceptor death than C57/BI6/J control mice.	NAD	66-72	retinal pigment epithelium 65	Mus musculus	23-28
22471832-1	2013	We report an unusual phenotype of congenital hemidysplasia with ichthyosiform erythroderma and limb defects syndrome most likely resulting from a novel X-chromosomal microdeletion encompassing the promoter region and exon 1 of the nicotinamide adenine dinucleotide phosphate steroid dehydrogenase-like protein gene, the neighboring gene CETN2, and more than 10 kb of noncoding deoxyribonucleic acid.	NAD	231-264	centrin 2	Homo sapiens	337-342
22452634-1	2013	AIMS: Nicotinamide phosphoribosyltransferase (Nampt) is a key enzyme for nicotinamide adenine dinucleotide (NAD(+)) biosynthesis, and recent evidence indicates its role in inflammatory processes.	NAD	108-115	nicotinamide phosphoribosyltransferase	Mus musculus	6-44
22452634-7	2013	The release of CXCL8 (human homolog of murine chemokine CXCL2) by human peripheral blood mononuclear cells (PBMCs) and Jurkat cells was also reduced by FK866, as well as by sirtuin (SIRT) inhibitors and SIRT6 silencing, implying a pivotal role for this NAD(+)-dependent deacetylase in the production of this chemokine.	NAD	253-259	C-X-C motif chemokine ligand 8	Homo sapiens	15-20
22452634-7	2013	The release of CXCL8 (human homolog of murine chemokine CXCL2) by human peripheral blood mononuclear cells (PBMCs) and Jurkat cells was also reduced by FK866, as well as by sirtuin (SIRT) inhibitors and SIRT6 silencing, implying a pivotal role for this NAD(+)-dependent deacetylase in the production of this chemokine.	NAD	253-259	chemokine (C-X-C motif) ligand 2	Mus musculus	56-61
23321587-4	2013	Sensitivity analysis of the factors in the enzyme system affecting dye removal examined by an artificial neural network model shows that the relative importance of enzyme ratio between azoreductase and glucose 1-dehydrogenase was 22%, followed by dye concentration (27%), NAD(+) concentration (23%) and glucose concentration (22%), indicating none of the variables could be ignored in the enzyme system.	NAD	272-278	NAD(P)H quinone dehydrogenase 1	Homo sapiens	185-197
23203961-2	2013	Inside the cell, Nampt (iNampt) functions as a rate-limiting enzyme in the NAD salvage pathway, and outside the cell (eNampt), it acts as a proinflammatory cytokine.	NAD	75-78	nicotinamide phosphoribosyltransferase	Mus musculus	17-22
23134369-3	2013	Of particular interest are the classical glycolytic enzymes GAPDH (glyceraldehyde-3-phosphate dehydrogenase) and LDH (lactate dehydrogenase), which utilize NAD(H) as coenzymes and not only moonlight (in their nuclear forms) to regulate the transcription of S-phase-specific histone genes, but also act as metabolic/redox sensors that link histone gene switching to DNA replication and S-phase progression.	NAD	156-162	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	60-65
23134369-3	2013	Of particular interest are the classical glycolytic enzymes GAPDH (glyceraldehyde-3-phosphate dehydrogenase) and LDH (lactate dehydrogenase), which utilize NAD(H) as coenzymes and not only moonlight (in their nuclear forms) to regulate the transcription of S-phase-specific histone genes, but also act as metabolic/redox sensors that link histone gene switching to DNA replication and S-phase progression.	NAD	156-162	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	67-107
23000657-4	2013	Close relations between complex I and group 4 membrane-bound [NiFe] hydrogenases and some subunits of multiple resistance to pH (Mrp) Na(+)/H(+) antiporters have been observed before and the suggestion that complex I arose from the association of a soluble nicotinamide adenine dinucleotide (NAD(+)) reducing hydrogenase with a Mrp-like antiporter has been put forward.	NAD	257-290	ATP binding cassette subfamily C member 1	Homo sapiens	129-132
23000657-4	2013	Close relations between complex I and group 4 membrane-bound [NiFe] hydrogenases and some subunits of multiple resistance to pH (Mrp) Na(+)/H(+) antiporters have been observed before and the suggestion that complex I arose from the association of a soluble nicotinamide adenine dinucleotide (NAD(+)) reducing hydrogenase with a Mrp-like antiporter has been put forward.	NAD	292-298	ATP binding cassette subfamily C member 1	Homo sapiens	129-132
23321587-2	2013	In this research, azoreductase and glucose 1-dehydrogenase were coupled for both continuous generation of the cofactor NADH and azo dye removal.	NAD	119-123	NAD(P)H quinone dehydrogenase 1	Homo sapiens	18-30
23321587-3	2013	The results show that 85% maximum relative activity of azoreductase in an integrated enzyme system was obtained at the conditions: 1U azoreductase:10U glucose 1-dehydrogenase, 250mM glucose, 1.0mM NAD(+) and 150muM methyl red.	NAD	197-203	NAD(P)H quinone dehydrogenase 1	Homo sapiens	55-67
23321587-3	2013	The results show that 85% maximum relative activity of azoreductase in an integrated enzyme system was obtained at the conditions: 1U azoreductase:10U glucose 1-dehydrogenase, 250mM glucose, 1.0mM NAD(+) and 150muM methyl red.	NAD	197-203	NAD(P)H quinone dehydrogenase 1	Homo sapiens	134-146
23631196-3	2013	FoxO1 is a downstream effector of insulin signaling and Sirt1 is an NAD(+)-dependent deacetylase, both of which work as energy sensors at the cellular level.	NAD	68-72	forkhead box O1	Homo sapiens	0-5
23301673-10	2013	SIRT1 has a role in the modulation of AKT activation and PARP1 has been described to be a gatekeeper for SIRT1 activity by limiting NAD+ availability.	NAD	132-136	poly(ADP-ribose) polymerase 1	Homo sapiens	57-62
22902320-3	2013	Ca(2+) is taken up by mitochondria via the mitochondrial Ca(2+) uniporter (MCU) where it stimulates key dehydrogenases of the Krebs cycle to match regeneration of NADH to its oxidation by the respiratory chain.	NAD	163-167	mitochondrial calcium uniporter	Homo sapiens	75-78
23138851-6	2013	OPA1-depleted cells exhibit decreased agonist-evoked mitochondrial Ca(2+) transients and corresponding reduction of NAD(+) to NADH, but the impairment in NADH oxidation leads to an overall more reduced mitochondrial NADH pool.	NAD	116-122	OPA1 mitochondrial dynamin like GTPase	Homo sapiens	0-4
23138851-6	2013	OPA1-depleted cells exhibit decreased agonist-evoked mitochondrial Ca(2+) transients and corresponding reduction of NAD(+) to NADH, but the impairment in NADH oxidation leads to an overall more reduced mitochondrial NADH pool.	NAD	126-130	OPA1 mitochondrial dynamin like GTPase	Homo sapiens	0-4
23138851-6	2013	OPA1-depleted cells exhibit decreased agonist-evoked mitochondrial Ca(2+) transients and corresponding reduction of NAD(+) to NADH, but the impairment in NADH oxidation leads to an overall more reduced mitochondrial NADH pool.	NAD	154-158	OPA1 mitochondrial dynamin like GTPase	Homo sapiens	0-4
23138851-6	2013	OPA1-depleted cells exhibit decreased agonist-evoked mitochondrial Ca(2+) transients and corresponding reduction of NAD(+) to NADH, but the impairment in NADH oxidation leads to an overall more reduced mitochondrial NADH pool.	NAD	154-158	OPA1 mitochondrial dynamin like GTPase	Homo sapiens	0-4
23378588-9	2013	On the other hand, if complex I is partially defective, the levels of NAD(+) may be sufficient to implement the Krebs cycle with higher levels of intermediates that stabilize HIF1alpha, thus favoring tumor malignancy.	NAD	70-76	hypoxia inducible factor 1 subunit alpha	Homo sapiens	175-184
22562958-2	2013	The mitochondrial NAD(+)-dependent protein deacetylase SIRT3 has previously been shown to be important in adapting to metabolic stress brought on by fasting and calorie restriction.	NAD	18-24	sirtuin 3	Homo sapiens	55-60
23146569-2	2013	Resveratrol has been reported to be an activator of NAD+-dependent deacetylase sirtuin 1 (SIRT1), which may regulate liver X receptor (LXR) activity, thereby upregulating the expression of genes crucial in reverse cholesterol transport (RCT).	NAD	52-55	nuclear receptor subfamily 1, group H, member 3	Mus musculus	117-133
23146569-2	2013	Resveratrol has been reported to be an activator of NAD+-dependent deacetylase sirtuin 1 (SIRT1), which may regulate liver X receptor (LXR) activity, thereby upregulating the expression of genes crucial in reverse cholesterol transport (RCT).	NAD	52-55	nuclear receptor subfamily 1, group H, member 3	Mus musculus	135-138
23237800-2	2013	Binding is prevented by NADH, suggesting that the coenzyme site is involved in the interaction LDH-A/ssDNA.	NAD	24-28	lactate dehydrogenase A	Homo sapiens	95-100
23237800-3	2013	We recently identified an inhibitor of LDH-A enzymatic activity (Galloflavin, GF) which occupies the NADH site.	NAD	101-105	lactate dehydrogenase A	Homo sapiens	39-44
23237800-9	2013	Our results suggest that: (i) inhibitors which bind the NADH site can exert their antiproliferative activity not only by blocking aerobic glycolysis but also by causing an inhibition of RNA synthesis independent from the effect on glycolysis; (ii) GF can be a useful tool to study the biological role of LDH-A binding to ssDNA.	NAD	56-60	lactate dehydrogenase A	Homo sapiens	304-309
23085506-10	2013	PARP-1 inhibition increased Sirt1 activity through an increased intracellular nicotinamide adenine dinucleotide (NAD(+)) level.	NAD	78-111	poly(ADP-ribose) polymerase 1	Homo sapiens	0-6
22851447-3	2013	This chapter describes the utilization of GAPDH"s enzymatic function for focal demands (i.e. ATP/ADP and NAD(+)/NADH), and offers a speculative role for GAPDH as perhaps moderating local concentrations of inorganic phosphate and hydrogen ions (i.e. co-substrate and co-product of the glycolytic reaction, respectively).	NAD	105-111	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	42-47
22851447-3	2013	This chapter describes the utilization of GAPDH"s enzymatic function for focal demands (i.e. ATP/ADP and NAD(+)/NADH), and offers a speculative role for GAPDH as perhaps moderating local concentrations of inorganic phosphate and hydrogen ions (i.e. co-substrate and co-product of the glycolytic reaction, respectively).	NAD	112-116	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	42-47
23085506-10	2013	PARP-1 inhibition increased Sirt1 activity through an increased intracellular nicotinamide adenine dinucleotide (NAD(+)) level.	NAD	113-119	poly(ADP-ribose) polymerase 1	Homo sapiens	0-6
23085506-13	2013	PARP-1 inhibition restored Sirt1 activity by increasing NAD(+) level and decreased iNOS and ICAM-1 expression by inhibiting NF-kappaB nuclear translocation and activity as well as NF-kappaB phosphorylation.	NAD	56-62	poly(ADP-ribose) polymerase 1	Homo sapiens	0-6
23832361-6	2013	Phytol increased the blood NAD level by suppressing ACMSD mRNA expression in the liver of the rats.	NAD	27-30	aminocarboxymuconate semialdehyde decarboxylase	Rattus norvegicus	52-57
23043339-9	2013	Overall, this evidence confirms that airborne particles induce decreases in intracellular NAD(P)H and NAD(+) through PARP-1 activation mediated by formation of DNA strand breaks.	NAD	102-108	poly(ADP-ribose) polymerase 1	Homo sapiens	117-123
23509928-5	2013	beta-NAD(+) inhibited the expression of MMP-1 and MMP-3 triggered by IL-1alpha at gene and protein levels.	NAD	0-11	matrix metallopeptidase 3	Homo sapiens	50-55
24171769-1	2013	SIRT6 is one of the seven members of the NAD-dependent family of sirtuins mammals.	NAD	41-44	sirtuin 6	Mus musculus	0-5
24171773-1	2013	Poly(ADP-ribose)polymerases (PARPs) catalyze a post-transcriptional modification of proteins, consisting in the attachment of mono, oligo or poly ADP-ribose units from NAD+ to specific polar residues of target proteins.	NAD	168-172	poly(ADP-ribose) polymerase 1	Homo sapiens	29-34
24222765-9	2013	E2 and PPT enhanced, but DPN inhibited, the migration and invasion of BCPAP cells in an in vitro experimental model system that is modulated by E-cadherin, vimentin, and MMP-9.	NAD	25-28	cadherin 1	Homo sapiens	144-154
23832361-1	2013	alpha-Amino-beta-carboxymuconate-epsilon-semialdehyde decarboxylase (ACMSD) plays a key role in the regulation of NAD biosynthesis or the production of quinolinate from tryptophan (Trp).	NAD	114-117	aminocarboxymuconate semialdehyde decarboxylase	Rattus norvegicus	0-67
23832361-1	2013	alpha-Amino-beta-carboxymuconate-epsilon-semialdehyde decarboxylase (ACMSD) plays a key role in the regulation of NAD biosynthesis or the production of quinolinate from tryptophan (Trp).	NAD	114-117	aminocarboxymuconate semialdehyde decarboxylase	Rattus norvegicus	69-74
23042952-2	2013	RSV targets and activates the NAD(+)-dependent protein deacetylase SIRT1; in turn, SIRT1 induces an intracellular antioxidative mechanism by inducing mitochondrial superoxide dismutase (SOD2).	NAD	30-36	superoxide dismutase 2, mitochondrial	Mus musculus	186-190
24512730-1	2013	It has been reported that upregulated SIRT1 (NAD(+)-dependent class III histone deacetylase) deacetylates the p53 protein, represses its function, and allows for tumor cell growth in various cancers.	NAD	45-51	tumor protein p53	Homo sapiens	110-113
23917125-1	2013	The poly(ADP-ribose) polymerase (PARP) family of proteins use NAD(+) as their substrate to modify acceptor proteins with ADP-ribose modifications.	NAD	62-68	poly(ADP-ribose) polymerase 1	Homo sapiens	4-31
23917125-1	2013	The poly(ADP-ribose) polymerase (PARP) family of proteins use NAD(+) as their substrate to modify acceptor proteins with ADP-ribose modifications.	NAD	62-68	poly(ADP-ribose) polymerase 1	Homo sapiens	33-37
24386592-5	2013	Poly(ADP-ribose) polymerase-1 (PARP-1) and sirtuins are key NAD(+)-consuming enzymes that mediate multiple biological processes.	NAD	60-66	poly(ADP-ribose) polymerase 1	Homo sapiens	0-29
23460848-9	2013	In addition, lactate dehydrogenase A and malate dehydrogenase 1 partially associate with human liver peroxisomes and enzyme activity profiles support the idea that NAD(+) becomes regenerated during fatty acid beta-oxidation by alternative shuttling processes in human peroxisomes involving lactate dehydrogenase and/or malate dehydrogenase.	NAD	164-170	lactate dehydrogenase A	Homo sapiens	13-36
23460848-9	2013	In addition, lactate dehydrogenase A and malate dehydrogenase 1 partially associate with human liver peroxisomes and enzyme activity profiles support the idea that NAD(+) becomes regenerated during fatty acid beta-oxidation by alternative shuttling processes in human peroxisomes involving lactate dehydrogenase and/or malate dehydrogenase.	NAD	164-170	malic enzyme 2	Homo sapiens	41-61
23011206-4	2013	Accordingly, PARP-1 inhibitors, acting by competing with its physiological substrate NAD(+), have been proposed to play a protective role in a wide range of inflammatory and ischemia/reperfusion-associated diseases.	NAD	85-91	poly(ADP-ribose) polymerase 1	Homo sapiens	13-19
24386592-5	2013	Poly(ADP-ribose) polymerase-1 (PARP-1) and sirtuins are key NAD(+)-consuming enzymes that mediate multiple biological processes.	NAD	60-66	poly(ADP-ribose) polymerase 1	Homo sapiens	31-37
23053940-2	2012	In addition to its pivotal role in energy metabolism, NAD(+) is also the indispensable substrate of poly (ADP-ribose) polymerase-1 (PARP-1) and sirtuin 1 (SIRT1).	NAD	54-60	poly(ADP-ribose) polymerase 1	Homo sapiens	100-130
23086932-6	2012	NQO1 in presence of its cofactor NADH protected C/EBPalpha against 20S degradation.	NAD	33-37	NAD(P)H quinone dehydrogenase 1	Homo sapiens	0-4
23086932-6	2012	NQO1 in presence of its cofactor NADH protected C/EBPalpha against 20S degradation.	NAD	33-37	CCAAT enhancer binding protein alpha	Homo sapiens	48-58
23086932-8	2012	Mutagenesis studies also revealed that NQO1Y127/Y129 required for NADH binding is essential for NQO1 stabilization of C/EBPalpha.	NAD	66-70	NAD(P)H quinone dehydrogenase 1	Homo sapiens	39-43
23086932-8	2012	Mutagenesis studies also revealed that NQO1Y127/Y129 required for NADH binding is essential for NQO1 stabilization of C/EBPalpha.	NAD	66-70	CCAAT enhancer binding protein alpha	Homo sapiens	118-128
23192029-1	2012	Quinolinate phosphoribosyltransferase (QAPRTase) is a key enzyme in NAD biosynthesis; it catalyzes the formation of nicotinate mononucleotide (NAMN) from quinolinate and 5-phosphoribosyl-1-pyrophosphate.	NAD	68-71	quinolinate phosphoribosyltransferase	Sus scrofa	0-37
23053940-4	2012	The NAD(+)-dependent modifications catalyzed by PARP-1 and SIRT1 liberate NAM, and NAM acts as feedback inhibitor of PARP-1 and SIRT1 through interacting with the enzymes at the binding site for NAD(+).	NAD	195-201	poly(ADP-ribose) polymerase 1	Homo sapiens	117-123
23201684-4	2012	Here, we show that the NAD-dependent deacetylase SIRT2 binds constitutively to RIP3 and that deletion or knockdown of SIRT2 prevents formation of the RIP1-RIP3 complex in mice.	NAD	23-26	receptor (TNFRSF)-interacting serine-threonine kinase 1	Mus musculus	150-154
24705085-3	2012	PARPs convert NAD+ molecules into PAR chains that interact covalently or noncovalently with target proteins and thereby modify their structure and functions.	NAD	14-18	poly(ADP-ribose) polymerase 1	Homo sapiens	0-5
23053940-2	2012	In addition to its pivotal role in energy metabolism, NAD(+) is also the indispensable substrate of poly (ADP-ribose) polymerase-1 (PARP-1) and sirtuin 1 (SIRT1).	NAD	54-60	poly(ADP-ribose) polymerase 1	Homo sapiens	132-138
23053940-4	2012	The NAD(+)-dependent modifications catalyzed by PARP-1 and SIRT1 liberate NAM, and NAM acts as feedback inhibitor of PARP-1 and SIRT1 through interacting with the enzymes at the binding site for NAD(+).	NAD	4-10	poly(ADP-ribose) polymerase 1	Homo sapiens	48-54
23053940-4	2012	The NAD(+)-dependent modifications catalyzed by PARP-1 and SIRT1 liberate NAM, and NAM acts as feedback inhibitor of PARP-1 and SIRT1 through interacting with the enzymes at the binding site for NAD(+).	NAD	4-10	poly(ADP-ribose) polymerase 1	Homo sapiens	117-123
23053940-4	2012	The NAD(+)-dependent modifications catalyzed by PARP-1 and SIRT1 liberate NAM, and NAM acts as feedback inhibitor of PARP-1 and SIRT1 through interacting with the enzymes at the binding site for NAD(+).	NAD	195-201	poly(ADP-ribose) polymerase 1	Homo sapiens	48-54
23146393-2	2012	The hemin/G-quadruplex formed by intercalating hemin into thrombin binding aptamer (TBA), firstly acted as a NADH oxidase, assisting the oxidation of NADH to NAD(+) accompanying with the generation of H(2)O(2) in the presence of dissolved O(2).	NAD	109-113	coagulation factor II, thrombin	Homo sapiens	58-66
23146393-2	2012	The hemin/G-quadruplex formed by intercalating hemin into thrombin binding aptamer (TBA), firstly acted as a NADH oxidase, assisting the oxidation of NADH to NAD(+) accompanying with the generation of H(2)O(2) in the presence of dissolved O(2).	NAD	158-164	coagulation factor II, thrombin	Homo sapiens	58-66
23076628-4	2012	PARP-1 is a DNA repair enzyme, normally activated by single strand breaks associated with oxidative stress, which catalyses the formation of poly ADP-ribose polymers from nicotinamide adenine dinucleotide (NAD(+)).	NAD	171-204	poly(ADP-ribose) polymerase 1	Homo sapiens	0-6
22563797-5	2012	The NADH overflow due to complex I inactivation induces TCA flux perturbations, leading to citrate production, triggering fatty acid synthase (FAS), and lipid peroxidation.	NAD	4-8	fatty acid synthase	Mus musculus	122-141
22563797-5	2012	The NADH overflow due to complex I inactivation induces TCA flux perturbations, leading to citrate production, triggering fatty acid synthase (FAS), and lipid peroxidation.	NAD	4-8	fatty acid synthase	Mus musculus	143-146
23086143-1	2012	The single-component type-II NADH dehydrogenases (NDH-2s) serve as alternatives to the multisubunit respiratory complex I (type-I NADH dehydrogenase (NDH-1), also called NADH:ubiquinone oxidoreductase; EC 1.6.5.3) in catalysing electron transfer from NADH to ubiquinone in the mitochondrial respiratory chain.	NAD	29-33	DExH-box helicase 9	Homo sapiens	50-55
23086143-1	2012	The single-component type-II NADH dehydrogenases (NDH-2s) serve as alternatives to the multisubunit respiratory complex I (type-I NADH dehydrogenase (NDH-1), also called NADH:ubiquinone oxidoreductase; EC 1.6.5.3) in catalysing electron transfer from NADH to ubiquinone in the mitochondrial respiratory chain.	NAD	130-134	DExH-box helicase 9	Homo sapiens	50-55
23076628-4	2012	PARP-1 is a DNA repair enzyme, normally activated by single strand breaks associated with oxidative stress, which catalyses the formation of poly ADP-ribose polymers from nicotinamide adenine dinucleotide (NAD(+)).	NAD	206-212	poly(ADP-ribose) polymerase 1	Homo sapiens	0-6
22941645-2	2012	Upon activation, PARP-1 uses NAD+ to generate large amounts of poly(ADP-ribose) (PAR), which facilitates the recruitment of DNA repair factors.	NAD	29-33	poly(ADP-ribose) polymerase 1	Homo sapiens	17-23
23076628-5	2012	The pathological over activation of PARP-1 causes depletion of NAD(+) and leads to cell death.	NAD	63-69	poly(ADP-ribose) polymerase 1	Homo sapiens	36-42
22750339-5	2012	Synthesized complexes have been tested for their SOD mimic activity using NBT/NADH/PMS system.	NAD	78-82	superoxide dismutase 1	Homo sapiens	49-52
22735644-1	2012	Human DBC1 (deleted in breast cancer-1; KIAA1967) is a nuclear protein that, in response to DNA damage, competitively inhibits the NAD(+)-dependent deacetylase SIRT1, a regulator of p53 apoptotic functions in response to genotoxic stress.	NAD	131-137	tumor protein p53	Homo sapiens	182-185
22955917-0	2012	Targeting NAD+ salvage pathway induces autophagy in multiple myeloma cells via mTORC1 and extracellular signal-regulated kinase (ERK1/2) inhibition.	NAD	10-14	mitogen-activated protein kinase 3	Homo sapiens	129-135
22960784-8	2012	The cyclic voltammogram (CV) displays two one-electron metal based processes: a quasi-reversible Co(III)/Co(II) oxidation wave at E(1/2) = -0.5 V vs. Fc(+)/Fc and a quasi-reversible Co(II)/Co(I) reduction wave at E(1/2) = -1.7 V. 1 reacts with CH(3)I, generating the mono S-methylated complex, [CoL(Me)I] (1(Me)).	NAD	189-194	mitochondrially encoded cytochrome c oxidase III	Homo sapiens	97-104
22960784-8	2012	The cyclic voltammogram (CV) displays two one-electron metal based processes: a quasi-reversible Co(III)/Co(II) oxidation wave at E(1/2) = -0.5 V vs. Fc(+)/Fc and a quasi-reversible Co(II)/Co(I) reduction wave at E(1/2) = -1.7 V. 1 reacts with CH(3)I, generating the mono S-methylated complex, [CoL(Me)I] (1(Me)).	NAD	189-194	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	97-102
22960784-8	2012	The cyclic voltammogram (CV) displays two one-electron metal based processes: a quasi-reversible Co(III)/Co(II) oxidation wave at E(1/2) = -0.5 V vs. Fc(+)/Fc and a quasi-reversible Co(II)/Co(I) reduction wave at E(1/2) = -1.7 V. 1 reacts with CH(3)I, generating the mono S-methylated complex, [CoL(Me)I] (1(Me)).	NAD	189-194	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	105-111
22781627-4	2012	Exposure of astrocytes to the ART2 substrate, NAD, induced calcium elevation, which was blocked by ART2 and P2X7 inhibitors.	NAD	46-49	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	108-112
22874065-3	2012	Dual oxidase 1 (DUOX1) and DUOX2, originally identified in the thyroid, are nicotinamide adenine dinucleotide phosphate (NADPH) oxidases that are necessary to produce the H2O2 required for thyroid hormone biosynthesis.	NAD	76-109	dual oxidase 1	Rattus norvegicus	0-14
22874065-3	2012	Dual oxidase 1 (DUOX1) and DUOX2, originally identified in the thyroid, are nicotinamide adenine dinucleotide phosphate (NADPH) oxidases that are necessary to produce the H2O2 required for thyroid hormone biosynthesis.	NAD	76-109	dual oxidase 1	Rattus norvegicus	16-21
22829588-3	2012	Indeed, NAD(+) led to increases in both active and latent cell-associated TGF-beta1 in RAW 264.7 mouse macrophages as well as in primary peritoneal macrophages isolated from both C3H/HeJ (TLR4-mutant) and C3H/HeOuJ (wild-type controls for C3H/HeJ) mice.	NAD	8-14	toll-like receptor 4	Mus musculus	188-192
22849721-3	2012	SIRT3 and SIRT5 are NAD-consuming enzymes that are potential therapeutic targets for the treatment of metabolic diseases and cancers.	NAD	20-23	sirtuin 3	Homo sapiens	0-5
22781627-0	2012	NAD induces astrocyte calcium flux and cell death by ART2 and P2X7 pathway.	NAD	0-3	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	62-66
22781627-7	2012	The harmful effect of ATP on astrocytes was inhibited by P2X7 and ART2 inhibitors, meaning that endogenous NAD release may occur.	NAD	107-110	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	57-61
22781627-9	2012	Collectively, to our knowledge, our study provides the first evidence that ART2 exists in mouse brain astrocytes and NAD induces calcium elevation and astrocyte death by an ART2 and P2X7-mediated mechanism.	NAD	117-120	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	182-186
22766154-2	2012	This study used an in vivo animal model to investigate UVA-excited fluorescence in the rabbit lens, which contains a high level of the UVA chromophore NADH, existing both free and bound to lambda-crystallin.	NAD	151-155	lambda-crystallin	Oryctolagus cuniculus	189-206
22766154-13	2012	It is concluded that UVA-induced loss of free NADH (which fluoresces blue) may have allowed the natural yellow fluorescence of lambda-crystallin and other proteins in the lens nucleus to become visible.	NAD	46-50	lambda-crystallin	Oryctolagus cuniculus	127-144
22553206-4	2012	By studying alternative variants of the mouse P2X7 receptor we show that sensitivity to NAD is mediated through the P2X7k variant, which has a much more restricted distribution than the P2X7a receptor, but is expressed in T lymphocytes.	NAD	88-91	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	46-59
22904041-8	2012	We then describe the role of NAD(+) and NADH as signal transducers through NAD(+)-dependent enzymes such as PARP-1 and Sirt1.	NAD	29-35	poly(ADP-ribose) polymerase 1	Homo sapiens	108-114
22904041-8	2012	We then describe the role of NAD(+) and NADH as signal transducers through NAD(+)-dependent enzymes such as PARP-1 and Sirt1.	NAD	40-44	poly(ADP-ribose) polymerase 1	Homo sapiens	108-114
22904041-8	2012	We then describe the role of NAD(+) and NADH as signal transducers through NAD(+)-dependent enzymes such as PARP-1 and Sirt1.	NAD	75-81	poly(ADP-ribose) polymerase 1	Homo sapiens	108-114
22904041-9	2012	PARP-1 is activated by damaged DNA in order to repair the DNA, which attenuates energy production through NAD(+) consumption; Sirt1 is activated by an increased NAD(+)/NADH ratio to facilitate signal transduction for metabolic adaption as well as stress responses.	NAD	106-112	poly(ADP-ribose) polymerase 1	Homo sapiens	0-6
22904041-9	2012	PARP-1 is activated by damaged DNA in order to repair the DNA, which attenuates energy production through NAD(+) consumption; Sirt1 is activated by an increased NAD(+)/NADH ratio to facilitate signal transduction for metabolic adaption as well as stress responses.	NAD	161-167	poly(ADP-ribose) polymerase 1	Homo sapiens	0-6
22904041-9	2012	PARP-1 is activated by damaged DNA in order to repair the DNA, which attenuates energy production through NAD(+) consumption; Sirt1 is activated by an increased NAD(+)/NADH ratio to facilitate signal transduction for metabolic adaption as well as stress responses.	NAD	168-172	poly(ADP-ribose) polymerase 1	Homo sapiens	0-6
22904042-5	2012	For instance, in many forms of heart disease a greater contribution from fatty acids for oxidative energy metabolism increases fatty acid beta-oxidation-derived NADH, which can activate pyruvate dehydrogenase (PDH) kinase isoforms that inhibit PDH and subsequent glucose oxidation.	NAD	161-165	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	186-208
22904042-5	2012	For instance, in many forms of heart disease a greater contribution from fatty acids for oxidative energy metabolism increases fatty acid beta-oxidation-derived NADH, which can activate pyruvate dehydrogenase (PDH) kinase isoforms that inhibit PDH and subsequent glucose oxidation.	NAD	161-165	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	210-213
22904042-5	2012	For instance, in many forms of heart disease a greater contribution from fatty acids for oxidative energy metabolism increases fatty acid beta-oxidation-derived NADH, which can activate pyruvate dehydrogenase (PDH) kinase isoforms that inhibit PDH and subsequent glucose oxidation.	NAD	161-165	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	244-247
22773876-4	2012	EPO increases the Sirt1 level, a NAD(+)-dependent deacetylase, and also induces the NAD(+)/NADH ratio that further increases Sirt1 activity.	NAD	33-39	erythropoietin	Homo sapiens	0-3
22553206-4	2012	By studying alternative variants of the mouse P2X7 receptor we show that sensitivity to NAD is mediated through the P2X7k variant, which has a much more restricted distribution than the P2X7a receptor, but is expressed in T lymphocytes.	NAD	88-91	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	46-50
22773876-4	2012	EPO increases the Sirt1 level, a NAD(+)-dependent deacetylase, and also induces the NAD(+)/NADH ratio that further increases Sirt1 activity.	NAD	91-95	erythropoietin	Homo sapiens	0-3
22553206-6	2012	Co-expression of P2X7k and P2X7a receptors reduced NAD sensitivity.	NAD	51-54	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	17-21
22863012-3	2012	Here we report that gain of function of the NAD-dependent deacetylase SirT1 or loss of function of its endogenous inhibitor Deleted in breast cancer-1 (Dbc1) promote "browning" of WAT by deacetylating peroxisome proliferator-activated receptor (Ppar)-gamma on Lys268 and Lys293.	NAD	44-47	peroxisome proliferator activated receptor gamma	Homo sapiens	201-256
22847419-4	2012	The Rossmann fold containing NAD(+) binding region on GAPDH is responsible for the interaction with TERC, whereas a lysine residue in the GAPDH catalytic domain is required for inhibiting telomerase activity and disrupting telomere maintenance.	NAD	29-35	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	54-59
22847419-4	2012	The Rossmann fold containing NAD(+) binding region on GAPDH is responsible for the interaction with TERC, whereas a lysine residue in the GAPDH catalytic domain is required for inhibiting telomerase activity and disrupting telomere maintenance.	NAD	29-35	telomerase RNA component	Homo sapiens	100-104
22465780-2	2012	SIRT1, a class III histone deacetylase, and PARP-1, a poly(ADP-ribose) polymerase, are two NAD(+)-dependent enzymes that have been shown to be involved in the regulation of the clock.	NAD	91-97	poly(ADP-ribose) polymerase 1	Homo sapiens	44-50
22476980-1	2012	Poly(ADP-ribose) polymerases (PARPs) are enzymes that catalyze the transfer of ADP-ribose units from beta-nicotinamide adenine dinucleotide (NAD(+)) to acceptor proteins.	NAD	101-139	poly(ADP-ribose) polymerase 1	Homo sapiens	30-35
22431722-1	2012	Adenosine diphosphate (ADP)-ribosylation is an important posttranslational modification catalyzed by a variety of enzymes, including poly (ADP ribose) polymerases (PARPs), which use nicotinamide adenine dinucleotide (NAD(+)) as a substrate to synthesize and transfer ADP-ribose units to acceptor proteins.	NAD	182-215	poly(ADP-ribose) polymerase 1	Homo sapiens	164-169
22431722-1	2012	Adenosine diphosphate (ADP)-ribosylation is an important posttranslational modification catalyzed by a variety of enzymes, including poly (ADP ribose) polymerases (PARPs), which use nicotinamide adenine dinucleotide (NAD(+)) as a substrate to synthesize and transfer ADP-ribose units to acceptor proteins.	NAD	217-223	poly(ADP-ribose) polymerase 1	Homo sapiens	164-169
22623791-3	2012	Members of the poly(ADP-ribose) polymerase (PARP) family of enzymes are major consumers of NAD(+), which they utilize to form poly(ADP-ribose) (PAR) chains on protein substrates in response to DNA damage.	NAD	91-97	poly(ADP-ribose) polymerase 1	Homo sapiens	15-42
22623791-3	2012	Members of the poly(ADP-ribose) polymerase (PARP) family of enzymes are major consumers of NAD(+), which they utilize to form poly(ADP-ribose) (PAR) chains on protein substrates in response to DNA damage.	NAD	91-97	poly(ADP-ribose) polymerase 1	Homo sapiens	44-48
22623791-5	2012	We report here that the HSV-1 infection-induced drop in NAD(+) levels required viral DNA replication, was associated with an increase in protein poly(ADP-ribosyl)ation (PARylation), and was blocked by pharmacological inhibition of PARP-1/PARP-2 (PARP-1/2).	NAD	56-62	poly(ADP-ribose) polymerase 1	Homo sapiens	231-235
22623791-5	2012	We report here that the HSV-1 infection-induced drop in NAD(+) levels required viral DNA replication, was associated with an increase in protein poly(ADP-ribosyl)ation (PARylation), and was blocked by pharmacological inhibition of PARP-1/PARP-2 (PARP-1/2).	NAD	56-62	poly(ADP-ribose) polymerase 1	Homo sapiens	238-242
22623791-5	2012	We report here that the HSV-1 infection-induced drop in NAD(+) levels required viral DNA replication, was associated with an increase in protein poly(ADP-ribosyl)ation (PARylation), and was blocked by pharmacological inhibition of PARP-1/PARP-2 (PARP-1/2).	NAD	56-62	poly(ADP-ribose) polymerase 1	Homo sapiens	238-242
22623791-8	2012	This work demonstrates that HSV-1 infection results in changes to NAD(+) metabolism by PARP-1/2 and PARG, and as PAR chain accumulation can induce caspase-independent apoptosis, we speculate that the decrease in PARG levels enhances the auto-PARylation-mediated inhibition of PARP, thereby avoiding premature death of the infected cell.	NAD	66-72	poly(ADP-ribose) polymerase 1	Homo sapiens	87-91
22623791-8	2012	This work demonstrates that HSV-1 infection results in changes to NAD(+) metabolism by PARP-1/2 and PARG, and as PAR chain accumulation can induce caspase-independent apoptosis, we speculate that the decrease in PARG levels enhances the auto-PARylation-mediated inhibition of PARP, thereby avoiding premature death of the infected cell.	NAD	66-72	poly(ADP-ribose) glycohydrolase	Homo sapiens	100-104
22430645-2	2012	However, the excessive activation of PARP-1 under pathological conditions may lead to an accumulation of poly(ADP-ribose) (PAR), a novel signaling molecule that induces programmed cell death, or to NAD depletion that induces energy crisis and necrotic cell death.	NAD	198-201	poly(ADP-ribose) polymerase 1	Homo sapiens	37-43
22476980-1	2012	Poly(ADP-ribose) polymerases (PARPs) are enzymes that catalyze the transfer of ADP-ribose units from beta-nicotinamide adenine dinucleotide (NAD(+)) to acceptor proteins.	NAD	141-148	poly(ADP-ribose) polymerase 1	Homo sapiens	30-35
22476980-4	2012	Upon binding, PARP-1 activity increases rapidly and cleaves NAD(+) into ADP-ribose and nicotinamide.	NAD	60-66	poly(ADP-ribose) polymerase 1	Homo sapiens	14-20
22476980-5	2012	Increased activity of PARP-1 can promote DNA repair and its interaction with several transcription factors, whereas hyperactivation of PARP-1 can result in poly(ADP-ribose) accumulation and depletion of NAD(+) and ATP which may lead to caspase independent apoptotic or necrotic cell death, respectively.	NAD	203-209	poly(ADP-ribose) polymerase 1	Homo sapiens	22-28
22476980-5	2012	Increased activity of PARP-1 can promote DNA repair and its interaction with several transcription factors, whereas hyperactivation of PARP-1 can result in poly(ADP-ribose) accumulation and depletion of NAD(+) and ATP which may lead to caspase independent apoptotic or necrotic cell death, respectively.	NAD	203-209	poly(ADP-ribose) polymerase 1	Homo sapiens	135-141
22739728-5	2012	Exposure to 30 mM glucose increased the activity of PARP1, which led to reduced cellular NAD content and insulin receptor phosphorylation.	NAD	89-92	poly(ADP-ribose) polymerase 1	Homo sapiens	52-57
22689570-4	2012	Molecular modeling, based on the structural coordinates of the homologous ClC-5 and CmClC proteins and in silico docking, suggest that NAD(+) binds with the adenine base deep in a cleft formed by ClC-1 intracellular cystathionine beta-synthase domains, and the nicotinamide base interacts with the membrane-embedded channel domain.	NAD	135-141	cystathionine beta-synthase	Homo sapiens	216-243
22689570-5	2012	Consistent with predictions from the models, mutation of residues in cystathionine beta-synthase and channel domains either attenuated (G200R, T636A, H847A) or abrogated (L848A) the effect of NAD(+).	NAD	192-198	cystathionine beta-synthase	Homo sapiens	69-96
22648412-9	2012	Expression of mutant Htt results in decreased deacetylase activity of SIRT3 and further leads to reduction in cellular NAD(+) levels and mitochondrial biogenesis in cells.	NAD	119-125	sirtuin 3	Homo sapiens	70-75
22523229-3	2012	The subsequent activation of the DNA nick sensor enzyme, poly(ADP-ribose) polymerase-1 (PARP-1), leads to the rapid depletion of ATP and NAD and the concomitant formation of poly(ADP-ribosylated) proteins (PARs).	NAD	137-140	poly(ADP-ribose) polymerase 1	Homo sapiens	57-86
22523229-3	2012	The subsequent activation of the DNA nick sensor enzyme, poly(ADP-ribose) polymerase-1 (PARP-1), leads to the rapid depletion of ATP and NAD and the concomitant formation of poly(ADP-ribosylated) proteins (PARs).	NAD	137-140	poly(ADP-ribose) polymerase 1	Homo sapiens	88-94
22742413-7	2012	NADH could also be the electron donor, while having a higher Km (220 muM) compared to that of NADPH (39 muM).	NAD	0-4	latexin	Homo sapiens	69-72
22742413-7	2012	NADH could also be the electron donor, while having a higher Km (220 muM) compared to that of NADPH (39 muM).	NAD	0-4	latexin	Homo sapiens	104-107
22394676-7	2012	Importantly, this biochemical phenotype develops concurrently with cardiac hypertrophy and is caused by inhibition of the NAD(+)-dependent SIRT3 deacetylase.	NAD	122-128	sirtuin 3	Homo sapiens	139-144
22609775-6	2012	Sirt3 overexpression reduced the intracellular NAD(+) level, repressed the ERK1/2 signaling pathway, and activated the Akt and JNK signaling pathways.	NAD	47-53	sirtuin 3	Homo sapiens	0-5
22394676-8	2012	This inhibition is caused by an 85-fold decrease in mitochondrial NAD(+)/NADH and direct carbonyl group modification of SIRT3, and is reversed with excess SIRT3 and NAD(+) in vitro.	NAD	66-72	sirtuin 3	Homo sapiens	155-160
22394676-8	2012	This inhibition is caused by an 85-fold decrease in mitochondrial NAD(+)/NADH and direct carbonyl group modification of SIRT3, and is reversed with excess SIRT3 and NAD(+) in vitro.	NAD	73-77	sirtuin 3	Homo sapiens	155-160
22394676-8	2012	This inhibition is caused by an 85-fold decrease in mitochondrial NAD(+)/NADH and direct carbonyl group modification of SIRT3, and is reversed with excess SIRT3 and NAD(+) in vitro.	NAD	165-171	sirtuin 3	Homo sapiens	120-125
22682224-2	2012	In line with this premise, decreased activity of PARP-1 or CD38-both NAD(+) consumers-increases NAD(+) bioavailability, resulting in SIRT1 activation and protection against metabolic disease.	NAD	69-75	poly(ADP-ribose) polymerase 1	Homo sapiens	49-55
22532167-4	2012	Elevated ROS levels cause extensive DNA lesions, PARP1 hyperactivation, and severe NAD+ /ATP depletion that stimulate Ca2+ -dependent programmed necrosis, unique to this new class of NQO1 "bioactivated" drugs.	NAD	83-87	NAD(P)H quinone dehydrogenase 1	Homo sapiens	183-187
22547068-8	2012	Finally, the presence of NAD(+) precursors up-regulated important T cell functions, such as proliferation and IL-2 release in response to mitogens.	NAD	25-31	interleukin 2	Homo sapiens	110-114
22682224-2	2012	In line with this premise, decreased activity of PARP-1 or CD38-both NAD(+) consumers-increases NAD(+) bioavailability, resulting in SIRT1 activation and protection against metabolic disease.	NAD	96-102	poly(ADP-ribose) polymerase 1	Homo sapiens	49-55
22417091-1	2012	Lactate dehydrogenase A (LDHA) catalyzes the conversion of pyruvate to lactate, utilizing NADH as a cofactor.	NAD	90-94	lactate dehydrogenase A	Homo sapiens	0-23
22559817-1	2012	3-Hydroxybenzoate 6-hydroxylase (3HB6H) from Rhodococcus jostii RHA1 is a nicotinamide adenine dinucleotide (NADH)-specific flavoprotein monooxygenase involved in microbial aromatic degradation.	NAD	74-107	3-hydroxybenzoate 6-hydroxylase	Rhodococcus jostii RHA1	0-38
22559817-1	2012	3-Hydroxybenzoate 6-hydroxylase (3HB6H) from Rhodococcus jostii RHA1 is a nicotinamide adenine dinucleotide (NADH)-specific flavoprotein monooxygenase involved in microbial aromatic degradation.	NAD	109-113	3-hydroxybenzoate 6-hydroxylase	Rhodococcus jostii RHA1	0-38
22129967-6	2012	The ATP hydrolysis activity tested by an ATP/NADH-coupled assay was increased after 48-h TGF-beta1 treatment.	NAD	45-49	transforming growth factor, beta 1	Rattus norvegicus	89-98
22453629-3	2012	In particular, the excessive activation of poly (ADP-ribose) polymerase-1 (PARP-1) consumes cytosolic nicotinamide adenine dinucleotide (NAD(+)), resulting in energy failure.	NAD	102-135	poly(ADP-ribose) polymerase 1	Homo sapiens	43-73
22453629-3	2012	In particular, the excessive activation of poly (ADP-ribose) polymerase-1 (PARP-1) consumes cytosolic nicotinamide adenine dinucleotide (NAD(+)), resulting in energy failure.	NAD	102-135	poly(ADP-ribose) polymerase 1	Homo sapiens	75-81
22453629-3	2012	In particular, the excessive activation of poly (ADP-ribose) polymerase-1 (PARP-1) consumes cytosolic nicotinamide adenine dinucleotide (NAD(+)), resulting in energy failure.	NAD	137-143	poly(ADP-ribose) polymerase 1	Homo sapiens	43-73
22453629-3	2012	In particular, the excessive activation of poly (ADP-ribose) polymerase-1 (PARP-1) consumes cytosolic nicotinamide adenine dinucleotide (NAD(+)), resulting in energy failure.	NAD	137-143	poly(ADP-ribose) polymerase 1	Homo sapiens	75-81
22453629-9	2012	Taken together, these results suggest an intriguing possibility: that increasing brain lactate following hypoglycemia offsets the decrease in NAD(+) due to overactivation of PARP-1 by acting as an alternative energy substrate that can effectively bypass glycolysis and be fed directly to the citric acid cycle to maintain cellular ATP levels.	NAD	142-148	poly(ADP-ribose) polymerase 1	Homo sapiens	174-180
22383490-2	2012	The purinergic receptor P2X7 is upstream of the nod-like receptor family, pryin domain containing-3 (NLRP3) inflammasome in immune cells and is activated by ATP and NAD that serve as damage-associated molecular patterns.	NAD	165-168	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	24-28
21794079-5	2012	P2X7 protein was also up-regulated and this was associated with altered function of P2X7 receptors producing increased responsiveness of cytoplasmic Ca(2+)  and extracellular signal-regulated kinase (ERK) phosphorylation to purinergic stimulation and altered sensitivity to NAD.	NAD	274-277	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	0-4
21794079-5	2012	P2X7 protein was also up-regulated and this was associated with altered function of P2X7 receptors producing increased responsiveness of cytoplasmic Ca(2+)  and extracellular signal-regulated kinase (ERK) phosphorylation to purinergic stimulation and altered sensitivity to NAD.	NAD	274-277	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	84-88
21794079-5	2012	P2X7 protein was also up-regulated and this was associated with altered function of P2X7 receptors producing increased responsiveness of cytoplasmic Ca(2+)  and extracellular signal-regulated kinase (ERK) phosphorylation to purinergic stimulation and altered sensitivity to NAD.	NAD	274-277	mitogen-activated protein kinase 1	Mus musculus	161-198
21794079-5	2012	P2X7 protein was also up-regulated and this was associated with altered function of P2X7 receptors producing increased responsiveness of cytoplasmic Ca(2+)  and extracellular signal-regulated kinase (ERK) phosphorylation to purinergic stimulation and altered sensitivity to NAD.	NAD	274-277	mitogen-activated protein kinase 1	Mus musculus	200-203
22399297-2	2012	Visfatin exhibits both an intracellular enzymatic activity (nicotinamide phosphoribosyltransferase, Nampt) leading to NAD synthesis and a cytokine function via the binding to its hypothetical receptor.	NAD	118-121	nicotinamide phosphoribosyltransferase	Mus musculus	0-8
22399297-2	2012	Visfatin exhibits both an intracellular enzymatic activity (nicotinamide phosphoribosyltransferase, Nampt) leading to NAD synthesis and a cytokine function via the binding to its hypothetical receptor.	NAD	118-121	nicotinamide phosphoribosyltransferase	Mus musculus	60-98
22326535-3	2012	We found that the expression of the SIRT3 gene was down-regulated in cybrids harboring mtDNA of the J haplogroup, which correlated with mitochondrial function, resulting in a decline of NAD(+)/NADH and ATP levels.	NAD	186-192	sirtuin 3	Homo sapiens	36-41
22326535-3	2012	We found that the expression of the SIRT3 gene was down-regulated in cybrids harboring mtDNA of the J haplogroup, which correlated with mitochondrial function, resulting in a decline of NAD(+)/NADH and ATP levels.	NAD	193-197	sirtuin 3	Homo sapiens	36-41
22417091-1	2012	Lactate dehydrogenase A (LDHA) catalyzes the conversion of pyruvate to lactate, utilizing NADH as a cofactor.	NAD	90-94	lactate dehydrogenase A	Homo sapiens	25-29
22404107-3	2012	Utilizing electron paramagnetic resonance spin trapping, we measured the role of AO in the generation of reactive oxygen species (ROS) through the oxidation of NADH and the effects of inhibitors of AO on NADH-mediated superoxide (O(2)( -)) generation.	NAD	160-164	aldehyde oxidase 1	Homo sapiens	81-83
22334709-1	2012	NMNAT-1 and PARP-1, two key enzymes in the NAD(+) metabolic pathway, localize to the nucleus where integration of their enzymatic activities has the potential to control a variety of nuclear processes.	NAD	43-49	poly(ADP-ribose) polymerase 1	Homo sapiens	12-18
22334709-3	2012	Specifically, we show that PARP-1 recruits NMNAT-1 to promoters where it produces NAD(+) to support PARP-1 catalytic activity, but also enhances the enzymatic activity of PARP-1 independently of NAD(+) production.	NAD	82-88	poly(ADP-ribose) polymerase 1	Homo sapiens	27-33
22334709-3	2012	Specifically, we show that PARP-1 recruits NMNAT-1 to promoters where it produces NAD(+) to support PARP-1 catalytic activity, but also enhances the enzymatic activity of PARP-1 independently of NAD(+) production.	NAD	82-88	poly(ADP-ribose) polymerase 1	Homo sapiens	100-106
22334709-3	2012	Specifically, we show that PARP-1 recruits NMNAT-1 to promoters where it produces NAD(+) to support PARP-1 catalytic activity, but also enhances the enzymatic activity of PARP-1 independently of NAD(+) production.	NAD	82-88	poly(ADP-ribose) polymerase 1	Homo sapiens	100-106
22334709-3	2012	Specifically, we show that PARP-1 recruits NMNAT-1 to promoters where it produces NAD(+) to support PARP-1 catalytic activity, but also enhances the enzymatic activity of PARP-1 independently of NAD(+) production.	NAD	195-201	poly(ADP-ribose) polymerase 1	Homo sapiens	27-33
22404107-3	2012	Utilizing electron paramagnetic resonance spin trapping, we measured the role of AO in the generation of reactive oxygen species (ROS) through the oxidation of NADH and the effects of inhibitors of AO on NADH-mediated superoxide (O(2)( -)) generation.	NAD	204-208	aldehyde oxidase 1	Homo sapiens	198-200
22404107-4	2012	NADH was found to be a good substrate for AO with apparent K(m) and V(max) values of 29 muM and 12 nmol min(-1) mg(-1), respectively.	NAD	0-4	aldehyde oxidase 1	Homo sapiens	42-44
22404107-5	2012	From O(2)( -) generation measurements by cytochrome c reduction the apparent K(m) and V(max) values of NADH for AO were 11 muM and 15 nmol min(-1) mg(-1), respectively.	NAD	103-107	cytochrome c, somatic	Homo sapiens	41-53
22431597-4	2012	Methylation of CoFeSP only occurs in the low-potential Co(I) state, which can be sporadically oxidized to the inactive Co(II) state, making its reductive reactivation necessary.	NAD	55-60	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	119-125
22404107-5	2012	From O(2)( -) generation measurements by cytochrome c reduction the apparent K(m) and V(max) values of NADH for AO were 11 muM and 15 nmol min(-1) mg(-1), respectively.	NAD	103-107	aldehyde oxidase 1	Homo sapiens	112-114
22404107-6	2012	With NADH oxidation by AO, &gt;=65% of the total electron flux led to O(2)( -) generation.	NAD	5-9	aldehyde oxidase 1	Homo sapiens	23-25
22404107-10	2012	Owing to the ubiquitous distribution of NADH, aldehydes, and other endogenous AO substrates, AO is predicted to have an important role in cellular redox stress and related disease pathogenesis.	NAD	40-44	aldehyde oxidase 1	Homo sapiens	93-95
21487704-5	2012	The NAD(+)(an oxidized form of NADH)/NADH ratio was maintained at a significantly higher level in cells overexpressing NQO1, consistent with enhanced levels of NQO1 activity.	NAD	4-10	NAD(P)H quinone dehydrogenase 1	Homo sapiens	119-123
21487704-5	2012	The NAD(+)(an oxidized form of NADH)/NADH ratio was maintained at a significantly higher level in cells overexpressing NQO1, consistent with enhanced levels of NQO1 activity.	NAD	4-10	NAD(P)H quinone dehydrogenase 1	Homo sapiens	160-164
21487704-5	2012	The NAD(+)(an oxidized form of NADH)/NADH ratio was maintained at a significantly higher level in cells overexpressing NQO1, consistent with enhanced levels of NQO1 activity.	NAD	31-35	NAD(P)H quinone dehydrogenase 1	Homo sapiens	119-123
21487704-5	2012	The NAD(+)(an oxidized form of NADH)/NADH ratio was maintained at a significantly higher level in cells overexpressing NQO1, consistent with enhanced levels of NQO1 activity.	NAD	31-35	NAD(P)H quinone dehydrogenase 1	Homo sapiens	160-164
21487704-5	2012	The NAD(+)(an oxidized form of NADH)/NADH ratio was maintained at a significantly higher level in cells overexpressing NQO1, consistent with enhanced levels of NQO1 activity.	NAD	37-41	NAD(P)H quinone dehydrogenase 1	Homo sapiens	119-123
21667072-1	2012	Molecular docking and structural analysis of the cofactor-protein interaction between NAD(+) and human (h) or mouse (m) 11beta-hydroxysteroid dehydrogenase type 2 (11betaHSD2) were performed with the molecular operating environment (MOE).	NAD	86-92	hydroxysteroid 11-beta dehydrogenase 2	Mus musculus	120-162
22499122-6	2012	Moreover, we have newly identified the two genes that are down-regulated in ESCC: monoamine oxidase A, an enzyme that catalyzes monoamines oxidation and 15-hydroxyprostaglandin dehydrogenase [NAD+], a prostaglandin-synthesizing enzyme that physiologically antagonizes COX-2.	NAD	192-196	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	268-273
22113495-3	2012	Activators of Sirt1 are known to improve mitochondrial function and the naturally occurring polyphenol resveratrol (RSV) has been shown to significantly increase Sirt1 activity by increasing its affinity to both NAD+ and the acetylated substrate.	NAD	212-216	sirtuin 1	Rattus norvegicus	14-19
22113495-3	2012	Activators of Sirt1 are known to improve mitochondrial function and the naturally occurring polyphenol resveratrol (RSV) has been shown to significantly increase Sirt1 activity by increasing its affinity to both NAD+ and the acetylated substrate.	NAD	212-216	sirtuin 1	Rattus norvegicus	162-167
22328989-5	2012	At an applied potential of 0.1 V, the sensor provides a linear response range for NADH from 5 x 10(-6) up to 1.5 x 10(-4) M with a sensitivity of 183.9 muA mM(-1) cm(-2), and detection and quantification limits of 0.6 and 5 muM (S/N = 3), respectively.	NAD	82-86	latexin	Homo sapiens	224-227
22198485-9	2012	Isolated mitochondria of A549 human transformed epithelial cells exhibited an improved resting bioenergetic status after stable lentiviral silencing of PARP1; these effects were associated with elevated resting mitochondrial NAD+ levels in PARP1 silenced cells.	NAD	225-229	poly(ADP-ribose) polymerase 1	Homo sapiens	152-157
22198485-9	2012	Isolated mitochondria of A549 human transformed epithelial cells exhibited an improved resting bioenergetic status after stable lentiviral silencing of PARP1; these effects were associated with elevated resting mitochondrial NAD+ levels in PARP1 silenced cells.	NAD	225-229	poly(ADP-ribose) polymerase 1	Homo sapiens	240-245
21678409-8	2012	Contrary, COX-2 expression levels significantly decreased nIDC and IDC respect to the nFA and nADH (P &lt; 0.001).	NAD	94-98	prostaglandin-endoperoxide synthase 2	Homo sapiens	10-15
22315217-6	2012	The colored Tat proteins were easily visible during purification, enabling identification of a highly active inverted membrane vesicle (IMV) fraction yielding transport rates with NADH almost an order of magnitude faster than previously reported.	NAD	180-184	twin-arginine translocation (TAT) pathway signal sequence domain protein	Escherichia coli	12-15
22008468-1	2012	Yeast NAD(+)-specific isocitrate dehydrogenase (IDH) is an octameric enzyme composed of four each of regulatory IDH1 and catalytic IDH2 subunits that share 42% sequence identity.	NAD	6-12	isocitrate dehydrogenase (NAD(+)) IDH1	Saccharomyces cerevisiae S288C	112-116
22267730-8	2012	Genetic deletion of AMPKalpha1 reduced NAD(+) levels and SIRT1 activity and significantly increased the levels of p53 and cell death.	NAD	39-45	protein kinase, AMP-activated, alpha 1 catalytic subunit	Mus musculus	20-30
22391446-4	2012	Many of PARP-1"s functions in stress response pathways are mediated by its regulated synthesis of PAR, a negatively charged polymer, using NAD(+) as a donor of ADP-ribose units.	NAD	139-145	poly(ADP-ribose) polymerase 1	Homo sapiens	8-14
22391446-5	2012	Thus, PARP-1"s functions are intimately tied to nuclear NAD(+) metabolism and the broader metabolic profile of the cell.	NAD	56-62	poly(ADP-ribose) polymerase 1	Homo sapiens	6-12
22090423-2	2012	However, recent data from a study using mice with knockout of the complex I subunit NADH:ubiquinone oxidoreductase iron-sulfur protein 4 (Ndufs4) has challenged this concept as these mice show degeneration of non-dopamine neurons.	NAD	84-88	NADH:ubiquinone oxidoreductase core subunit S4	Mus musculus	138-144
21667072-1	2012	Molecular docking and structural analysis of the cofactor-protein interaction between NAD(+) and human (h) or mouse (m) 11beta-hydroxysteroid dehydrogenase type 2 (11betaHSD2) were performed with the molecular operating environment (MOE).	NAD	86-92	hydroxysteroid 11-beta dehydrogenase 2	Mus musculus	164-174
21597922-6	2012	Common pathways for SFN treatment and KEAP1 knockdown were xenobiotic metabolism and antioxidants, glutathione metabolism, carbohydrate metabolism, and NADH/NADPH regeneration.	NAD	152-156	kelch like ECH associated protein 1	Homo sapiens	38-43
22297980-2	2012	The structure of TNKS1 in complex with PJ34 reveals two molecules of PJ34 bound in the NAD(+) donor pocket.	NAD	87-93	tankyrase	Homo sapiens	17-22
22297980-4	2012	Additionally, unlike the unliganded crystallization system, the TNKS1-PJ34 crystallization system has the NAD(+) donor site accessible to bulk solvent in the crystal, which allows displacement soaking.	NAD	106-112	tankyrase	Homo sapiens	64-69
22266671-4	2012	In human lung cells, MnCl(2) (&gt;=50 muM) decreased the levels of ATP, NAD(+) and NADH as well as the NAD(+)/NADH ratio.	NAD	83-87	latexin	Homo sapiens	38-41
22239987-0	2012	Malate-aspartate shuttle and exogenous NADH/cytochrome c electron transport pathway as two independent cytosolic reducing equivalent transfer systems.	NAD	39-43	cytochrome c, somatic	Homo sapiens	44-56
22239987-2	2012	Data never presented before show that the oxidation rate of exogenous NADH supported by the malate-aspartate shuttle system (reconstituted in vitro with isolated liver mitochondria) is comparable to the rate obtained on activation of the cytosolic NADH/cytochrome c electron transport pathway.	NAD	70-74	cytochrome c, somatic	Homo sapiens	253-265
22239987-4	2012	NADH oxidation induced by the malate-aspartate shuttle is inhibited by aminooxyacetate and by rotenone and/or antimycin A, two inhibitors of the respiratory chain, while the NADH/cytochrome c system remains insensitive to all of them.	NAD	0-4	cytochrome c, somatic	Homo sapiens	179-191
22239987-4	2012	NADH oxidation induced by the malate-aspartate shuttle is inhibited by aminooxyacetate and by rotenone and/or antimycin A, two inhibitors of the respiratory chain, while the NADH/cytochrome c system remains insensitive to all of them.	NAD	174-178	cytochrome c, somatic	Homo sapiens	179-191
22052811-6	2012	To determine the mechanism of action, we collected LDH-A and -B inhibition data in competition reactions with pyruvate or NADH and evaluated the results using software for enzyme kinetics analysis.	NAD	122-126	lactate dehydrogenase A	Homo sapiens	51-63
22204321-3	2012	The key NAD(+)-consuming enzyme--poly(ADP-ribose) polymerase-1 (PARP-1) and sirtuins--have also been shown to play important roles in cell death and aging, which are two key factors in the pathology of multiple major age-dependent neurological diseases: PARP-1 plays critical roles in both inflammation and oxidative stress-induced cell death; and sirtuins also mediate the process of aging, cell death and inflammation.	NAD	8-14	poly(ADP-ribose) polymerase 1	Homo sapiens	25-62
22204321-5	2012	For examples, the key NAD(+)-dependent enzymes SIRT1 and SIRT2 have been indicated to strongly affect the pathological changes of PD and AD; PARP-1 inhibition can profoundly reduce the brain injury in the animal models of multiple neurological diseases; and administration of either NAD(+) or nicotinamide can also decrease ischemic brain damage.	NAD	22-28	poly(ADP-ribose) polymerase 1	Homo sapiens	141-147
22204321-3	2012	The key NAD(+)-consuming enzyme--poly(ADP-ribose) polymerase-1 (PARP-1) and sirtuins--have also been shown to play important roles in cell death and aging, which are two key factors in the pathology of multiple major age-dependent neurological diseases: PARP-1 plays critical roles in both inflammation and oxidative stress-induced cell death; and sirtuins also mediate the process of aging, cell death and inflammation.	NAD	8-14	poly(ADP-ribose) polymerase 1	Homo sapiens	64-70
22204321-5	2012	For examples, the key NAD(+)-dependent enzymes SIRT1 and SIRT2 have been indicated to strongly affect the pathological changes of PD and AD; PARP-1 inhibition can profoundly reduce the brain injury in the animal models of multiple neurological diseases; and administration of either NAD(+) or nicotinamide can also decrease ischemic brain damage.	NAD	283-289	poly(ADP-ribose) polymerase 1	Homo sapiens	141-147
22204321-3	2012	The key NAD(+)-consuming enzyme--poly(ADP-ribose) polymerase-1 (PARP-1) and sirtuins--have also been shown to play important roles in cell death and aging, which are two key factors in the pathology of multiple major age-dependent neurological diseases: PARP-1 plays critical roles in both inflammation and oxidative stress-induced cell death; and sirtuins also mediate the process of aging, cell death and inflammation.	NAD	8-14	poly(ADP-ribose) polymerase 1	Homo sapiens	254-260
22302938-0	2012	Dietary obesity-associated Hif1alpha activation in adipocytes restricts fatty acid oxidation and energy expenditure via suppression of the Sirt2-NAD+ system.	NAD	145-149	hypoxia inducible factor 1 subunit alpha	Homo sapiens	27-36
22276961-5	2012	Western analysis demonstrates that CD38, a multifunctional protein that metabolizes beta-NAD(+) , is present on synaptosomal membranes and in the cytosol.	NAD	84-95	CD38 molecule	Rattus norvegicus	35-39
22128301-6	2012	EXPERIMENTAL DESIGN: Two chemical series of NAD(+)-competitive PARP inhibitors, iniparib and its C-nitroso metabolite, were analyzed in enzymatic and cellular assays.	NAD	44-50	poly(ADP-ribose) polymerase 1	Homo sapiens	63-67
21979946-0	2012	Germline SDHx variants modify breast and thyroid cancer risks in Cowden and Cowden-like syndrome via FAD/NAD-dependant destabilization of p53.	NAD	105-108	tumor protein p53	Homo sapiens	138-141
21979946-11	2012	This loss of p53 was regulated by MDM2-independent NADH quinone oxidoreductase 1-mediated protein degradation, likely due to the imbalance of flavin adenine dinucleotide/nicotinamide adenine dinucleotide in SDH(var+) cells.	NAD	170-203	tumor protein p53	Homo sapiens	13-16
22128301-10	2012	RESULTS: All NAD(+)-competitive inhibitors show robust activity in a PARP cellular assay, strongly potentiate the activity of temozolomide, and elicit robust cell killing in BRCA-deficient tumor cells in vitro and in vivo.	NAD	13-19	poly(ADP-ribose) polymerase 1	Homo sapiens	69-73
22126535-3	2012	This analog is stable and binds in the active site of a typical NAD-dependent enzyme formate dehydrogenase (FDH) with characteristics similar to those of natural NAD(+).	NAD	64-67	aldehyde dehydrogenase 1 family member L1	Homo sapiens	108-111
22265524-3	2012	Voltammetric studies revealed the increased electrochemical activity of the CNP-modified electrode toward various biologically important molecules, including dopamine, uric acid, dihydronicotinamide adenine dinucleotide, tyrosine, and serotonin, relative to those obtained using the unmodified electrode.	NAD	179-219	2',3'-cyclic nucleotide 3' phosphodiesterase	Homo sapiens	76-79
22126535-3	2012	This analog is stable and binds in the active site of a typical NAD-dependent enzyme formate dehydrogenase (FDH) with characteristics similar to those of natural NAD(+).	NAD	162-168	aldehyde dehydrogenase 1 family member L1	Homo sapiens	108-111
22089387-2	2012	The enzyme is known to be widely distributed in bacteria and eukarya, together with nicotinamide adenine dinucleotide (phosphate)-dependent P5C dehydrogenase, and to function in the metabolism of L-proline to L-glutamate.	NAD	84-117	aldehyde dehydrogenase 4 family member A1	Homo sapiens	140-157
22084251-7	2012	Inhibition of deacetylases, including the NAD+-dependent sirtuins, promotes Rictor acetylation and IGF-1-mediated Akt phosphorylation.	NAD	42-46	insulin like growth factor 1	Homo sapiens	99-104
22084251-7	2012	Inhibition of deacetylases, including the NAD+-dependent sirtuins, promotes Rictor acetylation and IGF-1-mediated Akt phosphorylation.	NAD	42-46	AKT serine/threonine kinase 1	Homo sapiens	114-117
22400117-1	2012	There is evidence for an unexpected role of diferric transferrin as a terminal oxidase for the transplasma membrane oxidation of cytosolic NADH.	NAD	139-143	transferrin	Homo sapiens	53-64
22400117-4	2012	The stimulation of cytosolic NADH oxidation by diferric transferrin indicates that the transferrin can act as a terminal oxidase for the transplasma membrane NADH oxidase or can bind to a site which activates the oxidase.	NAD	29-33	transferrin	Homo sapiens	56-67
22400117-4	2012	The stimulation of cytosolic NADH oxidation by diferric transferrin indicates that the transferrin can act as a terminal oxidase for the transplasma membrane NADH oxidase or can bind to a site which activates the oxidase.	NAD	29-33	transferrin	Homo sapiens	87-98
21840394-2	2012	The addition of polymers of adenosine diphosphate (ADP)-ribose (PAR), which are synthesized by PAR polymerases (PARPs) from nicotinamide adenine dinucleotide (NAD), is one such distinctive post-translational modification.	NAD	124-157	poly(ADP-ribose) polymerase 1	Homo sapiens	112-117
22359433-4	2012	Azoreductase belongs to the family of oxidoreductases, acting on other nitrogenous compounds as donors with NAD+ or NADP+ as acceptor.	NAD	108-112	NAD(P)H quinone dehydrogenase 1	Homo sapiens	0-12
21840394-2	2012	The addition of polymers of adenosine diphosphate (ADP)-ribose (PAR), which are synthesized by PAR polymerases (PARPs) from nicotinamide adenine dinucleotide (NAD), is one such distinctive post-translational modification.	NAD	159-162	poly(ADP-ribose) polymerase 1	Homo sapiens	112-117
22675360-3	2012	In highly respiring cells, the resulting NAD(+) accumulation then induces sirtuin-3-mediated activating IDH2 deacetylation, thus increasing its protective function.	NAD	41-47	isocitrate dehydrogenase (NADP(+)) 2	Homo sapiens	104-108
22201895-9	2012	They are flavin dependent NADH preferred azoreductase, flavin dependent NADPH preferred azoreductase, and flavin free NADPH preferred azoreductase.	NAD	26-30	NAD(P)H quinone dehydrogenase 1	Homo sapiens	41-53
22201895-9	2012	They are flavin dependent NADH preferred azoreductase, flavin dependent NADPH preferred azoreductase, and flavin free NADPH preferred azoreductase.	NAD	26-30	NAD(P)H quinone dehydrogenase 1	Homo sapiens	88-100
22201895-9	2012	They are flavin dependent NADH preferred azoreductase, flavin dependent NADPH preferred azoreductase, and flavin free NADPH preferred azoreductase.	NAD	26-30	NAD(P)H quinone dehydrogenase 1	Homo sapiens	88-100
23109907-5	2012	We find that nicotinamide riboside kinase 2b-mediated NAD+ biosynthesis, which functions as a small molecule agonist of muscle fiber-extracellular matrix adhesion, corrects dystrophic phenotypes in zebrafish lacking either a primary component of the dystrophin-glycoprotein complex or integrin alpha7.	NAD	54-58	integrin, alpha 7	Danio rerio	285-300
23939409-7	2012	Relationships among PGC-1alpha and its downstream targets NRF1 and TFAM were very similar in PD and CTL and were related to mitochondrial NADH-driven electron flow.	NAD	138-142	PPARG coactivator 1 alpha	Homo sapiens	20-30
23939409-7	2012	Relationships among PGC-1alpha and its downstream targets NRF1 and TFAM were very similar in PD and CTL and were related to mitochondrial NADH-driven electron flow.	NAD	138-142	transcription factor A, mitochondrial	Homo sapiens	67-71
23109907-10	2012	The surprising result that NAD+ supplementation ameliorates dystrophy in dystrophin-glycoprotein complex- or integrin alpha7-deficient zebrafish suggests the existence of an additional laminin receptor complex that anchors muscle fibers to the basement membrane.	NAD	27-31	integrin, alpha 7	Danio rerio	109-124
23284917-10	2012	However, during aging, the MRL/lpr T-cell population exhibits a drastically reduced sensitivity to ATP- or NAD-mediated stimulation of P2X7R, which parallels the increase in B220(+) DN T-cell numbers in lymphoid organs.	NAD	107-110	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	135-140
23226344-6	2012	Reduced expression of dCIA30 results in the loss of the complex I holoenzyme band in blue-native polyacrylamide gel electrophoresis and loss of NADH:ubiquinone oxidoreductase activity in isolated mitochondria.	NAD	144-148	Complex I intermediate-associated protein, 30 kDa	Drosophila melanogaster	22-28
22848760-2	2012	In genomic DNA, NAD(+) also represents the sole substrate for the nuclear repair enzyme, poly(ADP-ribose) polymerase (PARP) and the sirtuin family of NAD-dependent histone deacetylases.	NAD	16-22	poly(ADP-ribose) polymerase 1	Homo sapiens	89-116
23028781-6	2012	In contrast, we find similar values for Sirt5 and Sirt3 for the intrinsic NAD(+) affinity as well as the apparent NAD(+) affinity in presence of peptide.	NAD	74-80	sirtuin 3	Homo sapiens	50-55
22848760-2	2012	In genomic DNA, NAD(+) also represents the sole substrate for the nuclear repair enzyme, poly(ADP-ribose) polymerase (PARP) and the sirtuin family of NAD-dependent histone deacetylases.	NAD	16-22	poly(ADP-ribose) polymerase 1	Homo sapiens	118-122
22848760-3	2012	Age associated increases in oxidative nuclear damage have been associated with PARP-mediated NAD(+) depletion and loss of SIRT1 activity in rodents.	NAD	93-99	poly(ADP-ribose) polymerase 1	Homo sapiens	79-83
22848760-7	2012	PARP activity significantly increased with age in males (p&lt;0.0001; r = 0.768) and inversely correlated with tissue NAD(+) levels (p = 0.0003; r = -0.639).	NAD	118-124	poly(ADP-ribose) polymerase 1	Homo sapiens	0-4
22860104-1	2012	Sirtuins (SIRTs) and poly(ADP-ribose) polymerases (PARPs), NAD(+)-dependent enzymes, link cellular energy status with responses to environmental stresses.	NAD	59-65	poly(ADP-ribose) polymerase 1	Homo sapiens	51-56
22848760-11	2012	Strong positive correlations were also observed between lipid peroxidation and DNA damage (p&lt;0.0001; r = 0.4962), and PARP activity and NAD(+) levels (p = 0.0213; r = 0.5241) in post pubescent males.	NAD	139-145	poly(ADP-ribose) polymerase 1	Homo sapiens	121-125
22848760-12	2012	This study provides quantitative evidence in support of the hypothesis that hyperactivation of PARP due to an accumulation of oxidative damage to DNA during aging may be responsible for increased NAD(+) catabolism in human tissue.	NAD	196-202	poly(ADP-ribose) polymerase 1	Homo sapiens	95-99
22295107-5	2012	The treatment with estradiol (E2), anti-estrogenic agents 4-hydroxytamoxifen and ICI 182780, ERbeta specific ligand DPN and GPR30 agonist G1 led to a rapid activation of p-ERK1/2, suggesting the involvement of ERalpha36, ERbeta and GPR30 in the non-genomic signaling pathway in these cells.	NAD	116-119	mitogen-activated protein kinase 3	Homo sapiens	172-178
22848454-3	2012	Gating of murine P2X7 can be induced by the soluble ligand ATP, as well as by NAD(+)-dependent ADP-ribosylation of arginine 125, a posttranslational protein modification catalyzed by the toxin-related ecto-enzymes ART2.1 and ART2.2.	NAD	78-84	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	17-21
22848454-11	2012	Our results indicate that differential splicing of alternative exons encoding the N-terminal cytosolic and transmembrane domains of P2X7 control the sensitivity of different immune cells to extracellular NAD(+) and ATP.	NAD	204-210	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	132-136
21963991-3	2011	Among the proteins with high affinities for pyridine nucleotides that also inhibited 1,2-NQ-protein adduct formation in the presence of NADH, a 37-kDa protein was found and identified as glyceraldehyde-3-phosphate dehydrogenase (GAPDH).	NAD	136-140	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	187-227
22033928-0	2011	Connexin-43 hemichannels mediate cyclic ADP-ribose generation and its Ca2+-mobilizing activity by NAD+/cyclic ADP-ribose transport.	NAD	98-102	gap junction protein, alpha 1	Mus musculus	0-11
22153507-6	2011	This study also provides insight into how the GAPDH-CP12 complex is dissociated by a high NADP(H)/NAD(H) ratio.	NAD	98-104	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	46-51
21901281-1	2011	AIMS/HYPOTHESIS: Nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme for NAD(+) biosynthesis, exists as intracellular NAMPT (iNAMPT) and extracellular NAMPT (eNAMPT).	NAD	94-100	nicotinamide phosphoribosyltransferase	Mus musculus	17-55
21901281-1	2011	AIMS/HYPOTHESIS: Nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme for NAD(+) biosynthesis, exists as intracellular NAMPT (iNAMPT) and extracellular NAMPT (eNAMPT).	NAD	94-100	nicotinamide phosphoribosyltransferase	Mus musculus	57-62
21901281-1	2011	AIMS/HYPOTHESIS: Nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme for NAD(+) biosynthesis, exists as intracellular NAMPT (iNAMPT) and extracellular NAMPT (eNAMPT).	NAD	94-100	nicotinamide phosphoribosyltransferase	Mus musculus	139-144
21901281-1	2011	AIMS/HYPOTHESIS: Nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme for NAD(+) biosynthesis, exists as intracellular NAMPT (iNAMPT) and extracellular NAMPT (eNAMPT).	NAD	94-100	nicotinamide phosphoribosyltransferase	Mus musculus	139-144
21476963-1	2011	Poly(ADP-ribose) polymerases (PARPs) represent a family of enzymes which synthesize and bind branched polymers of ADP-ribose to acceptor proteins using NAD as a substrate.	NAD	152-155	poly(ADP-ribose) polymerase 1	Homo sapiens	30-35
21963991-3	2011	Among the proteins with high affinities for pyridine nucleotides that also inhibited 1,2-NQ-protein adduct formation in the presence of NADH, a 37-kDa protein was found and identified as glyceraldehyde-3-phosphate dehydrogenase (GAPDH).	NAD	136-140	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	229-234
21963991-4	2011	Using recombinant human GAPDH, we found that this glycolytic enzyme indeed catalyzes the two-electron reduction of 1,2-NQ accompanied by extensive NADH consumption under 20% oxygen conditions.	NAD	147-151	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	24-29
21963991-5	2011	When either 1,2-NQH(2) or 1,2-NQ was incubated with GAPDH in the presence of NADH, minimal covalent bonding to the enzyme occurred compared to that in its absence.	NAD	77-81	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	52-57
21963991-6	2011	These results indicate that GAPDH can inhibit 1,2-NQ-based electrophilic protein modification by conversion to the nonelectrophilic 1,2-NQH(2) via an NADH-dependent process.	NAD	150-154	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	28-33
21969607-0	2011	Tyrosine phosphorylation of lactate dehydrogenase A is important for NADH/NAD(+) redox homeostasis in cancer cells.	NAD	69-73	lactate dehydrogenase A	Homo sapiens	28-51
21488086-5	2011	Poly(ADP-ribose) polymerase (PARP) is considered to be a major NAD(+) degrading enzyme, particularly under conditions of extensive DNA damage.	NAD	63-69	poly(ADP-ribose) polymerase 1	Homo sapiens	0-27
21488086-5	2011	Poly(ADP-ribose) polymerase (PARP) is considered to be a major NAD(+) degrading enzyme, particularly under conditions of extensive DNA damage.	NAD	63-69	poly(ADP-ribose) polymerase 1	Homo sapiens	29-33
21969607-0	2011	Tyrosine phosphorylation of lactate dehydrogenase A is important for NADH/NAD(+) redox homeostasis in cancer cells.	NAD	74-80	lactate dehydrogenase A	Homo sapiens	28-51
21969607-2	2011	Lactate dehydrogenase A (LDH-A) regulates the last step of glycolysis that generates lactate and permits the regeneration of NAD(+).	NAD	125-131	lactate dehydrogenase A	Homo sapiens	0-23
22026918-1	2011	NADH pyrophosphatase (NudC) catalyses the hydrolysis of NAD(H) to AMP and NMN(H) [nicotinamide mononucleotide (reduced form)].	NAD	56-62	NADH pyrophosphatase	Mycobacterium tuberculosis H37Rv	22-26
21969607-2	2011	Lactate dehydrogenase A (LDH-A) regulates the last step of glycolysis that generates lactate and permits the regeneration of NAD(+).	NAD	125-131	lactate dehydrogenase A	Homo sapiens	25-30
21969607-6	2011	Phosphorylation at Y10 and Y83 enhances LDH-A activity by enhancing the formation of active, tetrameric LDH-A and the binding of LDH-A substrate NADH, respectively.	NAD	145-149	lactate dehydrogenase A	Homo sapiens	40-45
21969607-8	2011	Interestingly, cancer cells with stable knockdown of endogenous LDH-A and rescue expression of a catalytic hypomorph LDH-A mutant, Y10F, demonstrate increased respiration through mitochondrial complex I to sustain glycolysis by providing NAD(+).	NAD	238-244	lactate dehydrogenase A	Homo sapiens	64-69
21969607-8	2011	Interestingly, cancer cells with stable knockdown of endogenous LDH-A and rescue expression of a catalytic hypomorph LDH-A mutant, Y10F, demonstrate increased respiration through mitochondrial complex I to sustain glycolysis by providing NAD(+).	NAD	238-244	lactate dehydrogenase A	Homo sapiens	117-122
21969607-11	2011	Our findings suggest that tyrosine phosphorylation enhances LDH-A enzyme activity to promote the Warburg effect and tumor growth by regulating the NADH/NAD(+) redox homeostasis, representing an acute molecular mechanism underlying the enhanced lactate production in cancer cells.	NAD	147-151	lactate dehydrogenase A	Homo sapiens	60-65
21969607-11	2011	Our findings suggest that tyrosine phosphorylation enhances LDH-A enzyme activity to promote the Warburg effect and tumor growth by regulating the NADH/NAD(+) redox homeostasis, representing an acute molecular mechanism underlying the enhanced lactate production in cancer cells.	NAD	152-158	lactate dehydrogenase A	Homo sapiens	60-65
21942543-8	2011	-1.0 V vs SCE in cyclic voltammetry experiments for Co(dmgBF(2))(2) is more likely to correspond to the Co(II)H/Co(I)H reduction potential than the Co(III)H/Co(II)H reduction potential.	NAD	112-117	mitochondrially encoded cytochrome c oxidase III	Homo sapiens	151-154
21945626-6	2011	Involvement of the catalytic domain is restricted to its ability to poly(ADP-ribosyl)ate PARP-1 in the presence of NAD(+), likely through interference with DNA binding.	NAD	115-121	poly(ADP-ribose) polymerase 1	Homo sapiens	89-95
22332087-6	2011	Based on this synthesis, a model is proposed that links the FFA-rich environment of obesity/insulin resistance and T2DM with diminution of BCAA catabolic enzyme activity, changes in methionine oxidation and cysteine/cystine generation, and tissue redox balance (NADH/NAD+).	NAD	267-271	insulin	Homo sapiens	92-99
21812028-4	2011	We suppose that these effects were caused by age-related reduction of nicotinamide phosphoribosyltransferase (Nampt), the enzyme catalyzing NAD resynthesis from nicotinamide (NAM).	NAD	140-143	nicotinamide phosphoribosyltransferase	Mus musculus	70-108
22332087-6	2011	Based on this synthesis, a model is proposed that links the FFA-rich environment of obesity/insulin resistance and T2DM with diminution of BCAA catabolic enzyme activity, changes in methionine oxidation and cysteine/cystine generation, and tissue redox balance (NADH/NAD+).	NAD	262-266	insulin	Homo sapiens	92-99
21618469-11	2011	An increase in cell specific activity was also found for NAD(+)-dependent isocitrate dehydrogenase, glutamate dehydrogenase, and glutamine synthetase in MDCK cells grown with pyruvate.	NAD	57-63	glutamate-ammonia ligase	Canis lupus familiaris	129-149
22092810-5	2011	The detoxification system is constitutively expressed with a specific activity of 352 (+-18) nmol NADH oxidized min(-1)  (mg protein)(-1) .	NAD	98-102	CD59 molecule (CD59 blood group)	Homo sapiens	112-118
21807113-4	2011	Sirt1, a NAD-dependent class III histone deacetylase, has a paradoxical role in tumorigenesis by deacetylating several transcription factors, including p53, E2F1 and forkhead proteins.	NAD	9-12	tumor protein p53	Homo sapiens	152-155
21812028-4	2011	We suppose that these effects were caused by age-related reduction of nicotinamide phosphoribosyltransferase (Nampt), the enzyme catalyzing NAD resynthesis from nicotinamide (NAM).	NAD	140-143	nicotinamide phosphoribosyltransferase	Mus musculus	110-115
21812028-7	2011	Interestingly, although Nampt deficiency resulted in both decreased intracellular NAD(+) and increased NAM, the cell differentiation could be controlled only by regulation of NAM.	NAD	82-88	nicotinamide phosphoribosyltransferase	Mus musculus	24-29
21242068-2	2011	In yeast, NADP-dependent enzymes, encoded by GDH1 and GDH3, are reported to synthesize glutamate from alpha-ketoglutarate, while an NAD-dependent enzyme, encoded by GDH2, catalyzes the reverse.	NAD	10-13	glutamate dehydrogenase (NADP(+)) GDH3	Saccharomyces cerevisiae S288C	54-58
22017865-2	2011	demonstrate that loss of the NAD(+)-dependent deacetylase SIRT3 and resultant mitochondrial protein hyperacetylation play a critical role in the pathogenesis of metabolic syndrome, providing new insights into the therapeutic potential of SIRT3.	NAD	29-35	sirtuin 3	Homo sapiens	58-63
22017865-2	2011	demonstrate that loss of the NAD(+)-dependent deacetylase SIRT3 and resultant mitochondrial protein hyperacetylation play a critical role in the pathogenesis of metabolic syndrome, providing new insights into the therapeutic potential of SIRT3.	NAD	29-35	sirtuin 3	Homo sapiens	238-243
21242068-4	2011	In YNAceRaf the doubling time of wild type, gdh2Delta, and gdh3Delta cells was comparable at ~4 h. NADP-dependent GDH activity (Gdh1p+Gdh3p) in wild type, gdh2Delta, and gdh3Delta was decreased ~80% and NAD-dependent activity (Gdh2p) in wild type and gdh3Delta was increased ~20-fold in YNAceRaf as compared to glucose.	NAD	99-102	glutamate dehydrogenase (NADP(+)) GDH3	Saccharomyces cerevisiae S288C	134-139
21242068-5	2011	Cells carrying the gdh1Delta allele did not divide in YNAceRaf, yet both the NADP-dependent (Gdh3p) and NAD-dependent (Gdh2p) GDH activity was ~3-fold higher than in glucose.	NAD	77-80	glutamate dehydrogenase (NADP(+)) GDH3	Saccharomyces cerevisiae S288C	93-98
21913670-4	2011	The Co(II) complex derived from (Bz)NP2 displays dual coordination modes: one in the tetrahedral complex [((Bz)NP2)Co(I)(2)]; and the other in a square pyramidal variant, [((Bz)NP2)Co(I)(2)].	NAD	115-120	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	4-10
21913670-4	2011	The Co(II) complex derived from (Bz)NP2 displays dual coordination modes: one in the tetrahedral complex [((Bz)NP2)Co(I)(2)]; and the other in a square pyramidal variant, [((Bz)NP2)Co(I)(2)].	NAD	181-186	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	4-10
21567176-0	2011	Kinetic characterisation of recombinant Corynebacterium glutamicum NAD+-dependent LDH over-expressed in E. coli and its rescue of an lldD- phenotype in C. glutamicum: the issue of reversibility re-examined.	NAD	67-71	L-lactate dehydrogenase	Corynebacterium glutamicum ATCC 13032	82-85
21982712-3	2011	Here, we show that NAMPT-mediated NAD(+) biosynthesis is severely compromised in metabolic organs by high-fat diet (HFD).	NAD	34-40	nicotinamide phosphoribosyltransferase	Mus musculus	19-24
21982714-2	2011	We constructed a fluorescent biosensor of the cytosolic NADH-NAD(+) redox state by combining a circularly permuted GFP T-Sapphire with a bacterial NADH-binding protein, Rex.	NAD	56-60	rex	Mus musculus	169-172
21982714-2	2011	We constructed a fluorescent biosensor of the cytosolic NADH-NAD(+) redox state by combining a circularly permuted GFP T-Sapphire with a bacterial NADH-binding protein, Rex.	NAD	61-67	rex	Mus musculus	169-172
21982714-2	2011	We constructed a fluorescent biosensor of the cytosolic NADH-NAD(+) redox state by combining a circularly permuted GFP T-Sapphire with a bacterial NADH-binding protein, Rex.	NAD	147-151	rex	Mus musculus	169-172
21775503-11	2011	Binding of Hsp70 to GAPDH was nicotinamide adenine dinucleotide-dependent suggesting another type of association.	NAD	30-63	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	20-25
21739274-3	2011	The rate of cytosolic NADH/cyto-c electron transport pathway is also greatly stimulated.	NAD	22-26	cytochrome c, somatic	Homo sapiens	27-33
21567176-1	2011	The ldh gene of Corynebacterium glutamicum ATCC 13032 (gene symbol cg3219, encoding a 314 residue NAD+-dependent L-(+)-lactate dehydrogenase, EC 1.1.1.27) was cloned into the expression vector pKK388-1 and over-expressed in an ldhA-null E. coli TG1 strain upon isopropyl-beta-D-thiogalactopyranoside (IPTG) induction.	NAD	98-101	L-lactate dehydrogenase	Corynebacterium glutamicum ATCC 13032	4-7
21641039-8	2011	Exposure of ART2.2-transgenic T cells to low, submicromolar concentrations of NAD caused cell membrane alterations including uptake of propidium iodide, externalization of phosphatidylserine, and shedding of CD62L, while ART2.2-transgenic B cells were resistant to NAD.	NAD	78-81	selectin, lymphocyte	Mus musculus	208-213
21419845-3	2011	Spin-trapping studies of incubations containing RSF, 5,5-dimethyl-1-pyrroline N-oxide (DMPO) and NADH demonstrated, under irradiation with visible light, the production of the superoxide dismutase (SOD)-sensitive DMPO/( )OOH adduct.	NAD	97-101	superoxide dismutase 1	Homo sapiens	176-196
21571040-4	2011	CONCLUSIONS: Based on findings with metabolites, we conclude that apoptosis in cancer cell lines caused by ENOX2 inhibitors such as EGCG and phenoxodiol is a direct response to elevated levels of cytosolic NADH that result from ENOX2 inhibition.	NAD	206-210	ecto-NOX disulfide-thiol exchanger 2	Homo sapiens	107-112
21571040-4	2011	CONCLUSIONS: Based on findings with metabolites, we conclude that apoptosis in cancer cell lines caused by ENOX2 inhibitors such as EGCG and phenoxodiol is a direct response to elevated levels of cytosolic NADH that result from ENOX2 inhibition.	NAD	206-210	ecto-NOX disulfide-thiol exchanger 2	Homo sapiens	228-233
21571040-5	2011	GENERAL SIGNIFICANCE: The findings help to explain why increased NADH levels resulting from ENOX2 inhibition result in decreased prosurvival sphingosine-1-phosphate and increased proapoptotic ceramide, both of which may be important to initiation of the ENOX2 inhibitor-induced apoptotic cascade.	NAD	65-69	ecto-NOX disulfide-thiol exchanger 2	Homo sapiens	92-97
21571040-5	2011	GENERAL SIGNIFICANCE: The findings help to explain why increased NADH levels resulting from ENOX2 inhibition result in decreased prosurvival sphingosine-1-phosphate and increased proapoptotic ceramide, both of which may be important to initiation of the ENOX2 inhibitor-induced apoptotic cascade.	NAD	65-69	ecto-NOX disulfide-thiol exchanger 2	Homo sapiens	254-259
21502369-3	2011	beta-Lapachone (betaL), a well-known substrate of NAD(P)H:quinone oxidoreductase (NQO1), increases the cellular NAD(+)/NADH ratio via the activation of NQO1.	NAD	112-118	NAD(P)H quinone dehydrogenase 1	Homo sapiens	82-86
21502369-3	2011	beta-Lapachone (betaL), a well-known substrate of NAD(P)H:quinone oxidoreductase (NQO1), increases the cellular NAD(+)/NADH ratio via the activation of NQO1.	NAD	112-118	NAD(P)H quinone dehydrogenase 1	Homo sapiens	152-156
21502369-3	2011	beta-Lapachone (betaL), a well-known substrate of NAD(P)H:quinone oxidoreductase (NQO1), increases the cellular NAD(+)/NADH ratio via the activation of NQO1.	NAD	119-123	NAD(P)H quinone dehydrogenase 1	Homo sapiens	82-86
21502369-10	2011	CONCLUSION: This study is the first to demonstrate that NQO1 activation has a hypotensive effect mediated by eNOS activation via cellular NAD(+)/NADH ratio modulation in an animal model.	NAD	138-144	NAD(P)H quinone dehydrogenase 1	Homo sapiens	56-60
21502369-10	2011	CONCLUSION: This study is the first to demonstrate that NQO1 activation has a hypotensive effect mediated by eNOS activation via cellular NAD(+)/NADH ratio modulation in an animal model.	NAD	145-149	NAD(P)H quinone dehydrogenase 1	Homo sapiens	56-60
21419845-3	2011	Spin-trapping studies of incubations containing RSF, 5,5-dimethyl-1-pyrroline N-oxide (DMPO) and NADH demonstrated, under irradiation with visible light, the production of the superoxide dismutase (SOD)-sensitive DMPO/( )OOH adduct.	NAD	97-101	superoxide dismutase 1	Homo sapiens	198-201
20863819-2	2011	Reactive intermediates produced in the EtaA-catalyzed transformations of ethionamide and prothionamide result in NAD(+)/NADH adducts that inhibit the enoyl CoA reductase InhA, the ultimate target of these drugs.	NAD	113-119	inhibin subunit alpha	Homo sapiens	170-174
21545835-5	2011	Studies were performed to understand the related mechanisms of radical generation and NADH oxidation by Fe3+cyt c in the presence of H2O2.	NAD	86-90	cytochrome c, somatic	Homo sapiens	108-113
21545835-9	2011	The amount of superoxide radical adduct formed from the oxidation of NADH by the peroxidase activity of Fe3+cyt c increased with NADH and H2O2 concentration.	NAD	69-73	cytochrome c, somatic	Homo sapiens	108-113
21545835-9	2011	The amount of superoxide radical adduct formed from the oxidation of NADH by the peroxidase activity of Fe3+cyt c increased with NADH and H2O2 concentration.	NAD	129-133	cytochrome c, somatic	Homo sapiens	108-113
21545835-10	2011	From these results, we propose a mechanism in which the peroxidase activity of Fe3+cyt c oxidizes NADH to NAD( ), which in turn donates an electron to O2, resulting in superoxide radical formation.	NAD	98-102	cytochrome c, somatic	Homo sapiens	83-88
21545835-10	2011	From these results, we propose a mechanism in which the peroxidase activity of Fe3+cyt c oxidizes NADH to NAD( ), which in turn donates an electron to O2, resulting in superoxide radical formation.	NAD	106-112	cytochrome c, somatic	Homo sapiens	83-88
21545835-11	2011	A UV-visible spectroscopic study shows that Fe3+cyt c is reduced in the presence of both NADH and H2O2.	NAD	89-93	cytochrome c, somatic	Homo sapiens	48-53
20863819-2	2011	Reactive intermediates produced in the EtaA-catalyzed transformations of ethionamide and prothionamide result in NAD(+)/NADH adducts that inhibit the enoyl CoA reductase InhA, the ultimate target of these drugs.	NAD	120-124	inhibin subunit alpha	Homo sapiens	170-174
21721834-4	2011	In this study, we investigated the potential using NADH fluorescence intensity and/or lifetime to detect poly(adenosine-5"-diphosphate-ribose) polymerase-1 (PARP-1)-mediated cell death in HeLa cells.	NAD	51-55	poly(ADP-ribose) polymerase 1	Homo sapiens	157-163
21504897-5	2011	To visualize organellar NAD changes in cells, we targeted poly(ADP-ribose) polymerase activity into the mitochondrial matrix.	NAD	24-27	poly(ADP-ribose) polymerase 1	Homo sapiens	58-85
21721834-6	2011	The mechanism of PARP-1-mediated cell death has been well studied that extensive PARP-1 activation leads to cytosolic nicotinamide adenine dinucleotide depletion resulting in glycolytic inhibition, mitochondrial failure, and death.	NAD	118-151	poly(ADP-ribose) polymerase 1	Homo sapiens	17-23
21721834-6	2011	The mechanism of PARP-1-mediated cell death has been well studied that extensive PARP-1 activation leads to cytosolic nicotinamide adenine dinucleotide depletion resulting in glycolytic inhibition, mitochondrial failure, and death.	NAD	118-151	poly(ADP-ribose) polymerase 1	Homo sapiens	81-87
21721834-8	2011	Our results show that NADH fluorescence lifetime, not intensity, responded to PARP-1-mediated cell death and the rescue effect of pyruvate.	NAD	22-26	poly(ADP-ribose) polymerase 1	Homo sapiens	78-84
21296058-6	2011	The presence of coenzyme NAD(+) (10-50 muM) increased the extent of inactivation (60%) at 120 min of reaction, but the ligands betaine aldehyde (50 and 500 muM) and glycine betaine (100 mM) did not change the rate or extent of inactivation as compared to the reaction without ligand.	NAD	25-31	latexin	Homo sapiens	39-42
21463108-9	2011	The cells die by apoptosis, but the DNA strand breaks also cause the activation of poly(ADP-ribose) polymerase (PARP), with resultant cellular depletion of nicotinamide adenine dinucleotide (NAD) and ATP.	NAD	156-189	poly(ADP-ribose) polymerase 1	Homo sapiens	83-110
21463108-9	2011	The cells die by apoptosis, but the DNA strand breaks also cause the activation of poly(ADP-ribose) polymerase (PARP), with resultant cellular depletion of nicotinamide adenine dinucleotide (NAD) and ATP.	NAD	156-189	poly(ADP-ribose) polymerase 1	Homo sapiens	112-116
21463108-9	2011	The cells die by apoptosis, but the DNA strand breaks also cause the activation of poly(ADP-ribose) polymerase (PARP), with resultant cellular depletion of nicotinamide adenine dinucleotide (NAD) and ATP.	NAD	191-194	poly(ADP-ribose) polymerase 1	Homo sapiens	83-110
21463108-9	2011	The cells die by apoptosis, but the DNA strand breaks also cause the activation of poly(ADP-ribose) polymerase (PARP), with resultant cellular depletion of nicotinamide adenine dinucleotide (NAD) and ATP.	NAD	191-194	poly(ADP-ribose) polymerase 1	Homo sapiens	112-116
21738489-1	2011	The sirtuin Sirt6 is a NAD-dependent histone deacetylase that is implicated in gene regulation and lifespan control.	NAD	23-26	sirtuin 6	Mus musculus	12-17
21478153-1	2011	CD157, a member of the CD38 gene family, is an NAD-metabolizing ectoenzyme and a signaling molecule whose role in polarization, migration, and diapedesis of human granulocytes has been documented; however, the molecular events underpinning this role remain to be elucidated.	NAD	47-50	bone marrow stromal cell antigen 1	Homo sapiens	0-5
21441600-1	2011	Poly(ADP-ribose) polymerase-1 (PARP-1) is a NAD-consuming enzyme with an emerging key role in epigenetic regulation of gene transcription.	NAD	44-47	poly(ADP-ribose) polymerase 1	Homo sapiens	0-29
21441600-1	2011	Poly(ADP-ribose) polymerase-1 (PARP-1) is a NAD-consuming enzyme with an emerging key role in epigenetic regulation of gene transcription.	NAD	44-47	poly(ADP-ribose) polymerase 1	Homo sapiens	31-37
21354327-6	2011	The addition of dicoumarol, a DT-diaphorase inhibitor, decreased the number of danthron-induced histidine revertants by 35-39%, indicating that DT-diaphorase is involved in the metabolic activation of danthron in the presence of NADH as an electron donor.	NAD	229-233	NAD(P)H quinone dehydrogenase 1	Homo sapiens	144-157
21296058-6	2011	The presence of coenzyme NAD(+) (10-50 muM) increased the extent of inactivation (60%) at 120 min of reaction, but the ligands betaine aldehyde (50 and 500 muM) and glycine betaine (100 mM) did not change the rate or extent of inactivation as compared to the reaction without ligand.	NAD	25-31	latexin	Homo sapiens	156-159
21310944-7	2011	COX-2 induction was blocked in cells preincubated with an reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase inhibitor or by silencing p67PHOX, a subunit of NADPH oxidase.	NAD	66-99	prostaglandin-endoperoxide synthase 2	Homo sapiens	0-5
21531334-5	2011	Consequently, there is a marked decrease in NADH/NAD(+), oxidative phosphorylation, and ATP levels, which results in AMPK activation, p27(kip1) phosphorylation, and autophagy.	NAD	44-48	zinc ribbon domain containing 2	Homo sapiens	134-137
21531334-5	2011	Consequently, there is a marked decrease in NADH/NAD(+), oxidative phosphorylation, and ATP levels, which results in AMPK activation, p27(kip1) phosphorylation, and autophagy.	NAD	49-55	zinc ribbon domain containing 2	Homo sapiens	134-137
21360751-3	2011	Lack of Adh1p shifts the cellular redox balance towards excess NADH/NADPH and acetaldehyde, while absence of Adh2p does the opposite.	NAD	63-67	alcohol dehydrogenase ADH1	Saccharomyces cerevisiae S288C	8-13
21541336-9	2011	The strong positive correlation observed between DNA damage associated NAD+ depletion and Sirt1 activity suggests that adequate NAD+ concentrations may be an important longevity assurance factor.	NAD	71-75	sirtuin 1	Rattus norvegicus	90-95
21541336-9	2011	The strong positive correlation observed between DNA damage associated NAD+ depletion and Sirt1 activity suggests that adequate NAD+ concentrations may be an important longevity assurance factor.	NAD	128-132	sirtuin 1	Rattus norvegicus	90-95
20388721-4	2011	With respect to their immunological relevance, the importance and function of the major NAD+ metabolizing enzymes, namely CD38/CD157, ADP-ribosyltransferases (ARTs), poly-ADP-ribose-polymerases (PARPs), and sirtuins are summarized and roles of NAD+ and its main degradation product adenosine 5"-diphosphoribose (ADPR) in cell signaling are discussed.	NAD	88-92	bone marrow stromal cell antigen 1	Homo sapiens	127-132
21388966-6	2011	At the mechanistic level, expression profile analyses showed that LTKO livers had significantly down-regulated expression of the nicotinamide phosphoribosyltransferase (Nampt) gene encoding the rate-limiting enzyme in the salvage pathway of NAD(+) biosynthesis.	NAD	241-247	nicotinamide phosphoribosyltransferase	Mus musculus	129-167
21388966-6	2011	At the mechanistic level, expression profile analyses showed that LTKO livers had significantly down-regulated expression of the nicotinamide phosphoribosyltransferase (Nampt) gene encoding the rate-limiting enzyme in the salvage pathway of NAD(+) biosynthesis.	NAD	241-247	nicotinamide phosphoribosyltransferase	Mus musculus	169-174
21366272-7	2011	Determination of the levels of nicotinamide adenine dinucleotide (NAD+), the substrate for PAR synthesis and a coenzyme in cellular redox reactions, demonstrated a UV dose-dependent decrease in the level of NAD+ in wild-type cells, while NAD+ levels in PARG-null TS cells remained at higher levels.	NAD	31-64	poly(ADP-ribose) glycohydrolase	Homo sapiens	253-257
21366272-7	2011	Determination of the levels of nicotinamide adenine dinucleotide (NAD+), the substrate for PAR synthesis and a coenzyme in cellular redox reactions, demonstrated a UV dose-dependent decrease in the level of NAD+ in wild-type cells, while NAD+ levels in PARG-null TS cells remained at higher levels.	NAD	66-70	poly(ADP-ribose) glycohydrolase	Homo sapiens	253-257
21366272-7	2011	Determination of the levels of nicotinamide adenine dinucleotide (NAD+), the substrate for PAR synthesis and a coenzyme in cellular redox reactions, demonstrated a UV dose-dependent decrease in the level of NAD+ in wild-type cells, while NAD+ levels in PARG-null TS cells remained at higher levels.	NAD	207-211	poly(ADP-ribose) glycohydrolase	Homo sapiens	253-257
21366272-7	2011	Determination of the levels of nicotinamide adenine dinucleotide (NAD+), the substrate for PAR synthesis and a coenzyme in cellular redox reactions, demonstrated a UV dose-dependent decrease in the level of NAD+ in wild-type cells, while NAD+ levels in PARG-null TS cells remained at higher levels.	NAD	207-211	poly(ADP-ribose) glycohydrolase	Homo sapiens	253-257
21357538-5	2011	These immunoregulatory T cell populations are highly sensitive to NAD-induced cell death activated by ADP ribosyltransferase-2 (ART2)-mediated ADP ribosylation of P2X(7) receptors.	NAD	66-69	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	163-169
21329659-5	2011	SIRT1 (Sirtuin 1), a NAD-dependent class III histone deacetylase and a member of the sirtuin family of proteins, partially mediates deacetylation of PXR.	NAD	21-24	nuclear receptor subfamily 1 group I member 2	Homo sapiens	149-152
21284999-2	2011	A recent cancer genome-sequencing project revealed that more than 70% of low-grade gliomas bear mutations in one of two NAD(+)-dependent isocitrate dehydrogenase enzymes, namely, IDH1 and IDH2.	NAD	120-126	isocitrate dehydrogenase (NADP(+)) 2	Homo sapiens	188-192
21483791-10	2011	The circadian rhythm of nicotinamide phosphoryl-transferase (NAMPT) activity, which converts nicotinamide (NAM) to NAD+, is an important regulator of the circadian clock.	NAD	115-119	nicotinamide phosphoribosyltransferase	Mus musculus	24-59
21483791-10	2011	The circadian rhythm of nicotinamide phosphoryl-transferase (NAMPT) activity, which converts nicotinamide (NAM) to NAD+, is an important regulator of the circadian clock.	NAD	115-119	nicotinamide phosphoribosyltransferase	Mus musculus	61-66
21332213-5	2011	We have discovered new and efficient N-hydroxyindole-based inhibitors of LDH-A, which are isoform-selective (over LDH-B) and competitive with both the substrate (pyruvate) and the cofactor (NADH).	NAD	190-194	lactate dehydrogenase A	Homo sapiens	73-78
20583870-2	2011	The superoxide dismutase (SOD) like activity of the complexes were measured using an NBT/NADH/PMS system, these were expressed in terms of the concentration of complex which termianates the formation of formazan by 50% (IC50 value) and found to range from 0.781 to 1.354 muM.	NAD	89-93	superoxide dismutase 1	Homo sapiens	4-24
20583870-2	2011	The superoxide dismutase (SOD) like activity of the complexes were measured using an NBT/NADH/PMS system, these were expressed in terms of the concentration of complex which termianates the formation of formazan by 50% (IC50 value) and found to range from 0.781 to 1.354 muM.	NAD	89-93	superoxide dismutase 1	Homo sapiens	26-29
21245135-3	2011	After TLR4 signaling, SIRT1 rapidly accumulated at the promoters of TNF-alpha and IL-1beta, but not IkappaBalpha; SIRT1 promoter binding was dependent on its co-factor, NAD(+).	NAD	169-175	tumor necrosis factor	Homo sapiens	68-77
21245135-3	2011	After TLR4 signaling, SIRT1 rapidly accumulated at the promoters of TNF-alpha and IL-1beta, but not IkappaBalpha; SIRT1 promoter binding was dependent on its co-factor, NAD(+).	NAD	169-175	interleukin 1 beta	Homo sapiens	82-90
21224467-6	2011	HES1-induced PARP1 activation leads to self-ADP ribosylation of PARP1, consumption of nicotinamide adenine dinucleotide(+), diminished adenosine triphosphate levels, and translocation of apoptosis-inducing factor from mitochondria to the nucleus, resulting in apoptosis in B-ALL but not T-cell ALL.	NAD	86-119	poly(ADP-ribose) polymerase 1	Homo sapiens	13-18
21456871-7	2011	These findings suggest that the increased NADH fluorescence lifetime in STS-induced cell death occurred before the depletion of DeltaPsi and ATP and activation of caspase 3, and was not simply caused by cellular metabolic change.	NAD	42-46	caspase 3	Homo sapiens	163-172
21397863-3	2011	Here, we show that the mitochondrial NAD-dependent deacetylase SIRT3 is a crucial regulator of the Warburg effect.	NAD	37-40	sirtuin 3	Homo sapiens	63-68
21073854-8	2011	Both enzymes have a glycine-rich NAD(+)-binding domain at the N terminal and conserved catalytic triad of YxxxK residues, but substrate-binding residues of GME were not found in the ThrDH sequence.	NAD	33-39	GDP-D-mannose 3',5'-epimerase	Arabidopsis thaliana	156-159
21383081-6	2011	Enhanced rotenone toxicity to dopamine neurons from Ndufs4 knockout mice may involve enhanced dopamine synthesis caused by the accumulation of nicotinamide adenine dinucleotide reduced.	NAD	143-176	NADH:ubiquinone oxidoreductase core subunit S4	Mus musculus	52-58
21195744-0	2011	The general anesthetic sevoflurane affects the expression of clock gene mPer2 accompanying the change of NAD+ level in the suprachiasmatic nucleus of mice.	NAD	105-109	circadian locomotor output cycles kaput	Mus musculus	61-66
21195744-0	2011	The general anesthetic sevoflurane affects the expression of clock gene mPer2 accompanying the change of NAD+ level in the suprachiasmatic nucleus of mice.	NAD	105-109	period circadian clock 2	Mus musculus	72-77
21195744-8	2011	We also measured the NAD(+) level in the SCN, which was a mediator regulating the mPer2 expression.	NAD	21-27	period circadian clock 2	Mus musculus	82-87
21195744-10	2011	These results indicate that the anesthesia induces the increase of NAD(+), and consequently leads to the repression of mPer2 expression and modifies the circadian expression pattern and diurnal behavioral rhythm of mice.	NAD	67-73	period circadian clock 2	Mus musculus	119-124
20362304-2	2011	Nicotinamide adenine dinucleotide-dependent histone deacetylase sirtuin 1 (SIRT1) is also thought to play a pivotal role for such metabolic adaptations.	NAD	0-33	sirtuin 1	Rattus norvegicus	64-73
20362304-2	2011	Nicotinamide adenine dinucleotide-dependent histone deacetylase sirtuin 1 (SIRT1) is also thought to play a pivotal role for such metabolic adaptations.	NAD	0-33	sirtuin 1	Rattus norvegicus	75-80
21239112-2	2011	Activation of S1PR(1) has been reported to increase the formation of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase-derived superoxide (O(2)( -)) and nitric oxide synthase (NOS)-derived nitric oxide (NO).	NAD	69-102	sphingosine-1-phosphate receptor 1	Rattus norvegicus	14-21
21212137-7	2011	In theca-interstitial cells the expression of hydroxyprostaglandin dehydrogenase 15-(nicotinamide adenine dinucleotide) (Hpgd) was also inhibited by NFIL3 overexpression.	NAD	85-118	nuclear factor, interleukin 3 regulated	Homo sapiens	149-154
21149440-1	2011	Forkhead transcription factor FoxO1 and the NAD(+)-dependent histone deacetylase SIRT1 are evolutionarily conserved regulators of the development of aging, oxidative stress resistance, insulin resistance, and metabolism in species ranging from invertebrates to mammals.	NAD	44-50	insulin	Homo sapiens	185-192
21246601-9	2011	In neurons, Nampt positively modulated NAD(+) levels and thereby controlled SIRT1 activity.	NAD	39-45	nicotinamide phosphoribosyltransferase	Mus musculus	12-17
21236242-7	2011	In addition, nicotinamide-adenine dinucleotide (NAD), a coenzyme of GAPDH, inhibited the GAPDH-RNA binding.	NAD	13-46	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	68-73
21236242-7	2011	In addition, nicotinamide-adenine dinucleotide (NAD), a coenzyme of GAPDH, inhibited the GAPDH-RNA binding.	NAD	13-46	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	89-94
21236242-7	2011	In addition, nicotinamide-adenine dinucleotide (NAD), a coenzyme of GAPDH, inhibited the GAPDH-RNA binding.	NAD	48-51	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	68-73
21236242-7	2011	In addition, nicotinamide-adenine dinucleotide (NAD), a coenzyme of GAPDH, inhibited the GAPDH-RNA binding.	NAD	48-51	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	89-94
21247195-4	2011	Using a conventional photodetector, 2-(dibutylamino)ethanol (DBAE) and nicotinamide adenine dinucleotide (NADH) could be detected to levels of 0.9 muM and 72 muM, respectively.	NAD	71-104	latexin	Homo sapiens	147-150
21247195-4	2011	Using a conventional photodetector, 2-(dibutylamino)ethanol (DBAE) and nicotinamide adenine dinucleotide (NADH) could be detected to levels of 0.9 muM and 72 muM, respectively.	NAD	71-104	latexin	Homo sapiens	158-161
21247195-4	2011	Using a conventional photodetector, 2-(dibutylamino)ethanol (DBAE) and nicotinamide adenine dinucleotide (NADH) could be detected to levels of 0.9 muM and 72 muM, respectively.	NAD	106-110	latexin	Homo sapiens	147-150
21247195-4	2011	Using a conventional photodetector, 2-(dibutylamino)ethanol (DBAE) and nicotinamide adenine dinucleotide (NADH) could be detected to levels of 0.9 muM and 72 muM, respectively.	NAD	106-110	latexin	Homo sapiens	158-161
20940012-6	2011	Increased nicotinamide adenine dinucleotide phosphate (NADHP) oxidase activity and apoptosis induction, regulated by mitochondrial signal pathway through an increased pro-apoptotic Bax/BcL(2) ratio and caspase 3 activity, were demonstrated.	NAD	10-43	BCL2, apoptosis regulator	Rattus norvegicus	185-190
21068071-6	2011	Treatment of VSC4.1 motoneurons with PPT, DPN, or EST induced overexpression of ERalpha, ERbeta, or both, which contributed to neuroprotection by upregulating expression of anti-apoptotic proteins (p-AKT, p-CREB, Bcl-2, and p-Src).	NAD	42-45	estrogen receptor 1	Homo sapiens	80-87
21068071-6	2011	Treatment of VSC4.1 motoneurons with PPT, DPN, or EST induced overexpression of ERalpha, ERbeta, or both, which contributed to neuroprotection by upregulating expression of anti-apoptotic proteins (p-AKT, p-CREB, Bcl-2, and p-Src).	NAD	42-45	BCL2 apoptosis regulator	Homo sapiens	213-218
21068071-6	2011	Treatment of VSC4.1 motoneurons with PPT, DPN, or EST induced overexpression of ERalpha, ERbeta, or both, which contributed to neuroprotection by upregulating expression of anti-apoptotic proteins (p-AKT, p-CREB, Bcl-2, and p-Src).	NAD	42-45	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	226-229
21068071-11	2011	Taken together, our data indicate that both ERalpha and ERbeta contribute to PPT, DPN, or EST-mediated neuroprotection with similar signaling profiles.	NAD	82-85	estrogen receptor 1	Homo sapiens	44-51
21461238-6	2011	NAD(+)- and NADP(+)-mediated CCL2 release was significantly attenuated by SP6001250, U0126, LY294002, Akt inhibitor IV, RO318220, GF109203X, and diphenyleneiodium chloride.	NAD	0-6	AKT serine/threonine kinase 1	Homo sapiens	102-105
21205613-2	2011	In course of this high-throughput pathway, a peroxisomal transamination reaction converts serine to HP, most of which is subsequently reduced to glycerate by the NADH-dependent peroxisomal enzyme HP reductase (HPR1).	NAD	162-166	nuclear matrix protein-like protein	Arabidopsis thaliana	210-214
21245319-1	2011	Numerous studies indicate that Sirtuin 1 (SIRT1), a mammalian nicotinamide adenine dinucleotide (NAD(+))-dependent histone deacetylase (HDAC), plays a crucial role in p53-mediated stress responses by deacetylating p53.	NAD	62-95	tumor protein p53	Homo sapiens	167-170
21245319-1	2011	Numerous studies indicate that Sirtuin 1 (SIRT1), a mammalian nicotinamide adenine dinucleotide (NAD(+))-dependent histone deacetylase (HDAC), plays a crucial role in p53-mediated stress responses by deacetylating p53.	NAD	62-95	tumor protein p53	Homo sapiens	214-217
21245319-1	2011	Numerous studies indicate that Sirtuin 1 (SIRT1), a mammalian nicotinamide adenine dinucleotide (NAD(+))-dependent histone deacetylase (HDAC), plays a crucial role in p53-mediated stress responses by deacetylating p53.	NAD	97-103	tumor protein p53	Homo sapiens	167-170
21245319-1	2011	Numerous studies indicate that Sirtuin 1 (SIRT1), a mammalian nicotinamide adenine dinucleotide (NAD(+))-dependent histone deacetylase (HDAC), plays a crucial role in p53-mediated stress responses by deacetylating p53.	NAD	97-103	tumor protein p53	Homo sapiens	214-217
21224367-8	2011	Essential downstream mediators of lethality were as follows: (i) reactive oxygen species (ROS); (ii) single-strand DNA breaks induced by ROS; (iii) poly(ADP-ribose)polymerase-1 (PARP1) hyperactivation; (iv) dramatic NAD(+)/ATP depletion; and (v) programmed necrosis.	NAD	216-222	poly(ADP-ribose) polymerase 1	Homo sapiens	178-183
21586363-11	2011	Further, CD38 and changes in NAD(+) availability modulate ADP ribosylation of the cytolytic P2X7 receptor that deletes T regulatory cells.	NAD	29-35	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	92-105
21141881-2	2011	Preferential binding of the P- or M-helical conformer of bilirubin to dehydrogenases, catalase, alkaline phosphatase, and alpha-chymotrypsin is responsible for the characteristic exciton CD couplet that undergoes remarkable changes upon the addition of enzymatic cofactors (NADH, AMP) and an inhibitor (acridine).	NAD	274-278	catalase	Homo sapiens	86-94
21141881-3	2011	Alterations of the ICD spectra refer to a direct binding competition between bilirubin and NADH for a common binding site on alcohol dehydrogenase and catalase, suggesting a potential mechanism for the inhibitory effect of BR reported on NAD(P)H dependent enzymes.	NAD	91-95	catalase	Homo sapiens	151-159
21133413-1	2011	Yeast NAD(+)-specific isocitrate dehydrogenase (IDH) is an octameric enzyme composed of four heterodimers of regulatory IDH1 and catalytic IDH2 subunits.	NAD	6-12	isocitrate dehydrogenase (NAD(+)) IDH1	Saccharomyces cerevisiae S288C	120-124
21206019-1	2011	Quinolinate phosphoribosyltransferase (QPRTase) is a key NAD-biosynthetic enzyme which catalyzes the transfer of quinolinic acid to 5-phosphoribosyl-1-pyrophosphate, yielding nicotinic acid mononucleotide.	NAD	57-60	quinolinate phosphoribosyltransferase	Homo sapiens	0-37
21206019-1	2011	Quinolinate phosphoribosyltransferase (QPRTase) is a key NAD-biosynthetic enzyme which catalyzes the transfer of quinolinic acid to 5-phosphoribosyl-1-pyrophosphate, yielding nicotinic acid mononucleotide.	NAD	57-60	quinolinate phosphoribosyltransferase	Homo sapiens	39-46
21166830-7	2011	This was not explained by high cellular NADH levels or endogenous inhibitors; but rather because the activity of the beta1 and beta2 ADHs was constrained by the accumulation of acetaldehyde, as shown by the increased rate of ethanol oxidation by cell lines expressing beta2 ADH plus ALDH2.	NAD	40-44	potassium calcium-activated channel subfamily M regulatory beta subunit 1	Homo sapiens	117-122
21968702-1	2011	Poly(ADP-ribose) polymerase-1 (PARP-1) and PARP-2 belong to a family of enzymes that, using NAD(+) as a substrate, catalyze poly(ADP-ribosyl)ation of proteins.	NAD	92-98	poly(ADP-ribose) polymerase 1	Homo sapiens	0-29
21968702-1	2011	Poly(ADP-ribose) polymerase-1 (PARP-1) and PARP-2 belong to a family of enzymes that, using NAD(+) as a substrate, catalyze poly(ADP-ribosyl)ation of proteins.	NAD	92-98	poly(ADP-ribose) polymerase 1	Homo sapiens	31-37
21968702-1	2011	Poly(ADP-ribose) polymerase-1 (PARP-1) and PARP-2 belong to a family of enzymes that, using NAD(+) as a substrate, catalyze poly(ADP-ribosyl)ation of proteins.	NAD	92-98	poly(ADP-ribose) polymerase 2	Homo sapiens	43-49
21968702-5	2011	PARP inhibitors that compete with NAD+ at the highly conserved enzyme active site are arisen as new potential therapeutic strategies as chemo- and radiopotentiation and for the treatment of cancers with specific DNA repair defects as single-agent therapies.	NAD	34-38	poly(ADP-ribose) polymerase 1	Homo sapiens	0-4
22084601-5	2011	Competitive inhibition of indoleamine 2,3 dioxygenase (IDO), and quinolinic acid phosphoribosyltransferase (QPRT) activities with 1-methyl-L-Tryptophan (1-MT), and phthalic acid (PA) respectively, resulted in a dose-dependent decrease in intracellular NAD(+) levels and sirtuin deacetylase-1 (SIRT1) activity, and correlated directly with reduced cell viability.	NAD	252-258	quinolinate phosphoribosyltransferase	Homo sapiens	65-106
21372389-7	2011	The elevated expressions of p22(phox) and Nox-4 proteins (reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase subunits) were significantly decreased after kangen-karyu treatments.	NAD	66-99	dynein cytoplasmic 1 heavy chain 1	Mus musculus	28-31
21484571-2	2011	First identified in humans as a cytokine cytokine pre-B-cell colony enhancing factor pre-B cell colony enhancing factor (PBEF PBEF ) and subsequently described as an insulin-mimetic hormone visfatin visfatin , Nampt has recently excited the scientific interest of researchers from diverse fields, including NAD biology, metabolic regulation, and inflammation.	NAD	307-310	insulin	Homo sapiens	166-173
21568847-10	2011	The 115-kDa target protein was identified as PARP1 using NAD+-based functional testing.	NAD	57-61	poly(ADP-ribose) polymerase 1	Homo sapiens	45-50
21691086-0	2011	NAD blocks high glucose induced mesangial hypertrophy via activation of the sirtuins-AMPK-mTOR pathway.	NAD	0-3	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	85-89
21691086-8	2011	Activating Sirtuins by NAD blocked the activation of pro-hypertrophic Akt signaling, and augmented the activity of the antihypertrophic AMPK signaling in MCs, which prevented the subsequent induction of mTOR-mediated protein synthesis.	NAD	23-26	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	136-140
21691086-10	2011	In such, the NAD inhibited HG-induced mesangial hypertrophy whereas NAD lost its inhibitory effect in the presence of AMPK siRNA.	NAD	68-71	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	118-122
21479099-0	2011	Oxidative stress and PARP activation mediate the NADH-induced decrease in glioma cell survival.	NAD	49-53	poly(ADP-ribose) polymerase 1	Homo sapiens	21-25
21479099-4	2011	We found that treatment of C6 glioma cells with as low as 1 muM NADH for 24 hrs significantly decreased the survival of these cells, and that treatment of the cells with 1000 muM NADH for 4 days decreased the survival of the cells by nearly 90%.	NAD	64-68	latexin	Homo sapiens	60-63
21479099-4	2011	We found that treatment of C6 glioma cells with as low as 1 muM NADH for 24 hrs significantly decreased the survival of these cells, and that treatment of the cells with 1000 muM NADH for 4 days decreased the survival of the cells by nearly 90%.	NAD	179-183	latexin	Homo sapiens	60-63
21479099-4	2011	We found that treatment of C6 glioma cells with as low as 1 muM NADH for 24 hrs significantly decreased the survival of these cells, and that treatment of the cells with 1000 muM NADH for 4 days decreased the survival of the cells by nearly 90%.	NAD	179-183	latexin	Homo sapiens	175-178
21479099-6	2011	We also found that NADH treatment induced an increase in poly(ADP-ribose) polymerase (PARP) activity, and that PARP inhibitors decreased the effect of NADH on the survival of glioma cells.	NAD	19-23	poly(ADP-ribose) polymerase 1	Homo sapiens	57-84
21479099-6	2011	We also found that NADH treatment induced an increase in poly(ADP-ribose) polymerase (PARP) activity, and that PARP inhibitors decreased the effect of NADH on the survival of glioma cells.	NAD	19-23	poly(ADP-ribose) polymerase 1	Homo sapiens	86-90
22084601-5	2011	Competitive inhibition of indoleamine 2,3 dioxygenase (IDO), and quinolinic acid phosphoribosyltransferase (QPRT) activities with 1-methyl-L-Tryptophan (1-MT), and phthalic acid (PA) respectively, resulted in a dose-dependent decrease in intracellular NAD(+) levels and sirtuin deacetylase-1 (SIRT1) activity, and correlated directly with reduced cell viability.	NAD	252-258	quinolinate phosphoribosyltransferase	Homo sapiens	108-112
21479099-6	2011	We also found that NADH treatment induced an increase in poly(ADP-ribose) polymerase (PARP) activity, and that PARP inhibitors decreased the effect of NADH on the survival of glioma cells.	NAD	151-155	poly(ADP-ribose) polymerase 1	Homo sapiens	111-115
21479099-7	2011	These observations suggest that NADH reduces the cell survival at least partially by activating PARP.	NAD	32-36	poly(ADP-ribose) polymerase 1	Homo sapiens	96-100
21694451-6	2011	We found that Abeta peptides induced an increase in NAD+levels and a decrease in ATP levels, which was related with decreases in acetylated tubulin levels and tau hyperphosphorylation.	NAD	52-56	amyloid beta precursor protein	Homo sapiens	14-19
21697640-2	2011	Deficiency of cellular nicotinamide adenine dinucleotide (NAD(+)) content, consumed by PARP-1 to add ADP-ribose moieties onto target proteins, contributes to pathophysiological conditions.	NAD	23-56	poly(ADP-ribose) polymerase 1	Homo sapiens	87-93
21031461-10	2011	These data suggest that high-glucose-induced PARP1 activation might play a role in glucose toxicity by down-regulating SIRT1 and AMPK activity through NAD depletion and resulting in insulin insensitivity.	NAD	151-154	poly(ADP-ribose) polymerase 1	Homo sapiens	45-50
21697640-2	2011	Deficiency of cellular nicotinamide adenine dinucleotide (NAD(+)) content, consumed by PARP-1 to add ADP-ribose moieties onto target proteins, contributes to pathophysiological conditions.	NAD	58-65	poly(ADP-ribose) polymerase 1	Homo sapiens	87-93
21870251-2	2011	Since PARP-1 gene is expressed constitutively, its activation cannot be surmised from increased expression of its mRNA or protein, but by demonstrating the consequences of its catalytic -reaction which results in consumption of the substrate nicotinamide adenine dinucleotide (NAD(+)) and formation of three products, namely, polymer of ADP-ribose (pADPr or PAR), nicotinamide, and protons.	NAD	242-275	poly(ADP-ribose) polymerase 1	Homo sapiens	6-12
21870251-2	2011	Since PARP-1 gene is expressed constitutively, its activation cannot be surmised from increased expression of its mRNA or protein, but by demonstrating the consequences of its catalytic -reaction which results in consumption of the substrate nicotinamide adenine dinucleotide (NAD(+)) and formation of three products, namely, polymer of ADP-ribose (pADPr or PAR), nicotinamide, and protons.	NAD	277-283	poly(ADP-ribose) polymerase 1	Homo sapiens	6-12
21870251-3	2011	Here, we describe various approaches commonly used in our laboratory for detection of PARP-1 activation in vivo (cells, tissues, and tumors), in situ, and in vitro via assessment of formation of pADPr, depletion of the substrate NAD, or formation of protons resulting in rapid and reversible intracellular acidification.	NAD	229-232	poly(ADP-ribose) polymerase 1	Homo sapiens	86-92
21870258-3	2011	Overactivation of PARP, as reflected by increased poly-ADP-ribosylation, accumulation of pADPr-modified proteins or free pADPr, contributes to the depletion of NAD(+) and mitochondrial dysfunction, potentially leading to cell death via apoptosis or necrosis.	NAD	160-166	poly(ADP-ribose) polymerase 1	Homo sapiens	18-22
21870261-5	2011	PARP-1 and PARylation may (1) play dual roles in nuclear processes, depending on the levels of the substrate NAD and the presence of PARP-activating DNA breaks, (2) recruit acceptor proteins to certain sites or complexes through direct association or through binding to PAR and PAR-binding proteins, and (3) alters the nucleosomal structure of DNA by PARylation of nucleosomal proteins, such as histone H1 to destabilize higher order chromatin structures and promote access of DNA repair and replication enzymes as well as transcription factors to these sites.	NAD	109-112	poly(ADP-ribose) polymerase 1	Homo sapiens	0-6
21870261-5	2011	PARP-1 and PARylation may (1) play dual roles in nuclear processes, depending on the levels of the substrate NAD and the presence of PARP-activating DNA breaks, (2) recruit acceptor proteins to certain sites or complexes through direct association or through binding to PAR and PAR-binding proteins, and (3) alters the nucleosomal structure of DNA by PARylation of nucleosomal proteins, such as histone H1 to destabilize higher order chromatin structures and promote access of DNA repair and replication enzymes as well as transcription factors to these sites.	NAD	109-112	poly(ADP-ribose) polymerase 1	Homo sapiens	0-4
21870264-1	2011	PARP-1 is the most abundantly expressed member of a family of proteins that catalyze the transfer of ADP-ribose units from NAD(+) to target proteins.	NAD	123-129	poly(ADP-ribose) polymerase 1	Homo sapiens	0-6
21870266-1	2011	Poly (ADP-ribosyl)ation of proteins is a posttranslational modification mediated by poly (ADP-ribose) polymerases (PARPs) that uses NAD(+) as substrate to form the negatively charged polymer of poly (ADP-ribose) (PAR).	NAD	132-138	poly(ADP-ribose) polymerase 1	Homo sapiens	115-120
21870279-3	2011	However, most of them were designed to disrupt the DNA-dependent PARP1 protein activation pathway and were based on a competition with NAD for a binding site on PARP molecule and, therefore, on disruption of PARP-mediated enzymatic reaction.	NAD	135-138	poly(ADP-ribose) polymerase 1	Homo sapiens	65-70
21870279-3	2011	However, most of them were designed to disrupt the DNA-dependent PARP1 protein activation pathway and were based on a competition with NAD for a binding site on PARP molecule and, therefore, on disruption of PARP-mediated enzymatic reaction.	NAD	135-138	poly(ADP-ribose) polymerase 1	Homo sapiens	65-69
21870279-3	2011	However, most of them were designed to disrupt the DNA-dependent PARP1 protein activation pathway and were based on a competition with NAD for a binding site on PARP molecule and, therefore, on disruption of PARP-mediated enzymatic reaction.	NAD	135-138	poly(ADP-ribose) polymerase 1	Homo sapiens	161-165
21870279-4	2011	This limitation resulted in a discovery of mainly nucleotide-like PARP1 inhibitors which may target not only PARP, but also other pathways involving NAD and other nucleotides.	NAD	149-152	poly(ADP-ribose) polymerase 1	Homo sapiens	66-71
21870279-4	2011	This limitation resulted in a discovery of mainly nucleotide-like PARP1 inhibitors which may target not only PARP, but also other pathways involving NAD and other nucleotides.	NAD	149-152	poly(ADP-ribose) polymerase 1	Homo sapiens	66-70
21870279-6	2011	Besides the identification of NAD competitors in a small-molecule collection, this approach allows finding novel classes of PARP inhibitors that specifically disrupt H4-based PARP activation.	NAD	30-33	poly(ADP-ribose) polymerase 1	Homo sapiens	124-128
21870279-6	2011	Besides the identification of NAD competitors in a small-molecule collection, this approach allows finding novel classes of PARP inhibitors that specifically disrupt H4-based PARP activation.	NAD	30-33	poly(ADP-ribose) polymerase 1	Homo sapiens	175-179
21858060-6	2011	SDHA is hyperacetylated in SIRT3 KO mice and SIRT3 directly deacetylates SDHA in a NAD-dependent manner.	NAD	83-86	succinate dehydrogenase complex, subunit A, flavoprotein (Fp)	Mus musculus	73-77
22180829-1	2011	NAD-dependent Class III histone deacetylase SIRT1 is a multiple functional protein and has been demonstrated critically involved in stress response, cellular metabolism and aging through deacetylating variety of substrates including p53, forkhead transcription factors, PGC-1alpha, NF-kappaB, Ku70 and histones.	NAD	0-3	tumor protein p53	Homo sapiens	233-236
22180829-1	2011	NAD-dependent Class III histone deacetylase SIRT1 is a multiple functional protein and has been demonstrated critically involved in stress response, cellular metabolism and aging through deacetylating variety of substrates including p53, forkhead transcription factors, PGC-1alpha, NF-kappaB, Ku70 and histones.	NAD	0-3	PPARG coactivator 1 alpha	Homo sapiens	270-280
21858060-6	2011	SDHA is hyperacetylated in SIRT3 KO mice and SIRT3 directly deacetylates SDHA in a NAD-dependent manner.	NAD	83-86	succinate dehydrogenase complex, subunit A, flavoprotein (Fp)	Mus musculus	0-4
21675215-3	2011	We have found that injection of NAD+ in different doses immediately after IR causes an increased level of gamma-H2AX in mouse heart cells 20 min after IR at the dose of 3 Gy compared to control mice after IR exposure.	NAD	32-36	H2A.X variant histone	Mus musculus	106-116
20850412-1	2010	We have investigated whether increase in the oxidation rate of exogenous cytochrome c (cyto-c), induced by long-chain ceramides, might be due to an increased rate of cytosolic NADH/cyto-c electron transport pathway.	NAD	176-180	cytochrome c, somatic	Homo sapiens	73-85
21030595-4	2010	DBC1 has been previously identified as a regulator of some nuclear receptors, the methyltransferase SUV39H1, and the NAD-dependent deacetylase SIRT1.	NAD	117-120	cell cycle activator and apoptosis regulator 2	Mus musculus	0-4
20943658-1	2010	Nicotinamide mononucleotide (NMN) adenylyltransferase 2 (Nmnat2) catalyzes the synthesis of NAD from NMN and ATP.	NAD	92-95	nicotinamide nucleotide adenylyltransferase 2	Homo sapiens	0-55
20943658-1	2010	Nicotinamide mononucleotide (NMN) adenylyltransferase 2 (Nmnat2) catalyzes the synthesis of NAD from NMN and ATP.	NAD	92-95	nicotinamide nucleotide adenylyltransferase 2	Homo sapiens	57-63
21476439-6	2011	Our results show that the SDR domain of the WWOX protein has dehydrogenase activity and is reactive both in the presence of NAD+ and NADP+ for all examined steroid substrates.	NAD	124-128	WW domain containing oxidoreductase	Homo sapiens	44-48
20417190-3	2010	Despite the positive role of poly(ADP-ribosylation) in sensing and repairing DNA damage, generated also by ROS, PARP over-activation could allow NAD depletion and consequent necrosis, thus leading to an inflammatory condition in many diseases.	NAD	145-148	poly(ADP-ribose) polymerase 1	Homo sapiens	112-116
20850412-1	2010	We have investigated whether increase in the oxidation rate of exogenous cytochrome c (cyto-c), induced by long-chain ceramides, might be due to an increased rate of cytosolic NADH/cyto-c electron transport pathway.	NAD	176-180	cytochrome c, somatic	Homo sapiens	87-93
20850412-4	2010	However, the oxidation of added NADH, mediated by exogenous cyto-c and coupled to the generation of a membrane potential supporting the ATP synthesis, can also be stimulated by ceramide.	NAD	32-36	cytochrome c, somatic	Homo sapiens	60-66
20876576-7	2010	TiPARP overexpression reproduced TCDD effects on glucose output and NAD(+) levels whereas TiPARP silencing diminished them.	NAD	68-74	TCDD inducible poly(ADP-ribose) polymerase	Homo sapiens	0-6
20696207-12	2010	TRAIL addition to APO866 synergistically increased its activity in leukemia cells by enhancing NAD(+) depletion, DeltaPsi(m) dissipation, and ATP shortage.	NAD	95-101	TNF superfamily member 10	Homo sapiens	0-5
21212461-3	2010	Here we report that the NAD+-dependent deacetylase SIRT3 deacetylates the regulatory component of the mPTP, cyclophilin D (CypD) on lysine 166, adjacent to the binding site of cyclosporine A, a CypD inhibitor.	NAD	24-28	peptidylprolyl isomerase F (cyclophilin F)	Mus musculus	108-121
21212461-3	2010	Here we report that the NAD+-dependent deacetylase SIRT3 deacetylates the regulatory component of the mPTP, cyclophilin D (CypD) on lysine 166, adjacent to the binding site of cyclosporine A, a CypD inhibitor.	NAD	24-28	peptidylprolyl isomerase F (cyclophilin F)	Mus musculus	123-127
21212461-3	2010	Here we report that the NAD+-dependent deacetylase SIRT3 deacetylates the regulatory component of the mPTP, cyclophilin D (CypD) on lysine 166, adjacent to the binding site of cyclosporine A, a CypD inhibitor.	NAD	24-28	peptidylprolyl isomerase F (cyclophilin F)	Mus musculus	194-198
20485294-2	2010	By synthesizing NAD(+), PBEF functions to maintain an energy supply that has critical roles in cell survival.	NAD	16-22	nicotinamide phosphoribosyltransferase	Mus musculus	24-28
20725763-2	2010	The poly(ADP-ribose) polymerase (PARP) family catalyze the formation and addition onto proteins of negatively charged ADP-ribose polymers synthesized from NAD(+).	NAD	155-161	poly(ADP-ribose) polymerase 1	Homo sapiens	4-31
20725763-2	2010	The poly(ADP-ribose) polymerase (PARP) family catalyze the formation and addition onto proteins of negatively charged ADP-ribose polymers synthesized from NAD(+).	NAD	155-161	poly(ADP-ribose) polymerase 1	Homo sapiens	33-37
20725763-4	2010	PARP inhibitors that compete with NAD(+) at the enzyme"s activity site are effective chemo- and radiopotentiation agents and, in BRCA-deficient tumors, can be used as single-agent therapies acting through the principle of synthetic lethality.	NAD	34-40	poly(ADP-ribose) polymerase 1	Homo sapiens	0-4
21102443-4	2010	Loss of CtBP from the BRCA1 promoter through estrogen induction, depletion by RNA interference or increased NAD+/NADH ratio leads to HDAC1 dismissal, elevated histone acetylation and increased BRCA1 transcription.	NAD	108-112	histone deacetylase 1	Homo sapiens	133-138
20975043-0	2010	Extracellular NAD+ shapes the Foxp3+ regulatory T cell compartment through the ART2-P2X7 pathway.	NAD	14-18	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	84-88
20975043-2	2010	Nicotinamide adenine dinucleotide (NAD(+)) released during cell damage or inflammation results in ART2.2-mediated ADP-ribosylation of the cytolytic P2X7 receptor on T cells.	NAD	0-33	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	148-161
20975043-2	2010	Nicotinamide adenine dinucleotide (NAD(+)) released during cell damage or inflammation results in ART2.2-mediated ADP-ribosylation of the cytolytic P2X7 receptor on T cells.	NAD	35-42	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	148-161
20975043-8	2010	Collectively, our data demonstrate that NAD(+) influences survival, phenotype, and function of T reg cells and provide proof of principle that acting on the ART2-P2X7 pathway represents a new strategy to manipulate T reg cells in vivo.	NAD	40-46	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	162-166
20711239-3	2010	Similarly, the NAD-dependent poly(adenosine diphosphate)ribose polymerase 1 (PARP1) may affect p21 expression via its NAD-dependent enzymatic activity; we therefore asked if PARP1 and CtBP were functionally linked in regulating p21 transcription.	NAD	15-18	poly(ADP-ribose) polymerase 1	Homo sapiens	77-82
20711239-3	2010	Similarly, the NAD-dependent poly(adenosine diphosphate)ribose polymerase 1 (PARP1) may affect p21 expression via its NAD-dependent enzymatic activity; we therefore asked if PARP1 and CtBP were functionally linked in regulating p21 transcription.	NAD	15-18	cyclin dependent kinase inhibitor 1A	Homo sapiens	95-98
20711239-3	2010	Similarly, the NAD-dependent poly(adenosine diphosphate)ribose polymerase 1 (PARP1) may affect p21 expression via its NAD-dependent enzymatic activity; we therefore asked if PARP1 and CtBP were functionally linked in regulating p21 transcription.	NAD	15-18	poly(ADP-ribose) polymerase 1	Homo sapiens	174-179
20711239-3	2010	Similarly, the NAD-dependent poly(adenosine diphosphate)ribose polymerase 1 (PARP1) may affect p21 expression via its NAD-dependent enzymatic activity; we therefore asked if PARP1 and CtBP were functionally linked in regulating p21 transcription.	NAD	15-18	cyclin dependent kinase inhibitor 1A	Homo sapiens	228-231
20711239-3	2010	Similarly, the NAD-dependent poly(adenosine diphosphate)ribose polymerase 1 (PARP1) may affect p21 expression via its NAD-dependent enzymatic activity; we therefore asked if PARP1 and CtBP were functionally linked in regulating p21 transcription.	NAD	118-121	poly(ADP-ribose) polymerase 1	Homo sapiens	77-82
20798610-4	2010	In response to stress, FoxO1 dissociated from an NAD(+)-dependent histone deacetylase SIRT2 and FoxO1 thus became acetylated and in turn bound to Atg7, an E1-like protein, to influence the autophagic process leading to cell death.	NAD	49-55	forkhead box O1	Homo sapiens	23-28
20645413-3	2010	Recently, exogenous NAD(+) was reported to enter astrocytes via the P2X7 receptor (P2X7R)-associated channel/pore.	NAD	20-26	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	68-81
20645413-3	2010	Recently, exogenous NAD(+) was reported to enter astrocytes via the P2X7 receptor (P2X7R)-associated channel/pore.	NAD	20-26	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	83-88
20645413-8	2010	Taken together, these results indicate that exogenous NAD(+) is degraded by ectonucleotidases and that adenosine, as its metabolite, is taken up into astrocytes via the P2X7R-associated channel/pore.	NAD	54-60	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	169-174
20975832-1	2010	BACKGROUND: The NAD-dependent deacetylase SIRT1 is a nutrient-sensitive coordinator of stress-tolerance, multiple homeostatic processes and healthspan, while p53 is a stress-responsive transcription factor and our paramount tumour suppressor.	NAD	16-19	tumor protein p53	Homo sapiens	158-161
20846527-1	2010	Three of the conserved, membrane-bound subunits in NADH:ubiquinone oxidoreductase (complex I) are related to one another, and to Mrp sodium-proton antiporters.	NAD	51-55	ATP binding cassette subfamily C member 1	Homo sapiens	129-132
20715198-2	2010	A theoretical study of the protein dynamic effects on the hydride transfer between the formate anion and nicotinamide adenine dinucleotide (NAD(+)), catalyzed by formate dehydrogenase (FDH), is presented in this paper.	NAD	105-138	aldehyde dehydrogenase 1 family member L1	Homo sapiens	162-183
20715198-2	2010	A theoretical study of the protein dynamic effects on the hydride transfer between the formate anion and nicotinamide adenine dinucleotide (NAD(+)), catalyzed by formate dehydrogenase (FDH), is presented in this paper.	NAD	105-138	aldehyde dehydrogenase 1 family member L1	Homo sapiens	185-188
20715198-2	2010	A theoretical study of the protein dynamic effects on the hydride transfer between the formate anion and nicotinamide adenine dinucleotide (NAD(+)), catalyzed by formate dehydrogenase (FDH), is presented in this paper.	NAD	140-146	aldehyde dehydrogenase 1 family member L1	Homo sapiens	162-183
20715198-2	2010	A theoretical study of the protein dynamic effects on the hydride transfer between the formate anion and nicotinamide adenine dinucleotide (NAD(+)), catalyzed by formate dehydrogenase (FDH), is presented in this paper.	NAD	140-146	aldehyde dehydrogenase 1 family member L1	Homo sapiens	185-188
20655731-3	2010	It was found that ligand L was released from complex HgL by a ligand exchange process in the presence of GSH, which was enzymatic reduced from GSSG in the presence of NADH.	NAD	167-171	lipase F, gastric type	Homo sapiens	53-56
20942953-1	2010	BACKGROUND: The poly(ADP-ribose) polymerase (PARP) superfamily was originally identified as enzymes that catalyze the attachment of ADP-ribose subunits to target proteins using NAD+ as a substrate.	NAD	177-181	poly(ADP-ribose) polymerase 1	Homo sapiens	16-43
20942953-1	2010	BACKGROUND: The poly(ADP-ribose) polymerase (PARP) superfamily was originally identified as enzymes that catalyze the attachment of ADP-ribose subunits to target proteins using NAD+ as a substrate.	NAD	177-181	poly(ADP-ribose) polymerase 1	Homo sapiens	45-49
20798610-4	2010	In response to stress, FoxO1 dissociated from an NAD(+)-dependent histone deacetylase SIRT2 and FoxO1 thus became acetylated and in turn bound to Atg7, an E1-like protein, to influence the autophagic process leading to cell death.	NAD	49-55	forkhead box O1	Homo sapiens	96-101
20638297-5	2010	These studies suggest that insulin signaling underpins mitochondrial electron transport chain integrity and activity by suppressing FOXO1/HMOX1 and maintaining the NAD(+)/NADH ratio, the mediator of the SIRT1/PGC1alpha pathway for mitochondrial biogenesis and function.	NAD	164-170	insulin	Homo sapiens	27-34
20599792-1	2010	Poly(ADP-ribosyl)ation is a posttranslational modification of proteins, which is mainly catalyzed by poly(ADP-ribose) polymerase-1 (PARP-1) by using NAD(+) as substrate and is directly triggered by DNA strand breaks.	NAD	149-155	poly(ADP-ribose) polymerase 1	Homo sapiens	101-130
20599792-1	2010	Poly(ADP-ribosyl)ation is a posttranslational modification of proteins, which is mainly catalyzed by poly(ADP-ribose) polymerase-1 (PARP-1) by using NAD(+) as substrate and is directly triggered by DNA strand breaks.	NAD	149-155	poly(ADP-ribose) polymerase 1	Homo sapiens	132-138
20599792-2	2010	Under mild genotoxic stress poly(ADP-ribose) (PAR) formation plays an important role in DNA repair whereas severe genotoxic stress and the ensuing overactivation of PARP-1 induce cellular NAD(+) depletion, energy failure and ultimately cell death.	NAD	188-194	poly(ADP-ribose) polymerase 1	Homo sapiens	165-171
20659764-0	2010	Triggering the redox reaction of cytochrome c on a biomimetic layer and elimination of interferences for NADH detection.	NAD	105-109	cytochrome c, somatic	Homo sapiens	33-45
20659764-1	2010	Biomimetic layers triggering the redox process of cytochrome c (cyt c) by beta-nicotinamide adenine dinucleotide (NADH) were fabricated and applied for the detection of NADH.	NAD	74-112	cytochrome c, somatic	Homo sapiens	50-62
20659764-1	2010	Biomimetic layers triggering the redox process of cytochrome c (cyt c) by beta-nicotinamide adenine dinucleotide (NADH) were fabricated and applied for the detection of NADH.	NAD	74-112	cytochrome c, somatic	Homo sapiens	64-69
20659764-1	2010	Biomimetic layers triggering the redox process of cytochrome c (cyt c) by beta-nicotinamide adenine dinucleotide (NADH) were fabricated and applied for the detection of NADH.	NAD	114-118	cytochrome c, somatic	Homo sapiens	50-62
20659764-1	2010	Biomimetic layers triggering the redox process of cytochrome c (cyt c) by beta-nicotinamide adenine dinucleotide (NADH) were fabricated and applied for the detection of NADH.	NAD	114-118	cytochrome c, somatic	Homo sapiens	64-69
20659764-1	2010	Biomimetic layers triggering the redox process of cytochrome c (cyt c) by beta-nicotinamide adenine dinucleotide (NADH) were fabricated and applied for the detection of NADH.	NAD	169-173	cytochrome c, somatic	Homo sapiens	50-62
20659764-1	2010	Biomimetic layers triggering the redox process of cytochrome c (cyt c) by beta-nicotinamide adenine dinucleotide (NADH) were fabricated and applied for the detection of NADH.	NAD	169-173	cytochrome c, somatic	Homo sapiens	64-69
20638297-5	2010	These studies suggest that insulin signaling underpins mitochondrial electron transport chain integrity and activity by suppressing FOXO1/HMOX1 and maintaining the NAD(+)/NADH ratio, the mediator of the SIRT1/PGC1alpha pathway for mitochondrial biogenesis and function.	NAD	164-170	PPARG coactivator 1 alpha	Homo sapiens	209-218
20638297-5	2010	These studies suggest that insulin signaling underpins mitochondrial electron transport chain integrity and activity by suppressing FOXO1/HMOX1 and maintaining the NAD(+)/NADH ratio, the mediator of the SIRT1/PGC1alpha pathway for mitochondrial biogenesis and function.	NAD	171-175	insulin	Homo sapiens	27-34
20638297-5	2010	These studies suggest that insulin signaling underpins mitochondrial electron transport chain integrity and activity by suppressing FOXO1/HMOX1 and maintaining the NAD(+)/NADH ratio, the mediator of the SIRT1/PGC1alpha pathway for mitochondrial biogenesis and function.	NAD	171-175	PPARG coactivator 1 alpha	Homo sapiens	209-218
20824065-1	2010	Malic enzyme 2 (ME2) is a mitochondrial enzyme that catalyzes the conversion of malate to pyruvate and CO2 and uses NAD as a cofactor.	NAD	116-119	malic enzyme 2	Homo sapiens	0-14
20620150-1	2010	l-Gulonate 3-dehydrogenase (GDH) is a bifunctional dimeric protein that functions not only as an NAD(+)-dependent enzyme in the uronate cycle but also as a taxon-specific lambda-crystallin in rabbit lens.	NAD	97-103	lambda-crystallin	Oryctolagus cuniculus	0-26
20620150-1	2010	l-Gulonate 3-dehydrogenase (GDH) is a bifunctional dimeric protein that functions not only as an NAD(+)-dependent enzyme in the uronate cycle but also as a taxon-specific lambda-crystallin in rabbit lens.	NAD	97-103	lambda-crystallin	Oryctolagus cuniculus	28-31
20620150-2	2010	Here we report the first crystal structure of GDH in both apo form and NADH-bound holo form.	NAD	71-75	lambda-crystallin	Oryctolagus cuniculus	46-49
20824065-1	2010	Malic enzyme 2 (ME2) is a mitochondrial enzyme that catalyzes the conversion of malate to pyruvate and CO2 and uses NAD as a cofactor.	NAD	116-119	malic enzyme 2	Homo sapiens	16-19
20824065-8	2010	As might be expected, depletion of ME2 induced an increase in the NAD+/NADH ratio and ATP levels fell significantly.	NAD	66-70	malic enzyme 2	Homo sapiens	35-38
20824065-8	2010	As might be expected, depletion of ME2 induced an increase in the NAD+/NADH ratio and ATP levels fell significantly.	NAD	71-75	malic enzyme 2	Homo sapiens	35-38
20651248-5	2010	Resveratrol, an activator of the Nicotinamide adenine dinucleotide (NAD) dependent protein deacetylase SIRT1, reversed acetylation but not phosphorylation of Smad3 and inhibited TGF-beta1-induced up-regulation of collagen IV and fibronectin mRNA levels.	NAD	33-66	transforming growth factor beta 1	Homo sapiens	178-187
20651248-5	2010	Resveratrol, an activator of the Nicotinamide adenine dinucleotide (NAD) dependent protein deacetylase SIRT1, reversed acetylation but not phosphorylation of Smad3 and inhibited TGF-beta1-induced up-regulation of collagen IV and fibronectin mRNA levels.	NAD	68-71	transforming growth factor beta 1	Homo sapiens	178-187
20651248-5	2010	Resveratrol, an activator of the Nicotinamide adenine dinucleotide (NAD) dependent protein deacetylase SIRT1, reversed acetylation but not phosphorylation of Smad3 and inhibited TGF-beta1-induced up-regulation of collagen IV and fibronectin mRNA levels.	NAD	68-71	fibronectin 1	Homo sapiens	229-240
20471503-1	2010	NAD(+)-dependent Class III histone deacetylase SIRT1 is a multiple function protein critically involved in stress responses, cellular metabolism and aging through deacetylating a variety of substrates including p53, forkhead-box transcription factors, PGC-1alpha, NF-kappaB, Ku70 and histones.	NAD	0-6	tumor protein p53	Homo sapiens	211-214
20561255-4	2010	Prolonged ABA treatment increased the expression of the cox2 gene in complex IV and nad genes in complex I to a higher level than no ABA treatment in the wild type, but only to a moderate level in abo5, probably because abo5 already expressed high levels of mitochondrial-encoded cox2 and nad genes under no ABA treatment.	NAD	289-292	cytochrome c oxidase subunit 2	Arabidopsis thaliana	56-60
20669926-1	2010	Poly(ADP-ribose) polymerase-1 (PARP-1) is a molecular DNA damage sensor that catalyzes the synthesis of the complex biopolymer poly(ADP-ribose) (PAR) under consumption of NAD(+).	NAD	171-177	poly(ADP-ribose) polymerase 1	Homo sapiens	0-29
20669926-1	2010	Poly(ADP-ribose) polymerase-1 (PARP-1) is a molecular DNA damage sensor that catalyzes the synthesis of the complex biopolymer poly(ADP-ribose) (PAR) under consumption of NAD(+).	NAD	171-177	poly(ADP-ribose) polymerase 1	Homo sapiens	31-37
20518072-4	2010	Here we present a possible mechanism that explains how these substances result in apoptosis in cancer cells by ENOX2-mediated alterations of cytosolic amounts of NAD(+) and NADH.	NAD	162-168	ecto-NOX disulfide-thiol exchanger 2	Homo sapiens	111-116
20518072-4	2010	Here we present a possible mechanism that explains how these substances result in apoptosis in cancer cells by ENOX2-mediated alterations of cytosolic amounts of NAD(+) and NADH.	NAD	173-177	ecto-NOX disulfide-thiol exchanger 2	Homo sapiens	111-116
20518072-5	2010	When ENOX2 is inhibited, plasma membrane electron transport is diminished, and cytosolic NADH accumulates.	NAD	89-93	ecto-NOX disulfide-thiol exchanger 2	Homo sapiens	5-10
20518072-11	2010	Treatments that stimulate cytosolic NADH production potentiate the antiproliferative effects of ENOX2 inhibitors while those that attenuate NADH production or stimulate plasma membrane electron transport confer a survival advantage.	NAD	36-40	ecto-NOX disulfide-thiol exchanger 2	Homo sapiens	96-101
20631301-1	2010	The longevity-promoting NAD+-dependent class III histone deacetylase Sirtuin 1 (SIRT1) is involved in stem cell function by controlling cell fate decision and/or by regulating the p53-dependent expression of NANOG.	NAD	24-28	tumor protein p53	Homo sapiens	180-183
20633699-3	2010	PARP-1 works as DNA damage nick sensor, which uses NAD(+) to form polymers of ADP-ribose (PAR) and nicotinamide.	NAD	51-57	poly(ADP-ribose) polymerase 1	Homo sapiens	0-6
20804590-13	2010	Molecular docking studies at the active site of PARP showed 3-AB and NIC to interact with the binding site for the nicotinamide moiety of NAD+ and TAU to interact with the binding site for the adenine moiety of NAD+.	NAD	138-142	poly(ADP-ribose) polymerase 1	Homo sapiens	48-52
20804590-13	2010	Molecular docking studies at the active site of PARP showed 3-AB and NIC to interact with the binding site for the nicotinamide moiety of NAD+ and TAU to interact with the binding site for the adenine moiety of NAD+.	NAD	211-215	poly(ADP-ribose) polymerase 1	Homo sapiens	48-52
20060508-4	2010	SIRT4 can transfer the ADP-ribose group from NAD(+) onto acceptor proteins.	NAD	45-51	sirtuin 4	Homo sapiens	0-5
20471503-1	2010	NAD(+)-dependent Class III histone deacetylase SIRT1 is a multiple function protein critically involved in stress responses, cellular metabolism and aging through deacetylating a variety of substrates including p53, forkhead-box transcription factors, PGC-1alpha, NF-kappaB, Ku70 and histones.	NAD	0-6	PPARG coactivator 1 alpha	Homo sapiens	252-262
20608974-8	2010	Finally, we show that PPARgamma ligands increase NAD(+) production in primary human macrophages and that this regulation is dampened in the presence of visfatin small interfering RNA or by the visfatin-specific inhibitor FK866.	NAD	49-55	peroxisome proliferator activated receptor gamma	Homo sapiens	22-31
20608974-9	2010	Taken together, our results suggest that PPARgamma regulates the expression of visfatin in macrophages, leading to increased levels of NAD(+).	NAD	135-141	peroxisome proliferator activated receptor gamma	Homo sapiens	41-50
20679690-1	2010	Poly(ADP-ribose)polymerase-1 (PARP-1) catalyzes the polymerization of ADP-ribose units from NAD+ modules on target proteins, resulting in the attachment of linear or branched polymers.	NAD	92-96	poly(ADP-ribose) polymerase 1	Homo sapiens	0-28
20679690-1	2010	Poly(ADP-ribose)polymerase-1 (PARP-1) catalyzes the polymerization of ADP-ribose units from NAD+ modules on target proteins, resulting in the attachment of linear or branched polymers.	NAD	92-96	poly(ADP-ribose) polymerase 1	Homo sapiens	30-36
20453869-4	2010	Genistein"s mode of action on 3beta-HSD activity was competitive for the substrate pregnenolonrge and noncompetitive for the cofactor NAD(+).	NAD	134-140	hydroxy-delta-5-steroid dehydrogenase, 3 beta- and steroid delta-isomerase 1	Rattus norvegicus	30-39
20617556-2	2010	The anti-inflammatory function of Sirtuin 1 (SIRT1), a NAD-dependent class III histone/protein deacetylase, has been well documented, but how SIRT1 is regulated under inflammatory conditions is largely unknown.	NAD	55-58	sirtuin 1	Rattus norvegicus	34-43
20617556-2	2010	The anti-inflammatory function of Sirtuin 1 (SIRT1), a NAD-dependent class III histone/protein deacetylase, has been well documented, but how SIRT1 is regulated under inflammatory conditions is largely unknown.	NAD	55-58	sirtuin 1	Rattus norvegicus	45-50
20550106-3	2010	The activated state of PARP-1 was generated by treatment of cells with a DNA-damaging agent or by addition of NAD(+) to CFEs.	NAD	110-116	poly(ADP-ribose) polymerase 1	Homo sapiens	23-29
20725615-4	2010	Nicotinamide is the primary precursor of nicotinamide adenine dinucleotide (NAD(+)), an essential coenzyme in ATP production and the sole substrate of the nuclear enzyme poly-ADP-ribose polymerase-1 (PARP-1).	NAD	41-74	poly(ADP-ribose) polymerase 1	Homo sapiens	170-198
20725615-4	2010	Nicotinamide is the primary precursor of nicotinamide adenine dinucleotide (NAD(+)), an essential coenzyme in ATP production and the sole substrate of the nuclear enzyme poly-ADP-ribose polymerase-1 (PARP-1).	NAD	41-74	poly(ADP-ribose) polymerase 1	Homo sapiens	200-206
20725615-4	2010	Nicotinamide is the primary precursor of nicotinamide adenine dinucleotide (NAD(+)), an essential coenzyme in ATP production and the sole substrate of the nuclear enzyme poly-ADP-ribose polymerase-1 (PARP-1).	NAD	76-82	poly(ADP-ribose) polymerase 1	Homo sapiens	170-198
20725615-4	2010	Nicotinamide is the primary precursor of nicotinamide adenine dinucleotide (NAD(+)), an essential coenzyme in ATP production and the sole substrate of the nuclear enzyme poly-ADP-ribose polymerase-1 (PARP-1).	NAD	76-82	poly(ADP-ribose) polymerase 1	Homo sapiens	200-206
20558841-5	2010	The nicotinamide phosphoribosyl transferase (NAMPT) inhibitor APO866 (also called FK866 or WK175) selectively inhibits tumor growth through intracellular NAD depletion.	NAD	154-157	nicotinamide phosphoribosyltransferase	Mus musculus	4-43
20558841-5	2010	The nicotinamide phosphoribosyl transferase (NAMPT) inhibitor APO866 (also called FK866 or WK175) selectively inhibits tumor growth through intracellular NAD depletion.	NAD	154-157	nicotinamide phosphoribosyltransferase	Mus musculus	45-50
20543840-5	2010	In response to stress, FoxO1 was acetylated by dissociation from sirtuin-2 (SIRT2), a NAD(+)-dependent histone deacetylase, and the acetylated FoxO1 bound to Atg7, an E1-like protein, to influence the autophagic process leading to cell death.	NAD	86-92	forkhead box O1	Homo sapiens	23-28
20422640-5	2010	After adding exogenous cytochrome c, the sarcolemma isolated from myotubes had an ability to consume oxygen in the presence of NADH or succinate.	NAD	127-131	cytochrome c, somatic	Homo sapiens	23-35
20370672-6	2010	Its intracellular functions concentrate on the regulation of the activity of NAD-consuming enzymes such as various sirtuins thereby also affecting (TNFa) biosynthesis, cell life-span and longevity.	NAD	77-80	tumor necrosis factor	Homo sapiens	148-152
20550916-6	2010	To our knowledge, we obtained the first direct evidence that OmcA undergoes a redox state-dependent conformational change in solution whereby reduction decreases the overall length of OmcA by approximately 7 A (the maximum dimension was 96 A for oxidized OmcA, and 89 A for NADH and dithionite-reduced OmcA).	NAD	274-278	OmcA/MtrC family decaheme c-type cytochrome	Shewanella oneidensis MR-1	61-65
20498876-4	2010	Convenient voltammetric and chronoamperometric measurements of 0-3 mM ferrocyanide, 0-25 mM hydrogen peroxide, and 0-100 muM NADH have been documented.	NAD	125-129	latexin	Homo sapiens	121-124
20429690-2	2010	Resveratrol is a natural polyphenol that activates SIRT1, a novel cardioprotective and longevity factor having NAD(+)-dependent histone deacetylase activity.	NAD	111-117	sirtuin 1	Rattus norvegicus	51-56
20392873-9	2010	4) Within the liver, NAMPT/visfatin was located to hepatocytes, and our in vitro studies showed that NAMPT/visfatin exerts antiapoptotic effects in these cells, involving enzymatic synthesis of nicotinamide adenine dinucleotide.	NAD	194-227	nicotinamide phosphoribosyltransferase	Mus musculus	21-26
20392873-9	2010	4) Within the liver, NAMPT/visfatin was located to hepatocytes, and our in vitro studies showed that NAMPT/visfatin exerts antiapoptotic effects in these cells, involving enzymatic synthesis of nicotinamide adenine dinucleotide.	NAD	194-227	nicotinamide phosphoribosyltransferase	Mus musculus	27-35
20392873-9	2010	4) Within the liver, NAMPT/visfatin was located to hepatocytes, and our in vitro studies showed that NAMPT/visfatin exerts antiapoptotic effects in these cells, involving enzymatic synthesis of nicotinamide adenine dinucleotide.	NAD	194-227	nicotinamide phosphoribosyltransferase	Mus musculus	101-106
20392873-9	2010	4) Within the liver, NAMPT/visfatin was located to hepatocytes, and our in vitro studies showed that NAMPT/visfatin exerts antiapoptotic effects in these cells, involving enzymatic synthesis of nicotinamide adenine dinucleotide.	NAD	194-227	nicotinamide phosphoribosyltransferase	Mus musculus	107-115
20435741-7	2010	Each molecule of heterologously expressed HvUXE1 enzyme contained about one molecule of noncovalently bound NAD(+).	NAD	108-114	UXE1	Hordeum vulgare	42-48
22435614-8	2010	In experiments with surface NOX proteins released from HeLa cells, spectrophotometric measurements of the oxidation of NADH revealed inhibition of the cancer-specific ENOX2 activity by CLA and the omega-3 fatty acids, eicosapentaenoic, docosahexaenoic, and alpha-linolenic acids.	NAD	119-123	ecto-NOX disulfide-thiol exchanger 2	Homo sapiens	167-172
20411356-6	2010	However, hyperactivation of PARP-1 can result in depletion of NAD/ATP, and in PAR-dependent mitochondrial pore formation leading to release of apoptosis inducing factor and cell death.	NAD	62-65	poly(ADP-ribose) polymerase 1	Homo sapiens	28-34
20148352-10	2010	A 24-h fasting in mice increased mRNA and protein expression of both SIRT1 and PPARalpha in the livers, where the NAD(+) levels increased with increasing nicotinamide phosphoribosyltransferase (NAMPT) activity in the NAD(+) salvage pathway.	NAD	114-120	peroxisome proliferator activated receptor alpha	Mus musculus	79-88
20148352-10	2010	A 24-h fasting in mice increased mRNA and protein expression of both SIRT1 and PPARalpha in the livers, where the NAD(+) levels increased with increasing nicotinamide phosphoribosyltransferase (NAMPT) activity in the NAD(+) salvage pathway.	NAD	217-223	peroxisome proliferator activated receptor alpha	Mus musculus	79-88
20148352-10	2010	A 24-h fasting in mice increased mRNA and protein expression of both SIRT1 and PPARalpha in the livers, where the NAD(+) levels increased with increasing nicotinamide phosphoribosyltransferase (NAMPT) activity in the NAD(+) salvage pathway.	NAD	217-223	nicotinamide phosphoribosyltransferase	Mus musculus	154-192
20148352-10	2010	A 24-h fasting in mice increased mRNA and protein expression of both SIRT1 and PPARalpha in the livers, where the NAD(+) levels increased with increasing nicotinamide phosphoribosyltransferase (NAMPT) activity in the NAD(+) salvage pathway.	NAD	217-223	nicotinamide phosphoribosyltransferase	Mus musculus	194-199
20148352-11	2010	Treatment of Hepa1-6 cells in a low glucose medium conditions with NAD(+) or NADH showed that the mRNA expression of both SIRT1 and PPARalpha can be enhanced by addition of NAD(+), and decreased by increasing NADH levels.	NAD	67-73	peroxisome proliferator activated receptor alpha	Mus musculus	132-141
20148352-11	2010	Treatment of Hepa1-6 cells in a low glucose medium conditions with NAD(+) or NADH showed that the mRNA expression of both SIRT1 and PPARalpha can be enhanced by addition of NAD(+), and decreased by increasing NADH levels.	NAD	77-81	peroxisome proliferator activated receptor alpha	Mus musculus	132-141
20148352-11	2010	Treatment of Hepa1-6 cells in a low glucose medium conditions with NAD(+) or NADH showed that the mRNA expression of both SIRT1 and PPARalpha can be enhanced by addition of NAD(+), and decreased by increasing NADH levels.	NAD	173-179	peroxisome proliferator activated receptor alpha	Mus musculus	132-141
20148352-11	2010	Treatment of Hepa1-6 cells in a low glucose medium conditions with NAD(+) or NADH showed that the mRNA expression of both SIRT1 and PPARalpha can be enhanced by addition of NAD(+), and decreased by increasing NADH levels.	NAD	209-213	peroxisome proliferator activated receptor alpha	Mus musculus	132-141
20182695-2	2010	catalyzes the NAD-linked oxidation of formate to CO(2), and FDH transcript accumulation has been reported after various abiotic stresses.	NAD	14-17	formate dehydrogenase	Arabidopsis thaliana	60-63
20347206-2	2010	Visfatin is a recently described protein that functions both as a proinflammatory plasma cytokine and an intracellular enzyme within the nicotinamide adenine dinucleotide (NAD(+)) salvage pathway.	NAD	137-170	nicotinamide phosphoribosyltransferase	Mus musculus	0-8
20347206-2	2010	Visfatin is a recently described protein that functions both as a proinflammatory plasma cytokine and an intracellular enzyme within the nicotinamide adenine dinucleotide (NAD(+)) salvage pathway.	NAD	172-178	nicotinamide phosphoribosyltransferase	Mus musculus	0-8
20206212-0	2010	Quinolinate phosphoribosyl transferase, a key enzyme in de novo NAD(+) synthesis, suppresses spontaneous cell death by inhibiting overproduction of active-caspase-3.	NAD	64-70	quinolinate phosphoribosyltransferase	Homo sapiens	0-38
20463219-5	2010	We show that the flexible hinge 2 linker region of RIBEYE(B) domain that connects the nicotinamide adenine dinucleotide (NADH)-binding subdomain with the substrate-binding subdomain (SBD) binds to the C terminus of GCAP2.	NAD	86-119	C-terminal binding protein 2	Homo sapiens	51-57
20463219-5	2010	We show that the flexible hinge 2 linker region of RIBEYE(B) domain that connects the nicotinamide adenine dinucleotide (NADH)-binding subdomain with the substrate-binding subdomain (SBD) binds to the C terminus of GCAP2.	NAD	121-125	C-terminal binding protein 2	Homo sapiens	51-57
20463219-6	2010	We demonstrate that the RIBEYE-GCAP2 interaction is induced by the binding of NADH to RIBEYE.	NAD	78-82	C-terminal binding protein 2	Homo sapiens	24-30
20463219-6	2010	We demonstrate that the RIBEYE-GCAP2 interaction is induced by the binding of NADH to RIBEYE.	NAD	78-82	C-terminal binding protein 2	Homo sapiens	86-92
20544540-1	2010	The enzyme poly(ADP-ribose) polymerase (PARP-1, EC 2.4.2.30) is activated by DNA strand breaks caused by several agents and utilizes NAD to form polyADPR, bound to acceptor proteins.	NAD	133-136	poly(ADP-ribose) polymerase 1	Homo sapiens	11-38
20544540-1	2010	The enzyme poly(ADP-ribose) polymerase (PARP-1, EC 2.4.2.30) is activated by DNA strand breaks caused by several agents and utilizes NAD to form polyADPR, bound to acceptor proteins.	NAD	133-136	poly(ADP-ribose) polymerase 1	Homo sapiens	40-46
20544540-4	2010	Lower PARP-1 activity and higher NAD concentration were observed in pathological conditions than controls, supporting the role of PARP-1 activation in modulating NAD concentration.	NAD	162-165	poly(ADP-ribose) polymerase 1	Homo sapiens	130-136
20448901-2	2010	Employing the selective reduction of (rac)-2-phenylpropionaldehyde to (S)-phenyl-1-propanol as a model, we have demonstrated the successful co-immobilisation of the HLADH enzyme and co-factor NAD(H); with incorporation of the material into a continuous flow reactor facilitating the in situ electrochemical regeneration of NAD(H) for in excess of 100 h. Using this approach we have developed a reagent-less, atom efficient system applicable to the cost-effective, continuous biosynthesis of chiral compounds.	NAD	192-198	AKT serine/threonine kinase 1	Homo sapiens	38-41
20448901-2	2010	Employing the selective reduction of (rac)-2-phenylpropionaldehyde to (S)-phenyl-1-propanol as a model, we have demonstrated the successful co-immobilisation of the HLADH enzyme and co-factor NAD(H); with incorporation of the material into a continuous flow reactor facilitating the in situ electrochemical regeneration of NAD(H) for in excess of 100 h. Using this approach we have developed a reagent-less, atom efficient system applicable to the cost-effective, continuous biosynthesis of chiral compounds.	NAD	323-329	AKT serine/threonine kinase 1	Homo sapiens	38-41
20206212-0	2010	Quinolinate phosphoribosyl transferase, a key enzyme in de novo NAD(+) synthesis, suppresses spontaneous cell death by inhibiting overproduction of active-caspase-3.	NAD	64-70	caspase 3	Homo sapiens	155-164
20206212-1	2010	Quinolinate phosphoribosyl transferase (QPRT) is a key enzyme in de novo NAD(+) synthesis.	NAD	73-79	quinolinate phosphoribosyltransferase	Homo sapiens	0-38
20206212-1	2010	Quinolinate phosphoribosyl transferase (QPRT) is a key enzyme in de novo NAD(+) synthesis.	NAD	73-79	quinolinate phosphoribosyltransferase	Homo sapiens	40-44
20206212-3	2010	This study was designed to elucidate the functions of QPRT protein in addition to NAD(+) synthesis.	NAD	82-88	quinolinate phosphoribosyltransferase	Homo sapiens	54-58
20463295-5	2010	In models of acute stress, PARP-1 inhibition may protect cellular NAD pools and prevent nuclear factor-kappaB-dependent inflammatory signalling, while long-term protective roles for PARP-1 include DNA repair and regulation of chromatin structure.	NAD	66-69	poly(ADP-ribose) polymerase 1	Homo sapiens	27-33
20454697-11	2010	Out of the total 14 nonsynonymous changes observed in cases and controls, four (p.A52T in nicotinamide adenine dinucleotide [NADH] dehydrogenase [ND1] protein; p.L128Q in ND2; p.W48R in ATPase6; p.R340H in ND4 protein) were pathogenic.	NAD	90-123	mitochondrially encoded NADH dehydrogenase 1	Homo sapiens	146-149
20219917-1	2010	Poly(ADP-ribose) polymerase (PARP) is an abundant, chromatin-associated, NAD-dependent enzyme that functions in multiple chromosomal processes, including DNA replication and chromatin remodeling.	NAD	73-76	poly(ADP-ribose) polymerase 1	Homo sapiens	0-27
20219917-1	2010	Poly(ADP-ribose) polymerase (PARP) is an abundant, chromatin-associated, NAD-dependent enzyme that functions in multiple chromosomal processes, including DNA replication and chromatin remodeling.	NAD	73-76	poly(ADP-ribose) polymerase 1	Homo sapiens	29-33
20054824-7	2010	Immunofluorescence microscopy reveals more pronounced staining of cell-cell junctional protein VE-cadherin at the cellular periphery signifying increased tightness of the cell-cell contacts after beta-NAD stimulation.	NAD	196-204	cadherin 5	Homo sapiens	95-106
20081535-7	2010	MEASUREMENTS AND MAIN RESULTS: Acetylcholine-induced endothelium-dependent relaxation decreased, whereas nicotinamide adenine dinucleotide-stimulated superoxide radical production in the aorta and aortic p22phox, p47phox, gp91phox, NOX1, and NOX4 mRNA concentrations increased in trauma-hemorrhaged rats vs. sham rats.	NAD	105-138	cytochrome b-245 alpha chain	Rattus norvegicus	204-211
20047575-1	2010	The NAD+-dependent SIRT6 deacetylase is a therapeutic candidate against the emerging metabolic syndrome epidemic.	NAD	4-8	sirtuin 6	Mus musculus	19-24
20068143-11	2010	In THP-1 cells, high glucose and palmitate reduced SIRT1 and NAMPT expression and reduced the levels of intracellular NAD(+) through oxidative stress.	NAD	118-124	GLI family zinc finger 2	Homo sapiens	3-8
20054824-6	2010	Importantly, beta-NAD significantly attenuated thrombin-induced EC permeability as well as the barrier-compromising effects of Gram-negative and Gram-positive bacterial toxins representing the barrier-protective function of beta-NAD.	NAD	13-21	coagulation factor II, thrombin	Homo sapiens	47-55
20054824-9	2010	beta-NAD-treatment attenuates the lipopolysaccharide (LPS)-induced phosphorylation of myosin light chain (MLC) indicating its involvement in barrier protection.	NAD	0-8	modulator of VRAC current 1	Homo sapiens	86-104
20054824-9	2010	beta-NAD-treatment attenuates the lipopolysaccharide (LPS)-induced phosphorylation of myosin light chain (MLC) indicating its involvement in barrier protection.	NAD	0-8	modulator of VRAC current 1	Homo sapiens	106-109
20181750-2	2010	The level of NADH in Pro35S:AtNUDX6 and KO-nudx6 plants was decreased and increased, respectively, compared with that of the control plants, while the level of ADP-Rib was not changed in either plant.	NAD	13-17	nudix hydrolase homolog 6	Arabidopsis thaliana	28-35
20181750-2	2010	The level of NADH in Pro35S:AtNUDX6 and KO-nudx6 plants was decreased and increased, respectively, compared with that of the control plants, while the level of ADP-Rib was not changed in either plant.	NAD	13-17	nudix hydrolase homolog 6	Arabidopsis thaliana	43-48
20181750-3	2010	The activity of pyrophosphohydrolase toward NADH was enhanced and reduced in the Pro35S:AtNUDX6 and KO-nudx6 plants, respectively.	NAD	44-48	nudix hydrolase homolog 6	Arabidopsis thaliana	88-95
20181750-3	2010	The activity of pyrophosphohydrolase toward NADH was enhanced and reduced in the Pro35S:AtNUDX6 and KO-nudx6 plants, respectively.	NAD	44-48	nudix hydrolase homolog 6	Arabidopsis thaliana	103-108
20181750-4	2010	The decrease in the activity of NADH pyrophosphohydrolase and the increase in the level of NADH were observed in the rosette and cauline leaves, but not in the roots, of the KO-nudx6 plants.	NAD	32-36	nudix hydrolase homolog 6	Arabidopsis thaliana	177-182
20181750-10	2010	These results indicated that AtNUDX6 is a modulator of NADH rather than ADP-Rib metabolism and that, through induction of TRX-h5 expression, AtNUDX6 significantly impacts the plant immune response as a positive regulator of NPR1-dependent SA signaling pathways.	NAD	55-59	nudix hydrolase homolog 6	Arabidopsis thaliana	29-36
20181750-10	2010	These results indicated that AtNUDX6 is a modulator of NADH rather than ADP-Rib metabolism and that, through induction of TRX-h5 expression, AtNUDX6 significantly impacts the plant immune response as a positive regulator of NPR1-dependent SA signaling pathways.	NAD	55-59	nudix hydrolase homolog 6	Arabidopsis thaliana	141-148
20133733-7	2010	Our data suggest a mechanism for boundary formation whereby histone deacetylation by Rpd3 removes the substrate for the HDAC Sir2, so that Sir2 no longer can produce O-acetyl-ADP ribose (OAADPR) by consumption of NAD(+) in the deacetylation reaction.	NAD	213-219	histone deacetylase RPD3	Saccharomyces cerevisiae S288C	85-89
19795500-2	2010	Excessive oxidative DNA strand breaks lead to PARP-1-induced depletion of cellular NAD(+), glycolytic rate, ATP levels, and eventual cell death.	NAD	83-89	poly(ADP-ribose) polymerase 1	Homo sapiens	46-52
20042612-3	2010	Ribosome-associated SIRT3 was found to be responsible for deacetylation of MRPL10 in an NAD(+)-dependent manner.	NAD	88-94	mitochondrial ribosomal protein L10	Mus musculus	75-81
20181594-0	2010	NAD+ depletion is necessary and sufficient for poly(ADP-ribose) polymerase-1-mediated neuronal death.	NAD	0-4	poly(ADP-ribose) polymerase 1	Homo sapiens	47-76
19925161-2	2010	However, excessive activity of PARP-1 exacerbates brain injury via NAD+ depletion and energy failure.	NAD	67-71	poly(ADP-ribose) polymerase 1	Homo sapiens	31-37
20181594-2	2010	PARP-1 activation leads to cytosolic NAD(+) depletion and mitochondrial release of apoptosis-inducing factor (AIF), but the causal relationships between these two events have been difficult to resolve.	NAD	37-43	poly(ADP-ribose) polymerase 1	Homo sapiens	0-6
20181594-3	2010	Here, we examined this issue by using extracellular NAD(+) to restore neuronal NAD(+) levels after PARP-1 activation.	NAD	52-58	poly(ADP-ribose) polymerase 1	Homo sapiens	99-105
20181594-5	2010	Restoration of cytosolic NAD(+) by this means prevented the glycolytic inhibition, mitochondrial failure, AIF translocation, and neuron death that otherwise results from extensive PARP-1 activation.	NAD	25-31	poly(ADP-ribose) polymerase 1	Homo sapiens	180-186
20181594-7	2010	Conversely, depletion of cytosolic NAD(+) with NAD(+) glycohydrolase produced a block in glycolysis inhibition, mitochondrial depolarization, AIF translocation, and neuron death, independent of PARP-1 activation.	NAD	35-41	poly(ADP-ribose) polymerase 1	Homo sapiens	194-200
20181594-8	2010	These results establish NAD(+) depletion as a causal event in PARP-1-mediated cell death and place NAD(+) depletion and glycolytic failure upstream of mitochondrial AIF release.	NAD	24-30	poly(ADP-ribose) polymerase 1	Homo sapiens	62-68
20092359-1	2010	Poly-ADP-ribose polymerases (PARPs) catalyze transfer of ADP-ribose from NAD(+) to specific residues in their substrate proteins or to growing ADP-ribose chains.	NAD	73-79	poly(ADP-ribose) polymerase 1	Homo sapiens	29-34
19824993-10	2010	CONCLUSIONS: Considering the affinities for retinol and retinal of ADHs and ALDHs expressed in the rat esophagus, the NAD-dependent in situ retinoic acid supply system in the rat esophagus is thought to comprise Class IV ADH and ALDH 1A1.	NAD	118-121	aldehyde dehydrogenase 1 family, member A1	Rattus norvegicus	229-237
19928762-8	2010	Moreover, we also found that AMPK activity mediated by resveratrol in cancer cells was due to inducing the expression of Sirtuin type 1 (SIRT1) via elevation in the cellular NAD(+)/NADH in ER-positive cells.	NAD	174-180	estrogen receptor 1	Homo sapiens	189-191
19928762-8	2010	Moreover, we also found that AMPK activity mediated by resveratrol in cancer cells was due to inducing the expression of Sirtuin type 1 (SIRT1) via elevation in the cellular NAD(+)/NADH in ER-positive cells.	NAD	181-185	estrogen receptor 1	Homo sapiens	189-191
19902144-1	2010	Poly-ADP-ribose polymerases (PARPs) use NAD(+) as substrate to generate polymers of ADP-ribose.	NAD	40-46	poly(ADP-ribose) polymerase 1	Homo sapiens	29-34
19966022-1	2010	NAD-dependent butanediol dehydrogenase (Bdh1p) from Saccharomyces cerevisiae reversibly transforms acetoin to 2,3-butanediol in a stereospecific manner.	NAD	0-3	(R,R)-butanediol dehydrogenase	Saccharomyces cerevisiae S288C	40-45
19370397-0	2010	Nicotinamide adenine dinucleotide extends the lifespan of Caenorhabditis elegans mediated by sir-2.1 and daf-16.	NAD	0-33	Deacetylase sirtuin-type domain-containing protein;NAD-dependent protein deacetylase sir-2.1	Caenorhabditis elegans	93-100
19370397-6	2010	An RNA interference experiment revealed that life extension by NAD was sir-2.1 dependent.	NAD	63-66	Deacetylase sirtuin-type domain-containing protein;NAD-dependent protein deacetylase sir-2.1	Caenorhabditis elegans	71-78
19370397-10	2010	These results suggest that NAD affected lifespan through the activation of SIR-2.1 and DAF-16 along a signaling pathway, namely insulin-like signalling pathway (at least parts of it), different from that associated with caloric restriction.	NAD	27-30	Deacetylase sirtuin-type domain-containing protein;NAD-dependent protein deacetylase sir-2.1	Caenorhabditis elegans	75-82
19902144-2	2010	We targeted the catalytic domain of human PARP1 as molecular NAD(+) detector into cellular organelles.	NAD	61-67	poly(ADP-ribose) polymerase 1	Homo sapiens	42-47
20132432-1	2010	OBJECTIVE: Sirtuin 3 (SIRT3) is a nicotinamide adenine dinucleotide (NAD)(+)-dependent protein deacetylase localized on mitochondria and regulates the adaptive thermogenesis in brown adipocytes.	NAD	34-67	sirtuin 3	Homo sapiens	11-20
20132432-1	2010	OBJECTIVE: Sirtuin 3 (SIRT3) is a nicotinamide adenine dinucleotide (NAD)(+)-dependent protein deacetylase localized on mitochondria and regulates the adaptive thermogenesis in brown adipocytes.	NAD	34-67	sirtuin 3	Homo sapiens	22-27
20132432-1	2010	OBJECTIVE: Sirtuin 3 (SIRT3) is a nicotinamide adenine dinucleotide (NAD)(+)-dependent protein deacetylase localized on mitochondria and regulates the adaptive thermogenesis in brown adipocytes.	NAD	69-72	sirtuin 3	Homo sapiens	11-20
20132432-1	2010	OBJECTIVE: Sirtuin 3 (SIRT3) is a nicotinamide adenine dinucleotide (NAD)(+)-dependent protein deacetylase localized on mitochondria and regulates the adaptive thermogenesis in brown adipocytes.	NAD	69-72	sirtuin 3	Homo sapiens	22-27
19900402-6	2010	Further, the combination also reduced the overactivation of PARP as evident from increased NAD levels and decreased PAR immunopositivity in sciatic nerve microsections.	NAD	91-94	poly(ADP-ribose) polymerase 1	Homo sapiens	60-64
19887595-2	2010	NAD+ is an obligate cosubstrate for mammalian sirtuin-1 (SIRT1), a deacetylase that activates peroxisome proliferator-activated receptor-gamma coactivator-1alpha (PGC-1alpha), which in turn can activate mitochondrial biogenesis.	NAD	0-4	PPARG coactivator 1 alpha	Homo sapiens	94-161
19887595-2	2010	NAD+ is an obligate cosubstrate for mammalian sirtuin-1 (SIRT1), a deacetylase that activates peroxisome proliferator-activated receptor-gamma coactivator-1alpha (PGC-1alpha), which in turn can activate mitochondrial biogenesis.	NAD	0-4	PPARG coactivator 1 alpha	Homo sapiens	163-173
19915948-3	2010	By an alternative activity, AtXDH1 is capable of oxidizing NADH with concomitant formation of NAD(+) and superoxide.	NAD	59-63	xanthine dehydrogenase 1	Arabidopsis thaliana	28-34
19915948-3	2010	By an alternative activity, AtXDH1 is capable of oxidizing NADH with concomitant formation of NAD(+) and superoxide.	NAD	94-100	xanthine dehydrogenase 1	Arabidopsis thaliana	28-34
19915948-4	2010	Here we demonstrate that in comparison to the specific activity with xanthine as substrate, the specific activity of recombinant AtXDH1 with NADH as substrate is about 15-times higher accompanied by a doubling in superoxide production.	NAD	141-145	xanthine dehydrogenase 1	Arabidopsis thaliana	129-135
19915948-5	2010	The observation that NAD(+) inhibits NADH oxidase activity of AtXDH1 while NADH suppresses NAD(+)-dependent xanthine oxidation indicates that both NAD(+) and NADH compete for the same binding-site and that both sub-activities are not expressed at the same time.	NAD	21-27	xanthine dehydrogenase 1	Arabidopsis thaliana	62-68
19915948-5	2010	The observation that NAD(+) inhibits NADH oxidase activity of AtXDH1 while NADH suppresses NAD(+)-dependent xanthine oxidation indicates that both NAD(+) and NADH compete for the same binding-site and that both sub-activities are not expressed at the same time.	NAD	37-41	xanthine dehydrogenase 1	Arabidopsis thaliana	62-68
19819719-4	2010	In addition, NAD(+) indirectly activates peroxisome proliferator-activated receptor gamma coactivator 1alpha (PGC-1alpha) during fasting, whereas acetyl-CoA inactivates PGC-1alpha upon feeding.	NAD	13-19	PPARG coactivator 1 alpha	Homo sapiens	41-108
19819719-4	2010	In addition, NAD(+) indirectly activates peroxisome proliferator-activated receptor gamma coactivator 1alpha (PGC-1alpha) during fasting, whereas acetyl-CoA inactivates PGC-1alpha upon feeding.	NAD	13-19	PPARG coactivator 1 alpha	Homo sapiens	110-120
19940131-4	2010	NAD treatment blocked the activation of pro-hypertrophic Akt1 signaling, and augmented the activity of anti-hypertrophic LKB1-AMPK signaling in the heart, which prevented subsequent induction of mTOR-mediated protein synthesis.	NAD	0-3	thymoma viral proto-oncogene 1	Mus musculus	57-61
19940131-4	2010	NAD treatment blocked the activation of pro-hypertrophic Akt1 signaling, and augmented the activity of anti-hypertrophic LKB1-AMPK signaling in the heart, which prevented subsequent induction of mTOR-mediated protein synthesis.	NAD	0-3	serine/threonine kinase 11	Mus musculus	121-125
20000467-9	2010	Our findings constitute the first evidence of the regulation of Complex II activity by the reversible acetylation of the SdhA subunit as a novel substrate of the NAD(+)-dependent deacetylase, SIRT3.	NAD	162-168	sirtuin 3	Homo sapiens	192-197
20495288-9	2010	Therefore, the increase in the 1-methylnicotinamide level found when IFN-gamma is present in culture may be a consequence of increases in both the nicotinamide concentration and NNMT activity, whereas, 1-methylnicotinamide did not influence nicotinamide levels, NAD(+) levels, or cell viability per se.	NAD	262-268	interferon gamma	Homo sapiens	69-78
20423305-3	2010	Multiple studies have also suggested that NAD+ depletion mediates PARP-1 cytotoxicity, and NAD+ administration can decrease ischemic brain injury.	NAD	42-46	poly(ADP-ribose) polymerase 1	Homo sapiens	66-72
20423305-8	2010	It is increasingly likely that future studies on NAD- and NADP-dependent enzymes, such as NADPH oxidase, PARP-1, and sirtuins, would expose novel mechanisms underlying the roles of oxidative stress in cerebral ischemia, and suggest new therapeutic strategies for treating the debilitating disease.	NAD	49-52	poly(ADP-ribose) polymerase 1	Homo sapiens	105-111
20495288-5	2010	To clarify the mechanisms by which IFN-gamma increases 1-methylnicotinamide levels in these cells, we measured NNMT activity and the levels of NNMT expression, nicotinamide and nicotinamide adenine dinucleotide (NAD(+)) in the presence and absence of IFN-gamma.	NAD	212-218	interferon gamma	Homo sapiens	35-44
19682970-1	2009	Sirtuins are nicotinamide adenine dinucleotide (NAD(+))-dependent deacetylases that catalyze the deacetylation of proteins such as histones and p53.	NAD	13-46	tumor protein p53	Homo sapiens	144-147
19913571-5	2010	Exercise training induced SIRT1 activity due to the positive effect of exercise on the activity of nicotinamide phosphoribosyltransferase (NAMPT) and thereby the production of sirtuin-fueling NAD(+).	NAD	192-198	sirtuin 1	Rattus norvegicus	26-31
19913571-9	2010	Regular exercise decelerates the deleterious effects of the aging process via SIRT1-dependent pathways through the stimulation of NAD(+) biosynthesis by NAMPT.	NAD	130-136	sirtuin 1	Rattus norvegicus	78-83
19833096-4	2009	These effects were associated with decreased 8-iso-prostaglandin F(2alpha) and peroxynitrite formation, enhanced protein expression of NAD(+)-dependent class III histone deacetylase sirtuin (SIRT) 1, and downregulated protein expression of histone senescence factor p53.	NAD	135-141	tumor protein p53	Homo sapiens	266-269
19916945-3	2009	Partial inhibition of the Top1-DNA-adduct formation upon addition of poly(ADP-ribose) polymerase 1 in the absence of NAD+ was shown, whereas in the presence of NAD+ formation of a high molecular weight product, most likely corresponding to poly(ADP)-ribosylated Top1-DNA adduct, was observed.	NAD	117-121	poly(ADP-ribose) polymerase 1	Homo sapiens	69-98
19389396-1	2009	Poly(ADP-ribose) polymerases (PARPs) convert NAD to polymers of ADP-ribose that are converted to free ADP-ribose by poly(ADP-ribose) glycohydrolase (PARG).	NAD	45-48	poly(ADP-ribose) polymerase 1	Homo sapiens	30-35
19389396-1	2009	Poly(ADP-ribose) polymerases (PARPs) convert NAD to polymers of ADP-ribose that are converted to free ADP-ribose by poly(ADP-ribose) glycohydrolase (PARG).	NAD	45-48	poly(ADP-ribose) glycohydrolase	Homo sapiens	116-147
19389396-1	2009	Poly(ADP-ribose) polymerases (PARPs) convert NAD to polymers of ADP-ribose that are converted to free ADP-ribose by poly(ADP-ribose) glycohydrolase (PARG).	NAD	45-48	poly(ADP-ribose) glycohydrolase	Homo sapiens	149-153
19801639-6	2009	In the presence of typical aldehyde substrates or NADH, AO reduced nitrite to NO.	NAD	50-54	aldehyde oxidase 1	Homo sapiens	56-58
19801639-9	2009	Under aerobic conditions with the FAD site-binding substrate, NADH, AO-mediated NO production was largely maintained, although with aldehyde substrates oxygen-dependent inhibition was seen.	NAD	62-66	aldehyde oxidase 1	Homo sapiens	68-70
19729610-6	2009	Mice treated with the ERbeta-specific agonist, DPN had no effect on uterine weight but a 28% decrease in aortic lesion area in HSP27(o/e)apoE(-/-) compared to apoE(-/-) mice.	NAD	47-50	apolipoprotein E	Mus musculus	137-141
19936064-7	2009	We demonstrate that upregulation of the NAD(+)-degrading enzyme poly-(ADP-ribose)-polymerase (PARP) by activated T cells enhances their susceptibility to NAD(+) depletion.	NAD	40-46	poly(ADP-ribose) polymerase 1	Homo sapiens	64-92
19936064-7	2009	We demonstrate that upregulation of the NAD(+)-degrading enzyme poly-(ADP-ribose)-polymerase (PARP) by activated T cells enhances their susceptibility to NAD(+) depletion.	NAD	40-46	poly(ADP-ribose) polymerase 1	Homo sapiens	94-98
19936064-7	2009	We demonstrate that upregulation of the NAD(+)-degrading enzyme poly-(ADP-ribose)-polymerase (PARP) by activated T cells enhances their susceptibility to NAD(+) depletion.	NAD	154-160	poly(ADP-ribose) polymerase 1	Homo sapiens	64-92
19936064-7	2009	We demonstrate that upregulation of the NAD(+)-degrading enzyme poly-(ADP-ribose)-polymerase (PARP) by activated T cells enhances their susceptibility to NAD(+) depletion.	NAD	154-160	poly(ADP-ribose) polymerase 1	Homo sapiens	94-98
19855187-2	2009	NAD(+) also serves as a substrate for cellular enzymes, including poly (ADPribose) polymerase (PARP)-1 and Sirt1.	NAD	0-6	poly(ADP-ribose) polymerase 1	Homo sapiens	95-102
19855187-3	2009	Activation of PARP-1 by DNA damage depletes the cellular pool of NAD(+), leading to necrotic cell death.	NAD	65-71	poly(ADP-ribose) polymerase 1	Homo sapiens	14-20
19843166-1	2009	The enzyme alpha-amino-beta-carboxymuconate-epsilon-semialdehyde decarboxylase (ACMSD) is a zinc-dependent amidohydrolase that participates in picolinic acid (PA), quinolinic acid (QA) and NAD homeostasis.	NAD	189-192	aminocarboxymuconate semialdehyde decarboxylase	Homo sapiens	80-85
19744494-10	2009	Oxidative efficiency was also enhanced with SERCA1 as cytosolic NADH transport into the mitochondria was significantly greater compared to the PBS group.	NAD	64-68	ATPase sarcoplasmic/endoplasmic reticulum Ca2+ transporting 1	Rattus norvegicus	44-50
19744494-12	2009	These data demonstrate that metabolic coupling and NADH transport are significantly improved with SERCA1 treatment.	NAD	51-55	ATPase sarcoplasmic/endoplasmic reticulum Ca2+ transporting 1	Rattus norvegicus	98-104
19838201-5	2009	The expression of several forkhead box O1 (Foxo1) target genes increased in the DKO liver, including heme oxygenase-1 (Hmox1), which disrupts complex III and IV of the respiratory chain and lowers the NAD(+)/NADH ratio and ATP production.	NAD	201-207	heme oxygenase 1	Mus musculus	101-117
19838201-5	2009	The expression of several forkhead box O1 (Foxo1) target genes increased in the DKO liver, including heme oxygenase-1 (Hmox1), which disrupts complex III and IV of the respiratory chain and lowers the NAD(+)/NADH ratio and ATP production.	NAD	201-207	heme oxygenase 1	Mus musculus	119-124
19838201-5	2009	The expression of several forkhead box O1 (Foxo1) target genes increased in the DKO liver, including heme oxygenase-1 (Hmox1), which disrupts complex III and IV of the respiratory chain and lowers the NAD(+)/NADH ratio and ATP production.	NAD	208-212	heme oxygenase 1	Mus musculus	101-117
19838201-5	2009	The expression of several forkhead box O1 (Foxo1) target genes increased in the DKO liver, including heme oxygenase-1 (Hmox1), which disrupts complex III and IV of the respiratory chain and lowers the NAD(+)/NADH ratio and ATP production.	NAD	208-212	heme oxygenase 1	Mus musculus	119-124
19757771-3	2009	Successful integration of pentose phosphate, nicotinamide adenine dinucleotide biosynthesis, and cofactor recycling pathways with poly(ADP-ribose) polymerase-1 permitted labeling of PAR from (13)C-glucose and (13)C, (15)N-ATP in a single pot reaction.	NAD	45-78	poly(ADP-ribose) polymerase 1	Homo sapiens	130-159
19596275-5	2009	Only DPN administration regulated expression of AMPA receptor subunits GluR2 and GluR3, increasing and decreasing levels respectively.	NAD	5-8	glutamate ionotropic receptor AMPA type subunit 2	Rattus norvegicus	71-76
19764761-2	2009	Stimulated by binding to nicked DNA, PARP-1 catalyzes poly(ADP-ribosyl)ation of the acceptor proteins and itself using NAD(+) as a substrate.	NAD	119-125	poly(ADP-ribose) polymerase 1	Homo sapiens	37-43
19666841-7	2009	Because the enzymatic step catalyzed by GPD1L depends upon nicotinamide adenine dinucleotide, this GPD1L pathway links the metabolic state of the cell to I(Na) and excitability and may be important more generally in cardiac ischemia and heart failure.	NAD	59-92	glycerol-3-phosphate dehydrogenase 1 like	Homo sapiens	40-45
19666841-7	2009	Because the enzymatic step catalyzed by GPD1L depends upon nicotinamide adenine dinucleotide, this GPD1L pathway links the metabolic state of the cell to I(Na) and excitability and may be important more generally in cardiac ischemia and heart failure.	NAD	59-92	glycerol-3-phosphate dehydrogenase 1 like	Homo sapiens	99-104
19507198-1	2009	Saccharomyces cerevisiae NAD(H)-dependent 2,3-butanediol dehydrogenase (Bdh1), a medium chain dehydrogenase/reductase is the main enzyme catalyzing the reduction of acetoin to 2,3-butanediol.	NAD	25-31	(R,R)-butanediol dehydrogenase	Saccharomyces cerevisiae S288C	72-76
19507198-2	2009	In this work we focused on altering the coenzyme specificity of Bdh1 from NAD(H) to NADP(H).	NAD	74-80	(R,R)-butanediol dehydrogenase	Saccharomyces cerevisiae S288C	64-68
19507198-5	2009	The performance of the triple mutant for NADPH was close to that of native Bdh1 for NADH.	NAD	84-88	(R,R)-butanediol dehydrogenase	Saccharomyces cerevisiae S288C	75-79
19529948-3	2009	Overactivation of PARP-1 depletes NAD(+) and ATP, resulting in necrosis.	NAD	34-40	poly(ADP-ribose) polymerase 1	Homo sapiens	18-24
19596275-5	2009	Only DPN administration regulated expression of AMPA receptor subunits GluR2 and GluR3, increasing and decreasing levels respectively.	NAD	5-8	glutamate ionotropic receptor AMPA type subunit 3	Rattus norvegicus	81-86
19596275-6	2009	DPN also increased GluR2 expression in the other lamina of the CA1.	NAD	0-3	glutamate ionotropic receptor AMPA type subunit 2	Rattus norvegicus	19-24
19645416-1	2009	The tricarboxylic acid cycle NAD+-specific isocitrate dehydrogenase (IDH) of Saccharomyces cerevisiae is an octameric enzyme composed of four heterodimers of regulatory IDH1 and catalytic IDH2 subunits.	NAD	29-33	isocitrate dehydrogenase (NAD(+)) IDH1	Saccharomyces cerevisiae S288C	169-173
19618916-2	2009	The reactions of the catalytic cycle of the dimeric quinone reductase Lot6p from Saccharomyces cerevisiae were studied in anaerobic stopped-flow experiments at 4 degrees C. Both NADH and NADPH reacted similarly, reducing the FMN prosthetic group rapidly at saturation but binding with very low affinity.	NAD	178-182	flavin-dependent quinone reductase	Saccharomyces cerevisiae S288C	70-75
19615521-5	2009	The assay condition was optimized in terms of the conversion of 3HB-G into NADH by the enzymatic reactors when the reaction solution containing 3HB-G generated from 3HB-GGG (after the incubation with ACE) was repetitively injected into the FIA system.	NAD	75-79	angiotensin I converting enzyme	Homo sapiens	200-203
19555662-0	2009	Transcriptional activation of NAD+-dependent protein deacetylase SIRT1 by nuclear receptor TLX.	NAD	30-34	CD46 molecule	Homo sapiens	91-94
19661458-0	2009	Nicotinamide phosphoribosyltransferase regulates cell survival through NAD+ synthesis in cardiac myocytes.	NAD	71-75	nicotinamide phosphoribosyltransferase	Mus musculus	0-38
19506862-6	2009	Then, the genes encoding the NADH- and the NADPH-dependent HMF reductases, ADH1-S110P-Y295C and ADH6, respectively, were individually overexpressed in this background.	NAD	29-33	alcohol dehydrogenase ADH1	Saccharomyces cerevisiae S288C	75-79
19556422-1	2009	Human 17beta-hydroxysteroid dehydrogenase types 1 and 2 (17betaHSD1 and 17betaHSD2) regulate estrogen potency by catalyzing the interconversion of estrone (E1) and estradiol (E2) using nicotinamide adenine dinucleotide (phosphate) cofactors NAD(P)(H).	NAD	185-218	hydroxysteroid 17-beta dehydrogenase 1	Homo sapiens	57-67
19556422-5	2009	The shift to E2 oxidation parallels changes in apparent K(m) values for purified 17betaHSD1 proteins to favor NAD(H) over NADP(H).	NAD	110-116	hydroxysteroid 17-beta dehydrogenase 1	Homo sapiens	81-91
19666485-4	2009	Alc1 ATPase and chromatin remodeling activities are strongly activated by Parp1 and its substrate NAD and require an intact macrodomain capable of binding poly(ADP-ribose).	NAD	98-101	poly(ADP-ribose) polymerase 1	Homo sapiens	74-79
19344310-0	2009	Overexpression of the malate-aspartate NADH shuttle member Aralar1 in the clonal beta-cell line BRIN-BD11 enhances amino-acid-stimulated insulin secretion and cell metabolism.	NAD	39-43	insulin	Homo sapiens	137-144
19827131-1	2009	Previous studies have demonstrated that the NADH-dependent cytochrome b(5) electron transfer pathway can support some cytochrome P450 monooxygenases in vitro in the absence of their normal redox partner, NADPH-cytochrome P450 oxidoreductase.	NAD	44-48	cytochrome b, mitochondrial	Mus musculus	59-71
19587098-2	2009	In this study, we analyzed transgenic Arabidopsis (Arabidopsis thaliana) plants that overexpress NAD kinase2 (NADK2), an enzyme that catalyzes the synthesis of NADP from NAD in chloroplasts, to investigate the impacts of altering NADP level on plant metabolism.	NAD	97-100	NAD kinase 2	Arabidopsis thaliana	110-115
19661458-4	2009	OBJECTIVE: Here we investigated the role of Nampt in mediating NAD+ synthesis in cardiac myocytes and the function of Nampt in the heart in vivo.	NAD	63-67	nicotinamide phosphoribosyltransferase	Mus musculus	44-49
19661458-6	2009	Upregulation of Nampt significantly increased NAD+ and ATP concentrations, whereas downregulation of Nampt significantly decreased them.	NAD	46-50	nicotinamide phosphoribosyltransferase	Mus musculus	16-21
19661458-9	2009	Cardiac-specific overexpression of Nampt in transgenic mice increased NAD+ content in the heart, prevented downregulation of Nampt, and reduced the size of myocardial infarction and apoptosis in response to prolonged ischemia and ischemia/reperfusion.	NAD	70-74	nicotinamide phosphoribosyltransferase	Mus musculus	35-40
19661458-10	2009	CONCLUSIONS: Nampt critically regulates NAD+ and ATP contents, thereby playing an essential role in mediating cell survival by inhibiting apoptosis and stimulating autophagic flux in cardiac myocytes.	NAD	40-44	nicotinamide phosphoribosyltransferase	Mus musculus	13-18
19723034-1	2009	Poly(ADP-ribose) polymerase-1 (PARP-1) uses NAD(+) as a substrate to form ADP-ribose.	NAD	44-50	poly(ADP-ribose) polymerase 1	Homo sapiens	0-29
19531481-4	2009	Here we identify PARP1, a DNA-binding protein with an NAD+-dependent enzymatic activity, as a cofactor of Oct4 and Sox2 to regulate expression of their target gene FGF4.	NAD	54-58	poly(ADP-ribose) polymerase 1	Homo sapiens	17-22
19531481-4	2009	Here we identify PARP1, a DNA-binding protein with an NAD+-dependent enzymatic activity, as a cofactor of Oct4 and Sox2 to regulate expression of their target gene FGF4.	NAD	54-58	fibroblast growth factor 4	Homo sapiens	164-168
19723034-1	2009	Poly(ADP-ribose) polymerase-1 (PARP-1) uses NAD(+) as a substrate to form ADP-ribose.	NAD	44-50	poly(ADP-ribose) polymerase 1	Homo sapiens	31-37
19723034-2	2009	During apoptosis, caspases cleave PARP-1 to avoid excessive NAD consumption.	NAD	60-63	poly(ADP-ribose) polymerase 1	Homo sapiens	34-40
19519662-5	2009	Our results demonstrate that receptor-internalizing agonists (like DAMGO, beta-endorphin, methadone, piritramide, fentanyl, sufentanil, and etonitazene) strongly induce NADH/NADPH-mediated ROS synthesis via PLD-dependent signaling pathways, whereas agonists that do not induce MOPr endocytosis and PLD2 activation (like morphine, buprenorphine, hydromorphone, and oxycodone) failed to activate ROS synthesis in transfected human embryonic kidney 293 cells.	NAD	169-173	glycosylphosphatidylinositol specific phospholipase D1	Homo sapiens	207-210
19433264-6	2009	Further investigation confirmed that decreases in intracellular NAD(P)H in PCB-treated MDA cells are primarily due to reduction in intracellular NAD(+) pool mediated by poly(ADP-ribose)polymerase-1 activation through formation of DNA strand breaks.	NAD	145-151	pyruvate carboxylase	Homo sapiens	75-78
19578370-2	2009	Here we show that the acetyltransferase MOF (males absent on the first) acetylates TIP5, the largest subunit of NoRC, at a single lysine residue, K633, adjacent to the TIP5 RNA-binding domain, and that the NAD(+)-dependent deacetylase SIRT1 (sirtuin-1) removes the acetyl group from K633.	NAD	206-212	bromodomain adjacent to zinc finger domain 2A	Homo sapiens	83-87
19578370-2	2009	Here we show that the acetyltransferase MOF (males absent on the first) acetylates TIP5, the largest subunit of NoRC, at a single lysine residue, K633, adjacent to the TIP5 RNA-binding domain, and that the NAD(+)-dependent deacetylase SIRT1 (sirtuin-1) removes the acetyl group from K633.	NAD	206-212	bromodomain adjacent to zinc finger domain 2A	Homo sapiens	168-172
19376176-2	2009	The relationship between PARP activity and the intracellular concentration of its substrate nicotinamide adenine dinucleotide (NAD) is also investigated.	NAD	92-125	poly(ADP-ribose) polymerase 1	Homo sapiens	25-29
19362586-1	2009	Poly(ADP-ribose) polymerases (PARPs) are defined as cell signaling enzymes that catalyze the transfer of ADP-ribose units from NAD(+) to a number of acceptor proteins.	NAD	127-133	poly(ADP-ribose) polymerase 1	Homo sapiens	30-35
19376176-2	2009	The relationship between PARP activity and the intracellular concentration of its substrate nicotinamide adenine dinucleotide (NAD) is also investigated.	NAD	127-130	poly(ADP-ribose) polymerase 1	Homo sapiens	25-29
19376176-10	2009	An inverse relationship between PARP activity and NAD content was also observed.	NAD	50-53	poly(ADP-ribose) polymerase 1	Homo sapiens	32-36
19487957-5	2009	However, when NKA activity of the alpha1beta1 isoform was measured in membrane preparations from human kidney (reduced form of nicotinamide adenine dinucleotide-coupled assay, n = 3), a concentration-dependent full inhibition of the activity was induced by 8-methoxycoumestrol (IC50: 90 +/- 97 nM), similar to that observed for classical cardiac glycosides digitoxin, digoxin, methyldigoxin, and beta-acetyldigoxin (IC50 = 287 +/- 190 nM, 409 +/- 171 nM, 282 +/- 482 nM, 587 +/- 135 nM, P &gt; 0.05).	NAD	127-160	tachykinin precursor 1	Homo sapiens	14-17
19526301-5	2009	We have shown that the NMDA ion channel blockers, MK801 and memantine, and the nitric oxide synthase (NOS) inhibitor, L-NAME, significantly attenuate QUIN-mediated PARP activation, NAD(+) depletion, and LDH release in both neurons and astrocytes.	NAD	181-187	nitric oxide synthase 2	Homo sapiens	79-100
19542469-0	2009	Differential regulation of P2X7 receptor activation by extracellular nicotinamide adenine dinucleotide and ecto-ADP-ribosyltransferases in murine macrophages and T cells.	NAD	69-102	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	27-40
19542469-1	2009	Extracellular NAD induces the ATP-independent activation of the ionotropic P2X(7) purinergic receptor (P2X(7)R) in murine T lymphocytes via a novel covalent pathway involving ADP-ribosylation of arginine residues on the P2X(7)R ectodomain.	NAD	14-17	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	75-101
19542469-1	2009	Extracellular NAD induces the ATP-independent activation of the ionotropic P2X(7) purinergic receptor (P2X(7)R) in murine T lymphocytes via a novel covalent pathway involving ADP-ribosylation of arginine residues on the P2X(7)R ectodomain.	NAD	14-17	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	103-110
19542469-1	2009	Extracellular NAD induces the ATP-independent activation of the ionotropic P2X(7) purinergic receptor (P2X(7)R) in murine T lymphocytes via a novel covalent pathway involving ADP-ribosylation of arginine residues on the P2X(7)R ectodomain.	NAD	14-17	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	220-227
19542469-4	2009	Thus, we tested the hypothesis that extracellular NAD acts via ART2.1 to regulate P2X(7)R function in murine macrophages.	NAD	50-53	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	82-89
19542469-7	2009	Rather, NAD potentiated ATP-dependent P2X(7)R activation as indicated by a left shift in the ATP dose-response relationship.	NAD	8-11	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	38-45
19542469-8	2009	Thus, extracellular NAD regulates the P2X(7)R in both macrophages and T cells but via distinct mechanisms.	NAD	20-23	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	38-45
19542469-10	2009	These findings indicate that extracellular NAD and ATP can act synergistically to regulate P2X(7)R signaling in murine macrophages and also suggest that the cellular context in which P2X(7)R signaling occurs differs between myeloid and lymphoid leukocytes.	NAD	43-46	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	91-98
19542469-10	2009	These findings indicate that extracellular NAD and ATP can act synergistically to regulate P2X(7)R signaling in murine macrophages and also suggest that the cellular context in which P2X(7)R signaling occurs differs between myeloid and lymphoid leukocytes.	NAD	43-46	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	183-190
19185388-13	2009	Our results suggest that induction of NADH-GOGAT, NADH-GDH, AlaAT, and AspAT activities may compensate for the reduced Fd-GOGAT activity and serve as an alternative means of glutamate synthesis in wheat shoots under Ni stress.	NAD	38-42	aspartate aminotransferase, cytoplasmic	Triticum aestivum	71-76
19411252-1	2009	Upon massive DNA damage, hyperactivation of the nuclear enzyme poly(ADP-ribose) polymerase (PARP)-1 causes severe depletion of intracellular NAD and ATP pools as well as mitochondrial dysfunction.	NAD	141-144	poly(ADP-ribose) polymerase 1	Homo sapiens	63-99
19426698-7	2009	NMN increases in cells undergoing hyperactivation of the NAD-consuming enzyme poly(ADP-ribose) polymerase (PARP)-1, or exposed to gallotannin, a putative inhibitor of NMN-adenylyl transferases.	NAD	57-60	poly(ADP-ribose) polymerase 1	Homo sapiens	78-114
19372272-1	2009	Poly(ADP-ribose) polymerase 1 (PARP1) synthesizes poly(ADP-ribose) (PAR) using nicotinamide adenine dinucleotide (NAD) as a substrate.	NAD	79-112	poly(ADP-ribose) polymerase 1	Homo sapiens	0-29
19372272-1	2009	Poly(ADP-ribose) polymerase 1 (PARP1) synthesizes poly(ADP-ribose) (PAR) using nicotinamide adenine dinucleotide (NAD) as a substrate.	NAD	79-112	poly(ADP-ribose) polymerase 1	Homo sapiens	31-36
19372272-1	2009	Poly(ADP-ribose) polymerase 1 (PARP1) synthesizes poly(ADP-ribose) (PAR) using nicotinamide adenine dinucleotide (NAD) as a substrate.	NAD	114-117	poly(ADP-ribose) polymerase 1	Homo sapiens	0-29
19372272-1	2009	Poly(ADP-ribose) polymerase 1 (PARP1) synthesizes poly(ADP-ribose) (PAR) using nicotinamide adenine dinucleotide (NAD) as a substrate.	NAD	114-117	poly(ADP-ribose) polymerase 1	Homo sapiens	31-36
19372272-5	2009	The DNA-dependent interaction between the amino-terminal DNA-binding domain and the catalytic domain of PARP1 increased V(max) and decreased the K(m) for NAD.	NAD	154-157	poly(ADP-ribose) polymerase 1	Homo sapiens	104-109
19255877-1	2009	The homotrimeric P2X7 purinergic receptor has sparked interest because of its capacity to sense adenosine triphosphate (ATP) and nicotinamide adenine dinucleotide (NAD) released from cells and to induce calcium signaling and cell death.	NAD	129-162	purinergic receptor P2X 7	Homo sapiens	17-21
19255877-1	2009	The homotrimeric P2X7 purinergic receptor has sparked interest because of its capacity to sense adenosine triphosphate (ATP) and nicotinamide adenine dinucleotide (NAD) released from cells and to induce calcium signaling and cell death.	NAD	164-167	purinergic receptor P2X 7	Homo sapiens	17-21
19426698-9	2009	Importantly, NMN reduces NAD and ATP depletion in cells undergoing PARP-1 hyperactivation, significantly delaying cell death.	NAD	25-28	poly(ADP-ribose) polymerase 1	Homo sapiens	67-73
19299582-2	2009	Sirtuin 1 (SIRT1) is an NAD(+)-dependent class III protein deacetylase that is known to be involved in regulating production of proinflammatory cytokines including TNF-alpha.	NAD	24-30	sirtuin 1	Rattus norvegicus	0-9
20157531-2	2009	Reactive oxygen species, responsible for the most plausible and currently acceptable global mechanism to explain the aging process, strongly activate the enzymatic activity of PARP1 and the formation of poly(ADP-ribose) (PAR) from NAD(+).	NAD	231-237	poly(ADP-ribose) polymerase 1	Homo sapiens	176-181
20157531-3	2009	Consumption of NAD(+) links PARP1 to energy metabolism and to a large number of NAD(+)-dependent enzymes, such as the sirtuins.	NAD	15-21	poly(ADP-ribose) polymerase 1	Homo sapiens	28-33
19430704-3	2009	The characterization of the purified GAPDH reveals that the native enzyme is a homotetramer of ~150 kDa with an absolute specificity for the oxidized form of nicotinamide adenine dinucleotide (NAD(+)).	NAD	158-191	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	37-42
19430704-3	2009	The characterization of the purified GAPDH reveals that the native enzyme is a homotetramer of ~150 kDa with an absolute specificity for the oxidized form of nicotinamide adenine dinucleotide (NAD(+)).	NAD	193-199	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	37-42
19430704-6	2009	The kinetic parameters were also calculated: the Vmax was 4.3 U/mg and the Km values against G3P and NAD(+) were 20.7 and 17.8 muM, respectively.	NAD	101-107	latexin	Homo sapiens	127-130
19299582-2	2009	Sirtuin 1 (SIRT1) is an NAD(+)-dependent class III protein deacetylase that is known to be involved in regulating production of proinflammatory cytokines including TNF-alpha.	NAD	24-30	sirtuin 1	Rattus norvegicus	11-16
19299582-2	2009	Sirtuin 1 (SIRT1) is an NAD(+)-dependent class III protein deacetylase that is known to be involved in regulating production of proinflammatory cytokines including TNF-alpha.	NAD	24-30	tumor necrosis factor	Rattus norvegicus	164-173
19264808-5	2009	ER alpha and ER beta agonists PPT and DPN inhibited and 4-OHT increased miR-21 expression.	NAD	38-41	estrogen receptor 1	Homo sapiens	0-8
19329666-3	2009	Acetoin is reduced to 2,3-butanediol by the NADH-dependent 2,3-butanediol dehydrogenase Bdh1.	NAD	44-48	(R,R)-butanediol dehydrogenase	Saccharomyces cerevisiae S288C	88-92
19329666-4	2009	In order to investigate the influence of potential factors limiting this reaction, we overexpressed BDH1, coding for native NADH-dependent Bdh1, and the engineered gene BDH1(221,222,223), coding for an NADPH-dependent Bdh1 enzyme with the amino acid changes 221 EIA 223 to 221 SRS 223, in a glycerol-overproducing wine yeast.	NAD	124-128	(R,R)-butanediol dehydrogenase	Saccharomyces cerevisiae S288C	139-143
19426673-4	2009	In all cases, PARP-1 inhibition leads to suppressed poly-ADP-ribosylation of nuclear proteins, prevention of NAD(+) depletion and significant resistance against taxol induced caspase-3 activation and apoptotic cell death.	NAD	109-115	poly(ADP-ribose) polymerase 1	Homo sapiens	14-20
19297586-8	2009	AAO4 is able to oxidize BD without NAD(+), but its activity increases by 50% when this cofactor is added.	NAD	35-41	aldehyde oxidase 4	Arabidopsis thaliana	0-4
19286518-0	2009	Circadian control of the NAD+ salvage pathway by CLOCK-SIRT1.	NAD	25-29	circadian locomotor output cycles kaput	Mus musculus	49-54
19286518-2	2009	We have shown that the core circadian regulator, CLOCK, is a histone acetyltransferase whose activity is counterbalanced by the nicotinamide adenine dinucleotide (NAD+)-dependent histone deacetylase SIRT1.	NAD	128-161	circadian locomotor output cycles kaput	Mus musculus	49-54
19286518-2	2009	We have shown that the core circadian regulator, CLOCK, is a histone acetyltransferase whose activity is counterbalanced by the nicotinamide adenine dinucleotide (NAD+)-dependent histone deacetylase SIRT1.	NAD	163-167	circadian locomotor output cycles kaput	Mus musculus	49-54
19286518-3	2009	Here we show that intracellular NAD+ levels cycle with a 24-hour rhythm, an oscillation driven by the circadian clock.	NAD	32-36	circadian locomotor output cycles kaput	Mus musculus	112-117
19286518-4	2009	CLOCK:BMAL1 regulates the circadian expression of NAMPT (nicotinamide phosphoribosyltransferase), an enzyme that provides a rate-limiting step in the NAD+ salvage pathway.	NAD	150-154	circadian locomotor output cycles kaput	Mus musculus	0-5
19286518-4	2009	CLOCK:BMAL1 regulates the circadian expression of NAMPT (nicotinamide phosphoribosyltransferase), an enzyme that provides a rate-limiting step in the NAD+ salvage pathway.	NAD	150-154	nicotinamide phosphoribosyltransferase	Mus musculus	50-55
19286518-4	2009	CLOCK:BMAL1 regulates the circadian expression of NAMPT (nicotinamide phosphoribosyltransferase), an enzyme that provides a rate-limiting step in the NAD+ salvage pathway.	NAD	150-154	nicotinamide phosphoribosyltransferase	Mus musculus	57-95
19217932-4	2009	Increased NAD(P)H fluorescence in CA1 neurons during hypoxia and demonstration that NADH manipulation increases [Ca2+](i) in an IP3R-dependent manner revealed a primary role of cellular redox state in liberation of Ca2+ from the ER.	NAD	84-88	carbonic anhydrase 2	Rattus norvegicus	113-116
19217932-4	2009	Increased NAD(P)H fluorescence in CA1 neurons during hypoxia and demonstration that NADH manipulation increases [Ca2+](i) in an IP3R-dependent manner revealed a primary role of cellular redox state in liberation of Ca2+ from the ER.	NAD	84-88	carbonic anhydrase 2	Rattus norvegicus	215-218
19217932-6	2009	We conclude that the endoplasmic reticulum, acting via redox/NADH-dependent intracellular Ca2+ store release, is an important mediator of the neuroprotective response to hypoxic stress.	NAD	61-65	carbonic anhydrase 2	Rattus norvegicus	90-93
19460292-1	2009	Poly(ADP-ribose) polymerase (PARP) is an intracellular enzyme involved in DNA repair and in building poly-ADP-ribose polymers on nuclear proteins using NAD(+).	NAD	152-158	poly(ADP-ribose) polymerase 1	Homo sapiens	0-27
19188449-1	2009	The NAD(+)-dependent histone deacetylase hSirT1 regulates cell survival and stress responses by inhibiting p53-, NF-kappaB-, and E2F1-dependent transcription.	NAD	4-10	tumor protein p53	Homo sapiens	107-110
19460292-1	2009	Poly(ADP-ribose) polymerase (PARP) is an intracellular enzyme involved in DNA repair and in building poly-ADP-ribose polymers on nuclear proteins using NAD(+).	NAD	152-158	poly(ADP-ribose) polymerase 1	Homo sapiens	29-33
19460292-10	2009	The KGDH enzyme may, therefore, have a novel function as a PARP-like enzyme, which may play a role in regulating intramitochondrial NAD(+) and poly(ADP-ribose) homeostasis, with possible roles in physiology and pathophysiology.	NAD	132-138	poly(ADP-ribose) polymerase 1	Homo sapiens	59-63
19071213-1	2009	Resveratrol increases longevity through SirT1, which is activated with NAD(+) supplied by an anti-aging enzyme PBEF.	NAD	71-77	sirtuin 1	Rattus norvegicus	40-45
19234185-0	2009	NAD+ and ATP released from injured cells induce P2X7-dependent shedding of CD62L and externalization of phosphatidylserine by murine T cells.	NAD	0-4	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	48-52
19160423-6	2009	Kaempferol treatment increased the expression and the mitochondria localization of the NAD-dependent deacetylase SIRT3.	NAD	87-90	sirtuin 3	Homo sapiens	113-118
19234185-0	2009	NAD+ and ATP released from injured cells induce P2X7-dependent shedding of CD62L and externalization of phosphatidylserine by murine T cells.	NAD	0-4	selectin, lymphocyte	Mus musculus	75-80
19234185-3	2009	Although ATP acts as a soluble ligand to activate P2X(7), gating of P2X(7) by NAD(+) requires ecto-ADP-ribosyltransferase ART2.2-catalyzed transfer of the ADP-ribose moiety from NAD(+) onto Arg125 of P2X(7).	NAD	178-184	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	68-74
19234185-4	2009	Steady-state concentrations of NAD(+) and ATP in extracellular compartments are highly regulated and usually are well below the threshold required for activating P2X(7).	NAD	31-37	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	162-168
19234185-1	2009	Extracellular NAD(+) and ATP trigger the shedding of CD62L and the externalization of phosphatidylserine on murine T cells.	NAD	14-20	selectin, lymphocyte	Mus musculus	53-58
19234185-6	2009	We show that lysis of erythrocytes releases sufficient levels of NAD(+) and ATP to induce activation of P2X(7).	NAD	65-71	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	104-110
19234185-3	2009	Although ATP acts as a soluble ligand to activate P2X(7), gating of P2X(7) by NAD(+) requires ecto-ADP-ribosyltransferase ART2.2-catalyzed transfer of the ADP-ribose moiety from NAD(+) onto Arg125 of P2X(7).	NAD	78-84	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	50-56
19234185-8	2009	We further show that the routine preparation of primary lymph node and spleen cells induces the release of NAD(+) in sufficient concentrations for ART2.2 to ADP-ribosylate P2X(7), even at 4 degrees C. Gating of P2X(7) occurs when T cells are returned to 37 degrees C, rapidly inducing CD62L-shedding and PS-externalization by a substantial fraction of the cells.	NAD	107-113	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	172-178
19234185-8	2009	We further show that the routine preparation of primary lymph node and spleen cells induces the release of NAD(+) in sufficient concentrations for ART2.2 to ADP-ribosylate P2X(7), even at 4 degrees C. Gating of P2X(7) occurs when T cells are returned to 37 degrees C, rapidly inducing CD62L-shedding and PS-externalization by a substantial fraction of the cells.	NAD	107-113	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	211-217
19234185-3	2009	Although ATP acts as a soluble ligand to activate P2X(7), gating of P2X(7) by NAD(+) requires ecto-ADP-ribosyltransferase ART2.2-catalyzed transfer of the ADP-ribose moiety from NAD(+) onto Arg125 of P2X(7).	NAD	78-84	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	68-74
19234185-8	2009	We further show that the routine preparation of primary lymph node and spleen cells induces the release of NAD(+) in sufficient concentrations for ART2.2 to ADP-ribosylate P2X(7), even at 4 degrees C. Gating of P2X(7) occurs when T cells are returned to 37 degrees C, rapidly inducing CD62L-shedding and PS-externalization by a substantial fraction of the cells.	NAD	107-113	selectin, lymphocyte	Mus musculus	285-290
19234185-3	2009	Although ATP acts as a soluble ligand to activate P2X(7), gating of P2X(7) by NAD(+) requires ecto-ADP-ribosyltransferase ART2.2-catalyzed transfer of the ADP-ribose moiety from NAD(+) onto Arg125 of P2X(7).	NAD	78-84	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	68-74
19234185-3	2009	Although ATP acts as a soluble ligand to activate P2X(7), gating of P2X(7) by NAD(+) requires ecto-ADP-ribosyltransferase ART2.2-catalyzed transfer of the ADP-ribose moiety from NAD(+) onto Arg125 of P2X(7).	NAD	178-184	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	68-74
19049970-3	2009	This feature, associated with elevated cellular respiration and cytosolic ATP/ADP and NAD(+)/NADH ratios, was linked to a high expression and activity of mitochondrial glycerol-3-phosphate dehydrogenase.	NAD	86-92	glycerol-3-phosphate dehydrogenase 1	Rattus norvegicus	168-202
19052657-1	2009	Nicotinamide adenine dinucleotide (NAD(+)), a precursor of molecules involved in cell regulatory processes, is released in extra-cellular compartments after stress or inflammation.This study investigates the expression in the human cornea of CD38 and CD157, two NAD(+)-consuming ectoenzymes and surface receptors.	NAD	0-33	bone marrow stromal cell antigen 1	Homo sapiens	251-256
19052657-1	2009	Nicotinamide adenine dinucleotide (NAD(+)), a precursor of molecules involved in cell regulatory processes, is released in extra-cellular compartments after stress or inflammation.This study investigates the expression in the human cornea of CD38 and CD157, two NAD(+)-consuming ectoenzymes and surface receptors.	NAD	35-41	bone marrow stromal cell antigen 1	Homo sapiens	251-256
19049970-3	2009	This feature, associated with elevated cellular respiration and cytosolic ATP/ADP and NAD(+)/NADH ratios, was linked to a high expression and activity of mitochondrial glycerol-3-phosphate dehydrogenase.	NAD	93-97	glycerol-3-phosphate dehydrogenase 1	Rattus norvegicus	168-202
18848878-8	2009	The results suggest that NQO1 activity is more tightly coupled to the redox status of the NADPH/NADP(+) than NADH/NAD(+) redox pair, and that NADPH is the endogenous NQO1 electron donor.	NAD	109-113	NAD(P)H quinone dehydrogenase 1	Homo sapiens	25-29
19151729-0	2009	Intracellular NAD levels regulate tumor necrosis factor protein synthesis in a sirtuin-dependent manner.	NAD	14-17	tumor necrosis factor	Homo sapiens	34-55
19151729-3	2009	We show here that intracellular NAD concentration promotes TNF synthesis by activated immune cells.	NAD	32-35	tumor necrosis factor	Homo sapiens	59-62
19029946-3	2009	Furthermore, reduction of the FMN cofactor by either NADH or light irradiation results in the binding of the b-Zip transcription factor Yap4 to the Lot6-proteasome complex, indicating that recruitment of the transcription factor depends on the redox state of the quinone reductase.	NAD	53-57	flavin-dependent quinone reductase	Saccharomyces cerevisiae S288C	148-152
18848878-1	2009	The goal was to determine whether endogenous cytosolic NAD(P)H:quinone oxidoreductase 1 (NQO1) preferentially uses NADPH or NADH in intact pulmonary arterial endothelial cells in culture.	NAD	124-128	NAD(P)H quinone dehydrogenase 1	Homo sapiens	55-87
18848878-1	2009	The goal was to determine whether endogenous cytosolic NAD(P)H:quinone oxidoreductase 1 (NQO1) preferentially uses NADPH or NADH in intact pulmonary arterial endothelial cells in culture.	NAD	124-128	NAD(P)H quinone dehydrogenase 1	Homo sapiens	89-93
19060309-7	2009	Kinetic properties and sensitivity to 2-heptyl-4-hydroxyquinoline-N-oxide and aurachin C of NADH: ubiquinone reductase activity of Plasmodium NDH-II were similar to those of plant and fungus enzymes but it can oxidize NADPH and deamino-NADH.	NAD	92-96	DExH-box helicase 9	Homo sapiens	142-148
19151729-4	2009	Using a positive screen, we have identified Sirt6, a member of the sirtuin family, as the NAD-dependent enzyme able to regulate TNF production by acting at a post-transcriptional step.	NAD	90-93	tumor necrosis factor	Homo sapiens	128-131
18945963-4	2009	PlGF-mediated increased FLAP mRNA expression occurred via activation of phosphoinositide-3 (PI-3) kinase, nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, and hypoxia inducible factor-1alpha (HIF-1alpha).	NAD	106-139	placental growth factor	Homo sapiens	0-4
18945963-4	2009	PlGF-mediated increased FLAP mRNA expression occurred via activation of phosphoinositide-3 (PI-3) kinase, nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, and hypoxia inducible factor-1alpha (HIF-1alpha).	NAD	106-139	arachidonate 5-lipoxygenase activating protein	Homo sapiens	24-28
19273055-8	2009	A potential crosstalk between PARP1, PARP2 and other NAD+-dependent ADP-ribosyling enzymes such as Sirtuins and CD38 in cell death and survival pathways is discussed.	NAD	53-57	poly(ADP-ribose) polymerase 1	Homo sapiens	30-35
19055324-1	2008	ENOX (ECTO-NOX) proteins are growth-related cell surface proteins that catalyze both hydroquinone or NADH oxidation and protein disulfide-thiol interchange and exhibit both prion-like and time-keeping (clock) properties.	NAD	101-105	ecto-NOX disulfide-thiol exchanger 2	Homo sapiens	0-4
19273250-2	2009	For the past several years, studies on the mammalian NAD-dependent protein deacetylase SIRT1 and systemic NAD biosynthesis mediated by nicotinamide phosphoribosyltransferase (NAMPT) have demonstrated that these two regulatory components together play a critical role in the regulation of glucose homeostasis, particularly in the regulation of glucose-stimulated insulin secretion in pancreatic beta cells.	NAD	53-56	insulin	Homo sapiens	362-369
19273250-2	2009	For the past several years, studies on the mammalian NAD-dependent protein deacetylase SIRT1 and systemic NAD biosynthesis mediated by nicotinamide phosphoribosyltransferase (NAMPT) have demonstrated that these two regulatory components together play a critical role in the regulation of glucose homeostasis, particularly in the regulation of glucose-stimulated insulin secretion in pancreatic beta cells.	NAD	106-109	insulin	Homo sapiens	362-369
19273270-4	2009	Many macro domains, including those of the human histone macroH2A1.1, bind NAD metabolites such as ADP-ribose, suggesting that macro domains may function in the recognition of this and related molecules.	NAD	75-78	macroH2A.1 histone	Homo sapiens	49-68
19273109-1	2009	CD157 is a glycosylphosphatidylinositol-anchored molecule encoded by a member of the CD38/ADP-ribosyl cyclase gene family, involved in the metabolism of NAD.	NAD	153-156	bone marrow stromal cell antigen 1	Homo sapiens	0-5
19426866-3	2009	SIRT3 is therefore emerging as a metabolic sensor that responds to change in the energy status of the cell via NAD(+) and that modulates the activity of key metabolic enzymes via protein deacetylation.	NAD	111-117	sirtuin 3	Homo sapiens	0-5
18790050-9	2008	The binding of GAPDH to HCM significantly decreased after incubation with NAD+.	NAD	74-78	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	15-20
18954112-1	2008	Quinolinate phosphoribosyl transferase (QPRTase) is an essential enzyme that catalyzes the transformation of quinolinic acid (QA) to nicotinic acid mononucleotide (NAMN), a key step on the de novo pathway for nicotinamide adenine dinucleotide (NAD) biosynthesis.	NAD	209-242	quinolinate phosphoribosyltransferase	Homo sapiens	0-38
18954112-1	2008	Quinolinate phosphoribosyl transferase (QPRTase) is an essential enzyme that catalyzes the transformation of quinolinic acid (QA) to nicotinic acid mononucleotide (NAMN), a key step on the de novo pathway for nicotinamide adenine dinucleotide (NAD) biosynthesis.	NAD	209-242	quinolinate phosphoribosyltransferase	Homo sapiens	40-47
18954112-1	2008	Quinolinate phosphoribosyl transferase (QPRTase) is an essential enzyme that catalyzes the transformation of quinolinic acid (QA) to nicotinic acid mononucleotide (NAMN), a key step on the de novo pathway for nicotinamide adenine dinucleotide (NAD) biosynthesis.	NAD	244-247	quinolinate phosphoribosyltransferase	Homo sapiens	0-38
18954112-1	2008	Quinolinate phosphoribosyl transferase (QPRTase) is an essential enzyme that catalyzes the transformation of quinolinic acid (QA) to nicotinic acid mononucleotide (NAMN), a key step on the de novo pathway for nicotinamide adenine dinucleotide (NAD) biosynthesis.	NAD	244-247	quinolinate phosphoribosyltransferase	Homo sapiens	40-47
19016854-1	2008	Cytochrome c (cyto-c), added to isolated mitochondria, activates the oxidation of extramitochondrial NADH and the generation of a membrane potential, both linked to the activity of the cytosolic NADH/cyto-c electron transport pathway.	NAD	101-105	cytochrome c, somatic	Homo sapiens	0-12
19016854-1	2008	Cytochrome c (cyto-c), added to isolated mitochondria, activates the oxidation of extramitochondrial NADH and the generation of a membrane potential, both linked to the activity of the cytosolic NADH/cyto-c electron transport pathway.	NAD	101-105	cytochrome c, somatic	Homo sapiens	14-20
19016854-1	2008	Cytochrome c (cyto-c), added to isolated mitochondria, activates the oxidation of extramitochondrial NADH and the generation of a membrane potential, both linked to the activity of the cytosolic NADH/cyto-c electron transport pathway.	NAD	101-105	cytochrome c, somatic	Homo sapiens	200-206
19016854-1	2008	Cytochrome c (cyto-c), added to isolated mitochondria, activates the oxidation of extramitochondrial NADH and the generation of a membrane potential, both linked to the activity of the cytosolic NADH/cyto-c electron transport pathway.	NAD	195-199	cytochrome c, somatic	Homo sapiens	0-12
19016854-1	2008	Cytochrome c (cyto-c), added to isolated mitochondria, activates the oxidation of extramitochondrial NADH and the generation of a membrane potential, both linked to the activity of the cytosolic NADH/cyto-c electron transport pathway.	NAD	195-199	cytochrome c, somatic	Homo sapiens	14-20
19016854-1	2008	Cytochrome c (cyto-c), added to isolated mitochondria, activates the oxidation of extramitochondrial NADH and the generation of a membrane potential, both linked to the activity of the cytosolic NADH/cyto-c electron transport pathway.	NAD	195-199	cytochrome c, somatic	Homo sapiens	200-206
19016854-4	2008	We suggest that, in physiological low-amplitude swelling, magnesium ions may have the function, together with other factors, of modulating the amount of cyto-c molecules transferred from the mitochondrial intermembrane space into the cytosol, required for the correct execution of the apoptotic programme and/or the activation of the NADH/cyto-c electron transport pathway.	NAD	334-338	cytochrome c, somatic	Homo sapiens	153-159
18629638-11	2008	Recent findings suggest that several phytochemicals exhibit biphasic dose responses on cells with low doses activating signaling pathways that result in increased expression of vitagenes encoding survival proteins, as in the case of the Keap1/Nrf2/ARE pathway activated by curcumin and NAD/NADH-sirtuin-1 activated by resveratrol.	NAD	286-289	kelch like ECH associated protein 1	Homo sapiens	237-242
18629638-11	2008	Recent findings suggest that several phytochemicals exhibit biphasic dose responses on cells with low doses activating signaling pathways that result in increased expression of vitagenes encoding survival proteins, as in the case of the Keap1/Nrf2/ARE pathway activated by curcumin and NAD/NADH-sirtuin-1 activated by resveratrol.	NAD	286-289	NFE2 like bZIP transcription factor 2	Homo sapiens	243-247
18629638-11	2008	Recent findings suggest that several phytochemicals exhibit biphasic dose responses on cells with low doses activating signaling pathways that result in increased expression of vitagenes encoding survival proteins, as in the case of the Keap1/Nrf2/ARE pathway activated by curcumin and NAD/NADH-sirtuin-1 activated by resveratrol.	NAD	290-294	kelch like ECH associated protein 1	Homo sapiens	237-242
18629638-11	2008	Recent findings suggest that several phytochemicals exhibit biphasic dose responses on cells with low doses activating signaling pathways that result in increased expression of vitagenes encoding survival proteins, as in the case of the Keap1/Nrf2/ARE pathway activated by curcumin and NAD/NADH-sirtuin-1 activated by resveratrol.	NAD	290-294	NFE2 like bZIP transcription factor 2	Homo sapiens	243-247
18809674-5	2008	The G6PD enzymatic activity was increased, as were the levels of NADPH, NADH, and the GSH/GSSG ratio.	NAD	72-76	Zwischenferment	Drosophila melanogaster	4-8
18790050-10	2008	This suggests that the NAD binding domain on GAPDH may be related to binding to HCM.	NAD	23-26	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	45-50
18939989-1	2008	BACKGROUND: Mono-ADP-ribosyltransferase (ART) 1 belongs to a family of mammalian ectoenzymes that catalyze the transfer of ADP-ribose from NAD+ to a target protein.	NAD	139-143	ADP-ribosyltransferase 1	Homo sapiens	41-47
18775465-6	2008	The results indicate that a direct reaction between GAPDH and H(2)S does not occur and the observed decrease of GAPDH activity is to ascribe to the reaction between H(2)S and NAD(+)(H).	NAD	175-184	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	112-117
18854029-1	2008	BACKGROUND: Human ART4, carrier of the GPI-(glycosyl-phosphatidylinositol) anchored Dombrock blood group antigens, is an apparently inactive member of the mammalian mono-ADP-ribosyltransferase (ART) family named after the enzymatic transfer of a single ADP-ribose moiety from NAD+ to arginine residues of extracellular target proteins.	NAD	276-280	ADP-ribosyltransferase 4 (inactive) (Dombrock blood group)	Homo sapiens	18-22
18498245-9	2008	TD lymphoblasts showed increased expression of CD38, which hydrolyses NAD(+) into ADP-ribose, a trigger of Ca(2+) release from the endoplasmic reticulum that, in turn, facilitated CD20-induced apoptosis.	NAD	70-76	keratin 20	Homo sapiens	180-184
18775465-7	2008	This may lead to GAPDH inhibition by two ways, namely (i) cellular NAD(+)(H) reduced availability and (ii) catalytic site blockage.	NAD	67-73	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	17-22
18987575-7	2008	DNA damage is sensed by an important DNA repair enzyme, poly (ADP-ribose) polymerase (PARP); this enzyme repairs molecular damage by using nicotinamide adenine dinucleotide (NAD+) as a substrate.	NAD	139-172	poly(ADP-ribose) polymerase 1	Homo sapiens	56-84
18802071-5	2008	Analysis of hemizygous cells and in vitro cell lines expressing distinct levels of Nampt illustrates the critical role of this protein in regulating intracellular NAD levels.	NAD	163-166	nicotinamide phosphoribosyltransferase	Mus musculus	83-88
18802071-6	2008	Consequently, a clear relationship was found between intracellular Nampt levels and cell death in response to the genotoxic agent MNNG (N-methyl-N"-nitro-N-nitrosoguanidine), confirming that this enzyme represents a key regulator of cell sensitivity to NAD-consuming stress secondary to poly(ADP-ribose) polymerases overactivation.	NAD	253-256	nicotinamide phosphoribosyltransferase	Mus musculus	67-72
18987575-7	2008	DNA damage is sensed by an important DNA repair enzyme, poly (ADP-ribose) polymerase (PARP); this enzyme repairs molecular damage by using nicotinamide adenine dinucleotide (NAD+) as a substrate.	NAD	139-172	poly(ADP-ribose) polymerase 1	Homo sapiens	86-90
18987575-7	2008	DNA damage is sensed by an important DNA repair enzyme, poly (ADP-ribose) polymerase (PARP); this enzyme repairs molecular damage by using nicotinamide adenine dinucleotide (NAD+) as a substrate.	NAD	174-178	poly(ADP-ribose) polymerase 1	Homo sapiens	56-84
18987575-7	2008	DNA damage is sensed by an important DNA repair enzyme, poly (ADP-ribose) polymerase (PARP); this enzyme repairs molecular damage by using nicotinamide adenine dinucleotide (NAD+) as a substrate.	NAD	174-178	poly(ADP-ribose) polymerase 1	Homo sapiens	86-90
18987575-8	2008	Over-activation of PARP, due to severe DNA damage, consumes vast amounts of the respiratory coenzyme NAD+ leading to a cellular energy crisis.	NAD	101-105	poly(ADP-ribose) polymerase 1	Homo sapiens	19-23
18599483-4	2008	To better understand the molecular events leading to TRPM2 activation in lymphocytes, we analyzed oxidative stress-induced turnover of intracellular NAD, the metabolic precursor of adenine nucleotide 2nd messengers implicated in TRPM2 gating, and oxidative stress-induced TRPM2-mediated currents and Ca2+ transients in DT40 B cells.	NAD	149-152	transient receptor potential cation channel subfamily M member 2	Gallus gallus	229-234
18664567-5	2008	The PrBP/delta homology domain of Munc119 is essential for the interaction with the NADH binding region of RIBEYE(B) domain.	NAD	84-88	C-terminal binding protein 2	Homo sapiens	107-113
18664567-7	2008	A RIBEYE point mutant (RE(B)E844Q) that no longer interacted with Munc119 still bound NADH, arguing that binding of Munc119 and NADH to RIBEYE are independent from each other.	NAD	86-90	C-terminal binding protein 2	Homo sapiens	2-8
18768840-1	2008	The purinoreceptor P2X7 is expressed on subsets of T cells and mediates responses of these cells to extracellular nucleotides such as ATP or NAD(+).	NAD	141-147	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	19-23
18619469-2	2008	Next, Sir2/3/4 proteins propagate across these loci as histones are deacetylated by the NAD(+)-dependent histone deacetylase Sir2p, ultimately resulting in the cessation of transcription and in the loss of SET1- and DOT1-dependent methylation of histone H3 within silent chromatin.	NAD	88-94	histone methyltransferase DOT1	Saccharomyces cerevisiae S288C	216-220
18664567-7	2008	A RIBEYE point mutant (RE(B)E844Q) that no longer interacted with Munc119 still bound NADH, arguing that binding of Munc119 and NADH to RIBEYE are independent from each other.	NAD	128-132	C-terminal binding protein 2	Homo sapiens	136-142
18599483-4	2008	To better understand the molecular events leading to TRPM2 activation in lymphocytes, we analyzed oxidative stress-induced turnover of intracellular NAD, the metabolic precursor of adenine nucleotide 2nd messengers implicated in TRPM2 gating, and oxidative stress-induced TRPM2-mediated currents and Ca2+ transients in DT40 B cells.	NAD	149-152	transient receptor potential cation channel subfamily M member 2	Gallus gallus	229-234
18646819-1	2008	A theoretical study of the hydride transfer between formate anion and nicotinamide adenine dinucleotide (NAD(+)) catalyzed by the enzyme formate dehydrogenase (FDH) has been carried out by a combination of two hybrid quantum mechanics/molecular mechanics techniques: statistical simulation methods and internal energy minimizations.	NAD	70-103	aldehyde dehydrogenase 1 family member L1	Homo sapiens	137-158
18639906-9	2008	NAD(+) deficiency inhibits glycolysis and eventually oxidative metabolism, secondary to poly(ADP-ribose)polymerase (PARP) activity following DNA damage.	NAD	0-6	poly(ADP-ribose) polymerase 1	Homo sapiens	88-114
18639906-9	2008	NAD(+) deficiency inhibits glycolysis and eventually oxidative metabolism, secondary to poly(ADP-ribose)polymerase (PARP) activity following DNA damage.	NAD	0-6	poly(ADP-ribose) polymerase 1	Homo sapiens	116-120
18758064-0	2008	Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase-dependent activation of phosphoinositide 3-kinase and p38 mitogen-activated protein kinase signal pathways is required for lipopolysaccharide-induced microglial phagocytosis.	NAD	0-33	mitogen-activated protein kinase 14	Homo sapiens	114-150
18697942-7	2008	Surprisingly, the alternate ndh-2, but not -1, was shown to be the electron donor to the electron transport chain and to be essential to replenish the [NAD(+)] pool in hypoxic nonreplicating Mtb.	NAD	152-158	DExH-box helicase 9	Homo sapiens	28-33
18646819-1	2008	A theoretical study of the hydride transfer between formate anion and nicotinamide adenine dinucleotide (NAD(+)) catalyzed by the enzyme formate dehydrogenase (FDH) has been carried out by a combination of two hybrid quantum mechanics/molecular mechanics techniques: statistical simulation methods and internal energy minimizations.	NAD	70-103	aldehyde dehydrogenase 1 family member L1	Homo sapiens	160-163
18646819-1	2008	A theoretical study of the hydride transfer between formate anion and nicotinamide adenine dinucleotide (NAD(+)) catalyzed by the enzyme formate dehydrogenase (FDH) has been carried out by a combination of two hybrid quantum mechanics/molecular mechanics techniques: statistical simulation methods and internal energy minimizations.	NAD	105-111	aldehyde dehydrogenase 1 family member L1	Homo sapiens	137-158
18646819-1	2008	A theoretical study of the hydride transfer between formate anion and nicotinamide adenine dinucleotide (NAD(+)) catalyzed by the enzyme formate dehydrogenase (FDH) has been carried out by a combination of two hybrid quantum mechanics/molecular mechanics techniques: statistical simulation methods and internal energy minimizations.	NAD	105-111	aldehyde dehydrogenase 1 family member L1	Homo sapiens	160-163
18685021-7	2008	The docking site for RIBEYE(A) on RIBEYE(B) is topographically and functionally different from the RIBEYE(B) homodimerization interface and is negatively regulated by nicotinamide adenine dinucleotide.	NAD	167-200	C-terminal binding protein 2	Homo sapiens	34-40
18619441-1	2008	The H-bonded complex of ATP with Arg 34 of Zn2+ finger I of poly-ADP-ribose polymerase-1 (PARP-1) determines trans-oligo-ADP-ribosylation from NAD+ to proteins other than PARP-1.	NAD	143-147	poly(ADP-ribose) polymerase 1	Homo sapiens	60-88
18619441-1	2008	The H-bonded complex of ATP with Arg 34 of Zn2+ finger I of poly-ADP-ribose polymerase-1 (PARP-1) determines trans-oligo-ADP-ribosylation from NAD+ to proteins other than PARP-1.	NAD	143-147	poly(ADP-ribose) polymerase 1	Homo sapiens	90-96
18619441-1	2008	The H-bonded complex of ATP with Arg 34 of Zn2+ finger I of poly-ADP-ribose polymerase-1 (PARP-1) determines trans-oligo-ADP-ribosylation from NAD+ to proteins other than PARP-1.	NAD	143-147	poly(ADP-ribose) polymerase 1	Homo sapiens	171-177
18685021-7	2008	The docking site for RIBEYE(A) on RIBEYE(B) is topographically and functionally different from the RIBEYE(B) homodimerization interface and is negatively regulated by nicotinamide adenine dinucleotide.	NAD	167-200	C-terminal binding protein 2	Homo sapiens	34-40
18685021-7	2008	The docking site for RIBEYE(A) on RIBEYE(B) is topographically and functionally different from the RIBEYE(B) homodimerization interface and is negatively regulated by nicotinamide adenine dinucleotide.	NAD	167-200	C-terminal binding protein 2	Homo sapiens	21-27
18474219-7	2008	Saturation transfer to the ribose moieties is limited to the anomeric protons of E. coli SSADH suggesting that the NAD(+)/NADP(+) adenine and nicotinamide, but not the ribose moieties are important for the binding of the coenzymes.	NAD	115-121	Succinic semialdehyde dehydrogenase	Drosophila melanogaster	89-94
18046540-5	2008	In other contexts, overstimulation of PARP-1 triggers necrotic cell death because of rapid consumption of its substrate, beta-nicotinamide adenine dinucleotide (NAD+) and the consequent depletion of ATP.	NAD	161-165	poly(ADP-ribose) polymerase 1	Homo sapiens	38-44
18474219-5	2008	Epitope mapping by STD points to a strong interaction of the NAD(+)/NADP(+) adenine H2 proton with SSADH.	NAD	61-67	Succinic semialdehyde dehydrogenase	Drosophila melanogaster	99-104
18662547-0	2008	The NAD+-dependent deacetylase SIRT1 modulates CLOCK-mediated chromatin remodeling and circadian control.	NAD	4-8	circadian locomotor output cycles kaput	Mus musculus	47-52
18259858-3	2008	Hence, we tested the effects of ADPR, NAD+ and H2O2 on the activation of TRPM2 currents in transfected Chinese hamster ovary (CHO) cells.	NAD	38-42	transient receptor potential cation channel subfamily M member 2	Cricetulus griseus	73-78
18046540-5	2008	In other contexts, overstimulation of PARP-1 triggers necrotic cell death because of rapid consumption of its substrate, beta-nicotinamide adenine dinucleotide (NAD+) and the consequent depletion of ATP.	NAD	121-159	poly(ADP-ribose) polymerase 1	Homo sapiens	38-44
18537268-3	2008	The structure of the NAD (+)/CoASH-dependent aldehyde dehydrogenase subunit is similar to that of glyceraldehyde-3-phosphate dehydrogenase, with a Rossmann fold-based NAD (+) binding site observed in the NAD (+)-enzyme complex [Manjasetty, B.	NAD	21-28	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	98-138
18537268-3	2008	The structure of the NAD (+)/CoASH-dependent aldehyde dehydrogenase subunit is similar to that of glyceraldehyde-3-phosphate dehydrogenase, with a Rossmann fold-based NAD (+) binding site observed in the NAD (+)-enzyme complex [Manjasetty, B.	NAD	167-174	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	98-138
18537268-3	2008	The structure of the NAD (+)/CoASH-dependent aldehyde dehydrogenase subunit is similar to that of glyceraldehyde-3-phosphate dehydrogenase, with a Rossmann fold-based NAD (+) binding site observed in the NAD (+)-enzyme complex [Manjasetty, B.	NAD	167-174	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	98-138
18555842-2	2008	Although the oxidized form of nicotinamide adenine dinucloetide (NAD(+))-dependent histone deacetylase SIRT1 has been shown to mediate PGC-1alpha-induced metabolic adaptation, the effect of endurance exercise on the SIRT1 protein remains to be elucidated.	NAD	65-72	sirtuin 1	Rattus norvegicus	103-108
18555842-2	2008	Although the oxidized form of nicotinamide adenine dinucloetide (NAD(+))-dependent histone deacetylase SIRT1 has been shown to mediate PGC-1alpha-induced metabolic adaptation, the effect of endurance exercise on the SIRT1 protein remains to be elucidated.	NAD	65-72	PPARG coactivator 1 alpha	Rattus norvegicus	135-145
18555842-2	2008	Although the oxidized form of nicotinamide adenine dinucloetide (NAD(+))-dependent histone deacetylase SIRT1 has been shown to mediate PGC-1alpha-induced metabolic adaptation, the effect of endurance exercise on the SIRT1 protein remains to be elucidated.	NAD	65-72	sirtuin 1	Rattus norvegicus	216-221
18535182-3	2008	PARP overactivation depletes its substrate NAD(+), slowing the rate of glycolysis, electron transport, and ATP formation, eventually leading to functional impairment or death of cells, as well as up-regulation of various proinflammatory pathways.	NAD	43-49	poly(ADP-ribose) polymerase 1	Homo sapiens	0-4
18558727-3	2008	At noncytotoxic concentrations, E 2 induced dose-related reduction in intracellular NAD(P)H in MDA-MB-231 cells through decreases in intracellular NAD (+) mediated by poly(ADP-ribose) polymerase-1 (PARP-1) activation as determined by detection of the presence of polymers of ADP-ribose-modified PARP-1 using Western blotting.	NAD	147-154	poly(ADP-ribose) polymerase 1	Homo sapiens	167-196
18558727-5	2008	This evidence indicates that E 2 induces decreases in intracellular NAD(P)H and NAD (+) in MDA-MB-231 cells through PARP-1 activation mediated by the formation of DNA strand breaks.	NAD	80-87	poly(ADP-ribose) polymerase 1	Homo sapiens	116-122
18450439-2	2008	Poly(ADP-ribose) polymerase-1 (PARP-1), an abundant and ubiquitous nuclear enzyme that catalyzes the NAD(+)-dependent addition of ADP-ribose polymers on a variety of nuclear proteins, has been implicated in all of these functions.	NAD	101-107	poly(ADP-ribose) polymerase 1	Homo sapiens	0-29
18174234-5	2008	15-Hydroxyprostaglandin dehydrogenase [NAD(+)] (15-PGDH), a key enzyme in prostaglandin degradation, was identified as an upregulated protein in SGC7901 cells transfected with the COX-2siRNA plasmid.	NAD	39-45	prostaglandin-endoperoxide synthase 2	Homo sapiens	180-185
18450439-2	2008	Poly(ADP-ribose) polymerase-1 (PARP-1), an abundant and ubiquitous nuclear enzyme that catalyzes the NAD(+)-dependent addition of ADP-ribose polymers on a variety of nuclear proteins, has been implicated in all of these functions.	NAD	101-107	poly(ADP-ribose) polymerase 1	Homo sapiens	31-37
18493620-9	2008	Thus, NAMPT links NAD metabolism to inflammatory cytokine secretion by leukocytes, and its inhibition might therefore have therapeutic efficacy in immune-mediated inflammatory disorders.	NAD	18-21	nicotinamide phosphoribosyltransferase	Mus musculus	6-11
18452307-2	2008	Stimulated by binding to nicked DNA, PARP-1 catalyzes poly(ADP-ribosyl)ation of the acceptor proteins using NAD (+) as a substrate.	NAD	108-115	poly(ADP-ribose) polymerase 1	Homo sapiens	37-43
18452307-7	2008	Interestingly, domain C is essential for PARP-1 activity, since a mixture containing nicked DNA and the PARP-1 ABDEF domains has only basal enzymatic activity, while the addition of domain C to the mixture initiated NAD (+) hydrolysis and the formation of poly(ADP-ribose), as detected by an NMR-based assay and autoradiography.	NAD	216-223	poly(ADP-ribose) polymerase 1	Homo sapiens	41-47
18493620-0	2008	Pharmacological inhibition of nicotinamide phosphoribosyltransferase/visfatin enzymatic activity identifies a new inflammatory pathway linked to NAD.	NAD	145-148	nicotinamide phosphoribosyltransferase	Mus musculus	30-68
18493620-0	2008	Pharmacological inhibition of nicotinamide phosphoribosyltransferase/visfatin enzymatic activity identifies a new inflammatory pathway linked to NAD.	NAD	145-148	nicotinamide phosphoribosyltransferase	Mus musculus	69-77
18477242-3	2008	The recombinant proteins possess potent NAD+-dependent SSADH activity, while their catalytic efficiency for other aldehyde substrates is lower.	NAD	40-44	Succinic semialdehyde dehydrogenase	Drosophila melanogaster	55-60
18349103-5	2008	In the presence of camptothecin or its derivative topotecan, ATP (at up to 2 mM) inhibited PARP-1/NAD-facilitated TLD religation in a dose-dependent manner.	NAD	98-101	poly(ADP-ribose) polymerase 1	Homo sapiens	91-97
18349103-6	2008	This could be due to the suppression of topoisomerase I poly(ADP-ribosyl)ation through the competition with NAD for the binding site(s) on PARP-1.	NAD	108-111	poly(ADP-ribose) polymerase 1	Homo sapiens	139-145
18493620-1	2008	Nicotinamide phosphoribosyltransferase (NAMPT), also known as visfatin, is the rate-limiting enzyme in the salvage pathway of NAD biosynthesis from nicotinamide.	NAD	126-129	nicotinamide phosphoribosyltransferase	Mus musculus	0-38
18493620-1	2008	Nicotinamide phosphoribosyltransferase (NAMPT), also known as visfatin, is the rate-limiting enzyme in the salvage pathway of NAD biosynthesis from nicotinamide.	NAD	126-129	nicotinamide phosphoribosyltransferase	Mus musculus	40-45
18388260-4	2008	The mtDNA conferring high metastatic potential contained G13997A and 13885insC mutations in the gene encoding NADH (reduced form of nicotinamide adenine dinucleotide) dehydrogenase subunit 6 (ND6).	NAD	110-114	NADH dehydrogenase 6, mitochondrial	Mus musculus	192-195
18493620-1	2008	Nicotinamide phosphoribosyltransferase (NAMPT), also known as visfatin, is the rate-limiting enzyme in the salvage pathway of NAD biosynthesis from nicotinamide.	NAD	126-129	nicotinamide phosphoribosyltransferase	Mus musculus	62-70
18493620-7	2008	Moreover, NAMPT inhibition reduced intracellular NAD concentration in inflammatory cells and circulating TNFalpha levels during endotoxemia in mice.	NAD	49-52	nicotinamide phosphoribosyltransferase	Mus musculus	10-15
18493620-8	2008	In vitro pharmacological inhibition of NAMPT reduced the intracellular concentration of NAD and pro-inflammatory cytokine secretion by inflammatory cells.	NAD	88-91	nicotinamide phosphoribosyltransferase	Mus musculus	39-44
18485866-4	2008	They show that an altered NAD(+)/NADH ratio in response to glucose starvation regulates the silencing activity of eNoSC, a complex consisting of the NAD(+)-dependent histone deacetylase SIRT1, the histone methyltransferase SUV39H1, and a new protein called nucleomethylin (NML).	NAD	26-32	SUV39H1 histone lysine methyltransferase	Homo sapiens	223-230
18485866-4	2008	They show that an altered NAD(+)/NADH ratio in response to glucose starvation regulates the silencing activity of eNoSC, a complex consisting of the NAD(+)-dependent histone deacetylase SIRT1, the histone methyltransferase SUV39H1, and a new protein called nucleomethylin (NML).	NAD	33-37	SUV39H1 histone lysine methyltransferase	Homo sapiens	223-230
18485866-4	2008	They show that an altered NAD(+)/NADH ratio in response to glucose starvation regulates the silencing activity of eNoSC, a complex consisting of the NAD(+)-dependent histone deacetylase SIRT1, the histone methyltransferase SUV39H1, and a new protein called nucleomethylin (NML).	NAD	149-155	SUV39H1 histone lysine methyltransferase	Homo sapiens	223-230
18485871-6	2008	Both SIRT1 and SUV39H1 are required for energy-dependent transcriptional repression, suggesting that a change in the NAD(+)/NADH ratio induced by reduction of energy status could activate SIRT1, leading to deacetylation of histone H3 and dimethylation at Lys9 by SUV39H1, thus establishing silent chromatin in the rDNA locus.	NAD	117-123	SUV39H1 histone lysine methyltransferase	Homo sapiens	15-22
18485871-6	2008	Both SIRT1 and SUV39H1 are required for energy-dependent transcriptional repression, suggesting that a change in the NAD(+)/NADH ratio induced by reduction of energy status could activate SIRT1, leading to deacetylation of histone H3 and dimethylation at Lys9 by SUV39H1, thus establishing silent chromatin in the rDNA locus.	NAD	117-123	SUV39H1 histone lysine methyltransferase	Homo sapiens	263-270
18485871-6	2008	Both SIRT1 and SUV39H1 are required for energy-dependent transcriptional repression, suggesting that a change in the NAD(+)/NADH ratio induced by reduction of energy status could activate SIRT1, leading to deacetylation of histone H3 and dimethylation at Lys9 by SUV39H1, thus establishing silent chromatin in the rDNA locus.	NAD	124-128	SUV39H1 histone lysine methyltransferase	Homo sapiens	15-22
18485871-6	2008	Both SIRT1 and SUV39H1 are required for energy-dependent transcriptional repression, suggesting that a change in the NAD(+)/NADH ratio induced by reduction of energy status could activate SIRT1, leading to deacetylation of histone H3 and dimethylation at Lys9 by SUV39H1, thus establishing silent chromatin in the rDNA locus.	NAD	124-128	SUV39H1 histone lysine methyltransferase	Homo sapiens	263-270
18053578-1	2008	The standard assay for transketolase (E.C 2.2.1.1) has depended upon the use of D-xylulose 5-phosphate as the ketose donor substrate since the production of D-glyceraldehyde 3-phosphate can be readily coupled to a reaction that consumes NADH allowing the reaction to be followed spectrophotometrically.	NAD	237-241	transketolase	Homo sapiens	23-36
18316113-5	2008	Activity of DLDH dehydrogenase was measured as NAD+ oxidation of dihydrolipoamide.	NAD	47-51	dihydrolipoamide dehydrogenase	Rattus norvegicus	12-16
18399988-7	2008	The modified reductase arh1_A18G displayed spectroscopic characteristics similar to AdR and was shown to be capable of accepting electrons with no evident preference for NADH or NADPH, respectively.	NAD	170-174	low density lipoprotein receptor adaptor protein 1	Homo sapiens	23-27
18092337-7	2008	Immunoblotting and HPLC analysis showed considerable reduction in poly adenosyl ribosylation of VEGF associated with a significant decrease in the levels of NAD+, in cells maintained on Ln substrata.	NAD	157-161	vascular endothelial growth factor A	Homo sapiens	96-100
18092337-10	2008	It thus appears that Ln can affect aerobic metabolism of ECs by modulating the expression of LDH isoenzymes resulting in a decrease in the level of NAD+ that can cause a reduction in the poly adenosyl ribosylation of VEGF altering its angiogenic potency.	NAD	148-152	vascular endothelial growth factor A	Homo sapiens	217-221
18054108-2	2008	Excessive PARP-1 activation is known to lead to the depletion of intracellular NAD+ and ATP pools and hence to threat cell survival.	NAD	79-83	poly(ADP-ribose) polymerase 1	Homo sapiens	10-16
18239155-2	2008	By consuming NAD(+), PARP-1 activation can lead to ATP depletion and cell death.	NAD	13-19	poly(ADP-ribose) polymerase 1	Homo sapiens	21-27
18239155-6	2008	Here we investigated the hypothesis that PARP-1 inhibition protects human umbilical vein endothelial cells (HUVECs) from ROS- and RNS-induced cell death by limiting NAD(+) depletion and by activating a prosurvival signaling pathway via VEGFR2 phosphorylation.	NAD	165-171	poly(ADP-ribose) polymerase 1	Homo sapiens	41-47
18239155-8	2008	Both depleted HUVECs of NAD(+) and ATP, processes that were limited by the PARP-1 inhibitor, PJ34.	NAD	24-30	poly(ADP-ribose) polymerase 1	Homo sapiens	75-81
18239155-13	2008	CONCLUSIONS: PARP-1 inhibition prevents ROS- and RNS-induced HUVEC death by maintaining cellular energy in the form of NAD(+) and ATP, and also by activating a survival pathway via VEGFR2, Akt, and BAD phosphorylation.	NAD	119-125	poly(ADP-ribose) polymerase 1	Homo sapiens	13-19
18243466-5	2008	Once activated, PARP-1 catalyzes the formation of ADP-ribose polymers on acceptor proteins at the expense of NAD(+).	NAD	109-115	poly(ADP-ribose) polymerase 1	Homo sapiens	16-22
18243466-7	2008	Inhibitor of PARP-1 suppressed both overactivation of PARP-1 activity and NAD(+) depletion.	NAD	74-80	poly(ADP-ribose) polymerase 1	Homo sapiens	13-19
18322014-8	2008	In the absence of Txnip, oxidative inactivation of PTEN and subsequent activation of Akt attenuated mitochondrial respiration, resulting in the accumulation of NADH, a competitive inhibitor of thioredoxin NADPH-reductive activation of PTEN.	NAD	160-164	phosphatase and tensin homolog	Mus musculus	51-55
18322014-8	2008	In the absence of Txnip, oxidative inactivation of PTEN and subsequent activation of Akt attenuated mitochondrial respiration, resulting in the accumulation of NADH, a competitive inhibitor of thioredoxin NADPH-reductive activation of PTEN.	NAD	160-164	thymoma viral proto-oncogene 1	Mus musculus	85-88
18322014-8	2008	In the absence of Txnip, oxidative inactivation of PTEN and subsequent activation of Akt attenuated mitochondrial respiration, resulting in the accumulation of NADH, a competitive inhibitor of thioredoxin NADPH-reductive activation of PTEN.	NAD	160-164	phosphatase and tensin homolog	Mus musculus	235-239
18320257-1	2008	BACKGROUND: alpha-Amino-beta-carboxymuconate-epsilon-semialdehyde decarboxylase (ACMSD) is a key enzyme in NAD biosynthesis from tryptophan.	NAD	107-110	aminocarboxymuconate semialdehyde decarboxylase	Rattus norvegicus	12-79
18320257-1	2008	BACKGROUND: alpha-Amino-beta-carboxymuconate-epsilon-semialdehyde decarboxylase (ACMSD) is a key enzyme in NAD biosynthesis from tryptophan.	NAD	107-110	aminocarboxymuconate semialdehyde decarboxylase	Rattus norvegicus	81-86
18252249-2	2008	The identities of the NM_143151 gene product as NAD+-dependent SSADH and of the Aldh gene product as NAD+-dependent non-specific aldehyde dehydrogenase (ALDH, EC1.2.1.3) were established by substrate specificity studies using 30 different aldehydes.	NAD	101-105	Aldehyde dehydrogenase	Drosophila melanogaster	129-151
18252249-3	2008	In the case of D. melanogaster MalE-SSADH, the Michaelis constants (K(M)s) for the specific substrates succinic semialdehyde and NAD+ was 4.7 and 90.9 microM, respectively.	NAD	129-133	Succinic semialdehyde dehydrogenase	Drosophila melanogaster	36-41
18252249-4	2008	For D. melanogaster MalE-ALDH the K(M) of the putative in vivo substrate acetaldehyde was 0.9 microM while for NAD+, a K(M) of 62.7 microM was determined.	NAD	111-115	Aldehyde dehydrogenase	Drosophila melanogaster	25-29
18080092-6	2008	NAD and NADH diminished the GA-induced smearing of the G3PDH and GAPDH bands in different concentration-dependent manner.	NAD	0-3	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	65-70
18328572-8	2008	Interestingly, the ERbeta agonist, DPN significantly decreased IL-1beta following LPS treatment in young adult-derived microglia.	NAD	35-38	interleukin 1 beta	Rattus norvegicus	63-71
18344610-7	2008	When beta-NAD(+), a substrate of ADP-ribosyl cyclase, and cADPR were added to the medium, the former gradually increased [Ca(2+)](i) and the latter potentiated the fMLP-induced [Ca(2+)](i) rise.	NAD	5-16	formyl peptide receptor 1	Homo sapiens	164-168
18080092-6	2008	NAD and NADH diminished the GA-induced smearing of the G3PDH and GAPDH bands in different concentration-dependent manner.	NAD	8-12	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	65-70
20641814-3	2004	In mitochondria, one of the major pathways is the irreversible transformation of Pyr into acetyl-coenzyme A (acetyl-CoA) and CO2 by pyruvate dehydrogenase (PDH) in the presence of coenzyme nicotinamide adenine dinucleotide (NAD(+)/NADH).	NAD	189-222	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	156-159
20641814-3	2004	In mitochondria, one of the major pathways is the irreversible transformation of Pyr into acetyl-coenzyme A (acetyl-CoA) and CO2 by pyruvate dehydrogenase (PDH) in the presence of coenzyme nicotinamide adenine dinucleotide (NAD(+)/NADH).	NAD	224-230	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	156-159
20641814-3	2004	In mitochondria, one of the major pathways is the irreversible transformation of Pyr into acetyl-coenzyme A (acetyl-CoA) and CO2 by pyruvate dehydrogenase (PDH) in the presence of coenzyme nicotinamide adenine dinucleotide (NAD(+)/NADH).	NAD	231-235	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	156-159
19734127-1	2008	Phenoxodiol, an ENOX2 inhibitor, alters cytosolic NADH levels to initiate a regulatory cascade linking sphingolipid metabolism and the PI3K/Akt pathway to programmed cell death.	NAD	50-54	ecto-NOX disulfide-thiol exchanger 2	Homo sapiens	16-21
18082271-1	2008	The influence of de novo synthesis of nicotinamide adenine dinucleotide (NAD) through the kynurenine (KYN) pathway of tryptophan (TRP) degradation on gene transcription of inducible nitric oxide synthase (iNOS) and nitric oxide (NO) production in chicken interferon gamma (ChIFN-gamma)-stimulated and non-stimulated chicken macrophage cell line HD11 was investigated.	NAD	38-71	nitric oxide synthase 2	Gallus gallus	172-203
18082271-1	2008	The influence of de novo synthesis of nicotinamide adenine dinucleotide (NAD) through the kynurenine (KYN) pathway of tryptophan (TRP) degradation on gene transcription of inducible nitric oxide synthase (iNOS) and nitric oxide (NO) production in chicken interferon gamma (ChIFN-gamma)-stimulated and non-stimulated chicken macrophage cell line HD11 was investigated.	NAD	38-71	nitric oxide synthase 2	Gallus gallus	205-209
18082271-1	2008	The influence of de novo synthesis of nicotinamide adenine dinucleotide (NAD) through the kynurenine (KYN) pathway of tryptophan (TRP) degradation on gene transcription of inducible nitric oxide synthase (iNOS) and nitric oxide (NO) production in chicken interferon gamma (ChIFN-gamma)-stimulated and non-stimulated chicken macrophage cell line HD11 was investigated.	NAD	73-76	nitric oxide synthase 2	Gallus gallus	172-203
18082271-1	2008	The influence of de novo synthesis of nicotinamide adenine dinucleotide (NAD) through the kynurenine (KYN) pathway of tryptophan (TRP) degradation on gene transcription of inducible nitric oxide synthase (iNOS) and nitric oxide (NO) production in chicken interferon gamma (ChIFN-gamma)-stimulated and non-stimulated chicken macrophage cell line HD11 was investigated.	NAD	73-76	nitric oxide synthase 2	Gallus gallus	205-209
18082271-5	2008	Inhibition of poly(ADP-ribose) polymerase (PARP), a nuclear enzyme involved in DNA repair, replication and transcription, which cleaves NAD into nicotinamide and ADP-ribose, down regulated iNOS gene transcription and NO production in ChIFN-gamma-stimulated HD11 cells.	NAD	136-139	nitric oxide synthase 2	Gallus gallus	189-193
18082271-6	2008	Our results suggest that prevention of NAD depletion in HD11 cells by ChIFN-gamma-mediated induction of IDO facilitates iNOS transcription and NO production.	NAD	39-42	nitric oxide synthase 2	Gallus gallus	120-124
18082271-7	2008	This effect is most likely a result of PARP1 automodification in the presence of NAD, known to facilitate transcription by changing chromatin structure and to allow NFkappaB binding to iNOS promoter which is hindered by direct protein-protein interaction between NFkappaB and unmodified PARP1.	NAD	81-84	nitric oxide synthase 2	Gallus gallus	185-189
19023968-2	2008	The in vivo effects are in line with hypoxen capacity to accelerate in vitro oxidation of exogenous NADH in mitochondria by the non-rotenone-dependent pathway realized with participation of cytochrome C.	NAD	100-104	cytochrome c, somatic	Homo sapiens	190-202
18087619-4	2008	The resulting T. cruzi GAPDH-IMER was coupled to an analytical octyl column, which was used to achieve chromatographic separation of NAD(+) from NADH.	NAD	133-139	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	23-28
18087619-4	2008	The resulting T. cruzi GAPDH-IMER was coupled to an analytical octyl column, which was used to achieve chromatographic separation of NAD(+) from NADH.	NAD	145-149	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	23-28
18087619-5	2008	The production of NADH stimulated by d-glyceraldehyde-3-phosphate was used to investigate the activity and kinetic parameters of the immobilized T. cruzi GAPDH.	NAD	18-22	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	154-159
19734120-3	2008	The NADH-dependent system has been suggested to be involved in non-transferrin-bound iron (NTBI) reduction and uptake.	NAD	4-8	transferrin	Homo sapiens	67-78
19734127-1	2008	Phenoxodiol, an ENOX2 inhibitor, alters cytosolic NADH levels to initiate a regulatory cascade linking sphingolipid metabolism and the PI3K/Akt pathway to programmed cell death.	NAD	50-54	AKT serine/threonine kinase 1	Homo sapiens	140-143
19734127-8	2008	The prevailing hypothesis is that products of Akt activation, c-FLIP and XIAP, which exhibit anticaspase activities to block FAS signaling when sphingosine-1-phospate is elevated, are down regulated to permit apoptosis when sphingosine-1-phosphate is decreased by inhibition of sphingosine kinase under conditions of elevated cytosolic NADH associated with anticancer drug inhibition of ENOX2.	NAD	336-340	AKT serine/threonine kinase 1	Homo sapiens	46-49
19734127-8	2008	The prevailing hypothesis is that products of Akt activation, c-FLIP and XIAP, which exhibit anticaspase activities to block FAS signaling when sphingosine-1-phospate is elevated, are down regulated to permit apoptosis when sphingosine-1-phosphate is decreased by inhibition of sphingosine kinase under conditions of elevated cytosolic NADH associated with anticancer drug inhibition of ENOX2.	NAD	336-340	CASP8 and FADD like apoptosis regulator	Homo sapiens	62-68
17680234-18	2007	One enzyme is dependent on NAD+ for NMPA formation and is likely to be NADP(H):quinone oxidoreductase.	NAD	27-31	crystallin zeta	Rattus norvegicus	79-101
17981777-8	2008	A potential functional cross talk between PARP family members and other NAD+-consuming enzymes is discussed.	NAD	72-76	poly(ADP-ribose) polymerase 1	Homo sapiens	42-46
21558711-1	2008	The NAD(+)-dependent malic enzyme (DME) has been reported to play a key role supporting nitrogenase activity in bacteroids of Sinorhizobium meliloti.	NAD	4-10	NADP-dependent malic enzyme	Bradyrhizobium diazoefficiens USDA 110	35-38
17991898-3	2008	To functionally assess mitochondrial NAD metabolism, we overexpressed the catalytic domain of nuclear PAR polymerase 1 (PARP1) and targeted it to the matrix, which resulted in the constitutive presence of PAR within the organelles.	NAD	37-40	poly(ADP-ribose) polymerase 1	Homo sapiens	102-118
17991898-3	2008	To functionally assess mitochondrial NAD metabolism, we overexpressed the catalytic domain of nuclear PAR polymerase 1 (PARP1) and targeted it to the matrix, which resulted in the constitutive presence of PAR within the organelles.	NAD	37-40	poly(ADP-ribose) polymerase 1	Homo sapiens	120-125
17991898-10	2008	In addition, targeted PARP expression may serve as a compartment-specific "knock-down" of the NAD content which is readily detectable by PAR formation.	NAD	94-97	poly(ADP-ribose) polymerase 1	Homo sapiens	22-26
17981619-4	2008	Many studies, including the findings that poly(ADP-ribose) polymerase-1 mediates ischemic brain injury and that NAD+ administration can decrease ischemic brain damage, have suggested significant roles of NAD+ and NADH in the debilitating illness.	NAD	204-208	poly(ADP-ribose) polymerase 1	Homo sapiens	42-71
17981619-4	2008	Many studies, including the findings that poly(ADP-ribose) polymerase-1 mediates ischemic brain injury and that NAD+ administration can decrease ischemic brain damage, have suggested significant roles of NAD+ and NADH in the debilitating illness.	NAD	213-217	poly(ADP-ribose) polymerase 1	Homo sapiens	42-71
18071845-0	2008	Effectiveness of phenoxyl radicals generated by peroxidase/H2O2-catalyzed oxidation of caffeate, ferulate, and p-coumarate in cooxidation of ascorbate and NADH.	NAD	155-159	peroxidase	Glycine max	48-58
18071845-1	2008	The rate of ascorbate and nicotinamide adenine dinucleotide plus hydrogen (NADH) cooxidation (i.e., their nonenzymic oxidation by peroxidase/H2O2-generated phenoxyl radicals of three hydroxycinnamates: caffeate, ferulate and p-coumarate) was studied in vitro.	NAD	26-59	peroxidase	Glycine max	130-140
18071845-1	2008	The rate of ascorbate and nicotinamide adenine dinucleotide plus hydrogen (NADH) cooxidation (i.e., their nonenzymic oxidation by peroxidase/H2O2-generated phenoxyl radicals of three hydroxycinnamates: caffeate, ferulate and p-coumarate) was studied in vitro.	NAD	75-79	peroxidase	Glycine max	130-140
17954559-5	2008	Expression of the group 2 genes is selectively repressed by the NAD-dependent deacetylase SIRT1 in mature 3T3-L1 adipocytes, since knockdown of SIRT1 through the constitutive expression of a corresponding RNA interference enhances their expression without affecting the expression of classic adipogenic genes, such as adiponectin and FABP4/aP2.	NAD	64-67	adiponectin, C1Q and collagen domain containing	Homo sapiens	318-329
17935742-1	2008	ADP-ribose polymers are rapidly synthesized in cell nuclei by the poly(ADP-ribose) polymerases PARP-1 and PARP-2 in response to DNA strand interruptions, using NAD(+) as precursor.	NAD	160-166	poly(ADP-ribose) polymerase 1	Homo sapiens	95-101
17935742-1	2008	ADP-ribose polymers are rapidly synthesized in cell nuclei by the poly(ADP-ribose) polymerases PARP-1 and PARP-2 in response to DNA strand interruptions, using NAD(+) as precursor.	NAD	160-166	poly(ADP-ribose) polymerase 2	Homo sapiens	106-112
17514372-3	2008	Alternative or NDH-2-type NADH dehydrogenases are simple one subunit flavoenzymes that completely dissipate the redox energy of the NADH/quinone couple.	NAD	26-30	DExH-box helicase 9	Homo sapiens	15-20
18188525-8	2007	We propose that 4PYTP is formed by a novel route involving the oxidation of the intermediates of NAD turnover from quinolinic acid by aldehyde oxidase.	NAD	97-100	aldehyde oxidase 1	Homo sapiens	134-150
18021179-8	2007	DPN also elevated Bax expression.	NAD	0-3	BCL2 associated X, apoptosis regulator	Homo sapiens	18-21
17643414-9	2007	PARP-1 inhibition could have beneficial effects in such diseases as Chronic Obstructive Pulmonary Disease (COPD) and diabetes, by preservation of cellular NAD(+) levels and attenuating inflammatory conditions.	NAD	155-161	poly(ADP-ribose) polymerase 1	Homo sapiens	0-6
17936669-1	2007	Poly(ADP-ribose) polymerase (PARP) enzymes catalyze the conversion of NAD(+) to polymers of poly(ADP-ribose) (PAR).	NAD	70-76	poly(ADP-ribose) polymerase 1	Homo sapiens	0-27
17936669-1	2007	Poly(ADP-ribose) polymerase (PARP) enzymes catalyze the conversion of NAD(+) to polymers of poly(ADP-ribose) (PAR).	NAD	70-76	poly(ADP-ribose) polymerase 1	Homo sapiens	29-33
17957139-1	2007	SIRT3, one of seven mammalian sirtuins, is a NAD-dependent deacetylase.	NAD	45-48	sirtuin 3	Homo sapiens	0-5
17888864-3	2007	The substrate specificity differs from that of rat NAD+-dependent 3alpha-HSD (AKR1C17) that shares 95% sequence identity with AKR1C16.	NAD	51-55	aldo-keto reductase family 1, member C12-like 1	Rattus norvegicus	78-85
17888864-7	2007	AKR1C16 is also 92% identical with rat NAD+-dependent 17beta-HSD (AKR1C24), which possesses Tyr24.	NAD	39-43	hydroxysteroid (17-beta) dehydrogenase 3	Rattus norvegicus	54-64
17806102-1	2007	The NAD(+)-dependent protein deacetylase SIRT1 is linked to cellular survival pathways by virtue of keeping the tumor suppressor gene p53 and members of the forkhead transcription factor family deacetylated.	NAD	4-10	tumor protein p53	Homo sapiens	134-137
17803959-3	2007	In this study we tested our hypothesis that NADH can be transported across the plasma membranes of astrocytes by a P2X7 receptor (P2X7R)-mediated mechanism.	NAD	44-48	purinergic receptor P2X 7	Homo sapiens	115-128
17803959-3	2007	In this study we tested our hypothesis that NADH can be transported across the plasma membranes of astrocytes by a P2X7 receptor (P2X7R)-mediated mechanism.	NAD	44-48	purinergic receptor P2X 7	Homo sapiens	130-135
17803959-5	2007	Three lines of studies suggest that P2X7R mediates the NADH transport into astrocytes: the P2X receptor antagonist pyridoxalphosphate-6-azophenyl-2",4"-disulphonic acid (PPADS) blocked the NADH transport; RNAi knockdown of P2X7R led to decreased NADH transport; and transfection of HEK293 cells with mouse P2X7R cDNA led to increased NADH transport.	NAD	55-59	purinergic receptor P2X 7	Homo sapiens	36-41
17803959-5	2007	Three lines of studies suggest that P2X7R mediates the NADH transport into astrocytes: the P2X receptor antagonist pyridoxalphosphate-6-azophenyl-2",4"-disulphonic acid (PPADS) blocked the NADH transport; RNAi knockdown of P2X7R led to decreased NADH transport; and transfection of HEK293 cells with mouse P2X7R cDNA led to increased NADH transport.	NAD	189-193	purinergic receptor P2X 7	Homo sapiens	36-41
17803959-5	2007	Three lines of studies suggest that P2X7R mediates the NADH transport into astrocytes: the P2X receptor antagonist pyridoxalphosphate-6-azophenyl-2",4"-disulphonic acid (PPADS) blocked the NADH transport; RNAi knockdown of P2X7R led to decreased NADH transport; and transfection of HEK293 cells with mouse P2X7R cDNA led to increased NADH transport.	NAD	189-193	purinergic receptor P2X 7	Homo sapiens	36-41
17803959-5	2007	Three lines of studies suggest that P2X7R mediates the NADH transport into astrocytes: the P2X receptor antagonist pyridoxalphosphate-6-azophenyl-2",4"-disulphonic acid (PPADS) blocked the NADH transport; RNAi knockdown of P2X7R led to decreased NADH transport; and transfection of HEK293 cells with mouse P2X7R cDNA led to increased NADH transport.	NAD	189-193	purinergic receptor P2X 7	Homo sapiens	36-41
17803959-6	2007	Collectively, our study provides the first direct evidence demonstrating that NADH can be transported across the plasma membranes of astrocytes by a P2X7R-mediated mechanism.	NAD	78-82	purinergic receptor P2X 7	Homo sapiens	149-154
17983582-0	2007	Nampt/PBEF/Visfatin regulates insulin secretion in beta cells as a systemic NAD biosynthetic enzyme.	NAD	76-79	nicotinamide phosphoribosyltransferase	Mus musculus	0-5
17983582-0	2007	Nampt/PBEF/Visfatin regulates insulin secretion in beta cells as a systemic NAD biosynthetic enzyme.	NAD	76-79	nicotinamide phosphoribosyltransferase	Mus musculus	6-10
17785446-1	2007	We explored the mechanisms of chromatin compaction and transcriptional regulation by poly(ADP-ribose) polymerase 1 (PARP-1), a nucleosome-binding protein with an NAD(+)-dependent enzymatic activity.	NAD	162-168	poly(ADP-ribose) polymerase 1	Homo sapiens	85-114
17983582-0	2007	Nampt/PBEF/Visfatin regulates insulin secretion in beta cells as a systemic NAD biosynthetic enzyme.	NAD	76-79	nicotinamide phosphoribosyltransferase	Mus musculus	11-19
17983582-4	2007	Haplodeficiency and chemical inhibition of Nampt cause defects in NAD biosynthesis and glucose-stimulated insulin secretion in pancreatic islets in vivo and in vitro.	NAD	66-69	nicotinamide phosphoribosyltransferase	Mus musculus	43-48
17983582-7	2007	Our results demonstrate that Nampt-mediated systemic NAD biosynthesis is critical for beta cell function, suggesting a vital framework for the regulation of glucose homeostasis.	NAD	53-56	nicotinamide phosphoribosyltransferase	Mus musculus	29-34
17893042-7	2007	First, the ping-pong mechanism of NQO1 catalysis was utilized to overcome the problem of nonenzymatic reduction of the substrate by NADH.	NAD	132-136	NAD(P)H quinone dehydrogenase 1	Homo sapiens	34-38
17785446-1	2007	We explored the mechanisms of chromatin compaction and transcriptional regulation by poly(ADP-ribose) polymerase 1 (PARP-1), a nucleosome-binding protein with an NAD(+)-dependent enzymatic activity.	NAD	162-168	poly(ADP-ribose) polymerase 1	Homo sapiens	116-122
17975074-1	2007	Alcohol dehydrogenase 1 (Adh1)p catalyses the conversion of acetaldehyde to ethanol, regenerating NAD+.	NAD	98-102	alcohol dehydrogenase ADH1	Saccharomyces cerevisiae S288C	25-29
17803971-13	2007	The presence of the L-type Ca(2+) channel inhibitor, nifedipine (10 microM), partially inhibited 17beta-estradiol- and PPT-induced increase in phosphorylated ERK expression, whereas it induced a complete inhibition of DPN-induced increase in ERK phosphorylation.	NAD	218-221	tachykinin precursor 1	Homo sapiens	119-122
17562166-2	2007	Since the mechanisms that lead to TRPM2 inhibiting in response to ADPR and H(2)O(2) are not understood, I reviewed the effects of various inhibitors such as flufenamic acid and PARP inhibitors on ADPR, NAD(+) and H(2)O(2)-induced TRPM2 currents.	NAD	202-208	transient receptor potential cation channel subfamily M member 2	Cricetulus griseus	34-39
17562166-3	2007	In our experimental study, TRPM2 cation channels in chinese hamster ovary transected cells were gated both by ADPR and NAD(+).	NAD	119-125	transient receptor potential cation channel subfamily M member 2	Cricetulus griseus	27-32
17892301-0	2007	Copper ions inhibit S-adenosylhomocysteine hydrolase by causing dissociation of NAD+ cofactor.	NAD	80-84	adenosylhomocysteinase	Rattus norvegicus	20-52
17892301-5	2007	Binding of Cu2+ to SAHH resulted in the release of NAD+ cofactors, explaining the loss of the enzymatic activity of SAHH.	NAD	51-55	adenosylhomocysteinase	Rattus norvegicus	19-23
17892301-5	2007	Binding of Cu2+ to SAHH resulted in the release of NAD+ cofactors, explaining the loss of the enzymatic activity of SAHH.	NAD	51-55	adenosylhomocysteinase	Rattus norvegicus	116-120
17892301-6	2007	Further investigation by an ESR probe and computational simulation suggested that Cu2+ could bind at the central channel and interrupt the subunit interactions of SAHH, resulting in a large decrease in affinity to the NAD+ cofactor.	NAD	218-222	adenosylhomocysteinase	Rattus norvegicus	163-167
17803971-12	2007	Further analyses revealed that both PPT and DPN increased ERK phosphorylation, however, the temporal profile and magnitude of response were unique to each molecule.	NAD	44-47	mitogen-activated protein kinase 1	Homo sapiens	58-61
17595315-8	2007	Substitution of NADH for NADPH had a higher impact on C569Y and V608F mutants of POR.	NAD	16-20	cytochrome p450 oxidoreductase	Homo sapiens	81-84
17914902-6	2007	Thus, crystal structures of Nrk1 led to the identification of new pathways to NAD+.	NAD	78-82	nicotinamide riboside kinase 1	Homo sapiens	28-32
17629694-1	2007	The effects of flavonoids and quinones on NADPH- and NADH-dependent 20alpha-hydroxysteroid dehydrogenase (20alpha-HSD) activities were examined in cytosolic fractions from the liver and kidney of mice.	NAD	53-57	aldo-keto reductase family 1, member C18	Mus musculus	68-104
17629694-1	2007	The effects of flavonoids and quinones on NADPH- and NADH-dependent 20alpha-hydroxysteroid dehydrogenase (20alpha-HSD) activities were examined in cytosolic fractions from the liver and kidney of mice.	NAD	53-57	aldo-keto reductase family 1, member C18	Mus musculus	106-117
17629694-2	2007	Judging from the data for the inhibition of NADPH- and NADH-dependent 20alpha-HSD activities by flavonoids and quinones, enzyme catalyzing renal NADPH-dependent 20alpha-HSD activity was found to be distinct from enzyme(s) catalyzing hepatic NADPH- and NADH-dependent 20alpha-HSD activities.	NAD	55-59	aldo-keto reductase family 1, member C18	Mus musculus	70-81
17629694-2	2007	Judging from the data for the inhibition of NADPH- and NADH-dependent 20alpha-HSD activities by flavonoids and quinones, enzyme catalyzing renal NADPH-dependent 20alpha-HSD activity was found to be distinct from enzyme(s) catalyzing hepatic NADPH- and NADH-dependent 20alpha-HSD activities.	NAD	55-59	aldo-keto reductase family 1, member C18	Mus musculus	161-172
17629694-2	2007	Judging from the data for the inhibition of NADPH- and NADH-dependent 20alpha-HSD activities by flavonoids and quinones, enzyme catalyzing renal NADPH-dependent 20alpha-HSD activity was found to be distinct from enzyme(s) catalyzing hepatic NADPH- and NADH-dependent 20alpha-HSD activities.	NAD	55-59	aldo-keto reductase family 1, member C18	Mus musculus	161-172
17629694-2	2007	Judging from the data for the inhibition of NADPH- and NADH-dependent 20alpha-HSD activities by flavonoids and quinones, enzyme catalyzing renal NADPH-dependent 20alpha-HSD activity was found to be distinct from enzyme(s) catalyzing hepatic NADPH- and NADH-dependent 20alpha-HSD activities.	NAD	252-256	aldo-keto reductase family 1, member C18	Mus musculus	70-81
17629694-2	2007	Judging from the data for the inhibition of NADPH- and NADH-dependent 20alpha-HSD activities by flavonoids and quinones, enzyme catalyzing renal NADPH-dependent 20alpha-HSD activity was found to be distinct from enzyme(s) catalyzing hepatic NADPH- and NADH-dependent 20alpha-HSD activities.	NAD	252-256	aldo-keto reductase family 1, member C18	Mus musculus	161-172
17629694-2	2007	Judging from the data for the inhibition of NADPH- and NADH-dependent 20alpha-HSD activities by flavonoids and quinones, enzyme catalyzing renal NADPH-dependent 20alpha-HSD activity was found to be distinct from enzyme(s) catalyzing hepatic NADPH- and NADH-dependent 20alpha-HSD activities.	NAD	252-256	aldo-keto reductase family 1, member C18	Mus musculus	161-172
17629694-4	2007	Thus, enzyme catalyzing hepatic NADPH-dependent 20alpha-HSD activity appeared to be distinct from enzyme catalyzing hepatic NADH-dependent 20alpha-HSD activity.	NAD	124-128	aldo-keto reductase family 1, member C18	Mus musculus	48-59
17629694-4	2007	Thus, enzyme catalyzing hepatic NADPH-dependent 20alpha-HSD activity appeared to be distinct from enzyme catalyzing hepatic NADH-dependent 20alpha-HSD activity.	NAD	124-128	aldo-keto reductase family 1, member C18	Mus musculus	139-150
17629694-5	2007	The data for the pH profiles of hepatic NADPH- and NADH-dependent 20alpha-HSD activities also led us to the conclusion.	NAD	51-55	aldo-keto reductase family 1, member C18	Mus musculus	66-77
17629694-6	2007	Based on these results, we propose the possibility that several distinct enzymes catalyze NADPH- and NADH-dependent 20alpha-HSD activities in cytosolic fractions from the liver and kidney of mice.	NAD	101-105	aldo-keto reductase family 1, member C18	Mus musculus	116-127
17225077-8	2007	DNA damage causes PARP overactivation, resulting in the depletion of oxidized nicotinamide-adenine dinucleotide and adenosine triphosphate, and consequently in necrotic cell death.	NAD	78-111	poly(ADP-ribose) polymerase 1	Homo sapiens	18-22
17889652-4	2007	Increased Nampt provides protection against cell death and requires an intact mitochondrial NAD(+) salvage pathway as well as the mitochondrial NAD(+)-dependent deacetylases SIRT3 and SIRT4.	NAD	144-150	sirtuin 3	Homo sapiens	174-179
17889652-4	2007	Increased Nampt provides protection against cell death and requires an intact mitochondrial NAD(+) salvage pathway as well as the mitochondrial NAD(+)-dependent deacetylases SIRT3 and SIRT4.	NAD	144-150	sirtuin 4	Homo sapiens	184-189
17960110-0	2007	NADH photo-oxidation is enhanced by a partially purified lambda-crystallin fraction from rabbit lens.	NAD	0-4	lambda-crystallin	Oryctolagus cuniculus	57-74
17960110-1	2007	PURPOSE: In the rabbit lens, high levels of reduced nicotinamide adenine dinucleotide (NADH) can function as a near-ultraviolet light (near-UV) filter, an effect apparently achieved by specific nucleotide binding to lambda-crystallin.	NAD	52-85	lambda-crystallin	Oryctolagus cuniculus	216-233
17960110-1	2007	PURPOSE: In the rabbit lens, high levels of reduced nicotinamide adenine dinucleotide (NADH) can function as a near-ultraviolet light (near-UV) filter, an effect apparently achieved by specific nucleotide binding to lambda-crystallin.	NAD	87-91	lambda-crystallin	Oryctolagus cuniculus	216-233
17960110-2	2007	The present investigation asks whether lambda-crystallin enhances NADH photo-oxidation by superoxide radicals produced via a photosensitization reaction of near-UV with NADH.	NAD	66-70	lambda-crystallin	Oryctolagus cuniculus	39-56
17960110-2	2007	The present investigation asks whether lambda-crystallin enhances NADH photo-oxidation by superoxide radicals produced via a photosensitization reaction of near-UV with NADH.	NAD	169-173	lambda-crystallin	Oryctolagus cuniculus	39-56
17960110-7	2007	In contrast, NADH photo-oxidation was rapidly initiated in the presence of partially purified lambda-crystallin.	NAD	13-17	lambda-crystallin	Oryctolagus cuniculus	94-111
17960110-8	2007	This lambda-crystallin-enhanced NADH photo-oxidation was totally inhibited by adding superoxide dismutase.	NAD	32-36	lambda-crystallin	Oryctolagus cuniculus	5-22
17960110-9	2007	We also found that lambda-crystallin largely increased NADH oxidation by a superoxide that is generated enzymatically.	NAD	55-59	lambda-crystallin	Oryctolagus cuniculus	19-36
17960110-10	2007	These results indicate that NADH bound to lambda-crystallin rapidly reacts with superoxides.	NAD	28-32	lambda-crystallin	Oryctolagus cuniculus	42-59
17960110-12	2007	However, lambda-crystallin-enhanced NADH oxidation exceeded the superoxide levels generated by NADH photosensitization and xanthine/xanthine oxidase.	NAD	36-40	lambda-crystallin	Oryctolagus cuniculus	9-26
17960110-13	2007	CONCLUSIONS: We conclude that NADH binding to lambda-crystallin enhances NADH photo-oxidation through a radical chain reaction mechanism that is initiated by superoxides generated by NADH photosensitization and propagated by another superoxide from the molecule oxygen.	NAD	30-34	lambda-crystallin	Oryctolagus cuniculus	46-63
17960110-13	2007	CONCLUSIONS: We conclude that NADH binding to lambda-crystallin enhances NADH photo-oxidation through a radical chain reaction mechanism that is initiated by superoxides generated by NADH photosensitization and propagated by another superoxide from the molecule oxygen.	NAD	73-77	lambda-crystallin	Oryctolagus cuniculus	46-63
17960110-13	2007	CONCLUSIONS: We conclude that NADH binding to lambda-crystallin enhances NADH photo-oxidation through a radical chain reaction mechanism that is initiated by superoxides generated by NADH photosensitization and propagated by another superoxide from the molecule oxygen.	NAD	73-77	lambda-crystallin	Oryctolagus cuniculus	46-63
17960110-14	2007	High concentrations of NADH bound to lambda-crystallin may be beneficial to the rabbit lens in scavenging the low amounts of superoxide produced by near-UV absorption, since oxygen tension in the lens is very low.	NAD	23-27	lambda-crystallin	Oryctolagus cuniculus	37-54
17673460-9	2007	NDB2 and NDB4 fusion proteins were NADH-specific, and NDB2 was stimulated by Ca(2+).	NAD	35-39	NAD(P)H dehydrogenase B4	Arabidopsis thaliana	9-13
17554080-7	2007	Thus, a Ca(2+) influx in the principal piece through CATSPER channels can not only initiate hyperactivated motility, but can also trigger a tail-to-head Ca(2+) propagation that leads to an increase in [NADH] and may regulate ATP homeostasis.	NAD	202-206	cation channel, sperm associated 1	Mus musculus	53-60
17295209-5	2007	Prior inactivation of PARP protected both cell lines from the initial decrease in NAD+ and improved the survival of LNCaP cells following combined EGF and IR treatment.	NAD	82-86	poly(ADP-ribose) polymerase 1	Homo sapiens	22-26
17692540-4	2007	The ability of TCR-dependent Ca(2+) signals to stimulate mitochondrial NADH production in excess of that utilized for ATP synthesis was dependent on Bax and Bak.	NAD	71-75	BCL2 associated X, apoptosis regulator	Homo sapiens	149-152
17295209-2	2007	PARP activation was indicated by the appearance of polyADP-ribose, the incorporation of P32-labelled NADH, and by cellular NADH.	NAD	101-105	poly(ADP-ribose) polymerase 1	Homo sapiens	0-4
17295209-2	2007	PARP activation was indicated by the appearance of polyADP-ribose, the incorporation of P32-labelled NADH, and by cellular NADH.	NAD	123-127	poly(ADP-ribose) polymerase 1	Homo sapiens	0-4
17475203-0	2007	Rat NAD+-dependent 3alpha-hydroxysteroid dehydrogenase (AKR1C17): a member of the aldo-keto reductase family highly expressed in kidney cytosol.	NAD	4-7	aldo-keto reductase family 1, member C12-like 1	Rattus norvegicus	56-63
17475203-3	2007	The recombinant AKR1C17 efficiently oxidized 3alpha-hydroxysteroids and bile acids using NAD(+) as the preferred coenzyme at an optimal pH of 7.4-9.5, and was inhibited by ketamine and organic anions.	NAD	89-95	aldo-keto reductase family 1, member C12-like 1	Rattus norvegicus	16-23
17475203-5	2007	Thus, AKR1C17 represents a novel NAD(+)-dependent type of cytosolic 3alpha-HSD with unique inhibitor sensitivity and tissue distribution.	NAD	33-39	aldo-keto reductase family 1, member C12-like 1	Rattus norvegicus	6-13
17635179-2	2007	In the endoplasmic reticulum a single nicotinamide adenine dinucleotide phosphate (NADPH) P450 oxidoreductase (POR) supplies electrons to all microsomal P450s for catalytic activity.	NAD	38-71	cytochrome p450 oxidoreductase	Homo sapiens	111-114
17490600-1	2007	We have developed a highly sensitive assay of MEK-mediated ATP hydrolysis by coupling the formation of ADP to NADH oxidation through the enzymes pyruvate kinase and lactate dehydrogenase.	NAD	110-114	mitogen-activated protein kinase kinase 7	Homo sapiens	46-49
17676935-2	2007	The three-dimensional structure of dimeric EhGAPDH in complex with cofactor NAD(+) has been generated by homology modeling based on the crystal structure of human liver GAPDH.	NAD	76-82	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	45-50
17728843-5	2007	Excessive levels of free, ionic zinc can initiate DNA damage and the subsequent activation of poly(ADP-ribose) polymerase 1 (PARP-1), which in turn lead to NAD+ and ATP depletion when DNA damage is extensive.	NAD	156-160	poly(ADP-ribose) polymerase 1	Homo sapiens	94-123
17508915-2	2007	Our studies suggest that cytosolic NADH reductive stress under high glucose is largely caused by increased flux of glucose through polyol (sorbitol) pathway consisting of aldose reductase and sorbitol dehydrogenase.	NAD	35-39	aldo-keto reductase family 1 member B	Homo sapiens	171-187
17508915-2	2007	Our studies suggest that cytosolic NADH reductive stress under high glucose is largely caused by increased flux of glucose through polyol (sorbitol) pathway consisting of aldose reductase and sorbitol dehydrogenase.	NAD	35-39	sorbitol dehydrogenase	Homo sapiens	192-214
17508915-6	2007	In addition, it has been shown that the NADH utilizing enzyme, glyceraldehyde-3-phosphate dehydrogenase, participates as transcriptional regulator.	NAD	40-44	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	63-103
17555402-6	2007	In combination with the hypoxia-induced expression of LDHA (lactate dehydrogenase A), which converts pyruvate into lactate, PDK1 reduces the delivery of acetyl-CoA to the tricarboxylic acid cycle, thus reducing the levels of NADH and FADH2 delivered to the electron-transport chain.	NAD	225-229	lactate dehydrogenase A	Homo sapiens	54-58
17555402-6	2007	In combination with the hypoxia-induced expression of LDHA (lactate dehydrogenase A), which converts pyruvate into lactate, PDK1 reduces the delivery of acetyl-CoA to the tricarboxylic acid cycle, thus reducing the levels of NADH and FADH2 delivered to the electron-transport chain.	NAD	225-229	lactate dehydrogenase A	Homo sapiens	60-83
17521358-5	2007	Addition of PARP-specific inhibitors such as 3-aminobenzamide to RCD-promoting media restored the intracellular NAD(+) levels and thereby prevented RCD.	NAD	112-118	poly(ADP-ribose) polymerase 1	Homo sapiens	12-16
17669606-10	2007	Overall, this evidence confirms that TCDD induces decreases in intracellular NAD(P)H and NAD(+) through PARP-1 activation mediated by formation of DNA strand breaks.	NAD	89-95	poly(ADP-ribose) polymerase 1	Homo sapiens	104-110
17728843-5	2007	Excessive levels of free, ionic zinc can initiate DNA damage and the subsequent activation of poly(ADP-ribose) polymerase 1 (PARP-1), which in turn lead to NAD+ and ATP depletion when DNA damage is extensive.	NAD	156-160	poly(ADP-ribose) polymerase 1	Homo sapiens	125-131
17347665-2	2007	However, activation of the DNA repair system, poly(ADP-ribose) polymerase (PARP-1), is thought to cause neuronal death through NAD+ depletion and mitochondrial membrane potential (delta psi(m)) depolarization.	NAD	127-131	poly(ADP-ribose) polymerase 1	Homo sapiens	46-73
17579037-2	2007	In vitro, ADP-ribosylation by ART2 activates the P2X7 ATP receptor and is responsible for NAD(+)-induced T cell death (NICD).	NAD	90-96	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	49-53
17579037-6	2007	Intravenous injection of NAD(+) used to exacerbate NICD in vivo results in fast and dramatic ART2- and P2X7-dependent depletion of CD4+ and CD8+ T lymphocytes, which can affect up to 80% of peripheral T cells in CD38(-/-) mice.	NAD	25-31	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	103-107
17452319-0	2007	Characterization of Arabidopsis thaliana SufE2 and SufE3: functions in chloroplast iron-sulfur cluster assembly and Nad synthesis.	NAD	116-119	sulfur E2	Arabidopsis thaliana	41-46
17347665-2	2007	However, activation of the DNA repair system, poly(ADP-ribose) polymerase (PARP-1), is thought to cause neuronal death through NAD+ depletion and mitochondrial membrane potential (delta psi(m)) depolarization.	NAD	127-131	poly(ADP-ribose) polymerase 1	Homo sapiens	75-81
17347665-4	2007	Only in severe oxidative stress does PARP-1 activation result in NAD+ and ATP depletion and neuronal death.	NAD	65-69	poly(ADP-ribose) polymerase 1	Homo sapiens	37-43
17405841-1	2007	CONTEXT: We have previously identified nicotinamide adenine dinucleotide phosphate:quinone oxidoreductase 1 (NQO1), an enzyme involved in the protection against oxidative stress, as a gene predominantly expressed in human adipocytes.	NAD	39-72	NAD(P)H quinone dehydrogenase 1	Homo sapiens	109-113
17529993-2	2007	Here we uncover a positive role for SET in dislodging DEK and PARP1, which restrict access to chromatin in the absence of SET and the PARP1 substrate NAD(+).	NAD	150-156	poly(ADP-ribose) polymerase 1	Homo sapiens	62-67
17336418-8	2007	PPT/DPN reduced nitrate/nitrite production and iNOS mRNA in Kupffer cells following trauma-hemorrhage; however, these levels in DPN-treated animals remained higher than sham.	NAD	4-7	nitric oxide synthase 2	Rattus norvegicus	47-51
17567466-7	2007	These studies identify a critical role for nicotinamide adenine dinucleotide phosphate (NADPH) oxidase-derived reactive oxygen species in the activation of ERK1/2 and subsequent production of TNFalpha in Kupffer cells after chronic ethanol feeding.	NAD	43-76	tumor necrosis factor	Mus musculus	192-200
17529993-2	2007	Here we uncover a positive role for SET in dislodging DEK and PARP1, which restrict access to chromatin in the absence of SET and the PARP1 substrate NAD(+).	NAD	150-156	poly(ADP-ribose) polymerase 1	Homo sapiens	134-139
17529993-5	2007	In the presence of NAD(+), PARP1 poly(ADP-ribosyl)ates and evicts DEK (and itself) from chromatin to permit Mediator loading and transcription independent of SET.	NAD	19-25	poly(ADP-ribose) polymerase 1	Homo sapiens	27-32
17455910-3	2007	The indolequinones with 4-nitrophenoxy, 4-pyridinyloxy, and acetoxy substituents at the (indol-3-yl)methyl position were NADH-dependent inhibitors of recombinant human NQO1, indicative of mechanism-based inhibition.	NAD	121-125	NAD(P)H quinone dehydrogenase 1	Homo sapiens	168-172
17221190-8	2007	Additionally, the NADH-producing pathway from acetaldehyde to acetate was analysed by overexpressing the stress-induced gene ALD3.	NAD	18-22	aldehyde dehydrogenase (NAD(+)) ALD3	Saccharomyces cerevisiae S288C	125-129
17395143-9	2007	Interference by NAD analogs (e.g., NAAD, NADP) in the sample was eliminated prior to running the assay by treating the sample with NADS and NAD nucleosidase (NADase).	NAD	16-19	bone marrow stromal cell antigen 1	Homo sapiens	140-156
17320039-6	2007	This report strengthens the proposal, supported by previously published data that in isotonic medium the exogenous NADH/cyto-c electron transport system is catalyzed by intact mitochondria, not permeable to added cyto-c.	NAD	115-119	cytochrome c, somatic	Homo sapiens	120-126
17320039-6	2007	This report strengthens the proposal, supported by previously published data that in isotonic medium the exogenous NADH/cyto-c electron transport system is catalyzed by intact mitochondria, not permeable to added cyto-c.	NAD	115-119	cytochrome c, somatic	Homo sapiens	213-219
17470521-1	2007	Cortisol-cortisone metabolism is catalysed by the bi-directional NADP(H)-dependent type 1 11beta-hydroxysteroid dehydrogenase (11betaHSD1) enzyme and the oxidative NAD(+)-dependent type 2 11betaHSD (11betaHSD2).	NAD	164-170	hydroxysteroid 11-beta dehydrogenase 2	Bos taurus	199-209
17167776-6	2007	Isolated VEGF, when blotted and subsequently probed with anti-PAR antibody, revealed considerable reduction in poly-adenosyl ribosylation of VEGF associated with a significant decrease in the levels of NAD(+), in presence of lactate.	NAD	202-208	vascular endothelial growth factor A	Homo sapiens	9-13
17167776-6	2007	Isolated VEGF, when blotted and subsequently probed with anti-PAR antibody, revealed considerable reduction in poly-adenosyl ribosylation of VEGF associated with a significant decrease in the levels of NAD(+), in presence of lactate.	NAD	202-208	vascular endothelial growth factor A	Homo sapiens	141-145
17163414-5	2007	Indeed, NAD(+) is rapidly and severely depleted, a fact most probably related to a strong Poly(ADP-ribose) polymerase (PARP) activation, as shown by the high amount of poly-ADP-ribosylated proteins.	NAD	8-14	poly(ADP-ribose) polymerase 1	Homo sapiens	90-117
17084037-3	2007	When activated by DNA damage, PARP-1 consumes nicotinamide adenine dinucleotide (NAD+) to form branched polymers of ADP-ribose on target proteins.	NAD	46-79	poly(ADP-ribose) polymerase 1	Homo sapiens	30-36
17084037-3	2007	When activated by DNA damage, PARP-1 consumes nicotinamide adenine dinucleotide (NAD+) to form branched polymers of ADP-ribose on target proteins.	NAD	81-85	poly(ADP-ribose) polymerase 1	Homo sapiens	30-36
17430113-12	2007	NAD depletion mediated by peroxynitrate PARP1 activation is one of the few established mechanisms of necrosis.	NAD	0-3	poly(ADP-ribose) polymerase 1	Homo sapiens	40-45
17430113-13	2007	Chronic elevation of TNFalpha leading to necrotic events by NAD depletion in autoimmune disease likely occurs via combination of persistent IDO activation and iNOS-peroxynitrate activation of PARP1 both of which deplete NAD.	NAD	60-63	tumor necrosis factor	Homo sapiens	21-29
17430113-13	2007	Chronic elevation of TNFalpha leading to necrotic events by NAD depletion in autoimmune disease likely occurs via combination of persistent IDO activation and iNOS-peroxynitrate activation of PARP1 both of which deplete NAD.	NAD	60-63	poly(ADP-ribose) polymerase 1	Homo sapiens	192-197
17430113-13	2007	Chronic elevation of TNFalpha leading to necrotic events by NAD depletion in autoimmune disease likely occurs via combination of persistent IDO activation and iNOS-peroxynitrate activation of PARP1 both of which deplete NAD.	NAD	220-223	tumor necrosis factor	Homo sapiens	21-29
17430113-13	2007	Chronic elevation of TNFalpha leading to necrotic events by NAD depletion in autoimmune disease likely occurs via combination of persistent IDO activation and iNOS-peroxynitrate activation of PARP1 both of which deplete NAD.	NAD	220-223	poly(ADP-ribose) polymerase 1	Homo sapiens	192-197
17430113-17	2007	Distinct among the NAD precursors, nicotinic acid specifically activates the g-protein coupled receptor (GPCR) GPR109a to produce the IDO-inducing tolerogenic prostaglandins PGE(2) and PGD(2).	NAD	19-22	hydroxycarboxylic acid receptor 2	Homo sapiens	111-118
17454128-2	2007	We demonstrated that UVA-irradiated NADH induced damage to (32)P-labeled DNA fragments obtained from the p53 gene in the presence of Cu(II).	NAD	36-40	tumor protein p53	Homo sapiens	105-108
17302434-5	2007	Compared to other members of the ALDH family, FDH demonstrates a new mode of binding of the 2"-phosphate group of NADP via a water-mediated contact with Gln600 that may contribute to the specificity of the enzyme for NADP over NAD.	NAD	114-117	aldehyde dehydrogenase 1 family, member L1	Rattus norvegicus	46-49
17437997-0	2007	SirT3 is a nuclear NAD+-dependent histone deacetylase that translocates to the mitochondria upon cellular stress.	NAD	19-22	sirtuin 3	Homo sapiens	0-5
17430113-6	2007	Approaches to cell specific therapeutic IDO induction with NAD precursor supplementation to prevent the collateral non-T cell pathogenesis due to chronic TNFalpha-IDO activated tryptophan depletion in autoimmune diseases are reviewed.	NAD	59-62	tumor necrosis factor	Homo sapiens	154-162
17520094-3	2007	Upon binding to DNA breaks, activated PARP cleaves NAD+ into nicotinamide and ADP-ribose and polymerizes the latter onto nuclear acceptor proteins including histones, transcription factors and PARP itself.	NAD	51-55	poly(ADP-ribose) polymerase 1	Homo sapiens	38-42
17520094-3	2007	Upon binding to DNA breaks, activated PARP cleaves NAD+ into nicotinamide and ADP-ribose and polymerizes the latter onto nuclear acceptor proteins including histones, transcription factors and PARP itself.	NAD	51-55	poly(ADP-ribose) polymerase 1	Homo sapiens	193-197
17163414-5	2007	Indeed, NAD(+) is rapidly and severely depleted, a fact most probably related to a strong Poly(ADP-ribose) polymerase (PARP) activation, as shown by the high amount of poly-ADP-ribosylated proteins.	NAD	8-14	poly(ADP-ribose) polymerase 1	Homo sapiens	119-123
17360427-0	2007	Regulation of poly(ADP-ribose) polymerase 1 activity by the phosphorylation state of the nuclear NAD biosynthetic enzyme NMN adenylyl transferase 1.	NAD	97-100	poly(ADP-ribose) polymerase 1	Homo sapiens	14-43
17309261-9	2007	These observations confirm NAD as the substrate for THI4 and elucidate the early steps of this unique biosynthesis of the thiazole moiety of thiamin in eukaryotes.	NAD	27-30	thiamine thiazole synthase	Saccharomyces cerevisiae S288C	52-56
17224139-12	2007	Overall, results from our investigation suggest that while NHQ and 1,4-NQ are more efficient in the induction of cell death, NCAT and 1,2-NQ are prone to induce depletion of NAD(P)H and NAD(+) mediated by PARP-1 activation through formation of DNA single-strand breaks in human cultured cells.	NAD	186-192	poly(ADP-ribose) polymerase 1	Homo sapiens	205-211
17896587-1	2007	During tryptophan-niacin conversion, hepatic alpha-amino-beta-carboxymuconate-epsilon-semialdehyde decarboxylase (ACMSD) [EC4.1.1.45] plays a key role in regulating NAD biosynthesis.	NAD	165-168	aminocarboxymuconate semialdehyde decarboxylase	Rattus norvegicus	114-119
18404420-9	2007	Since ART expression is limited to naive/resting T cells, P2X7-mediated NAD-induced cell death (NICD) specifically targets this cell population.	NAD	72-75	purinergic receptor P2X 7	Homo sapiens	58-62
17217379-1	2007	BACKGROUND: Polyadenosine diphosphate-ribose (poly(ADP-ribose)) is a nuclear polymer which is derived from nicotinamide adenine dinucleotide (NAD(+)) catalysed by poly(ADP-ribose) polymerase 1 (PARP-1).	NAD	107-140	poly(ADP-ribose) polymerase 1	Homo sapiens	163-192
17141279-3	2007	Reduction of expression of PARP-1 by siRNA increased cellular NAD(+) level and decreased general poly(ADP-ribosyl)ation of proteins.	NAD	62-68	poly(ADP-ribose) polymerase 1	Homo sapiens	27-33
17217379-1	2007	BACKGROUND: Polyadenosine diphosphate-ribose (poly(ADP-ribose)) is a nuclear polymer which is derived from nicotinamide adenine dinucleotide (NAD(+)) catalysed by poly(ADP-ribose) polymerase 1 (PARP-1).	NAD	107-140	poly(ADP-ribose) polymerase 1	Homo sapiens	194-200
17217379-1	2007	BACKGROUND: Polyadenosine diphosphate-ribose (poly(ADP-ribose)) is a nuclear polymer which is derived from nicotinamide adenine dinucleotide (NAD(+)) catalysed by poly(ADP-ribose) polymerase 1 (PARP-1).	NAD	142-148	poly(ADP-ribose) polymerase 1	Homo sapiens	163-192
17217379-1	2007	BACKGROUND: Polyadenosine diphosphate-ribose (poly(ADP-ribose)) is a nuclear polymer which is derived from nicotinamide adenine dinucleotide (NAD(+)) catalysed by poly(ADP-ribose) polymerase 1 (PARP-1).	NAD	142-148	poly(ADP-ribose) polymerase 1	Homo sapiens	194-200
17392604-9	2007	Intra-cellular, PBEF/visfatin acts as a cytosolic enzyme involved in nicotinamide adenine dinucleotide (NAD) synthesis.	NAD	69-102	nicotinamide phosphoribosyltransferase	Mus musculus	16-20
17392604-9	2007	Intra-cellular, PBEF/visfatin acts as a cytosolic enzyme involved in nicotinamide adenine dinucleotide (NAD) synthesis.	NAD	69-102	nicotinamide phosphoribosyltransferase	Mus musculus	21-29
17392604-9	2007	Intra-cellular, PBEF/visfatin acts as a cytosolic enzyme involved in nicotinamide adenine dinucleotide (NAD) synthesis.	NAD	104-107	nicotinamide phosphoribosyltransferase	Mus musculus	16-20
17392604-9	2007	Intra-cellular, PBEF/visfatin acts as a cytosolic enzyme involved in nicotinamide adenine dinucleotide (NAD) synthesis.	NAD	104-107	nicotinamide phosphoribosyltransferase	Mus musculus	21-29
17595514-1	2007	It has been reported that p53 acetylation, which promotes cellular senescence, can be regulated by the NAD(+)-dependent deacetylase SIRT1, the human homolog of yeast Sir2, a protein that modulates lifespan.	NAD	103-109	tumor protein p53	Homo sapiens	26-29
17222007-3	2007	The CNF-coated electrode thus allowed highly sensitive amperometric detection of NADH with a low limit of detection (0.11 muM), low applied potential (+0.06 V), and minimization of surface fouling.	NAD	81-85	latexin	Homo sapiens	122-125
17595514-5	2007	Pre-incubation with the poly (ADP-ribose) polymerase (PARP) inhibitor resulted in preservation of intracellular NAD(+) levels.	NAD	112-118	poly(ADP-ribose) polymerase 1	Homo sapiens	24-52
17595514-5	2007	Pre-incubation with the poly (ADP-ribose) polymerase (PARP) inhibitor resulted in preservation of intracellular NAD(+) levels.	NAD	112-118	poly(ADP-ribose) polymerase 1	Homo sapiens	54-58
17617028-2	2007	PARPs catalyze the formation of long chains of poly(ADP-ribose) onto protein acceptors using NAD(+) as a substrate.	NAD	93-99	tankyrase	Homo sapiens	0-5
17901563-7	2007	The NADH/NADPH-dependent inhibition of pyrogallol autooxidation by the cytosols was completely abolished by the NQO1-specific inhibitor, ES936, suggesting that the endogenously expressed NQO1 could scavenge O2(.-).	NAD	4-8	NAD(P)H quinone dehydrogenase 1	Rattus norvegicus	112-116
17901563-7	2007	The NADH/NADPH-dependent inhibition of pyrogallol autooxidation by the cytosols was completely abolished by the NQO1-specific inhibitor, ES936, suggesting that the endogenously expressed NQO1 could scavenge O2(.-).	NAD	4-8	NAD(P)H quinone dehydrogenase 1	Rattus norvegicus	187-191
17504138-3	2007	PARP-1 act as a DNA nick sensor and is activated by DNA breaks to cleave NAD(+) into nicotinamide and ADP-ribose to synthesize long branching poly(ADP-ribose) polymers (PAR) covalently attached to nuclear acceptor proteins.	NAD	73-79	poly(ADP-ribose) polymerase 1	Homo sapiens	0-6
17430191-3	2007	PARP-1, the best characterised member, works as a DNA damage nick-sensor protein that uses beta-NAD(+) to form polymers of ADP-ribose and has been implicated in DNA repair, maintenance of genomic integrity and mammalian longevity.	NAD	91-102	poly(ADP-ribose) polymerase 1	Homo sapiens	0-6
17430191-4	2007	The generation of free radicals, reactive oxygen species, and peroxynitrite causes overactivation of PARP resulting in the depletion of NAD(+) and ATP and consequently in necrotic cell death and organ dysfunction.	NAD	136-142	poly(ADP-ribose) polymerase 1	Homo sapiens	101-105
17306600-6	2007	Maximal cytochrome c release correlated with mitochondrial dysfunction and complete NAD+ deletion.	NAD	84-88	cytochrome c, somatic	Homo sapiens	8-20
18467771-4	2007	Comparison of the NAD;{+} binding pocket of the modeled TvGAPDH with human GAPDH (hGAPDH) reveals the presence of a hydrophobic pocket near the N-6 position of adenine ring as well as a hydrophobic cleft near O-2" of the adenosine ribose that are absent in the human enzyme.	NAD	18-25	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	58-63
18467771-4	2007	Comparison of the NAD;{+} binding pocket of the modeled TvGAPDH with human GAPDH (hGAPDH) reveals the presence of a hydrophobic pocket near the N-6 position of adenine ring as well as a hydrophobic cleft near O-2" of the adenosine ribose that are absent in the human enzyme.	NAD	18-25	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	82-88
17380790-3	2007	Activation of PARP may dramatically lower the intracellular concentration of its substrate, NAD thus slowing the rate of glycolysis, electron transport and subsequently ATP formation.	NAD	92-95	poly(ADP-ribose) polymerase 1	Homo sapiens	14-18
17484123-1	2007	Poly(ADP-ribose) Polymerase-1 (PARP-1) is the prototypical and most abundantly expressed member of a family of PARPs that catalyze the polymerization of ADP-ribose (ADPR) units from donor NAD" molecules on target proteins.	NAD	188-192	poly(ADP-ribose) polymerase 1	Homo sapiens	0-29
17484123-1	2007	Poly(ADP-ribose) Polymerase-1 (PARP-1) is the prototypical and most abundantly expressed member of a family of PARPs that catalyze the polymerization of ADP-ribose (ADPR) units from donor NAD" molecules on target proteins.	NAD	188-192	poly(ADP-ribose) polymerase 1	Homo sapiens	111-116
21469509-2	2007	Previous research indicates that the cytotoxicity caused by CCl4 may be mediated by the rapid induction of PARP-1, a nuclear repair enzyme, which results in celluar depletion of NAD+ and ATP.	NAD	178-182	poly(ADP-ribose) polymerase 1	Homo sapiens	107-113
17484123-1	2007	Poly(ADP-ribose) Polymerase-1 (PARP-1) is the prototypical and most abundantly expressed member of a family of PARPs that catalyze the polymerization of ADP-ribose (ADPR) units from donor NAD" molecules on target proteins.	NAD	188-192	poly(ADP-ribose) polymerase 1	Homo sapiens	31-37
17396564-1	2007	Phytogenous flavonoid-containing agents (PFCA) are able to initiate electron flow bypassing the NAD-dependent region of respiratory chain, which is related with the activity of DT-diaphorase catalyzing two-electron reduction of quinones to hydroquinones and hydrogen peroxide in the presence of NADH and oxygen.	NAD	295-299	NAD(P)H quinone dehydrogenase 1	Homo sapiens	177-190
17158952-3	2006	We report that mitochondrial respiration defects lead to activation of the Akt survival pathway through a novel mechanism mediated by NADH.	NAD	134-138	AKT serine/threonine kinase 1	Homo sapiens	75-78
17396564-1	2007	Phytogenous flavonoid-containing agents (PFCA) are able to initiate electron flow bypassing the NAD-dependent region of respiratory chain, which is related with the activity of DT-diaphorase catalyzing two-electron reduction of quinones to hydroquinones and hydrogen peroxide in the presence of NADH and oxygen.	NAD	96-99	NAD(P)H quinone dehydrogenase 1	Homo sapiens	177-190
17158952-6	2006	The increase in NADH caused by respiratory deficiency inactivates PTEN through a redox modification mechanism, leading to Akt activation.	NAD	16-20	AKT serine/threonine kinase 1	Homo sapiens	122-125
17099246-1	2006	The nicotinamide adenine dinucleotide (NAD(+))-dependent protein deacetylase SIRT1 has been linked to fatty acid metabolism via suppression of peroxysome proliferator-activated receptor gamma (PPAR-gamma) and to inflammatory processes by deacetylating the transcription factor NF-kappaB.	NAD	4-37	peroxisome proliferator activated receptor gamma	Homo sapiens	143-191
17089016-9	2006	The activity of PARP was calculated by measurement of tritiated NAD incorporation.	NAD	64-67	poly(ADP-ribose) polymerase 1	Homo sapiens	16-20
17099246-1	2006	The nicotinamide adenine dinucleotide (NAD(+))-dependent protein deacetylase SIRT1 has been linked to fatty acid metabolism via suppression of peroxysome proliferator-activated receptor gamma (PPAR-gamma) and to inflammatory processes by deacetylating the transcription factor NF-kappaB.	NAD	4-37	nuclear factor kappa B subunit 1	Homo sapiens	277-286
17099246-1	2006	The nicotinamide adenine dinucleotide (NAD(+))-dependent protein deacetylase SIRT1 has been linked to fatty acid metabolism via suppression of peroxysome proliferator-activated receptor gamma (PPAR-gamma) and to inflammatory processes by deacetylating the transcription factor NF-kappaB.	NAD	39-46	peroxisome proliferator activated receptor gamma	Homo sapiens	143-191
17032644-5	2006	MTHFR was not inhibited by S-adenosylmethionine and, uniquely among folate-metabolizing enzymes, showed dual-cofactor specificity with NADH and NADPH under physiological conditions.	NAD	135-139	methylenetetrahydrofolate reductase	Mus musculus	0-5
17142987-5	2006	The results, together with the intracellular high ratio of NAD+/NADH, suggest that AKR1C12 functions as a dehydrogenase for the endogenous hydroxysteroids and geranylgeraniol in mouse stomach and myeloid cells.	NAD	59-63	aldo-keto reductase family 1, member C12	Mus musculus	83-90
17142987-5	2006	The results, together with the intracellular high ratio of NAD+/NADH, suggest that AKR1C12 functions as a dehydrogenase for the endogenous hydroxysteroids and geranylgeraniol in mouse stomach and myeloid cells.	NAD	64-68	aldo-keto reductase family 1, member C12	Mus musculus	83-90
17099246-1	2006	The nicotinamide adenine dinucleotide (NAD(+))-dependent protein deacetylase SIRT1 has been linked to fatty acid metabolism via suppression of peroxysome proliferator-activated receptor gamma (PPAR-gamma) and to inflammatory processes by deacetylating the transcription factor NF-kappaB.	NAD	39-46	peroxisome proliferator activated receptor gamma	Homo sapiens	193-203
17099246-1	2006	The nicotinamide adenine dinucleotide (NAD(+))-dependent protein deacetylase SIRT1 has been linked to fatty acid metabolism via suppression of peroxysome proliferator-activated receptor gamma (PPAR-gamma) and to inflammatory processes by deacetylating the transcription factor NF-kappaB.	NAD	4-37	peroxisome proliferator activated receptor gamma	Homo sapiens	193-203
17099246-1	2006	The nicotinamide adenine dinucleotide (NAD(+))-dependent protein deacetylase SIRT1 has been linked to fatty acid metabolism via suppression of peroxysome proliferator-activated receptor gamma (PPAR-gamma) and to inflammatory processes by deacetylating the transcription factor NF-kappaB.	NAD	39-46	nuclear factor kappa B subunit 1	Homo sapiens	277-286
16931513-9	2006	Furthermore, ART2.2 IELs are more resistant to NAD-induced cell death than ART2.1 IELs that do not have multimeric auto-ADP-ribosylation activity.	NAD	47-50	ADP-ribosyltransferase 2b	Rattus norvegicus	13-17
17227547-3	2006	We identified one of the mutations by positional cloning as a single base pair change in a gene encoding NADH:cytochrome b5 reductase (CBR1, At5g17770).	NAD	105-109	NADH:cytochrome B5 reductase 1	Arabidopsis thaliana	135-139
16920718-1	2006	After genotoxic stress poly(ADP-ribose) polymerase-1 (PARP-1) can be hyperactivated, causing (ADP-ribosyl)ation of nuclear proteins (including itself), resulting in NAD(+) and ATP depletion and cell death.	NAD	165-171	poly(ADP-ribose) polymerase 1	Homo sapiens	23-52
16920718-1	2006	After genotoxic stress poly(ADP-ribose) polymerase-1 (PARP-1) can be hyperactivated, causing (ADP-ribosyl)ation of nuclear proteins (including itself), resulting in NAD(+) and ATP depletion and cell death.	NAD	165-171	poly(ADP-ribose) polymerase 1	Homo sapiens	54-60
17052202-6	2006	UCP2 induction may also alter fatty acid metabolism by altering NAD/NADH or by facilitating cycling of fatty acid anions.	NAD	64-67	uncoupling protein 2 (mitochondrial, proton carrier)	Mus musculus	0-4
17052202-6	2006	UCP2 induction may also alter fatty acid metabolism by altering NAD/NADH or by facilitating cycling of fatty acid anions.	NAD	68-72	uncoupling protein 2 (mitochondrial, proton carrier)	Mus musculus	0-4
16923962-5	2006	Human SIRT1 (hSIRT1) repression of DHT-induced AR signaling requires the NAD-dependent catalytic function of hSIRT1 and the AR lysine residues deacetylated by SIRT1.	NAD	73-76	androgen receptor	Homo sapiens	47-49
17088420-3	2006	The NAD+ -dependent isoform (11HSD2) is an oxidase that restrains the effect of hormones due to 11beta-oxidation of cortisol and corticosterone to their 11-oxo derivatives.	NAD	4-8	hydroxysteroid 11-beta dehydrogenase 2	Mus musculus	29-35
16294211-5	2006	The necrotic component is caspase 3-independent and is caused by PARP-induced [ATP](i)/NAD(+) depletion, resulting in membrane permeabilization.	NAD	87-93	poly(ADP-ribose) polymerase 1	Homo sapiens	65-69
17150157-5	2006	Paradoxically, when stressful conditions similar to those experienced during vascular reconstructions result in overactivation of PARP, depletion of cellular levels of adenosine triphosphate and nicotinamide adenine dinucleotide can result in exacerbation of tissue injury.	NAD	195-228	poly(ADP-ribose) polymerase 1	Homo sapiens	130-134
17132781-11	2006	Studies will be described where the NADH binding and oxidation kinetics at complex I in the intact mitochondria were determined using fluorescence lifetime and enzyme dependent-fluorescence recovery after photo-oxidation (ED-FRAP) techniques.	NAD	36-40	mechanistic target of rapamycin kinase	Homo sapiens	225-229
16870158-2	2006	PARP-1 overactivation and the subsequent extensive turnover of its substrate NAD+ put a large demand on mitochondrial ATP-production.	NAD	77-81	poly(ADP-ribose) polymerase 1	Homo sapiens	0-6
16923992-5	2006	The increase in NADPH oxidase activity and the expression of p22(phox), a reduced nicotinamide-adenine dinucleotide/reduced nicotinamide-adenine dinucleotide phosphate oxidase subunit, after cuff placement was also attenuated in ATRAP-Tg mice.	NAD	82-115	dynein cytoplasmic 1 heavy chain 1	Mus musculus	61-64
16807375-0	2006	Regulation of mouse hepatic alpha-amino-beta-carboxymuconate-epsilon-semialdehyde decarboxylase, a key enzyme in the tryptophan-nicotinamide adenine dinucleotide pathway, by hepatocyte nuclear factor 4alpha and peroxisome proliferator-activated receptor alpha.	NAD	128-161	peroxisome proliferator activated receptor alpha	Mus musculus	211-259
16964967-5	2006	Additionally, the Thi4 structure reveals the first protein structure with a GR(2) domain that binds NAD instead of FAD, raising interesting questions about how this protein evolved from a flavoenzyme to a NAD binding enzyme.	NAD	100-103	thiamine thiazole synthase	Saccharomyces cerevisiae S288C	18-22
16908017-8	2006	Generation of superoxide (O(2)(-)) of the smooth muscle cells (with NADH presence), measured using the lucigenin-enhanced chemiluminescence, was markedly increased by angiotensin II (100 nM) and homocysteine (30 microM).	NAD	68-72	angiotensinogen	Homo sapiens	167-181
16964967-5	2006	Additionally, the Thi4 structure reveals the first protein structure with a GR(2) domain that binds NAD instead of FAD, raising interesting questions about how this protein evolved from a flavoenzyme to a NAD binding enzyme.	NAD	205-208	thiamine thiazole synthase	Saccharomyces cerevisiae S288C	18-22
16884682-1	2006	Yeast NAD+-specific isocitrate dehydrogenase (IDH) is an octamer of four IDH1 and four IDH2 subunits, and the basic structural unit of the enzyme is an IDH1/IDH2 heterodimer.	NAD	6-10	isocitrate dehydrogenase (NAD(+)) IDH1	Saccharomyces cerevisiae S288C	73-77
16884682-1	2006	Yeast NAD+-specific isocitrate dehydrogenase (IDH) is an octamer of four IDH1 and four IDH2 subunits, and the basic structural unit of the enzyme is an IDH1/IDH2 heterodimer.	NAD	6-10	isocitrate dehydrogenase (NAD(+)) IDH1	Saccharomyces cerevisiae S288C	152-156
16905135-0	2006	Bradykinin activates ADP-ribosyl cyclase in neuroblastoma cells: intracellular concentration decrease in NAD and increase in cyclic ADP-ribose.	NAD	105-108	kininogen 1	Homo sapiens	0-10
16905135-3	2006	Application of 300nM BK to living NGPM1-27 cells decreased NAD(+) to 78% of the prestimulation level at 30s.	NAD	59-65	kininogen 1	Homo sapiens	21-23
16961761-7	2006	(2) Non-drinker rats carry a previously unreported allele of aldehyde dehydrogenase-2 (Aldh2) that encodes an enzyme with a low affinity for Nicotinamide-adenine-dinuclectide (NAD+) (Aldh2(2)), while drinker rats present two Aldh2 alleles (Aldh2(1) and Aldh2(3)) with four- to fivefold higher affinities for NAD+.	NAD	176-180	aldehyde dehydrogenase 1 family, member A1	Rattus norvegicus	61-85
16961761-7	2006	(2) Non-drinker rats carry a previously unreported allele of aldehyde dehydrogenase-2 (Aldh2) that encodes an enzyme with a low affinity for Nicotinamide-adenine-dinuclectide (NAD+) (Aldh2(2)), while drinker rats present two Aldh2 alleles (Aldh2(1) and Aldh2(3)) with four- to fivefold higher affinities for NAD+.	NAD	176-180	aldehyde dehydrogenase 1 family, member A1	Rattus norvegicus	87-92
16961761-7	2006	(2) Non-drinker rats carry a previously unreported allele of aldehyde dehydrogenase-2 (Aldh2) that encodes an enzyme with a low affinity for Nicotinamide-adenine-dinuclectide (NAD+) (Aldh2(2)), while drinker rats present two Aldh2 alleles (Aldh2(1) and Aldh2(3)) with four- to fivefold higher affinities for NAD+.	NAD	176-180	aldehyde dehydrogenase 1 family, member A1	Rattus norvegicus	183-188
16961761-7	2006	(2) Non-drinker rats carry a previously unreported allele of aldehyde dehydrogenase-2 (Aldh2) that encodes an enzyme with a low affinity for Nicotinamide-adenine-dinuclectide (NAD+) (Aldh2(2)), while drinker rats present two Aldh2 alleles (Aldh2(1) and Aldh2(3)) with four- to fivefold higher affinities for NAD+.	NAD	176-180	aldehyde dehydrogenase 1 family, member A1	Rattus norvegicus	183-188
16906506-2	2006	Using HEK, intracellular 3H-labeled NAD+ (3H-adenine) was metabolically generated and then these cells were exposed to SM (1 mM).	NAD	36-40	EPH receptor A3	Homo sapiens	6-9
16961761-7	2006	(2) Non-drinker rats carry a previously unreported allele of aldehyde dehydrogenase-2 (Aldh2) that encodes an enzyme with a low affinity for Nicotinamide-adenine-dinuclectide (NAD+) (Aldh2(2)), while drinker rats present two Aldh2 alleles (Aldh2(1) and Aldh2(3)) with four- to fivefold higher affinities for NAD+.	NAD	308-312	aldehyde dehydrogenase 1 family, member A1	Rattus norvegicus	61-85
16961761-7	2006	(2) Non-drinker rats carry a previously unreported allele of aldehyde dehydrogenase-2 (Aldh2) that encodes an enzyme with a low affinity for Nicotinamide-adenine-dinuclectide (NAD+) (Aldh2(2)), while drinker rats present two Aldh2 alleles (Aldh2(1) and Aldh2(3)) with four- to fivefold higher affinities for NAD+.	NAD	308-312	aldehyde dehydrogenase 1 family, member A1	Rattus norvegicus	87-92
16961761-11	2006	Studies also show that the low alcohol consumption phenotype of Aldh2(2)/Aldh2(2) animals depends on the existence of a maternally derived low-activity mitochondrial reduced form of nicotinamide-adenine-dinucleotide (NADH)-ubiquinone complex I.	NAD	182-215	aldehyde dehydrogenase 1 family, member A1	Rattus norvegicus	64-69
16961761-11	2006	Studies also show that the low alcohol consumption phenotype of Aldh2(2)/Aldh2(2) animals depends on the existence of a maternally derived low-activity mitochondrial reduced form of nicotinamide-adenine-dinucleotide (NADH)-ubiquinone complex I.	NAD	182-215	aldehyde dehydrogenase 1 family, member A1	Rattus norvegicus	73-78
17286969-1	2006	Contact of T lymphocytes with nicotinamide adenine dinucleotide (NAD) or ATP causes cell death that requires expression of purinergic receptor P2X(7) (P2X(7)R).	NAD	30-63	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	151-158
17286969-1	2006	Contact of T lymphocytes with nicotinamide adenine dinucleotide (NAD) or ATP causes cell death that requires expression of purinergic receptor P2X(7) (P2X(7)R).	NAD	65-68	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	151-158
16762039-6	2006	Here, we show that HIC1 interacts with both CtBP1 and CtBP2 and that this interaction is stimulated by agents increasing NADH levels.	NAD	121-125	C-terminal binding protein 2	Homo sapiens	54-59
16814740-1	2006	Cytochrome b5 reductase (cb5r), a member of the flavoprotein transhydrogenase family of oxidoreductase enzymes, catalyzes the transfer of reducing equivalents from the physiological electron donor, NADH, to two molecules of cytochrome b5.	NAD	198-202	cytochrome b5 reductase 3	Canis lupus familiaris	25-29
16873119-1	2006	Dihydrofolate reductase (DHFR) maintains the intracellular pool of tetrahydrofolate through catalysis of hydrogen transfer from reduced nicotinamide adenine dinucleotide to 7,8-dihydrofolate.	NAD	136-169	dihydrofolate reductase	Escherichia coli	25-29
16884709-3	2006	At non-cytotoxic concentrations both PCB153 and PCB126 induced decreases in intracellular NAD(P)H and NAD+ in T47D and MDA-MB-231 cells where T47D cells were more resistant to PCB-induced reduction in intracellular NAD(P)H than MDA-MB-231 cells.	NAD	102-106	pyruvate carboxylase	Homo sapiens	37-40
16884709-5	2006	These results imply that decreases in intracellular NAD(P)H in PCB-treated cells may be, in part, due to depletion of intracellular NAD+ pool mediated by PARP-1 activation through formation of DNA strand breaks.	NAD	132-136	pyruvate carboxylase	Homo sapiens	63-66
16884709-5	2006	These results imply that decreases in intracellular NAD(P)H in PCB-treated cells may be, in part, due to depletion of intracellular NAD+ pool mediated by PARP-1 activation through formation of DNA strand breaks.	NAD	132-136	poly(ADP-ribose) polymerase 1	Homo sapiens	154-160
16854233-1	2006	BACKGROUND: Poly(ADP-ribosyl)ation is a posttranslational modification of nuclear proteins catalysed by poly(ADP-ribose) polymerases (PARPs), using NAD+ as a substrate.	NAD	148-152	poly(ADP-ribose) polymerase 1	Homo sapiens	134-139
16829982-1	2006	The addition to proteins of the negatively charged polymer of ADP-ribose (PAR), which is synthesized by PAR polymerases (PARPs) from NAD(+), is a unique post-translational modification.	NAD	133-139	poly(ADP-ribose) polymerase 1	Homo sapiens	121-126
16453289-7	2006	When soluble ART2 was incubated with serum proteins in the presence of [32P]-labeled NAD, several serum proteins were ADP-ribosylated in a thiol-specific manner.	NAD	85-88	ADP-ribosyltransferase 1	Homo sapiens	13-17
16497729-4	2006	The acetylation of ERalpha by p300 is reversed by native cellular deacetylases, including trichostatin A-sensitive enzymes (i.e. class I and II deacetylases) and nicotinamide adenine dinucleotide-dependent/nicotinamide-sensitive enzymes (i.e. class III deacetylases, such as sirtuin 1).	NAD	162-195	estrogen receptor 1	Homo sapiens	19-26
16604373-8	2006	Our data indicate that NAD metabolites accumulate in plasma of children with CRF and their combined effect could lead to the inhibition of PARP-1 activity.	NAD	23-26	poly(ADP-ribose) polymerase 1	Homo sapiens	139-145
16805776-9	2006	During pathological conditions activation of the NAD(+)-consuming enzyme poly(APD-ribose) polymerase-1 (PARP-1) is also a likely mechanism for NO-mediated energy failure and neurotoxicity.	NAD	49-55	poly(ADP-ribose) polymerase 1	Homo sapiens	73-102
16805776-9	2006	During pathological conditions activation of the NAD(+)-consuming enzyme poly(APD-ribose) polymerase-1 (PARP-1) is also a likely mechanism for NO-mediated energy failure and neurotoxicity.	NAD	49-55	poly(ADP-ribose) polymerase 1	Homo sapiens	104-110
16807528-0	2006	NADH binding properties of rabbit lens lambda-crystallin.	NAD	0-4	lambda-crystallin	Oryctolagus cuniculus	39-56
16807528-1	2006	PURPOSE: The present investigation aims to evaluate the NADH binding ability of lambda-crystallin, a taxon-specific enzyme-crystallin, in the rabbit lens.	NAD	56-60	lambda-crystallin	Oryctolagus cuniculus	80-97
16807528-3	2006	Analysis of NADH bound to the lambda-crystallin preparation was performed using spectrophotometric and enzymological methods.	NAD	12-16	lambda-crystallin	Oryctolagus cuniculus	30-47
16807528-10	2006	Additional looser binding of added NADH to lambda-crystallin was observed in both the lambda/betaL1-crystallin fraction (including the full-length 33 kDa protein: 34%; 25-30 kDa proteins, most of which might be generated by cleavage of the 33 kDa protein: 64%) and the partially purified enzyme-crystallin.	NAD	35-39	lambda-crystallin	Oryctolagus cuniculus	43-60
16807528-13	2006	CONCLUSIONS: From the present study, we conclude that lambda-crystallin plays a sufficiently important role as a NADH binding protein to maintain high levels of this nucleotide in the rabbit lens.	NAD	113-117	lambda-crystallin	Oryctolagus cuniculus	54-71
16740659-2	2006	In this study, we found that hypoxia increased free NADH levels in cancer cells, promoting CtBP recruitment to the E-cadherin promoter.	NAD	52-56	cadherin 1	Homo sapiens	115-125
16604373-2	2006	Our research was aimed at establishing whether chronic renal failure (CRF) in children leads to the elevation of plasma NAD metabolites sufficient to inhibit PARP-1 activity.	NAD	120-123	poly(ADP-ribose) polymerase 1	Homo sapiens	158-164
16604373-4	2006	The effect of these NAD metabolites on PARP-1 activity was studied in vitro.	NAD	20-23	poly(ADP-ribose) polymerase 1	Homo sapiens	39-45
16376922-1	2006	We have investigated the electrocatalytic dehalogenation of beta-methylallyl chloride (beta-mAC), widely used in the polymer industry, using [Co(I)(bpy)3]+ (where bpy=2,2"-bipyridine) electrochemically generated in situ from [Co(II)(bpy)3]2+ at a glassy carbon electrode in the presence of three different cationic surfactants in aqueous solution.	NAD	142-147	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	226-231
16444750-9	2006	The presented results suggest that GAPDH and LDH have a functional interaction that can affect NAD(+)/NADH metabolism and glycolysis in living cells.	NAD	95-101	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	35-40
16444750-9	2006	The presented results suggest that GAPDH and LDH have a functional interaction that can affect NAD(+)/NADH metabolism and glycolysis in living cells.	NAD	102-106	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	35-40
16516847-0	2006	TNF regulates cellular NAD+ metabolism in primary macrophages.	NAD	23-27	tumor necrosis factor	Homo sapiens	0-3
16892389-0	2006	Poly(ADP-ribose)-polymerase-catalyzed hydrolysis of NAD+: QM/MM simulation of the enzyme reaction.	NAD	52-56	poly(ADP-ribose) polymerase 1	Homo sapiens	0-27
16892389-1	2006	Poly(ADP-ribose) polymerase (PARP) is a nuclear enzyme which uses NAD+ as substrate and catalyzes the transfer of multiple units of ADP-ribose to target proteins.	NAD	66-70	poly(ADP-ribose) polymerase 1	Homo sapiens	0-27
16892389-1	2006	Poly(ADP-ribose) polymerase (PARP) is a nuclear enzyme which uses NAD+ as substrate and catalyzes the transfer of multiple units of ADP-ribose to target proteins.	NAD	66-70	poly(ADP-ribose) polymerase 1	Homo sapiens	29-33
16892389-3	2006	Herein, we use the PARP-catalyzed reaction of NAD+ hydrolysis as a model for gaining insight into the molecular details of the catalytic mechanism of PARP.	NAD	46-50	poly(ADP-ribose) polymerase 1	Homo sapiens	19-23
16892389-3	2006	Herein, we use the PARP-catalyzed reaction of NAD+ hydrolysis as a model for gaining insight into the molecular details of the catalytic mechanism of PARP.	NAD	46-50	poly(ADP-ribose) polymerase 1	Homo sapiens	150-154
16913409-0	2006	Stimulation by cytochrome c of the external pathway of NADH oxidation and ascorbate oxidation in the presence of TMPD.	NAD	55-59	cytochrome c, somatic	Homo sapiens	15-27
16376383-3	2006	In liver cytosol, both NADPH and NADH were effective as cofactors for 20alpha-HSD activity, although NADPH was better than NADH for the enzyme activity.	NAD	33-37	aldo-keto reductase family 1, member C18	Mus musculus	70-81
17048193-0	2006	Differential effects of pyrazinamide and clofibrate on gene expression of rat hepatic alpha-amino-beta-carboxymuconate-epsilon-semialdehyde decarboxylase, a key enzyme of the tryptophan-NAD pathway.	NAD	186-189	aminocarboxymuconate semialdehyde decarboxylase	Rattus norvegicus	86-153
17048193-1	2006	Hepatic alpha-amino-beta-carboxymuconate-epsilon-semialdehyde decarboxylase (ACMSD) [EC4.1.1.45] plays a key role in regulating NAD biosynthesis from tryptophan.	NAD	128-131	aminocarboxymuconate semialdehyde decarboxylase	Rattus norvegicus	8-75
17048193-1	2006	Hepatic alpha-amino-beta-carboxymuconate-epsilon-semialdehyde decarboxylase (ACMSD) [EC4.1.1.45] plays a key role in regulating NAD biosynthesis from tryptophan.	NAD	128-131	aminocarboxymuconate semialdehyde decarboxylase	Rattus norvegicus	77-82
16516847-7	2006	Treatment of macrophages with TNF decreased NAD(+) levels over time, suggesting that increases in NAD(+)-degrading enzymes were dominant.	NAD	44-50	tumor necrosis factor	Homo sapiens	30-33
16516847-7	2006	Treatment of macrophages with TNF decreased NAD(+) levels over time, suggesting that increases in NAD(+)-degrading enzymes were dominant.	NAD	98-104	tumor necrosis factor	Homo sapiens	30-33
16516847-8	2006	To evaluate whether this was the case, we measured TNF-mediated changes in NAD(+) levels in animals where CD38 was genetically deleted.	NAD	75-81	tumor necrosis factor	Homo sapiens	51-54
16516847-9	2006	In CD38-/- macrophages, the effects of TNF were reversed, with TNF increasing NAD(+) levels over time.	NAD	78-84	tumor necrosis factor	Homo sapiens	63-66
16516847-10	2006	The significance of our findings is threefold: (1) we establish that TNF affects NAD(+) metabolism by regulating the expression of major NAD(+) metabolic enzymes, (2) TNF-induced decreases in cellular NAD(+) levels were carried out through the up-regulation of extracellularly situated enzymes, and (3) we provide a mechanism for the observed clinical connection of TNF-dependent diseases to tissue reductions in NAD(+) content.	NAD	81-87	tumor necrosis factor	Homo sapiens	69-72
16516847-10	2006	The significance of our findings is threefold: (1) we establish that TNF affects NAD(+) metabolism by regulating the expression of major NAD(+) metabolic enzymes, (2) TNF-induced decreases in cellular NAD(+) levels were carried out through the up-regulation of extracellularly situated enzymes, and (3) we provide a mechanism for the observed clinical connection of TNF-dependent diseases to tissue reductions in NAD(+) content.	NAD	81-87	tumor necrosis factor	Homo sapiens	167-170
16516847-10	2006	The significance of our findings is threefold: (1) we establish that TNF affects NAD(+) metabolism by regulating the expression of major NAD(+) metabolic enzymes, (2) TNF-induced decreases in cellular NAD(+) levels were carried out through the up-regulation of extracellularly situated enzymes, and (3) we provide a mechanism for the observed clinical connection of TNF-dependent diseases to tissue reductions in NAD(+) content.	NAD	81-87	tumor necrosis factor	Homo sapiens	167-170
16516847-10	2006	The significance of our findings is threefold: (1) we establish that TNF affects NAD(+) metabolism by regulating the expression of major NAD(+) metabolic enzymes, (2) TNF-induced decreases in cellular NAD(+) levels were carried out through the up-regulation of extracellularly situated enzymes, and (3) we provide a mechanism for the observed clinical connection of TNF-dependent diseases to tissue reductions in NAD(+) content.	NAD	137-143	tumor necrosis factor	Homo sapiens	69-72
16516847-10	2006	The significance of our findings is threefold: (1) we establish that TNF affects NAD(+) metabolism by regulating the expression of major NAD(+) metabolic enzymes, (2) TNF-induced decreases in cellular NAD(+) levels were carried out through the up-regulation of extracellularly situated enzymes, and (3) we provide a mechanism for the observed clinical connection of TNF-dependent diseases to tissue reductions in NAD(+) content.	NAD	137-143	tumor necrosis factor	Homo sapiens	167-170
16516847-10	2006	The significance of our findings is threefold: (1) we establish that TNF affects NAD(+) metabolism by regulating the expression of major NAD(+) metabolic enzymes, (2) TNF-induced decreases in cellular NAD(+) levels were carried out through the up-regulation of extracellularly situated enzymes, and (3) we provide a mechanism for the observed clinical connection of TNF-dependent diseases to tissue reductions in NAD(+) content.	NAD	137-143	tumor necrosis factor	Homo sapiens	167-170
16516847-2	2006	Despite a well-established connection of TNF to metabolism, the relationship between TNF and NAD(+) metabolism remains unclear.	NAD	93-99	tumor necrosis factor	Homo sapiens	85-88
16516847-10	2006	The significance of our findings is threefold: (1) we establish that TNF affects NAD(+) metabolism by regulating the expression of major NAD(+) metabolic enzymes, (2) TNF-induced decreases in cellular NAD(+) levels were carried out through the up-regulation of extracellularly situated enzymes, and (3) we provide a mechanism for the observed clinical connection of TNF-dependent diseases to tissue reductions in NAD(+) content.	NAD	137-143	tumor necrosis factor	Homo sapiens	69-72
16516847-10	2006	The significance of our findings is threefold: (1) we establish that TNF affects NAD(+) metabolism by regulating the expression of major NAD(+) metabolic enzymes, (2) TNF-induced decreases in cellular NAD(+) levels were carried out through the up-regulation of extracellularly situated enzymes, and (3) we provide a mechanism for the observed clinical connection of TNF-dependent diseases to tissue reductions in NAD(+) content.	NAD	137-143	tumor necrosis factor	Homo sapiens	167-170
16516847-3	2006	In this report, we evaluated the effects of TNF on NAD(+) metabolism in cells that are TNF"s primary autocrine target-macrophages.	NAD	51-57	tumor necrosis factor	Homo sapiens	44-47
16516847-10	2006	The significance of our findings is threefold: (1) we establish that TNF affects NAD(+) metabolism by regulating the expression of major NAD(+) metabolic enzymes, (2) TNF-induced decreases in cellular NAD(+) levels were carried out through the up-regulation of extracellularly situated enzymes, and (3) we provide a mechanism for the observed clinical connection of TNF-dependent diseases to tissue reductions in NAD(+) content.	NAD	137-143	tumor necrosis factor	Homo sapiens	167-170
16516847-3	2006	In this report, we evaluated the effects of TNF on NAD(+) metabolism in cells that are TNF"s primary autocrine target-macrophages.	NAD	51-57	tumor necrosis factor	Homo sapiens	87-90
16516847-10	2006	The significance of our findings is threefold: (1) we establish that TNF affects NAD(+) metabolism by regulating the expression of major NAD(+) metabolic enzymes, (2) TNF-induced decreases in cellular NAD(+) levels were carried out through the up-regulation of extracellularly situated enzymes, and (3) we provide a mechanism for the observed clinical connection of TNF-dependent diseases to tissue reductions in NAD(+) content.	NAD	137-143	tumor necrosis factor	Homo sapiens	69-72
16516847-10	2006	The significance of our findings is threefold: (1) we establish that TNF affects NAD(+) metabolism by regulating the expression of major NAD(+) metabolic enzymes, (2) TNF-induced decreases in cellular NAD(+) levels were carried out through the up-regulation of extracellularly situated enzymes, and (3) we provide a mechanism for the observed clinical connection of TNF-dependent diseases to tissue reductions in NAD(+) content.	NAD	137-143	tumor necrosis factor	Homo sapiens	167-170
16516847-10	2006	The significance of our findings is threefold: (1) we establish that TNF affects NAD(+) metabolism by regulating the expression of major NAD(+) metabolic enzymes, (2) TNF-induced decreases in cellular NAD(+) levels were carried out through the up-regulation of extracellularly situated enzymes, and (3) we provide a mechanism for the observed clinical connection of TNF-dependent diseases to tissue reductions in NAD(+) content.	NAD	137-143	tumor necrosis factor	Homo sapiens	167-170
16516847-4	2006	We designed real-time PCR primers to all NAD(+) metabolic enzymes, which we used to examine TNF-induced changes over time.	NAD	41-47	tumor necrosis factor	Homo sapiens	92-95
16516847-5	2006	We found that TNF paradoxically up-regulated enzymes that served to increase NAD(+) levels, such as IDO and PBEF, as well as enzymes that decrease NAD(+) levels, such as CD38 and CD157.	NAD	77-83	tumor necrosis factor	Homo sapiens	14-17
16516847-5	2006	We found that TNF paradoxically up-regulated enzymes that served to increase NAD(+) levels, such as IDO and PBEF, as well as enzymes that decrease NAD(+) levels, such as CD38 and CD157.	NAD	147-153	tumor necrosis factor	Homo sapiens	14-17
16516847-6	2006	The significance of these mRNA changes was evaluated by examining TNF-mediated changes in cellular NAD(+) levels.	NAD	99-105	tumor necrosis factor	Homo sapiens	66-69
16618762-1	2006	SIRT1 and other NAD-dependent deacetylases have been implicated in control of cellular responses to stress and in tumorigenesis through deacetylation of important regulatory proteins, including p53 and the BCL6 oncoprotein.	NAD	16-19	tumor protein p53	Homo sapiens	194-197
16442077-12	2006	Physiologically, therefore, modulation of the expression of the NAD(+)-sensing enzyme, CD38, by Ca(2+), cAMP, and cytokines, such as TNF-alpha may contribute to coupling the intense metabolic activity of osteoclasts and osteoblasts to their respective bone-resorbing and bone-forming functions.	NAD	64-70	tumor necrosis factor	Mus musculus	133-142
16628003-2	2006	Sirtuins (SIRTs) are deacetylases that promote cell survival whereas poly(ADP-ribose) polymerases (PARPs) can act both as survival and death inducing factor and the two protein families are strictly dependent on NAD(+) for their activities.	NAD	212-218	poly(ADP-ribose) polymerase 1	Homo sapiens	99-104
16677153-2	2006	It is hypothesized that activation of the receptor for advanced glycation end products (RAGE) might contribute to acetaminophen-induced liver toxicity by virtue of its ability to generate reactive oxygen species, at least in part via nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, and thereby activate downstream signaling pathways leading to cellular injury.	NAD	234-267	advanced glycosylation end product-specific receptor	Mus musculus	88-92
20641312-7	2004	The hyperactivation of poly(ADP-ribose) polymerase 1 (PARP-1) followed by depletion of NAD(+) pools is thought to be the mechanism taking place specifically during necrosis, and probing PARP-1 activity is currently being investigated as a possible route for imaging and evaluating cellular death through necrosis.	NAD	87-93	poly(ADP-ribose) polymerase 1	Homo sapiens	54-60
20641312-7	2004	The hyperactivation of poly(ADP-ribose) polymerase 1 (PARP-1) followed by depletion of NAD(+) pools is thought to be the mechanism taking place specifically during necrosis, and probing PARP-1 activity is currently being investigated as a possible route for imaging and evaluating cellular death through necrosis.	NAD	87-93	poly(ADP-ribose) polymerase 1	Homo sapiens	186-192
16172904-10	2006	Cytochrome c and liver microsomes also reduced satraplatin to JM118 in a manner that depended upon the presence of NADH and was inhibited by carbon monoxide.	NAD	115-119	cytochrome c, somatic	Homo sapiens	0-12
16337154-9	2006	All these data suggest that contrary to the original view, which considered preservation of NAD+ and consequently ATP pools as the exclusive underlying mechanism for the cytoprotective effect of PARP inhibitors, the activation of PI3-kinase/Akt pathway and related processes are at least equally important in the cardioprotective effects of PARP inhibitors during ischemia-reperfusion.	NAD	92-96	poly(ADP-ribose) polymerase 1	Homo sapiens	195-199
16041576-8	2006	In addition, genes involved in NAD metabolism, i.e. BNA2, BNA3, BNA4 and BNA6, or those involved in the TCA cycle and glutamate metabolism, i.e. MEU1, CIT1, CIT2, KDG1 and KDG2, displayed significant changes in expression.	NAD	31-34	kynurenine 3-monooxygenase	Saccharomyces cerevisiae S288C	64-68
16111903-3	2006	Activation of PARP may dramatically lower the intracellular concentration of its substrate, nicotinamide adenine dinucleotide, thus slowing the rate of glycolysis, electron transport, and subsequently ATP formation.	NAD	92-125	poly(ADP-ribose) polymerase 1	Homo sapiens	14-18
16356938-1	2006	CtBP family members, CtBP1 and CtBP2, are unique transcriptional regulators that adapt a metabolic enzyme fold, and their activities are regulated by NAD(H)-binding.	NAD	150-156	C-terminal binding protein 2	Homo sapiens	31-36
16529497-3	2006	In the first, the Co-C bond cleaves to produce Co(I) and a chlorovinyl radical, while the second pathway results in the formation of Co(II) and a chlorovinyl anion.	NAD	47-52	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	133-139
16227345-6	2006	Fluorescent spectrometric analysis demonstrated that incubation of SR with NADH time dependently produced O2-*, which could be substantially blocked by the specific NAD(P)H oxidase inhibitors diphenylene iodonium and apocynin and by SOD or its mimetic tiron.	NAD	75-79	superoxide dismutase 1	Homo sapiens	233-236
16227345-8	2006	In experiments of lipid bilayer channel reconstitution, addition of NADH to the cis solution significantly increased the activity of RyR/Ca2+ release channels from these SR preparations from CASM, with a maximal increase in channel open probability from 0.0044 +/- 0.0005 to 0.0213 +/- 0.0018; this effect of NADH was markedly blocked in the presence of SOD or tiron or the NAD(P)H oxidase inhibitors diphenylene iodonium, N-vanillylnonanamide, and apocynin.	NAD	68-72	ryanodine receptor 1	Homo sapiens	133-136
16227345-8	2006	In experiments of lipid bilayer channel reconstitution, addition of NADH to the cis solution significantly increased the activity of RyR/Ca2+ release channels from these SR preparations from CASM, with a maximal increase in channel open probability from 0.0044 +/- 0.0005 to 0.0213 +/- 0.0018; this effect of NADH was markedly blocked in the presence of SOD or tiron or the NAD(P)H oxidase inhibitors diphenylene iodonium, N-vanillylnonanamide, and apocynin.	NAD	68-72	superoxide dismutase 1	Homo sapiens	354-357
16227345-8	2006	In experiments of lipid bilayer channel reconstitution, addition of NADH to the cis solution significantly increased the activity of RyR/Ca2+ release channels from these SR preparations from CASM, with a maximal increase in channel open probability from 0.0044 +/- 0.0005 to 0.0213 +/- 0.0018; this effect of NADH was markedly blocked in the presence of SOD or tiron or the NAD(P)H oxidase inhibitors diphenylene iodonium, N-vanillylnonanamide, and apocynin.	NAD	309-313	ryanodine receptor 1	Homo sapiens	133-136
16359865-1	2006	A series of novel pyrrolocarbazole lactams was identified as potent PARP-1 inhibitors in vitro and in a PC12 cellular NAD(+) depletion assay.	NAD	118-124	poly(ADP-ribose) polymerase 1	Homo sapiens	68-74
16337154-1	2006	Poly(ADP-ribose) polymerase (PARP) inhibitors protect hearts from ischemia-reperfusion (IR)-induced damages by limiting nicotinamide adenine dinucleotide (NAD+) and ATP depletion, and by other, not yet elucidated mechanisms.	NAD	120-153	poly(ADP-ribose) polymerase 1	Homo sapiens	0-27
16337154-1	2006	Poly(ADP-ribose) polymerase (PARP) inhibitors protect hearts from ischemia-reperfusion (IR)-induced damages by limiting nicotinamide adenine dinucleotide (NAD+) and ATP depletion, and by other, not yet elucidated mechanisms.	NAD	120-153	poly(ADP-ribose) polymerase 1	Homo sapiens	29-33
16337154-1	2006	Poly(ADP-ribose) polymerase (PARP) inhibitors protect hearts from ischemia-reperfusion (IR)-induced damages by limiting nicotinamide adenine dinucleotide (NAD+) and ATP depletion, and by other, not yet elucidated mechanisms.	NAD	155-159	poly(ADP-ribose) polymerase 1	Homo sapiens	0-27
16337154-1	2006	Poly(ADP-ribose) polymerase (PARP) inhibitors protect hearts from ischemia-reperfusion (IR)-induced damages by limiting nicotinamide adenine dinucleotide (NAD+) and ATP depletion, and by other, not yet elucidated mechanisms.	NAD	155-159	poly(ADP-ribose) polymerase 1	Homo sapiens	29-33
16415206-4	2006	We found that the gpdhc1 T-DNA insertional mutants exhibited increased NADH/NAD+ ratios compared with wild-type plants under standard growth conditions, as well as impaired adjustment of NADH/NAD+ ratios under stress simulated by abscisic acid treatment.	NAD	71-75	6-phosphogluconate dehydrogenase family protein	Arabidopsis thaliana	18-24
16195541-9	2006	Akt phosphorylation and cell proliferation were also blocked by the antioxidants, N-acetyl-l-cysteine, Ginko biloba 501, and tiron, the reduced nicotinamide adenine dinucleotide phosphate oxidase inhibitor, diphenyleneiodonium, and the 5-HT2 receptor antagonists ketanserin and mianserin, but not by the 5-HT serotonin transporter or 5-HT 1B/1D receptor antagonists.	NAD	144-177	AKT serine/threonine kinase 1	Homo sapiens	0-3
16415206-4	2006	We found that the gpdhc1 T-DNA insertional mutants exhibited increased NADH/NAD+ ratios compared with wild-type plants under standard growth conditions, as well as impaired adjustment of NADH/NAD+ ratios under stress simulated by abscisic acid treatment.	NAD	76-80	6-phosphogluconate dehydrogenase family protein	Arabidopsis thaliana	18-24
16415206-4	2006	We found that the gpdhc1 T-DNA insertional mutants exhibited increased NADH/NAD+ ratios compared with wild-type plants under standard growth conditions, as well as impaired adjustment of NADH/NAD+ ratios under stress simulated by abscisic acid treatment.	NAD	187-191	6-phosphogluconate dehydrogenase family protein	Arabidopsis thaliana	18-24
16415206-4	2006	We found that the gpdhc1 T-DNA insertional mutants exhibited increased NADH/NAD+ ratios compared with wild-type plants under standard growth conditions, as well as impaired adjustment of NADH/NAD+ ratios under stress simulated by abscisic acid treatment.	NAD	192-196	6-phosphogluconate dehydrogenase family protein	Arabidopsis thaliana	18-24
16385446-8	2006	In an application to asthma case-control data from the Children"s Health Study, FITF identified a significant multilocus effect between the nicotinamide adenine dinucleotide (phosphate) reduced:quinone oxidoreductase gene (NQO1), myeloperoxidase gene (MPO), and catalase gene (CAT) (unadjusted P = .00026), three genes that are involved in the oxidative stress pathway.	NAD	140-173	NAD(P)H quinone dehydrogenase 1	Homo sapiens	223-227
16385446-8	2006	In an application to asthma case-control data from the Children"s Health Study, FITF identified a significant multilocus effect between the nicotinamide adenine dinucleotide (phosphate) reduced:quinone oxidoreductase gene (NQO1), myeloperoxidase gene (MPO), and catalase gene (CAT) (unadjusted P = .00026), three genes that are involved in the oxidative stress pathway.	NAD	140-173	myeloperoxidase	Homo sapiens	230-245
16385446-8	2006	In an application to asthma case-control data from the Children"s Health Study, FITF identified a significant multilocus effect between the nicotinamide adenine dinucleotide (phosphate) reduced:quinone oxidoreductase gene (NQO1), myeloperoxidase gene (MPO), and catalase gene (CAT) (unadjusted P = .00026), three genes that are involved in the oxidative stress pathway.	NAD	140-173	myeloperoxidase	Homo sapiens	252-255
16385446-8	2006	In an application to asthma case-control data from the Children"s Health Study, FITF identified a significant multilocus effect between the nicotinamide adenine dinucleotide (phosphate) reduced:quinone oxidoreductase gene (NQO1), myeloperoxidase gene (MPO), and catalase gene (CAT) (unadjusted P = .00026), three genes that are involved in the oxidative stress pathway.	NAD	140-173	catalase	Homo sapiens	262-270
16385446-8	2006	In an application to asthma case-control data from the Children"s Health Study, FITF identified a significant multilocus effect between the nicotinamide adenine dinucleotide (phosphate) reduced:quinone oxidoreductase gene (NQO1), myeloperoxidase gene (MPO), and catalase gene (CAT) (unadjusted P = .00026), three genes that are involved in the oxidative stress pathway.	NAD	140-173	catalase	Homo sapiens	277-280
17002793-9	2006	These cytokines have previously been shown to independently regulate the frequency (IFN-gamma) and amplitude (IL-8) of the oscillations of key metabolites in neutrophils, including nicotinamide adenine dinucleotide (phosphate) (NAD(P)H) and superoxide ion.	NAD	181-214	C-X-C motif chemokine ligand 8	Homo sapiens	110-114
16720433-5	2006	This mechanism, dubbed "NAD-induced cell death" or NICD, is initiated when ART2 ADP-ribosylates the cytolytic P2X7 purinergic receptor, inducing formation of a cation channel, opening of a nonselective pore, shedding of CD62L from the cell surface, exposure of phosphatidylserine on the outer leaflet of the plasma membrane, breakdown of the mitochondrial membrane potential, and DNA-fragmentation.	NAD	24-27	ADP-ribosyltransferase 1	Homo sapiens	75-79
16720433-5	2006	This mechanism, dubbed "NAD-induced cell death" or NICD, is initiated when ART2 ADP-ribosylates the cytolytic P2X7 purinergic receptor, inducing formation of a cation channel, opening of a nonselective pore, shedding of CD62L from the cell surface, exposure of phosphatidylserine on the outer leaflet of the plasma membrane, breakdown of the mitochondrial membrane potential, and DNA-fragmentation.	NAD	24-27	purinergic receptor P2X 7	Homo sapiens	110-114
16720433-8	2006	We propose that ART2-catalyzed ADP-ribosylation of P2X7 represents the paradigm of a regulatory mechanism by which ART-expressing cells can sense and respond to the release of NAD from damaged cells.	NAD	176-179	ADP-ribosyltransferase 1	Homo sapiens	16-20
16720433-8	2006	We propose that ART2-catalyzed ADP-ribosylation of P2X7 represents the paradigm of a regulatory mechanism by which ART-expressing cells can sense and respond to the release of NAD from damaged cells.	NAD	176-179	purinergic receptor P2X 7	Homo sapiens	51-55
18221025-5	2006	However, in the case of extensive DNA damage PARP-1 overactivation induces a decrease of NAD+ and ATP levels leading to cell dysfunction or even to necrotic cell death.	NAD	89-93	poly(ADP-ribose) polymerase 1	Homo sapiens	45-51
16918420-3	2006	Activation of PARP can dramatically lower the intracellular concentration of its substrate, nicotinamide adenine dinucleotide, thus slowing the rate of glycolysis, electron transport and subsequently ATP formation.	NAD	92-125	poly(ADP-ribose) polymerase 1	Homo sapiens	14-18
16380493-14	2006	In conclusion, leucine culture upregulates glucokinase, which increases NAD(P)H level, and ATPSbeta, which increases oxidation of NADH and production of ATP.	NAD	130-134	ATP synthase F1 subunit beta	Homo sapiens	91-99
16289176-4	2006	In mouse liver, trans, trans-muconaldehyde is predominantly reduced by an NADH-dependent enzyme, which was identified as alcohol dehydrogenase (Adh1).	NAD	74-78	alcohol dehydrogenase 1 (class I)	Mus musculus	144-148
16289039-3	2005	Inhibition of PARP-1 results in preservation of the intracellular NAD+ pool, and of NAD+-dependent cellular processes.	NAD	66-70	poly(ADP-ribose) polymerase 1	Homo sapiens	14-20
16289039-3	2005	Inhibition of PARP-1 results in preservation of the intracellular NAD+ pool, and of NAD+-dependent cellular processes.	NAD	84-88	poly(ADP-ribose) polymerase 1	Homo sapiens	14-20
16289039-4	2005	In this study, PARP-1 activation by hydrogen peroxide decreased intracellular NAD+ levels in human pulmonary epithelial cells, which was found to be prevented in a dose-dependent manner by theophylline, a widely used compound in the treatment of COPD.	NAD	78-82	poly(ADP-ribose) polymerase 1	Homo sapiens	15-21
16198644-9	2005	GRHPR had a higher affinity for NADPH than NADH (K(M) 0.011 mM vs. 2.42 mM).	NAD	43-47	glyoxylate and hydroxypyruvate reductase	Homo sapiens	0-5
16207712-0	2005	Poly(ADP-ribose) polymerase-1-dependent cardiac myocyte cell death during heart failure is mediated by NAD+ depletion and reduced Sir2alpha deacetylase activity.	NAD	103-107	poly(ADP-ribose) polymerase 1	Homo sapiens	0-29
16207712-2	2005	Here, we show that depletion of myocyte NAD levels and the subsequent reduction of Sir2alpha deacetylase activity are the sequential steps contributing to PARP-mediated myocyte cell death.	NAD	40-43	poly(ADP-ribose) polymerase 1	Homo sapiens	155-159
16207712-4	2005	Myocyte cell death induced by PARP activation was prevented by repletion of cellular NAD levels either by adding NAD directly to the culture medium or by overexpressing NAD biosynthetic enzymes.	NAD	85-88	poly(ADP-ribose) polymerase 1	Homo sapiens	30-34
16207712-4	2005	Myocyte cell death induced by PARP activation was prevented by repletion of cellular NAD levels either by adding NAD directly to the culture medium or by overexpressing NAD biosynthetic enzymes.	NAD	113-116	poly(ADP-ribose) polymerase 1	Homo sapiens	30-34
16207712-4	2005	Myocyte cell death induced by PARP activation was prevented by repletion of cellular NAD levels either by adding NAD directly to the culture medium or by overexpressing NAD biosynthetic enzymes.	NAD	113-116	poly(ADP-ribose) polymerase 1	Homo sapiens	30-34
16207712-7	2005	NAD repletion also prevented loss of the transcriptional regulatory activity of the Sir2alpha catalytic core domain resulting from PARP activation.	NAD	0-3	poly(ADP-ribose) polymerase 1	Homo sapiens	131-135
16207712-9	2005	These data demonstrate that, in stressed cardiac myocytes, depletion of cellular NAD levels forms a link between PARP activation and reduced Sir2alpha deacetylase activity, contributing to myocyte cell death during heart failure.	NAD	81-84	poly(ADP-ribose) polymerase 1	Homo sapiens	113-117
16292346-5	2005	This role of BARS requires its interaction with ARFGAP1, which is in turn regulated oppositely by p-coA and nicotinamide adenine dinucleotide, which act as cofactors of BARS.	NAD	108-141	ADP ribosylation factor GTPase activating protein 1	Homo sapiens	48-55
16198644-6	2005	For the oxidation of glyoxylate, K(M) values were 0.18 mM and 0.26 mM for LDHA and LDHB respectively with NAD+ as cofactor.	NAD	106-110	lactate dehydrogenase A	Homo sapiens	74-78
16239728-3	2005	The liver GAPDH structure consists of a homotetramer, each subunit of which is bound to a nicotinamide adenine dinucleotide (NAD+) molecule.	NAD	90-123	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	10-15
16262266-1	2005	In response to DNA strand breaks in the genome of higher eukaryotes, poly(ADP-ribose)polymerase 1 (PARP-1) catalyses the covalent attachment of ADP-ribose units from NAD(+) to various nuclear acceptor proteins including PARP-1 itself.	NAD	166-172	poly(ADP-ribose) polymerase 1	Homo sapiens	69-97
16262266-1	2005	In response to DNA strand breaks in the genome of higher eukaryotes, poly(ADP-ribose)polymerase 1 (PARP-1) catalyses the covalent attachment of ADP-ribose units from NAD(+) to various nuclear acceptor proteins including PARP-1 itself.	NAD	166-172	poly(ADP-ribose) polymerase 1	Homo sapiens	99-105
16262266-1	2005	In response to DNA strand breaks in the genome of higher eukaryotes, poly(ADP-ribose)polymerase 1 (PARP-1) catalyses the covalent attachment of ADP-ribose units from NAD(+) to various nuclear acceptor proteins including PARP-1 itself.	NAD	166-172	poly(ADP-ribose) polymerase 1	Homo sapiens	220-226
16306806-0	2005	Flow-independent myocardial ischemia induced by endothelin-1: an NADH fluorescence analysis.	NAD	65-69	endothelin 1	Canis lupus familiaris	48-60
16239728-3	2005	The liver GAPDH structure consists of a homotetramer, each subunit of which is bound to a nicotinamide adenine dinucleotide (NAD+) molecule.	NAD	125-129	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	10-15
16356120-3	2005	PARP activation, on the one hand, depletes its substrate, NAD+, slowing the rate of glycolysis, electron transport, and ATP formation.	NAD	58-62	poly(ADP-ribose) polymerase 1	Homo sapiens	0-4
16249673-7	2005	Myocardial tissue content of nicotinamide adenine dinucleotide served as a marker for mPTP opening.	NAD	29-62	protein tyrosine phosphatase, receptor type, U	Mus musculus	86-90
16249673-11	2005	LY294002 inhibited isoflurane-induced phosphorylation of protein kinase B/Akt and glycogen synthase kinase 3beta and opened mPTP as determined by nicotinamide adenine dinucleotide measurements.	NAD	146-179	protein tyrosine phosphatase, receptor type, U	Mus musculus	124-128
16344601-10	2005	The third element essential to the cycle is the generation of NAD to support the oxidation of alcohol by alcohol dehydrogenase.	NAD	62-65	aldo-keto reductase family 1 member A1	Rattus norvegicus	105-126
16357945-6	2005	Here, we report the development and the validation of a nonisotopic PARP-1 assay suitable for HTS by converting a biotinylated NAD-based colorimetric assay to a miniaturized 384-well plate format.	NAD	127-130	poly(ADP-ribose) polymerase 1	Homo sapiens	68-74
16115861-1	2005	According to the classical view, the cytoprotective effect of inhibitors of poly(ADP-ribose)polymerase (PARP) in oxidative stress was based on the prevention of NAD+ and ATP depletion, thus the attenuation of necrosis.	NAD	161-165	poly(ADP-ribose) polymerase 1	Homo sapiens	76-102
16244666-1	2005	Poly(ADP-ribose) (PAR) is a large, negatively charged post-translational modification that is produced by polymerization of NAD+ by PAR polymerases (PARPs).	NAD	124-128	tankyrase	Homo sapiens	149-154
16386505-2	2005	Poly (ADP-Ribose) polymerase (PARP-1) overactivation leads to massive NAD+ consumption and ATP depletion with induction of cellular necrosis under ischemic conditions, which may lead to an increase in acute tubular necrosis (ATN) and a delay in total recovery of renal function (RFR) of the transplanted organ.	NAD	70-74	poly(ADP-ribose) polymerase 1	Homo sapiens	0-28
16386505-2	2005	Poly (ADP-Ribose) polymerase (PARP-1) overactivation leads to massive NAD+ consumption and ATP depletion with induction of cellular necrosis under ischemic conditions, which may lead to an increase in acute tubular necrosis (ATN) and a delay in total recovery of renal function (RFR) of the transplanted organ.	NAD	70-74	poly(ADP-ribose) polymerase 1	Homo sapiens	30-36
16115861-1	2005	According to the classical view, the cytoprotective effect of inhibitors of poly(ADP-ribose)polymerase (PARP) in oxidative stress was based on the prevention of NAD+ and ATP depletion, thus the attenuation of necrosis.	NAD	161-165	poly(ADP-ribose) polymerase 1	Homo sapiens	104-108
16179389-4	2005	PARP-1 is a NAD(+)-dependent enzyme that plays a multifunctional role in DNA damage detection and repair and maintenance of genomic stability.	NAD	12-18	poly(ADP-ribose) polymerase 1	Homo sapiens	0-6
16140981-0	2005	Poly(ADP-ribosyl)ation by PARP-1: "PAR-laying" NAD+ into a nuclear signal.	NAD	47-51	poly(ADP-ribose) polymerase 1	Homo sapiens	26-32
16150419-0	2005	NAD- and NADP-dependent mitochondrially targeted methylenetetrahydrofolate dehydrogenase-cyclohydrolases can rescue mthfd2 null fibroblasts.	NAD	0-3	methylenetetrahydrofolate dehydrogenase (NAD+ dependent), methenyltetrahydrofolate cyclohydrolase	Mus musculus	116-122
16150419-1	2005	Mouse fibroblasts in which the mthfd2 gene encoding mitochondrial NAD-dependent methylenetetrahydrofolate dehydrogenase-cyclohydrolase (NMDMC) was previously inactivated were infected with retroviral expression constructs of dehydrogenase/cyclohydrolase cDNA.	NAD	66-69	methylenetetrahydrofolate dehydrogenase (NAD+ dependent), methenyltetrahydrofolate cyclohydrolase	Mus musculus	31-37
16150419-1	2005	Mouse fibroblasts in which the mthfd2 gene encoding mitochondrial NAD-dependent methylenetetrahydrofolate dehydrogenase-cyclohydrolase (NMDMC) was previously inactivated were infected with retroviral expression constructs of dehydrogenase/cyclohydrolase cDNA.	NAD	66-69	methylenetetrahydrofolate dehydrogenase (NAD+ dependent), methenyltetrahydrofolate cyclohydrolase	Mus musculus	136-141
16122695-7	2005	The interaction between CtBP and CBP is functionally important and leads to impairment of histone H3 acetylation by CBP at specific lysine residues (Lys9, Lys14, and Lys18) in a dose-dependent and NADH-dependent manner.	NAD	197-201	CREB binding protein	Homo sapiens	116-119
16154098-2	2005	We show that the forkhead protein FoxO1 protects beta cells against oxidative stress by forming a complex with the promyelocytic leukemia protein Pml and the NAD-dependent deacetylase Sirt1 to activate expression of NeuroD and MafA, two Insulin2 (Ins2) gene transcription factors.	NAD	158-161	forkhead box O1	Homo sapiens	34-39
16140404-1	2005	Mono-ADP-ribosyltransferase (ART) 4 belongs to a family of ectoenzymes that catalyze the transfer of ADP-ribose from NAD+ to a target protein.	NAD	117-121	ADP-ribosyltransferase 4 (inactive) (Dombrock blood group)	Homo sapiens	29-35
16122695-7	2005	The interaction between CtBP and CBP is functionally important and leads to impairment of histone H3 acetylation by CBP at specific lysine residues (Lys9, Lys14, and Lys18) in a dose-dependent and NADH-dependent manner.	NAD	197-201	CREB binding protein	Homo sapiens	33-36
16140981-1	2005	Poly(ADP-ribose) (PAR) and the PAR polymerases (PARPs) that catalyze its synthesis from donor nicotinamide adenine dinucleotide (NAD+) molecules have received considerable attention in the recent literature.	NAD	94-127	poly(ADP-ribose) polymerase 1	Homo sapiens	48-53
16140981-1	2005	Poly(ADP-ribose) (PAR) and the PAR polymerases (PARPs) that catalyze its synthesis from donor nicotinamide adenine dinucleotide (NAD+) molecules have received considerable attention in the recent literature.	NAD	129-133	poly(ADP-ribose) polymerase 1	Homo sapiens	48-53
16140981-5	2005	In addition, connections between nuclear NAD+ metabolism and nuclear signaling through PARP-1 are discussed.	NAD	41-45	poly(ADP-ribose) polymerase 1	Homo sapiens	87-93
16076959-2	2005	We previously reported that Foxo1, a member of the FOXO family, is regulated through reversible acetylation catalyzed by histone acetyltransferase cAMP-response element-binding protein (CREB)-binding protein (CBP) and NAD-dependent histone deacetylase silent information regulator 2, and that the acetylation at Lys-242, Lys-245, and Lys-262 of Foxo1 attenuates its transcriptional activity.	NAD	218-221	forkhead box O1	Homo sapiens	28-33
15967408-2	2005	Mitochondrial glycerophosphate dehydrogenase (mGPDH) participates in the reoxidation of cytosolic NADH by delivering reducing equivalents from this molecule into the electron transport chain, thus sustaining glycolysis.	NAD	98-102	glycerol-3-phosphate dehydrogenase 2	Homo sapiens	0-44
15967791-9	2005	Addition of oxidants of NADH was found to decrease the expression of CTT1 induced by myxothiazol treatment, suggesting that the accumulation of NADH caused by the inhibition of the respiratory chain may be involved in the signaling pathway from the mitochondria to the transcription factor.	NAD	24-28	catalase T	Saccharomyces cerevisiae S288C	69-73
15967791-9	2005	Addition of oxidants of NADH was found to decrease the expression of CTT1 induced by myxothiazol treatment, suggesting that the accumulation of NADH caused by the inhibition of the respiratory chain may be involved in the signaling pathway from the mitochondria to the transcription factor.	NAD	144-148	catalase T	Saccharomyces cerevisiae S288C	69-73
16076959-2	2005	We previously reported that Foxo1, a member of the FOXO family, is regulated through reversible acetylation catalyzed by histone acetyltransferase cAMP-response element-binding protein (CREB)-binding protein (CBP) and NAD-dependent histone deacetylase silent information regulator 2, and that the acetylation at Lys-242, Lys-245, and Lys-262 of Foxo1 attenuates its transcriptional activity.	NAD	218-221	forkhead box O1	Homo sapiens	51-55
16076959-2	2005	We previously reported that Foxo1, a member of the FOXO family, is regulated through reversible acetylation catalyzed by histone acetyltransferase cAMP-response element-binding protein (CREB)-binding protein (CBP) and NAD-dependent histone deacetylase silent information regulator 2, and that the acetylation at Lys-242, Lys-245, and Lys-262 of Foxo1 attenuates its transcriptional activity.	NAD	218-221	CREB binding protein	Homo sapiens	209-212
16076959-2	2005	We previously reported that Foxo1, a member of the FOXO family, is regulated through reversible acetylation catalyzed by histone acetyltransferase cAMP-response element-binding protein (CREB)-binding protein (CBP) and NAD-dependent histone deacetylase silent information regulator 2, and that the acetylation at Lys-242, Lys-245, and Lys-262 of Foxo1 attenuates its transcriptional activity.	NAD	218-221	forkhead box O1	Homo sapiens	345-350
16082197-4	2005	Recent findings suggest that p53 also undergoes ubiquitin-independent degradation by the 20S proteasomes and that this process is regulated by NAD(P)H quinone oxidoreductase 1 (NQO1) together with NADH.	NAD	197-201	tumor protein p53	Homo sapiens	29-32
16012350-0	2005	NADH can enter into astrocytes and block poly(ADP-ribose) polymerase-1-mediated astrocyte death.	NAD	0-4	poly(ADP-ribose) polymerase 1	Homo sapiens	41-70
16012350-1	2005	Poly(ADP-ribose) polymerase-1 consumes NAD to catalyze poly(ADP-ribosyl)ation of target proteins, which modulates various biological functions.	NAD	39-42	poly(ADP-ribose) polymerase 1	Homo sapiens	0-29
16012350-3	2005	Our recent studies have indicated that NAD can enter into astrocytes to prevent poly(ADP-ribose) polymerase-1 cytotoxicity.	NAD	39-42	poly(ADP-ribose) polymerase 1	Homo sapiens	80-109
16012350-4	2005	In this study, we show that NADH can also enter into astrocytes, which can significantly decrease poly(ADP-ribose) polymerase-1-induced astrocyte death even when applied 3-4 h after poly(ADP-ribose) polymerase-1 activation.	NAD	28-32	poly(ADP-ribose) polymerase 1	Homo sapiens	98-127
16012350-4	2005	In this study, we show that NADH can also enter into astrocytes, which can significantly decrease poly(ADP-ribose) polymerase-1-induced astrocyte death even when applied 3-4 h after poly(ADP-ribose) polymerase-1 activation.	NAD	28-32	poly(ADP-ribose) polymerase 1	Homo sapiens	182-211
16012350-6	2005	These results provide novel information suggesting that NADH can be used for decreasing poly(ADP-ribose) polymerase-1 toxicity, and extracellular NADH can enter into astrocytes to influence cellular functions.	NAD	56-60	poly(ADP-ribose) polymerase 1	Homo sapiens	88-117
15864308-7	2005	This is consistent with the hypothesis that before the Adh1-Adh2 duplication, yeast did not accumulate ethanol for later consumption but rather used Adh(A) to recycle NADH generated in the glycolytic pathway.	NAD	167-171	alcohol dehydrogenase ADH1	Saccharomyces cerevisiae S288C	55-59
15946639-2	2005	The rate of oxidation of NADH by Co(II) plus H(2)O(2), in Tris or phosphate, was markedly enhanced by CO(2)/HCO(3)(-).	NAD	25-29	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	33-39
16026317-4	2005	PARP-1 activated by DNA breaks cleaves NAD(+) into nicotinamide and ADP-ribose and uses the latter to synthesize long branching PAR polymers covalently attached to acceptor proteins including histones, DNA repair enzymes, transcription factors and PARP-1.	NAD	39-45	poly(ADP-ribose) polymerase 1	Homo sapiens	0-6
16026317-4	2005	PARP-1 activated by DNA breaks cleaves NAD(+) into nicotinamide and ADP-ribose and uses the latter to synthesize long branching PAR polymers covalently attached to acceptor proteins including histones, DNA repair enzymes, transcription factors and PARP-1.	NAD	39-45	poly(ADP-ribose) polymerase 1	Homo sapiens	248-254
16026318-3	2005	The activation of PARP leads to an energy consuming inefficient repair cycle with subsequent depletion of NAD(+) and ATP pools and necrotic cell death.	NAD	106-112	poly(ADP-ribose) polymerase 1	Homo sapiens	18-22
16026325-3	2005	Following excessive activation, PARP-1 depletes the intracellular stores of its substrate, nicotinamide adenine dinucleotide, thus slowing glycolysis, generation of high energy phosphates, and mitochondrial electron transport.	NAD	91-124	poly(ADP-ribose) polymerase 1	Homo sapiens	32-38
15911332-1	2005	Free radical and oxidant production in cardiac myocytes during ischemia/reperfusion, cardiomyopathy, cardiotoxic drug exposure and ageing leads to DNA strand-breakage which activates the nuclear enzyme poly(ADP-ribose) polymerase (PARP) and initiates an energy consuming, inefficient cellular metabolic cycle with transfer of the ADP-ribosyl moiety of NAD+ to protein acceptors.	NAD	352-356	poly(ADP-ribose) polymerase 1	Homo sapiens	202-229
15911332-1	2005	Free radical and oxidant production in cardiac myocytes during ischemia/reperfusion, cardiomyopathy, cardiotoxic drug exposure and ageing leads to DNA strand-breakage which activates the nuclear enzyme poly(ADP-ribose) polymerase (PARP) and initiates an energy consuming, inefficient cellular metabolic cycle with transfer of the ADP-ribosyl moiety of NAD+ to protein acceptors.	NAD	352-356	poly(ADP-ribose) polymerase 1	Homo sapiens	231-235
15911333-8	2005	Overactivation of PARP in conditions such as ischemic renal injury leads to cellular depletion of its substrate NAD+ and consequently ATP.	NAD	112-116	poly(ADP-ribose) polymerase 1	Homo sapiens	18-22
15911334-3	2005	Both during the pathogenesis of diabetes and during the pathogenesis of diabetic complications, free radical and oxidant production leads to DNA strand-breakage which activates the nuclear enzyme PARP and initiates an energy consuming, inefficient cellular metabolic cycle with transfer of the ADP-ribosyl moiety of NAD+ to protein acceptors.	NAD	316-320	poly(ADP-ribose) polymerase 1	Homo sapiens	196-200
15795229-8	2005	However, purified recombinant mSIRT6 did catalyze the robust transfer of radiolabel from [32P]NAD to mSIRT6.	NAD	94-97	sirtuin 6	Mus musculus	30-36
15795229-8	2005	However, purified recombinant mSIRT6 did catalyze the robust transfer of radiolabel from [32P]NAD to mSIRT6.	NAD	94-97	sirtuin 6	Mus musculus	101-107
15959561-4	2005	When activated by DNA breaks, these PARPs use NAD+ to catalyze their automodification with negatively charged, long and branched ADP-ribose polymers.	NAD	46-50	poly(ADP-ribose) polymerase 1	Homo sapiens	36-41
15870696-6	2005	Three members of the NAD-dependent deacetylases, the sirtuins, are upregulated by VPA and by TSA and sirtuin activity contributes to loss of ERalpha expression.	NAD	21-24	estrogen receptor 1	Homo sapiens	141-148
15925280-3	2005	ROS-induced DNA strand breaks lead to overactivation of the nuclear enzyme poly(ADP-ribose) polymerase-1 (PARP-1; EC 2.4.2.30), causing excessive use of energetic substrates such as NAD(+) and ATP, inducing cell death either by apoptosis or by necrosis.	NAD	182-188	poly(ADP-ribose) polymerase 1	Homo sapiens	75-104
15925280-3	2005	ROS-induced DNA strand breaks lead to overactivation of the nuclear enzyme poly(ADP-ribose) polymerase-1 (PARP-1; EC 2.4.2.30), causing excessive use of energetic substrates such as NAD(+) and ATP, inducing cell death either by apoptosis or by necrosis.	NAD	182-188	poly(ADP-ribose) polymerase 1	Homo sapiens	106-112
15867389-7	2005	This data suggests that PARP-1 destabilizes the topoisomerase I-camptothecin-DNA complex with the participation of the NH2-terminal domain of topoisomerase I. Poly(ADP-ribosyl)ation of topoisomerase I by PARP-1 in the presence its substrate, NAD, could also promote the religation activity of full-length topoisomerase I as well as NH2 terminus-truncated topoisomerase I.	NAD	242-245	poly(ADP-ribose) polymerase 1	Homo sapiens	24-30
15788719-3	2005	In testing this hypothesis, we show here that, if supplied with glutathione (GSH), NAD, and glycolytic substrate, the mixture of purified GAPDH and PGK indeed catalyzes the reduction of AsV.	NAD	83-86	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	138-143
15788719-5	2005	The GAPDH-catalyzed AsV reduction required GSH, NAD, and glyceraldehyde-3-phosphate.	NAD	48-51	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	4-9
15788719-9	2005	Inactivation of GAPDH by KA abolished AsV reduction in intact RBC as well as in the hemolysate and the liver cytosol, when GAPDH in the latter extracts was abundantly supplied with exogenous NAD and glycolytic substrate.	NAD	191-194	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	16-21
15788719-9	2005	Inactivation of GAPDH by KA abolished AsV reduction in intact RBC as well as in the hemolysate and the liver cytosol, when GAPDH in the latter extracts was abundantly supplied with exogenous NAD and glycolytic substrate.	NAD	191-194	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	123-128
15788719-11	2005	In conclusion, the key glycolytic enzyme GAPDH can fortuitously catalyze the reduction of AsV to AsIII, if GSH, NAD, and glycolytic substrate are available.	NAD	112-115	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	41-46
15855333-4	2005	Activated PARP-1 consumes cytosolic NAD, and because NAD is required for glycolysis, hypoglycemia-induced PARP-1 activation may render cells unable to use glucose even when glucose availability is restored.	NAD	36-39	poly(ADP-ribose) polymerase 1	Homo sapiens	10-16
15750180-8	2005	PARP-1 inhibitors rescued ATP (but not NAD(H) levels) in cells undergoing hyper-poly(ADP-ribosyl)ation.	NAD	39-45	poly(ADP-ribose) polymerase 1	Homo sapiens	0-6
15868400-2	2005	Activated PARP-1 cleaves NAD into nicotinamide and ADP-ribose and polymerizes the latter covalently coupled to nuclear acceptor proteins.	NAD	25-28	poly(ADP-ribose) polymerase 1	Homo sapiens	10-16
15703174-1	2005	Poly(ADP-ribose) polymerase-1 (PARP-1) influences numerous cellular processes, including DNA repair, transcriptional regulation, and caspase-independent cell death, by utilizing NAD(+) to synthesize long chains of poly(ADP-ribose) (PAR) on target proteins, including itself.	NAD	178-184	poly(ADP-ribose) polymerase 1	Homo sapiens	0-29
15703174-1	2005	Poly(ADP-ribose) polymerase-1 (PARP-1) influences numerous cellular processes, including DNA repair, transcriptional regulation, and caspase-independent cell death, by utilizing NAD(+) to synthesize long chains of poly(ADP-ribose) (PAR) on target proteins, including itself.	NAD	178-184	poly(ADP-ribose) polymerase 1	Homo sapiens	31-37
15703174-7	2005	Indeed, PARP-1, in the presence of NAD(+), significantly decreased DFF40 activity on plasmid substrates.	NAD	35-41	poly(ADP-ribose) polymerase 1	Homo sapiens	8-14
15703174-9	2005	The inhibition of DFF40 activity in the presence of NAD(+) was reduced by co-incubation with poly(ADP-ribose) glycohydrolase and a PARP inhibitor.	NAD	52-58	poly(ADP-ribose) glycohydrolase	Homo sapiens	93-124
15703174-9	2005	The inhibition of DFF40 activity in the presence of NAD(+) was reduced by co-incubation with poly(ADP-ribose) glycohydrolase and a PARP inhibitor.	NAD	52-58	poly(ADP-ribose) polymerase 1	Homo sapiens	131-135
15703174-10	2005	Additionally, caspase-cleaved PARP-1, in the presence of NAD(+), did not inhibit DFF40 activity significantly.	NAD	57-63	poly(ADP-ribose) polymerase 1	Homo sapiens	30-36
15716268-4	2005	In PC12 cells, increased expression of the NAD-dependent deacetylase SIRT1 reduces cellular oxygen consumption by approximately 25%.	NAD	43-46	sirtuin 1	Rattus norvegicus	69-74
15744310-5	2005	We find that once SIRT1 is induced, it interacts with and deacetylates PGC-1alpha at specific lysine residues in an NAD(+)-dependent manner.	NAD	116-122	PPARG coactivator 1 alpha	Homo sapiens	71-81
15752713-1	2005	Cytochrome c (cyto-c) added to isolated mitochondria promotes the oxidation of extra-mitochondrial NADH and the reduction of molecular oxygen associated to the generation of an electrochemical membrane potential available for ATP synthesis.	NAD	99-103	cytochrome c, somatic	Homo sapiens	0-12
15752713-1	2005	Cytochrome c (cyto-c) added to isolated mitochondria promotes the oxidation of extra-mitochondrial NADH and the reduction of molecular oxygen associated to the generation of an electrochemical membrane potential available for ATP synthesis.	NAD	99-103	cytochrome c, somatic	Homo sapiens	14-20
15752713-3	2005	Dextran sulfate (500 kDa), known to interact with porin (the voltage-dependent anion channel), other than to inhibit the release of ATP synthesized inside the mitochondria, greatly decreases the activity of exogenous NADH/cyto-c system of intact mitochondria but has no effect on the reconstituted system made of mitoplasts and external membrane preparations.	NAD	217-221	cytochrome c, somatic	Homo sapiens	222-228
15752713-5	2005	The proposal is put forward that the bi-trans-membrane electron transport chain activated by cytosolic cyto-c becomes, in physio-pathological conditions: (i) functional in removing the excess of cytosolic NADH; (ii) essential for cell survival in the presence of an impairment of the first three respiratory complexes; and (iii) an additional source of energy at the beginning of apoptosis.	NAD	205-209	cytochrome c, somatic	Homo sapiens	103-109
15749861-2	2005	Upon exposure of T cells to NAD, the substrate for ADP-ribosylation, ART2 catalyzes ADP-ribosylation of the P2X7 purinoceptor and other functionally important cell surface proteins.	NAD	28-31	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	108-125
15694256-2	2005	The quinone oxidoreductases, nicotinamide adenine dinucleotide (phosphate) (NAD[P]H): quinone oxidoreductase 1 (NQO1) and dihydronicotinamide riboside (NRH): quinone oxidoreductase 2 (NQO2) detoxify quinones and quinonoid compounds.	NAD	29-62	NAD(P)H quinone dehydrogenase 1	Homo sapiens	112-116
15857303-3	2005	Upon binding to DNA breaks, activated PARP cleaves NAD+ into nicotinamide and ADP-ribose and polymerizes the latter on nuclear acceptor proteins including histones, transcription factors and PARP itself.	NAD	51-55	poly(ADP-ribose) polymerase 1	Homo sapiens	38-42
15857303-3	2005	Upon binding to DNA breaks, activated PARP cleaves NAD+ into nicotinamide and ADP-ribose and polymerizes the latter on nuclear acceptor proteins including histones, transcription factors and PARP itself.	NAD	51-55	poly(ADP-ribose) polymerase 1	Homo sapiens	191-195
15857303-6	2005	Overactivation of PARP consumes NAD+ and ATP culminating in cell dysfunction and necrosis.	NAD	32-36	poly(ADP-ribose) polymerase 1	Homo sapiens	18-22
15551062-8	2005	The rate of ethanol, 2-ethoxyethanol (2-EE), ethylene glycol, 2-phenoxyethanol (2-PE) and 2-BE conversion to alkoxyacetic acid by ADH/ALDH in these fractions was continuously monitored by UV spectrophotometry via the conversion of NAD+ to NADH at 340 nm.	NAD	231-235	aldo-keto reductase family 1 member A1	Rattus norvegicus	130-133
15551062-8	2005	The rate of ethanol, 2-ethoxyethanol (2-EE), ethylene glycol, 2-phenoxyethanol (2-PE) and 2-BE conversion to alkoxyacetic acid by ADH/ALDH in these fractions was continuously monitored by UV spectrophotometry via the conversion of NAD+ to NADH at 340 nm.	NAD	239-243	aldo-keto reductase family 1 member A1	Rattus norvegicus	130-133
15747064-3	2005	Here we report that alpha-crystallin, in the presence of the SDH pyridine cofactor NAD(H), can exert a remarkable chaperone action by favoring the recovery of the enzyme activity from chemically denaturated SDH up to 77%.	NAD	83-89	sorbitol dehydrogenase	Homo sapiens	61-64
15747064-3	2005	Here we report that alpha-crystallin, in the presence of the SDH pyridine cofactor NAD(H), can exert a remarkable chaperone action by favoring the recovery of the enzyme activity from chemically denaturated SDH up to 77%.	NAD	83-89	sorbitol dehydrogenase	Homo sapiens	207-210
15809331-1	2005	L-Gulonate 3-dehydrogenase (GDH) catalyzes the NAD(+)-linked dehydrogenation of L-gulonate into dehydro-L-gulonate in the uronate cycle.	NAD	47-53	lambda-crystallin	Oryctolagus cuniculus	0-26
15683711-8	2005	The addition of the biological electron donors NADH, NADPH, or ascorbate enhanced the reduction rate of cytochrome c approximately 30-fold.	NAD	47-51	cytochrome c, somatic	Homo sapiens	104-116
15809331-1	2005	L-Gulonate 3-dehydrogenase (GDH) catalyzes the NAD(+)-linked dehydrogenation of L-gulonate into dehydro-L-gulonate in the uronate cycle.	NAD	47-53	lambda-crystallin	Oryctolagus cuniculus	28-31
15561723-5	2005	Hypoxia-induced channels are inhibited by NADH, an agent that inhibits large conductance channels produced by a pro-apoptotic fragment of BCL-xL in these synaptic mitochondria.	NAD	42-46	BCL2 like 1	Homo sapiens	138-144
15962096-3	2005	PARP activation, on one hand, depletes its substrate, NAD+, slowing the rate of glycolysis, electron transport and ATP formation.	NAD	54-58	poly(ADP-ribose) polymerase 1	Homo sapiens	0-4
15856945-5	2005	Only in the case of (CCTTT)n marker of NOS2 gene we have found a tendency for the association of 14 allele with DPN development.	NAD	112-115	nitric oxide synthase 2	Homo sapiens	39-43
15574424-1	2005	Cyclic ADP-ribose (cADPR) is an intracellular calcium mobilizer generated from NAD(+) by the ADP-ribosyl cyclases CD38 and BST-1.	NAD	79-85	bone marrow stromal cell antigen 1	Homo sapiens	123-128
15711971-6	2005	Recombinant AtNADK-1 utilises ATP to phosphorylate both NAD and NADH, showing a two-fold preference for NADH.	NAD	64-68	NAD kinase 1	Arabidopsis thaliana	12-20
15711971-6	2005	Recombinant AtNADK-1 utilises ATP to phosphorylate both NAD and NADH, showing a two-fold preference for NADH.	NAD	104-108	NAD kinase 1	Arabidopsis thaliana	12-20
15699125-0	2005	P2X7 receptor-dependent and -independent T cell death is induced by nicotinamide adenine dinucleotide.	NAD	68-101	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	0-13
15699125-3	2005	Low NAD concentrations (&lt;10 microM) suffice to trigger rapid cell death, which is associated with annexin V binding and membrane pore formation, is not blocked by the caspase inhibitor Z-VADfmk, and requires functional P2X7 receptors.	NAD	4-7	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	222-226
15684044-5	2005	Overexpression of Ezh2 in tissue culture promotes formation of a previously undescribed PRC complex, PRC4, that contains the NAD+-dependent histone deacetylase SirT1 and isoform 2 of the PRC component Eed.	NAD	125-129	enhancer of zeste 2 polycomb repressive complex 2 subunit	Homo sapiens	18-22
15680246-5	2005	Pre-incubation of DTx with a 2000-fold excess of NAD, the natural substrate for the toxin"s ADP-ribosyltransferase (ADPrT) activity, inhibited the transfer of radiolabeled ADP-ribose to elongation factor 2 but had no effect on the degradation of radiolabeled DNA.	NAD	49-52	poly(ADP-ribose) polymerase 1	Homo sapiens	92-114
15680246-5	2005	Pre-incubation of DTx with a 2000-fold excess of NAD, the natural substrate for the toxin"s ADP-ribosyltransferase (ADPrT) activity, inhibited the transfer of radiolabeled ADP-ribose to elongation factor 2 but had no effect on the degradation of radiolabeled DNA.	NAD	49-52	poly(ADP-ribose) polymerase 1	Homo sapiens	116-121
15792370-3	2005	Protein interaction assays revealed that the 73 kDa CaMKIIbeta(C) binds GAPDH to modulate the production of NADH in a Ca2+/CaM dependent reaction.	NAD	108-112	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	72-77
15677321-2	2005	We report selective binding of IP3R to GAPDH, whose activity leads to the local generation of NADH to regulate intracellular calcium signaling.	NAD	94-98	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	39-44
15581900-1	2005	Drosophila alcohol dehydrogenase (DADH) is an NAD+-dependent enzyme that catalyzes the oxidation of alcohols to aldehydes/ketones and that is also able to further oxidize aldehydes to their corresponding carboxylic acids.	NAD	46-49	Alcohol dehydrogenase	Drosophila melanogaster	0-32
15677321-0	2005	Inositol 1,4,5-trisphosphate receptor/GAPDH complex augments Ca2+ release via locally derived NADH.	NAD	94-98	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	38-43
15531583-10	2005	MPO potentiation was inhibited by NADH, but not azide, suggesting oxidative nitrosylation with NO(2)(.)	NAD	34-38	myeloperoxidase	Homo sapiens	0-3
15581900-1	2005	Drosophila alcohol dehydrogenase (DADH) is an NAD+-dependent enzyme that catalyzes the oxidation of alcohols to aldehydes/ketones and that is also able to further oxidize aldehydes to their corresponding carboxylic acids.	NAD	46-49	Alcohol dehydrogenase	Drosophila melanogaster	34-38
16873929-3	2005	When tNOX is active, coenzyme Q(10) (ubiquinone) of the plasma membrane is oxidized and NADH is oxidized at the cytosolic surface of the plasma membrane.	NAD	88-92	ecto-NOX disulfide-thiol exchanger 2	Homo sapiens	5-9
16873929-4	2005	However, when tNOX is inhibited and plasma membrane electron transport is diminished, both reduced coenzyme Q(10) (ubiquinol) and NADH would be expected to accumulate.	NAD	130-134	ecto-NOX disulfide-thiol exchanger 2	Homo sapiens	14-18
15953818-1	2005	Poly(ADP-ribose) polymerase (PARP)-1 is a DNA nick sensor that transforms ADP-ribose from betaNAD+ in the form of polymer to over 40 nuclear proteins, particularly to histones, several transcription factors, and PARP itself, modulating their activities and functions.	NAD	90-98	poly(ADP-ribose) polymerase 1	Homo sapiens	0-36
16245207-4	2005	PARP-1 activity was estimated radiochemically using egzogenous substrate adenine[14C]NAD.	NAD	85-88	poly(ADP-ribose) polymerase 1	Homo sapiens	0-6
15389540-5	2005	We demonstrated that specific inhibition of poly(ADP-ribose) polymerase activity via 3-aminobenzamide (3ABA) or NAD+ deprivation prevents FGF2-mediated uPA mRNA over-expression and cell-associated plasminogen activator (PA) production in GM7373 endothelial cell line.	NAD	112-116	fibroblast growth factor 2	Bos taurus	138-142
16181138-1	2005	The poly(ADP-ribose)polymerases (PARPs) catalyse the transfer of ADP-ribose units from the substrate NAD(+) to acceptor proteins, biosynthesising polyanionic poly(ADP-ribose) polymers.	NAD	101-107	poly(ADP-ribose) polymerase 1	Homo sapiens	33-38
16181138-4	2005	Most PARP-1 inhibitors mimic the nicotinamide of NAD(+) and the structure-activity relationships are understood in terms of the structure of the catalytic site.	NAD	49-55	poly(ADP-ribose) polymerase 1	Homo sapiens	5-11
15960671-7	2005	CONCLUSIONS: The NAD+-dependant aldehyde dehydrogenase encoded by ALD3 appears to contribute to acetic acid production during Icewine fermentation.	NAD	17-21	aldehyde dehydrogenase (NAD(+)) ALD3	Saccharomyces cerevisiae S288C	66-70
15520447-10	2005	We demonstrate an effect of Txnip on the redox status, as the Txnip-deficient mice in the fed state had a significant increase in the ratio of NADH to NAD(+).	NAD	143-147	thioredoxin interacting protein	Mus musculus	28-33
15520447-10	2005	We demonstrate an effect of Txnip on the redox status, as the Txnip-deficient mice in the fed state had a significant increase in the ratio of NADH to NAD(+).	NAD	151-157	thioredoxin interacting protein	Mus musculus	28-33
15953818-1	2005	Poly(ADP-ribose) polymerase (PARP)-1 is a DNA nick sensor that transforms ADP-ribose from betaNAD+ in the form of polymer to over 40 nuclear proteins, particularly to histones, several transcription factors, and PARP itself, modulating their activities and functions.	NAD	90-98	poly(ADP-ribose) polymerase 1	Homo sapiens	29-33
15953818-4	2005	Excessive activation of PARP-1 by peroxynitrate-evoked DNA damage during oxidative stress can cause cell death by NAD+/ATP depletion after ischemia-reperfusion injury, inflammation, and diabetes mellitus.	NAD	114-118	poly(ADP-ribose) polymerase 1	Homo sapiens	24-30
15610352-4	2005	Here, we show that in plants stresses such as drought, high light and heat activate PARP causing NAD(+) breakdown and ATP consumption.	NAD	97-103	poly(ADP-ribose) polymerase 1	Homo sapiens	84-88
15381699-0	2004	The NAD biosynthesis pathway mediated by nicotinamide phosphoribosyltransferase regulates Sir2 activity in mammalian cells.	NAD	4-7	nicotinamide phosphoribosyltransferase	Mus musculus	41-79
15607977-0	2004	NAD+-dependent modulation of chromatin structure and transcription by nucleosome binding properties of PARP-1.	NAD	0-4	poly(ADP-ribose) polymerase 1	Homo sapiens	103-109
15607977-1	2004	PARP-1 is the most abundantly expressed member of a family of proteins that catalyze the transfer of ADP-ribose units from NAD+ to target proteins.	NAD	123-127	poly(ADP-ribose) polymerase 1	Homo sapiens	0-6
15607977-3	2004	PARP-1 binds in a specific manner to nucleosomes and modulates chromatin structure through NAD+-dependent automodification, without modifying core histones or promoting the disassembly of nucleosomes.	NAD	91-95	poly(ADP-ribose) polymerase 1	Homo sapiens	0-6
15607977-5	2004	The NAD+-dependent activities of PARP-1 are reversed by PARG, a poly(ADP-ribose) glycohydrolase, and are inhibited by ATP.	NAD	4-8	poly(ADP-ribose) polymerase 1	Homo sapiens	33-39
15607977-5	2004	The NAD+-dependent activities of PARP-1 are reversed by PARG, a poly(ADP-ribose) glycohydrolase, and are inhibited by ATP.	NAD	4-8	poly(ADP-ribose) glycohydrolase	Homo sapiens	56-60
15381699-4	2004	In this study, we determined the kinetics of the NAD biosynthesis mediated by nicotinamide phosphoribosyltransferase (Nampt) and nicotinamide/nicotinic acid mononucleotide adenylyltransferase (Nmnat), and we examined its effects on the transcriptional regulatory function of the mouse Sir2 ortholog, Sir2alpha, in mouse fibroblasts.	NAD	49-52	nicotinamide phosphoribosyltransferase	Mus musculus	78-116
15381699-4	2004	In this study, we determined the kinetics of the NAD biosynthesis mediated by nicotinamide phosphoribosyltransferase (Nampt) and nicotinamide/nicotinic acid mononucleotide adenylyltransferase (Nmnat), and we examined its effects on the transcriptional regulatory function of the mouse Sir2 ortholog, Sir2alpha, in mouse fibroblasts.	NAD	49-52	nicotinamide phosphoribosyltransferase	Mus musculus	118-123
15381699-6	2004	Increased dosage of Nampt, but not Nmnat, increased the total cellular NAD level and enhanced the transcriptional regulatory activity of the catalytic domain of Sir2alpha recruited onto a reporter gene in mouse fibroblasts.	NAD	71-74	nicotinamide phosphoribosyltransferase	Mus musculus	20-25
15566299-1	2004	Type 2 human sirtuin (SIRT2) is a NAD(+)-dependent cytoplasmic protein that is colocalized with HDAC6 on microtubules.	NAD	34-40	histone deacetylase 6	Homo sapiens	96-101
15381699-8	2004	These findings suggest that NAD biosynthesis mediated by Nampt regulates the function of Sir2alpha and thereby plays an important role in controlling various biological events in mammals.	NAD	28-31	nicotinamide phosphoribosyltransferase	Mus musculus	57-62
15790542-2	2004	describes how alkylating agents kill cells by a process they term "programmed necrosis," induced by excessive activation of PARP resulting in degradation of cytosolic NAD(+) and inhibition of glycolysis.	NAD	167-173	poly(ADP-ribose) polymerase 1	Homo sapiens	124-128
15448140-6	2004	Loss of MOC1 causes a high light-sensitive phenotype and disrupts the transcription and expression profiles of the mitochondrial respiratory complexes causing, as compared with wild type, light-mediated changes in the expression levels of nuclear and mitochondrial encoded cytochrome c oxidase subunits and ubiquinone-NAD subunits.	NAD	318-321	uncharacterized protein	Chlamydomonas reinhardtii	8-12
15506920-3	2004	We have determined the X-ray crystal structure of a Sir2 homologue from yeast Hst2 (yHst2), in various liganded forms, including the yHst2/acetyl-Lys-16 histone H4/NAD(+) ternary complex; we have also performed related biochemical studies to address the conserved mode of catalysis by these enzymes as well as the distinguishing features that allow different members of the family to target their respective cognate substrates.	NAD	164-170	histone deacetylase HST2	Saccharomyces cerevisiae S288C	78-82
15506920-3	2004	We have determined the X-ray crystal structure of a Sir2 homologue from yeast Hst2 (yHst2), in various liganded forms, including the yHst2/acetyl-Lys-16 histone H4/NAD(+) ternary complex; we have also performed related biochemical studies to address the conserved mode of catalysis by these enzymes as well as the distinguishing features that allow different members of the family to target their respective cognate substrates.	NAD	164-170	histone deacetylase HST2	Saccharomyces cerevisiae S288C	84-89
15470234-14	2004	This appears to require the supply of GSH, NAD, and substrate to one or more of the glycolytic enzymes localized between GAPDH and enolase.	NAD	43-46	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	121-126
15522828-1	2004	Hepatic alpha-amino-beta-carboxymuconate-epsilon-semialdehyde decarboxylase (ACMSD; formerly termed picolinic carboxylase) [EC4.1.1.45] plays a key role in regulating NAD biosynthesis and the generation of quinolinate (quinolinic acid) from tryptophan.	NAD	167-170	aminocarboxymuconate semialdehyde decarboxylase	Rattus norvegicus	8-75
15522828-1	2004	Hepatic alpha-amino-beta-carboxymuconate-epsilon-semialdehyde decarboxylase (ACMSD; formerly termed picolinic carboxylase) [EC4.1.1.45] plays a key role in regulating NAD biosynthesis and the generation of quinolinate (quinolinic acid) from tryptophan.	NAD	167-170	aminocarboxymuconate semialdehyde decarboxylase	Rattus norvegicus	77-82
15509798-0	2004	NAD+ modulates p53 DNA binding specificity and function.	NAD	0-4	tumor protein p53	Homo sapiens	15-18
15464726-1	2004	We have studied the peroxidase-oxidase reaction catalyzed by human myeloperoxidase in an open system where both substrates-molecular oxygen and NADH-are supplied continuously to the reaction mixture.	NAD	144-148	myeloperoxidase	Homo sapiens	67-82
15578928-4	2004	In addition to Sir2, yeast have four additional NAD-dependent histone deacetylases Hst1-4 (for homologue of Sir2), with distinct cellular roles.	NAD	48-51	histone deacetylase HST2	Saccharomyces cerevisiae S288C	83-89
15582275-1	2004	Poly(ADP-ribosyl)ation is a DNA strand break-driven post-translational modification of proteins catalyzed by poly(ADP-ribose) polymerase-1 (PARP-1), with NAD+ serving as substrate.	NAD	154-158	poly(ADP-ribose) polymerase 1	Homo sapiens	109-138
15582275-1	2004	Poly(ADP-ribosyl)ation is a DNA strand break-driven post-translational modification of proteins catalyzed by poly(ADP-ribose) polymerase-1 (PARP-1), with NAD+ serving as substrate.	NAD	154-158	poly(ADP-ribose) polymerase 1	Homo sapiens	140-146
15509798-7	2004	Small-molecule manipulation of p53 DNA binding activity has been an elusive goal, but here we show that NAD(+) binds to p53 tetramers, induces a conformational change, and modulates p53 DNA binding specificity in vitro.	NAD	104-110	tumor protein p53	Homo sapiens	31-34
15509798-7	2004	Small-molecule manipulation of p53 DNA binding activity has been an elusive goal, but here we show that NAD(+) binds to p53 tetramers, induces a conformational change, and modulates p53 DNA binding specificity in vitro.	NAD	104-110	tumor protein p53	Homo sapiens	120-123
15509798-7	2004	Small-molecule manipulation of p53 DNA binding activity has been an elusive goal, but here we show that NAD(+) binds to p53 tetramers, induces a conformational change, and modulates p53 DNA binding specificity in vitro.	NAD	104-110	tumor protein p53	Homo sapiens	120-123
15509798-9	2004	These effects are likely due to a direct effect of NAD(+) on p53, as a molecule structurally related to part of NAD(+), TDP, also inhibits p53 DNA binding, and the TDP precursor, thiamine (vitamin B(1)), inhibits intracellular p53 activity.	NAD	51-57	tumor protein p53	Homo sapiens	61-64
15509798-9	2004	These effects are likely due to a direct effect of NAD(+) on p53, as a molecule structurally related to part of NAD(+), TDP, also inhibits p53 DNA binding, and the TDP precursor, thiamine (vitamin B(1)), inhibits intracellular p53 activity.	NAD	51-57	tumor protein p53	Homo sapiens	139-142
15509798-9	2004	These effects are likely due to a direct effect of NAD(+) on p53, as a molecule structurally related to part of NAD(+), TDP, also inhibits p53 DNA binding, and the TDP precursor, thiamine (vitamin B(1)), inhibits intracellular p53 activity.	NAD	51-57	tumor protein p53	Homo sapiens	139-142
15509798-9	2004	These effects are likely due to a direct effect of NAD(+) on p53, as a molecule structurally related to part of NAD(+), TDP, also inhibits p53 DNA binding, and the TDP precursor, thiamine (vitamin B(1)), inhibits intracellular p53 activity.	NAD	112-118	tumor protein p53	Homo sapiens	61-64
15509798-9	2004	These effects are likely due to a direct effect of NAD(+) on p53, as a molecule structurally related to part of NAD(+), TDP, also inhibits p53 DNA binding, and the TDP precursor, thiamine (vitamin B(1)), inhibits intracellular p53 activity.	NAD	112-118	tumor protein p53	Homo sapiens	139-142
15509798-9	2004	These effects are likely due to a direct effect of NAD(+) on p53, as a molecule structurally related to part of NAD(+), TDP, also inhibits p53 DNA binding, and the TDP precursor, thiamine (vitamin B(1)), inhibits intracellular p53 activity.	NAD	112-118	tumor protein p53	Homo sapiens	139-142
15229365-2	2004	ACMS decarboxylase (ACMSD) directs ACMS to acetyl CoA; otherwise ACMS is non-enzymatically converted to quinolinate (QA), leading to the formation of NAD and its degradation products.	NAD	150-153	aminocarboxymuconate semialdehyde decarboxylase	Rattus norvegicus	0-18
15481984-4	2004	The compounds were designed to optimize space-filling and atomic interactions within the NAD+ binding site of PARP-1.	NAD	89-93	poly(ADP-ribose) polymerase 1	Homo sapiens	110-116
15466236-13	2004	)OH produced by endogenous cell wall peroxidase in the presence of NADH and H(2)O(2).	NAD	67-71	peroxidase 1	Zea mays	37-47
15229365-2	2004	ACMS decarboxylase (ACMSD) directs ACMS to acetyl CoA; otherwise ACMS is non-enzymatically converted to quinolinate (QA), leading to the formation of NAD and its degradation products.	NAD	150-153	aminocarboxymuconate semialdehyde decarboxylase	Rattus norvegicus	20-25
15313399-2	2004	In this paper, the main features of this process have been reviewed, focusing on the best known poly(ADP-ribose) polymerizing enzyme, PARP-1, a DNA nick-sensor protein that uses beta-NAD+ to form polymers of ADP-ribose.	NAD	178-187	poly(ADP-ribose) polymerase 1	Homo sapiens	134-140
15633931-7	2004	This review devoted to late diabetic complications will summarize recent findings about proximal hyperglycaemia-induced alterations leading to common pathogenic action - inhibition of glycolysis on the level of GAPDH due to increased ratio NADH/NAD+, generation of superoxide and intracellular accumulation of dicarbonyls.	NAD	240-244	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	211-216
15633931-7	2004	This review devoted to late diabetic complications will summarize recent findings about proximal hyperglycaemia-induced alterations leading to common pathogenic action - inhibition of glycolysis on the level of GAPDH due to increased ratio NADH/NAD+, generation of superoxide and intracellular accumulation of dicarbonyls.	NAD	245-249	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	211-216
15329937-4	2004	Transport experiments in a twin chamber diffusion cell showed that as NAD was added to the donor side, the dissociation of the binding sites between the Cibacron blue and the lysozyme led to an increase in protein diffusion through the hydrogel.	NAD	70-73	lysozyme	Homo sapiens	175-183
15329937-5	2004	The results showed that addition of NAD caused a saturable concentration-dependent increase in the transport of both cytochrome C and hemoglobin.	NAD	36-39	cytochrome c, somatic	Homo sapiens	117-129
15245332-7	2004	On the other hand, Lys-435 and/or Lys-436 are implicated in the coenzyme specificity (NADP(+) versus NAD(+)) of maize NADP(+)-ME by interacting with the 2"-phosphate group of the ribose ring.	NAD	101-108	NADP-dependent malic enzyme	Zea mays	118-128
15342906-8	2004	Consistent with this idea, the large channels induced by N-truncated BCL-xL are inhibited by NADH and require the presence of VDAC, a voltage-dependent anion channel present in the outer mitochondrial membrane.	NAD	93-97	BCL2 like 1	Homo sapiens	69-75
15342116-1	2004	Deletion of the gene encoding NAD-dependent methylenetetrahydrofolate dehydrogenase-cyclohydrolase (NMDMC) in mice was demonstrated previously to result in failure to establish definitive erythropoiesis in the developing liver.	NAD	30-33	methylenetetrahydrofolate dehydrogenase (NAD+ dependent), methenyltetrahydrofolate cyclohydrolase	Mus musculus	100-105
15377859-7	2004	While decrements in ATP and NAD are readily observed following PARP activation, it is not yet clear whether loss of ATP and NAD contribute to the neuronal death cascade or are simply a biochemical marker for PARP-1 activation.	NAD	28-31	poly(ADP-ribose) polymerase 1	Homo sapiens	63-67
15342727-9	2004	Rundown was significantly reduced by the addition of GAPDH or its reduced cofactor NADH and nearly abolished by the addition of its substrate glyceraldehyde-3-phosphate (G3P).	NAD	83-87	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	53-58
15275834-2	2004	A unique feature of TRPM2 is its activation by ADP-ribose and chemical species that arise during oxidative stress, for example, NAD(+) and H(2)O(2).	NAD	128-134	transient receptor potential cation channel, subfamily M, member 2	Rattus norvegicus	20-25
15226311-11	2004	Furthermore, pyridoxal 4-dehydrogenase prefers NAD(+) to NADP(+) as a cofactor, although AKRs generally show higher affinities for the latter.	NAD	47-53	aldo/keto reductase	Agrobacterium tumefaciens	13-38
15377872-5	2004	Channel activity induced by cleaved BCL-xL or by hypoxia is attenuated by NADH, an inhibitor of the voltage-dependent anion channel (VDAC) of mitochondrial outer membranes.	NAD	74-78	BCL2 like 1	Homo sapiens	36-42
15239654-5	2004	Molecular modifications of the ligand NAD moiety, including nonpolar groups and hydrogen bond donor and acceptor groups, seemingly improve ligand interactions with amino acid residues of the InhA active site.	NAD	38-41	inhibin subunit alpha	Homo sapiens	191-195
15282175-3	2004	The consumption of cellular NAD(+) by PARP-1 is accompanied by ATP depletion, mitochondrial depolarization and release of proapoptotic proteins, but whether a causal relationship exists among these events remains an open question.	NAD	28-34	poly(ADP-ribose) polymerase 1	Homo sapiens	38-44
15254249-7	2004	Four genes (encoding Nop56, the NADH SDAP subunit, and two novel sequences) were found to be down-regulated in EMT-6 spheroids and four (encoding 2-oxoglutarate carrier protein, JTV-1, and two novel sequences) were up-regulated.	NAD	32-36	aminoacyl tRNA synthetase complex-interacting multifunctional protein 2	Mus musculus	111-183
15163630-4	2004	Simultaneous imaging of mitochondrial redox state (NADH and flavoprotein autofluorescence) and [Ca2+]i revealed that sperm-triggered [Ca2+] oscillations are transmitted to the mitochondria where they directly stimulate mitochondrial activity.	NAD	51-55	carbonic anhydrase 2	Mus musculus	134-137
15100216-0	2004	A new crystal structure of deoxyhypusine synthase reveals the configuration of the active enzyme and of an enzyme.NAD.inhibitor ternary complex.	NAD	114-117	deoxyhypusine synthase	Homo sapiens	27-49
15100216-9	2004	This first structure of a deoxyhypusine synthase.NAD.inhibitor ternary complex under physiological conditions now provides a structural context to discuss the results of previous biochemical investigations of the deoxyhypusine synthase reaction mechanism.	NAD	49-52	deoxyhypusine synthase	Homo sapiens	26-48
15100216-9	2004	This first structure of a deoxyhypusine synthase.NAD.inhibitor ternary complex under physiological conditions now provides a structural context to discuss the results of previous biochemical investigations of the deoxyhypusine synthase reaction mechanism.	NAD	49-52	deoxyhypusine synthase	Homo sapiens	213-235
33873776-4	2004	NAD kinases catalyse the transfer of a phosphate group from ATP to NAD to form NADP and are well characterised in plants in their requirement for the calcium binding protein calmodulin, thereby putatively linking their regulation to stress-induced intracellular calcium release.	NAD	0-3	calmodulin 1	Homo sapiens	174-184
15241181-0	2004	The NAD+ precursor nicotinamide governs neuronal survival during oxidative stress through protein kinase B coupled to FOXO3a and mitochondrial membrane potential.	NAD	4-8	forkhead box O3	Homo sapiens	118-124
15110392-6	2004	Furthermore, we show that cytochrome c is reduced by TrxR2 in vitro, not only by using NADPH as an electron donor but also by using NADH, pointing at TrxR2 as an important redox protein on complex III impairment.	NAD	132-136	cytochrome c, somatic	Homo sapiens	26-38
15150415-3	2004	To provide structural insights into the chemistry catalyzed by Sir2 proteins we report the high-resolution ternary structure of yeast Hst2 (homologue of Sir two 2) with an acetyllysine histone H4 peptide and a nonhydrolyzable NAD(+) analogue, carba-NAD(+), as well as an analogous ternary complex with a reaction intermediate analog formed immediately after nicotinamide hydrolysis, ADP-ribose.	NAD	226-232	histone deacetylase HST2	Saccharomyces cerevisiae S288C	134-138
15126114-5	2004	Further analyses showed that both PPT and DPN enhanced Bcl-2 expression in hippocampal neurons, with an efficacy comparable to their neuroprotective capacity.	NAD	42-45	BCL2 apoptosis regulator	Homo sapiens	55-60
15145826-5	2004	Cell death is determined by the effect of PARP-mediated beta-nicotinamide adenine dinucleotide (NAD) consumption on cellular metabolism.	NAD	56-94	poly(ADP-ribose) polymerase 1	Homo sapiens	42-46
15145826-5	2004	Cell death is determined by the effect of PARP-mediated beta-nicotinamide adenine dinucleotide (NAD) consumption on cellular metabolism.	NAD	96-99	poly(ADP-ribose) polymerase 1	Homo sapiens	42-46
15110392-6	2004	Furthermore, we show that cytochrome c is reduced by TrxR2 in vitro, not only by using NADPH as an electron donor but also by using NADH, pointing at TrxR2 as an important redox protein on complex III impairment.	NAD	132-136	thioredoxin reductase 2	Homo sapiens	53-58
15110392-6	2004	Furthermore, we show that cytochrome c is reduced by TrxR2 in vitro, not only by using NADPH as an electron donor but also by using NADH, pointing at TrxR2 as an important redox protein on complex III impairment.	NAD	132-136	thioredoxin reductase 2	Homo sapiens	150-155
15193131-6	2004	In the presence of NAD+ and single-strand breaks in DNA, PARP-1 catalyzes the synthesis of poly(ADP-ribose) covalently attached to the enzyme, and this automodification is thought to provide for dissociation of PARP-1 from DNA.	NAD	19-23	poly(ADP-ribose) polymerase 1	Homo sapiens	57-63
15193131-6	2004	In the presence of NAD+ and single-strand breaks in DNA, PARP-1 catalyzes the synthesis of poly(ADP-ribose) covalently attached to the enzyme, and this automodification is thought to provide for dissociation of PARP-1 from DNA.	NAD	19-23	poly(ADP-ribose) polymerase 1	Homo sapiens	211-217
14734561-10	2004	In the presence of DNA and NAD(+), PARP-1 poly(ADP-ribosyl)ates itself and Ku70/80 but not WRN, and gel-shift assays showed that poly-(ADP-ribosyl)ation of Ku70/80 decreases the DNA-binding affinity of this factor.	NAD	27-33	poly(ADP-ribose) polymerase 1	Homo sapiens	35-41
14749354-0	2004	Synergistic induction of the nicotinamide adenine dinucleotide-linked 15-hydroxyprostaglandin dehydrogenase by an androgen and interleukin-6 or forskolin in human prostate cancer cells.	NAD	29-62	interleukin 6	Homo sapiens	127-140
15102952-1	2004	Experiments using purified recombinant human NAD(P)H:quinone oxidoreductase 1 (NQO1) revealed that the auto-oxidation of fully reduced protein resulted in a 1:1 stoichiometry of oxygen consumption to NADH oxidation with the production of hydrogen peroxide.	NAD	200-204	NAD(P)H quinone dehydrogenase 1	Homo sapiens	45-77
15102952-1	2004	Experiments using purified recombinant human NAD(P)H:quinone oxidoreductase 1 (NQO1) revealed that the auto-oxidation of fully reduced protein resulted in a 1:1 stoichiometry of oxygen consumption to NADH oxidation with the production of hydrogen peroxide.	NAD	200-204	NAD(P)H quinone dehydrogenase 1	Homo sapiens	79-83
15102952-5	2004	Kinetic parameters for the reduction of O(2)(*)(-) by NQO1 were estimated using xanthine/xanthine oxidase as the source of O(2)(*)(-) and after NQO1-dependent NADH oxidation at 340 nm.	NAD	159-163	NAD(P)H quinone dehydrogenase 1	Homo sapiens	54-58
15102952-5	2004	Kinetic parameters for the reduction of O(2)(*)(-) by NQO1 were estimated using xanthine/xanthine oxidase as the source of O(2)(*)(-) and after NQO1-dependent NADH oxidation at 340 nm.	NAD	159-163	NAD(P)H quinone dehydrogenase 1	Homo sapiens	144-148
15066826-5	2004	Second, differential expression of many genes involved in redox metabolism indicates that increased cytosolic NADPH formation and NADH consumption enable a higher flux through the two-step oxidoreductase reaction of xylose to xylulose in the mutant.	NAD	130-134	oxidoreductase	Saccharomyces cerevisiae S288C	189-203
19641691-2	2004	Single-strand DNA breaks are the most potent activators of poly(ADP-ribose) polymerase (PARP); prolonged action of PARP culminates in intracellular oxidized nicotinamide adenine dinucleotide (NAD(+)) and ATP depletion.	NAD	157-190	poly(ADP-ribose) polymerase 1	Homo sapiens	59-86
19641691-2	2004	Single-strand DNA breaks are the most potent activators of poly(ADP-ribose) polymerase (PARP); prolonged action of PARP culminates in intracellular oxidized nicotinamide adenine dinucleotide (NAD(+)) and ATP depletion.	NAD	157-190	poly(ADP-ribose) polymerase 1	Homo sapiens	88-92
19641691-2	2004	Single-strand DNA breaks are the most potent activators of poly(ADP-ribose) polymerase (PARP); prolonged action of PARP culminates in intracellular oxidized nicotinamide adenine dinucleotide (NAD(+)) and ATP depletion.	NAD	157-190	poly(ADP-ribose) polymerase 1	Homo sapiens	115-119
19641691-2	2004	Single-strand DNA breaks are the most potent activators of poly(ADP-ribose) polymerase (PARP); prolonged action of PARP culminates in intracellular oxidized nicotinamide adenine dinucleotide (NAD(+)) and ATP depletion.	NAD	192-198	poly(ADP-ribose) polymerase 1	Homo sapiens	88-92
19641691-2	2004	Single-strand DNA breaks are the most potent activators of poly(ADP-ribose) polymerase (PARP); prolonged action of PARP culminates in intracellular oxidized nicotinamide adenine dinucleotide (NAD(+)) and ATP depletion.	NAD	192-198	poly(ADP-ribose) polymerase 1	Homo sapiens	115-119
14769338-0	2004	An enzymatic assay for poly(ADP-ribose) polymerase-1 (PARP-1) via the chemical quantitation of NAD(+): application to the high-throughput screening of small molecules as potential inhibitors.	NAD	95-101	poly(ADP-ribose) polymerase 1	Homo sapiens	23-52
15037661-0	2004	The CtBP2 co-repressor is regulated by NADH-dependent dimerization and possesses a novel N-terminal repression domain.	NAD	39-43	C-terminal binding protein 2	Homo sapiens	4-9
15037661-5	2004	Here we extend the functional characterization of CtBP by demonstrating that amino acid substitutions at Gly189 in the conserved NAD+-binding fold both abrogate the ability of CtBP2 to homodimerize and are associated with a dramatic loss of co-repressor activity.	NAD	129-133	C-terminal binding protein 2	Homo sapiens	176-181
15037661-8	2004	Our results suggest a model in which CtBP2 co-repressor function is regulated, at least in part, through the effect of NADH on CtBP2 homodimerization.	NAD	119-123	C-terminal binding protein 2	Homo sapiens	37-42
15037661-8	2004	Our results suggest a model in which CtBP2 co-repressor function is regulated, at least in part, through the effect of NADH on CtBP2 homodimerization.	NAD	119-123	C-terminal binding protein 2	Homo sapiens	127-132
14769338-0	2004	An enzymatic assay for poly(ADP-ribose) polymerase-1 (PARP-1) via the chemical quantitation of NAD(+): application to the high-throughput screening of small molecules as potential inhibitors.	NAD	95-101	poly(ADP-ribose) polymerase 1	Homo sapiens	54-60
14769338-1	2004	The enzyme poly(adenosine 5"-diphosphate (ADP)-ribose) polymerase (PARP-1) catalyzes the formation of (ADP)-ribose polymers on a variety of protein acceptors in a NAD+ -dependent manner.	NAD	163-167	poly(ADP-ribose) polymerase 1	Homo sapiens	67-73
14769338-2	2004	While PARP-1 is activated by DNA damage and plays a critical role in cellular survival mechanisms, its overactivation leads to a depletion of NAD+/ATP energy stores and ultimately to necrotic cell death.	NAD	142-146	poly(ADP-ribose) polymerase 1	Homo sapiens	6-12
14769338-5	2004	Described herein is a highly sensitive, inexpensive, and operationally simple assay for the rapid assessment of PARP activity that relies on the conversion of NAD+ into a highly fluorescent compound.	NAD	159-163	poly(ADP-ribose) polymerase 1	Homo sapiens	112-116
14769338-8	2004	As existing PARP assays utilize specialized reagents such as radiolabeled/biotinylated NAD+ or antibodies to poly(ADP-ribose), the chemical quantitation method described herein offers a highly sensitive and convenient alternative for rapidly screening compound collections for PARP inhibition.	NAD	87-91	poly(ADP-ribose) polymerase 1	Homo sapiens	12-16
15026183-1	2004	As first observed in rat adrenal glomerulosa cells, cytoplasmic Ca(2+) signal, induced by K(+), angiotensin II or vasopressin, evokes an increase in the level of reduced mitochondrial pyridine nucleotides, NADH and NADPH.	NAD	206-210	angiotensinogen	Rattus norvegicus	96-110
14987257-3	2004	Overactivation of PARP-1 leads to cell dysfunction and cell death mainly due to depletion of NAD(+) (the substrate of PARP-1) and ATP.	NAD	93-99	poly(ADP-ribose) polymerase 1	Homo sapiens	18-24
14987257-3	2004	Overactivation of PARP-1 leads to cell dysfunction and cell death mainly due to depletion of NAD(+) (the substrate of PARP-1) and ATP.	NAD	93-99	poly(ADP-ribose) polymerase 1	Homo sapiens	118-124
15076227-2	2004	Since cardiomyocytes can be protected from ischemia-reoxygenation injury by poly(ADP-ribose) polymerase (PARP) inhibitors mimicking the adenine/ADP part of NAD, their structural resemblance to ADP may also enable the blockade of platelet aggregation via binding to ADP receptors.	NAD	156-159	poly(ADP-ribose) polymerase 1	Homo sapiens	76-103
15076227-2	2004	Since cardiomyocytes can be protected from ischemia-reoxygenation injury by poly(ADP-ribose) polymerase (PARP) inhibitors mimicking the adenine/ADP part of NAD, their structural resemblance to ADP may also enable the blockade of platelet aggregation via binding to ADP receptors.	NAD	156-159	poly(ADP-ribose) polymerase 1	Homo sapiens	105-109
15026183-1	2004	As first observed in rat adrenal glomerulosa cells, cytoplasmic Ca(2+) signal, induced by K(+), angiotensin II or vasopressin, evokes an increase in the level of reduced mitochondrial pyridine nucleotides, NADH and NADPH.	NAD	206-210	arginine vasopressin	Rattus norvegicus	114-125
15009710-5	2004	Here we show for the first time that concentrations of less than 30 microM H2O2 increase DHPR activities, whereas levels greater than 30 microM H2O2 deactivate the enzyme based on the oxidation of Met146 and Met151 in the sequence, consequently leading to disruption of the NADH-dependent enzyme active site.	NAD	274-278	quinoid dihydropteridine reductase	Homo sapiens	89-93
14962478-2	2004	Free radical and oxidant production and related cytotoxicity during ischemia/reperfusion leads to DNA strand breakage which activates the nuclear enzyme PARP and initiates an energy-consuming, inefficient cellular metabolic cycle with transfer of the ADP-ribosyl moiety of NAD+ to protein acceptors.	NAD	273-277	poly(ADP-ribose) polymerase 1	Homo sapiens	153-157
14965227-1	2004	Sorbitol dehydrogenase (SDH), a member of the medium-chain dehydrogenase/reductase protein family and the second enzyme of the polyol pathway of glucose metabolism, converts sorbitol to fructose strictly using NAD(+) as coenzyme.	NAD	210-216	sorbitol dehydrogenase	Homo sapiens	0-22
14965227-1	2004	Sorbitol dehydrogenase (SDH), a member of the medium-chain dehydrogenase/reductase protein family and the second enzyme of the polyol pathway of glucose metabolism, converts sorbitol to fructose strictly using NAD(+) as coenzyme.	NAD	210-216	sorbitol dehydrogenase	Homo sapiens	24-27
14516279-11	2004	These data suggest that the unique tissue-expression patterns of hNMNAT-2 reflect distinct functions for the isoforms in the regulation of NAD metabolism.	NAD	139-142	nicotinamide nucleotide adenylyltransferase 2	Homo sapiens	65-73
15586663-2	2004	Several conditions (e.g., ischemia-reperfusion or chemical-induced injury) have been shown to overactivate PARP-1, causing neurodegeneration and necrotic or apoptotic cell death from NAD+ and ATP depletion.	NAD	183-187	poly(ADP-ribose) polymerase 1	Homo sapiens	107-113
14705947-9	2004	The inhibitory mechanism of ATP on PARP-1 consists of a noncompetitive interaction with the NAD site and competition with the coenzymic DNA binding site.	NAD	92-95	poly(ADP-ribose) polymerase 1	Homo sapiens	35-41
15586663-9	2004	Thus, PARP-1 inhibition by DMSO depends on NAD+ concentration and in some pathological processes might be significant even at low DMSO concentrations.	NAD	43-47	poly(ADP-ribose) polymerase 1	Homo sapiens	6-12
14695307-0	2004	NADH enzyme-dependent fluorescence recovery after photobleaching (ED-FRAP): applications to enzyme and mitochondrial reaction kinetics, in vitro.	NAD	0-4	mechanistic target of rapamycin kinase	Homo sapiens	69-73
15706060-1	2004	Capsaicin and the principal green tea catechin, (-)-epigallocatechin-3-gallate (EGCg), target tNOX, a tumor (cancer)-specific surface hydroquinone (NADH) oxidase with protein disulfide-thiol interchange activity (ECTO-NOX protein).	NAD	148-152	ecto-NOX disulfide-thiol exchanger 2	Homo sapiens	94-98
14695307-1	2004	NADH enzyme-dependent fluorescence recovery after photobleaching (ED-FRAP) was evaluated for studying enzyme kinetics in vitro and in isolated mitochondria.	NAD	0-4	mechanistic target of rapamycin kinase	Homo sapiens	69-73
14529457-3	2003	PARP-1 uses NAD+ as a substrate and is activated during stressful circumstances, mainly in the nucleus.	NAD	12-16	poly(ADP-ribose) polymerase 1	Homo sapiens	0-6
15720822-5	2004	Superoxide dismutase (SOD) and aminooxyacetate (AOA), a malate/aspartate shuttle inhibitor, strongly inhibited WST-1 reduction and reduced DCIP reduction by 40-60%, but failed to affect FeCN reduction, indicating involvement of mitochondrial TCA cycle-derived NADH and a possible role for superoxide in WST-1 but not FeCN reduction.	NAD	260-264	superoxide dismutase 1	Homo sapiens	0-20
15033737-2	2003	Exposure of T cells to NAD, the substrate for ART2-catalyzed ADP-ribosylation, induces exposure of phosphatidylserine, uptake of propidium iodide, and fragmentation of DNA.	NAD	23-26	ADP-ribosyltransferase 1	Homo sapiens	46-50
15033737-3	2003	ART2-specific antibodies raised by gene gun immunization block NAD-induced apoptosis.	NAD	63-66	ADP-ribosyltransferase 1	Homo sapiens	0-4
15622856-0	2004	Fluorescence measurements of steady state peroxynitrite production upon SIN-1 decomposition: NADH versus dihydrodichlorofluorescein and dihydrorhodamine 123.	NAD	93-97	MAPK associated protein 1	Homo sapiens	72-77
15622856-1	2004	The production of peroxynitrite during 3-morpholinosydnonimine (SIN-1) decomposition can be continuously monitored, with a sensitivity &lt; or = 0.1 microM, from the kinetics of NADH fluorescence quenching in phosphate buffers, as well as in buffers commonly used with cell cultures, like Locke"s buffer or Dulbecco"s modified Eagle"s medium (DMEM-F12).	NAD	178-182	MAPK associated protein 1	Homo sapiens	64-69
15622856-5	2004	NADH was found to be less sensitive than dihydrorhodamine 123 and 2",7"-dichlorodihydrofluorescein diacetate to oxidation by H2O2, which is produced during SIN-1 decomposition in common buffers.	NAD	0-4	MAPK associated protein 1	Homo sapiens	156-161
15588129-8	2004	Reaction of FAL with diaphorase was lowered with SOD by 38 % indicating the partial participation of superoxide anion probably generated by the reaction of diaphorase with NADH or NADPH.	NAD	172-176	superoxide dismutase 1	Homo sapiens	49-52
14659887-0	2003	Identification of NAD+-dependent isocitrate dehydrogenase 3 gamma-like (IDH3GL) gene and its genetic polymorphisms.	NAD	18-21	neural EGFL like 1	Homo sapiens	33-70
14659887-0	2003	Identification of NAD+-dependent isocitrate dehydrogenase 3 gamma-like (IDH3GL) gene and its genetic polymorphisms.	NAD	18-21	neural EGFL like 1	Homo sapiens	72-78
14529457-4	2003	PARP-1 inhibitors are well known for blocking the excessive consumption of NAD+, thereby preserving energy metabolism.	NAD	75-79	poly(ADP-ribose) polymerase 1	Homo sapiens	0-6
14525943-6	2003	The tissue lactate/pyruvate ratio, a measure of cytosolic NADH/NAD+, was reduced by SDH inhibition under both normoxic and ischemic conditions.	NAD	58-62	sorbitol dehydrogenase	Homo sapiens	84-87
14525943-6	2003	The tissue lactate/pyruvate ratio, a measure of cytosolic NADH/NAD+, was reduced by SDH inhibition under both normoxic and ischemic conditions.	NAD	63-67	sorbitol dehydrogenase	Homo sapiens	84-87
14646967-7	2003	CONCLUSIONS: These results suggest that rat esophagus has an nicotinamide adenine dinucleotide-dependent all-trans retinoic acid formation pathway in which alcohol dehydrogenase is involved.	NAD	61-94	aldo-keto reductase family 1 member A1	Rattus norvegicus	156-177
19087393-1	2003	Poly(ADP-ribose) synthetase/polymerase (PARP) activation causes NAD+ depletion in pancreatic beta-cells, which results in necrotic cell death.	NAD	64-68	poly(ADP-ribose) polymerase 1	Homo sapiens	0-38
19087393-1	2003	Poly(ADP-ribose) synthetase/polymerase (PARP) activation causes NAD+ depletion in pancreatic beta-cells, which results in necrotic cell death.	NAD	64-68	poly(ADP-ribose) polymerase 1	Homo sapiens	40-44
14981915-3	2003	The addition of antioxidants (N-acetyl-Lcysteine, sodium ascorbate, catalase) reduced the cytotoxicity of BHA/BHT or BMP against HSC-2 cells, but not that of BHA or BHT, whereas the addition of NADH, a quinone reductase to BMP, enhanced the cytotoxicity.	NAD	194-198	catalase	Homo sapiens	68-76
12969868-1	2003	Nicotinamide adenine dinucleotide (phosphate) reduced:quinone oxidoreductase (NQO1) and glutathione S-transferase (GST) M1 are phase II enzymes important in response to oxidative stress, such as occurs during exposure to ozone.	NAD	0-33	NAD(P)H quinone dehydrogenase 1	Homo sapiens	78-82
14612543-7	2003	Certain tissues, however, have a high turnover of NAD+ through its cleavage by enzymes like poly(ADP-ribose) polymerase.	NAD	50-54	poly(ADP-ribose) polymerase 1	Homo sapiens	92-119
12975482-1	2003	In the course of other experiments, we serendipitously observed that extracellular nicotinamide adenine dinucleotide (NAD+) ameliorated the development of epithelial hyperpermeability when monolayers of Caco-2 enterocyte-like cells were incubated with cytomix, a mixture containing interferon-gamma, interleukin-1beta, and tumor necrosis factor-alpha.	NAD	83-116	interferon gamma	Homo sapiens	282-298
12975482-7	2003	Treatment of cytomix-stimulated cells with NAD+ also blocked nuclear factor-kappaB (NF-kappaB) activation, inducible nitric-oxide synthase induction, and increased production of nitric oxide (NO.).	NAD	43-47	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	61-82
12975482-7	2003	Treatment of cytomix-stimulated cells with NAD+ also blocked nuclear factor-kappaB (NF-kappaB) activation, inducible nitric-oxide synthase induction, and increased production of nitric oxide (NO.).	NAD	43-47	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	84-93
12975482-11	2003	Thus, extracellular NAD+ seems to ameliorate inflammation-induced intestinal epithelial barrier dysfunction by inhibiting NF-kappaB activation and increased NO.	NAD	20-24	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	122-131
12975482-1	2003	In the course of other experiments, we serendipitously observed that extracellular nicotinamide adenine dinucleotide (NAD+) ameliorated the development of epithelial hyperpermeability when monolayers of Caco-2 enterocyte-like cells were incubated with cytomix, a mixture containing interferon-gamma, interleukin-1beta, and tumor necrosis factor-alpha.	NAD	83-116	interleukin 1 beta	Homo sapiens	300-317
12975482-1	2003	In the course of other experiments, we serendipitously observed that extracellular nicotinamide adenine dinucleotide (NAD+) ameliorated the development of epithelial hyperpermeability when monolayers of Caco-2 enterocyte-like cells were incubated with cytomix, a mixture containing interferon-gamma, interleukin-1beta, and tumor necrosis factor-alpha.	NAD	83-116	tumor necrosis factor	Homo sapiens	323-350
12975482-1	2003	In the course of other experiments, we serendipitously observed that extracellular nicotinamide adenine dinucleotide (NAD+) ameliorated the development of epithelial hyperpermeability when monolayers of Caco-2 enterocyte-like cells were incubated with cytomix, a mixture containing interferon-gamma, interleukin-1beta, and tumor necrosis factor-alpha.	NAD	118-122	interferon gamma	Homo sapiens	282-298
12975482-1	2003	In the course of other experiments, we serendipitously observed that extracellular nicotinamide adenine dinucleotide (NAD+) ameliorated the development of epithelial hyperpermeability when monolayers of Caco-2 enterocyte-like cells were incubated with cytomix, a mixture containing interferon-gamma, interleukin-1beta, and tumor necrosis factor-alpha.	NAD	118-122	interleukin 1 beta	Homo sapiens	300-317
12975482-1	2003	In the course of other experiments, we serendipitously observed that extracellular nicotinamide adenine dinucleotide (NAD+) ameliorated the development of epithelial hyperpermeability when monolayers of Caco-2 enterocyte-like cells were incubated with cytomix, a mixture containing interferon-gamma, interleukin-1beta, and tumor necrosis factor-alpha.	NAD	118-122	tumor necrosis factor	Homo sapiens	323-350
14594650-2	2003	PARP mediates the transfer of poly-ADP-ribose moieties on itself and other nuclear proteins by the breakdown of NAD+.	NAD	112-116	poly(ADP-ribose) polymerase 1	Homo sapiens	0-4
14604530-4	2003	Comparison of the ternary complex with the yHst2/NAD(+) complex, also reported here, and nascent yHst2 structure also reveals that NAD(+) binding accompanies intramolecular loop rearrangement for more stable NAD(+) and acetyl-lysine binding, and that acetyl-lysine peptide binding induces a trimer-monomer protein transition involving nonconserved Sir2 residues.	NAD	49-55	histone deacetylase HST2	Saccharomyces cerevisiae S288C	43-48
14604530-4	2003	Comparison of the ternary complex with the yHst2/NAD(+) complex, also reported here, and nascent yHst2 structure also reveals that NAD(+) binding accompanies intramolecular loop rearrangement for more stable NAD(+) and acetyl-lysine binding, and that acetyl-lysine peptide binding induces a trimer-monomer protein transition involving nonconserved Sir2 residues.	NAD	131-137	histone deacetylase HST2	Saccharomyces cerevisiae S288C	43-48
14604530-4	2003	Comparison of the ternary complex with the yHst2/NAD(+) complex, also reported here, and nascent yHst2 structure also reveals that NAD(+) binding accompanies intramolecular loop rearrangement for more stable NAD(+) and acetyl-lysine binding, and that acetyl-lysine peptide binding induces a trimer-monomer protein transition involving nonconserved Sir2 residues.	NAD	131-137	histone deacetylase HST2	Saccharomyces cerevisiae S288C	97-102
14604530-4	2003	Comparison of the ternary complex with the yHst2/NAD(+) complex, also reported here, and nascent yHst2 structure also reveals that NAD(+) binding accompanies intramolecular loop rearrangement for more stable NAD(+) and acetyl-lysine binding, and that acetyl-lysine peptide binding induces a trimer-monomer protein transition involving nonconserved Sir2 residues.	NAD	131-137	histone deacetylase HST2	Saccharomyces cerevisiae S288C	43-48
14604530-4	2003	Comparison of the ternary complex with the yHst2/NAD(+) complex, also reported here, and nascent yHst2 structure also reveals that NAD(+) binding accompanies intramolecular loop rearrangement for more stable NAD(+) and acetyl-lysine binding, and that acetyl-lysine peptide binding induces a trimer-monomer protein transition involving nonconserved Sir2 residues.	NAD	131-137	histone deacetylase HST2	Saccharomyces cerevisiae S288C	97-102
14594650-6	2003	Both PARP inhibitors delayed the drop in WST-1 reduction and retained NAD+ and ATP levels required for apoptosis.	NAD	70-74	poly(ADP-ribose) polymerase 1	Homo sapiens	5-9
14580859-1	2003	The human sirtuin 3 (SIRT3) gene encodes a putative mitochondrial NAD-dependent deacetylase (SIRT3) which belongs to the evolutionary conserved family of sirtuin 2 proteins.	NAD	66-69	sirtuin 3	Homo sapiens	10-19
12871940-5	2003	Pi oxidized cytochrome b (cyto-b) and reduced cytochrome c (cyto-c), potentially improving the coupling between the NADH free energy and the proton motive force.	NAD	116-120	cytochrome c, somatic	Homo sapiens	60-66
12930846-5	2003	To investigate the effect of this association on PARP-1 activity, an assay based on the incorporation of radioactive NAD was performed.	NAD	117-120	poly(ADP-ribose) polymerase 1	Homo sapiens	49-55
12871940-5	2003	Pi oxidized cytochrome b (cyto-b) and reduced cytochrome c (cyto-c), potentially improving the coupling between the NADH free energy and the proton motive force.	NAD	116-120	cytochrome c, somatic	Homo sapiens	46-58
14529360-3	2003	Massive PARP-1 activation, however, can deplete the cell of NAD(+) and ATP, ultimately leading to energy failure and cell death.	NAD	60-66	poly(ADP-ribose) polymerase 1	Homo sapiens	8-14
14580859-1	2003	The human sirtuin 3 (SIRT3) gene encodes a putative mitochondrial NAD-dependent deacetylase (SIRT3) which belongs to the evolutionary conserved family of sirtuin 2 proteins.	NAD	66-69	sirtuin 3	Homo sapiens	21-26
14580859-1	2003	The human sirtuin 3 (SIRT3) gene encodes a putative mitochondrial NAD-dependent deacetylase (SIRT3) which belongs to the evolutionary conserved family of sirtuin 2 proteins.	NAD	66-69	sirtuin 3	Homo sapiens	93-98
12963490-0	2003	Inhibition of indoleamine 2,3-dioxygenase activity in IFN-gamma stimulated astroglioma cells decreases intracellular NAD levels.	NAD	117-120	interferon gamma	Homo sapiens	54-63
12972620-10	2003	Transcript array analysis shows that reduction in cellular NAD(+) levels preferentially affects Hst1p-regulated genes in comparison to genes regulated with other NAD(+)-dependent deacetylases (Sir2p, Hst2p, Hst3p, and Hst4p).	NAD	59-65	histone deacetylase HST2	Saccharomyces cerevisiae S288C	200-205
14502267-2	2003	The X-ray crystal structure of the full-length yHst2 protein reveals a central catalytic core domain fold that is characteristic of the other Sir2 homologs, and C- and N-terminal extensions that interact with the NAD(+) and acetyl-lysine substrate-binding sites, respectively, suggesting an autoregulatory function for these domains.	NAD	213-219	histone deacetylase HST2	Saccharomyces cerevisiae S288C	47-52
14563321-0	2003	NAD-induced T cell death: ADP-ribosylation of cell surface proteins by ART2 activates the cytolytic P2X7 purinoceptor.	NAD	0-3	ADP-ribosyltransferase 1	Homo sapiens	71-75
14563321-0	2003	NAD-induced T cell death: ADP-ribosylation of cell surface proteins by ART2 activates the cytolytic P2X7 purinoceptor.	NAD	0-3	purinergic receptor P2X 7	Homo sapiens	100-104
14563321-4	2003	Interestingly, much lower NAD than ATP concentrations are required to activate P2X7.	NAD	26-29	purinergic receptor P2X 7	Homo sapiens	79-83
14517300-8	2003	Nevertheless, expression of Glut1 and HK1 promoted increased cytosolic NADH and NADPH levels relative to those of the control cells upon growth factor withdrawal, prevented activation of Bax, and promoted growth factor-independent survival.	NAD	71-75	hexokinase 1	Homo sapiens	38-41
14527731-2	2003	The ADP-ribose polymers, synthesized by the diverse PARP enzymes by cleavage of NAD(+), are involved in the regulation of multiple cellular functions.	NAD	80-86	poly(ADP-ribose) polymerase 1	Homo sapiens	52-56
14527731-3	2003	At present, only a single enzyme, poly (ADP-ribose) glycohydrolase (PARG), has been identified to catalyze ADP-ribose polymer hydrolysis in the cell causing a rapid turnover of the biopolymer which may ultimately result in lethal depletion of cellular NAD(+) pools.	NAD	252-258	poly(ADP-ribose) glycohydrolase	Homo sapiens	34-66
14527731-3	2003	At present, only a single enzyme, poly (ADP-ribose) glycohydrolase (PARG), has been identified to catalyze ADP-ribose polymer hydrolysis in the cell causing a rapid turnover of the biopolymer which may ultimately result in lethal depletion of cellular NAD(+) pools.	NAD	252-258	poly(ADP-ribose) glycohydrolase	Homo sapiens	68-72
12927790-5	2003	Here, we used primary astrocyte cultures to directly test this proposal, utilizing the endogenous expression of connexin-43 hemichannels by astrocytes to manipulate intracellular NAD(+) concentrations.	NAD	179-185	gap junction protein, alpha 1	Mus musculus	112-123
13679179-1	2003	An excessive activation of poly(ADP-ribose) polymerase-1 (PARP-1), a nuclear enzyme able to catalyze the transfer of ADP-ribose from NAD to acceptor proteins, is involved in the progression of neuronal damage after brain insult.	NAD	133-136	poly(ADP-ribose) polymerase 1	Homo sapiens	27-56
14500388-3	2003	NQO(1) gene regulation may be up-regulated in some tumors to accommodate the needs of rapidly metabolizing cells to regenerate NAD(+).	NAD	127-133	NAD(P)H quinone dehydrogenase 1	Homo sapiens	0-6
14650208-5	2003	In the energostim treated group, there is a correlation between the SOD activity and the content of cytochrome C in mitochondria (R 6.1, p &lt; 0.01): a change in the level of cytochrome C during 2-h acute ischemia is correlated with the decrease in redox potential (NAD/NADH) and in the ratio of glutathione peroxidase to Mn-dependent SOD (r 0.64, p &lt; 0.01).	NAD	267-270	cytochrome c, somatic	Homo sapiens	100-112
14650208-5	2003	In the energostim treated group, there is a correlation between the SOD activity and the content of cytochrome C in mitochondria (R 6.1, p &lt; 0.01): a change in the level of cytochrome C during 2-h acute ischemia is correlated with the decrease in redox potential (NAD/NADH) and in the ratio of glutathione peroxidase to Mn-dependent SOD (r 0.64, p &lt; 0.01).	NAD	267-270	cytochrome c, somatic	Homo sapiens	176-188
14650208-5	2003	In the energostim treated group, there is a correlation between the SOD activity and the content of cytochrome C in mitochondria (R 6.1, p &lt; 0.01): a change in the level of cytochrome C during 2-h acute ischemia is correlated with the decrease in redox potential (NAD/NADH) and in the ratio of glutathione peroxidase to Mn-dependent SOD (r 0.64, p &lt; 0.01).	NAD	271-275	cytochrome c, somatic	Homo sapiens	100-112
14650208-5	2003	In the energostim treated group, there is a correlation between the SOD activity and the content of cytochrome C in mitochondria (R 6.1, p &lt; 0.01): a change in the level of cytochrome C during 2-h acute ischemia is correlated with the decrease in redox potential (NAD/NADH) and in the ratio of glutathione peroxidase to Mn-dependent SOD (r 0.64, p &lt; 0.01).	NAD	271-275	cytochrome c, somatic	Homo sapiens	176-188
14570268-4	2003	However, overexpression of the MDH3 gene that was involved in the reoxidation of NADH during fatty acid beta-oxidation caused a decrease in cell viability of AKD321 to H2O2 stress, while the 746 rho0 mutant had no such effect.	NAD	81-85	malate dehydrogenase MDH3	Saccharomyces cerevisiae S288C	31-35
13679179-1	2003	An excessive activation of poly(ADP-ribose) polymerase-1 (PARP-1), a nuclear enzyme able to catalyze the transfer of ADP-ribose from NAD to acceptor proteins, is involved in the progression of neuronal damage after brain insult.	NAD	133-136	poly(ADP-ribose) polymerase 1	Homo sapiens	58-64
12788913-7	2003	Purified human deoxyhypusine synthase also exhibited homospermidine synthesis activity when incubated with spermidine, NAD, and putrescine.	NAD	119-122	deoxyhypusine synthase	Homo sapiens	15-37
15969098-2	2003	Assimilatory NADH: nitrate reductase (NR, EC 1.6.6.1), a complex Mo-pterin-, cytochrome b(557)- and FAD-containing protein, catalyzes the regulated and rate-limiting step in the utilization of inorganic nitrogen by higher plants.	NAD	13-17	nitrate reductase [NADH]	Solanum lycopersicum	19-36
12967857-1	2003	PURPOSE: To evaluate the relationship of lambda-crystallin to reduced nicotinamide adenine dinucleotide (NADH)-dependent dehydroascorbate (DHA) reductase found specifically in the rabbit lens.	NAD	70-103	lambda-crystallin	Oryctolagus cuniculus	41-58
12967857-1	2003	PURPOSE: To evaluate the relationship of lambda-crystallin to reduced nicotinamide adenine dinucleotide (NADH)-dependent dehydroascorbate (DHA) reductase found specifically in the rabbit lens.	NAD	105-109	lambda-crystallin	Oryctolagus cuniculus	41-58
12788913-5	2003	When eIF5A([3H]Dhp), radiolabeled in the 4-aminobutyl portion of its deoxyhypusine residue, was incubated with human deoxyhypusine synthase, NAD, and 1,3-diaminopropane, [3H]spermidine was formed by a rapid transfer of the radiolabeled 4-aminobutyl side chain of the [3H]deoxyhypusine residue to 1,3-diaminopropane.	NAD	141-144	dihydropyrimidinase	Homo sapiens	15-18
12893257-3	2003	Both NAD and NADH-the cofactors of GAPDH-inhibited the GAPDH-RNA (DNA) interaction, though NAD was much less effective than NADH in the case of oxidized GAPDH.	NAD	124-128	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	35-40
12748170-0	2003	Evidence for the role of a peroxidase compound I-type intermediate in the oxidation of glutathione, NADH, ascorbate, and dichlorofluorescin by cytochrome c/H2O2.	NAD	100-104	cytochrome c, somatic	Homo sapiens	143-155
12700160-2	2003	The NAD+-dependent type 2 (11betaHSD2) enzyme is an oxidase that inactivates cortisol and corticosterone, conferring extrinsic specificity of the mineralocorticoid receptor for aldosterone.	NAD	4-8	nuclear receptor subfamily 3, group C, member 2	Rattus norvegicus	146-172
12893257-3	2003	Both NAD and NADH-the cofactors of GAPDH-inhibited the GAPDH-RNA (DNA) interaction, though NAD was much less effective than NADH in the case of oxidized GAPDH.	NAD	124-128	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	55-60
12893257-3	2003	Both NAD and NADH-the cofactors of GAPDH-inhibited the GAPDH-RNA (DNA) interaction, though NAD was much less effective than NADH in the case of oxidized GAPDH.	NAD	124-128	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	55-60
12879452-2	2003	Overstimulation of PARP-1 by extensive DNA damage, however, can result in cell death, as prolonged PARP-1 activation depletes NAD(+), a substrate, and elevates nicotinamide, a product.	NAD	126-132	poly(ADP-ribose) polymerase 1	Homo sapiens	19-25
12918120-8	2003	NADH could not only eliminate the apoptosis induced by X-ray irradiation, but also up-regulate expression of bcl-2 protein and down-regulate expression of p53, bax, fas and fasL proteins (P&lt;0.05).	NAD	0-4	BCL2 apoptosis regulator	Homo sapiens	109-114
12879452-2	2003	Overstimulation of PARP-1 by extensive DNA damage, however, can result in cell death, as prolonged PARP-1 activation depletes NAD(+), a substrate, and elevates nicotinamide, a product.	NAD	126-132	poly(ADP-ribose) polymerase 1	Homo sapiens	99-105
12879452-5	2003	It is conceivable that poly(ADP-ribosyl)ation by PARP-1, which is induced by DNA damage, could modulate protein deacetylation by Sir2 via the NAD(+)/nicotinamide connection.	NAD	142-148	poly(ADP-ribose) polymerase 1	Homo sapiens	49-55
12893257-3	2003	Both NAD and NADH-the cofactors of GAPDH-inhibited the GAPDH-RNA (DNA) interaction, though NAD was much less effective than NADH in the case of oxidized GAPDH.	NAD	5-8	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	35-40
12893257-3	2003	Both NAD and NADH-the cofactors of GAPDH-inhibited the GAPDH-RNA (DNA) interaction, though NAD was much less effective than NADH in the case of oxidized GAPDH.	NAD	5-8	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	55-60
12893257-3	2003	Both NAD and NADH-the cofactors of GAPDH-inhibited the GAPDH-RNA (DNA) interaction, though NAD was much less effective than NADH in the case of oxidized GAPDH.	NAD	5-8	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	55-60
12893257-3	2003	Both NAD and NADH-the cofactors of GAPDH-inhibited the GAPDH-RNA (DNA) interaction, though NAD was much less effective than NADH in the case of oxidized GAPDH.	NAD	13-17	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	35-40
12893257-3	2003	Both NAD and NADH-the cofactors of GAPDH-inhibited the GAPDH-RNA (DNA) interaction, though NAD was much less effective than NADH in the case of oxidized GAPDH.	NAD	13-17	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	55-60
12893257-3	2003	Both NAD and NADH-the cofactors of GAPDH-inhibited the GAPDH-RNA (DNA) interaction, though NAD was much less effective than NADH in the case of oxidized GAPDH.	NAD	13-17	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	55-60
12893257-3	2003	Both NAD and NADH-the cofactors of GAPDH-inhibited the GAPDH-RNA (DNA) interaction, though NAD was much less effective than NADH in the case of oxidized GAPDH.	NAD	13-16	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	35-40
12893257-3	2003	Both NAD and NADH-the cofactors of GAPDH-inhibited the GAPDH-RNA (DNA) interaction, though NAD was much less effective than NADH in the case of oxidized GAPDH.	NAD	13-16	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	55-60
12893257-3	2003	Both NAD and NADH-the cofactors of GAPDH-inhibited the GAPDH-RNA (DNA) interaction, though NAD was much less effective than NADH in the case of oxidized GAPDH.	NAD	13-16	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	55-60
14599119-3	2003	Enzyme activity of 11beta-HSD1 and 2 in lung tissue homogenate were determined as NADP(+)- and NAD(+)-dependent conversion of corticosterone to 11-dehydrocorticosterone, respectively.	NAD	95-101	hydroxy-delta-5-steroid dehydrogenase, 3 beta- and steroid delta-isomerase 5	Rattus norvegicus	19-36
12928715-8	2003	NADH-TR staining was employed to distinguish nuclear bag1, nuclear bag2, and nuclear chain intrafusal muscle fibers.	NAD	0-4	BAG cochaperone 1	Rattus norvegicus	53-57
12739149-3	2003	This hypothesis was investigated by supplying cell walls of maize ( Zea mays L.) coleoptiles and sunflower ( Helianthus annuus L.) hypocotyls with external NADH, an artificial substrate known to cause *OH generation by POD in vitro.	NAD	156-160	peroxidase 1	Zea mays	219-222
12739149-5	2003	NADH mediates cell wall extension in vitro and in vivo in an H2O2-dependent reaction that shows the characteristic features of POD.	NAD	0-4	peroxidase 1	Zea mays	127-130
12739149-8	2003	Apoplastic consumption of external NADH by living coleoptiles can be traced back to the superimposed action of two enzymatic reactions, a KCN-sensitive reaction mediated by POD operating in the *OH-forming mode, and a KCN-insensitive reaction with the kinetic properties of a superoxide-producing plasma-membrane NADH oxidase the activity of which can be promoted by auxin.	NAD	35-39	peroxidase 1	Zea mays	173-176
12739149-9	2003	Under natural conditions, i.e. in the absence of external NADH, this enzyme may provide superoxide (O2*-) (and H2O2 utilized by POD for) *OH production in the cell wall.	NAD	58-62	peroxidase 1	Zea mays	128-131
12893257-4	2003	Oxidation of GAPDH strongly decreased its affinity to NAD but not to NADH.	NAD	54-57	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	13-18
12893257-4	2003	Oxidation of GAPDH strongly decreased its affinity to NAD but not to NADH.	NAD	69-73	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	13-18
12918120-8	2003	NADH could not only eliminate the apoptosis induced by X-ray irradiation, but also up-regulate expression of bcl-2 protein and down-regulate expression of p53, bax, fas and fasL proteins (P&lt;0.05).	NAD	0-4	tumor protein p53	Homo sapiens	155-158
12918120-8	2003	NADH could not only eliminate the apoptosis induced by X-ray irradiation, but also up-regulate expression of bcl-2 protein and down-regulate expression of p53, bax, fas and fasL proteins (P&lt;0.05).	NAD	0-4	BCL2 associated X, apoptosis regulator	Homo sapiens	160-163
12918120-10	2003	CONCLUSION: NADH has marked anti-radiation effect, its mechanism may be associated with up-regulation of bcl-2 expression and down-regulation of p53, bax fas and fasL expression, as well as decline of intracellular ROS.	NAD	12-16	BCL2 apoptosis regulator	Homo sapiens	105-110
12918120-10	2003	CONCLUSION: NADH has marked anti-radiation effect, its mechanism may be associated with up-regulation of bcl-2 expression and down-regulation of p53, bax fas and fasL expression, as well as decline of intracellular ROS.	NAD	12-16	tumor protein p53	Homo sapiens	145-148
12918120-10	2003	CONCLUSION: NADH has marked anti-radiation effect, its mechanism may be associated with up-regulation of bcl-2 expression and down-regulation of p53, bax fas and fasL expression, as well as decline of intracellular ROS.	NAD	12-16	BCL2 associated X, apoptosis regulator	Homo sapiens	150-153
12887926-3	2003	Surprisingly, p38 represents a nuclear form of glyceraldehyde-3-phosphate dehydrogenase, and binding to Oct-1, as well as OCA-S function, is stimulated by NAD(+) but inhibited by NADH.	NAD	155-161	mitogen-activated protein kinase 14	Homo sapiens	14-17
12887926-3	2003	Surprisingly, p38 represents a nuclear form of glyceraldehyde-3-phosphate dehydrogenase, and binding to Oct-1, as well as OCA-S function, is stimulated by NAD(+) but inhibited by NADH.	NAD	179-183	mitogen-activated protein kinase 14	Homo sapiens	14-17
12887926-3	2003	Surprisingly, p38 represents a nuclear form of glyceraldehyde-3-phosphate dehydrogenase, and binding to Oct-1, as well as OCA-S function, is stimulated by NAD(+) but inhibited by NADH.	NAD	155-161	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	47-87
12721285-1	2003	Mono-ADP-ribosyltransferases (ART1-7) transfer ADP-ribose from NAD+ to proteins (transferase activity) or water (NAD glycohydrolase activity).	NAD	63-67	ADP-ribosyltransferase 1	Mus musculus	30-34
12860382-2	2003	NADH decreased cardiac RyR activity, which was counteracted by NAD+.	NAD	0-4	ryanodine receptor 1	Homo sapiens	23-26
12860382-2	2003	NADH decreased cardiac RyR activity, which was counteracted by NAD+.	NAD	63-67	ryanodine receptor 1	Homo sapiens	23-26
12867035-6	2003	This interaction, and consequent repression of p53-dependent transcription, is relieved under hypoxia or hypoxia-mimicking conditions that are known to increase levels of intracellular NADH.	NAD	185-189	tumor protein p53	Homo sapiens	47-50
12758076-6	2003	We found a similarity between the MWFE homologues and the C-terminal part of the nqrA subunit of bacterial Na(+)-translocating NADH:quinone oxidoreductases (Na(+)-NQR), suggesting a link between proton-pumping and sodium-pumping NADH dehydrogenases.	NAD	127-131	NADH:ubiquinone oxidoreductase subunit A1	Homo sapiens	34-38
12823559-7	2003	Both enzymes were specific for NADH as electron donor, but with different apparent Km values (NoxA-1, 0.13 mm; NoxB-1, 0.011 mm).	NAD	31-35	NADPH oxidase activator 1	Homo sapiens	94-100
12909186-2	2003	HYPOTHESIS: We hypothesised that this was due to the following effects of alcohol: (1) alcohol metabolism increases NADH, leading to a reduction in hepatic gluconeogenesis; (2) increased glycogen phosphorylase activity depletes hepatic glycogen stores; (3) after the alcohol is metabolised, hepatic insulin sensitivity is increased, leading to the restoration of glycogen stores and reduction in blood glucose levels; and (4) consequently, after several hours, glycogen stores and insulin sensitivity return to normal.	NAD	116-120	insulin	Homo sapiens	299-306
12843783-7	2003	Glycerol 3-phosphate dehydrogenase, which is involved in mitochondrial reoxidation of glycolysis derived NADH, was regulated more than 60-fold.	NAD	105-109	glycerol-3-phosphate dehydrogenase 1	Rattus norvegicus	0-34
12787027-5	2003	In relaxation experiments performed with CPR reduced at the two-electron level with NADH, the observed rate of internal electron transfer (1/tau = 18 +/- 0.7 s-1) is intermediate in value between those seen with dithionite-reduced and NADPH-reduced enzyme, indicating that the presence of the 2"-phosphate is important for enhancing internal electron transfer.	NAD	84-88	cytochrome p450 oxidoreductase	Homo sapiens	41-44
12787027-8	2003	Reduction of CPR at the two-electron level by NADPH, NADH or dithionite generates the same spectral species, consistent with an electron distribution that is equivalent regardless of reductant at the initiation of the temperature jump.	NAD	53-57	cytochrome p450 oxidoreductase	Homo sapiens	13-16
12649291-8	2003	Incubation with NAD and auto-ADP-ribosylation decreased the NADase activities of wild-type ART2b and ART2b (R204W), whereas activity of ART2b(R204K), which is not auto-modified, was unchanged by NAD.	NAD	16-19	ADP-ribosyltransferase 2b	Rattus norvegicus	91-96
12649291-8	2003	Incubation with NAD and auto-ADP-ribosylation decreased the NADase activities of wild-type ART2b and ART2b (R204W), whereas activity of ART2b(R204K), which is not auto-modified, was unchanged by NAD.	NAD	16-19	ADP-ribosyltransferase 2b	Rattus norvegicus	101-106
12649291-8	2003	Incubation with NAD and auto-ADP-ribosylation decreased the NADase activities of wild-type ART2b and ART2b (R204W), whereas activity of ART2b(R204K), which is not auto-modified, was unchanged by NAD.	NAD	16-19	ADP-ribosyltransferase 2b	Rattus norvegicus	101-106
12649291-8	2003	Incubation with NAD and auto-ADP-ribosylation decreased the NADase activities of wild-type ART2b and ART2b (R204W), whereas activity of ART2b(R204K), which is not auto-modified, was unchanged by NAD.	NAD	60-63	ADP-ribosyltransferase 2b	Rattus norvegicus	91-96
12649291-8	2003	Incubation with NAD and auto-ADP-ribosylation decreased the NADase activities of wild-type ART2b and ART2b (R204W), whereas activity of ART2b(R204K), which is not auto-modified, was unchanged by NAD.	NAD	60-63	ADP-ribosyltransferase 2b	Rattus norvegicus	101-106
12649291-8	2003	Incubation with NAD and auto-ADP-ribosylation decreased the NADase activities of wild-type ART2b and ART2b (R204W), whereas activity of ART2b(R204K), which is not auto-modified, was unchanged by NAD.	NAD	60-63	ADP-ribosyltransferase 2b	Rattus norvegicus	101-106
12766240-4	2003	We therefore investigated whether NAD and NADP interact with both Kir6.2 and SUR1 subunits of the KATP channel by comparing the potency of these agents on recombinant Kir6.2DeltaC and Kir6.2/SUR1 channels expressed in Xenopus oocytes.	NAD	34-37	ATP-binding cassette sub-family C member 8	Xenopus laevis	77-81
12766240-5	2003	Our results show that, at physiological concentrations, NAD and NADP interact with the nucleotide inhibitory site of Kir6.2 to inhibit Kir6.2/SUR1 currents.	NAD	56-59	ATP-binding cassette sub-family C member 8	Xenopus laevis	142-146
12853070-2	2003	PARP-1 is highly activated by reactive oxygen species-induced DNA strand breaks, upon which it forms extensive poly(ADP-ribose) (PAR) polymers from its substrate NAD(+).	NAD	162-168	poly(ADP-ribose) polymerase 1	Homo sapiens	0-6
12929742-2	2003	The measurements indicated that the enzymes located in the Golgi apparatus (uridine 5"-diphosphate galactosyl transferase) and in the endoplasmic reticulum (ER) (nicotinamide adenine dinucleotide [reduced] [NADH] cytochrome c [cyt c] reductase) are inactivated by the treatment, whereas mitochondrial marker enzymes (cyt c oxidase and dehydrogenases) were unaffected.	NAD	162-195	cytochrome c, somatic	Homo sapiens	213-225
12929742-2	2003	The measurements indicated that the enzymes located in the Golgi apparatus (uridine 5"-diphosphate galactosyl transferase) and in the endoplasmic reticulum (ER) (nicotinamide adenine dinucleotide [reduced] [NADH] cytochrome c [cyt c] reductase) are inactivated by the treatment, whereas mitochondrial marker enzymes (cyt c oxidase and dehydrogenases) were unaffected.	NAD	162-195	cytochrome c, somatic	Homo sapiens	227-232
12929742-2	2003	The measurements indicated that the enzymes located in the Golgi apparatus (uridine 5"-diphosphate galactosyl transferase) and in the endoplasmic reticulum (ER) (nicotinamide adenine dinucleotide [reduced] [NADH] cytochrome c [cyt c] reductase) are inactivated by the treatment, whereas mitochondrial marker enzymes (cyt c oxidase and dehydrogenases) were unaffected.	NAD	162-195	cytochrome c, somatic	Homo sapiens	317-322
12857389-5	2003	Using NAD(+) and (3)H-NAD(+) as substrate, activated PARP-1 synthesizes labeled poly(ADP-ribose) chains.	NAD	6-12	poly(ADP-ribose) polymerase 1	Homo sapiens	53-59
12834290-5	2003	These activities contained assimilatory type NADPH (or NADH)-dependent NO3- reductase (aNar), dissimilatory nitrite reductase (dNir), and nitric oxide reductase (P450nor), but did not contain ubiquinol-dependent, dissimilatory NO3- reductase (dNar).	NAD	55-59	NBL1, DAN family BMP antagonist	Homo sapiens	71-74
12642583-2	2003	Upon binding to the site of DNA strand breakage, PARP-1 is activated, leading to rapid and transient poly(ADP-ribosyl)ation of nuclear proteins using NAD+ as substrate.	NAD	150-154	poly(ADP-ribose) polymerase 1	Homo sapiens	49-55
12853316-2	2003	Upon activation, the enzyme hydrolyzes NAD(+) to nicotinamide and transfers ADP ribose units to a variety of nuclear proteins, including histones and PARP-1 itself.	NAD	39-45	poly(ADP-ribose) polymerase 1	Homo sapiens	150-156
12853316-4	2003	However, excessive activation of PARP-1 can lead to significant decrements in NAD(+), and ATP depletion, and cell death (suicide hypothesis).	NAD	78-84	poly(ADP-ribose) polymerase 1	Homo sapiens	33-39
12615520-1	2003	The polyol pathway consists of two enzymes aldose reductase (AR) and sorbitol dehydrogenase (SDH); the former is the first enzyme in the polyol pathway, that catalyzes the reduction of glucose to sorbitol, the latter is the second one, that converts sorbitol to fructose using by NAD(+) as a cofactor.	NAD	280-286	aldo-keto reductase family 1 member B	Homo sapiens	43-59
12716823-7	2003	Poly(ADP-ribose) polymerase activation in turn depletes the intracellular concentration of its substrate NAD(+), slowing the rate of glycolysis, electron transport, and ATP formation, and produces an ADP-ribosylation of the GAPDH.	NAD	105-111	poly(ADP-ribose) polymerase 1	Homo sapiens	0-27
14596340-4	2003	For the quantification of beta-HADH activity, the rate of conversion of reduced beta-nicotinamide adenine dinucleotide (NADH) to beta-nicotinamide adenine dinucleotide (NAD+) was calculated by determining NAD+ at 260 nm.	NAD	129-167	hydroxyacyl-CoA dehydrogenase	Homo sapiens	31-35
14596340-4	2003	For the quantification of beta-HADH activity, the rate of conversion of reduced beta-nicotinamide adenine dinucleotide (NADH) to beta-nicotinamide adenine dinucleotide (NAD+) was calculated by determining NAD+ at 260 nm.	NAD	169-173	hydroxyacyl-CoA dehydrogenase	Homo sapiens	31-35
14596340-4	2003	For the quantification of beta-HADH activity, the rate of conversion of reduced beta-nicotinamide adenine dinucleotide (NADH) to beta-nicotinamide adenine dinucleotide (NAD+) was calculated by determining NAD+ at 260 nm.	NAD	205-209	hydroxyacyl-CoA dehydrogenase	Homo sapiens	31-35
14596340-6	2003	Accurate quantification of beta-HADH activity was achieved since on-line monitoring allowed us to account for the NAD+ produced from NADH degradation by applying a correction factor.	NAD	114-118	hydroxyacyl-CoA dehydrogenase	Homo sapiens	32-36
14596340-6	2003	Accurate quantification of beta-HADH activity was achieved since on-line monitoring allowed us to account for the NAD+ produced from NADH degradation by applying a correction factor.	NAD	133-137	hydroxyacyl-CoA dehydrogenase	Homo sapiens	32-36
12676457-6	2003	Activated PARP-1 cleaves NAD(+) into nicotinamide and ADP-ribose and polymerizes the latter on nuclear acceptor proteins.	NAD	25-31	poly(ADP-ribose) polymerase 1	Homo sapiens	10-16
12676457-7	2003	Peroxynitrite-induced overactivation of PARP consumes NAD(+) and consequently ATP culminating in cell dysfunction, apoptosis or necrosis.	NAD	54-60	poly(ADP-ribose) polymerase 1	Homo sapiens	40-44
14596340-4	2003	For the quantification of beta-HADH activity, the rate of conversion of reduced beta-nicotinamide adenine dinucleotide (NADH) to beta-nicotinamide adenine dinucleotide (NAD+) was calculated by determining NAD+ at 260 nm.	NAD	80-118	hydroxyacyl-CoA dehydrogenase	Homo sapiens	31-35
14596340-4	2003	For the quantification of beta-HADH activity, the rate of conversion of reduced beta-nicotinamide adenine dinucleotide (NADH) to beta-nicotinamide adenine dinucleotide (NAD+) was calculated by determining NAD+ at 260 nm.	NAD	120-124	hydroxyacyl-CoA dehydrogenase	Homo sapiens	31-35
12562755-1	2003	Yeast NAD(+)-specific isocitrate dehydrogenase (IDH) is an allosterically regulated octameric enzyme composed of two types of homologous subunits designated IDH1 and IDH2.	NAD	6-12	isocitrate dehydrogenase (NAD(+)) IDH1	Saccharomyces cerevisiae S288C	157-161
12605957-4	2003	One of the immediate eukaryotic cellular responses to DNA breakage is the covalent post-translational modification of nuclear proteins with poly(ADP-ribose) from NAD+ as precursor, mostly catalysed by poly(ADP-ribose) polymerase-1 (PARP-1).	NAD	162-166	poly(ADP-ribose) polymerase 1	Homo sapiens	201-230
12605957-4	2003	One of the immediate eukaryotic cellular responses to DNA breakage is the covalent post-translational modification of nuclear proteins with poly(ADP-ribose) from NAD+ as precursor, mostly catalysed by poly(ADP-ribose) polymerase-1 (PARP-1).	NAD	162-166	poly(ADP-ribose) polymerase 1	Homo sapiens	232-238
12657979-3	2003	This genetic damage triggers the activation of the nuclear enzyme poly(ADP-ribose) polymerase 1, which, in turn, cleaves the respiratory coenzyme nicotinamide adenine dinucleotide into nicotinamide and ADP ribose.	NAD	146-179	poly(ADP-ribose) polymerase 1	Homo sapiens	66-95
12615520-1	2003	The polyol pathway consists of two enzymes aldose reductase (AR) and sorbitol dehydrogenase (SDH); the former is the first enzyme in the polyol pathway, that catalyzes the reduction of glucose to sorbitol, the latter is the second one, that converts sorbitol to fructose using by NAD(+) as a cofactor.	NAD	280-286	aldo-keto reductase family 1 member B	Homo sapiens	61-63
12615520-1	2003	The polyol pathway consists of two enzymes aldose reductase (AR) and sorbitol dehydrogenase (SDH); the former is the first enzyme in the polyol pathway, that catalyzes the reduction of glucose to sorbitol, the latter is the second one, that converts sorbitol to fructose using by NAD(+) as a cofactor.	NAD	280-286	sorbitol dehydrogenase	Homo sapiens	69-91
12615520-1	2003	The polyol pathway consists of two enzymes aldose reductase (AR) and sorbitol dehydrogenase (SDH); the former is the first enzyme in the polyol pathway, that catalyzes the reduction of glucose to sorbitol, the latter is the second one, that converts sorbitol to fructose using by NAD(+) as a cofactor.	NAD	280-286	sorbitol dehydrogenase	Homo sapiens	93-96
12820363-8	2003	The metabolic Achilles" heel of the tumor metabolome is its sensitivity to a reduction of NAD levels caused by activation of poly(ADP-ribose) polymerase after DNA damage.	NAD	90-93	poly(ADP-ribose) polymerase 1	Homo sapiens	125-152
12556353-12	2003	The increased activation of PDH was not explained by changes in muscle pyruvate or the ATP/ADP ratio but may be related to a decrease in the NADH/NAD(+) ratio or an epinephrine-induced increase in calcium concentration.	NAD	141-145	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	28-31
12556353-12	2003	The increased activation of PDH was not explained by changes in muscle pyruvate or the ATP/ADP ratio but may be related to a decrease in the NADH/NAD(+) ratio or an epinephrine-induced increase in calcium concentration.	NAD	146-152	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	28-31
12724214-6	2003	Histone deacetylases (HDACs) are divided into three classes: class I HDACs (HDACs 1, 2, 3, and 8) are similar to the yeast RPD3 protein and localize to the nucleus; class II HDACs (HDACs 4, 5, 6, 7, 9, and 10) are homologous to the yeast HDA1 protein and are found in both the nucleus and cytoplasm; and class III HDACs form a structurally distinct class of NAD-dependent enzymes that are similar to the yeast SIR2 proteins.	NAD	358-361	histone deacetylase RPD3	Saccharomyces cerevisiae S288C	123-127
15206771-9	2003	Tryptophan-NAD pathway was initiated by cleavage of indole ring of tryptophan by TDO in the liver and IDO in many organs.	NAD	11-14	tryptophan 2,3-dioxygenase	Rattus norvegicus	81-84
12573279-0	2003	Cytochrome c-induced cytosolic nicotinamide adenine dinucleotide oxidation, mitochondrial permeability transition, and apoptosis.	NAD	31-64	cytochrome c, somatic	Homo sapiens	0-12
12573279-1	2003	A catalytic amount of cytochrome c (cyto-c) added to the incubation medium of isolated mitochondria promotes the transfer of reducing equivalents from extramitochondrial nicotinamide adenine dinucleotide in its reduced state (NADH) to molecular oxygen inside the mitochondria, a process coupled to the generation of a membrane potential.	NAD	170-203	cytochrome c, somatic	Homo sapiens	22-34
12573279-1	2003	A catalytic amount of cytochrome c (cyto-c) added to the incubation medium of isolated mitochondria promotes the transfer of reducing equivalents from extramitochondrial nicotinamide adenine dinucleotide in its reduced state (NADH) to molecular oxygen inside the mitochondria, a process coupled to the generation of a membrane potential.	NAD	170-203	cytochrome c, somatic	Homo sapiens	36-42
12573279-1	2003	A catalytic amount of cytochrome c (cyto-c) added to the incubation medium of isolated mitochondria promotes the transfer of reducing equivalents from extramitochondrial nicotinamide adenine dinucleotide in its reduced state (NADH) to molecular oxygen inside the mitochondria, a process coupled to the generation of a membrane potential.	NAD	226-230	cytochrome c, somatic	Homo sapiens	22-34
12573279-1	2003	A catalytic amount of cytochrome c (cyto-c) added to the incubation medium of isolated mitochondria promotes the transfer of reducing equivalents from extramitochondrial nicotinamide adenine dinucleotide in its reduced state (NADH) to molecular oxygen inside the mitochondria, a process coupled to the generation of a membrane potential.	NAD	226-230	cytochrome c, somatic	Homo sapiens	36-42
12573279-6	2003	In the early stages of apoptosis cytosolic cyto-c participates in the activation of caspases and at the same time can promote the oxidation of cytosolic NADH, making more energy available for the correct execution of the cell death program.	NAD	153-157	cytochrome c, somatic	Homo sapiens	43-49
12594242-5	2003	In addition, NOS3 overexpression impaired neuronal Mt function as demonstrated by the reduced levels of 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide and nicotinamide adenine dinucleotide (reduced form)-tetrazolium reductase activities and MitoTracker Red fluorescence.	NAD	169-202	nitric oxide synthase 3	Homo sapiens	13-17
15206738-7	2003	In 1993, we found that cyclic ADP-ribose (cADPR), a metabolite of NAD+, is a second messenger for intracellular Ca2+ mobilization for insulin secretion by glucose, and proposed a novel mechanism of insulin secretion, the CD38-cADPR signal system.	NAD	66-70	CD38 molecule	Rattus norvegicus	221-225
12688429-3	2003	In these conditions, and in the absence of 3-AB treatment, clear signs of oxidative stress, such as lipid peroxidation, increase in protein carbonyls and DNA strand breaks, were evident; PARP was markedly activated in concomitance with a significant NAD+ and ATP depletion.	NAD	250-254	poly(ADP-ribose) polymerase 1	Homo sapiens	187-191
12570705-3	2003	Upon binding to DNA breaks, activated PARP cleaves NAD(+) into nicotinamide and ADP-ribose and polymerizes the latter onto nuclear acceptor proteins including histones, transcription factors and PARP itself.	NAD	51-57	poly(ADP-ribose) polymerase 1	Homo sapiens	38-42
12570705-3	2003	Upon binding to DNA breaks, activated PARP cleaves NAD(+) into nicotinamide and ADP-ribose and polymerizes the latter onto nuclear acceptor proteins including histones, transcription factors and PARP itself.	NAD	51-57	poly(ADP-ribose) polymerase 1	Homo sapiens	195-199
12570705-5	2003	In addition, oxidative stress-induced overactivation of PARP consumes NAD(+) and consequently ATP, culminating in cell dysfunction or necrosis.	NAD	70-76	poly(ADP-ribose) polymerase 1	Homo sapiens	56-60
12519059-3	2003	In vitro inhibition of PARP-1 was confirmed by direct measurement of NAD+ depletion and ADP-ribose polymer formation caused by chemically induced DNA damage.	NAD	69-73	poly(ADP-ribose) polymerase 1	Homo sapiens	23-29
14594189-6	2003	In pathophysiological conditions associated with oxidative stress (such as various forms of inflammation and reperfusion injury), activation of the nuclear enzyme poly(ADP-ribose) polymerase (PARP) occurs, with subsequent, substantial fall in cellular NAD+ and ATP levels, which can determine the viability and function of the affected cells.	NAD	252-256	poly(ADP-ribose) polymerase 1	Homo sapiens	163-190
14594189-6	2003	In pathophysiological conditions associated with oxidative stress (such as various forms of inflammation and reperfusion injury), activation of the nuclear enzyme poly(ADP-ribose) polymerase (PARP) occurs, with subsequent, substantial fall in cellular NAD+ and ATP levels, which can determine the viability and function of the affected cells.	NAD	252-256	poly(ADP-ribose) polymerase 1	Homo sapiens	192-196
15206789-1	2003	Hepatic ACMSD [EC4.1.1.45] plays a key role in regulating NAD biosynthesis from tryptophan.	NAD	58-61	aminocarboxymuconate semialdehyde decarboxylase	Rattus norvegicus	8-13
12415565-5	2002	Both molecules are involved in the metabolism of NAD(+), and the CD157 gene is synthenic on 4p15 with CD38, with which it also shares a unique genomic organization.	NAD	49-55	bone marrow stromal cell antigen 1	Homo sapiens	65-70
14695936-7	2003	The rate of formation of the CoQ1 sulfate conjugate was markedly increased by the addition of NADH and was prevented by dicumarol, a DT-diaphorase (NQO1) inhibitor.	NAD	94-98	NAD(P)H quinone dehydrogenase 1	Rattus norvegicus	133-146
14695936-7	2003	The rate of formation of the CoQ1 sulfate conjugate was markedly increased by the addition of NADH and was prevented by dicumarol, a DT-diaphorase (NQO1) inhibitor.	NAD	94-98	NAD(P)H quinone dehydrogenase 1	Rattus norvegicus	148-152
12766354-2	2003	Nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d) reactivity was markedly reduced in the hippocampal CA1, CA2 and CA3 sectors as well as in the dentate gyrus, suggesting a suppression of NO production in these areas.	NAD	0-33	carbonic anhydrase 2	Rattus norvegicus	121-124
12589775-7	2003	nPG prevented the H(2)O(2)-induced growth inhibition, membrane blebbing, drop in NAD(+) and single-strand breaks in DNA.	NAD	81-87	OPA1 mitochondrial dynamin like GTPase	Homo sapiens	0-3
12485408-5	2003	The activity of 3beta-HSD in homogenates was evaluated using 3H-labelled PREG as a substrate and NAD+ as a cofactor, the levels of steroids formed were calculated either by extrapolating the relationship between tritiated peaks obtained by TLC to the initial amount of PREG, or by gas chromatography/mass spectrometry determination.	NAD	97-101	hydroxy-delta-5-steroid dehydrogenase, 3 beta- and steroid delta-isomerase 1	Rattus norvegicus	16-25
12180906-3	2002	In the current study, we demonstrate that loss of cytochrome c by mitochondria oxidizing NAD(+)-linked substrates results in a dramatic increase of ROS production and respiratory inhibition.	NAD	89-95	cytochrome c, somatic	Homo sapiens	50-62
14715435-4	2003	In this study, we examined the effects of nanomolar levels of acrolein on the activities of pyruvate dehydrogenase (PDH) and Alpha-ketoglutarate dehydrogenase (KGDH), both reduced nicotinamide adenine dinucleotide (NADH)-linked mitochondrial enzymes.	NAD	180-213	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	92-114
14715435-4	2003	In this study, we examined the effects of nanomolar levels of acrolein on the activities of pyruvate dehydrogenase (PDH) and Alpha-ketoglutarate dehydrogenase (KGDH), both reduced nicotinamide adenine dinucleotide (NADH)-linked mitochondrial enzymes.	NAD	180-213	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	116-119
14715435-4	2003	In this study, we examined the effects of nanomolar levels of acrolein on the activities of pyruvate dehydrogenase (PDH) and Alpha-ketoglutarate dehydrogenase (KGDH), both reduced nicotinamide adenine dinucleotide (NADH)-linked mitochondrial enzymes.	NAD	215-219	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	92-114
14715435-4	2003	In this study, we examined the effects of nanomolar levels of acrolein on the activities of pyruvate dehydrogenase (PDH) and Alpha-ketoglutarate dehydrogenase (KGDH), both reduced nicotinamide adenine dinucleotide (NADH)-linked mitochondrial enzymes.	NAD	215-219	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	116-119
12381719-8	2002	In a recombinant cytochrome P-450 2E1 Ames bacterial mutagenicity assay, the R597M/W677A protein increased the sensitivity to dimethylnitrosamine by approximately 2-fold, suggesting that the ability to use NADH afforded a significant advantage in this in vivo assay.	NAD	206-210	cytochrome P450 family 2 subfamily E member 1	Homo sapiens	17-37
12450807-7	2002	In the presence of NADH, His-tagged CarAc was reduced by His-tagged CarAd.	NAD	19-23	carAc	Pseudomonas resinovorans	36-41
12213537-15	2002	Excessive PARP activity consumes NAD leading to energy depletion and neuronal damage.	NAD	33-36	poly(ADP-ribose) polymerase 1	Homo sapiens	10-14
12493070-5	2002	Recently, however, our laboratory has obtained data to suggest that the most important mechanism underlying the development of cytopathic hypoxia is depletion of cellular stores of nicotinamide adenine dinucleotide (NAD+/NADH) as a result of activation of the enzyme, poly(ADP-ribose) polymerase-1.	NAD	181-214	poly(ADP-ribose) polymerase 1	Homo sapiens	268-297
12493070-5	2002	Recently, however, our laboratory has obtained data to suggest that the most important mechanism underlying the development of cytopathic hypoxia is depletion of cellular stores of nicotinamide adenine dinucleotide (NAD+/NADH) as a result of activation of the enzyme, poly(ADP-ribose) polymerase-1.	NAD	216-221	poly(ADP-ribose) polymerase 1	Homo sapiens	268-297
12429500-7	2002	With an aspartic acid at position 58 in 17beta-HSD-3 occupying the equivalent space in the cofactor binding pocket as arginine 224 in glutathione reductase or serine 12 in 17beta-HSD-1, there was an expectation that some of the mutants might use NADH as a cofactor.	NAD	246-250	hydroxysteroid 17-beta dehydrogenase 3	Homo sapiens	40-52
12582889-2	2002	Myo-inositol 1-phosphate synthase (MIPS; EC 5.5.1.4) converts glucose 6-phosphate to myo-inositol 1-phosphate in the presence of NAD(+).	NAD	129-135	myo-inositol-3-phosphate synthase	Glycine max	0-33
12582889-2	2002	Myo-inositol 1-phosphate synthase (MIPS; EC 5.5.1.4) converts glucose 6-phosphate to myo-inositol 1-phosphate in the presence of NAD(+).	NAD	129-135	myo-inositol-3-phosphate synthase	Glycine max	35-39
12555668-3	2002	Recently, a bacterial protein encoded by nadV, a gene from the prokaryote Haemophilus ducreyi displaying significant homology with PBEF, has been identified as a nicotinamide phosphoribosyltranferase (NAmPRTase), an enzyme involved in nicotinamide adenine dinucleotide (NAD) biosynthesis.	NAD	235-268	nicotinamide phosphoribosyltransferase	Mus musculus	131-135
12555668-3	2002	Recently, a bacterial protein encoded by nadV, a gene from the prokaryote Haemophilus ducreyi displaying significant homology with PBEF, has been identified as a nicotinamide phosphoribosyltranferase (NAmPRTase), an enzyme involved in nicotinamide adenine dinucleotide (NAD) biosynthesis.	NAD	235-268	nicotinamide phosphoribosyltransferase	Mus musculus	201-210
12555668-3	2002	Recently, a bacterial protein encoded by nadV, a gene from the prokaryote Haemophilus ducreyi displaying significant homology with PBEF, has been identified as a nicotinamide phosphoribosyltranferase (NAmPRTase), an enzyme involved in nicotinamide adenine dinucleotide (NAD) biosynthesis.	NAD	270-273	nicotinamide phosphoribosyltransferase	Mus musculus	131-135
12555668-3	2002	Recently, a bacterial protein encoded by nadV, a gene from the prokaryote Haemophilus ducreyi displaying significant homology with PBEF, has been identified as a nicotinamide phosphoribosyltranferase (NAmPRTase), an enzyme involved in nicotinamide adenine dinucleotide (NAD) biosynthesis.	NAD	270-273	nicotinamide phosphoribosyltransferase	Mus musculus	201-210
12555668-4	2002	Using a panel of antibodies to murine PBEF, we demonstrate in this work that, similarly to its microbial counterpart, the murine protein is a NAmPRTase, catalyzing the condensation of nicotinamide with 5-phosphoribosyl-1-pyrophosphate to yield nicotinamide mononucleotide, an intermediate in the biosynthesis of NAD.	NAD	312-315	nicotinamide phosphoribosyltransferase	Mus musculus	38-42
12555668-4	2002	Using a panel of antibodies to murine PBEF, we demonstrate in this work that, similarly to its microbial counterpart, the murine protein is a NAmPRTase, catalyzing the condensation of nicotinamide with 5-phosphoribosyl-1-pyrophosphate to yield nicotinamide mononucleotide, an intermediate in the biosynthesis of NAD.	NAD	312-315	nicotinamide phosphoribosyltransferase	Mus musculus	142-151
12555668-5	2002	The role of PBEF as a NAmPRTase was further confirmed by showing that the mouse gene was able to confer the ability to grow in the absence of NAD to a NAmPRTase-defective bacterial strain.	NAD	142-145	nicotinamide phosphoribosyltransferase	Mus musculus	12-16
12555668-5	2002	The role of PBEF as a NAmPRTase was further confirmed by showing that the mouse gene was able to confer the ability to grow in the absence of NAD to a NAmPRTase-defective bacterial strain.	NAD	142-145	nicotinamide phosphoribosyltransferase	Mus musculus	22-31
12555668-5	2002	The role of PBEF as a NAmPRTase was further confirmed by showing that the mouse gene was able to confer the ability to grow in the absence of NAD to a NAmPRTase-defective bacterial strain.	NAD	142-145	nicotinamide phosphoribosyltransferase	Mus musculus	151-160
12270706-7	2002	This correspondence and the nicotinamide position were used to model the binding structure of the whole substrate NAD(+) at ART2.2.	NAD	114-120	ADP-ribosyltransferase 2b	Rattus norvegicus	124-128
12374852-0	2002	SIRT3, a human SIR2 homologue, is an NAD-dependent deacetylase localized to mitochondria.	NAD	37-40	sirtuin 3	Homo sapiens	0-5
12429187-3	2002	Inhibitors of PARP/PARG attenuated both zinc-induced NAD/ATP depletion and cell death, thereby implicating the PARP/PARG cascade in these processes.	NAD	53-56	poly(ADP-ribose) polymerase 1	Homo sapiens	14-18
12429187-3	2002	Inhibitors of PARP/PARG attenuated both zinc-induced NAD/ATP depletion and cell death, thereby implicating the PARP/PARG cascade in these processes.	NAD	53-56	poly(ADP-ribose) glycohydrolase	Homo sapiens	19-23
12429187-3	2002	Inhibitors of PARP/PARG attenuated both zinc-induced NAD/ATP depletion and cell death, thereby implicating the PARP/PARG cascade in these processes.	NAD	53-56	poly(ADP-ribose) polymerase 1	Homo sapiens	111-115
12429187-3	2002	Inhibitors of PARP/PARG attenuated both zinc-induced NAD/ATP depletion and cell death, thereby implicating the PARP/PARG cascade in these processes.	NAD	53-56	poly(ADP-ribose) glycohydrolase	Homo sapiens	116-120
12429187-7	2002	The present study demonstrates that induction of NADPH oxidase and nNOS actively contributes to PARP/PARG-mediated NAD/ATP depletion and cell death induced by zinc in cortical culture.	NAD	49-52	poly(ADP-ribose) polymerase 1	Homo sapiens	96-100
12429187-7	2002	The present study demonstrates that induction of NADPH oxidase and nNOS actively contributes to PARP/PARG-mediated NAD/ATP depletion and cell death induced by zinc in cortical culture.	NAD	49-52	poly(ADP-ribose) glycohydrolase	Homo sapiens	101-105
12383592-4	2002	Angiotensin II stimulates nicotinamide adenine dinucleotide phosphate (NADPH)/nicotinamide adenine dinucleotide (NADH) oxidase in endothelium, smooth muscle cells, and the adventitia of blood vessels to generate reactive oxygen species, leading to endothelial dysfunction, growth, and inflammation.	NAD	26-59	angiotensinogen	Homo sapiens	0-14
12383592-4	2002	Angiotensin II stimulates nicotinamide adenine dinucleotide phosphate (NADPH)/nicotinamide adenine dinucleotide (NADH) oxidase in endothelium, smooth muscle cells, and the adventitia of blood vessels to generate reactive oxygen species, leading to endothelial dysfunction, growth, and inflammation.	NAD	113-117	angiotensinogen	Homo sapiens	0-14
12236714-4	2002	Upon the addition of NADH to the buffer solution of rMb(1) in the presence of SOD and catalase, the oxymyoglobin was rapidly formed.	NAD	21-25	superoxide dismutase 1	Homo sapiens	78-94
12393208-4	2002	In the present study, we found that the anaerobic growth of the strain disrupted for both the FRDS and OSM1 genes was fully restored by adding the oxidized form of methylene blue or phenazine methosulfate, which non-enzymatically oxidize cellular NADH to NAD(+).	NAD	247-251	fumarate reductase	Saccharomyces cerevisiae S288C	103-107
12393208-4	2002	In the present study, we found that the anaerobic growth of the strain disrupted for both the FRDS and OSM1 genes was fully restored by adding the oxidized form of methylene blue or phenazine methosulfate, which non-enzymatically oxidize cellular NADH to NAD(+).	NAD	255-261	fumarate reductase	Saccharomyces cerevisiae S288C	103-107
12164482-2	2002	In response to genotoxic injury, PARP catalyses the synthesis of poly (ADP-ribose), from its substrate beta-NAD+ and this polymer is covalently attached to several nuclear proteins and PARP itself.	NAD	103-112	poly(ADP-ribose) polymerase 1	Homo sapiens	33-37
12440774-1	2002	Mammalian poly(ADP-ribose)polymerase 1 (PARP-1) is an abundant nuclear chromatin-associated protein and belongs to a large family of enzymes that catalyzes the transfer of ADP-ribose units from its substrate beta-nicotinamide adenine dinucleotide (NAD+) covalently to itself and other nuclear chromatin-associated proteins.	NAD	208-246	poly(ADP-ribose) polymerase 1	Homo sapiens	10-38
12440774-1	2002	Mammalian poly(ADP-ribose)polymerase 1 (PARP-1) is an abundant nuclear chromatin-associated protein and belongs to a large family of enzymes that catalyzes the transfer of ADP-ribose units from its substrate beta-nicotinamide adenine dinucleotide (NAD+) covalently to itself and other nuclear chromatin-associated proteins.	NAD	208-246	poly(ADP-ribose) polymerase 1	Homo sapiens	40-46
12440774-1	2002	Mammalian poly(ADP-ribose)polymerase 1 (PARP-1) is an abundant nuclear chromatin-associated protein and belongs to a large family of enzymes that catalyzes the transfer of ADP-ribose units from its substrate beta-nicotinamide adenine dinucleotide (NAD+) covalently to itself and other nuclear chromatin-associated proteins.	NAD	248-252	poly(ADP-ribose) polymerase 1	Homo sapiens	10-38
12440774-1	2002	Mammalian poly(ADP-ribose)polymerase 1 (PARP-1) is an abundant nuclear chromatin-associated protein and belongs to a large family of enzymes that catalyzes the transfer of ADP-ribose units from its substrate beta-nicotinamide adenine dinucleotide (NAD+) covalently to itself and other nuclear chromatin-associated proteins.	NAD	248-252	poly(ADP-ribose) polymerase 1	Homo sapiens	40-46
12218169-5	2002	Consistent with the prediction of an oxidoreductase domain, RyR1 binds [3H]NAD+, supporting a model in which RyR1 has a oxidoreductase-like domain that could function as a type of redox sensor.	NAD	75-79	ryanodine receptor 1	Homo sapiens	60-64
12218169-5	2002	Consistent with the prediction of an oxidoreductase domain, RyR1 binds [3H]NAD+, supporting a model in which RyR1 has a oxidoreductase-like domain that could function as a type of redox sensor.	NAD	75-79	ryanodine receptor 1	Homo sapiens	109-113
12093799-2	2002	mGPD in combination with the cytosolic glycerol phosphate dehydrogenase (cGPD) is proposed to form the glycerol phosphate shuttle, catalyzing the interconversion of dihydroxyacetone phosphate and glycerol phosphate with net oxidation of cytosolic NADH.	NAD	247-251	atypical chemokine receptor 1 (Duffy blood group)	Mus musculus	0-4
12093799-10	2002	The phenotype may be secondary to consequences of the obligatory production of cytosolic NADH from glycerol metabolism in the mGPD knockout animal.	NAD	89-93	atypical chemokine receptor 1 (Duffy blood group)	Mus musculus	126-130
12164482-2	2002	In response to genotoxic injury, PARP catalyses the synthesis of poly (ADP-ribose), from its substrate beta-NAD+ and this polymer is covalently attached to several nuclear proteins and PARP itself.	NAD	103-112	poly(ADP-ribose) polymerase 1	Homo sapiens	185-189
12356164-2	2002	A NAD-dependent isolate 46 (C-3) of Haemophilus paragallinarum, which was previously demonstrated to be of high virulence, was transformed to NAD independence using a plasmid isolated from a naturally occurring NAD-independent isolate of H. paragallinarum.	NAD	2-5	complement component 3	Gallus gallus	28-31
12356164-2	2002	A NAD-dependent isolate 46 (C-3) of Haemophilus paragallinarum, which was previously demonstrated to be of high virulence, was transformed to NAD independence using a plasmid isolated from a naturally occurring NAD-independent isolate of H. paragallinarum.	NAD	142-145	complement component 3	Gallus gallus	28-31
12356164-2	2002	A NAD-dependent isolate 46 (C-3) of Haemophilus paragallinarum, which was previously demonstrated to be of high virulence, was transformed to NAD independence using a plasmid isolated from a naturally occurring NAD-independent isolate of H. paragallinarum.	NAD	142-145	complement component 3	Gallus gallus	28-31
12356164-4	2002	The transformed NAD-independent serovar C-3 isolate and the wild-type serovar C-3 isolate were used to experimentally infect vaccinated layer chickens.	NAD	16-19	complement component 3	Gallus gallus	40-43
12356164-5	2002	It was shown that the transformation to NAD independence significantly altered the virulence of the serovar C-3 isolate that was used in the transformation experiment.	NAD	40-43	complement component 3	Gallus gallus	108-111
12065597-4	2002	Cysteine is utilized by the cysteine desulfurase Nfs1p to release sulfan sulfur; ATP presumably reflects the function of the Hsp70 family chaperone Ssq1p; and NADH is used for reduction of the ferredoxin Yah1p involved in Fe/S protein biogenesis.	NAD	159-163	cysteine desulfurase	Saccharomyces cerevisiae S288C	49-54
12223530-3	2002	Upon binding to DNA breaks, activated PARP cleaves NAD(+) into nicotinamide and ADP-ribose and polymerizes the latter onto nuclear acceptor proteins including histones, transcription factors, and PARP itself.	NAD	51-57	poly(ADP-ribose) polymerase 1	Homo sapiens	38-42
12223530-3	2002	Upon binding to DNA breaks, activated PARP cleaves NAD(+) into nicotinamide and ADP-ribose and polymerizes the latter onto nuclear acceptor proteins including histones, transcription factors, and PARP itself.	NAD	51-57	poly(ADP-ribose) polymerase 1	Homo sapiens	196-200
12223530-5	2002	On the other hand, oxidative stress-induced overactivation of PARP consumes NAD(+) and consequently ATP, culminating in cell dysfunction or necrosis.	NAD	76-82	poly(ADP-ribose) polymerase 1	Homo sapiens	62-66
12068015-7	2002	The levels of NAD(+), a PARP substrate, were significantly decreased in HL-60 cells after a 3-h incubation with TAS-103.	NAD	14-20	poly(ADP-ribose) polymerase 1	Homo sapiens	24-28
12051667-1	2002	Poly(ADP-ribose) polymerase (PARP) is a nuclear enzyme which is activated in response to genotoxic insults by binding damaged DNA and attaching polymers of ADP-ribose to nuclear proteins at the expense of its substrate NAD+.	NAD	219-223	poly(ADP-ribose) polymerase 1	Homo sapiens	0-27
12140175-8	2002	Cotreatment with a PARP inhibitor, 3-aminobenzamide, decreased beta-lapachone-induced PARP activation and provided significant protection from necrosis by preventing depletion of intracellular NAD(+) and ATP.	NAD	193-199	poly(ADP-ribose) polymerase 1	Homo sapiens	19-23
12238047-0	2002	[Role of NADH shuttle system in glucose-stimulated insulin secretion].	NAD	9-13	insulin	Homo sapiens	51-58
12051667-1	2002	Poly(ADP-ribose) polymerase (PARP) is a nuclear enzyme which is activated in response to genotoxic insults by binding damaged DNA and attaching polymers of ADP-ribose to nuclear proteins at the expense of its substrate NAD+.	NAD	219-223	poly(ADP-ribose) polymerase 1	Homo sapiens	29-33
12051667-6	2002	The improvement of cellular growth and NAD+ levels in A-T cells with PARP inhibition suggests that the cellular metabolic status of A-T cells is compromised and the inhibition of PARP may relieve some of the drain on cellular pyridine nucleotides and ATP.	NAD	39-43	poly(ADP-ribose) polymerase 1	Homo sapiens	69-73
12051667-6	2002	The improvement of cellular growth and NAD+ levels in A-T cells with PARP inhibition suggests that the cellular metabolic status of A-T cells is compromised and the inhibition of PARP may relieve some of the drain on cellular pyridine nucleotides and ATP.	NAD	39-43	poly(ADP-ribose) polymerase 1	Homo sapiens	179-183
11790791-8	2002	The prevention of PARP cleavage by inhibition of caspase-3 resulted in a 10-fold activation of the enzyme and a resultant depletion of NAD and ATP.	NAD	135-138	poly(ADP-ribose) polymerase 1	Homo sapiens	18-22
11925444-1	2002	Previously we have demonstrated that activation of p38 mitogen-activated protein kinase (MAPK) and induction of DNA synthesis in response to receptor tyrosine kinase (RTK) and G protein-coupled receptor (GPCR) agonists require NADH/NADPH-like oxidase activity in vascular smooth muscle cells (VSMC).	NAD	227-231	mitogen-activated protein kinase 14	Homo sapiens	51-87
12166075-4	2002	Glycolysis was markedly retarded in the patient"s muscle in the glyceraldehyde 3-phosphate dehydrogenase(GAPDH) step, possibly due to the impaired reoxidation of NADH produced by GAPDH activity.	NAD	162-166	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	64-104
12166075-4	2002	Glycolysis was markedly retarded in the patient"s muscle in the glyceraldehyde 3-phosphate dehydrogenase(GAPDH) step, possibly due to the impaired reoxidation of NADH produced by GAPDH activity.	NAD	162-166	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	105-110
12166075-4	2002	Glycolysis was markedly retarded in the patient"s muscle in the glyceraldehyde 3-phosphate dehydrogenase(GAPDH) step, possibly due to the impaired reoxidation of NADH produced by GAPDH activity.	NAD	162-166	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	179-184
11966438-8	2002	NAD has important regulatory role in repair of DNA damage and cell growth since it is a substrate for poly(ADP-ribose) polymerase (PARP).	NAD	0-3	poly(ADP-ribose) polymerase 1	Homo sapiens	102-129
11966438-8	2002	NAD has important regulatory role in repair of DNA damage and cell growth since it is a substrate for poly(ADP-ribose) polymerase (PARP).	NAD	0-3	poly(ADP-ribose) polymerase 1	Homo sapiens	131-135
11966438-14	2002	Presumably, the shared IMP-NAD active site of IMPDH has a similar architecture to the NAD-binding pocket of PARP.	NAD	27-30	poly(ADP-ribose) polymerase 1	Homo sapiens	108-112
11966438-14	2002	Presumably, the shared IMP-NAD active site of IMPDH has a similar architecture to the NAD-binding pocket of PARP.	NAD	86-89	poly(ADP-ribose) polymerase 1	Homo sapiens	108-112
11966440-1	2002	Benzamide riboside (BR) after anabolism to an analogue of NAD, was shown to inhibit the activity of NAD-dependent enzymes such as inosine 5"-monophosphate dehydrogenase (IMPDH), the rate limiting enzyme in de novo guanylate biosynthesis, and malate dehydrogenase which is involved in the citric cycle and respiratory chain.	NAD	58-61	malic enzyme 2	Homo sapiens	242-262
11966440-1	2002	Benzamide riboside (BR) after anabolism to an analogue of NAD, was shown to inhibit the activity of NAD-dependent enzymes such as inosine 5"-monophosphate dehydrogenase (IMPDH), the rate limiting enzyme in de novo guanylate biosynthesis, and malate dehydrogenase which is involved in the citric cycle and respiratory chain.	NAD	100-103	malic enzyme 2	Homo sapiens	242-262
11991201-5	2002	In 1993, we found that cyclic ADP-ribose (cADPR), a product synthesized from NAD+, is a second messenger for intracellular Ca2+ mobilization for insulin secretion by glucose, and proposed a novel mechanism of insulin secretion, the CD38-cADPR signal system.	NAD	77-81	CD38 molecule	Rattus norvegicus	232-236
11790791-8	2002	The prevention of PARP cleavage by inhibition of caspase-3 resulted in a 10-fold activation of the enzyme and a resultant depletion of NAD and ATP.	NAD	135-138	caspase 3	Homo sapiens	49-58
11790791-9	2002	The PARP inhibitor 3-AB prevented the loss of NAD and ATP.	NAD	46-49	poly(ADP-ribose) polymerase 1	Homo sapiens	4-8
12039737-2	2002	In tpi1-null mutants, intracellular accumulation of dihydroxyacetone phosphate might be prevented if the cytosolic NADH generated in glycolysis by glyceraldehyde-3-phosphate dehydrogenase were quantitatively used to reduce dihydroxyacetone phosphate to glycerol.	NAD	115-119	triose-phosphate isomerase TPI1	Saccharomyces cerevisiae S288C	3-7
12039737-3	2002	We hypothesize that the growth defect of tpi1-null mutants is caused by mitochondrial reoxidation of cytosolic NADH, thus rendering it unavailable for dihydroxyacetone-phosphate reduction.	NAD	111-115	triose-phosphate isomerase TPI1	Saccharomyces cerevisiae S288C	41-45
12297471-9	2002	CONCLUSION: I/R might induce apoptosis in L02 cells by up-regulating the expression of p16, p21, p53 and down-regulating the expression of Bcl-2, and the protective effect of NADH against I/R-induced apoptosis may lie in the expression regulation of the proteins concerned.	NAD	175-179	BCL2 apoptosis regulator	Homo sapiens	139-144
12677203-3	2002	Upon binding to DNA breaks, activated PARP cleaves NAD(+) into nicotinamide and ADP-ribose and polymerizes the latter onto nuclear acceptor proteins including histones, transcription factors and PARP itself.	NAD	51-57	poly(ADP-ribose) polymerase 1	Homo sapiens	38-42
12677203-3	2002	Upon binding to DNA breaks, activated PARP cleaves NAD(+) into nicotinamide and ADP-ribose and polymerizes the latter onto nuclear acceptor proteins including histones, transcription factors and PARP itself.	NAD	51-57	poly(ADP-ribose) polymerase 1	Homo sapiens	195-199
11929639-3	2002	Reduced forms of the nicotinamide adenine dinucleotide cofactors, NADH and NADPH, protect TH from inhibition by ONOO(-) and prevent nitration of tyrosine residues.	NAD	21-54	tyrosine hydroxylase	Homo sapiens	90-92
11929639-3	2002	Reduced forms of the nicotinamide adenine dinucleotide cofactors, NADH and NADPH, protect TH from inhibition by ONOO(-) and prevent nitration of tyrosine residues.	NAD	66-70	tyrosine hydroxylase	Homo sapiens	90-92
12069106-10	2002	This suggests that CoQ1 or menadione cytoprotection also involves the NQO1 catalysed reoxidation of NADH that accumulates as a result of complex I inhibition.	NAD	100-104	NAD(P)H quinone dehydrogenase 1	Homo sapiens	70-74
11941457-3	2002	Backbone cleavage of cell wall polysaccharides can be accomplished in vitro by (*OH) produced from H2O2 in a Fenton reaction or in a reaction catalyzed by peroxidase supplied with O2 and NADH.	NAD	187-191	peroxidase 1	Zea mays	155-165
11869830-8	2002	Both single-stranded DNA and RNA inhibited the esterase activity of GAPDH, an activity that requires the absence of NAD+, in a process that was relieved at higher polynucleotide concentrations.	NAD	116-120	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	68-73
12390773-4	2002	RESULT: NADH not only inhibited the apoptosis induced by UVB irradiation, but also up-regulated the expression of Bcl-2 protein and down-regulated expressions of p53 and Bax proteins (P&lt;0.01).	NAD	8-12	BCL2 apoptosis regulator	Homo sapiens	114-119
12390773-4	2002	RESULT: NADH not only inhibited the apoptosis induced by UVB irradiation, but also up-regulated the expression of Bcl-2 protein and down-regulated expressions of p53 and Bax proteins (P&lt;0.01).	NAD	8-12	tumor protein p53	Homo sapiens	162-165
12390773-4	2002	RESULT: NADH not only inhibited the apoptosis induced by UVB irradiation, but also up-regulated the expression of Bcl-2 protein and down-regulated expressions of p53 and Bax proteins (P&lt;0.01).	NAD	8-12	BCL2 associated X, apoptosis regulator	Homo sapiens	170-173
12390773-6	2002	CONCLUSION: NADH significantly inhibits apoptosis induced by UVB irradiation possibly by the mechanism of up-regulating Bcl-2 expression and down-regulating p53 and Bax expressions.	NAD	12-16	BCL2 apoptosis regulator	Homo sapiens	120-125
12390773-6	2002	CONCLUSION: NADH significantly inhibits apoptosis induced by UVB irradiation possibly by the mechanism of up-regulating Bcl-2 expression and down-regulating p53 and Bax expressions.	NAD	12-16	tumor protein p53	Homo sapiens	157-160
12390773-6	2002	CONCLUSION: NADH significantly inhibits apoptosis induced by UVB irradiation possibly by the mechanism of up-regulating Bcl-2 expression and down-regulating p53 and Bax expressions.	NAD	12-16	BCL2 associated X, apoptosis regulator	Homo sapiens	165-168
12418547-4	2002	In fibroblast and myoblast cultures cAMP-dependent phosphorylation of the 18 kDa protein is associated with stimulation of complex I and overall respiratory activity with NAD-linked substrates.	NAD	171-174	cathelicidin antimicrobial peptide	Homo sapiens	36-40
11942325-7	2002	Although O2- was not able to alter EGFR mRNA expression, O2- at the concentration of 18 micromol/l NADH and 4 micromol/l PMS reduced EGFR protein expression.	NAD	99-103	epidermal growth factor receptor	Homo sapiens	133-137
11864782-5	2002	NADH cytochrome c reductase activity was decreased and superoxide production rates with NADH as substrate were increased.	NAD	0-4	cytochrome c, somatic	Homo sapiens	5-17
11935355-1	2002	The equilibrium constants and the thermodynamic parameters enthalpy and entropy of the interaction between Ni(II) and Co(II) with NAD(+) in aqueous solution were determined by calorimetry and potentiometry methods (ionic strength adjusted to 0.1 with sodium nitrate at 25 degrees C).	NAD	130-136	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	118-124
11846617-1	2002	Poly(ADP-ribose) polymerases (PARPs) are defined as cell signaling enzymes that catalyze the transfer of ADP-ribose units from NAD(+)to a number of acceptor proteins.	NAD	127-133	poly(ADP-ribose) polymerase 1	Homo sapiens	30-35
11952169-1	2002	Intracellular catabolism of NAD in mammalian cells occurs mainly via reaction catalyzed by poly(ADP-ribose) polymerase (PARP) with the release of nicotinamide, which is then metabolized predominantly to N-methyl-2-pyridone-5-carboxamide (2PY).	NAD	28-31	poly(ADP-ribose) polymerase 1	Homo sapiens	91-118
11952169-1	2002	Intracellular catabolism of NAD in mammalian cells occurs mainly via reaction catalyzed by poly(ADP-ribose) polymerase (PARP) with the release of nicotinamide, which is then metabolized predominantly to N-methyl-2-pyridone-5-carboxamide (2PY).	NAD	28-31	poly(ADP-ribose) polymerase 1	Homo sapiens	120-124
11846617-5	2002	Conversely, in the case of massive DNA injury, elevated PARP-1 activation leads to rapid NAD(+)/ATP consumption and cell death by necrosis.	NAD	89-95	poly(ADP-ribose) polymerase 1	Homo sapiens	56-62
11853409-1	2002	Poly(ADP-ribose) polymerase-1 (PARP-1) is a chromatin-associated enzyme that is activated by DNA strand breaks and catalyzes the transfer of ADP-ribose groups from NAD to itself and other nuclear proteins.	NAD	164-167	poly(ADP-ribose) polymerase 1	Homo sapiens	0-29
11825606-10	2002	It is proposed that these residues serve to deliver the catalytic water molecule required for hydrolysis of the cysteine-bound XMP* intermediate formed after oxidation by NAD.	NAD	171-174	epithelial membrane protein 2	Homo sapiens	127-131
11785971-6	2002	The DFF45(-/-) cells regained the ability to fragment their DNA into 50-kb pieces in response to TNF, which resulted in a marked activation of PARP-1 and a concomitant depletion of intracellular NAD.	NAD	195-198	tumor necrosis factor	Homo sapiens	97-100
11853409-1	2002	Poly(ADP-ribose) polymerase-1 (PARP-1) is a chromatin-associated enzyme that is activated by DNA strand breaks and catalyzes the transfer of ADP-ribose groups from NAD to itself and other nuclear proteins.	NAD	164-167	poly(ADP-ribose) polymerase 1	Homo sapiens	31-37
11741702-3	2002	The method most commonly employed to determine phosphofructokinase-1 activity is based on oxidation of NADH by the use of aldolase, triosephosphate isomerase, and alpha-glycerophosphate dehydrogenase.	NAD	103-107	triosephosphate isomerase 1	Homo sapiens	132-157
11804836-7	2002	Results: (i) GAPD was recovered from the plasma-membrane-enriched fraction, in internal membranes, and in the cytosol; (ii) GAPD could be phosphorylated, a phenomenon inhibited by both GAP and NADH; and (iii) GAPD exhibits ADP-ribosyltransferase activity, which is stimulated by nitric oxide in a concentration-dependent manner.	NAD	193-197	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	13-17
11756665-1	2002	In response to high levels of DNA damage, catalytic activation of the nuclear enzyme poly(ADP-ribose) polymerase (PARP) triggers necrotic death because of rapid consumption of its substrate beta-nicotinamide adenine dinucleotide and consequent depletion of ATP.	NAD	190-228	poly(ADP-ribose) polymerase 1	Homo sapiens	85-112
11756665-1	2002	In response to high levels of DNA damage, catalytic activation of the nuclear enzyme poly(ADP-ribose) polymerase (PARP) triggers necrotic death because of rapid consumption of its substrate beta-nicotinamide adenine dinucleotide and consequent depletion of ATP.	NAD	190-228	poly(ADP-ribose) polymerase 1	Homo sapiens	114-118
11756665-3	2002	Here, we show that PARP activation reaction in vitro becomes acidic with release of protons during hydrolysis of beta-nicotinamide adenine dinucleotide.	NAD	113-151	poly(ADP-ribose) polymerase 1	Homo sapiens	19-23
11684688-4	2002	Here we report that PARP can bind to the DNA secondary structures (hairpins) in heteroduplex DNA in a DNA end-independent fashion and that automodification of PARP in the presence of NAD+ inhibited its hairpin binding activity.	NAD	183-187	poly(ADP-ribose) polymerase 1	Homo sapiens	20-24
11684688-4	2002	Here we report that PARP can bind to the DNA secondary structures (hairpins) in heteroduplex DNA in a DNA end-independent fashion and that automodification of PARP in the presence of NAD+ inhibited its hairpin binding activity.	NAD	183-187	poly(ADP-ribose) polymerase 1	Homo sapiens	159-163
12200960-5	2002	Our results show that shear-induced synchronized expression of processes control oxidant production; these changes included upregulation of NADH-producing enzymes (Krebs cycle dehydrogenases and glyceraldehyde-3-phosphate dehydrogenase [GAPDH]) accompanied by simultaneous decrease in NADH-depleting pathways (e.g., lactate dehydrogenase [LDH]) and diminished production of lactate.	NAD	140-144	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	195-235
12200960-5	2002	Our results show that shear-induced synchronized expression of processes control oxidant production; these changes included upregulation of NADH-producing enzymes (Krebs cycle dehydrogenases and glyceraldehyde-3-phosphate dehydrogenase [GAPDH]) accompanied by simultaneous decrease in NADH-depleting pathways (e.g., lactate dehydrogenase [LDH]) and diminished production of lactate.	NAD	140-144	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	237-242
11694507-5	2002	In an in vitro system based on purified recombinant proteins and NAD, caspase-3 prevented the inhibition of DNAS1L3 endonuclease activity by wild-type PARP-1 but not that induced by a caspase-3-resistant PARP-1 mutant.	NAD	65-68	caspase 3	Homo sapiens	70-79
11694507-5	2002	In an in vitro system based on purified recombinant proteins and NAD, caspase-3 prevented the inhibition of DNAS1L3 endonuclease activity by wild-type PARP-1 but not that induced by a caspase-3-resistant PARP-1 mutant.	NAD	65-68	poly(ADP-ribose) polymerase 1	Homo sapiens	151-157
11694507-10	2002	These results indicate that PARP-1 cleavage during apoptosis is not simply required to prevent excessive depletion of NAD and ATP but is also necessary to release DNAS1L3 from poly(ADP-ribosyl)ation-mediated inhibition.	NAD	118-121	poly(ADP-ribose) polymerase 1	Homo sapiens	28-34
11804836-7	2002	Results: (i) GAPD was recovered from the plasma-membrane-enriched fraction, in internal membranes, and in the cytosol; (ii) GAPD could be phosphorylated, a phenomenon inhibited by both GAP and NADH; and (iii) GAPD exhibits ADP-ribosyltransferase activity, which is stimulated by nitric oxide in a concentration-dependent manner.	NAD	193-197	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	124-128
11804836-7	2002	Results: (i) GAPD was recovered from the plasma-membrane-enriched fraction, in internal membranes, and in the cytosol; (ii) GAPD could be phosphorylated, a phenomenon inhibited by both GAP and NADH; and (iii) GAPD exhibits ADP-ribosyltransferase activity, which is stimulated by nitric oxide in a concentration-dependent manner.	NAD	193-197	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	124-128
11738065-8	2001	Predominance of NADPH- over NADH-dependent O(2)(-) production was confirmed in cell homogenates and by cytochrome c reduction assay.	NAD	28-32	cytochrome c, somatic	Homo sapiens	103-115
11735396-7	2001	The control NQO1 protein had a mass of 30864 +/- 6 Da (n = 20, theoretical, 30868.6 Da) which increased by 217 Da after ES936 treatment (31081 +/- 7 Da, n = 20) in the presence of NADH.	NAD	180-184	NAD(P)H quinone dehydrogenase 1	Homo sapiens	12-16
11577079-4	2001	Electrophoretic mobility shift assays showed that, when PARP-1 was present, NF-kappaB-p50 DNA binding was dependent on the presence of betaNAD+.	NAD	135-143	poly(ADP-ribose) polymerase 1	Homo sapiens	56-62
11577079-4	2001	Electrophoretic mobility shift assays showed that, when PARP-1 was present, NF-kappaB-p50 DNA binding was dependent on the presence of betaNAD+.	NAD	135-143	nuclear factor kappa B subunit 1	Homo sapiens	76-89
11577079-8	2001	Co-immunoprecipitation and immunoblot analysis revealed that PARP-1 physically interacts with NF-kappaB-p50 with high specificity in the absence of betaNAD+.	NAD	148-156	poly(ADP-ribose) polymerase 1	Homo sapiens	61-67
11602597-0	2001	A self-restricted CD38-connexin 43 cross-talk affects NAD+ and cyclic ADP-ribose metabolism and regulates intracellular calcium in 3T3 fibroblasts.	NAD	54-58	gap junction protein, alpha 1	Mus musculus	23-34
11602597-1	2001	Connexin 43 (Cx43) hexameric hemichannels, recently demonstrated to mediate NAD(+) transport, functionally interact in the plasma membrane of several cells with the ectoenzyme CD38 that converts NAD(+) to the universal calcium mobilizer cyclic ADP-ribose (cADPR).	NAD	76-82	gap junction protein, alpha 1	Mus musculus	0-11
11602597-1	2001	Connexin 43 (Cx43) hexameric hemichannels, recently demonstrated to mediate NAD(+) transport, functionally interact in the plasma membrane of several cells with the ectoenzyme CD38 that converts NAD(+) to the universal calcium mobilizer cyclic ADP-ribose (cADPR).	NAD	195-201	gap junction protein, alpha 1	Mus musculus	0-11
11714283-1	2001	Yeast NAD(+)-specific isocitrate dehydrogenase is an allosterically regulated octameric enzyme composed of four each of two homologous but nonidentical subunits designated IDH1 and IDH2.	NAD	6-12	isocitrate dehydrogenase (NAD(+)) IDH1	Saccharomyces cerevisiae S288C	172-176
11885779-8	2001	Alternatively, the increased AST activity may be connected with an increased transport of NADH from the cytosol to mitochondria, while the increased ALT activity would represent the transformation of pyruvate to alanine as a consequence of increased glycolysis.	NAD	90-94	glutamic-oxaloacetic transaminase 2	Rattus norvegicus	29-32
11672702-8	2001	Quantified were NAD-linked oxidation of benzaldehyde catalyzed by nALDH3A1 and tALDH3A1, and NAD-linked oxidation of acetaldehyde catalyzed by rALDH1A1 and rALDH2, all at 37 degrees C and pH 8.1, and in the presence and absence of inhibitor.	NAD	93-96	aldehyde dehydrogenase 1 family, member A1	Rattus norvegicus	143-151
11765140-10	2001	When liver cytosol or blood was separated by DEAE-cellulose column chromatography, the fractions with the reducing activity in the presence of both NADH and FAD also showed catalase activity.	NAD	148-152	catalase	Oryctolagus cuniculus	173-181
11708925-1	2001	Through an effort to develop novel ligands that have subtype selectivity for the estrogen receptors alpha (ERalpha) and beta (ERbeta), we have found that 2,3-bis(4-hydroxyphenyl)propionitrile (DPN) acts as an agonist on both ER subtypes, but has a 70-fold higher relative binding affinity and 170-fold higher relative potency in transcription assays with ERbeta than with ERalpha.	NAD	193-196	estrogen receptor 1	Homo sapiens	107-114
11708925-1	2001	Through an effort to develop novel ligands that have subtype selectivity for the estrogen receptors alpha (ERalpha) and beta (ERbeta), we have found that 2,3-bis(4-hydroxyphenyl)propionitrile (DPN) acts as an agonist on both ER subtypes, but has a 70-fold higher relative binding affinity and 170-fold higher relative potency in transcription assays with ERbeta than with ERalpha.	NAD	193-196	estrogen receptor 1	Homo sapiens	372-379
11696370-2	2001	We observed (i) NAD-dependent enzyme activity and mRNA for 11beta-HSD2, but not 11beta-HSD1, (ii) increasing 11beta-HSD2 activity with increasing degree of differentiation and (iii) a concentration-dependent down-regulation by TNF-alpha, phorbol myristate acetate (PMA) or glucose of activity and mRNA of 11beta-HSD2.	NAD	16-19	tumor necrosis factor	Homo sapiens	227-236
11570811-1	2001	Poly(ADP-ribose) polymerase-1 (PARP-1) plays the active role of "nick sensor" during DNA repair and apoptosis, when it synthesizes ADP-ribose from NAD(+) in the presence of DNA strand breaks.	NAD	147-153	poly(ADP-ribose) polymerase 1	Homo sapiens	0-29
11672522-3	2001	Nicotinamide (Vitamin B3) inhibits an NAD-dependent p53 deacetylation induced by Sir2alpha, and also enhances the p53 acetylation levels in vivo.	NAD	38-41	tumor protein p53	Homo sapiens	52-55
11672523-0	2001	hSIR2(SIRT1) functions as an NAD-dependent p53 deacetylase.	NAD	29-32	tumor protein p53	Homo sapiens	43-46
11461900-7	2001	The TNF-induced activation of poly(ADP-ribose) polymerase (PARP), which requires PARP binding to DNA strand breaks, and the consequent depletion of the PARP substrate NAD were markedly delayed in DFF45(-/-) cells, suggesting a role for DFF in PARP activation.	NAD	167-170	tumor necrosis factor	Mus musculus	4-7
11570811-1	2001	Poly(ADP-ribose) polymerase-1 (PARP-1) plays the active role of "nick sensor" during DNA repair and apoptosis, when it synthesizes ADP-ribose from NAD(+) in the presence of DNA strand breaks.	NAD	147-153	poly(ADP-ribose) polymerase 1	Homo sapiens	31-37
11511974-4	2001	PARP in turn depletes the intracellular concentration of its substrate, NAD+, slowing the rate of glycolysis, electron transport, and ATP formation.	NAD	72-76	poly(ADP-ribose) polymerase 1	Homo sapiens	0-4
11513952-1	2001	Proton-pumping nicotinamide nucleotide transhydrogenase (Nnt) is a membrane-bound enzyme that catalyzes the reversible reduction of NADP(+) by NADH.	NAD	143-147	nicotinamide nucleotide transhydrogenase	Mus musculus	57-60
11489987-0	2001	Nicotinamide adenine dinucleotide (NAD) and its metabolites inhibit T lymphocyte proliferation: role of cell surface NAD glycohydrolase and pyrophosphatase activities.	NAD	0-33	ADP-ribosyltransferase 2b	Rattus norvegicus	117-135
11489987-0	2001	Nicotinamide adenine dinucleotide (NAD) and its metabolites inhibit T lymphocyte proliferation: role of cell surface NAD glycohydrolase and pyrophosphatase activities.	NAD	35-38	ADP-ribosyltransferase 2b	Rattus norvegicus	117-135
11489987-1	2001	The presence of NAD-metabolizing enzymes (e.g., ADP-ribosyltransferase (ART)2) on the surface of immune cells suggests a potential immunomodulatory activity for ecto-NAD or its metabolites at sites of inflammation and cell lysis where extracellular levels of NAD may be high.	NAD	16-19	ADP-ribosyltransferase 2b	Rattus norvegicus	48-77
11489987-1	2001	The presence of NAD-metabolizing enzymes (e.g., ADP-ribosyltransferase (ART)2) on the surface of immune cells suggests a potential immunomodulatory activity for ecto-NAD or its metabolites at sites of inflammation and cell lysis where extracellular levels of NAD may be high.	NAD	166-169	ADP-ribosyltransferase 2b	Rattus norvegicus	48-77
11489987-1	2001	The presence of NAD-metabolizing enzymes (e.g., ADP-ribosyltransferase (ART)2) on the surface of immune cells suggests a potential immunomodulatory activity for ecto-NAD or its metabolites at sites of inflammation and cell lysis where extracellular levels of NAD may be high.	NAD	166-169	ADP-ribosyltransferase 2b	Rattus norvegicus	48-77
11668012-4	2001	The activity of PDH was measured in the presence of acetaldehyde (10 microM-1 mM) by measuring the formation of the reduced form of nicotinamide-adenine dinucleotide at 340 nm.	NAD	132-165	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	16-19
11498506-2	2001	Arginine-specific ADP-ribosyltransferase (ART1) is expressed on the surface of a number of cell types, and catalyses the transfer of ADP-ribose from NAD(+) to target proteins.	NAD	149-155	ADP-ribosyltransferase 1	Homo sapiens	42-46
11684461-4	2001	Poly(ADP)-ribose polymerase (PARP-1) is the enzyme responsible for much of the NAD degradation following DNA damage, although numerous other PARPs have been discovered recently that await functional characterization.	NAD	79-82	poly(ADP-ribose) polymerase 1	Homo sapiens	0-27
11684461-4	2001	Poly(ADP)-ribose polymerase (PARP-1) is the enzyme responsible for much of the NAD degradation following DNA damage, although numerous other PARPs have been discovered recently that await functional characterization.	NAD	79-82	poly(ADP-ribose) polymerase 1	Homo sapiens	29-35
11536292-1	2001	One of the immediate eukaryotic cellular responses to DNA breakage is the covalent post-translational modification of nuclear proteins with poly(ADP-ribose) from NAD+ as precursor, mostly catalysed by poly(ADP-ribose) polymerase-1 (PARP-1).	NAD	162-166	poly(ADP-ribose) polymerase 1	Homo sapiens	201-230
11536292-1	2001	One of the immediate eukaryotic cellular responses to DNA breakage is the covalent post-translational modification of nuclear proteins with poly(ADP-ribose) from NAD+ as precursor, mostly catalysed by poly(ADP-ribose) polymerase-1 (PARP-1).	NAD	162-166	poly(ADP-ribose) polymerase 1	Homo sapiens	232-238
11536292-5	2001	The pathophysiology effects are mediated through PARP-1 overactivity, which can cause cell suicide by NAD+ depletion.	NAD	102-106	poly(ADP-ribose) polymerase 1	Homo sapiens	49-55
11470445-7	2001	The Michaelis constants for L-threonine and NAD for partially purified chicken hepatic TDH are 5.38 and 0.19 mM, respectively.	NAD	44-47	L-threonine dehydrogenase (pseudogene)	Gallus gallus	87-90
11444838-2	2001	However, we have found that NAD, as a coenzyme of d-glyceraldehyde-3-phosphate dehydrogenase (GAPDH), also stimulates the discharge of GAPDH folding intermediate from its stable complex with GroEL formed in the absence of ATP and assists refolding with the same yield as ATP/Mg(2+) does.	NAD	28-31	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	50-92
11444838-2	2001	However, we have found that NAD, as a coenzyme of d-glyceraldehyde-3-phosphate dehydrogenase (GAPDH), also stimulates the discharge of GAPDH folding intermediate from its stable complex with GroEL formed in the absence of ATP and assists refolding with the same yield as ATP/Mg(2+) does.	NAD	28-31	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	94-99
11444838-2	2001	However, we have found that NAD, as a coenzyme of d-glyceraldehyde-3-phosphate dehydrogenase (GAPDH), also stimulates the discharge of GAPDH folding intermediate from its stable complex with GroEL formed in the absence of ATP and assists refolding with the same yield as ATP/Mg(2+) does.	NAD	28-31	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	135-140
11444838-5	2001	Different from ATP, NAD triggers the release of GAPDH intermediates bound by GroEL via binding with GAPDH itself but not with GroEL, and the released intermediates all folded to native molecules without the formation of aggregation.	NAD	20-23	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	48-53
11444838-5	2001	Different from ATP, NAD triggers the release of GAPDH intermediates bound by GroEL via binding with GAPDH itself but not with GroEL, and the released intermediates all folded to native molecules without the formation of aggregation.	NAD	20-23	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	100-105
15995937-1	2001	Poly(ADP-ribose) polymerase (PARP) catalyzes the biochemical conversion of nicotinamide adenine dinucleotide (NAD+) to poly(ADP-ribose) and nicotinamide, which is a weak feedback inhibitor of the enzyme.	NAD	75-108	poly(ADP-ribose) polymerase 1	Homo sapiens	0-27
11441146-0	2001	Regulation of clock and NPAS2 DNA binding by the redox state of NAD cofactors.	NAD	64-67	neuronal PAS domain protein 2	Homo sapiens	24-29
11441146-3	2001	Here we show that the DNA-binding activity of the Clock:BMAL1 and NPAS2:BMAL1 heterodimers is regulated by the redox state of nicotinamide adenine dinucleotide (NAD) cofactors in a purified system.	NAD	126-159	neuronal PAS domain protein 2	Homo sapiens	66-71
11441146-3	2001	Here we show that the DNA-binding activity of the Clock:BMAL1 and NPAS2:BMAL1 heterodimers is regulated by the redox state of nicotinamide adenine dinucleotide (NAD) cofactors in a purified system.	NAD	161-164	neuronal PAS domain protein 2	Homo sapiens	66-71
11418099-5	2001	However, there were striking exceptions where an apparent interaction was found between the PSST and ND1 subunits: preincubation with NADH increases PSST labeling and decreases ND1 labeling; the very weak complex I inhibitor 1-methyl-4-phenylpyridinium ion (MPP(+)) and the semiquinone analogue stigmatellin show the opposite effect with increased labeling at ND1 coupled to decreased labeling at PSST in a concentration- and time-dependent manner.	NAD	134-138	mitochondrially encoded NADH dehydrogenase 1	Homo sapiens	101-104
11418099-5	2001	However, there were striking exceptions where an apparent interaction was found between the PSST and ND1 subunits: preincubation with NADH increases PSST labeling and decreases ND1 labeling; the very weak complex I inhibitor 1-methyl-4-phenylpyridinium ion (MPP(+)) and the semiquinone analogue stigmatellin show the opposite effect with increased labeling at ND1 coupled to decreased labeling at PSST in a concentration- and time-dependent manner.	NAD	134-138	mitochondrially encoded NADH dehydrogenase 1	Homo sapiens	177-180
11418099-5	2001	However, there were striking exceptions where an apparent interaction was found between the PSST and ND1 subunits: preincubation with NADH increases PSST labeling and decreases ND1 labeling; the very weak complex I inhibitor 1-methyl-4-phenylpyridinium ion (MPP(+)) and the semiquinone analogue stigmatellin show the opposite effect with increased labeling at ND1 coupled to decreased labeling at PSST in a concentration- and time-dependent manner.	NAD	134-138	mitochondrially encoded NADH dehydrogenase 1	Homo sapiens	177-180
15995937-1	2001	Poly(ADP-ribose) polymerase (PARP) catalyzes the biochemical conversion of nicotinamide adenine dinucleotide (NAD+) to poly(ADP-ribose) and nicotinamide, which is a weak feedback inhibitor of the enzyme.	NAD	75-108	poly(ADP-ribose) polymerase 1	Homo sapiens	29-33
15995937-1	2001	Poly(ADP-ribose) polymerase (PARP) catalyzes the biochemical conversion of nicotinamide adenine dinucleotide (NAD+) to poly(ADP-ribose) and nicotinamide, which is a weak feedback inhibitor of the enzyme.	NAD	110-114	poly(ADP-ribose) polymerase 1	Homo sapiens	0-27
15995937-1	2001	Poly(ADP-ribose) polymerase (PARP) catalyzes the biochemical conversion of nicotinamide adenine dinucleotide (NAD+) to poly(ADP-ribose) and nicotinamide, which is a weak feedback inhibitor of the enzyme.	NAD	110-114	poly(ADP-ribose) polymerase 1	Homo sapiens	29-33
11469679-4	2001	Results obtained were consistent with the hypothesis that carboplatin and hyperthermia perturbation of NAD + pools results in down-regulation of GRP78 with subsequent modulation of VP-16 cytotoxicity.	NAD	103-108	heat shock protein 5	Mus musculus	145-150
12638607-2	2001	Alterations to the cellular metabolism induced by exposure to microgravity are evidentiated in the modification of PARP activity (strongly dependent to the presence of DNA damages and to the altered gene expression), in the modification of the repair ability and in the cell"s energy homeostasis (NAD and ATP).	NAD	297-300	poly(ADP-ribose) polymerase 1	Homo sapiens	115-119
12666944-5	2001	The AST measurements were based on the establishment absorbency coefficient of NADH.	NAD	79-83	solute carrier family 17 member 5	Homo sapiens	4-7
12666944-6	2001	The rate of decrease in the concentration of NADH is directly proportional to the AST activity in the sample.	NAD	45-49	solute carrier family 17 member 5	Homo sapiens	82-85
11425472-3	2001	UTR1p specifically phosphorylated NAD in the presence of ATP, dATP, or CTP as phosphoryl donors, and was most active at pH 8.0, 30 degrees C. Km values of UTR1p for NAD and ATP were determined to be 0.50 mM and 0.60 mM, respectively.	NAD	34-37	NADH/NAD(+) kinase	Saccharomyces cerevisiae S288C	0-5
12090349-3	2001	We hypothesized that treatments with liposome encapsulated ATP or NAD+ would protect human endothelial cells exposed to endotoxin (LPS) and interferon-gamma (IFN-gamma) from energy failure.	NAD	66-70	interferon gamma	Homo sapiens	140-156
12090349-3	2001	We hypothesized that treatments with liposome encapsulated ATP or NAD+ would protect human endothelial cells exposed to endotoxin (LPS) and interferon-gamma (IFN-gamma) from energy failure.	NAD	66-70	interferon gamma	Homo sapiens	158-167
11442316-10	2001	Furthermore, a significant reduction of suppression of mitochondrial respiration, DNA strand breakage, and reduction of cellular levels of NAD+ was observed in ex vivo macrophages harvested from the peritoneal cavity of iNOS -/- mice subjected to zymosan-induced non-septic shock.	NAD	139-143	nitric oxide synthase 2, inducible	Mus musculus	220-224
11425472-3	2001	UTR1p specifically phosphorylated NAD in the presence of ATP, dATP, or CTP as phosphoryl donors, and was most active at pH 8.0, 30 degrees C. Km values of UTR1p for NAD and ATP were determined to be 0.50 mM and 0.60 mM, respectively.	NAD	34-37	NADH/NAD(+) kinase	Saccharomyces cerevisiae S288C	155-160
11425472-3	2001	UTR1p specifically phosphorylated NAD in the presence of ATP, dATP, or CTP as phosphoryl donors, and was most active at pH 8.0, 30 degrees C. Km values of UTR1p for NAD and ATP were determined to be 0.50 mM and 0.60 mM, respectively.	NAD	165-168	NADH/NAD(+) kinase	Saccharomyces cerevisiae S288C	0-5
11516724-12	2001	Likewise, only cofactors of PHS, arachidonic acid and hydrogen peroxide, supported the DNA adduct formation of AAI and AAII, while NADPH and NADH were ineffective.	NAD	141-145	pterin-4 alpha-carbinolamine dehydratase 1	Homo sapiens	28-31
11425472-3	2001	UTR1p specifically phosphorylated NAD in the presence of ATP, dATP, or CTP as phosphoryl donors, and was most active at pH 8.0, 30 degrees C. Km values of UTR1p for NAD and ATP were determined to be 0.50 mM and 0.60 mM, respectively.	NAD	165-168	NADH/NAD(+) kinase	Saccharomyces cerevisiae S288C	155-160
11394900-1	2001	Poly(ADP-ribose) polymerase 1 (PARP-1) is a nuclear enzyme that catalyzes the synthesis of ADP-ribose polymers from NAD(+).	NAD	116-122	poly(ADP-ribose) polymerase 1	Homo sapiens	0-29
11405646-2	2001	Crystal structures of Trypanosoma brucei, Trypanosoma cruzi, Leishmania mexicana, and human GAPDH"s provided details of how the adenosyl moiety of NAD(+) interacts with the proteins, and this facilitated the understanding of the relative affinities of a series of adenosine analogues for the various GAPDH"s.	NAD	147-153	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	92-97
11405646-2	2001	Crystal structures of Trypanosoma brucei, Trypanosoma cruzi, Leishmania mexicana, and human GAPDH"s provided details of how the adenosyl moiety of NAD(+) interacts with the proteins, and this facilitated the understanding of the relative affinities of a series of adenosine analogues for the various GAPDH"s.	NAD	147-153	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	300-305
11274199-2	2001	Recently, hexameric connexin 43 (Cx43) hemichannels have been shown to release cytosolic NAD(+) from isolated murine fibroblasts (Bruzzone, S., Guida, L., Zocchi, E., Franco, L. and De Flora, A.	NAD	89-95	gap junction protein, alpha 1	Mus musculus	20-31
11394900-1	2001	Poly(ADP-ribose) polymerase 1 (PARP-1) is a nuclear enzyme that catalyzes the synthesis of ADP-ribose polymers from NAD(+).	NAD	116-122	poly(ADP-ribose) polymerase 1	Homo sapiens	31-37
11259441-6	2001	Consistent with these findings, when ADP-induced oxidative phosphorylation is limited by exogenous beta-NADH, recombinant Bcl-x(L) can sustain outer mitochondrial membrane permeability to ADP.	NAD	99-108	BCL2 like 1	Homo sapiens	122-130
11259315-2	2001	We describe the use of confocal microscopy in conjunction with enzyme-dependent fluorescence recovery after photobleaching (ED-FRAP) of NADH as a topological assay of NADH generation capacity within living cardiac myocytes.	NAD	136-140	mechanistic target of rapamycin kinase	Homo sapiens	127-131
11295153-1	2001	Nicotinic acid (NA) and nicotinamide (NAM), commonly called niacin, are the dietary precursors for NAD(+) (nicotinamide adenine dinucleotide), which is required for DNA synthesis, as well as for the activity of the enzyme poly(ADP-ribose) polymerase-1 (PARP-1; EC 2.4.2.30) for which NAD(+) is the sole substrate.	NAD	99-105	poly(ADP-ribose) polymerase 1	Homo sapiens	222-251
11295153-1	2001	Nicotinic acid (NA) and nicotinamide (NAM), commonly called niacin, are the dietary precursors for NAD(+) (nicotinamide adenine dinucleotide), which is required for DNA synthesis, as well as for the activity of the enzyme poly(ADP-ribose) polymerase-1 (PARP-1; EC 2.4.2.30) for which NAD(+) is the sole substrate.	NAD	99-105	poly(ADP-ribose) polymerase 1	Homo sapiens	253-259
11295153-1	2001	Nicotinic acid (NA) and nicotinamide (NAM), commonly called niacin, are the dietary precursors for NAD(+) (nicotinamide adenine dinucleotide), which is required for DNA synthesis, as well as for the activity of the enzyme poly(ADP-ribose) polymerase-1 (PARP-1; EC 2.4.2.30) for which NAD(+) is the sole substrate.	NAD	107-140	poly(ADP-ribose) polymerase 1	Homo sapiens	222-251
11295153-1	2001	Nicotinic acid (NA) and nicotinamide (NAM), commonly called niacin, are the dietary precursors for NAD(+) (nicotinamide adenine dinucleotide), which is required for DNA synthesis, as well as for the activity of the enzyme poly(ADP-ribose) polymerase-1 (PARP-1; EC 2.4.2.30) for which NAD(+) is the sole substrate.	NAD	107-140	poly(ADP-ribose) polymerase 1	Homo sapiens	253-259
11295153-4	2001	Since NAD(+) is important for PARP-1 activity, various aspects of PARP-1 in relation to DNA synthesis and repair, and regulation of gene expression are addressed.	NAD	6-12	poly(ADP-ribose) polymerase 1	Homo sapiens	30-36
11295153-4	2001	Since NAD(+) is important for PARP-1 activity, various aspects of PARP-1 in relation to DNA synthesis and repair, and regulation of gene expression are addressed.	NAD	6-12	poly(ADP-ribose) polymerase 1	Homo sapiens	66-72
11295153-6	2001	In vitro studies show that PARP-1 function is impaired and genomic stability decreased when cells are either depleted from NAD(+) or incubated with high concentrations of NAM which is a PARP-1 inhibitor.	NAD	123-129	poly(ADP-ribose) polymerase 1	Homo sapiens	27-33
11361135-1	2001	The NPY1 nudix hydrolase gene of Saccharomyces cerevisiae has been cloned and shown to encode a diphosphatase (pyrophosphatase) with NADH as the preferred substrate, giving NMNH and AMP as products.	NAD	133-137	NAD(+) diphosphatase	Saccharomyces cerevisiae S288C	4-8
11410692-1	2001	The effects of thyroid hormone on hepatic and gastric alcohol dehydrogenase (ADH) activities (nM of NADH/min/mg of cytosolic protein) have been investigated in male Sprague Dawley rats treated with thyroxine (1 mg/kg, po) for 14 days.	NAD	100-104	aldo-keto reductase family 1 member A1	Rattus norvegicus	77-80
11353811-2	2001	ROS and peroxynitrite induce single-strand DNA break formation and PARP activation, resulting in NAD(+) and ATP depletion, which can lead to cell death.	NAD	97-103	poly(ADP-ribose) polymerase 1	Homo sapiens	67-71
11353811-3	2001	Although protection of cardiac muscle by PARP inhibitors can be explained by their attenuating effect on NAD(+) and ATP depletion, there are data indicating that PARP inhibitors also protect mitochondria from oxidant-induced injury.	NAD	105-111	poly(ADP-ribose) polymerase 1	Homo sapiens	41-45
11353811-7	2001	Therefore, PARP inhibitors, in addition to their important primary effect of decreasing the activity of nuclear PARP and decreasing NAD(+) and ATP consumption, reduce ischemia-reperfusion-induced endogenous ROS production and protect the respiratory complexes from ROS induced inactivation, providing an additional mechanism by which they can protect heart from oxidative damages.	NAD	132-138	poly(ADP-ribose) polymerase 1	Homo sapiens	11-15
11327708-2	2001	In contrast, the gap1-encoded GAPDH1, which is the other NAD-dependent cyanobacterial GAPDH, is virtually absent in both cell types.	NAD	57-60	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	30-35
11311149-0	2001	Structure-function studies of human deoxyhypusine synthase: identification of amino acid residues critical for the binding of spermidine and NAD.	NAD	141-144	deoxyhypusine synthase	Homo sapiens	36-58
11311149-2	2001	The crystal structure of human deoxyhypusine synthase in complex with NAD revealed four NAD-binding sites per enzyme tetramer, and led to a prediction of the spermidine-binding pocket.	NAD	70-73	deoxyhypusine synthase	Homo sapiens	31-53
11311149-2	2001	The crystal structure of human deoxyhypusine synthase in complex with NAD revealed four NAD-binding sites per enzyme tetramer, and led to a prediction of the spermidine-binding pocket.	NAD	88-91	deoxyhypusine synthase	Homo sapiens	31-53
11311149-9	2001	These findings permit the positive identification of amino acid residues critical for binding of spermidine and NAD, and provide a new insight into the complex molecular interactions involved in the deoxyhypusine synthase reaction.	NAD	112-115	deoxyhypusine synthase	Homo sapiens	199-221
11259315-2	2001	We describe the use of confocal microscopy in conjunction with enzyme-dependent fluorescence recovery after photobleaching (ED-FRAP) of NADH as a topological assay of NADH generation capacity within living cardiac myocytes.	NAD	167-171	mechanistic target of rapamycin kinase	Homo sapiens	127-131
11259315-5	2001	In addition, NADH ED-FRAP was correlated with flavin adenine dinucleotide (FAD(+)) fluorescence.	NAD	13-17	mechanistic target of rapamycin kinase	Homo sapiens	21-25
11259315-6	2001	These data, coupled with the cellular patterns of NADH ED-FRAP changes with dehydrogenase stimulation, suggest that NADH ED-FRAP is localized to the mitochondria.	NAD	50-54	mechanistic target of rapamycin kinase	Homo sapiens	58-62
11259315-6	2001	These data, coupled with the cellular patterns of NADH ED-FRAP changes with dehydrogenase stimulation, suggest that NADH ED-FRAP is localized to the mitochondria.	NAD	50-54	mechanistic target of rapamycin kinase	Homo sapiens	124-128
11259315-7	2001	These results suggest that ED-FRAP enables measurement of regional dynamics of mitochondrial NADH production in intact cells, thus providing information regarding region-specific intracellular redox reactions and energy metabolism.	NAD	93-97	mechanistic target of rapamycin kinase	Homo sapiens	30-34
11330877-1	2001	OBJECTIVES: To investigate the basal and NADH-stimulated superoxide (.O2-) production and inactivation by Cu/Zn superoxide dismutase (SOD) in aorta from spontaneously hypertensive rats (SHR) and from desoxycorticosterone acetate (DOCA)-salt hypertensive (DOCA-HT) rats.	NAD	41-45	superoxide dismutase 1	Rattus norvegicus	134-137
11206479-0	2001	A disubstituted NAD+ analogue is a nanomolar inhibitor of trypanosomal glyceraldehyde-3-phosphate dehydrogenase.	NAD	16-20	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	71-111
11295358-9	2001	Stimulation with angiotensin II and platelet-derived growth factor also predominantly increased the NADPH-driven signal (101 +/- 8% and 83 +/- 1% increase above control, respectively), with less of an effect on NADH-dependent O2*- (17 +/- 3% and 36 +/- 5% increase, respectively).	NAD	211-215	angiotensinogen	Homo sapiens	17-31
11253920-1	2001	The influence of various phenolic compounds on the lactoperoxidase (LPO)/hydrogen peroxide (H2O2)-catalyzed oxidation of biochemical reductants such as reduced beta-nicotinamide adenine dinucleotide (NADH), reduced beta-nicotinamide adenine dinucleotide phosphate (NADPH) or reduced glutathione (GSH) was investigated by electron spin resonance (ESR) spectroscopy.	NAD	160-198	lactoperoxidase	Homo sapiens	51-66
11253920-1	2001	The influence of various phenolic compounds on the lactoperoxidase (LPO)/hydrogen peroxide (H2O2)-catalyzed oxidation of biochemical reductants such as reduced beta-nicotinamide adenine dinucleotide (NADH), reduced beta-nicotinamide adenine dinucleotide phosphate (NADPH) or reduced glutathione (GSH) was investigated by electron spin resonance (ESR) spectroscopy.	NAD	160-198	lactoperoxidase	Homo sapiens	68-71
11253920-1	2001	The influence of various phenolic compounds on the lactoperoxidase (LPO)/hydrogen peroxide (H2O2)-catalyzed oxidation of biochemical reductants such as reduced beta-nicotinamide adenine dinucleotide (NADH), reduced beta-nicotinamide adenine dinucleotide phosphate (NADPH) or reduced glutathione (GSH) was investigated by electron spin resonance (ESR) spectroscopy.	NAD	200-204	lactoperoxidase	Homo sapiens	51-66
11253920-1	2001	The influence of various phenolic compounds on the lactoperoxidase (LPO)/hydrogen peroxide (H2O2)-catalyzed oxidation of biochemical reductants such as reduced beta-nicotinamide adenine dinucleotide (NADH), reduced beta-nicotinamide adenine dinucleotide phosphate (NADPH) or reduced glutathione (GSH) was investigated by electron spin resonance (ESR) spectroscopy.	NAD	200-204	lactoperoxidase	Homo sapiens	68-71
11306038-8	2001	Quantified were NAD-linked oxidation of benzaldehyde catalyzed by nALDH3A1 and tALDH3A1, and NAD-linked oxidation of acetaldehyde catalyzed by rALDH1A1 and rALDH2, all at 37 degrees C and pH 8.1, and in the presence and absence of inhibitor.	NAD	93-96	aldehyde dehydrogenase 1 family, member A1	Rattus norvegicus	143-151
11042198-1	2001	Yeast mitochondrial NAD(+)-specific isocitrate dehydrogenase is an octamer composed of four each of two nonidentical but related subunits designated IDH1 and IDH2.	NAD	20-26	isocitrate dehydrogenase (NAD(+)) IDH1	Saccharomyces cerevisiae S288C	149-153
11341957-9	2001	Competition experiments with increasing concentration of NAD(+) co-factor indicate that the GAPDH Rossmann fold is a docking site for antisense oligonucleotides containing a TAAAT motif.	NAD	57-63	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	92-97
11226170-0	2001	A cytosolic NAD-dependent deacetylase, Hst2p, can modulate nucleolar and telomeric silencing in yeast.	NAD	12-15	histone deacetylase HST2	Saccharomyces cerevisiae S288C	39-44
11136248-7	2001	Furthermore, NADPH was a potent inhibitor of the W676A NADH-dependent cytochrome c reduction and CYP1A2 activity.	NAD	55-59	cytochrome c, somatic	Homo sapiens	70-82
11136248-8	2001	Overall, the results show that Trp-676 of human CPR plays a major role in cofactor discrimination, and substitution of this conserved aromatic residue with alanine results in an efficient NADH-dependent cytochrome P450 system.	NAD	188-192	cytochrome p450 oxidoreductase	Homo sapiens	48-51
11136248-1	2001	A functional human NADH-dependent cytochrome P450 system has been developed by altering the cofactor preference of human NADPH cytochrome P450 reductase (CPR), the redox partner for P450s.	NAD	19-23	cytochrome p450 oxidoreductase	Homo sapiens	121-152
11136248-1	2001	A functional human NADH-dependent cytochrome P450 system has been developed by altering the cofactor preference of human NADPH cytochrome P450 reductase (CPR), the redox partner for P450s.	NAD	19-23	cytochrome p450 oxidoreductase	Homo sapiens	154-157
11217149-6	2001	PARP activity in WI-26 (a type I-like cell line) and A549 (a type II-like cell line) cells was assessed by the uptake of labeled NAD over 4 hours and confirmed on the basis of the reduction of PARP levels in the presence of a PARP inhibitor, 3-aminobenzamide (3-ABA).	NAD	129-132	poly(ADP-ribose) polymerase 1	Homo sapiens	0-4
11136248-3	2001	Of the mutations made, the substitution of Trp-676 with alanine (W676A) resulted in a functional NADH-dependent enzyme, which catalyzed the reduction of cytochrome c and ferricyanide as well as facilitated the metabolism of 7-ethoxyresorufin by CYP1A2.	NAD	97-101	cytochrome c, somatic	Homo sapiens	153-165
11136248-4	2001	Kinetic analysis measuring cytochrome c activity revealed that the NADH-dependent k(cat) of W676A is equivalent (90%) to the NADPH-dependent k(cat) of the wild-type enzyme, with W676A having an approximately 1,000-fold higher specificity for NADH.	NAD	67-71	cytochrome c, somatic	Homo sapiens	27-39
11846007-1	2001	During apoptosis, the nuclear enzyme Poly(ADP-Ribose) Polymerase-1 (PARP-1) catalyzes the rapid and transient synthesis of poly(ADP-ribose) from NAD+ and becomes inactive when cleaved by caspases.	NAD	145-149	poly(ADP-ribose) polymerase 1	Homo sapiens	37-66
11846007-1	2001	During apoptosis, the nuclear enzyme Poly(ADP-Ribose) Polymerase-1 (PARP-1) catalyzes the rapid and transient synthesis of poly(ADP-ribose) from NAD+ and becomes inactive when cleaved by caspases.	NAD	145-149	poly(ADP-ribose) polymerase 1	Homo sapiens	68-74
11149897-4	2001	Upon binding to broken DNA, PARP cleaves NAD+ into nicotinamide and ADP-ribose and polymerizes the latter on nuclear acceptor proteins such as histones and PARP itself.	NAD	41-45	poly(ADP-ribose) polymerase 1	Homo sapiens	28-32
11149897-4	2001	Upon binding to broken DNA, PARP cleaves NAD+ into nicotinamide and ADP-ribose and polymerizes the latter on nuclear acceptor proteins such as histones and PARP itself.	NAD	41-45	poly(ADP-ribose) polymerase 1	Homo sapiens	156-160
11149897-5	2001	Overactivation of PARP depletes cellular NAD+ and ATP stores and causes necrotic cell death.	NAD	41-45	poly(ADP-ribose) polymerase 1	Homo sapiens	18-22
11847482-0	2001	Influence of reduced nicotinamide adenine dinucleotide on the production of interleukin-6 by peripheral human blood leukocytes.	NAD	21-54	interleukin 6	Homo sapiens	76-89
11847482-6	2001	RESULTS: In PBLs from the 18 healthy donors, NADH significantly stimulated the dose-dependent release of IL-6, ranging from 6.25 to 400 microg/ml, compared to medium-treated cells (p &lt; 0.001).	NAD	45-49	interleukin 6	Homo sapiens	105-109
11847482-7	2001	An amount of 1,000 pg/ml IL-6 was induced by NADH concentrations ranging from 3.1 to &gt;25 microg/ml.	NAD	45-49	interleukin 6	Homo sapiens	25-29
11113971-5	2000	At high demand for NADH reoxidation, a strong induction was seen not only of the GPD2 gene, but also of GPP1, encoding one of the molecular forms of glycerol-3-phosphatase.	NAD	19-23	glycerol-1-phosphatase RHR2	Saccharomyces cerevisiae S288C	104-108
11216837-4	2001	The maize NADH-dependent O2*--synthase activity could clearly be differentiated from peroxidase-mediated O2*--synthesizing activity by its insensitivity to cyanide and azide, as well as by its much higher affinity to O2.	NAD	10-14	peroxidase 1	Zea mays	85-95
11104695-0	2000	Human deoxyhypusine synthase: interrelationship between binding of NAD and substrates.	NAD	67-70	deoxyhypusine synthase	Homo sapiens	6-28
11104695-1	2000	Deoxyhypusine synthase catalyses the NAD-dependent transfer of the butylamine moiety from the polyamine, spermidine, to a specific lysine residue of a single cellular protein, eukaryotic translation-initiation factor 5A (eIF5A) precursor.	NAD	37-40	deoxyhypusine synthase	Homo sapiens	0-22
11095743-5	2000	Two genes appear to participate in feedback loops that modulate HDAC activity: ZRT1 encodes a zinc transporter and is repressed by RPD3 (Rpd3p is zinc-dependent); BNA1 encodes a nicotinamide adenine dinucleotide (NAD)-biosynthesis enzyme and is repressed by SIR2 (Sir2p is NAD-dependent).	NAD	178-211	histone deacetylase RPD3	Saccharomyces cerevisiae S288C	137-142
11095743-5	2000	Two genes appear to participate in feedback loops that modulate HDAC activity: ZRT1 encodes a zinc transporter and is repressed by RPD3 (Rpd3p is zinc-dependent); BNA1 encodes a nicotinamide adenine dinucleotide (NAD)-biosynthesis enzyme and is repressed by SIR2 (Sir2p is NAD-dependent).	NAD	213-216	high-affinity Zn(2+) transporter ZRT1	Saccharomyces cerevisiae S288C	79-83
11095743-5	2000	Two genes appear to participate in feedback loops that modulate HDAC activity: ZRT1 encodes a zinc transporter and is repressed by RPD3 (Rpd3p is zinc-dependent); BNA1 encodes a nicotinamide adenine dinucleotide (NAD)-biosynthesis enzyme and is repressed by SIR2 (Sir2p is NAD-dependent).	NAD	213-216	histone deacetylase RPD3	Saccharomyces cerevisiae S288C	137-142
11095743-5	2000	Two genes appear to participate in feedback loops that modulate HDAC activity: ZRT1 encodes a zinc transporter and is repressed by RPD3 (Rpd3p is zinc-dependent); BNA1 encodes a nicotinamide adenine dinucleotide (NAD)-biosynthesis enzyme and is repressed by SIR2 (Sir2p is NAD-dependent).	NAD	273-276	high-affinity Zn(2+) transporter ZRT1	Saccharomyces cerevisiae S288C	79-83
11095743-5	2000	Two genes appear to participate in feedback loops that modulate HDAC activity: ZRT1 encodes a zinc transporter and is repressed by RPD3 (Rpd3p is zinc-dependent); BNA1 encodes a nicotinamide adenine dinucleotide (NAD)-biosynthesis enzyme and is repressed by SIR2 (Sir2p is NAD-dependent).	NAD	273-276	histone deacetylase RPD3	Saccharomyces cerevisiae S288C	137-142
11090589-11	2000	The reduced PDH activation with elevated FFA during the rest-to-exercise transition was related to higher mitochondrial NADH at rest and 1 min of exercise and lower muscle pyruvate at rest.	NAD	120-124	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	12-15
11123719-2	2000	The process of poly(ADP-ribosyl)ation in response to DNA damage is mediated by poly(ADP-ribose) polymerase (PARP) and results in NAD+ depletion.	NAD	129-133	poly(ADP-ribose) polymerase 1	Homo sapiens	79-106
11123719-2	2000	The process of poly(ADP-ribosyl)ation in response to DNA damage is mediated by poly(ADP-ribose) polymerase (PARP) and results in NAD+ depletion.	NAD	129-133	poly(ADP-ribose) polymerase 1	Homo sapiens	108-112
11163272-5	2000	The A domain mediates assembly of RIBEYE into large structures, whereas the B domain binds NAD(+) with high affinity, similar to 2-hydroxyacid dehydrogenases.	NAD	91-97	C-terminal binding protein 2	Homo sapiens	34-40
11113971-7	2000	At low demand for NADH reoxidation via glycerol formation, the GPD1, GPD2, GPP1, and GPP2 genes were all expressed at basal levels.	NAD	18-22	glycerol-1-phosphatase RHR2	Saccharomyces cerevisiae S288C	75-79
11074273-6	2000	Formate dehydrogenase from Arabidopsis was partially purified and K(m) values for formate and NAD(+) were determined to be 10 mM and 65 microM, respectively; the K(i) for NADH was 17 microM.	NAD	94-100	formate dehydrogenase	Arabidopsis thaliana	0-21
11074273-6	2000	Formate dehydrogenase from Arabidopsis was partially purified and K(m) values for formate and NAD(+) were determined to be 10 mM and 65 microM, respectively; the K(i) for NADH was 17 microM.	NAD	171-175	formate dehydrogenase	Arabidopsis thaliana	0-21
11074273-7	2000	We conclude that formate dehydrogenase is normally present in Arabidopsis chloroplasts and that sensitivity to inhibition by NADH may play a role in whether cellular formate is assimilated or dissimilated.	NAD	125-129	formate dehydrogenase	Arabidopsis thaliana	17-38
10965046-3	2000	The PARP inhibitor, 3-aminobenzamide (3-ABA), prevents the depletion in NAD(+) and ATP levels and concomitantly protects U937 cells from the lysis that follows ricin treatment.	NAD	72-78	poly(ADP-ribose) polymerase 1	Homo sapiens	4-8
11112844-5	2000	Both the inhibition of repair and the protective effect of nicotinamide against necrotic death indicate that the repair process and related poly(ADP-ribose)polymerase (PARP) activation induce a decrease in intracellular NAD+ and ATP contents below the threshold at which necrosis becomes the preferential mechanism of cell death.	NAD	220-224	poly(ADP-ribose) polymerase 1	Homo sapiens	140-166
11112844-5	2000	Both the inhibition of repair and the protective effect of nicotinamide against necrotic death indicate that the repair process and related poly(ADP-ribose)polymerase (PARP) activation induce a decrease in intracellular NAD+ and ATP contents below the threshold at which necrosis becomes the preferential mechanism of cell death.	NAD	220-224	poly(ADP-ribose) polymerase 1	Homo sapiens	168-172
10973923-2	2000	We previously reported on the ability of TGF-beta1 to activate a cell surface-associated NADH:flavin:O(2) oxidoreductase (NADH oxidase) that generates extracellular H(2)O(2).	NAD	89-93	transforming growth factor beta 1	Homo sapiens	41-50
11198422-1	2000	Quinolate acid phosphoribosyltransferase (QPRTase), a key enzyme in nicotinamide adenine dinucleotide (NAD) biosynthesis, also plays an important role in ensuring nicotinic acid is available for the synthesis of defensive pyridine alkaloids in Nicotiana species.	NAD	68-101	nicotinate-nucleotide pyrophosphorylase [carboxylating], chloroplastic-like	Nicotiana tabacum	42-49
11198422-1	2000	Quinolate acid phosphoribosyltransferase (QPRTase), a key enzyme in nicotinamide adenine dinucleotide (NAD) biosynthesis, also plays an important role in ensuring nicotinic acid is available for the synthesis of defensive pyridine alkaloids in Nicotiana species.	NAD	103-106	nicotinate-nucleotide pyrophosphorylase [carboxylating], chloroplastic-like	Nicotiana tabacum	42-49
10913437-2	2000	A site-directed mutagenesis, D244E, of S-adenosylhomocysteine hydrolase (AdoHcyase) changes drastically the nature of the protein, especially the NAD(+) binding affinity.	NAD	146-152	adenosylhomocysteinase	Rattus norvegicus	39-71
10913437-2	2000	A site-directed mutagenesis, D244E, of S-adenosylhomocysteine hydrolase (AdoHcyase) changes drastically the nature of the protein, especially the NAD(+) binding affinity.	NAD	146-152	adenosylhomocysteinase	Rattus norvegicus	73-82
10987821-1	2000	Using mRNA differential display, we found that the gene for NAD(+)-dependent glycerol phosphate dehydrogenase (GPDH; EC 1.1.1.8) is induced in rat brain following seizure activity.	NAD	60-66	glycerol-3-phosphate dehydrogenase 1	Rattus norvegicus	77-109
10987821-1	2000	Using mRNA differential display, we found that the gene for NAD(+)-dependent glycerol phosphate dehydrogenase (GPDH; EC 1.1.1.8) is induced in rat brain following seizure activity.	NAD	60-66	glycerol-3-phosphate dehydrogenase 1	Rattus norvegicus	111-115
10970744-1	2000	The structure of mouse class II alcohol dehydrogenase (ADH2) has been determined in a binary complex with the coenzyme NADH and in a ternary complex with both NADH and the inhibitor N-cyclohexylformamide to 2.2 A and 2.1 A resolution, respectively.	NAD	119-123	alcohol dehydrogenase 4 (class II), pi polypeptide	Mus musculus	55-59
10970744-1	2000	The structure of mouse class II alcohol dehydrogenase (ADH2) has been determined in a binary complex with the coenzyme NADH and in a ternary complex with both NADH and the inhibitor N-cyclohexylformamide to 2.2 A and 2.1 A resolution, respectively.	NAD	159-163	alcohol dehydrogenase 4 (class II), pi polypeptide	Mus musculus	55-59
10961901-4	2000	The CML cell-mediated inhibition of NK cells required triggering of reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase-mediated formation of reactive oxygen species (ROS) and was prevented by catalase, a scavenger of ROS, and by histamine, acting via H(2)-receptor-mediated inhibition of ROS production in CML cells.	NAD	76-109	catalase	Homo sapiens	209-217
10944198-4	2000	In damaged cells, poly(ADP-ribose) polymerase binds to DNA breaks and automodifies itself in the presence of NAD(+), resulting in poly(ADP-ribose) polymerase inactivation.	NAD	109-115	poly(ADP-ribose) polymerase 1	Homo sapiens	18-45
10944198-4	2000	In damaged cells, poly(ADP-ribose) polymerase binds to DNA breaks and automodifies itself in the presence of NAD(+), resulting in poly(ADP-ribose) polymerase inactivation.	NAD	109-115	poly(ADP-ribose) polymerase 1	Homo sapiens	130-157
10837478-5	2000	PGR/LTB(4)DH catalyzed the NADH-dependent reduction of 15-oxo-LXA(4) to yield 13,14-dihydro-15-oxo-LXA(4).	NAD	27-31	prostaglandin reductase 1	Homo sapiens	4-12
10964654-0	2000	Identification of the NAD(+)-binding fold of glyceraldehyde-3-phosphate dehydrogenase as a novel RNA-binding domain.	NAD	22-28	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	45-85
10964654-5	2000	We established that the N-terminal 43 amino acid residues of GAPDH, which correspond to the first mononucleotide-binding domain of the NAD(+)-binding fold is sufficient to confer RNA-binding.	NAD	135-141	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	61-66
11035256-1	2000	DT-diaphorase, also referred to as NQO1 or NAD(P)H: quinone acceptor oxidoreductase, is a flavoprotein that catalyzes the two-electron reduction of quinones and quinonoid compounds to hydroquinones, using either NADH or NADPH as the electron donor.	NAD	212-216	NAD(P)H quinone dehydrogenase 1	Homo sapiens	0-13
10972187-0	2000	Thermotoga maritima AglA, an extremely thermostable NAD+-, Mn2+-, and thiol-dependent alpha-glucosidase.	NAD	52-56	alpha-glucosidase/alpha-galactosidase	Thermotoga maritima MSB8	86-103
10945628-4	2000	Because poly(ADP-ribose) polymerase (PARP)-mediated NAD+/ATP depletion has been implicated in the nucleoside-induced killing of normal resting lymphocytes, we postulated that this mechanism might account for the p53-independent component of nucleoside cytotoxicity in CLL.	NAD	52-56	poly(ADP-ribose) polymerase 1	Homo sapiens	8-35
10945628-4	2000	Because poly(ADP-ribose) polymerase (PARP)-mediated NAD+/ATP depletion has been implicated in the nucleoside-induced killing of normal resting lymphocytes, we postulated that this mechanism might account for the p53-independent component of nucleoside cytotoxicity in CLL.	NAD	52-56	poly(ADP-ribose) polymerase 1	Homo sapiens	37-41
10945628-4	2000	Because poly(ADP-ribose) polymerase (PARP)-mediated NAD+/ATP depletion has been implicated in the nucleoside-induced killing of normal resting lymphocytes, we postulated that this mechanism might account for the p53-independent component of nucleoside cytotoxicity in CLL.	NAD	52-56	tumor protein p53	Homo sapiens	212-215
10972187-4	2000	The T. maritima alpha-glucosidase has the unusual property of requiring NAD+ and Mn2+ for activity.	NAD	72-76	alpha-glucosidase/alpha-galactosidase	Thermotoga maritima MSB8	16-33
11185961-0	2000	Chain length analysis of ADP-ribose polymers generated by poly(ADP-ribose) polymerase (PARP) as a function of beta-NAD+ and enzyme concentrations.	NAD	110-119	poly(ADP-ribose) polymerase 1	Homo sapiens	58-85
10972187-6	2000	T. maritima AglA represents the first example of a maltodextrin-degrading alpha-glucosidase with NAD+ and Mn2+ requirement.	NAD	97-101	alpha-glucosidase/alpha-galactosidase	Thermotoga maritima MSB8	74-91
11185961-0	2000	Chain length analysis of ADP-ribose polymers generated by poly(ADP-ribose) polymerase (PARP) as a function of beta-NAD+ and enzyme concentrations.	NAD	110-119	poly(ADP-ribose) polymerase 1	Homo sapiens	87-91
11185961-1	2000	Bireactant autopoly(ADP-ribosyl)ation of poly(ADP-ribose) polymerase (PARP) (EC 2.4.2.30) was carried out by using either increasing concentrations of beta-NAD+ (donor substrate) at a fixed protein concentration or increasing concentrations of PARP (acceptor substrate) at a fixed beta-NAD+ concentration.	NAD	151-160	poly(ADP-ribose) polymerase 1	Homo sapiens	41-68
11185961-1	2000	Bireactant autopoly(ADP-ribosyl)ation of poly(ADP-ribose) polymerase (PARP) (EC 2.4.2.30) was carried out by using either increasing concentrations of beta-NAD+ (donor substrate) at a fixed protein concentration or increasing concentrations of PARP (acceptor substrate) at a fixed beta-NAD+ concentration.	NAD	151-160	poly(ADP-ribose) polymerase 1	Homo sapiens	70-74
11185961-1	2000	Bireactant autopoly(ADP-ribosyl)ation of poly(ADP-ribose) polymerase (PARP) (EC 2.4.2.30) was carried out by using either increasing concentrations of beta-NAD+ (donor substrate) at a fixed protein concentration or increasing concentrations of PARP (acceptor substrate) at a fixed beta-NAD+ concentration.	NAD	281-290	poly(ADP-ribose) polymerase 1	Homo sapiens	41-68
11185961-1	2000	Bireactant autopoly(ADP-ribosyl)ation of poly(ADP-ribose) polymerase (PARP) (EC 2.4.2.30) was carried out by using either increasing concentrations of beta-NAD+ (donor substrate) at a fixed protein concentration or increasing concentrations of PARP (acceptor substrate) at a fixed beta-NAD+ concentration.	NAD	281-290	poly(ADP-ribose) polymerase 1	Homo sapiens	70-74
10911953-1	2000	Poly(ADP-ribosyl)ation is a DNA strandbreak-driven posttranslational modification of nuclear proteins that is catalyzed by poly(ADP-ribose) polymerase-1 (PARP-1), with NAD+ serving as substrate.	NAD	168-172	poly(ADP-ribose) polymerase 1	Homo sapiens	123-152
11229527-3	2000	DT-diaphorase also reduces CoQ, although through a two-electron reaction mechanism using both NADH and NADPH, which may be particularly important under oxidative stress conditions.	NAD	94-98	NAD(P)H quinone dehydrogenase 1	Homo sapiens	0-13
10860495-2	2000	When activated by DNA damage, PARP synthesizes poly(ADP-ribose) from NAD.	NAD	69-72	poly(ADP-ribose) polymerase 1	Homo sapiens	30-34
10860495-3	2000	Conventional radioactive PARP enzyme assay requires the separation of the polymer product from the NAD substrate, a rate-limiting step that hampers large-scale chemical library screening to identify novel small-molecule PARP inhibitors.	NAD	99-102	poly(ADP-ribose) polymerase 1	Homo sapiens	25-29
10860495-3	2000	Conventional radioactive PARP enzyme assay requires the separation of the polymer product from the NAD substrate, a rate-limiting step that hampers large-scale chemical library screening to identify novel small-molecule PARP inhibitors.	NAD	99-102	poly(ADP-ribose) polymerase 1	Homo sapiens	220-224
10860495-4	2000	By using biotinylated NAD, we have developed a scintillation proximity assay (SPA) for PARP.	NAD	22-25	poly(ADP-ribose) polymerase 1	Homo sapiens	87-91
10748119-5	2000	SIN-1 (150 micrometer)-mediated oxidation of NADH (200 micrometer) was half-maximally inhibited by low ascorbate concentrations (61-75 micrometer), both in the absence and presence of CO(2).	NAD	45-49	MAPK associated protein 1	Homo sapiens	0-5
10964595-2	2000	Overactivation of PARP by cellular insults depletes its substrate NAD(+) and then ATP, leading to a major energy deficit and cell death.	NAD	66-72	poly(ADP-ribose) polymerase 1	Homo sapiens	18-22
10889035-0	2000	Functional comparison of the NAD binding cleft of ADP-ribosylating toxins.	NAD	29-32	poly(ADP-ribose) polymerase 1	Homo sapiens	50-66
10889035-2	2000	To explain differences in their mechanisms of NAD binding and hydrolysis, the functional interrelationship of residues predicted to perform similar functions in the beta3-strand of the NAD binding cleft of different ADPRT toxins was compared.	NAD	185-188	poly(ADP-ribose) polymerase 1	Homo sapiens	216-221
10911953-1	2000	Poly(ADP-ribosyl)ation is a DNA strandbreak-driven posttranslational modification of nuclear proteins that is catalyzed by poly(ADP-ribose) polymerase-1 (PARP-1), with NAD+ serving as substrate.	NAD	168-172	poly(ADP-ribose) polymerase 1	Homo sapiens	154-160
10818064-13	2000	These findings suggest that an association exists between p22phox gene overexpression and NADH/NADPH overactivity in the aortas of adult SHR.	NAD	90-94	cytochrome b-245 alpha chain	Rattus norvegicus	58-65
10814540-4	2000	MALDI-MS analysis and amino acid sequencing identified the ferric reductase as being related to the 26 kDa liver NADH-dependent quinoid dihydropteridine reductase (DHPR).	NAD	113-117	quinoid dihydropteridine reductase	Homo sapiens	136-162
10814540-4	2000	MALDI-MS analysis and amino acid sequencing identified the ferric reductase as being related to the 26 kDa liver NADH-dependent quinoid dihydropteridine reductase (DHPR).	NAD	113-117	quinoid dihydropteridine reductase	Homo sapiens	164-168
10814540-5	2000	The NADH-dependent DHPR ferric reductase activity was found to be pteridine-independent since exhaustive dialysis did not reduce activity and heat-inactivation destroyed activity.	NAD	4-8	quinoid dihydropteridine reductase	Homo sapiens	19-23
10814540-7	2000	Thus, DHPR appears to be a dual function enzyme, a NADH-dependent dihydopteridine reductase and an iron-regulated, NADH-dependent, pteridine-independent ferric reductase.	NAD	51-55	quinoid dihydropteridine reductase	Homo sapiens	6-10
10699858-5	2000	NAD(H) covalently bound to polyethylene glycol with a molecular weight of 10(4) [PEG-10,000-NAD(H)] was used as coenzyme.	NAD	0-6	paternally expressed 10	Homo sapiens	81-87
10814955-1	2000	Poly(ADP-ribose) polymerase (PARP) catalyzes the transfer of successive units of ADP-ribose moiety from NAD(+) covalently to itself and other nuclear acceptor proteins.	NAD	104-110	poly(ADP-ribose) polymerase 1	Homo sapiens	0-27
10814955-1	2000	Poly(ADP-ribose) polymerase (PARP) catalyzes the transfer of successive units of ADP-ribose moiety from NAD(+) covalently to itself and other nuclear acceptor proteins.	NAD	104-110	poly(ADP-ribose) polymerase 1	Homo sapiens	29-33
10734052-0	2000	Deoxyhypusine synthase generates and uses bound NADH in a transient hydride transfer mechanism.	NAD	48-52	deoxyhypusine synthase	Homo sapiens	0-22
10734052-3	2000	In the initial step of this reaction, deoxyhypusine synthase catalyzes the production of NADH through dehydrogenation of spermidine.	NAD	89-93	deoxyhypusine synthase	Homo sapiens	38-60
10699858-5	2000	NAD(H) covalently bound to polyethylene glycol with a molecular weight of 10(4) [PEG-10,000-NAD(H)] was used as coenzyme.	NAD	92-98	paternally expressed 10	Homo sapiens	81-87
10699858-8	2000	Formate dehydrogenase (FDH) was used for the regeneration of NADH.	NAD	61-65	aldehyde dehydrogenase 1 family member L1	Homo sapiens	0-21
10699858-8	2000	Formate dehydrogenase (FDH) was used for the regeneration of NADH.	NAD	61-65	aldehyde dehydrogenase 1 family member L1	Homo sapiens	23-26
10713134-6	2000	The inhibition of the cellular PARP activity might prevent cellular NAD(+) depletion and stimulate apoptosis by maintaining the basal cellular energy level required for the completion of apoptosis.	NAD	68-74	poly(ADP-ribose) polymerase 1	Homo sapiens	31-35
10683268-7	2000	Nonetheless, GSH was decreased in the FGF-1-transduced cells along with high energy phosphates, adenine nucleotides, NADH, and the redox poise.	NAD	117-121	fibroblast growth factor 1	Homo sapiens	38-43
10662717-7	2000	The increased PDH(a) may have resulted from alterations in the acetyl-CoA, ADP(f), pyruvate, NADH, and H(+) concentrations leading to a lower relative activity of PDH kinase, whereas the similar values at 75% VO(2 max) may have reflected maximal activation.	NAD	93-97	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	14-17
10745276-3	2000	NaDOC induces DNA damage and activates poly(ADP-ribose) polymerase (PARP), an enzyme that utilizes NAD+ as a substrate to repair DNA.	NAD	99-103	poly(ADP-ribose) polymerase 1	Homo sapiens	39-66
10745276-3	2000	NaDOC induces DNA damage and activates poly(ADP-ribose) polymerase (PARP), an enzyme that utilizes NAD+ as a substrate to repair DNA.	NAD	99-103	poly(ADP-ribose) polymerase 1	Homo sapiens	68-72
10662717-7	2000	The increased PDH(a) may have resulted from alterations in the acetyl-CoA, ADP(f), pyruvate, NADH, and H(+) concentrations leading to a lower relative activity of PDH kinase, whereas the similar values at 75% VO(2 max) may have reflected maximal activation.	NAD	93-97	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	163-166
10597301-1	1999	Poly(ADP-ribose) polymerase (PARP4) catalyzes the formation of ADP-ribose polymers covalently attached to proteins by using NAD+ as substrate.	NAD	124-128	poly(ADP-ribose) polymerase 1	Homo sapiens	0-27
10562410-3	1999	The aim of this study was to investigate the effect of interferon-gamma treatment on intracellular NAD concentration in the murine macrophage cell line, RAW 264.7.	NAD	99-102	interferon gamma	Mus musculus	55-71
10562410-4	1999	A significant increase in intracellular NAD concentration was observed following 24 h exposure to interferon-gamma.	NAD	40-43	interferon gamma	Mus musculus	98-114
11205159-3	2000	As part of the conversion, GAPDH converts NAD+ to the high-energy electron carrier NADH.	NAD	42-46	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	27-32
11205159-3	2000	As part of the conversion, GAPDH converts NAD+ to the high-energy electron carrier NADH.	NAD	83-87	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	27-32
10939283-2	2000	Inflammation within the CNS increases the concentration of oxidative metabolites and, therefore, the potential for NAD depletion through increased poly-(ADP-ribose) polymerase (PARP) activity.	NAD	115-118	poly(ADP-ribose) polymerase 1	Homo sapiens	147-175
10939283-2	2000	Inflammation within the CNS increases the concentration of oxidative metabolites and, therefore, the potential for NAD depletion through increased poly-(ADP-ribose) polymerase (PARP) activity.	NAD	115-118	poly(ADP-ribose) polymerase 1	Homo sapiens	177-181
10939283-6	2000	Intracellular NAD levels also increased significantly after treatment with IFN-gamma in the presence of a PARP inhibitor.	NAD	14-17	interferon gamma	Homo sapiens	75-84
10939283-6	2000	Intracellular NAD levels also increased significantly after treatment with IFN-gamma in the presence of a PARP inhibitor.	NAD	14-17	poly(ADP-ribose) polymerase 1	Homo sapiens	106-110
10939283-7	2000	Pretreatment of astroglial cells with IFN-gamma significantly moderated both the drop in intracellular NAD concentration and cell death following exposure to hydrogen peroxide.	NAD	103-106	interferon gamma	Homo sapiens	38-47
10585740-3	1999	Eight factors influenced CYP3A4-mediated NIF activity: buffer type, pH, temperature, Mg/EDTA, cytochrome b5, NADPH-P450 reductase, NADH, and solvent.	NAD	131-135	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	25-31
10562410-8	1999	These results provide evidence for the first time that de novo synthesis of NAD from tryptophan is increased concomitantly with free radical production in RAW 264.7 macrophages stimulated with interferon-gamma.	NAD	76-79	interferon gamma	Mus musculus	193-209
10597301-1	1999	Poly(ADP-ribose) polymerase (PARP4) catalyzes the formation of ADP-ribose polymers covalently attached to proteins by using NAD+ as substrate.	NAD	124-128	poly(ADP-ribose) polymerase family member 4	Homo sapiens	29-34
10564760-3	1999	Electron paramagnetic resonance studies confirm that BQ-II is reductively activated by NADH:cytochrome c reductase to superoxide anion radical.	NAD	87-91	cytochrome c, somatic	Homo sapiens	92-104
10551851-4	1999	Recombinant MVDP was functional and displayed kinetic properties distinct from those of murine AR toward various substrates, a preference for NADH, and insensitivity to AR inhibitors.	NAD	142-146	aldo-keto reductase family 1, member B7	Mus musculus	12-16
10551851-7	1999	We demonstrate that in Y1 cells, forskolin-induced MVDP expression enhanced NADH-linked ICR activity by 5-6-fold, whereas no variation in ICR-linked NADPH activity was observed in the same experiment.	NAD	76-80	aldo-keto reductase family 1, member B7	Mus musculus	51-55
10551851-8	1999	In cells stably transfected with MVDP antisense cDNA, NADH-linked ICR activity was abolished even in the presence of forskolin, and the isocaproaldehyde toxicity was increased compared with that of intact Y1 cells, as measured by isocaproaldehyde LD(50).	NAD	54-58	aldo-keto reductase family 1, member B7	Mus musculus	33-37
10615405-0	1999	Angiotensin II-induced superoxide anion generation in human vascular endothelial cells: role of membrane-bound NADH-/NADPH-oxidases.	NAD	111-115	angiotensinogen	Homo sapiens	0-14
10516124-9	1999	Reduced PDH activity occurred with ACID and may have resulted from alterations in the concentrations of acetyl-CoA, free ADP, pyruvate, NADH, and H(+), leading to greater relative activity of the kinase.	NAD	136-140	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	8-11
10614722-9	1999	CONCLUSIONS: A cytotoxic mechanism was proposed where the sustained increase in NADH levels, resulting from ethanol metabolism, maintains CYP2E1 in a more reduced state that increases ROS formation.	NAD	80-84	cytochrome P450 family 2 subfamily E member 1	Homo sapiens	138-144
10697561-5	1999	The identification of DNA-fragmentation and p53 and Ki-67 genes expression suggest that the mechanism of NADH action is different from disregulation of genes considered as check-points in cell cycle.	NAD	105-109	tumor protein p53	Homo sapiens	44-47
10615405-9	1999	In addition, our lucigenin-enhanced chemiluminescence assay showed that the activity of plasma membrane-bound NADH-/NADPH-oxidases derived from ANG II-treated cells was also significantly increased, this effect was reduced in cells pretreated with losartan or to lesser extent by PD123319.	NAD	110-114	angiotensinogen	Homo sapiens	144-150
10615405-12	1999	CONCLUSION: ANG II induces O2- release in HVECs via activation of membrane-bound NADH-/NADPH-oxidase, an effect, that is mediated by both AT-1 and AT-2 receptors.	NAD	81-85	angiotensinogen	Homo sapiens	12-18
10455133-12	1999	First, the efficiency of NADH oxidation increased to 60-90% regardless of the presence of HCO(3)(-)/CO(2), along with an increase of H(2)O(2) formation to about 23 and 35% relative to the amounts of added SIN-1 and NADH.	NAD	25-29	MAPK associated protein 1	Homo sapiens	205-210
10548046-6	1999	Presented here are the corrected amino acid sequence and the high resolution crystal structure determined for pig heart SCHAD complexed with its NAD+ cofactor (2.8 A; R(cryst) = 22.4%, R(free) = 28.8%).	NAD	145-149	hydroxyacyl-CoA dehydrogenase	Homo sapiens	120-125
10471325-2	1999	Activation of poly(ADP-ribose) polymerase (PARP) occurs early in oxidant-induced EC injury and putatively mediates cell death by depleting its substrate, NAD(+).	NAD	154-160	poly(ADP-ribose) polymerase 1	Homo sapiens	14-41
10471325-2	1999	Activation of poly(ADP-ribose) polymerase (PARP) occurs early in oxidant-induced EC injury and putatively mediates cell death by depleting its substrate, NAD(+).	NAD	154-160	poly(ADP-ribose) polymerase 1	Homo sapiens	43-47
10455133-13	1999	Second, and more interesting, the peroxynitrite scavenger glutathione (GSH) was needed in a 75-fold surplus to inhibit the SIN-1-dependent oxidation of NADH half-maximal in the presence of HCO(3)(-)/CO(2).	NAD	152-156	MAPK associated protein 1	Homo sapiens	123-128
10486578-4	1999	On the basis of previous findings obtained in the same neuronal population undergoing excitotoxic death, it is hypothesized that release of cyt c may be part of a cellular attempt to maintain production of ATP via cytochrome oxidase, which is reduced by cytosolic NADH in a cytochrome b5-soluble cyt c-mediated fashion.	NAD	264-268	cytochrome c, somatic	Homo sapiens	140-145
10391925-5	1999	This effect of thrombin was accompanied by increased O-2 and H2O2 generation and NADH/NADPH consumption.	NAD	81-85	coagulation factor II, thrombin	Homo sapiens	15-23
10438458-5	1999	This inactivation of PARP has been proposed to prevent depletion of NAD (a PARP substrate) and ATP, which are thought to be required for later events in apoptosis.	NAD	68-71	poly(ADP-ribose) polymerase 1	Homo sapiens	21-25
10419545-5	1999	With NADH as the electron donor and menadione as the electron acceptor, the k(cat) values for the wild-type human DT-diaphorase, hY155F, hH161Q, and hP187S were measured as 66 +/- 1, 23 +/- 0, 5 +/- 0 and 8 +/- 2 x 10(3) min(-1), respectively.	NAD	5-9	NAD(P)H quinone dehydrogenase 1	Homo sapiens	114-127
10423172-3	1999	Both FAA and DMXAA are competitive inhibitors of the enzyme DT-diaphorase (NAD(P)H:Quinone oxidoreductase EC 1.6.99.2) with respect to NADH, with Ki values of 75 and 20 microM, respectively.	NAD	135-139	NAD(P)H quinone dehydrogenase 1	Homo sapiens	60-73
10391884-0	1999	Thiols mediate superoxide-dependent NADH modification of glyceraldehyde-3-phosphate dehydrogenase.	NAD	36-40	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	57-97
10391884-1	1999	Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) is covalently modified by NAD in the presence of nitric oxide (NO) and dithiothreitol.	NAD	75-78	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	0-40
10391884-1	1999	Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) is covalently modified by NAD in the presence of nitric oxide (NO) and dithiothreitol.	NAD	75-78	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	42-47
10438458-5	1999	This inactivation of PARP has been proposed to prevent depletion of NAD (a PARP substrate) and ATP, which are thought to be required for later events in apoptosis.	NAD	68-71	poly(ADP-ribose) polymerase 1	Homo sapiens	75-79
10391884-9	1999	Thus, linkage of GAPDH to NADH, in contrast to NAD, occurs in the presence of thiol, is independent of NO, and is mediated by superoxide.	NAD	26-30	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	17-22
10391884-9	1999	Thus, linkage of GAPDH to NADH, in contrast to NAD, occurs in the presence of thiol, is independent of NO, and is mediated by superoxide.	NAD	26-29	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	17-22
10398706-0	1999	Simultaneous expression of NAD-dependent isocitrate dehydrogenase and other krebs cycle genes after nitrate resupply to short-term nitrogen-starved tobacco Mitochondrial NAD-dependent (IDH) and cytosolic NADP-dependent isocitrate dehydrogenases have been considered as candidates for the production of 2-oxoglutarate required by the glutamine synthetase/glutamate synthase cycle.	NAD	28-31	isocitrate dehydrogenase [NADP]	Nicotiana tabacum	186-189
10373561-1	1999	Activation of poly(ADP-ribose) polymerase (PARP) by DNA breaks catalyzes poly(ADP-ribosyl)ation and results in depletion of NAD+ and ATP, which is thought to induce necrosis.	NAD	124-128	poly(ADP-ribose) polymerase 1	Homo sapiens	14-41
10373561-1	1999	Activation of poly(ADP-ribose) polymerase (PARP) by DNA breaks catalyzes poly(ADP-ribosyl)ation and results in depletion of NAD+ and ATP, which is thought to induce necrosis.	NAD	124-128	poly(ADP-ribose) polymerase 1	Homo sapiens	43-47
10373561-5	1999	This enhanced cell death is attributable to the induction of necrosis and an increased apoptosis and was coupled with depletion of NAD+ and ATP that occurred only in cells expressing caspase-resistant PARP.	NAD	131-135	poly(ADP-ribose) polymerase 1	Homo sapiens	201-205
10373561-6	1999	The PARP inhibitor 3-aminobenzamide prevented the NAD+ drop and concomitantly inhibited necrosis and the elevated apoptosis.	NAD	50-54	poly(ADP-ribose) polymerase 1	Homo sapiens	4-8
10373561-7	1999	These data indicate that this accelerated cell death is due to NAD+ depletion, a mechanism known to kill various cell types, caused by activation of uncleaved PARP after DNA fragmentation.	NAD	63-67	poly(ADP-ribose) polymerase 1	Homo sapiens	159-163
10391884-2	1999	Replacement of NAD with NADH in the presence of SIN-1 (3-morpholinosydnonimine) and dithiothreitol increased modification 25-fold.	NAD	15-18	MAPK associated protein 1	Homo sapiens	48-53
10391884-2	1999	Replacement of NAD with NADH in the presence of SIN-1 (3-morpholinosydnonimine) and dithiothreitol increased modification 25-fold.	NAD	24-28	MAPK associated protein 1	Homo sapiens	48-53
10391884-3	1999	We now demonstrate that in contrast to NO-mediated attachment of NAD, covalent attachment of NADH to GAPDH proceeds in the presence of low molecular weight thiols, independent of NO.	NAD	93-97	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	101-106
10391884-5	1999	Electrospray mass spectrometry showed covalent linkage of the NADH molecule to GAPDH.	NAD	62-66	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	79-84
10391884-6	1999	Characterization of the product of phosphodiesterase cleavage demonstrated that linkage to GAPDH occurred through the nicotinamide of NADH.	NAD	134-138	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	91-96
10391884-7	1999	Lys-C digestion of GAPDH, followed by peptide isolation by high performance liquid chromatography, matrix-assisted laser desorption ionization time-of-flight analysis, and Edman sequencing, demonstrated that NADH attachment occurred at Cys-149, the active-site thiol.	NAD	208-212	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	19-24
10383895-2	1999	We speculate that other loci that determine response to oxidative stress, such as NAD(H):quinone oxidoreductase (NQO1) are candidates.	NAD	82-88	NAD(P)H quinone dehydrogenase 1	Homo sapiens	113-117
10398706-0	1999	Simultaneous expression of NAD-dependent isocitrate dehydrogenase and other krebs cycle genes after nitrate resupply to short-term nitrogen-starved tobacco Mitochondrial NAD-dependent (IDH) and cytosolic NADP-dependent isocitrate dehydrogenases have been considered as candidates for the production of 2-oxoglutarate required by the glutamine synthetase/glutamate synthase cycle.	NAD	28-31	glutamine synthetase	Nicotiana tabacum	334-354
10362112-6	1999	This suggested that our results were due to inhibition of glyceraldehyde-3-phosphate dehydrogenase, possibly as a consequence of NAD depletion following poly(ADP-ribose) polymerase activation.	NAD	129-132	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	58-98
10356292-9	1999	When NADH was used as a substrate, lucigenin inhibited the SOD-dependent component of cytochrome c reduction and enhanced both the SOD-independent cytochrome c reduction and NADH oxidation, being a sole acceptor of an electron from the enzyme.	NAD	5-9	cytochrome c, somatic	Homo sapiens	86-98
10381378-8	1999	Recombinant E. coli cobB and human SIRT2 sirtuin proteins were able to cause radioactivity to be transferred from [32P]NAD to bovine serum albumin (BSA).	NAD	119-122	albumin	Homo sapiens	133-146
10364460-1	1999	The nuclear enzyme poly(ADP-ribosyl) transferase (pADPRT) catalyzes the formation of poly(ADP-ribose) from NAD+.	NAD	107-111	poly(ADP-ribose) polymerase 1	Homo sapiens	19-48
10364460-1	1999	The nuclear enzyme poly(ADP-ribosyl) transferase (pADPRT) catalyzes the formation of poly(ADP-ribose) from NAD+.	NAD	107-111	poly(ADP-ribose) polymerase 1	Homo sapiens	50-56
10366509-1	1999	Drosophila alcohol dehydrogenase (DADH) is an NAD+-dependent enzyme that catalyzes the oxidation of alcohols to aldehydes/ketones.	NAD	46-50	Alcohol dehydrogenase	Drosophila melanogaster	0-32
10366509-1	1999	Drosophila alcohol dehydrogenase (DADH) is an NAD+-dependent enzyme that catalyzes the oxidation of alcohols to aldehydes/ketones.	NAD	46-50	Alcohol dehydrogenase	Drosophila melanogaster	34-38
10366509-15	1999	The p Kavalue of 9-9.5 obtained by kinetic measurements on apo DADH can be assigned to a protonated Tyr151 which is converted to an unprotonated tyrosinate (p Ka7.6) by the influence of the positively charged nicotinamide ring in the binary enzyme-NAD+form.	NAD	248-252	Alcohol dehydrogenase	Drosophila melanogaster	63-67
10231530-1	1999	Human heart short chain L-3-hydroxyacyl-CoA dehydrogenase (SCHAD) catalyzes the oxidation of the hydroxyl group of L-3-hydroxyacyl-CoA to a keto group, concomitant with the reduction of NAD+ to NADH, as part of the beta-oxidation pathway.	NAD	186-190	hydroxyacyl-CoA dehydrogenase	Homo sapiens	12-57
10231530-1	1999	Human heart short chain L-3-hydroxyacyl-CoA dehydrogenase (SCHAD) catalyzes the oxidation of the hydroxyl group of L-3-hydroxyacyl-CoA to a keto group, concomitant with the reduction of NAD+ to NADH, as part of the beta-oxidation pathway.	NAD	186-190	hydroxyacyl-CoA dehydrogenase	Homo sapiens	59-64
10231530-1	1999	Human heart short chain L-3-hydroxyacyl-CoA dehydrogenase (SCHAD) catalyzes the oxidation of the hydroxyl group of L-3-hydroxyacyl-CoA to a keto group, concomitant with the reduction of NAD+ to NADH, as part of the beta-oxidation pathway.	NAD	194-198	hydroxyacyl-CoA dehydrogenase	Homo sapiens	12-57
10231530-1	1999	Human heart short chain L-3-hydroxyacyl-CoA dehydrogenase (SCHAD) catalyzes the oxidation of the hydroxyl group of L-3-hydroxyacyl-CoA to a keto group, concomitant with the reduction of NAD+ to NADH, as part of the beta-oxidation pathway.	NAD	194-198	hydroxyacyl-CoA dehydrogenase	Homo sapiens	59-64
10231530-3	1999	The dissociation constants of NAD+ and NADH have been determined over a broad pH range and indicate that SCHAD binds reduced cofactor preferentially.	NAD	30-34	hydroxyacyl-CoA dehydrogenase	Homo sapiens	105-110
10231530-3	1999	The dissociation constants of NAD+ and NADH have been determined over a broad pH range and indicate that SCHAD binds reduced cofactor preferentially.	NAD	39-43	hydroxyacyl-CoA dehydrogenase	Homo sapiens	105-110
10231530-5	1999	The crystal structure of SCHAD complexed with NAD+ has been solved using multiwavelength anomalous diffraction techniques and a selenomethionine-substituted analogue of the enzyme.	NAD	46-50	hydroxyacyl-CoA dehydrogenase	Homo sapiens	25-30
10092604-4	1999	In agreement with our previous findings, the following results were obtained: (i) When ISP/cytochrome c1 were prereduced or SMP were treated with a P-side inhibitor, the high potential heme bH was fully and rapidly reduced by NADH or succinate, whereas the low potential heme bL was only partially reduced.	NAD	226-230	cytochrome c1	Bos taurus	91-104
10334203-5	1999	Using 32P-5"-end-labeled DNA fragments obtained from human p53 tumor suppressor gene and c-Ha-ras-1 protooncogene, we showed that PBQ plus NADH, and also PHQ, induced DNA damage frequently at thymine residues, in the presence of Cu(II).	NAD	139-143	tumor protein p53	Homo sapiens	59-62
10100603-1	1999	Poly(ADP-ribose)polymerase is a nuclear NAD-dependent enzyme and an essential nick sensor involved in cellular processes where nicking and rejoining of DNA strands are required.	NAD	40-43	poly(ADP-ribose) polymerase 1	Homo sapiens	0-26
10082530-1	1999	Mammalian poly(ADP-ribose) polymerase (PARP) is a nuclear chromatin-associated protein with a molecular mass of 114 kDa that catalyzes the transfer of ADP-ribose units from NAD+ to nuclear proteins that are located within chromatin.	NAD	173-177	poly(ADP-ribose) polymerase 1	Homo sapiens	10-37
10082530-1	1999	Mammalian poly(ADP-ribose) polymerase (PARP) is a nuclear chromatin-associated protein with a molecular mass of 114 kDa that catalyzes the transfer of ADP-ribose units from NAD+ to nuclear proteins that are located within chromatin.	NAD	173-177	poly(ADP-ribose) polymerase 1	Homo sapiens	39-43
10322503-2	1999	Excessive activation of PARP, however, can deplete tissue stores of nicotinamide adenine dinucleotide (NAD), the PARP substrate which, with the resultant depletion of ATP, leads to cell death.	NAD	68-101	poly(ADP-ribose) polymerase 1	Homo sapiens	24-28
10322503-2	1999	Excessive activation of PARP, however, can deplete tissue stores of nicotinamide adenine dinucleotide (NAD), the PARP substrate which, with the resultant depletion of ATP, leads to cell death.	NAD	68-101	poly(ADP-ribose) polymerase 1	Homo sapiens	113-117
10322503-2	1999	Excessive activation of PARP, however, can deplete tissue stores of nicotinamide adenine dinucleotide (NAD), the PARP substrate which, with the resultant depletion of ATP, leads to cell death.	NAD	103-106	poly(ADP-ribose) polymerase 1	Homo sapiens	24-28
10322503-2	1999	Excessive activation of PARP, however, can deplete tissue stores of nicotinamide adenine dinucleotide (NAD), the PARP substrate which, with the resultant depletion of ATP, leads to cell death.	NAD	103-106	poly(ADP-ribose) polymerase 1	Homo sapiens	113-117
10100603-4	1999	We now describe a novel protein that includes (i) a so-called BRCT domain found in many proteins involved in DNA repair, (ii) an area that is homologous to the NAD-dependent catalytic domain of poly(ADP-ribose)polymerase, (iii) an area that is homologous to the upper two thirds of precursor polypeptides H1P-H4P and (iv) a proline-rich region with a potential nuclear localization signal.	NAD	160-163	poly(ADP-ribose) polymerase 1	Homo sapiens	194-220
10103001-8	1999	O2.- and H2O2 can be produced by the oxidase reaction of horseradish peroxidase in the presence of NADH.	NAD	99-103	peroxidase	Glycine max	69-79
10097894-6	1999	Suppression of PARP activity by nicotinamide not only decreases consumption of NAD+, the substrate of PARP, but also has major regulatory effects on gene expression, as shown for the major histocompatibility complex class II gene.	NAD	79-83	poly(ADP-ribose) polymerase 1	Homo sapiens	15-19
10097894-6	1999	Suppression of PARP activity by nicotinamide not only decreases consumption of NAD+, the substrate of PARP, but also has major regulatory effects on gene expression, as shown for the major histocompatibility complex class II gene.	NAD	79-83	poly(ADP-ribose) polymerase 1	Homo sapiens	102-106
10037463-10	1999	Sodium nitroprusside-induced NAD labeling of nuclear GAPDH showed a 60% loss of GAPDH labeling after AraC treatment, suggesting that the active site of GAPDH may be covalently modified, denatured, or improperly folded.	NAD	29-32	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	53-58
10218656-1	1999	We report that a lactoperoxidase (LPO) metabolite derived from nitrite (NO2-) catalyses one-electron oxidation of biological electron donors and antioxidants such as NADH, NADPH, cysteine, glutathione, ascorbate, and Trolox C.	NAD	166-170	lactoperoxidase	Homo sapiens	17-32
10218656-1	1999	We report that a lactoperoxidase (LPO) metabolite derived from nitrite (NO2-) catalyses one-electron oxidation of biological electron donors and antioxidants such as NADH, NADPH, cysteine, glutathione, ascorbate, and Trolox C.	NAD	166-170	lactoperoxidase	Homo sapiens	34-37
10037463-10	1999	Sodium nitroprusside-induced NAD labeling of nuclear GAPDH showed a 60% loss of GAPDH labeling after AraC treatment, suggesting that the active site of GAPDH may be covalently modified, denatured, or improperly folded.	NAD	29-32	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	80-85
10037463-10	1999	Sodium nitroprusside-induced NAD labeling of nuclear GAPDH showed a 60% loss of GAPDH labeling after AraC treatment, suggesting that the active site of GAPDH may be covalently modified, denatured, or improperly folded.	NAD	29-32	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	80-85
11864456-4	1999	Activity of poly (ADP-ribose) polymerase (PARP) was determined by [(3)H]-NAD incorporating method.	NAD	73-76	poly(ADP-ribose) polymerase 1	Homo sapiens	12-40
10331640-2	1999	We show that nicotinamide and the resulting cellular NAD concentration modulate expression of the tumor suppressor protein, p53, in human breast, skin, and lung cells.	NAD	53-56	tumor protein p53	Homo sapiens	124-127
10331640-5	1999	Since NAD is important in modulating ADP-ribose polymer metabolism, cyclic ADP-ribose synthesis, and stress response proteins, such as p53, following DNA damage, understanding how NAD metabolism is regulated in the human has important implications in developing both prevention and treatment strategies in carcinogenesis.	NAD	6-9	tumor protein p53	Homo sapiens	135-138
10331640-5	1999	Since NAD is important in modulating ADP-ribose polymer metabolism, cyclic ADP-ribose synthesis, and stress response proteins, such as p53, following DNA damage, understanding how NAD metabolism is regulated in the human has important implications in developing both prevention and treatment strategies in carcinogenesis.	NAD	180-183	tumor protein p53	Homo sapiens	135-138
10331646-8	1999	These findings are consistent with the existence at the carboxyl terminus of ART1 of a catalytically active domain, capable of hydrolyzing NAD, but not of transferring ADP-ribose to a guanidino acceptor.	NAD	139-142	ADP-ribosyltransferase 1	Homo sapiens	77-81
10082668-0	1999	The NAD+ precursors, nicotinic acid and nicotinamide upregulate glyceraldehyde-3-phosphate dehydrogenase and glucose-6-phosphate dehydrogenase mRNA in Jurkat cells.	NAD	4-8	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	64-104
10082668-4	1999	Our findings suggest that the NAD+ precursors may protect against oxidative stress and DNA damage by up-regulating the stress response genes GAPDH and G6PD.	NAD	30-34	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	141-146
10331651-6	1999	On the other hand, in a reconstituted reaction system, purified PARP from human placenta suppressed the pRB-phosphorylation activity in the presence of NAD and damaged DNA.	NAD	152-155	poly(ADP-ribose) polymerase 1	Homo sapiens	64-68
11864456-4	1999	Activity of poly (ADP-ribose) polymerase (PARP) was determined by [(3)H]-NAD incorporating method.	NAD	73-76	poly(ADP-ribose) polymerase 1	Homo sapiens	42-46
9895226-7	1999	The data obtained suggests that: (1) expression of ADH and XOR or AOX in breast tissue provides the enzymes that generate ROS; (2) metabolism of alcohol produces acetaldehyde and NADH that can both be substrates for XOR or AOX and thereby result in ROS formation; and (3) ROS generated by XOR or AOX can induce the carcinogenic mutations and DNA damage found in breast cancer.	NAD	179-183	aldehyde oxidase 1	Homo sapiens	66-69
9895226-7	1999	The data obtained suggests that: (1) expression of ADH and XOR or AOX in breast tissue provides the enzymes that generate ROS; (2) metabolism of alcohol produces acetaldehyde and NADH that can both be substrates for XOR or AOX and thereby result in ROS formation; and (3) ROS generated by XOR or AOX can induce the carcinogenic mutations and DNA damage found in breast cancer.	NAD	179-183	aldehyde oxidase 1	Homo sapiens	223-226
9895226-7	1999	The data obtained suggests that: (1) expression of ADH and XOR or AOX in breast tissue provides the enzymes that generate ROS; (2) metabolism of alcohol produces acetaldehyde and NADH that can both be substrates for XOR or AOX and thereby result in ROS formation; and (3) ROS generated by XOR or AOX can induce the carcinogenic mutations and DNA damage found in breast cancer.	NAD	179-183	aldehyde oxidase 1	Homo sapiens	223-226
10216966-8	1999	The K(m) and Vmax values for the cofactor NADH in the presence of saturating concentration of cytochrome b5 were found to be 0.0017 mM NADH and 6944 nmol cytochrome b5 reduced/min/mg enzyme, respectively.	NAD	42-46	cytochrome b5	Ovis aries	94-107
10216966-8	1999	The K(m) and Vmax values for the cofactor NADH in the presence of saturating concentration of cytochrome b5 were found to be 0.0017 mM NADH and 6944 nmol cytochrome b5 reduced/min/mg enzyme, respectively.	NAD	42-46	cytochrome b5	Ovis aries	154-167
10196734-5	1999	The deduced amino acid sequence of the cDNA shared 60% identity with sheep NAD(+)-dependent sorbitol dehydrogenase (SDH).	NAD	75-81	L-iditol 2-dehydrogenase	Ovis aries	92-114
10216966-8	1999	The K(m) and Vmax values for the cofactor NADH in the presence of saturating concentration of cytochrome b5 were found to be 0.0017 mM NADH and 6944 nmol cytochrome b5 reduced/min/mg enzyme, respectively.	NAD	135-139	cytochrome b5	Ovis aries	94-107
10196734-5	1999	The deduced amino acid sequence of the cDNA shared 60% identity with sheep NAD(+)-dependent sorbitol dehydrogenase (SDH).	NAD	75-81	L-iditol 2-dehydrogenase	Ovis aries	116-119
9930932-2	1999	CD38 has both ADP-ribosyl cyclase, which catalyzes the formation of cyclic ADP-ribose from NAD+, and cyclic ADP-ribose hydrolase, which converts cyclic ADP-ribose to ADP-ribose.	NAD	91-95	CD38 molecule	Rattus norvegicus	0-4
9920281-4	1999	Inhibition of poly(ADP-ribose) polymerase (PARP, EC 2.4.2.30) by 3-aminobenzamide prevented the depletion of NAD+.	NAD	109-113	poly(ADP-ribose) polymerase 1	Homo sapiens	14-41
9920281-4	1999	Inhibition of poly(ADP-ribose) polymerase (PARP, EC 2.4.2.30) by 3-aminobenzamide prevented the depletion of NAD+.	NAD	109-113	poly(ADP-ribose) polymerase 1	Homo sapiens	43-47
9920281-7	1999	The chelation of intracellular calcium by bis-(o-aminophenoxy)-ethane-N,N,N1,N1-tetraacidic acid/tetraacetoxymethyl) ester also prevented the dramatic loss of NAD+, demonstrating that Ca2+ is an activating factor in PARP-mediated cell killing.	NAD	159-163	poly(ADP-ribose) polymerase 1	Homo sapiens	216-220
9989455-15	1999	Over-activation of PARP, with resulting depletion of NAD+, has been shown to make a major contribution to brain damage after transient focal ischemia in experimental animals.	NAD	53-57	poly(ADP-ribose) polymerase 1	Homo sapiens	19-23
10071053-1	1999	Experimental studies indicate that overactivation of the DNA repair protein poly(ADP-ribose) polymerase (PARP) in response to oxidative damage to DNA can cause cell death due to depletion of NAD+.	NAD	191-195	poly(ADP-ribose) polymerase 1	Homo sapiens	76-103
10071053-1	1999	Experimental studies indicate that overactivation of the DNA repair protein poly(ADP-ribose) polymerase (PARP) in response to oxidative damage to DNA can cause cell death due to depletion of NAD+.	NAD	191-195	poly(ADP-ribose) polymerase 1	Homo sapiens	105-109
16232608-0	1999	Effect of NAD+-dependent isocitrate dehydrogenase gene (IDH1, IDH2) disruption of sake yeast on organic acid composition in sake mash.	NAD	10-14	isocitrate dehydrogenase (NAD(+)) IDH1	Saccharomyces cerevisiae S288C	56-60
10445046-1	1999	Dimethyl sulfoxide (DMSO), a solvent popularly used for dissolving water-insoluble compounds, is a weak inhibitor of poly(ADP-ribose) synthetase, that is a nuclear enzyme producing (ADP-ribose)n from NAD+.	NAD	200-204	poly(ADP-ribose) polymerase 1	Homo sapiens	117-144
9880378-4	1999	The recombinant NADH-Cyt b5 reductase was functionally active and displayed strict specificity to NADH for the reduction of a recombinant Cyt b5 (AtB5-A), whereas no Cyt b5 reduction was observed when NADPH was used as the electron donor.	NAD	16-20	cytochrome B5 	Arabidopsis thaliana	146-152
9893134-0	1999	Increased NAD(P)H oxidase-mediated superoxide production in renovascular hypertension: evidence for an involvement of protein kinase C. BACKGROUND: Angiotensin II infusion has been shown to cause hypertension and endothelial dysfunction and to increase superoxide (O-.2) production in vascular tissue, mainly via an activation of nicotinamide adenine dinucleotide (phosphate) [NAD(P)H]-dependent oxidase, the most significant O-.2 source in endothelial and/or smooth muscle cells.	NAD	330-363	angiotensinogen	Rattus norvegicus	148-162
9851831-5	1998	Glycerol-3-phosphate dehydrogenase purified from muscle cytosol contains tightly bound NADH-X, NAD, and ADP-ribose, each in amounts of about 0.1 mol per mole of enzyme polypeptide chain.	NAD	87-90	glycerol-3-phosphate dehydrogenase 1	Rattus norvegicus	0-34
10232052-3	1999	11 beta-HSD2 is a high affinity NAD-dependent dehydrogenase that protects the mineralocorticoid receptor from glucocorticoid excess; mutations in the HSD11B2 gene explain an inherited form of hypertension, the syndrome of apparent mineralocorticoid excess in which cortisol acts as a potent mineralocorticoid.	NAD	32-35	hydroxysteroid 11-beta dehydrogenase 1	Homo sapiens	0-7
9722602-2	1998	We have previously described a cell surface-associated H2O2-generating NADH:flavin:O2 oxidoreductase (referred to as NADH oxidase) activity in human lung fibroblasts induced by TGF-beta1 (Thannickal, V. J., and Fanburg, B. L. (1995) J. Biol.	NAD	71-75	transforming growth factor beta 1	Homo sapiens	177-186
9841866-0	1998	Molecular characterization and expression of the gene for mouse NAD+:arginine ecto-mono(ADP-ribosyl)transferase, Art1.	NAD	64-68	ADP-ribosyltransferase 1	Mus musculus	113-117
9865591-6	1998	On the other hand, stimulators of H2O2 generation (xanthine oxidase, glucose oxidase, NADH, NADPH) lowered Epo production in hypoxic cultures.	NAD	86-90	erythropoietin	Homo sapiens	107-110
9853008-7	1998	Thus, the possibility exists that activation of PARP leads to NAD+ depletion and thereby alters mitochondrial redox status.	NAD	62-66	poly(ADP-ribose) polymerase 1	Homo sapiens	48-52
9735295-4	1998	The initial model was improved by crystallographic refinement accompanied by electron density averaging, R-factor=20.5%, R-free=23.8%.DADH subunits show an alpha/beta single domain structure with a characteristic NAD(H) binding motif (Rossmann fold).	NAD	213-219	Alcohol dehydrogenase	Drosophila melanogaster	134-138
9850147-1	1998	In the infant brain, ischemia-induced ionic and enzyme mechanisms may independently lead to cell death by energy depletion: resequestration of calcium mobilized from intracellular stores consumes ATP, and activated poly(ADP-ribose) polymerase (PARP) uses oxidized nicotinamide adenine dinucleotide to form polyADP-ribosyl nuclear proteins associated with DNA damage.	NAD	264-297	poly(ADP-ribose) polymerase 1	Homo sapiens	215-242
9823314-8	1998	Although p53 was not endogenously poly (ADP-ribosyl)ated in situ, incubation of cell extracts with full-length PARP from calf thymus and [32P]beta NAD+ resulted in its time-dependent poly(ADP-ribosyl)ation.	NAD	147-151	tumor protein p53	Homo sapiens	9-12
9823314-8	1998	Although p53 was not endogenously poly (ADP-ribosyl)ated in situ, incubation of cell extracts with full-length PARP from calf thymus and [32P]beta NAD+ resulted in its time-dependent poly(ADP-ribosyl)ation.	NAD	147-151	poly(ADP-ribose) polymerase 1	Homo sapiens	111-115
9774627-0	1998	In situ staining for poly(ADP-ribose) polymerase activity using an NAD analogue.	NAD	67-70	poly(ADP-ribose) polymerase 1	Homo sapiens	21-48
9774627-1	1998	Poly(ADP-ribose) polymerase (PARP) is a highly abundant nuclear enzyme which metabolizes NAD, in response to DNA strand breakage, to produce chains of poly(ADP-ribose) attached to nuclear proteins.	NAD	89-92	poly(ADP-ribose) polymerase 1	Homo sapiens	0-27
9774627-1	1998	Poly(ADP-ribose) polymerase (PARP) is a highly abundant nuclear enzyme which metabolizes NAD, in response to DNA strand breakage, to produce chains of poly(ADP-ribose) attached to nuclear proteins.	NAD	89-92	poly(ADP-ribose) polymerase 1	Homo sapiens	29-33
9774627-3	1998	We have modified an existing in situ method for detection of PARP activity by using an NAD analogue in which adenine is modified by an "etheno" (vinyl) bridge.	NAD	87-90	poly(ADP-ribose) polymerase 1	Homo sapiens	61-65
9727014-6	1998	Electrons could be transferred from NADPH and NADH as measured in the cytochrome c reduction assay.	NAD	46-50	cytochrome c, somatic	Homo sapiens	70-82
9793073-10	1998	The activation of PARP results in depletion of NAD and ATP.	NAD	47-50	poly(ADP-ribose) polymerase 1	Homo sapiens	18-22
9740615-0	1998	Role of NADH/NADPH oxidase-derived H2O2 in angiotensin II-induced vascular hypertrophy.	NAD	8-12	angiotensinogen	Homo sapiens	43-57
9855679-1	1998	The cellular coenzymatic role of NAD, being a pleiotropic cofactor for diverse cellular reactions, is extended to poly(ADP-ribose) and to the highly abundant nuclear protein, poly(ADP-ribose) polymerase, with special focus on the pharmacological action of ligands on the latter.	NAD	33-36	poly(ADP-ribose) polymerase 1	Homo sapiens	175-202
9721847-3	1998	Automodification of PARP in the presence of NAD+ resulted in its dissociation from the DNA fragments, which, nevertheless, remained physically aligned.	NAD	44-48	poly(ADP-ribose) polymerase 1	Homo sapiens	20-24
9721847-4	1998	A recombinant 28-kDa fragment of PARP containing the DNA binding domain but lacking the automodification domain irreversibly bound to and linked DNA fragments in the absence or presence of NAD+.	NAD	189-193	poly(ADP-ribose) polymerase 1	Homo sapiens	33-37
9825918-6	1998	This reveals that both NGD+ and NAD+ are converted by CD38 to their cyclic nucleotides.	NAD	32-36	CD38 molecule	Rattus norvegicus	54-58
9666055-1	1998	The structural organization of the NDUFS8 gene coding for the TYKY subunit of the human mitochondrial NADH:ubiquinone oxidoreductase (Complex I) has been determined by sequencing of a genomic fragment cloned from a cosmid library.	NAD	102-106	NADH:ubiquinone oxidoreductase core subunit S8	Homo sapiens	35-41
9666055-1	1998	The structural organization of the NDUFS8 gene coding for the TYKY subunit of the human mitochondrial NADH:ubiquinone oxidoreductase (Complex I) has been determined by sequencing of a genomic fragment cloned from a cosmid library.	NAD	102-106	NADH:ubiquinone oxidoreductase core subunit S8	Homo sapiens	62-66
9675019-1	1998	The only major structural difference between aldehyde reductase, a primarily NADPH-dependent aldo-keto reductase, and aldose reductase, a dually coenzyme-specific (NADPH/NADH) member of the same superfamily, is an additional eight amino acid residues in the substrate/inhibitor binding site (C-terminal region) of aldehyde reductase.	NAD	170-174	aldo-keto reductase family 1 member B	Homo sapiens	118-134
9675145-6	1998	Stimulation of vessels with NADH (200 microM) increased CLA enhanced chemiluminescence, which was inhibited by low concentrations of superoxide dismutase (20U/ml).	NAD	28-32	superoxide dismutase 1	Homo sapiens	133-153
9603959-5	1998	The protein kinase activity of DNA-PK can be stimulated by PARP in the presence of NAD+ in a reaction that is blocked by the PARP inhibitor 1, 5-dihydroxyisoquinoline.	NAD	83-87	protein kinase, DNA-activated, catalytic subunit	Homo sapiens	31-37
9647766-3	1998	We cloned the cDNA of three remaining human NADH:ubiquinone oxidoreductase subunits of this IP fraction: the NDUFS2 (49 kDa), NDUFS3 (30 kDa), and NDUFS6 (13 kDa) subunits.	NAD	44-48	NADH:ubiquinone oxidoreductase core subunit S2	Homo sapiens	109-115
9647766-3	1998	We cloned the cDNA of three remaining human NADH:ubiquinone oxidoreductase subunits of this IP fraction: the NDUFS2 (49 kDa), NDUFS3 (30 kDa), and NDUFS6 (13 kDa) subunits.	NAD	44-48	NADH:ubiquinone oxidoreductase subunit S6	Homo sapiens	147-153
9680129-8	1998	Interestingly, capsid protein phosphorylation decreased in a concentration-dependent manner (at concentrations of 5-30 mM) in the presence of specific inhibitors for GAPD-PK (NADH and GAP).	NAD	175-179	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	166-170
9603959-5	1998	The protein kinase activity of DNA-PK can be stimulated by PARP in the presence of NAD+ in a reaction that is blocked by the PARP inhibitor 1, 5-dihydroxyisoquinoline.	NAD	83-87	poly(ADP-ribose) polymerase 1	Homo sapiens	59-63
9603959-5	1998	The protein kinase activity of DNA-PK can be stimulated by PARP in the presence of NAD+ in a reaction that is blocked by the PARP inhibitor 1, 5-dihydroxyisoquinoline.	NAD	83-87	poly(ADP-ribose) polymerase 1	Homo sapiens	125-129
10191393-8	1998	Furthermore, IL-6 and glucagon caused an increase in the ketone-body ratio (KBR = [acetoacetate]/[beta-hydroxybutyrate]), which is in equilibrium with the intramitochondrial NAD+/NADH.	NAD	174-178	interleukin 6	Rattus norvegicus	13-17
29710893-1	1998	Just like in biological systems, the GAPDH-catalyzed oxidation of aldehyde to carboxylate proceeds in conjunction with 1,4-selective reduction of NAD+ to NADH model compounds [Eq. (1)].	NAD	146-150	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	37-42
29710893-1	1998	Just like in biological systems, the GAPDH-catalyzed oxidation of aldehyde to carboxylate proceeds in conjunction with 1,4-selective reduction of NAD+ to NADH model compounds [Eq. (1)].	NAD	154-158	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	37-42
29710893-2	1998	The combination of GAPDH- and LDH-type transfer reactions is also described here as a system mimic for the NAD+ /NADH redox cycle in anaerobic glycolysis.	NAD	107-111	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	19-24
29710893-2	1998	The combination of GAPDH- and LDH-type transfer reactions is also described here as a system mimic for the NAD+ /NADH redox cycle in anaerobic glycolysis.	NAD	113-117	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	19-24
9633603-1	1998	The NAD(+)-dependent isocitrate dehydrogenase of Saccharomyces cerevisiae is an octamer composed of four Idh1p subunits and four Idh2p subunits.	NAD	4-8	isocitrate dehydrogenase (NAD(+)) IDH1	Saccharomyces cerevisiae S288C	105-110
9593711-9	1998	Subsequent degradation of PARP by caspase-3-like proteases may prevent depletion of NAD and ATP or release certain nuclear proteins from poly(ADP-ribosyl)ation-induced inhibition, both of which might be required for late stages of apoptosis.	NAD	84-87	poly(ADP-ribose) polymerase 1	Homo sapiens	26-30
9593711-9	1998	Subsequent degradation of PARP by caspase-3-like proteases may prevent depletion of NAD and ATP or release certain nuclear proteins from poly(ADP-ribosyl)ation-induced inhibition, both of which might be required for late stages of apoptosis.	NAD	84-87	caspase 3	Homo sapiens	34-43
9635838-5	1998	Concomitantly, the intracellular levels of NAD+--the substrate for the PARP--and the reduced counterpart NADH were determined using an enzymatic cycling assay 30 min after [60Co] gamma-ray cells irradiation.	NAD	43-47	poly(ADP-ribose) polymerase 1	Homo sapiens	71-75
9635838-6	1998	Our results demonstrate that a marked stimulation of PARP activity is produced upon radiation of the cells from healthy subjects but not in the FAP leucocytes, which concomitantly show a marked decrease in total NAD-/NADH content.	NAD	212-216	poly(ADP-ribose) polymerase 1	Homo sapiens	53-57
9635838-6	1998	Our results demonstrate that a marked stimulation of PARP activity is produced upon radiation of the cells from healthy subjects but not in the FAP leucocytes, which concomitantly show a marked decrease in total NAD-/NADH content.	NAD	217-221	poly(ADP-ribose) polymerase 1	Homo sapiens	53-57
9571033-1	1998	The binding site for the acceptor substrate poly(ADP-ribose) in the elongation reaction of the ADP-ribosyl transferase poly(ADP-ribose) polymerase (PARP) was detected by cocrystallizing the enzyme with an NAD+ analogue.	NAD	205-209	poly(ADP-ribose) polymerase 1	Homo sapiens	119-146
9571033-1	1998	The binding site for the acceptor substrate poly(ADP-ribose) in the elongation reaction of the ADP-ribosyl transferase poly(ADP-ribose) polymerase (PARP) was detected by cocrystallizing the enzyme with an NAD+ analogue.	NAD	205-209	poly(ADP-ribose) polymerase 1	Homo sapiens	148-152
9683009-2	1998	Rapid activation of PARS depletes the intracellular concentration of its substrate, NAD+, slowing the rate of glycolysis, electron transport and ATP formation.	NAD	84-88	poly(ADP-ribose) polymerase 1	Homo sapiens	20-24
10191393-8	1998	Furthermore, IL-6 and glucagon caused an increase in the ketone-body ratio (KBR = [acetoacetate]/[beta-hydroxybutyrate]), which is in equilibrium with the intramitochondrial NAD+/NADH.	NAD	179-183	interleukin 6	Rattus norvegicus	13-17
9568479-10	1998	Removal of cellular GAPDH by exposing erythrocyte membranes to NADH prior to membrane resealing neither affects ATP modulation of sugar transport nor reduces biphasic net sugar uptake to a single phase.	NAD	63-67	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	20-25
9787766-3	1998	At pH 7.4 and 25 degrees C, the major and minor components of the E3 isozyme catalyzed the reaction with Vmax of 1.1 and 0.8 mumol NADH min-1 mg-1 protein, respectively, compared to 0.067 and 0.060 mumol NADH min-1 mg-1 protein for the E1 and E2 isozymes, respectively.	NAD	131-135	CD59 molecule (CD59 blood group)	Homo sapiens	136-146
9787766-3	1998	At pH 7.4 and 25 degrees C, the major and minor components of the E3 isozyme catalyzed the reaction with Vmax of 1.1 and 0.8 mumol NADH min-1 mg-1 protein, respectively, compared to 0.067 and 0.060 mumol NADH min-1 mg-1 protein for the E1 and E2 isozymes, respectively.	NAD	131-135	CD59 molecule (CD59 blood group)	Homo sapiens	209-219
9787766-3	1998	At pH 7.4 and 25 degrees C, the major and minor components of the E3 isozyme catalyzed the reaction with Vmax of 1.1 and 0.8 mumol NADH min-1 mg-1 protein, respectively, compared to 0.067 and 0.060 mumol NADH min-1 mg-1 protein for the E1 and E2 isozymes, respectively.	NAD	204-208	CD59 molecule (CD59 blood group)	Homo sapiens	136-146
9586947-8	1998	Upon reconstitution, human liver b5 plus NADH:b5 reductase and CYP2C9 plus NADPH:P450 reductase were both effective catalysts of AZT reduction, which was also supported when CYP2A6 or CYP2E1 was substituted for CYP2C9.	NAD	41-45	cytochrome P450 family 2 subfamily E member 1	Homo sapiens	184-190
9496941-1	1998	BACKGROUND &amp; AIMS: Peroxynitrite induces cytotoxicity by generating DNA single-strand breaks and activating poly(ADP-ribose) synthetase (PARS), a nuclear enzyme that consumes oxidized nicotinamide adenine dinucleotide (NAD+) and depletes cellular adenosine triphosphate (ATP).	NAD	188-221	poly(ADP-ribose) polymerase 1	Homo sapiens	112-139
9496941-1	1998	BACKGROUND &amp; AIMS: Peroxynitrite induces cytotoxicity by generating DNA single-strand breaks and activating poly(ADP-ribose) synthetase (PARS), a nuclear enzyme that consumes oxidized nicotinamide adenine dinucleotide (NAD+) and depletes cellular adenosine triphosphate (ATP).	NAD	188-221	poly(ADP-ribose) polymerase 1	Homo sapiens	141-145
9521710-0	1998	Inhibitor and NAD+ binding to poly(ADP-ribose) polymerase as derived from crystal structures and homology modeling.	NAD	14-18	poly(ADP-ribose) polymerase 1	Homo sapiens	30-57
9568479-6	1998	GAPDH is released from erythrocyte membranes upon exposure to Mg.ATP or to NADH.	NAD	75-79	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	0-5
9496941-1	1998	BACKGROUND &amp; AIMS: Peroxynitrite induces cytotoxicity by generating DNA single-strand breaks and activating poly(ADP-ribose) synthetase (PARS), a nuclear enzyme that consumes oxidized nicotinamide adenine dinucleotide (NAD+) and depletes cellular adenosine triphosphate (ATP).	NAD	223-227	poly(ADP-ribose) polymerase 1	Homo sapiens	112-139
9570746-10	1998	NADH and NADPH (5 mM) triggered sperm capacitation and phosphorylation of p105/p81, but these processes were not prevented by SOD or catalase, nor were they associated with an increased O2.- production.	NAD	0-4	nuclear factor kappa B subunit 1	Homo sapiens	74-78
9496941-1	1998	BACKGROUND &amp; AIMS: Peroxynitrite induces cytotoxicity by generating DNA single-strand breaks and activating poly(ADP-ribose) synthetase (PARS), a nuclear enzyme that consumes oxidized nicotinamide adenine dinucleotide (NAD+) and depletes cellular adenosine triphosphate (ATP).	NAD	223-227	poly(ADP-ribose) polymerase 1	Homo sapiens	141-145
9496941-5	1998	Both SIN-1 and SNAP reduced [ATP], but only SIN-1 reduced [NAD+].	NAD	59-63	MAPK associated protein 1	Homo sapiens	44-49
9496941-6	1998	Inhibition of PARS activity by the PARS inhibitors 5-iodo-6-amino 1,2-benzopyrone or 3-aminobenzamide prevented the SIN-1-induced reduction in [NAD+] and [ATP] but had no effect on the SNAP-induced reduction in [ATP].	NAD	144-148	poly(ADP-ribose) polymerase 1	Homo sapiens	14-18
9496941-6	1998	Inhibition of PARS activity by the PARS inhibitors 5-iodo-6-amino 1,2-benzopyrone or 3-aminobenzamide prevented the SIN-1-induced reduction in [NAD+] and [ATP] but had no effect on the SNAP-induced reduction in [ATP].	NAD	144-148	poly(ADP-ribose) polymerase 1	Homo sapiens	35-39
9445395-4	1998	Dose-response experiments for NADH showed an upward shift of the curve for TNF-alpha-treated cells, suggesting that TNF-alpha increased the amount of available enzyme.	NAD	30-34	tumor necrosis factor	Rattus norvegicus	75-84
9484215-1	1998	Poly(ADP-ribosyl) transferase (ADPRT) is a nuclear enzyme that catalyzes the synthesis of ADP-ribose polymers from NAD+ as well as the transfer of these polymers onto acceptor proteins.	NAD	115-119	poly(ADP-ribose) polymerase 1	Homo sapiens	0-29
9484215-1	1998	Poly(ADP-ribosyl) transferase (ADPRT) is a nuclear enzyme that catalyzes the synthesis of ADP-ribose polymers from NAD+ as well as the transfer of these polymers onto acceptor proteins.	NAD	115-119	poly(ADP-ribose) polymerase 1	Homo sapiens	31-36
9445395-4	1998	Dose-response experiments for NADH showed an upward shift of the curve for TNF-alpha-treated cells, suggesting that TNF-alpha increased the amount of available enzyme.	NAD	30-34	tumor necrosis factor	Rattus norvegicus	116-125
9538194-6	1998	Increased NAD levels were found in both IFN gamma-treated and non-treated hepatocytes following the addition of PUFAs, but clofibrate, a peroxisome proliferator, bromophenacyl bromide (BPB), an inhibitor of phospholipase, nordihydroguaiaretic acid (NDGA), an inhibitor of lipoxygenase, and arachidonic acid, a metabolite of linoleic acid, did not inhibit IFN gamma-induced cellular injury.	NAD	10-13	interferon gamma	Homo sapiens	40-49
9538194-6	1998	Increased NAD levels were found in both IFN gamma-treated and non-treated hepatocytes following the addition of PUFAs, but clofibrate, a peroxisome proliferator, bromophenacyl bromide (BPB), an inhibitor of phospholipase, nordihydroguaiaretic acid (NDGA), an inhibitor of lipoxygenase, and arachidonic acid, a metabolite of linoleic acid, did not inhibit IFN gamma-induced cellular injury.	NAD	10-13	interferon gamma	Homo sapiens	355-364
9520268-12	1998	KOD1-GDH utilized both coenzymes NADH and NADPH, as do most eukaryal GDHs.	NAD	33-37	Glu/Leu/Phe/Val dehydrogenase	Thermococcus kodakarensis KOD1	5-8
9493264-0	1998	Crystal structure of the NAD complex of human deoxyhypusine synthase: an enzyme with a ball-and-chain mechanism for blocking the active site.	NAD	25-28	deoxyhypusine synthase	Homo sapiens	46-68
9454604-1	1998	The role of noncovalent interactions in the catalytic mechanism of aldose reductase from the yeast Candida tenuis was determined by steady-state kinetic analysis of the NADH-dependent reduction of various aldehydes, differing in hydrophobicity and the hydrogen bonding capability with the binary enzyme-NADH complex.	NAD	169-173	aldo-keto reductase family 1 member B	Homo sapiens	67-83
9454604-1	1998	The role of noncovalent interactions in the catalytic mechanism of aldose reductase from the yeast Candida tenuis was determined by steady-state kinetic analysis of the NADH-dependent reduction of various aldehydes, differing in hydrophobicity and the hydrogen bonding capability with the binary enzyme-NADH complex.	NAD	303-307	aldo-keto reductase family 1 member B	Homo sapiens	67-83
9473669-1	1998	Mammalian quinolinate phosphoribosyltransferase (QPRTase) (EC 2.4.2.19) is a key enzyme in catabolism of quinolinate, an intermediate in the tryptophan-nicotinamide adenine dinucleotide (NAD) pathway.	NAD	152-185	quinolinate phosphoribosyltransferase	Homo sapiens	10-47
9473669-1	1998	Mammalian quinolinate phosphoribosyltransferase (QPRTase) (EC 2.4.2.19) is a key enzyme in catabolism of quinolinate, an intermediate in the tryptophan-nicotinamide adenine dinucleotide (NAD) pathway.	NAD	152-185	quinolinate phosphoribosyltransferase	Homo sapiens	49-56
9435273-2	1998	Mitochondria isolated from yeast cells deleted for the POR1 gene (delta por1) had a profoundly reduced outer membrane permeability as measured by the ability of an intermembrane space dehydrogenase to oxidize exogenously added NADH.	NAD	227-231	porin POR1	Saccharomyces cerevisiae S288C	55-59
9493264-5	1998	RESULTS: The crystal structure of human DHS with bound NAD cofactor has been determined and refined at 2.2 A resolution.	NAD	55-58	deoxyhypusine synthase	Homo sapiens	40-43
9405293-13	1998	Isoenzyme PDK4 was activated almost 2-fold by NADH, but NADH plus acetyl-CoA did not activate above the level seen with NADH alone.	NAD	46-50	pyruvate dehydrogenase kinase 4	Homo sapiens	10-14
9706251-9	1998	The MPO/NADH/halide systems, where NADH replaced H2O2, also inactivated LADH.	NAD	8-12	myeloperoxidase	Homo sapiens	4-7
9923724-10	1998	Kinetic analysis indicated that the chronic ethanol-induced decrease in the glycerol 3-phosphate dehydrogenase reaction was due to a decreased rate of NADH reoxidation in the liver, likely owing to a decrease in oxygen supply or utilization in the ethanol-treated rats.	NAD	151-155	glycerol-3-phosphate dehydrogenase 1	Rattus norvegicus	76-110
9706251-9	1998	The MPO/NADH/halide systems, where NADH replaced H2O2, also inactivated LADH.	NAD	35-39	myeloperoxidase	Homo sapiens	4-7
9706251-10	1998	Native (not denatured) catalase completely prevented the MPO/NADH/Kl system effect (Table 1), in close agreement with H2O2 production by the LADH-catalysed NADH oxidation and the role of H2O2 in LADH inactivation.	NAD	61-65	myeloperoxidase	Homo sapiens	57-60
9706251-10	1998	Native (not denatured) catalase completely prevented the MPO/NADH/Kl system effect (Table 1), in close agreement with H2O2 production by the LADH-catalysed NADH oxidation and the role of H2O2 in LADH inactivation.	NAD	156-160	myeloperoxidase	Homo sapiens	57-60
9919621-1	1998	As a substrate for poly(ADP-ribose) polymerase (PARP; EC, 2.4.2.30), an enzyme that is activated by DNA strand breaks and is thought to facilitate efficient DNA repair, NAD+ and its precursor nicotinic acid (niacin) are involved in the cellular defense against DNA damage by genotoxic compounds.	NAD	169-173	poly(ADP-ribose) polymerase 1	Homo sapiens	19-46
9919621-1	1998	As a substrate for poly(ADP-ribose) polymerase (PARP; EC, 2.4.2.30), an enzyme that is activated by DNA strand breaks and is thought to facilitate efficient DNA repair, NAD+ and its precursor nicotinic acid (niacin) are involved in the cellular defense against DNA damage by genotoxic compounds.	NAD	169-173	poly(ADP-ribose) polymerase 1	Homo sapiens	48-52
9432004-0	1997	Mechanism of NADH transfer between alcohol dehydrogenase and glyceraldehyde-3-phosphate dehydrogenase.	NAD	13-17	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	61-101
9494059-2	1997	The object of the study is to evaluate the erythrocytes superoxide dismutase (SOD) activity in two groups of persons (Group I, healthy blood donors; Group II, lung cancer patients), using the spectrophotometric assay of NADH oxidation and the indirect method.	NAD	220-224	superoxide dismutase 1	Homo sapiens	56-76
9494059-2	1997	The object of the study is to evaluate the erythrocytes superoxide dismutase (SOD) activity in two groups of persons (Group I, healthy blood donors; Group II, lung cancer patients), using the spectrophotometric assay of NADH oxidation and the indirect method.	NAD	220-224	superoxide dismutase 1	Homo sapiens	78-81
9367520-2	1997	To investigate the specificity and target proteins of the arginine-specific mono-ADP-ribosyltransferase (mADP-RT) in rabbit skeletal muscle T-tubules (TT) biotin- or digoxigenin-coupled NAD-derivatives were synthesized.	NAD	186-189	ADP-ribosyltransferase 1	Mus musculus	105-112
9367520-6	1997	Under the appropriate reaction conditions, the radioactive [adenylate-14C]NAD and [32P]NAD were found to be solely consumed by the arginine-specific mADP-RT of skeletal muscle TT.	NAD	74-77	ADP-ribosyltransferase 1	Mus musculus	149-156
11774666-6	1998	(4) exogenous NAD+ attenuates stimulated collagen synthesis by IGF1 on PDL cells.	NAD	14-18	insulin like growth factor 1	Homo sapiens	63-67
11774666-7	1998	CONCLUSION: IGF1 stimulates collagen synthesis of PDL cells through inhibiting PADPR synthesis by acting at increasing lactate production which lowers intracellular NAD+ level and at suppressing PADPR synthetase activity.	NAD	165-169	insulin like growth factor 1	Homo sapiens	12-16
9448751-11	1997	These results suggest that inactivation of GAPDH induced by ferrylMb is predominantly due to oxidation of the essential cysteine 149, and that NAD protects the active site from oxidative attack of ferrylMb.	NAD	143-146	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	43-48
9432004-1	1997	Steady-state and transient-state kinetic experiments have been performed to test the proposal that there is a direct (channelled) transfer of NADH from glyceraldehyde-3-phosphate dehydrogenase to alcohol dehydrogenase.	NAD	142-146	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	152-192
9367892-1	1997	Poly(ADP-ribosyl) transferase (ADPRT) is a nuclear enzyme that catalyzes the synthesis of ADP-ribose polymers from NAD+ as well as the transfer of these polymers onto acceptor proteins.	NAD	115-119	poly(ADP-ribose) polymerase 1	Homo sapiens	0-29
9367892-1	1997	Poly(ADP-ribosyl) transferase (ADPRT) is a nuclear enzyme that catalyzes the synthesis of ADP-ribose polymers from NAD+ as well as the transfer of these polymers onto acceptor proteins.	NAD	115-119	poly(ADP-ribose) polymerase 1	Homo sapiens	31-36
9305729-4	1997	The nitrate reductase contains 1 mol FAD per mole of enzyme and also reduces cytochrome c or dichlorophenol indophenol with NADH as the electron donor.	NAD	124-128	cytochrome c, somatic	Homo sapiens	77-89
9371836-6	1997	NO increases the binding of NAD, a G3PD cofactor, to G3PD and inhibits its activity as also found by others.	NAD	28-31	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	35-39
9371836-6	1997	NO increases the binding of NAD, a G3PD cofactor, to G3PD and inhibits its activity as also found by others.	NAD	28-31	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	53-57
9371836-7	1997	The increased NAD binding resulted in an increase in G3PD binding to actin.	NAD	14-17	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	53-57
9355754-0	1997	Co-oxidation of NADH and NADPH by a mammalian 15-lipoxygenase: inhibition of lipoxygenase activity at near-physiological NADH concentrations.	NAD	16-20	arachidonate 15-lipoxygenase	Homo sapiens	46-61
9355754-0	1997	Co-oxidation of NADH and NADPH by a mammalian 15-lipoxygenase: inhibition of lipoxygenase activity at near-physiological NADH concentrations.	NAD	121-125	arachidonate 15-lipoxygenase	Homo sapiens	46-61
9355754-1	1997	The purified 15-lipoxygenase from rabbit reticulocytes is capable of oxidizing NADH in the presence of linoleic acid and oxygen.	NAD	79-83	arachidonate 15-lipoxygenase	Homo sapiens	13-28
9307017-2	1997	During growth on d-xylose the yeast Candida tenuis produces one aldose reductase that is active with both NADPH and NADH as coenzyme.	NAD	116-120	aldo-keto reductase family 1 member B	Homo sapiens	64-80
9200678-1	1997	Poly(ADP-ribosyl)transferase (pADPRT) is a nuclear protein which catalyzes the polymerization of ADP-ribose using NAD+ as substrate, as well as the transfer of ADP-ribose polymers to itself and other protein acceptors.	NAD	114-118	poly(ADP-ribose) polymerase 1	Homo sapiens	0-28
9361705-9	1997	However, Ca2+ is only effective in helping gluconeogenesis stimulation by glucagon at highly negative redox potentials of the cytosolic NAD(+)-NADH system.	NAD	136-142	carbonic anhydrase 2	Rattus norvegicus	9-12
9361705-9	1997	However, Ca2+ is only effective in helping gluconeogenesis stimulation by glucagon at highly negative redox potentials of the cytosolic NAD(+)-NADH system.	NAD	143-147	carbonic anhydrase 2	Rattus norvegicus	9-12
9247708-9	1997	It has been suggested that aldolase and GPDH form a 1:1 complex of dissociation constant equal to or less than 5 x 10(-8) M. The complex was found to dissociate in the presence of KCl, (NH4)2SO4, ATP and NADH whereas its formation was favoured by fructose-1,6-bisphosphate, glyceraldehyde-3-phosphate, NAD+, ADP, AMP and phosphate ions.	NAD	204-208	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	40-44
9247708-9	1997	It has been suggested that aldolase and GPDH form a 1:1 complex of dissociation constant equal to or less than 5 x 10(-8) M. The complex was found to dissociate in the presence of KCl, (NH4)2SO4, ATP and NADH whereas its formation was favoured by fructose-1,6-bisphosphate, glyceraldehyde-3-phosphate, NAD+, ADP, AMP and phosphate ions.	NAD	302-306	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	40-44
9200678-1	1997	Poly(ADP-ribosyl)transferase (pADPRT) is a nuclear protein which catalyzes the polymerization of ADP-ribose using NAD+ as substrate, as well as the transfer of ADP-ribose polymers to itself and other protein acceptors.	NAD	114-118	poly(ADP-ribose) polymerase 1	Homo sapiens	30-36
9200678-6	1997	Varying the concentration of NAD+, two different forms of automodified pADPRT were obtained: oligo(ADP-ribosyl)ated pADPRT with less than 20 ADP-ribose units per chain, and poly(ADP-ribosyl)ated pADPRT with polymer lengths of up to 200 ADP-ribose residues.	NAD	29-33	poly(ADP-ribose) polymerase 1	Homo sapiens	71-77
9165033-4	1997	In contrast, type II, which is postulated to confer specificity in mineralocorticoid receptor (MR)-mediated responses, acts as an NAD-dependent oxidase that is potently inhibited by both end product and CBX.	NAD	130-133	nuclear receptor subfamily 3, group C, member 2	Rattus norvegicus	67-93
9165033-4	1997	In contrast, type II, which is postulated to confer specificity in mineralocorticoid receptor (MR)-mediated responses, acts as an NAD-dependent oxidase that is potently inhibited by both end product and CBX.	NAD	130-133	nuclear receptor subfamily 3, group C, member 2	Rattus norvegicus	95-97
9298712-6	1997	Adriamycin cross-linked to diferric transferrin and other impermeant supports also was effective in inhibition of NADH oxidation by isolated plasma membrane vesicles and in inhibition of growth of cultured cells.	NAD	114-118	transferrin	Rattus norvegicus	36-47
27406960-4	1997	PARP overexpression may result in a rapid drop of intracellular NAD(+) and ATP concentration, thus contributing to cellular redox imbalance.	NAD	64-70	poly(ADP-ribose) polymerase 1	Homo sapiens	0-4
9354374-0	1997	Nitric oxide-induced modification of glyceraldehyde-3-phosphate dehydrogenase with NAD+ is not ADP-ribosylation.	NAD	83-87	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	37-77
9354374-3	1997	To determine whether or not NO really activates ADP-ribosylation, we re-examined the NO-induced modification of GAPDH with NAD+.	NAD	123-127	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	112-117
9354374-4	1997	GAPDH was modified equally with [adenosine-14C]NAD+ and [carbonyl-14C]NAD+, indicating that the glycoside bond of NAD+ between ADP-ribose and nicotinamide is intact.	NAD	47-51	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	0-5
9354374-4	1997	GAPDH was modified equally with [adenosine-14C]NAD+ and [carbonyl-14C]NAD+, indicating that the glycoside bond of NAD+ between ADP-ribose and nicotinamide is intact.	NAD	70-74	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	0-5
9354374-4	1997	GAPDH was modified equally with [adenosine-14C]NAD+ and [carbonyl-14C]NAD+, indicating that the glycoside bond of NAD+ between ADP-ribose and nicotinamide is intact.	NAD	70-74	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	0-5
9099752-8	1997	LTC4-[125I]ASA binding to the NAD+ site was confirmed by V8 protease digestion of purified GAPDH labeled with LTC4-[125I]ASA or PNBG-[125I]ASA, with both labels localized to the 6.8-kDa N-terminal fragment.	NAD	30-34	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	91-96
9193784-2	1997	It was associated with inhibition of the NAD-dependent secondary alcohol-dehydrogenase (A-D II) histochemical reaction in the Leydig cells.	NAD	41-44	aldo-keto reductase family 1 member A1	Rattus norvegicus	65-86
9168807-13	1997	These results suggest a negative regulatory role for PARP during apoptosis, which in turn may reflect the requirement for adequate NAD and ATP during the later stages of programmed cell death.	NAD	131-134	poly(ADP-ribose) polymerase 1	Homo sapiens	53-57
9142237-0	1997	Rat T cell differentiation alloantigens RT6.1 and RT6.2 are NAD(+)-metabolizing ecto-enzymes that differ in their enzymatic activities.	NAD	60-66	ADP-ribosyltransferase 2b	Rattus norvegicus	40-45
9142237-0	1997	Rat T cell differentiation alloantigens RT6.1 and RT6.2 are NAD(+)-metabolizing ecto-enzymes that differ in their enzymatic activities.	NAD	60-66	ADP-ribosyltransferase 2b	Rattus norvegicus	50-55
9163701-8	1997	NADH consumption was accompanied by dicumarol-sensitive oxygen uptake both with the purified enzyme and with cytosol from human melanoma cells with high levels of DT-diaphorase activity.	NAD	0-4	NAD(P)H quinone dehydrogenase 1	Homo sapiens	163-176
9378521-4	1997	Thus any substance which autoregulate the activity of hexokinase and maintains critical level of G-6P necessary for generation of ATP and coenzymes (NADPH &amp; NAD+) in the prevailing hyperglycemic state can be a potential therapeutic agent for diabetic patients.	NAD	161-165	hexokinase 1	Homo sapiens	54-64
9092577-9	1997	Both FDH and its COOH-terminal domain also bound NAD+ (Kd 11 and 16 microM, respectively) as measured by fluorescence titration.	NAD	49-53	aldehyde dehydrogenase 1 family, member L1	Rattus norvegicus	5-8
9092577-12	1997	NAD+ at physiological concentrations stimulated the aldehyde dehydrogenase reaction performed by FDH or its COOH-terminal domain using NADP+.	NAD	0-4	aldehyde dehydrogenase 1 family, member L1	Rattus norvegicus	97-100
9083059-1	1997	The critical role of domain I. NAD kinase is a Ca2+/calmodulin (CaM)-dependent enzyme capable of converting cellular NAD to NADP.	NAD	31-34	calmodulin	Glycine max	52-62
9083059-14	1997	Thus, our data suggest that domain I of CaM plays a key role in the differential activation of NAD kinase exhibited by SCaM-1 and SCaM-4.	NAD	95-98	calmodulin	Glycine max	119-125
9112779-12	1997	Likewise, the relative difference in the level of alpha or beta subunits was correlated with changes in the level of GDH1 or GDH2 transcript detected in each sample, suggesting that NAD(H)-GDH activity is controlled at least in part at the transcriptional level.	NAD	182-188	glutamate dehydrogenase 2	Arabidopsis thaliana	125-129
9242981-3	1997	For instance, when eucaryotic cells are exposed to high concentrations of DNA-damaging agents, the resulting DNA strand breaks may stimulate the nuclear enzyme poly(ADP-ribose) polymerase (PARP) to such an extent that the cellular pool of NAD+, which is the substrate for this enzyme, is severely depleted, possibly leading to acute cell death.	NAD	239-243	poly(ADP-ribose) polymerase 1	Homo sapiens	160-187
9242981-3	1997	For instance, when eucaryotic cells are exposed to high concentrations of DNA-damaging agents, the resulting DNA strand breaks may stimulate the nuclear enzyme poly(ADP-ribose) polymerase (PARP) to such an extent that the cellular pool of NAD+, which is the substrate for this enzyme, is severely depleted, possibly leading to acute cell death.	NAD	239-243	poly(ADP-ribose) polymerase 1	Homo sapiens	189-193
9242981-5	1997	This additional NAD+ is indeed available for PARP to synthesize higher-than-normal amounts of poly(ADP-ribose) after treatment with the alkylating agent N-methyl-N"-nitro-N-nitrosoguanidine.	NAD	16-20	poly(ADP-ribose) polymerase 1	Homo sapiens	45-49
9083690-3	1997	Secondly, the CW-EPR spectra of N epsilon-spin-labeled coenzyme NAD+ bound to microcrystalline, tetrameric glyceraldehyde-3-phosphate dehydrogenase (GAPDH) have been collected at 9.8, 34, and 94 GHz.	NAD	64-68	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	107-147
9083690-3	1997	Secondly, the CW-EPR spectra of N epsilon-spin-labeled coenzyme NAD+ bound to microcrystalline, tetrameric glyceraldehyde-3-phosphate dehydrogenase (GAPDH) have been collected at 9.8, 34, and 94 GHz.	NAD	64-68	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	149-154
9173879-3	1997	Incubation of transformed cells with FGF-2 and [adenylate-32P]nicotinamide-adenine dinucleotide (NAD) resulted in the rapid incorporation of [32P]ADP-ribose into FGF-2 in a time- and concentration-dependent manner, with labelling averaging 3 mol of ADP-ribose/mol of FGF-2.	NAD	62-95	fibroblast growth factor 2	Homo sapiens	162-167
9173879-3	1997	Incubation of transformed cells with FGF-2 and [adenylate-32P]nicotinamide-adenine dinucleotide (NAD) resulted in the rapid incorporation of [32P]ADP-ribose into FGF-2 in a time- and concentration-dependent manner, with labelling averaging 3 mol of ADP-ribose/mol of FGF-2.	NAD	62-95	fibroblast growth factor 2	Homo sapiens	162-167
9163530-1	1997	Deoxyhypusine synthase catalyzes the NAD+-dependent formation of deoxyhypusine in the eIF-5A precursor protein by transferring the 4-aminobutyl moiety of spermidine.	NAD	37-41	deoxyhypusine synthase	Saccharomyces cerevisiae S288C	0-22
9078247-1	1997	A human liver 3 alpha-hydroxysteroid dehydrogenase isoenzyme, a member of the aldo-keto reductase family, shows a marked preference for NADP(H) over NAD(H), and is activated by sulphobromophthalein, which increases the Km values for both NADP(H) and substrates.	NAD	149-155	aldo-keto reductase family 1 member C3	Homo sapiens	14-50
9099907-7	1997	Using an in-house mouse 11beta-HSD2 cDNA and NAD-dependent activity studies, 11 beta-HSD2 was expressed in epithelial cells of colon, renal collecting ducts, ovary, and adrenal, but was absent in liver, spleen, testis and heart.	NAD	45-48	hydroxysteroid 11-beta dehydrogenase 2	Mus musculus	77-89
9000707-12	1997	These data indicate that inhibition of aldose reductase activity preserves high-energy phosphates, maintains a lower cytosolic NADH/NAD+ ratio, and markedly protects both diabetic and nondiabetic hearts during ischemia and reperfusion.	NAD	127-131	aldo-keto reductase family 1 member B1	Rattus norvegicus	39-55
9018047-1	1997	The crystal structure of the human class III chi chi alcohol dehydrogenase (ADH) in a binary complex with NAD+(gamma) was solved to 2.7 A resolution by molecular replacement with human class I beta1 beta1 ADH.	NAD	106-110	alcohol dehydrogenase 5 (class III), chi polypeptide	Homo sapiens	76-79
9018047-9	1997	The position for residue His47 in the chi chi ADH structure suggests His47 may function both as a catalytic base for proton transfer and in the binding of the adenosine phosphate of NAD(H).	NAD	182-188	alcohol dehydrogenase 5 (class III), chi polypeptide	Homo sapiens	46-49
9000707-12	1997	These data indicate that inhibition of aldose reductase activity preserves high-energy phosphates, maintains a lower cytosolic NADH/NAD+ ratio, and markedly protects both diabetic and nondiabetic hearts during ischemia and reperfusion.	NAD	132-136	aldo-keto reductase family 1 member B1	Rattus norvegicus	39-55
10072900-4	1997	The activities of GPI and GAPDH in the cysts were measured by the formation of NADH or NADPH.	NAD	79-83	glucose-6-phosphate isomerase 1	Mus musculus	18-21
27396879-1	1997	A conjugated enzyme system, alanine dehydrogenase (AIDH) for stereospecific reduction of pyruvate to l-alanine and glucose dehydrogenase (GDH) for regeneration of NADH, were coimmobilized in a nanofiltration membrane bioreactor (NFMBR) for the continuous production of l-alanine from pyruvate with NADH regeneration.	NAD	163-167	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	115-136
8950170-1	1996	The cDNA for mouse NAD+ dependent 15-hydroxyprostaglandin dehydrogenase (15-PGDH) was isolated from a lung cDNA library.	NAD	19-23	hydroxyprostaglandin dehydrogenase 15 (NAD)	Mus musculus	73-80
8883403-0	1996	Development and validation of a spectrophotometric assay for measuring the activity of NADH: cytochrome b5 reductase in human tumour cells.	NAD	87-91	cytochrome b5 reductase 3	Homo sapiens	104-116
8883403-1	1996	As part of an "enzyme-directed" approach to bioreductive drug development, we have measured the activity of NADH: cytochrome b5 reductase (B5R) in human cancer cell lines in order to assess the role of this enzyme in activating bioreductive drugs, and thus in influencing the cytotoxicity of these compounds.	NAD	108-112	cytochrome b5 reductase 3	Homo sapiens	125-137
27396879-1	1997	A conjugated enzyme system, alanine dehydrogenase (AIDH) for stereospecific reduction of pyruvate to l-alanine and glucose dehydrogenase (GDH) for regeneration of NADH, were coimmobilized in a nanofiltration membrane bioreactor (NFMBR) for the continuous production of l-alanine from pyruvate with NADH regeneration.	NAD	163-167	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	138-141
8883403-1	1996	As part of an "enzyme-directed" approach to bioreductive drug development, we have measured the activity of NADH: cytochrome b5 reductase (B5R) in human cancer cell lines in order to assess the role of this enzyme in activating bioreductive drugs, and thus in influencing the cytotoxicity of these compounds.	NAD	108-112	cytochrome b5 reductase 3	Homo sapiens	139-142
8883403-2	1996	At present, there is no validated assay reported in the literature for measuring the activity of B5R in tumour cells, and current measurements have assumed that the enzyme activity can be measured either as the NADH-dependent reduction of cytochrome c or as the non-dicoumarol-inhibitable activity in the DT-diaphorase assay.	NAD	211-215	cytochrome b5 reductase 3	Homo sapiens	97-100
9048929-1	1997	NADH-cytochrome b5 reductase (b5R) is a member of a flavoenzyme family of dehydrogenases-electron transferases that participates in the transfer of electrons from the NADH generated in glycolysis to cytochrome b5.	NAD	0-4	cytochrome b5 reductase 3	Homo sapiens	30-33
8871630-12	1996	These effects are not seen in cells from which the ADPRT was removed by phospholipase C. Moreover, cells lacking the cell surface ADPRT are not inhibited by NAD in the cell adhesion assay, but gain this property upon transfection with the ADPRT gene.	NAD	157-160	ADP-ribosyltransferase 3 (inactive)	Homo sapiens	130-135
9193645-9	1997	In contrast to Yac-1, the Yac-2 enzyme had significant NAD glycohydrolase activity and may preferentially hydrolyze NAD.	NAD	55-58	ADP-ribosyltransferase 5	Mus musculus	26-31
8883403-3	1996	Using p-hydroxymercuribenzoate (pHMB) as an inhibitor of B5R, we have quantified the contribution of B5R to the NADH-dependent reduction of cytochrome c and to the overall reduction of cytochrome c in the DT-diaphorase assay.	NAD	112-116	cytochrome b5 reductase 3	Homo sapiens	101-104
8883403-5	1996	Thus, simply measuring the NADH-dependent reduction of cytochrome c consistently overestimated B5R activity.	NAD	27-31	cytochrome b5 reductase 3	Homo sapiens	95-98
8883403-7	1996	Therefore, we have developed a spectrophotometric assay for measuring B5R activity as the pHMB-inhibitable NADH-dependent reduction of cytochrome c.	NAD	107-111	cytochrome b5 reductase 3	Homo sapiens	70-73
8871630-12	1996	These effects are not seen in cells from which the ADPRT was removed by phospholipase C. Moreover, cells lacking the cell surface ADPRT are not inhibited by NAD in the cell adhesion assay, but gain this property upon transfection with the ADPRT gene.	NAD	157-160	ADP-ribosyltransferase 3 (inactive)	Homo sapiens	130-135
8923738-0	1996	Reduced pyruvate decarboxylase and increased glycerol-3-phosphate dehydrogenase [NAD+] levels enhance glycerol production in Saccharomyces cerevisiae.	NAD	81-85	glycerol-3-phosphate dehydrogenase	Saccharomyces cerevisiae S288C	45-79
8923738-2	1996	In particular, the impact of reduced pyruvate-decarboxylase (PDC) and increased NAD-dependent glycerol-3-phosphate dehydrogenase (GPD) levels was studied.	NAD	80-83	glycerol-3-phosphate dehydrogenase	Saccharomyces cerevisiae S288C	94-128
8923738-2	1996	In particular, the impact of reduced pyruvate-decarboxylase (PDC) and increased NAD-dependent glycerol-3-phosphate dehydrogenase (GPD) levels was studied.	NAD	80-83	glycerol-3-phosphate dehydrogenase	Saccharomyces cerevisiae S288C	130-133
8703012-8	1996	The deduced amino acid sequence of the Yac-2 transferase contained consensus regions common to several bacterial toxin and mammalian transferases and NAD glycohydrolases, consistent with the hypothesis that there is a common mechanism of NAD binding and catalysis among ADP-ribosyltransferases.	NAD	150-153	ADP-ribosyltransferase 5	Mus musculus	39-44
8811894-1	1996	Using 1,N6-etheno NAD, a fluorescent analog of NAD, we extended an existing assay for NAD glycohydrolase to the measurement of mono-ADP-ribosyltransferase (mADP-RT) activity using agmatine as acceptor for ADP-ribose.	NAD	18-21	ecto-ADP-ribosyltransferase 3	Oryctolagus cuniculus	127-154
8706705-5	1996	Zinc ions inhibited the NAD+ glycohydrolase reaction catalyzed by MBP-CD38 in an uncompetitive manner, whereas they enhanced the ADP-ribosyl cyclase reaction without affecting the Km value for NAD+.	NAD	24-28	myelin basic protein	Homo sapiens	66-69
8727261-10	1996	The cofactor NAD, in a concentration-dependent manner, protected ALDH from inhibition by MeDTC sulfoxide and MeDTC sulfone.	NAD	13-16	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	65-69
8664262-2	1996	Studies of the CDP-D-glucose 4,6-dehydratase (Eod) from Yersinia had shown that this dimeric protein binds only 1 equiv of NAD+/mol of enzyme and, unlike other enzymes of the same class, displays a unique NAD+ requirement for full catalytic activity.	NAD	123-127	cut like homeobox 1	Homo sapiens	15-18
8664262-2	1996	Studies of the CDP-D-glucose 4,6-dehydratase (Eod) from Yersinia had shown that this dimeric protein binds only 1 equiv of NAD+/mol of enzyme and, unlike other enzymes of the same class, displays a unique NAD+ requirement for full catalytic activity.	NAD	205-209	cut like homeobox 1	Homo sapiens	15-18
8664262-11	1996	Interestingly, the sequestered NADH is released upon binding with CDP-D-glucose.	NAD	31-35	cut like homeobox 1	Homo sapiens	66-69
8709006-5	1996	Islet-activating protein (IAP, pertussis toxin, PTX) catalyses the transfer of the ADP-ribose moiety of NAD to the alpha subunit of Gi, resulting in a complete loss of the Gi functions.	NAD	104-107	islet amyloid polypeptide	Homo sapiens	0-24
8709006-5	1996	Islet-activating protein (IAP, pertussis toxin, PTX) catalyses the transfer of the ADP-ribose moiety of NAD to the alpha subunit of Gi, resulting in a complete loss of the Gi functions.	NAD	104-107	islet amyloid polypeptide	Homo sapiens	26-29
8852039-1	1996	NMN adenylyltransferase (NAD pyrophosphorylase; NMNAT) reversibly catalyzes the synthesis of NAD from ATP and NMN.	NAD	25-28	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	48-53
12893455-5	1996	AcH metabolism by liver mitochondrial aldehyde dehydrogenase (ALDH) was studied by following AcH disappearance rate and the formation of NADH at 340 nm in the incubation medium.	NAD	137-141	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	62-66
12893455-8	1996	Kinetic studies of mitochondrial ALDH show that low-Km mitochondrial ALDH from UChB rats exhibits a higher affinity for NAD than UChA rats.	NAD	120-123	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	33-37
12893455-8	1996	Kinetic studies of mitochondrial ALDH show that low-Km mitochondrial ALDH from UChB rats exhibits a higher affinity for NAD than UChA rats.	NAD	120-123	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	69-73
12893455-9	1996	This observation could explain the different inhibition of ALDH by both drugs, assuming that the inhibitors reduce NAD availability, the rate limiting step in the mitochondrial ALDH oxidation.	NAD	115-118	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	59-63
12893455-9	1996	This observation could explain the different inhibition of ALDH by both drugs, assuming that the inhibitors reduce NAD availability, the rate limiting step in the mitochondrial ALDH oxidation.	NAD	115-118	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	177-181
8924602-2	1996	The rat hepatic microsomal aldehyde dehydrogenase (mALDH) metabolizes aliphatic and aromatic aldehydes to the corresponding acids with NAD as the optimal cofactor.	NAD	135-138	aldehyde dehydrogenase family 3, subfamily A1	Mus musculus	51-56
8689937-10	1995	The drug, after addition of NADH, was a substrate of the human liver recombinant UGT1*6 that presents a strict specificity toward planar phenolic substances, but not that of UGT2B4 and UGT2B1 expressed in V79 fibroblasts.	NAD	28-32	UDP glucuronosyltransferase family 1 member A6	Homo sapiens	81-87
8553368-2	1995	We report here on the ability of ATA to inhibit the activity of several NAD(H)/NADP(H)-requiring enzymes (purified or cellular homogenates), including lactic dehydrogenase, alcohol dehydrogenase, cytochrome c reductase, ethoxycoumarin o-dealkylase, isocitric dehydrogenase, glutathione reductase and glucose-6-phosphate dehydrogenase.	NAD	72-78	glucose-6-phosphate dehydrogenase	Rattus norvegicus	300-333
8521845-10	1995	Purified recombinant S. solfataricus PGK and GraP-DH showed half lives of 39 min and 17 h, respectively, at 80 degrees C. Unlike bacterial GraP-DH enzymes, S. solfataricus GraP-DH was able to use both NAD+ and NADP+ as cofactors, but exhibited a marked preference for NADP+.	NAD	201-205	SULA_RS08180	Saccharolobus solfataricus	45-52
7576437-0	1995	Amperometric thin film biosensors based on glucose dehydrogenase and Toluidine Blue O as catalyst for NADH electrooxidation.	NAD	102-106	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	43-64
7576437-1	1995	Amperometric glucose sensors were constructed based on solid graphite electrodes, surface-modified with NAD+ dependent glucose dehydrogenase (GDH), Toluidine Blue O (TBO), and protective ionic polymers.	NAD	104-107	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	119-140
7622845-4	1995	NADH diaphorase enzymatic activity co-migrated with complexes of Mn SOD on a non-denaturing gel.	NAD	0-4	superoxide dismutase 2	Homo sapiens	65-71
8979347-1	1997	Mutants of Saccharomyces cerevisiae, in which one or both of the genes encoding the two isoforms of NAD-dependent glycerol-3-phosphate dehydrogenase had been deleted, were studied in aerobic batch cultures and in aerobic-anaerobic step change experiments.	NAD	100-103	glycerol-3-phosphate dehydrogenase	Saccharomyces cerevisiae S288C	114-148
27396879-1	1997	A conjugated enzyme system, alanine dehydrogenase (AIDH) for stereospecific reduction of pyruvate to l-alanine and glucose dehydrogenase (GDH) for regeneration of NADH, were coimmobilized in a nanofiltration membrane bioreactor (NFMBR) for the continuous production of l-alanine from pyruvate with NADH regeneration.	NAD	298-302	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	138-141
8874222-0	1996	Two novel mutations in the reduced nicotinamide adenine dinucleotide (NADH)-cytochrome b5 reductase gene of a patient with generalized type, hereditary methemoglobinemia.	NAD	35-68	cytochrome b5 reductase 3	Homo sapiens	87-99
8874222-0	1996	Two novel mutations in the reduced nicotinamide adenine dinucleotide (NADH)-cytochrome b5 reductase gene of a patient with generalized type, hereditary methemoglobinemia.	NAD	70-74	cytochrome b5 reductase 3	Homo sapiens	87-99
8874222-1	1996	Hereditary methemoglobinemia due to reduced nicotinamide adenine dinucleotide (NADH) cytochrome b5 reductase (b5R) deficiency is classified into two types, an erythrocyte (type I) and a generalized (type II).	NAD	44-77	cytochrome b5 reductase 3	Homo sapiens	96-108
8874222-1	1996	Hereditary methemoglobinemia due to reduced nicotinamide adenine dinucleotide (NADH) cytochrome b5 reductase (b5R) deficiency is classified into two types, an erythrocyte (type I) and a generalized (type II).	NAD	44-77	cytochrome b5 reductase 3	Homo sapiens	110-113
8874222-1	1996	Hereditary methemoglobinemia due to reduced nicotinamide adenine dinucleotide (NADH) cytochrome b5 reductase (b5R) deficiency is classified into two types, an erythrocyte (type I) and a generalized (type II).	NAD	79-83	cytochrome b5 reductase 3	Homo sapiens	96-108
8874222-1	1996	Hereditary methemoglobinemia due to reduced nicotinamide adenine dinucleotide (NADH) cytochrome b5 reductase (b5R) deficiency is classified into two types, an erythrocyte (type I) and a generalized (type II).	NAD	79-83	cytochrome b5 reductase 3	Homo sapiens	110-113
8660950-9	1996	Our results showed that incorporation of isotope into this protein band from [32P]NAD is due to ADP-ribosylation of desmin.	NAD	82-85	desmin	Gallus gallus	116-122
8679568-9	1996	The K(m)s for NAD+ and (R)-3-hydroxybutyrate (R-HOB) of expressed BDH are similar to those for bovine heart or rat liver BDH in mitochondria.	NAD	14-18	3-hydroxybutyrate dehydrogenase 1	Bos taurus	66-69
8631807-6	1996	Immunoprecipitation of recombinant Rt6-1 and Rt6-2 with anti-FLAG M2 antibody followed by incubation with [32P]NAD+ leads to rapid and covalent incorporation of radioactivity into the light chain of the M2 antibody.	NAD	111-115	ADP-ribosyltransferase 2a	Mus musculus	35-50
8631807-8	1996	These results demonstrate that Rt6-1 and RT6-2 possess the enzymatic activities typical for NAD+-dependent arginine/protein mono(ADPribosyl)transferases (EC 2.4.2.31).	NAD	92-96	ADP-ribosyltransferase 2a	Mus musculus	31-46
8602879-8	1996	Similarly, two selective inhibitors of NADH: cytochrome b5 reductase, pHMB and PTU, completely inhibited both NADH and NADPH-dependent reduction of RB90740.	NAD	39-43	cytochrome b5 type A (microsomal)	Mus musculus	45-58
8602879-8	1996	Similarly, two selective inhibitors of NADH: cytochrome b5 reductase, pHMB and PTU, completely inhibited both NADH and NADPH-dependent reduction of RB90740.	NAD	110-114	cytochrome b5 type A (microsomal)	Mus musculus	45-58
8600980-12	1996	In microsomes from phenobarbital-treated rats, anti-CYP2B1/B2 IgG completely prevented the NADPH- and NADH-dependent increases in reactive oxygen formation produced by ferritin.	NAD	102-106	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	52-58
8631352-4	1996	Malarial glutathione reductase, a homodimer of 110 kDa with a pH optimum of 6.8 and a high preference for NADPH over NADH, was shown to contain FAD as its prosthetic group.	NAD	117-121	glutathione-disulfide reductase	Homo sapiens	9-30
8631357-3	1996	BVR is unique among enzymes characterized to date in that it has dual pH/cofactor (NADH, NADPH) specificity.	NAD	83-87	biliverdin reductase A	Homo sapiens	0-3
7563128-2	1995	One strand ORF is 1,929 nucleotides long and exhibits great identity (87.5% at the nucleotide level and 94% at the amino acid level) with the hsp70 gene copies of D. melanogaster, while the second strand ORF, in antiparallel in-frame register arrangement, is 1,839 nucleotides long and exhibits 32% identity with a putative, recently identified, NAD(+)-dependent glutamate dehydrogenase (NAD(+)-GDH).	NAD	346-352	Heat-shock-protein-70Ab	Drosophila melanogaster	142-147
7783663-6	1995	These results suggest that ethanol inhibits xanthine dehydrogenase presumably by an ethanol-induced increase in the cytosolic concentration of NADH in the liver.	NAD	143-147	xanthine dehydrogenase	Homo sapiens	44-66
7728971-9	1995	DES quinone was also reduced to DES by pure diaphorase, a mitochondrial reducing enzyme, in the presence of NADH.	NAD	108-112	dihydrolipoamide dehydrogenase	Homo sapiens	44-54
7696266-10	1995	Inhibition of ethanol oxidation by sigma sigma and beta 2 beta 2 with varied NAD+ was competitive.	NAD	77-81	potassium calcium-activated channel subfamily M regulatory beta subunit 2	Homo sapiens	51-57
7696266-10	1995	Inhibition of ethanol oxidation by sigma sigma and beta 2 beta 2 with varied NAD+ was competitive.	NAD	77-81	potassium calcium-activated channel subfamily M regulatory beta subunit 2	Homo sapiens	58-64
7696266-11	1995	These results, together with the cimetidine inhibition kinetics of acetaldehyde reduction by sigma sigma and beta 2 beta 2, with either varied NADH or varied acetaldehyde, are consistent with cimetidine binding to two enzyme species.	NAD	143-147	potassium calcium-activated channel subfamily M regulatory beta subunit 2	Homo sapiens	116-122
7822839-3	1994	The resulting NAD was measured by using a redox enzymatic recycling system of alcohol dehydrogenase, diaphorase and iodonitrotetrazolium as chromogen.	NAD	14-17	dihydrolipoamide dehydrogenase	Homo sapiens	101-111
7721724-3	1994	k-1 was accelerated several orders of magnitude by NADH oxidation.	NAD	51-55	keratin 1	Homo sapiens	0-3
7819143-7	1994	Analysis of the BP-3 cDNA sequence indicates that it represents a previously undescribed gene that shares significant homology with genes encoding nicotinamide adenine dinucleotide (NAD) glycohydrolase of Aplysia californica and the CD38 antigens in mouse and human.	NAD	147-180	bone marrow stromal cell antigen 1	Mus musculus	16-20
8806601-2	1996	Although their amino acid sequences are 54% identical, these enzymes have different cofactor specificities: rat retinol dehydrogenase uses NADP+, while cow 11-cis retinol dehydrogenase uses NAD+.	NAD	190-194	retinol dehydrogenase 5	Homo sapiens	156-184
8806601-7	1996	This suggests that aspartic acid-37 and threonine-61 are important in the specificity of 11-cis retinol dehydrogenase for NAD+.	NAD	122-126	retinol dehydrogenase 5	Homo sapiens	89-117
8759717-4	1996	Two other nucleotide-hydrolyzing activities were induced on the T cell surface concomitantly with CD38: the human PC-1 molecule, a nucleotide phosphodiesterase/pyrophosphatase that produces AMP from NAD or ADP-ribose, and a nucleotidase that produces adenosine from AMP, but which may be distinct from the CD73 5"-nucleotidase.	NAD	199-202	5'-nucleotidase ecto	Homo sapiens	306-310
8769129-4	1996	Under equivalent conditions at 20 degrees C, pH 8.0, mammalian TR reduced lipoic acid by NADPH 15 times more efficiently than the corresponding NADH dependent reduction catalyzed by LipDH (297 min-1 for TR vs. 20.3 min-1 for LipDH).	NAD	144-148	dihydrolipoamide dehydrogenase	Homo sapiens	182-187
8769129-6	1996	In contrast, LipDH was only 0.048 times as efficient in the forward reaction as compared to the reverse reaction (using NADH and NAD+).	NAD	120-124	dihydrolipoamide dehydrogenase	Homo sapiens	13-18
8769129-6	1996	In contrast, LipDH was only 0.048 times as efficient in the forward reaction as compared to the reverse reaction (using NADH and NAD+).	NAD	129-133	dihydrolipoamide dehydrogenase	Homo sapiens	13-18
8634235-6	1996	113Cd NMR spectra of [113Cd]HDH were measured as complexes with two substrates (L-histidinol and DL-histidinal) and four inhibitors (imidazole, histamine, L-histidine, and DL-4-(4-imidazolyl)-3-amino-2-butanone) in the absence and presence of NAD+.	NAD	243-247	histidinol dehydrogenase, chloroplastic	Brassica oleracea	28-31
8605194-8	1996	This also follows from data on substrate inhibition and activation, effects of NAD+ on ALDH-catalyzed hydrolysis of p-nitrophenyl esters, substrate specificity toward aldehydes and p-nitrophenyl esters, and inhibition by disulfiram in relation to oxidation and hydrolysis catalyzed by the ALDHs.	NAD	79-83	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	87-91
7945680-2	1994	We show both photometrically by NADH+H+ oxidation and by HPLC product analysis that this enantiomer is rapidly reduced by NADH+H+ catalyzed by porcine heart lipoamide dehydrogenase/diaphorase.	NAD	32-36	dihydrolipoamide dehydrogenase	Homo sapiens	157-180
7945680-2	1994	We show both photometrically by NADH+H+ oxidation and by HPLC product analysis that this enantiomer is rapidly reduced by NADH+H+ catalyzed by porcine heart lipoamide dehydrogenase/diaphorase.	NAD	32-36	dihydrolipoamide dehydrogenase	Homo sapiens	181-191
7945680-2	1994	We show both photometrically by NADH+H+ oxidation and by HPLC product analysis that this enantiomer is rapidly reduced by NADH+H+ catalyzed by porcine heart lipoamide dehydrogenase/diaphorase.	NAD	122-126	dihydrolipoamide dehydrogenase	Homo sapiens	157-180
7945680-2	1994	We show both photometrically by NADH+H+ oxidation and by HPLC product analysis that this enantiomer is rapidly reduced by NADH+H+ catalyzed by porcine heart lipoamide dehydrogenase/diaphorase.	NAD	122-126	dihydrolipoamide dehydrogenase	Homo sapiens	181-191
18966494-6	1996	The diaphorase electrode thus obtained responds to NADH at 0 V. The sensitivity and detection limit of this biosensor are 11.2 mA M(-1) cm(-2) and 1 muM respectively.	NAD	51-55	dihydrolipoamide dehydrogenase	Homo sapiens	4-14
8593807-2	1996	The cultured stromal cells displayed both NADP(+)-dependent (type 1) and NAD(+)-dependent (type 2) 11 beta HSD activities under basal conditions.	NAD	73-79	carbohydrate sulfotransferase 3	Homo sapiens	107-110
8201622-5	1994	A naturally occurring variant of beta 1 alcohol dehydrogenase, found in approximately 50% of the Asian population, possesses a His at position 47 (beta 2 or beta 47H) and was crystallized in a complex with NAD+ and the inhibitor 4-iodopyrazole.	NAD	206-210	potassium calcium-activated channel subfamily M regulatory beta subunit 2	Homo sapiens	147-153
11666971-9	1996	The substituent effects are qualitatively similar to the substrate-induced electrostatic effects on the nicotinamide ring of NAD(+) at the active site of UDP-galactose 4-epimerase (Burke, J. R.; Frey, P. A. Biochemistry 1993, 32, 13220-13230).	NAD	125-131	UDP-galactose-4-epimerase	Homo sapiens	154-179
8191539-6	1994	This review examines the attributes of these 11 beta-hydroxysteroid dehydrogenase isozymes and suggests reasons why a high affinity, NAD-dependent enzyme appears to be the most likely candidate to endow specificity on the mineralocorticoid receptor.	NAD	133-136	nuclear receptor subfamily 3 group C member 2	Homo sapiens	222-248
7616299-2	1995	Xanthine dehydrogenase uses NAD as the electron acceptor to catalyze a reaction which does not produce any oxygen free radicals and may depress the conversion of xanthine dehydrogenase to xanthine oxidase.	NAD	28-31	xanthine dehydrogenase	Rattus norvegicus	0-22
7616299-2	1995	Xanthine dehydrogenase uses NAD as the electron acceptor to catalyze a reaction which does not produce any oxygen free radicals and may depress the conversion of xanthine dehydrogenase to xanthine oxidase.	NAD	28-31	xanthine dehydrogenase	Rattus norvegicus	162-184
8567127-9	1996	This activity was also distinct from xanthine oxidoreductase and NADH-cytochrome b5 reductase, 2 other enzymes that catalyze metabolic activation of MMC, because the unique activity was not inhibited by allopurinol (an inhibitor of xanthine oxidoreductase) and its activity was the same with NADH and NADPH (cytochrome b5 reductase is specific to NADH).	NAD	65-69	xanthine dehydrogenase	Homo sapiens	232-255
8572289-1	1995	NMN adenylyltransferase (NMNAT) reversibly catalyzes the synthesis of NAD+ or NaAD+ from ATP and NMN or NaMN.	NAD	70-74	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	0-23
8572289-1	1995	NMN adenylyltransferase (NMNAT) reversibly catalyzes the synthesis of NAD+ or NaAD+ from ATP and NMN or NaMN.	NAD	70-74	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	25-30
8821708-3	1994	With this isoform, the Km values were estimated to be 330 mumol/l for NAD and 30 mumol/l for MBP, and the optimal pH for ADP-ribosylation was 8.5.	NAD	70-73	myelin basic protein	Gallus gallus	93-96
8274146-8	1993	The inhibition of ALDH and the resulting decrease in the redox effect on the NAD system bound to alcohol dehydrogenase (EC 1.1.1.1) could explain the protective effect of methylene blue against metabolic redox effects of ethanol.	NAD	77-80	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	18-22
8237468-1	1993	We have developed a chemiluminescent flow injection method for analysis of bile acid, glucose and ATP using the chemiluminescent assay of NADH using 1-methoxy-5-methylphenazinium methyl sulphate (1-MPMS)/isoluminol(IL)/microperoxidase (m-POD) system and immobilized enzyme reactors such as 3 alpha-hydroxysteroid dehydrogenase, glucose-dehydrogenase, hexokinase and glucose-6-phosphate dehydrogenase.	NAD	138-142	aldo-keto reductase family 1 member C3	Homo sapiens	290-326
8237468-1	1993	We have developed a chemiluminescent flow injection method for analysis of bile acid, glucose and ATP using the chemiluminescent assay of NADH using 1-methoxy-5-methylphenazinium methyl sulphate (1-MPMS)/isoluminol(IL)/microperoxidase (m-POD) system and immobilized enzyme reactors such as 3 alpha-hydroxysteroid dehydrogenase, glucose-dehydrogenase, hexokinase and glucose-6-phosphate dehydrogenase.	NAD	138-142	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	328-349
8567127-9	1996	This activity was also distinct from xanthine oxidoreductase and NADH-cytochrome b5 reductase, 2 other enzymes that catalyze metabolic activation of MMC, because the unique activity was not inhibited by allopurinol (an inhibitor of xanthine oxidoreductase) and its activity was the same with NADH and NADPH (cytochrome b5 reductase is specific to NADH).	NAD	292-296	xanthine dehydrogenase	Homo sapiens	37-60
8936052-4	1996	Both forms of purified b5R could reduce cytochrome b5 and both could use NADH or NADPH as an electron donor, although NADH was more efficient.	NAD	73-77	cytochrome b5 reductase 3	Homo sapiens	23-26
8364410-1	1993	Covalent adducts of NAD+ with pyruvate and 2-oxoglutarate have been reported to inhibit differentially the activities of bovine glutamate dehydrogenase (GDH) towards these two oxoacid substrates, implying separate active sites.	NAD	20-24	glutamate dehydrogenase 1, mitochondrial	Bos taurus	128-151
8364410-1	1993	Covalent adducts of NAD+ with pyruvate and 2-oxoglutarate have been reported to inhibit differentially the activities of bovine glutamate dehydrogenase (GDH) towards these two oxoacid substrates, implying separate active sites.	NAD	20-24	glutamate dehydrogenase 1, mitochondrial	Bos taurus	153-156
7810686-7	1994	Microsomes catalyzed an NADH-mediated reduction of several electron acceptor dyes, cytochrome c (rotenone insensitive) and methemoglobin.	NAD	24-28	LOC104968582	Bos taurus	83-95
7896566-1	1994	Xanthine oxidoreductase is an enzyme which has the unusual property that it can exist in a dehydrogenase form which uses NAD+ and an oxidase form which uses oxygen as electron acceptor.	NAD	121-125	xanthine dehydrogenase	Homo sapiens	0-23
8936052-4	1996	Both forms of purified b5R could reduce cytochrome b5 and both could use NADH or NADPH as an electron donor, although NADH was more efficient.	NAD	118-122	cytochrome b5 reductase 3	Homo sapiens	23-26
1426237-1	1992	N"-Methylnicotinamide and nicotinamide, which decreased in vitro ADP-ribosylation of nuclear proteins and/or cellular NAD+ content, selectively increased the basal expression of the rat growth hormone (GH) gene promoter and its response to triiodothyronine (T3).	NAD	118-122	gonadotropin releasing hormone receptor	Rattus norvegicus	186-200
1426237-1	1992	N"-Methylnicotinamide and nicotinamide, which decreased in vitro ADP-ribosylation of nuclear proteins and/or cellular NAD+ content, selectively increased the basal expression of the rat growth hormone (GH) gene promoter and its response to triiodothyronine (T3).	NAD	118-122	gonadotropin releasing hormone receptor	Rattus norvegicus	202-204
8835944-3	1996	Oxalate caused non-competitive inhibition (Ki app = IC50 = 0.15 mM) of the forward reaction, NADH was more effective in blocking inhibition by GAA than pyruvate.	NAD	93-97	alpha glucosidase	Homo sapiens	143-146
1524439-0	1992	NAD biosynthesis in human placenta: purification and characterization of homogeneous NMN adenylyltransferase.	NAD	0-3	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	85-108
7499374-8	1995	It was found that NAD+ binding influences the interaction between the flavin and the reduced disulfide in the 2"-F-arabino-FAD-lipoamide dehydrogenase, presumably by altering the relative oxidation-reduction potentials.	NAD	18-22	dihydrolipoamide dehydrogenase	Homo sapiens	127-150
16668941-7	1992	Ultraviolet and visible spectra of oxidized and NADH-reduced recombinant cytochrome c reductase were nearly identical with those of maize leaf NADH:nitrate reductase.	NAD	48-52	cytochrome c	Zea mays	73-85
16668941-8	1992	These two enzyme forms also had very similar kinetic properties with respect to NADH-dependent cytochrome c and ferricyanide reduction.	NAD	80-84	cytochrome c	Zea mays	95-107
8777059-0	1995	Aqueous soluble tetrazolium/formazan MTS as an indicator of NADH- and NADPH-dependent dehydrogenase activity.	NAD	60-64	MLRL	Homo sapiens	37-40
24178072-6	1992	The results indicate that the increase in NADH-GDH specific activity was due to de-novo synthesis of the alpha-subunit of GDH and the assembly of only the more anodic isoenzymes.	NAD	42-46	L-galactose dehydrogenase	Vitis vinifera	47-50
24178072-6	1992	The results indicate that the increase in NADH-GDH specific activity was due to de-novo synthesis of the alpha-subunit of GDH and the assembly of only the more anodic isoenzymes.	NAD	42-46	L-galactose dehydrogenase	Vitis vinifera	122-125
8777059-4	1995	In cell-free studies, MTS was reduce to the soluble formazan in the presence of NADH and NADPH, and reaction were compared to those with dithiothreitol (DTT) or 2-mercaptoethanol (2-ME).	NAD	80-84	MLRL	Homo sapiens	22-25
8777059-7	1995	Generation of either NADH or NADPH in solution by malate dehydrogenase or isocitrate dehydrogenase, respectively, was monitored by the MTS reduction reaction.	NAD	21-25	MLRL	Homo sapiens	135-138
1350433-2	1992	An enzyme layer composed of glutamate dehydrogenase (GDH) and glutamate-pyruvate transaminase (GPT) is used to produce reduced nicotinamide adenine dinucleotide (NADH) at the tip of a fiber-optic probe.	NAD	127-160	glutamic--pyruvic transaminase	Homo sapiens	62-93
8777059-9	1995	This system represents a useful tool for evaluating reaction kinetics in solutions of NAD- or NADP-dependent dehydrogenase enzymes, and these reactions can be performed in typical biological buffers containing reducing agents without significant interference to the MTS/formazan system.	NAD	86-89	MLRL	Homo sapiens	266-269
1350433-2	1992	An enzyme layer composed of glutamate dehydrogenase (GDH) and glutamate-pyruvate transaminase (GPT) is used to produce reduced nicotinamide adenine dinucleotide (NADH) at the tip of a fiber-optic probe.	NAD	127-160	glutamic--pyruvic transaminase	Homo sapiens	95-98
7631008-6	1995	Radiolabeling of control and irradiated samples with [32P]NAD or [32P]orthophosphoric acid revealed the acidic species of B23 to be both ADP-ribosylated and phosphorylated.	NAD	58-61	nucleophosmin 1	Homo sapiens	122-125
1350433-2	1992	An enzyme layer composed of glutamate dehydrogenase (GDH) and glutamate-pyruvate transaminase (GPT) is used to produce reduced nicotinamide adenine dinucleotide (NADH) at the tip of a fiber-optic probe.	NAD	162-166	glutamic--pyruvic transaminase	Homo sapiens	62-93
1350433-2	1992	An enzyme layer composed of glutamate dehydrogenase (GDH) and glutamate-pyruvate transaminase (GPT) is used to produce reduced nicotinamide adenine dinucleotide (NADH) at the tip of a fiber-optic probe.	NAD	162-166	glutamic--pyruvic transaminase	Homo sapiens	95-98
7619054-4	1995	The enzymes alcohol dehydrogenase and diaphorase are used to cycle beta-NAD+ in the presence of ethanol and p-Iodonitrotetrazolium Violet.	NAD	67-76	dihydrolipoamide dehydrogenase	Homo sapiens	38-48
1314540-0	1992	Superoxide generated by glutathione reductase initiates a vanadate-dependent free radical chain oxidation of NADH.	NAD	109-113	glutathione-disulfide reductase	Homo sapiens	24-45
7721768-2	1995	This NAD-dependent enzyme catalyzes the formation of deoxyhypusine by transfer of the butylamine portion of spermidine to the epsilon-amino group of a specific lysine residue in the eIF-5A precursor.	NAD	5-8	eukaryotic translation initiation factor 5A	Rattus norvegicus	182-188
1313365-13	1992	When purified EF-2 from pyBHK cells was incubated with [carbonyl-14C]nicotinamide and diphtheria toxin fragment A, under conditions for reversal of the ADP-ribosylation reaction, [14C]NAD was generated.	NAD	184-187	elongation factor 2	Cricetulus griseus	14-18
7887984-10	1995	The substrate (acetaldehyde, 80 microM) and cofactor (NAD, 0.5 mM) together completely protected ALDH from inhibition by MeDTC sulfone; substrate alone partially protected the enzyme.	NAD	54-57	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	97-101
1898092-9	1991	These results suggest that S-acylation of the enzyme prevents a stabilizing conformational change induced in MMSDH by NAD+ binding.	NAD	118-122	aldehyde dehydrogenase 6 family, member A1	Rattus norvegicus	109-114
7757200-5	1995	NADH and ADP (not NAD+ or ATP) enhanced LADH inactivation by Cu(II).	NAD	0-4	dihydrolipoamide dehydrogenase	Sus scrofa	40-44
1888731-1	1991	Kinetic parameters and primary deuterium kinetic isotope effects for NADH and five pyridine nucleotide substrates have been determined at pH 8.1 for human erythrocyte glutathione reductase.	NAD	69-73	glutathione-disulfide reductase	Homo sapiens	167-188
1888336-13	1991	Catalysis by AHD-2 accounted for more than 90% of the total NAD-dependent activity.	NAD	60-63	aldehyde dehydrogenase family 1, subfamily A1	Mus musculus	13-18
7588404-3	1995	11 beta HSD1 is a low affinity NADP dependent enzyme, while 11 beta HSD2 is a high affinity NAD dependent species thought to be responsible for endowing specificity on the mineralocorticoid receptor and for protecting the fetus from high circulating levels of maternal glucocorticoids.	NAD	31-34	RNA, U1 small nuclear 1	Homo sapiens	8-12
1864360-1	1991	Studies on the osmotic induction of glycerol production and glycerol-3-phosphate dehydrogenase (NAD+) Production of glycerol and a key enzyme in glycerol production, glycerol 3-phosphate dehydrogenase (NAD+) (GPD), was studied in Saccharomyces cerevisiae cultured in basal media or media of high salinity, with glucose, raffinose or ethanol as the sole carbon source.	NAD	96-100	glycerol-3-phosphate dehydrogenase	Saccharomyces cerevisiae S288C	60-94
1864360-1	1991	Studies on the osmotic induction of glycerol production and glycerol-3-phosphate dehydrogenase (NAD+) Production of glycerol and a key enzyme in glycerol production, glycerol 3-phosphate dehydrogenase (NAD+) (GPD), was studied in Saccharomyces cerevisiae cultured in basal media or media of high salinity, with glucose, raffinose or ethanol as the sole carbon source.	NAD	96-100	glycerol-3-phosphate dehydrogenase	Saccharomyces cerevisiae S288C	166-200
7827022-3	1995	At variable NAD, rS1, C204, and C180 ADP-ribosylated alpha i3C20 with similar initial velocities which followed Michaelis-Menten kinetics.	NAD	12-15	retinoschisin 1	Rattus norvegicus	17-20
1646634-2	1991	It is concluded that: (1) The decrease of output flow of the transhydrogenase proton pump, defined as the rate of reduction of NADP+ by NADH, is linearily correlated with the decrease of input force, delta mu H+, in an extended range of delta mu H+, independently of whether the H(+)-generating pump is the ATPase or a redox pump, or whether delta mu H+ is depressed by inhibitors of the H(+)-generating pump such as oligomycin or malonate, or by uncouplers.	NAD	136-140	dynein axonemal heavy chain 8	Homo sapiens	307-313
7822295-2	1995	Pseudomonas aeruginosa exotoxin A (ETA) is a member of the family of bacterial ADP-ribosylating toxins which use NAD+ as the ADP-ribose donor.	NAD	113-117	endothelin receptor type A	Homo sapiens	23-33
1708393-6	1991	TCII has no homology with the amino-terminal region of R-IF that has been reported to have significant primary as well as secondary structural homology with the nucleotide-binding domain of NAD-dependent oxidoreductases.	NAD	190-193	transcobalamin 2	Homo sapiens	0-4
7822295-2	1995	Pseudomonas aeruginosa exotoxin A (ETA) is a member of the family of bacterial ADP-ribosylating toxins which use NAD+ as the ADP-ribose donor.	NAD	113-117	endothelin receptor type A	Homo sapiens	35-38
7542321-1	1995	The enzyme S-adenosylhomocysteine hydrolase (E.C.3.3.1.1) occurs in two forms in bovine liver: Type A, which carries four moles of NAD+ per mole of enzyme tetramer, and Type B, which carries two moles of NAD+ per mole of tetramer.	NAD	131-135	adenosylhomocysteinase	Bos taurus	11-43
1912072-6	1991	Thus, incubation of the alpha-ketoglutarate dehydrogenase complex with NADH has been found to induce the conversion from the non-cooperative form to the cooperative one, presumably through the reduction of lipoic acid bound to the complex in the reaction catalyzed by lipoyl dehydrogenase, the third component of the complex.	NAD	71-75	dihydrolipoamide dehydrogenase	Homo sapiens	268-288
7542321-1	1995	The enzyme S-adenosylhomocysteine hydrolase (E.C.3.3.1.1) occurs in two forms in bovine liver: Type A, which carries four moles of NAD+ per mole of enzyme tetramer, and Type B, which carries two moles of NAD+ per mole of tetramer.	NAD	204-208	adenosylhomocysteinase	Bos taurus	11-43
1934310-2	1991	It is now shown that the perplexity may be due to the possibility that the coenzyme (NAD) required for UDPG-D activity, may be acting as a substrate for a second dehydrogenase, namely xanthine dehydrogenase, which may utilize NAD as its substrate.	NAD	85-88	UDP-glucose 6-dehydrogenase	Homo sapiens	103-109
7721724-2	1994	The affinity of the membrane-bound enzyme for ATP during NADH oxidation was calculated from the ratio of the rate constants for the forward binding step (k+1) and the reverse dissociation step (k-1).	NAD	57-61	keratin 1	Homo sapiens	194-197
7721724-4	1994	In the presence of NADH and ADP an additional enhancement of k-1 was observed.	NAD	19-23	keratin 1	Homo sapiens	61-64
1999388-9	1991	The activity determined by the C-terminal region of the XylA sequence may be the reduction of the oxidized form of ferredoxin by concomitant oxidation of NADH.	NAD	154-158	xylose isomerase	Pseudomonas putida	56-60
7815897-8	1994	Co-incubation with 2-CdA and the poly-ADP-ribose synthetase inhibitor 3-MOB, which is known to render cells resistant to 2-CdA toxicity by preventing cellular nicotinamide adenine dinucleotide (NAD)- and adenosine triphosphase-depletion, also reversed the effect of 2-CdA on lipid accumulation.	NAD	159-192	sphingomyelin synthase 1	Mus musculus	72-75
2001241-8	1991	However, previously accumulated oxaloacetate transitorily decreased the level of the reduction of the NAD+ driven by succinate, by causing the reversal of the malate dehydrogenase reaction.	NAD	102-106	NAD-dependent malic enzyme 62 kDa isoform, mitochondrial	Solanum tuberosum	159-179
7815897-8	1994	Co-incubation with 2-CdA and the poly-ADP-ribose synthetase inhibitor 3-MOB, which is known to render cells resistant to 2-CdA toxicity by preventing cellular nicotinamide adenine dinucleotide (NAD)- and adenosine triphosphase-depletion, also reversed the effect of 2-CdA on lipid accumulation.	NAD	194-197	sphingomyelin synthase 1	Mus musculus	72-75
8034647-1	1994	The reductive half-reaction of milk xanthine dehydrogenase (XDH) with NADH and with xanthine has been studied at pH 7.5, 25 degree C. NADH reduces XDH to the two-electron reduced form at a rate of 18 s-1, independent of NADH concentration over the range studied.	NAD	70-74	xanthine dehydrogenase	Homo sapiens	36-58
1955295-7	1991	It was concluded that in the hepatic dysfunction caused by the dietary products of lipid peroxidation the incorporated decomposed products in the liver directly inactivated the mitochondrial NAD-dependent aldehyde dehydrogenase and glucose-6-phosphate dehydrogenase, destroyed coenzyme A, and disturbed the synthetic system of glucokinase.	NAD	191-194	glucose-6-phosphate dehydrogenase	Rattus norvegicus	232-265
1955295-7	1991	It was concluded that in the hepatic dysfunction caused by the dietary products of lipid peroxidation the incorporated decomposed products in the liver directly inactivated the mitochondrial NAD-dependent aldehyde dehydrogenase and glucose-6-phosphate dehydrogenase, destroyed coenzyme A, and disturbed the synthetic system of glucokinase.	NAD	191-194	glucokinase	Rattus norvegicus	327-338
8034647-1	1994	The reductive half-reaction of milk xanthine dehydrogenase (XDH) with NADH and with xanthine has been studied at pH 7.5, 25 degree C. NADH reduces XDH to the two-electron reduced form at a rate of 18 s-1, independent of NADH concentration over the range studied.	NAD	70-74	xanthine dehydrogenase	Homo sapiens	60-63
8034647-1	1994	The reductive half-reaction of milk xanthine dehydrogenase (XDH) with NADH and with xanthine has been studied at pH 7.5, 25 degree C. NADH reduces XDH to the two-electron reduced form at a rate of 18 s-1, independent of NADH concentration over the range studied.	NAD	70-74	xanthine dehydrogenase	Homo sapiens	147-150
8034647-1	1994	The reductive half-reaction of milk xanthine dehydrogenase (XDH) with NADH and with xanthine has been studied at pH 7.5, 25 degree C. NADH reduces XDH to the two-electron reduced form at a rate of 18 s-1, independent of NADH concentration over the range studied.	NAD	134-138	xanthine dehydrogenase	Homo sapiens	36-58
8034647-1	1994	The reductive half-reaction of milk xanthine dehydrogenase (XDH) with NADH and with xanthine has been studied at pH 7.5, 25 degree C. NADH reduces XDH to the two-electron reduced form at a rate of 18 s-1, independent of NADH concentration over the range studied.	NAD	134-138	xanthine dehydrogenase	Homo sapiens	60-63
8034647-1	1994	The reductive half-reaction of milk xanthine dehydrogenase (XDH) with NADH and with xanthine has been studied at pH 7.5, 25 degree C. NADH reduces XDH to the two-electron reduced form at a rate of 18 s-1, independent of NADH concentration over the range studied.	NAD	134-138	xanthine dehydrogenase	Homo sapiens	147-150
8034647-1	1994	The reductive half-reaction of milk xanthine dehydrogenase (XDH) with NADH and with xanthine has been studied at pH 7.5, 25 degree C. NADH reduces XDH to the two-electron reduced form at a rate of 18 s-1, independent of NADH concentration over the range studied.	NAD	134-138	xanthine dehydrogenase	Homo sapiens	36-58
8034647-1	1994	The reductive half-reaction of milk xanthine dehydrogenase (XDH) with NADH and with xanthine has been studied at pH 7.5, 25 degree C. NADH reduces XDH to the two-electron reduced form at a rate of 18 s-1, independent of NADH concentration over the range studied.	NAD	134-138	xanthine dehydrogenase	Homo sapiens	60-63
8034647-1	1994	The reductive half-reaction of milk xanthine dehydrogenase (XDH) with NADH and with xanthine has been studied at pH 7.5, 25 degree C. NADH reduces XDH to the two-electron reduced form at a rate of 18 s-1, independent of NADH concentration over the range studied.	NAD	134-138	xanthine dehydrogenase	Homo sapiens	147-150
8034647-4	1994	The four-electron reduced species reached through reduction by NADH is the same as the species obtained upon reaction of NAD with fully reduced XDH.	NAD	63-67	xanthine dehydrogenase	Homo sapiens	144-147
8034647-4	1994	The four-electron reduced species reached through reduction by NADH is the same as the species obtained upon reaction of NAD with fully reduced XDH.	NAD	63-66	xanthine dehydrogenase	Homo sapiens	144-147
8034647-9	1994	The reductive half-reaction of XDH with xanthine is rate-limiting in xanthine/NAD turnover, which appears to occur between the two- and four-electron reduced enzyme species.	NAD	78-81	xanthine dehydrogenase	Homo sapiens	31-34
8031116-0	1994	Kinetic properties of NAD-dependent glyceraldehyde-3-phosphate dehydrogenase from the host fraction of soybean root nodules.	NAD	22-25	glyceraldehyde-3-phosphate dehydrogenase	Glycine max	36-76
8031116-1	1994	The kinetic mechanism of NAD-dependent glyceraldehyde-3-phosphate dehydrogenase [D-glyceraldehyde-3-phosphate:NAD+ oxidoreductase (phosphorylating), EC 1.2.1.12] from the host cytosolic fraction of soybean (Glycine max L. Merr.	NAD	25-28	glyceraldehyde-3-phosphate dehydrogenase	Glycine max	39-79
8031116-8	1994	The possible role of these properties in the regulation of NAD-dependent glyceraldehyde-3-phosphate dehydrogenase in the host cytosol of soybean nodules is discussed.	NAD	59-62	glyceraldehyde-3-phosphate dehydrogenase	Glycine max	73-113
8196651-2	1994	We have cloned a gene encoding the key enzyme of glycerol synthesis, the NADH-dependent cytosolic glycerol-3-phosphate dehydrogenase, and we named it GPD1.	NAD	73-77	glycerol-3-phosphate dehydrogenase	Saccharomyces cerevisiae S288C	98-132
8155713-4	1994	The Michaelis constants for ALDH-1 and -2, determined from initial velocities (for ALDH-1) and single reaction progress curves (for ALDH-2), are 180 +/- 10 microM and 0.20 +/- 0.02 microM, respectively (pH 7.5 and 9.5, saturating NAD+ in both cases).	NAD	230-234	aldehyde dehydrogenase 2 family member	Homo sapiens	132-138
8132639-2	1994	We have proposed that cytidine monophospho-N-acetylneuraminic acid (CMP-NeuAc) hydroxylation is carried out by a multienzyme system involving CMP-NeuAc hydroxylase (the terminal enzyme of the system), cytochrome b5, and an NADH-dependent cytochrome b5-reducing factor (Kozutsumi, Y., Kawano, T., Yamakawa, T., and Suzuki, A.	NAD	223-227	cytidine monophospho-N-acetylneuraminic acid hydroxylase	Mus musculus	142-163
8297331-9	1994	NADH/lipoamide-stimulated vitamin K epoxide reduction is uncoupled by traces of Triton X-100, suggesting that microsomal lipoamide reductase and vitamin K epoxide reductase are associated.	NAD	0-4	dihydrolipoamide dehydrogenase	Homo sapiens	121-140
8297331-10	1994	The results suggest that the vitamin K cycle obtains reducing equivalents from NADH through microsomal lipoamide reductase.	NAD	79-83	dihydrolipoamide dehydrogenase	Homo sapiens	103-122
8138543-6	1993	All the Cys-112 mutant HDHs catalyzed both the alcohol dehydrogenase and aldehyde dehydrogenase reactions, producing 1 mol of L-histidine during the reduction of 2 mol of NAD+, as did the wild type HDH.	NAD	171-175	histidinol dehydrogenase, chloroplastic	Brassica oleracea	23-26
8227023-1	1993	The reduction of milk xanthine dehydrogenase by salicylate anion radical (SL-), nicotinamide adenine dinucleotide radical (NAD.), and 1-methylnicotinamide (NMA) radicals was investigated by the use of pulse radiolysis.	NAD	123-127	xanthine dehydrogenase	Homo sapiens	22-44
7873673-1	1994	Almost complete slow activation of the deactivated purified Complex I was observed after the steady-state NADH: cytochrome c reductase reaction turnovers catalyzed by the endogenous (tightly-bound) ubiquinone and contaminant Complex III.	NAD	106-110	LOC104968582	Bos taurus	112-124
8221687-5	1993	MMC interaction with XDH was also assessed by monitoring the ability of MMC to inhibit XDH-mediated uric acid and NADH formation.	NAD	114-118	xanthine dehydrogenase	Homo sapiens	87-90
7767879-2	1994	ATPase activity was measured using a phosphoenolpyruvate-pyruvate kinase regenerating system for ATP that was monitored by NADH fluorescence changes, and Ca2+ was measured using fura 2 fluorescence.	NAD	123-127	dynein axonemal heavy chain 8	Homo sapiens	0-6
8221687-9	1993	Stimulation of uric acid formation and decreases in NADH formation by XDH in the presence of MMC suggest that MMC interaction with XDH may occur at the NAD(+)-binding region of the enzyme.	NAD	52-56	xanthine dehydrogenase	Homo sapiens	70-73
8221687-9	1993	Stimulation of uric acid formation and decreases in NADH formation by XDH in the presence of MMC suggest that MMC interaction with XDH may occur at the NAD(+)-binding region of the enzyme.	NAD	52-56	xanthine dehydrogenase	Homo sapiens	131-134
8221687-9	1993	Stimulation of uric acid formation and decreases in NADH formation by XDH in the presence of MMC suggest that MMC interaction with XDH may occur at the NAD(+)-binding region of the enzyme.	NAD	152-158	xanthine dehydrogenase	Homo sapiens	70-73
8037463-1	1994	Cabbage histidinol dehydrogenase (HDH) oxidizes L-histidinol to L-histidine through two sequential NAD(+)-linked reactions via an alkaline-labile, L-histidinaldehyde intermediate.	NAD	99-105	histidinol dehydrogenase, chloroplastic	Brassica oleracea	34-37
8221687-9	1993	Stimulation of uric acid formation and decreases in NADH formation by XDH in the presence of MMC suggest that MMC interaction with XDH may occur at the NAD(+)-binding region of the enzyme.	NAD	152-158	xanthine dehydrogenase	Homo sapiens	131-134
8248161-4	1993	Analysis of potential NAD binding sites suggested a simple hypothesis for the conversion of human XD into the oxygen metabolite forming xanthine oxidase (XO; xanthine:oxygen oxidoreductase, EC 1.1.3.22).	NAD	22-25	xanthine dehydrogenase	Homo sapiens	98-100
8248161-4	1993	Analysis of potential NAD binding sites suggested a simple hypothesis for the conversion of human XD into the oxygen metabolite forming xanthine oxidase (XO; xanthine:oxygen oxidoreductase, EC 1.1.3.22).	NAD	22-25	hydroxysteroid 17-beta dehydrogenase 6	Homo sapiens	174-188
8160299-6	1993	The apparent values Km and V have been calculated for aldehyde dehydrogenase 1 in people and aldehyde dehydrogenase 2 in rats when using acetaldehyde and NAD as the reaction substrates.	NAD	154-157	aldehyde dehydrogenase 2 family member	Homo sapiens	93-117
8369428-0	1993	NADH fluorescence of isolated ventricular myocytes: effects of pacing, myoglobin, and oxygen supply.	NAD	0-4	myoglobin	Rattus norvegicus	71-80
8369428-8	1993	However, NAD reduction increased reversibly in response to electrically paced contractions when: (a) myoglobin was inactivated with sodium nitrite (37 +/- 7%; n = 48); or (b) cells were more densely layered and gassed with 20% O2/5% CO2 (48 +/- 3%; n = 30).	NAD	9-12	myoglobin	Rattus norvegicus	101-110
8369428-9	1993	We conclude that (a) the ratio NADH/NAD is decreased in well-oxygenated cells with increased work; (b) steady-state NAD reduction is increased with increased work when oxygen delivery is limited; and (c) functional myoglobin ensures an oxygen supply to the mitochondria of working cells.	NAD	31-35	myoglobin	Rattus norvegicus	215-224
8369428-9	1993	We conclude that (a) the ratio NADH/NAD is decreased in well-oxygenated cells with increased work; (b) steady-state NAD reduction is increased with increased work when oxygen delivery is limited; and (c) functional myoglobin ensures an oxygen supply to the mitochondria of working cells.	NAD	31-34	myoglobin	Rattus norvegicus	215-224
8369428-9	1993	We conclude that (a) the ratio NADH/NAD is decreased in well-oxygenated cells with increased work; (b) steady-state NAD reduction is increased with increased work when oxygen delivery is limited; and (c) functional myoglobin ensures an oxygen supply to the mitochondria of working cells.	NAD	36-39	myoglobin	Rattus norvegicus	215-224
8311938-2	1993	The basis of the detection system for the assay is the electrochemical oxidation of NADH produced by G6PDH-labelled theophylline at a potential of +150 mV vs Ag/AgCl using platinised activated carbon (PACE) electrodes.	NAD	84-88	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	101-106
1328233-6	1992	XDH can be converted back to the XO form by the addition of three to four equivalents of the disulfide-forming reagent 4,4"-dithiodipyridine, suggesting that, in the XDH form of the enzyme, disulfide bonds are broken; this may cause a conformational change which creates a binding site for NAD and changes the protein structure near the flavin.	NAD	290-293	xanthine dehydrogenase	Homo sapiens	0-3
1328233-6	1992	XDH can be converted back to the XO form by the addition of three to four equivalents of the disulfide-forming reagent 4,4"-dithiodipyridine, suggesting that, in the XDH form of the enzyme, disulfide bonds are broken; this may cause a conformational change which creates a binding site for NAD and changes the protein structure near the flavin.	NAD	290-293	xanthine dehydrogenase	Homo sapiens	166-169
1562584-1	1992	Holo-CRBP (cellular retinol binding protein) is recognized specifically by an NADP-dependent microsomal retinol dehydrogenase and protects retinol from conversion into retinal by NAD and NADPH dependent dehydrogenases.	NAD	78-81	retinol binding protein 1	Homo sapiens	5-9
1311164-2	1992	ESR measurements demonstrated that deferoxamine can efficiently reduce the concentration of the Cr(V) intermediate as formed in the reduction of Cr(VI) by NAD(P)H or a flavoenzyme glutathione reductase/NADH.	NAD	202-206	glutathione-disulfide reductase	Homo sapiens	180-201
1319549-1	1992	The activity of pure calf-liver and Escherichia coli thioredoxin reductases decreased drastically in the presence of NADPH or NADH, while NADP+, NAD+ and oxidized E. coli thioredoxin activated both enzymes significantly, particularly the bacterial one.	NAD	126-130	thioredoxin	Bos taurus	53-64
1319549-1	1992	The activity of pure calf-liver and Escherichia coli thioredoxin reductases decreased drastically in the presence of NADPH or NADH, while NADP+, NAD+ and oxidized E. coli thioredoxin activated both enzymes significantly, particularly the bacterial one.	NAD	145-149	thioredoxin	Bos taurus	53-64
1319549-3	1992	Oxidized E. coli thioredoxin fully protected both enzymes from inactivation, and also promoted their complete reactivation after only 30 min incubation at 30 degrees C. Lower but significant protection and reactivation was also observed with NADP+ and NAD+.	NAD	252-256	thioredoxin	Bos taurus	17-28
1748655-3	1991	In contrast, titration of transducin in the presence of a constant concentration of NAD (25 nM) showed that rS1 possessed a lower Kmapp(transducin) and greater kcat than either C195 or C180.	NAD	84-87	retinoschisin 1	Rattus norvegicus	108-111
1911436-8	1991	FSA is a cofactor site-directed reagent that binds with similar affinity as a competitive inhibitor of NAD+ reduction by dehydrogenase (Ki = 162 microM) or as a stimulator of isomerase (Km = 153 microM).	NAD	103-107	bridge-like lipid transfer protein family member 1	Homo sapiens	0-3
8127183-6	1994	Spectroscopic scans demonstrated consistently that RA-treated MTS exhibit a decrease in the peak associated with reduced nicotinamide-adenine dinucleotide (NADH) and an increase in the peaks associated with flavins, tryptophan, and cytokeratins when compared to controls.	NAD	121-154	MLRL	Homo sapiens	62-65
8127183-6	1994	Spectroscopic scans demonstrated consistently that RA-treated MTS exhibit a decrease in the peak associated with reduced nicotinamide-adenine dinucleotide (NADH) and an increase in the peaks associated with flavins, tryptophan, and cytokeratins when compared to controls.	NAD	156-160	MLRL	Homo sapiens	62-65
1979936-10	1990	An increase of the NADP-linked enzymes glucose-6-phosphate dehydrogenase (G6PDH), malic enzyme, extra-mitochondrial ICDH as well as an enhancement of NAD-dependent alpha-G3PDH and lactate dehydrogenase were found following DEHP administration.	NAD	19-22	glucose-6-phosphate dehydrogenase	Rattus norvegicus	39-72
1979936-10	1990	An increase of the NADP-linked enzymes glucose-6-phosphate dehydrogenase (G6PDH), malic enzyme, extra-mitochondrial ICDH as well as an enhancement of NAD-dependent alpha-G3PDH and lactate dehydrogenase were found following DEHP administration.	NAD	19-22	glucose-6-phosphate dehydrogenase	Rattus norvegicus	74-79
2387845-0	1990	Proteolytic conversion of xanthine dehydrogenase from the NAD-dependent type to the O2-dependent type.	NAD	58-61	xanthine dehydrogenase	Rattus norvegicus	26-48
2375745-1	1990	The relationship between the NADH:lipoamide reductase and NADH:quinone reductase reactions of pig heart lipoamide dehydrogenase (EC 1.6.4.3) was investigated.	NAD	29-33	dihydrolipoamide dehydrogenase	Sus scrofa	104-127
2293579-7	1990	A corresponding rise of nicotinamide adenine dinucleotide (reduced form) in vitro inhibited xanthine dehydrogenase activity by 60%-76%.	NAD	24-57	xanthine dehydrogenase	Rattus norvegicus	92-114
2293579-8	1990	Increased purine degradation, possibly associated with a shift from the dehydrogenase to the xanthine oxidase pathway (secondary to nicotinamide adenine dinucleotide [reduced form]-mediated inhibition of xanthine dehydrogenase activity) is proposed as a possible mechanism for ethanol-stimulated free radical production.	NAD	132-165	xanthine dehydrogenase	Rattus norvegicus	204-226
17038483-4	2007	Recently, we reported that the yeast single-subunit nicotinamide adenine dinucleotide (reduced) dehydrogenase (NDI1) is resistant to rotenone, a complex I inhibitor that produces a parkinsonian syndrome in rats, and that overexpression of NDI1 in SK-N-MC cells prevents the toxicity of rotenone.	NAD	52-85	NADH-ubiquinone reductase (H(+)-translocating) NDI1	Saccharomyces cerevisiae S288C	111-115
17038483-4	2007	Recently, we reported that the yeast single-subunit nicotinamide adenine dinucleotide (reduced) dehydrogenase (NDI1) is resistant to rotenone, a complex I inhibitor that produces a parkinsonian syndrome in rats, and that overexpression of NDI1 in SK-N-MC cells prevents the toxicity of rotenone.	NAD	52-85	NADH-ubiquinone reductase (H(+)-translocating) NDI1	Saccharomyces cerevisiae S288C	239-243
34453970-3	2022	Treatment of CGS-exposed dams with the NAD+-stabilizing agent P7C3-A20 during pregnancy and postpartum, however, preserved normal maternal care behavior.	NAD	39-43	TNF alpha induced protein 3	Homo sapiens	67-70
34919052-5	2021	Mechanistic analysis suggests that NMNAT interferes with DNA damage-p53-caspase-3 apoptosis signaling pathway by enhancing NAD+-dependent posttranslational modifications (PTMs) poly(ADP-ribosyl)ation (PARylation) and deacetylation of p53.	NAD	123-127	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	35-40
34919052-7	2021	Our findings reveal a novel tumorigenic mechanism involving protein complex formation of p53 with NAD+ synthetic enzyme NMNAT and NAD+-dependent PTM enzymes that regulates glioma growth.	NAD	98-102	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	120-125
34938344-0	2021	Jian-Pi-Yi-Shen Formula Alleviates Chronic Kidney Disease in Two Rat Models by Modulating QPRT/NAD+/SIRT3/Mitochondrial Dynamics Pathway.	NAD	95-99	quinolinate phosphoribosyltransferase	Rattus norvegicus	90-94
34938344-11	2021	In addition, CKD rats exhibited suppressed QPRT/NAD+/SIRT3 signal, increased mitochondrial fission, and decreased mitochondrial fusion.	NAD	48-52	quinolinate phosphoribosyltransferase	Rattus norvegicus	43-47
34938344-13	2021	Conclusion: In conclusion, administration of JPYSF effectively alleviated CKD progression in two rat models, which may be related with regulation of the QPRT/NAD+/SIRT3/mitochondrial dynamics pathway.	NAD	158-162	quinolinate phosphoribosyltransferase	Rattus norvegicus	153-157
34878972-0	2021	Nuclear NAD+-biosynthetic enzyme NMNAT1 facilitates development and early survival of retinal neurons.	NAD	8-12	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	33-39
1897001-8	1991	These results are consistent with the idea that conversion of NAD(+)-dependent xanthine dehydrogenase to xanthine oxidase is involved in the zone-specific hepatotoxicity of allyl alcohol.	NAD	62-68	xanthine dehydrogenase	Rattus norvegicus	79-101
1993675-2	1991	Purified rS1 and C180 peptide, a deletion peptide which contains amino acids 1-180 of rS1, had Km values for NAD of 24 and 13 microM and kcat values of 22 and 24 h-1, respectively, in the NAD glycohydrolase reaction.	NAD	109-112	retinoschisin 1	Rattus norvegicus	9-12
1993675-2	1991	Purified rS1 and C180 peptide, a deletion peptide which contains amino acids 1-180 of rS1, had Km values for NAD of 24 and 13 microM and kcat values of 22 and 24 h-1, respectively, in the NAD glycohydrolase reaction.	NAD	109-112	retinoschisin 1	Rattus norvegicus	86-89
1993675-10	1991	These studies indicate that (i) rS1, purified from Escherichia coli, possesses biochemical properties similar to S1 subunit purified from pertussis toxin, (ii) amino acids 1-180 of the S1 subunit contain residues required for NAD binding, N-glycosidic cleavage, and transfer of ADP-ribose to transducin, and (iii) residues between 181 and 219 of the S1 subunit are required for efficient ADP-ribosyltransferase activity.	NAD	226-229	retinoschisin 1	Rattus norvegicus	32-35
2060039-3	1991	The cytosolic ALDH activity of the liver was determined either with propionaldehyde and NAD (P/NAD), or with benzaldehyde and NADP (B/NADP).	NAD	95-99	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	14-18
1858346-4	1991	Apparent Ki value for NADH constituted 0.88-0.10 mM, thus demonstrating the effective regulation of the lipoamide dehydrogenase activity by end products.	NAD	22-26	dihydrolipoamide dehydrogenase	Homo sapiens	104-127
2253346-1	1990	We describe a kinetic enzymic method for serum bicarbonate analysis, using wheat germ phosphoenolpyruvate carboxylase (EC 4.1.1.31) coupled through oxaloacetate reduction with NADH in the presence of malate dehydrogenase (EC 1.1.1.37).	NAD	176-180	phosphoenolpyruvate carboxylase 2	Triticum aestivum	86-117
34461505-5	2021	Computational and biochemical studies indicated that these compounds exhibited competitive SIRT5 inhibition with respect to the glutaryl-lysine substrate rather than nicotinamide adenine dinucleotide cofactor.	NAD	166-199	sirtuin 5	Homo sapiens	91-96
1964451-4	1990	An antibody against cytochrome b5 markedly reduced the CMP-NeuAc hydroxylase activity when added to incubation mixture containing either NADH or NADPH as an electron donor.	NAD	137-141	cytidine monophospho-N-acetylneuraminic acid hydroxylase, pseudogene	Homo sapiens	55-76
34899370-2	2021	Moreover, caloric restriction is believed to slow down aging by boosting the activity of some sirtuins through activating adenosine monophosphate-activated protein kinase (AMPK), thus raising the level of intracellular nicotinamide adenine dinucleotide (NAD+) by stimulating NAD+ biosynthesis.	NAD	219-252	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	122-170
2400809-6	1990	Levels of aldehyde dehydrogenase (ALDH), which inactivates CY by prevention of formation of PhM, were significantly elevated in these CY-resistant AML cells: cytosolic and particulate ALDH fractions from these cells were 11 to 13 times control with NAD cofactor and propanal substrate and three to four times control with NADP cofactor and benzaldehyde substrate.	NAD	249-252	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	10-32
34899370-2	2021	Moreover, caloric restriction is believed to slow down aging by boosting the activity of some sirtuins through activating adenosine monophosphate-activated protein kinase (AMPK), thus raising the level of intracellular nicotinamide adenine dinucleotide (NAD+) by stimulating NAD+ biosynthesis.	NAD	219-252	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	172-176
34899370-2	2021	Moreover, caloric restriction is believed to slow down aging by boosting the activity of some sirtuins through activating adenosine monophosphate-activated protein kinase (AMPK), thus raising the level of intracellular nicotinamide adenine dinucleotide (NAD+) by stimulating NAD+ biosynthesis.	NAD	254-258	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	122-170
34899370-2	2021	Moreover, caloric restriction is believed to slow down aging by boosting the activity of some sirtuins through activating adenosine monophosphate-activated protein kinase (AMPK), thus raising the level of intracellular nicotinamide adenine dinucleotide (NAD+) by stimulating NAD+ biosynthesis.	NAD	254-258	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	172-176
34899370-2	2021	Moreover, caloric restriction is believed to slow down aging by boosting the activity of some sirtuins through activating adenosine monophosphate-activated protein kinase (AMPK), thus raising the level of intracellular nicotinamide adenine dinucleotide (NAD+) by stimulating NAD+ biosynthesis.	NAD	275-279	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	122-170
34899370-2	2021	Moreover, caloric restriction is believed to slow down aging by boosting the activity of some sirtuins through activating adenosine monophosphate-activated protein kinase (AMPK), thus raising the level of intracellular nicotinamide adenine dinucleotide (NAD+) by stimulating NAD+ biosynthesis.	NAD	275-279	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	172-176
8129726-9	1994	The converse effects of glycerol and dihydroxy-acetone suggest a role for the cytosolic NADH/NAD+ redox state in controlling glucokinase translocation.	NAD	88-92	glucokinase	Rattus norvegicus	125-136
8129726-9	1994	The converse effects of glycerol and dihydroxy-acetone suggest a role for the cytosolic NADH/NAD+ redox state in controlling glucokinase translocation.	NAD	93-97	glucokinase	Rattus norvegicus	125-136
2400809-6	1990	Levels of aldehyde dehydrogenase (ALDH), which inactivates CY by prevention of formation of PhM, were significantly elevated in these CY-resistant AML cells: cytosolic and particulate ALDH fractions from these cells were 11 to 13 times control with NAD cofactor and propanal substrate and three to four times control with NADP cofactor and benzaldehyde substrate.	NAD	249-252	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	34-38
16667675-2	1990	The antiserum recognized the seven isoenzymes of NADH-GDH and precipitated all the enzyme activity from the three tissues tested.	NAD	49-53	L-galactose dehydrogenase	Vitis vinifera	54-57
8129740-4	1994	Any activity of monoamine oxidase-A towards this substrate was too low to allow accurate determinations to be made by either luminometric determination of H2O2 formation or spectrophotometric coupling of aldehyde formation to NAD+ reduction in the presence of aldehyde dehydrogenase.	NAD	226-230	monoamine oxidase A	Rattus norvegicus	16-35
8297331-3	1994	The study shows that microsomes contain NADH-dependent lipoamide reductase activity.	NAD	40-44	dihydrolipoamide dehydrogenase	Homo sapiens	55-74
8130648-7	1994	Increasingly enough, patients with NAD displayed high IL-5 but low IL-4 levels.	NAD	35-38	interleukin 5	Homo sapiens	54-58
34758883-0	2021	Down-regulation of EPB41L4A-AS1 mediated the brain aging and neurodegenerative diseases via damaging synthesis of NAD+ and ATP.	NAD	114-118	EPB41L4A antisense RNA 1	Homo sapiens	19-31
34758883-8	2021	EPB41L4A-AS1 related genes were found to be enriched in the electron transport chain and NAD+ synthesis pathway.	NAD	89-93	EPB41L4A antisense RNA 1	Homo sapiens	0-12
34758883-10	2021	In addition, biological experiments proved that the downregulation of EPB41L4A-AS1 could reduce the expression of these genes via histone H3 lysine 27 acetylation, resulting in decreased NAD+ and ATP levels, while EPB41L4A-AS1 overexpression and nicotinamide riboside treatment could restore the NAD+ and ATP levels.	NAD	187-191	EPB41L4A antisense RNA 1	Homo sapiens	70-82
34758883-10	2021	In addition, biological experiments proved that the downregulation of EPB41L4A-AS1 could reduce the expression of these genes via histone H3 lysine 27 acetylation, resulting in decreased NAD+ and ATP levels, while EPB41L4A-AS1 overexpression and nicotinamide riboside treatment could restore the NAD+ and ATP levels.	NAD	296-300	EPB41L4A antisense RNA 1	Homo sapiens	70-82
34758883-10	2021	In addition, biological experiments proved that the downregulation of EPB41L4A-AS1 could reduce the expression of these genes via histone H3 lysine 27 acetylation, resulting in decreased NAD+ and ATP levels, while EPB41L4A-AS1 overexpression and nicotinamide riboside treatment could restore the NAD+ and ATP levels.	NAD	296-300	EPB41L4A antisense RNA 1	Homo sapiens	214-226
34758883-11	2021	CONCLUSIONS: Downregulation of EPB41L4A-AS1 not only disturbs NAD+ biosynthesis but also affects ATP synthesis.	NAD	62-66	EPB41L4A antisense RNA 1	Homo sapiens	31-43
16667675-3	1990	Western blot following SDS-PAGE revealed the same protein band for the three tissues, with a molecular mass of 42.5 kilodaltons corresponding to NADH-GDH subunit.	NAD	145-149	L-galactose dehydrogenase	Vitis vinifera	150-153
34758883-13	2021	However, overexpression of EPB41L4A-AS1 and nicotinamide riboside, a substrate of NAD+ synthesis, can reduce EPB41L4A-AS1 downregulation-mediated decrease of NAD+ and ATP synthesis.	NAD	82-86	EPB41L4A antisense RNA 1	Homo sapiens	27-39
16667675-4	1990	Results, based on the immunological studies, revealed that NADH-GDH from leaf, shoot, and root tissues are closely related proteins.	NAD	59-63	L-galactose dehydrogenase	Vitis vinifera	64-67
34758883-13	2021	However, overexpression of EPB41L4A-AS1 and nicotinamide riboside, a substrate of NAD+ synthesis, can reduce EPB41L4A-AS1 downregulation-mediated decrease of NAD+ and ATP synthesis.	NAD	82-86	EPB41L4A antisense RNA 1	Homo sapiens	109-121
34758883-13	2021	However, overexpression of EPB41L4A-AS1 and nicotinamide riboside, a substrate of NAD+ synthesis, can reduce EPB41L4A-AS1 downregulation-mediated decrease of NAD+ and ATP synthesis.	NAD	158-162	EPB41L4A antisense RNA 1	Homo sapiens	27-39
16667675-5	1990	Furthermore, addition of ammonium ions to the culture medium of in vitro grown explants resulted in a significant increase in NADH-GDH activity in root, shoot, and leaf tissues.	NAD	126-130	L-galactose dehydrogenase	Vitis vinifera	131-134
34758883-13	2021	However, overexpression of EPB41L4A-AS1 and nicotinamide riboside, a substrate of NAD+ synthesis, can reduce EPB41L4A-AS1 downregulation-mediated decrease of NAD+ and ATP synthesis.	NAD	158-162	EPB41L4A antisense RNA 1	Homo sapiens	109-121
8188630-1	1994	Histidinol dehydrogenase (HDH), a Zn-metalloenzyme, produces His from histidinol through two successive oxidation reactions with NAD+ as a coenzyme.	NAD	129-133	histidinol dehydrogenase, chloroplastic	Brassica oleracea	0-24
2390066-4	1990	Inactivation of 3 alpha-hydroxysteroid dehydrogenase by compound (I) displays an NAD+ concentration optimum.	NAD	81-85	aldo-keto reductase family 1 member C3	Homo sapiens	16-52
8188630-1	1994	Histidinol dehydrogenase (HDH), a Zn-metalloenzyme, produces His from histidinol through two successive oxidation reactions with NAD+ as a coenzyme.	NAD	129-133	histidinol dehydrogenase, chloroplastic	Brassica oleracea	26-29
2119895-7	1990	Aldose reductase utilized both reduced nicotinamide adenine dinucleotide phosphate (NADPH) and reduced nicotinamide adenine dinucleotide (NADH) as coenzymes, whereas aldehyde reductase utilized only NADPH.	NAD	39-72	aldo-keto reductase family 1 member B1	Rattus norvegicus	0-16
8241177-1	1993	UDP-galactose 4-epimerase contains NAD+ irreversibly but noncovalently bound to the active site.	NAD	35-39	UDP-galactose-4-epimerase	Homo sapiens	0-25
34975119-0	2021	Nicotinamide adenine dinucleotide promotes synaptic plasticity gene expression through regulation N-methyl-D-aspartate receptor/Ca2+/Erk1/2 pathway.	NAD	0-33	mitogen-activated protein kinase 3	Mus musculus	133-139
34975119-4	2021	Moreover, NADH significantly increased intracellular Ca2+ levels and the phosphorylation of Erk1/2, a downstream molecule of the NMDAR.	NAD	10-14	mitogen-activated protein kinase 3	Mus musculus	92-98
34975119-6	2021	In conclusion, this study indicates that NADH can promote the expression of synaptic plasticity-related IEGs through the NMDAR/Ca2+/Erk1/2 pathway, which provides a new way to understand the regulatory role of NADH in synaptic plasticity.	NAD	41-45	mitogen-activated protein kinase 3	Mus musculus	132-138
34975119-6	2021	In conclusion, this study indicates that NADH can promote the expression of synaptic plasticity-related IEGs through the NMDAR/Ca2+/Erk1/2 pathway, which provides a new way to understand the regulatory role of NADH in synaptic plasticity.	NAD	210-214	mitogen-activated protein kinase 3	Mus musculus	132-138
34403688-4	2021	However, with injury or disease the levels of the NAD+ biosynthetic enzyme NMNAT2 drop, increasing the NMN/ NAD+ ratio and thereby promoting NMN binding to the SARM1 allosteric site, which in turn induces a conformational change activating the SARM1 NAD+ hydrolase.	NAD	50-54	sterile alpha and TIR motif containing 1	Homo sapiens	160-165
34403688-4	2021	However, with injury or disease the levels of the NAD+ biosynthetic enzyme NMNAT2 drop, increasing the NMN/ NAD+ ratio and thereby promoting NMN binding to the SARM1 allosteric site, which in turn induces a conformational change activating the SARM1 NAD+ hydrolase.	NAD	50-54	sterile alpha and TIR motif containing 1	Homo sapiens	244-249
34403688-4	2021	However, with injury or disease the levels of the NAD+ biosynthetic enzyme NMNAT2 drop, increasing the NMN/ NAD+ ratio and thereby promoting NMN binding to the SARM1 allosteric site, which in turn induces a conformational change activating the SARM1 NAD+ hydrolase.	NAD	108-112	sterile alpha and TIR motif containing 1	Homo sapiens	244-249
8405427-4	1993	Our findings have pointed out that the most suitable electron acceptor for the NADH:CoQ reductase assay is the homolog CoQ1.	NAD	79-83	decaprenyl diphosphate synthase subunit 1	Homo sapiens	119-123
34403688-5	2021	Hence, NAD+ metabolites both regulate the activation of SARM1 and, in turn, are regulated by the SARM1 NAD+ hydrolase.	NAD	7-11	sterile alpha and TIR motif containing 1	Homo sapiens	56-61
2119895-7	1990	Aldose reductase utilized both reduced nicotinamide adenine dinucleotide phosphate (NADPH) and reduced nicotinamide adenine dinucleotide (NADH) as coenzymes, whereas aldehyde reductase utilized only NADPH.	NAD	138-142	aldo-keto reductase family 1 member B1	Rattus norvegicus	0-16
34403688-5	2021	Hence, NAD+ metabolites both regulate the activation of SARM1 and, in turn, are regulated by the SARM1 NAD+ hydrolase.	NAD	7-11	sterile alpha and TIR motif containing 1	Homo sapiens	97-102
1972335-0	1990	Purification and characterization of glycerol-3-phosphate dehydrogenase (NAD+) in the salt-tolerant yeast Debaryomyces hansenii.	NAD	73-77	glycerol-3-phosphate dehydrogenase	Saccharomyces cerevisiae S288C	37-71
34403688-5	2021	Hence, NAD+ metabolites both regulate the activation of SARM1 and, in turn, are regulated by the SARM1 NAD+ hydrolase.	NAD	103-107	sterile alpha and TIR motif containing 1	Homo sapiens	56-61
34403688-5	2021	Hence, NAD+ metabolites both regulate the activation of SARM1 and, in turn, are regulated by the SARM1 NAD+ hydrolase.	NAD	103-107	sterile alpha and TIR motif containing 1	Homo sapiens	97-102
34403688-6	2021	This dual upstream and downstream role for NAD+ metabolites in SARM1 function has hindered mechanistic understanding of axoprotective mechanisms that manipulate the NAD+ metabolome.	NAD	43-47	sterile alpha and TIR motif containing 1	Homo sapiens	63-68
34403688-8	2021	We find that these approaches not only lead to a decrease in the levels of the SARM1 activator NMN, but also an increase in the levels of the NAD+ precursor nicotinic acid mononucleotide (NaMN).	NAD	142-146	sterile alpha and TIR motif containing 1	Homo sapiens	79-84
34403688-11	2021	Together, these results demonstrate that the SARM1 allosteric pocket can bind a diverse set of metabolites including NMN, NAD+, and NaMN to monitor cellular NAD+ homeostasis and regulate SARM1 NAD+ hydrolase activity.	NAD	122-126	sterile alpha and TIR motif containing 1	Homo sapiens	45-50
34403688-11	2021	Together, these results demonstrate that the SARM1 allosteric pocket can bind a diverse set of metabolites including NMN, NAD+, and NaMN to monitor cellular NAD+ homeostasis and regulate SARM1 NAD+ hydrolase activity.	NAD	122-126	sterile alpha and TIR motif containing 1	Homo sapiens	187-192
34403688-11	2021	Together, these results demonstrate that the SARM1 allosteric pocket can bind a diverse set of metabolites including NMN, NAD+, and NaMN to monitor cellular NAD+ homeostasis and regulate SARM1 NAD+ hydrolase activity.	NAD	157-161	sterile alpha and TIR motif containing 1	Homo sapiens	45-50
34403688-11	2021	Together, these results demonstrate that the SARM1 allosteric pocket can bind a diverse set of metabolites including NMN, NAD+, and NaMN to monitor cellular NAD+ homeostasis and regulate SARM1 NAD+ hydrolase activity.	NAD	193-197	sterile alpha and TIR motif containing 1	Homo sapiens	45-50
34403688-11	2021	Together, these results demonstrate that the SARM1 allosteric pocket can bind a diverse set of metabolites including NMN, NAD+, and NaMN to monitor cellular NAD+ homeostasis and regulate SARM1 NAD+ hydrolase activity.	NAD	193-197	sterile alpha and TIR motif containing 1	Homo sapiens	187-192
8394740-6	1993	Cell- and membrane-mediated reduction of CoQ1 was enhanced by NADH, FAD, or human plasma.	NAD	62-66	decaprenyl diphosphate synthase subunit 1	Homo sapiens	41-45
8397143-1	1993	MPP+ has been reported to inhibit reduced nicotinamide adenine dinucleotide (NADH) dehydrogenase in mitochondria, which results in the formation of O2(.-).	NAD	42-75	M-phase phosphoprotein 6	Homo sapiens	0-3
8284816-3	1993	An increase of activity of NAD(+)- and NADP(+)-dependent isoforms of ALDH-II 60 min after their injection in a dose of 2.5 and 4.5 g/kg also contributes to this effect.	NAD	27-33	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	69-73
8284816-6	1993	Activity of NAD(+)-dependent ALDH-II mitochondria decreased with 2.5 g/kg at the 30th and 60th min, respectively.	NAD	12-18	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	29-33
8439315-2	1993	Synthesis of [32P]ADPribulose from [32P]NAD+ by the combined activities of commercial NAD+ glycohydrolase and phosphoriboisomerase allowed us to use it as a labeled internal standard throughout the procedure of purification from trichloroacetic acid extracts of human red blood cells.	NAD	40-44	ribose 5-phosphate isomerase A	Homo sapiens	110-130
8357577-15	1993	A much higher response of the GDH immobilized 2 microm microelectrode was obtained when not only ferricyanide but also diaphorase was employed to reoxidize the NADH produced by the enzyme reaction of GDH.	NAD	160-164	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	30-33
8357577-15	1993	A much higher response of the GDH immobilized 2 microm microelectrode was obtained when not only ferricyanide but also diaphorase was employed to reoxidize the NADH produced by the enzyme reaction of GDH.	NAD	160-164	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	200-203
1429615-3	1992	However, GDH from P. furiosus is inactive at temperatures below 40 degrees C and undergoes heat activation above 40 degrees C. Both NAD+ and NADP+ are utilized as cofactors.	NAD	132-136	glutamate dehydrogenase 1, mitochondrial	Bos taurus	9-12
1328233-2	1992	Unlike XO, which reacts rapidly only with oxygen and not with NAD, the XDH form of the enzyme reacts rapidly with NAD.	NAD	114-117	xanthine dehydrogenase	Homo sapiens	71-74
1328233-3	1992	XDH has a turnover number for the NAD-dependent conversion of xanthine to urate of 380 mol/min/mol at pH 7.5, 25 degrees C, with a Km = &lt; or = 1 microM for xanthine and a Km = 7 microM for NAD, but has very little O2-dependent activity.	NAD	34-37	xanthine dehydrogenase	Homo sapiens	0-3
1328233-3	1992	XDH has a turnover number for the NAD-dependent conversion of xanthine to urate of 380 mol/min/mol at pH 7.5, 25 degrees C, with a Km = &lt; or = 1 microM for xanthine and a Km = 7 microM for NAD, but has very little O2-dependent activity.	NAD	192-195	xanthine dehydrogenase	Homo sapiens	0-3
1417986-5	1992	In contrast, levels of aldehyde dehydrogenase (ALDH) (propionaldehyde, NAD+) which were expressed constitutively in all strains of rats were induced by PB in only two of the eight strains (ACI, Copenhagen).	NAD	71-75	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	23-45
1417986-5	1992	In contrast, levels of aldehyde dehydrogenase (ALDH) (propionaldehyde, NAD+) which were expressed constitutively in all strains of rats were induced by PB in only two of the eight strains (ACI, Copenhagen).	NAD	71-75	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	47-51
1417986-7	1992	These results imply that induction of ALDH (propionaldehyde, NAD+) is associated with the PB pleiotropic response in Copenhagen rats.	NAD	61-65	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	38-42
1456954-4	1992	The role of flavin in the nitroreductase activity was supported by (a) the nitrofuran effect on the spectral properties of anaerobic, arsenite-inhibited, NADH-reduced LipDH; (b) FAD catalytic activity in a NADH-nitrofuran model system; and (c) the nitroreductase activity of LipDH monomer.	NAD	154-158	dihydrolipoamide dehydrogenase	Homo sapiens	167-172
1483503-7	1992	BCP 54 preferentially oxidizes aromatic aldehyde such as benzaldehyde with NAD as coenzyme, but cannot oxidize phenylacetaldehyde.	NAD	75-78	aldehyde dehydrogenase 3 family member A1	Bos taurus	0-6
1435769-6	1992	Addition of NADH (marginally effective on its own) or H2O2 (effective alone) dramatically enhanced the effect of vanadate on c-jun gene expression.	NAD	12-16	jun proto-oncogene	Mus musculus	125-130
16669085-4	1992	Kinetic studies of the purified enzyme suggested that nicotinamide adenine dinucleotide phosphate(+) inhibited P5CR activity, whereas nicotinamide adenine dinucleotide(+) did not.	NAD	54-87	pyrroline-5-carboxylate reductase	Glycine max	111-115
16668941-0	1992	Expression in Escherichia coli of Cytochrome c Reductase Activity from a Maize NADH:Nitrate Reductase Complementary DNA.	NAD	79-83	cytochrome c	Zea mays	34-46
16668941-4	1992	The cell lysate contained NADH:cytochrome c reductase activity, which is a characteristic partial activity of NADH:nitrate reductase dependent on the cytochrome b and flavin adenine dinucleotide domains.	NAD	26-30	cytochrome c	Zea mays	31-43
16668941-4	1992	The cell lysate contained NADH:cytochrome c reductase activity, which is a characteristic partial activity of NADH:nitrate reductase dependent on the cytochrome b and flavin adenine dinucleotide domains.	NAD	110-114	cytochrome c	Zea mays	31-43
16668941-6	1992	The purified cytochrome c reductase, which had a major size of 43 kilodaltons, was inhibited by polyclonal antibodies for maize leaf NADH:nitrate reductase and bound these antibodies when blotted to nitrocellulose.	NAD	133-137	cytochrome c	Zea mays	13-25
1585367-2	1992	In the presence of NAD(+)-fortified ALDH, the mono-oxidation product (acid/aldehyde) was the primary metabolite formed with trace amounts of the dioxidation product (trans,trans-muconic acid).	NAD	19-25	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	36-40
1585367-5	1992	Unexpectedly, an additional metabolite was detected, which was a major product in both NAD(+)- and NADH-fortified systems containing ALDH and ADH in combination and whose formation could be inhibited by pyrazole (an ADH inhibitor).	NAD	87-93	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	133-137
1585367-5	1992	Unexpectedly, an additional metabolite was detected, which was a major product in both NAD(+)- and NADH-fortified systems containing ALDH and ADH in combination and whose formation could be inhibited by pyrazole (an ADH inhibitor).	NAD	99-103	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	133-137
1554695-1	1992	Lipoamide dehydrogenase is a flavoprotein which catalyzes the reversible oxidation of dihydrolipoamide, Lip(SH)2, by NAD+.	NAD	117-121	dihydrolipoamide dehydrogenase	Sus scrofa	0-23
1551461-2	1992	Modification of histidine residue(s) of xanthine dehydrogenase from hen liver by DEP and photooxidation results in loss of the ability to transfer electrons from xanthine to NAD+ and also from NADH to 2,6-dichlorophenolindophenol (DCIP).	NAD	174-178	xanthine dehydrogenase	Homo sapiens	40-62
1551461-2	1992	Modification of histidine residue(s) of xanthine dehydrogenase from hen liver by DEP and photooxidation results in loss of the ability to transfer electrons from xanthine to NAD+ and also from NADH to 2,6-dichlorophenolindophenol (DCIP).	NAD	193-197	xanthine dehydrogenase	Homo sapiens	40-62
1551239-2	1992	An enzymatic reaction involving alkaline phosphatase (EC 3.1.3.1) and galactose dehydrogenase (EC 1.1.1.48) produces NADH, which is coupled with diaphorase (EC 1.8.1.4) and iodonitrotetrazolium violet (INT).	NAD	117-121	dihydrolipoamide dehydrogenase	Homo sapiens	145-155
1296570-2	1992	NAD-H, NADP-H-diaphorase, acid phosphatase and ATPase were revealed in the fungi, the activity of these enzymes depended on the state of the fungus.	NAD	0-5	dynein axonemal heavy chain 8	Homo sapiens	47-53
1751496-9	1991	Turnover in the dihydrolipoamide/NAD+ reaction is decreased by 10-fold and in the NADH/lipoamide reaction by 2-fold in I184Y lipoamide dehydrogenase.	NAD	33-37	dihydrolipoamide dehydrogenase	Homo sapiens	125-148
1751496-9	1991	Turnover in the dihydrolipoamide/NAD+ reaction is decreased by 10-fold and in the NADH/lipoamide reaction by 2-fold in I184Y lipoamide dehydrogenase.	NAD	82-86	dihydrolipoamide dehydrogenase	Homo sapiens	125-148
1664494-2	1991	The following parameters are evaluated: (a) content of respiratory components, namely ubiquinone, cytochrome b, cytochrome c1, cytochrome c; (b) specific activity of enzymes, namely citrate synthase, succinate dehydrogenase, rotenone-sensitive NADH: cytochrome c reductase, cytochrome oxidase; (c) concentration of reduced glutathione (GSH).	NAD	244-248	citrate synthase	Rattus norvegicus	182-198
1667626-2	1991	In the first step, pyruvate kinase (ATP: pyruvate 2-O-phosphotransferase, EC 2.7.1.40) and lactate dehydrogenase (L-lactate: NAD+ oxidoreductase, EC 1.1.1.27) were used to eliminate endogenous constituents (ADP and pyruvate) in the presence of phosphoenolpyruvate and NADH.	NAD	268-272	hydroxysteroid 17-beta dehydrogenase 6	Homo sapiens	130-144
1723851-5	1991	The NADH formed in the oxidative deamination of methionine reacts with PMS and NBT to form a blue band on the surface of the gel coincident with glutamine transaminase K activity.	NAD	4-8	kynurenine aminotransferase 1	Rattus norvegicus	145-169
1897001-3	1991	A microassay for NAD(+)-dependent xanthine dehydrogenase, based on measuring the production of NADH fluorometrically under anaerobic conditions, was developed and used to examine the actions of allyl alcohol on this activity in periportal and pericentral regions of the liver lobule.	NAD	95-99	xanthine dehydrogenase	Rattus norvegicus	34-56
1661206-1	1991	The NAD- and NADP-dependent aldehyde dehydrogenase (ALDH) activities were evaluated in two rat hepatoma cell lines, namely the well-differentiated MH1C1 line and the less differentiated HTC line.	NAD	4-7	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	52-56
1680656-2	1991	The effect of the concentrations of NAD+ at different concentrations of catalase on the inactivation of ALDH by cyanamide (20 and 200 microM) in vitro point to an ALDH-NAD(+)-catalase complex prior to the binding to cyanamide to form the holoenzyme-inhibitor complex.	NAD	36-40	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	104-108
1680656-2	1991	The effect of the concentrations of NAD+ at different concentrations of catalase on the inactivation of ALDH by cyanamide (20 and 200 microM) in vitro point to an ALDH-NAD(+)-catalase complex prior to the binding to cyanamide to form the holoenzyme-inhibitor complex.	NAD	36-40	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	163-167
1848777-0	1991	Spatial arrangement of coenzyme and substrates bound to L-3-hydroxyacyl-CoA dehydrogenase as studied by spin-labeled analogues of NAD+ and CoA.	NAD	130-134	enoyl-CoA hydratase and 3-hydroxyacyl CoA dehydrogenase	Homo sapiens	56-89
1848777-12	1991	NAD+, spin-labeled at N6 of the adenine ring, is an active coenzyme of L-3-hydroxyacyl-CoA dehydrogenase (60% vmax).	NAD	0-4	enoyl-CoA hydratase and 3-hydroxyacyl CoA dehydrogenase	Homo sapiens	71-104
1652585-1	1991	The oxidase reaction of lipoamide dehydrogenase with NADH generates superoxide radicals and hydrogen peroxide under aerobic conditions.	NAD	53-57	dihydrolipoamide dehydrogenase	Homo sapiens	24-47
1993675-10	1991	These studies indicate that (i) rS1, purified from Escherichia coli, possesses biochemical properties similar to S1 subunit purified from pertussis toxin, (ii) amino acids 1-180 of the S1 subunit contain residues required for NAD binding, N-glycosidic cleavage, and transfer of ADP-ribose to transducin, and (iii) residues between 181 and 219 of the S1 subunit are required for efficient ADP-ribosyltransferase activity.	NAD	226-229	retinoschisin 1	Rattus norvegicus	33-35
1989691-1	1991	The activity of the pH 7.5 NADH-linked nitrate reductase isoform from soybeans is termed inducible.	NAD	27-31	inducible nitrate reductase [NADH] 1	Glycine max	39-56
2173592-13	1990	The nitroreductase activity was inhibited by p-chloromercuribenzoate and enhanced by cadmium and arsenite, whereas the NADH-induced LADH inactivation failed to affect the nitroreductase activity.	NAD	119-123	dihydrolipoamide dehydrogenase	Homo sapiens	132-136
2096889-6	1990	Formation of various binary, ternary and quaternary complexes of bovine liver glutamate dehydrogenase (GDH) with glutamate, NADPH, NADH, and ADP was also investigated using immobilized GDH.	NAD	131-135	glutamate dehydrogenase 1, mitochondrial	Bos taurus	78-101
2096889-6	1990	Formation of various binary, ternary and quaternary complexes of bovine liver glutamate dehydrogenase (GDH) with glutamate, NADPH, NADH, and ADP was also investigated using immobilized GDH.	NAD	131-135	glutamate dehydrogenase 1, mitochondrial	Bos taurus	103-106
2124130-3	1990	Drosophila melanogaster DHFR can use folate and NADH at acidic pH values, but at a much lower rate than the preferred substrate and cofactor.	NAD	48-52	Dihydrofolate reductase	Drosophila melanogaster	24-28
2359406-1	1990	In the presence of Mg2+, pure glutamate dehydrogenase is more reactive with NADPH than with NADH and is markedly activated by elevations in the ADP/ATP ratio or the addition of leucine.	NAD	92-96	mucin 7, secreted	Homo sapiens	19-22
2199815-1	1990	We have isolated several cDNA clones encoding delta 1-pyrroline-5-carboxylate reductase (P5CR, L-proline: NAD(P)+ 5-oxidoreductase, EC 1.5.1.2) which catalyzes the terminal step in proline biosynthesis, by direct complementation of a proC mutation in Escherichia coli with an expression library of soybean root nodule cDNA.	NAD	106-110	pyrroline-5-carboxylate reductase	Glycine max	89-93
34164859-1	2021	Dihydrolipoamide dehydrogenase (DLDH) is a homodimeric flavin-dependent enzyme that catalyzes the NAD+ -dependent oxidation of dihydrolipoamide.	NAD	98-102	dihydrolipoamide dehydrogenase	Homo sapiens	0-30
34164859-1	2021	Dihydrolipoamide dehydrogenase (DLDH) is a homodimeric flavin-dependent enzyme that catalyzes the NAD+ -dependent oxidation of dihydrolipoamide.	NAD	98-102	dihydrolipoamide dehydrogenase	Homo sapiens	32-36
34619528-8	2021	Doxorubicin and IR caused metabolic changes with nicotinamide adenine dinucleotide depletion and ensuing mitochondrial stunning (reversible mitochondria dysfunction without showing any cell death under ATP depletion) via p90RSK-ERK5 modulation and poly (ADP-ribose) polymerase (PARP) activation, which formed a nucleus-mitochondria positive feedback loop.	NAD	49-82	mitogen-activated protein kinase 7	Mus musculus	228-232
34645816-8	2021	Sirt1 activity, dependent on the cytoplasmic glycolysis product NAD+, directly interacts with p107, impeding its mitochondrial localization.	NAD	64-68	RB transcriptional corepressor like 1	Homo sapiens	94-98
34399423-1	2021	Nicotinamide phosphoribosyltransferase (NAMPT) is the key rate-limiting enzyme in the regulation of nicotinamide adenine dinucleotide (NAD) biosynthesis, and its activity is critical for the replenishment of NAD level as well as cell survival or death.	NAD	100-133	nicotinamide phosphoribosyltransferase	Homo sapiens	0-38
34399423-1	2021	Nicotinamide phosphoribosyltransferase (NAMPT) is the key rate-limiting enzyme in the regulation of nicotinamide adenine dinucleotide (NAD) biosynthesis, and its activity is critical for the replenishment of NAD level as well as cell survival or death.	NAD	100-133	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
34399423-1	2021	Nicotinamide phosphoribosyltransferase (NAMPT) is the key rate-limiting enzyme in the regulation of nicotinamide adenine dinucleotide (NAD) biosynthesis, and its activity is critical for the replenishment of NAD level as well as cell survival or death.	NAD	135-138	nicotinamide phosphoribosyltransferase	Homo sapiens	0-38
34399423-1	2021	Nicotinamide phosphoribosyltransferase (NAMPT) is the key rate-limiting enzyme in the regulation of nicotinamide adenine dinucleotide (NAD) biosynthesis, and its activity is critical for the replenishment of NAD level as well as cell survival or death.	NAD	135-138	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
34399423-1	2021	Nicotinamide phosphoribosyltransferase (NAMPT) is the key rate-limiting enzyme in the regulation of nicotinamide adenine dinucleotide (NAD) biosynthesis, and its activity is critical for the replenishment of NAD level as well as cell survival or death.	NAD	208-211	nicotinamide phosphoribosyltransferase	Homo sapiens	0-38
34399423-1	2021	Nicotinamide phosphoribosyltransferase (NAMPT) is the key rate-limiting enzyme in the regulation of nicotinamide adenine dinucleotide (NAD) biosynthesis, and its activity is critical for the replenishment of NAD level as well as cell survival or death.	NAD	208-211	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
34399423-5	2021	On the other hand, NAMPT downregulation and NAD depletion could induce cell death in oral squamous cell cancer, suggesting that a combination of NAMPT inhibitor and radiotherapy presents a promising therapeutic strategy for cancer treatment.	NAD	44-47	nicotinamide phosphoribosyltransferase	Homo sapiens	145-150
34680055-3	2021	In this review, we discuss the evidence supporting a role for NNMT in the progression of the cancer phenotype and how it achieves this by driving the activity of pro-oncogenic NAD+-consuming enzymes.	NAD	176-180	nicotinamide N-methyltransferase	Homo sapiens	62-66
34573442-2	2021	The mammalian SIRT6 protein, a member of the Class III HDAC Sirtuin family of NAD+-dependent enzymes, plays pivotal roles in aging, metabolism, and cancer biology.	NAD	78-82	sirtuin 6	Homo sapiens	14-19
34465625-3	2021	Activation of ALC1 cryptic ATPase activity and the subsequent nucleosome remodeling requires binding of its macrodomain to PAR chains synthesized by PARP1 and NAD+ A key question is whether PARP1 has a role(s) in ALC1-dependent nucleosome remodeling beyond simply synthesizing the PAR chains needed to activate the ALC1 ATPase.	NAD	159-163	chromodomain helicase DNA binding protein 1 like	Homo sapiens	14-18
34174704-8	2021	NAD+ intervention relieved inflammatory infiltration and CD3+ and CD4+ cell infiltration and decreased the number and activation of microglia and astrocytes in the optic nerve.	NAD	0-4	CD3 antigen, epsilon polypeptide	Mus musculus	57-60
34504490-1	2021	Mouse T cells express the ecto-ADP-ribosyltransferase ARTC2.2, which can transfer the ADP-ribose group of extracellular nicotinamide adenine dinucleotide (NAD+) to arginine residues of various cell surface proteins thereby influencing their function.	NAD	120-153	ADP-ribosyltransferase 2a	Mus musculus	54-59
34504490-1	2021	Mouse T cells express the ecto-ADP-ribosyltransferase ARTC2.2, which can transfer the ADP-ribose group of extracellular nicotinamide adenine dinucleotide (NAD+) to arginine residues of various cell surface proteins thereby influencing their function.	NAD	155-159	ADP-ribosyltransferase 2a	Mus musculus	54-59
34489954-1	2021	On murine T cells, mono-ADP ribosyltransferase ARTC2.2 catalyzes ADP-ribosylation of various surface proteins when nicotinamide adenine dinucleotide (NAD+) is released into the extracellular compartment.	NAD	115-148	ADP-ribosyltransferase 2a	Mus musculus	47-52
34489954-1	2021	On murine T cells, mono-ADP ribosyltransferase ARTC2.2 catalyzes ADP-ribosylation of various surface proteins when nicotinamide adenine dinucleotide (NAD+) is released into the extracellular compartment.	NAD	150-154	ADP-ribosyltransferase 2a	Mus musculus	47-52
34445574-3	2021	Our previous results suggest that NMNAT1, a key enzyme in nuclear NAD+ synthesis, facilitates the survival of cisplatin-treated osteosarcoma cells.	NAD	66-70	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	34-40
34445574-7	2021	The reduced NAD+ content in NMNAT1 KO cells was further decreased by ActD, which partially inhibited NAD+-dependent enzymes, including the DNA nick sensor enzyme PARP1 and the NAD+-dependent deacetylase SIRT1.	NAD	12-16	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	28-34
34445574-7	2021	The reduced NAD+ content in NMNAT1 KO cells was further decreased by ActD, which partially inhibited NAD+-dependent enzymes, including the DNA nick sensor enzyme PARP1 and the NAD+-dependent deacetylase SIRT1.	NAD	101-105	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	28-34
34175654-5	2021	The field is converging on a model whereby SARM1 acts as a sensor for metabolic changes that occur after injury and then drives catastrophic NAD+ loss to promote degeneration.	NAD	141-145	sterile alpha and TIR motif containing 1	Homo sapiens	43-48
34130091-0	2021	Restoring NAD+ by NAMPT is essential for the SIRT1/p53-mediated survival of UVA- and UVB-irradiated epidermal keratinocytes.	NAD	10-14	nicotinamide phosphoribosyltransferase	Homo sapiens	18-23
34307460-3	2021	This is an axonal NAD-related signaling mechanism mainly regulated by the two key proteins with opposing roles: the NAD-synthesizing enzyme NMNAT2, and SARM1, a protein with NADase and related activities.	NAD	18-21	sterile alpha and TIR motif containing 1	Homo sapiens	152-157
34101492-0	2021	MiR-613 Promotes Cell Death in Breast Cancer Cells by Downregulation of Nicotinamide Phosphoribosyltransferase and Reduction of NAD.	NAD	128-131	microRNA 613	Homo sapiens	0-7
34101492-1	2021	NAD is mainly biosynthesized by the enzymatic action of nicotinamide phosphoribosyltransferase (NAMPT) through the salvage pathway.	NAD	0-3	nicotinamide phosphoribosyltransferase	Homo sapiens	56-94
34101492-1	2021	NAD is mainly biosynthesized by the enzymatic action of nicotinamide phosphoribosyltransferase (NAMPT) through the salvage pathway.	NAD	0-3	nicotinamide phosphoribosyltransferase	Homo sapiens	96-101
34101492-3	2021	Our previous researches revealed that inhibition of NAMPT by miRNA (miR) could suppress NAD levels and thereby hinder the growth and promotion of breast cancer (BC).	NAD	88-91	nicotinamide phosphoribosyltransferase	Homo sapiens	52-57
34101492-8	2021	Inhibition of NAMPT led to a remarkable reduction in the concentration of NAD in the BC cells NAMPT.	NAD	74-77	nicotinamide phosphoribosyltransferase	Homo sapiens	14-19
34101492-8	2021	Inhibition of NAMPT led to a remarkable reduction in the concentration of NAD in the BC cells NAMPT.	NAD	74-77	nicotinamide phosphoribosyltransferase	Homo sapiens	94-99
34101492-11	2021	Targeting the NAMPT-mediated NAD salvage pathway by miR-613 is a novel approach for managing BC, which is worth further investigation.	NAD	29-32	nicotinamide phosphoribosyltransferase	Homo sapiens	14-19
34101492-11	2021	Targeting the NAMPT-mediated NAD salvage pathway by miR-613 is a novel approach for managing BC, which is worth further investigation.	NAD	29-32	microRNA 613	Homo sapiens	52-59
34097876-8	2021	Interestingly, silencing the NAD+-sensor enzyme SIRT1 prevented eNAD+-dependent transcriptional repression of CD73, Slc12a8, and NRK1, as well as iNAD+ resetting.	NAD	29-33	5'-nucleotidase ecto	Homo sapiens	110-114
34198503-9	2021	With the realization that SLC25A51 (or MCART1) represents the major mitochondrial NAD+ carrier in mammals, a long-standing mystery in NAD+ biology has been resolved.	NAD	82-86	solute carrier family 25 member 51	Homo sapiens	26-34
34198503-9	2021	With the realization that SLC25A51 (or MCART1) represents the major mitochondrial NAD+ carrier in mammals, a long-standing mystery in NAD+ biology has been resolved.	NAD	82-86	solute carrier family 25 member 51	Homo sapiens	39-45
34198503-9	2021	With the realization that SLC25A51 (or MCART1) represents the major mitochondrial NAD+ carrier in mammals, a long-standing mystery in NAD+ biology has been resolved.	NAD	134-138	solute carrier family 25 member 51	Homo sapiens	26-34
34198503-9	2021	With the realization that SLC25A51 (or MCART1) represents the major mitochondrial NAD+ carrier in mammals, a long-standing mystery in NAD+ biology has been resolved.	NAD	134-138	solute carrier family 25 member 51	Homo sapiens	39-45
34094839-1	2021	The recent discovery of activator compounds binding to an allosteric site on the NAD+-dependent protein lysine deacetylase, sirtuin 6 (SIRT6) has attracted interest and presents a pharmaceutical target for aging-related and cancer diseases.	NAD	81-84	sirtuin 6	Homo sapiens	124-133
34094839-1	2021	The recent discovery of activator compounds binding to an allosteric site on the NAD+-dependent protein lysine deacetylase, sirtuin 6 (SIRT6) has attracted interest and presents a pharmaceutical target for aging-related and cancer diseases.	NAD	81-84	sirtuin 6	Homo sapiens	135-140
35447542-3	2022	Recently, it has been shown that NADH binds to a specific pocket in the inner surface of VDAC1, also conserved in VDAC2 and 3, closing the channel.	NAD	33-37	voltage dependent anion channel 1	Homo sapiens	89-94
35447542-3	2022	Recently, it has been shown that NADH binds to a specific pocket in the inner surface of VDAC1, also conserved in VDAC2 and 3, closing the channel.	NAD	33-37	voltage dependent anion channel 2	Homo sapiens	114-125
35588716-0	2022	Correction to: Intestinal Epithelial NAD+ Biosynthesis Regulates GLP-1 Production and Postprandial Glucose Metabolism in Mice.	NAD	37-41	glucagon	Mus musculus	65-70
35500221-4	2022	Transcriptional profiling revealed that this oxidative phenotype was driven by IFNgamma-induced reprogramming of NAD+ metabolism, which is dependent on nicotinamide phosphoribosyltransferase (NAMPT)-mediated NAD+ salvage to generate NADH and NADPH for oxidation by mitochondrial complex I and NADPH oxidase, respectively.	NAD	113-117	nicotinamide phosphoribosyltransferase	Homo sapiens	152-190
35500221-4	2022	Transcriptional profiling revealed that this oxidative phenotype was driven by IFNgamma-induced reprogramming of NAD+ metabolism, which is dependent on nicotinamide phosphoribosyltransferase (NAMPT)-mediated NAD+ salvage to generate NADH and NADPH for oxidation by mitochondrial complex I and NADPH oxidase, respectively.	NAD	113-117	nicotinamide phosphoribosyltransferase	Homo sapiens	192-197
35500221-4	2022	Transcriptional profiling revealed that this oxidative phenotype was driven by IFNgamma-induced reprogramming of NAD+ metabolism, which is dependent on nicotinamide phosphoribosyltransferase (NAMPT)-mediated NAD+ salvage to generate NADH and NADPH for oxidation by mitochondrial complex I and NADPH oxidase, respectively.	NAD	208-212	nicotinamide phosphoribosyltransferase	Homo sapiens	152-190
35500221-4	2022	Transcriptional profiling revealed that this oxidative phenotype was driven by IFNgamma-induced reprogramming of NAD+ metabolism, which is dependent on nicotinamide phosphoribosyltransferase (NAMPT)-mediated NAD+ salvage to generate NADH and NADPH for oxidation by mitochondrial complex I and NADPH oxidase, respectively.	NAD	208-212	nicotinamide phosphoribosyltransferase	Homo sapiens	192-197
35500221-4	2022	Transcriptional profiling revealed that this oxidative phenotype was driven by IFNgamma-induced reprogramming of NAD+ metabolism, which is dependent on nicotinamide phosphoribosyltransferase (NAMPT)-mediated NAD+ salvage to generate NADH and NADPH for oxidation by mitochondrial complex I and NADPH oxidase, respectively.	NAD	233-237	nicotinamide phosphoribosyltransferase	Homo sapiens	152-190
35500221-4	2022	Transcriptional profiling revealed that this oxidative phenotype was driven by IFNgamma-induced reprogramming of NAD+ metabolism, which is dependent on nicotinamide phosphoribosyltransferase (NAMPT)-mediated NAD+ salvage to generate NADH and NADPH for oxidation by mitochondrial complex I and NADPH oxidase, respectively.	NAD	233-237	nicotinamide phosphoribosyltransferase	Homo sapiens	192-197
35276409-4	2022	In this study, we isolated a new mutant allele of FLAGELLIN-INSENSITIVE 4 (FIN4), which encodes the first enzyme in de novo NAD biosynthesis.	NAD	124-127	L-aspartate oxidase	Arabidopsis thaliana	50-73
35276409-4	2022	In this study, we isolated a new mutant allele of FLAGELLIN-INSENSITIVE 4 (FIN4), which encodes the first enzyme in de novo NAD biosynthesis.	NAD	124-127	L-aspartate oxidase	Arabidopsis thaliana	75-79
35276409-6	2022	However, FIN4 and other genes involved in NAD- and NADPH-generating pathways are not highly upregulated upon elicitor treatment, raising a possibility that a cytosolic NADP-linked dehydrogenase might be post-transcriptionally activated to maintain the NADPH supply close to RBOHD.	NAD	42-45	L-aspartate oxidase	Arabidopsis thaliana	9-13
35150808-2	2022	Heat shock response (HSR) was altered in the absence of the NAD-dependent glycerol 3-phosphate dehydrogenase (Gpd1).	NAD	60-63	glycerol-3-phosphate dehydrogenase	Saccharomyces cerevisiae S288C	74-108
35150861-6	2022	Besides, Rd strengthened the interaction between AMPK and SIRT1 by increasing NAD+/NADH levels and LKB1 deacetylation in endothelial cells.	NAD	78-82	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	49-53
35150861-6	2022	Besides, Rd strengthened the interaction between AMPK and SIRT1 by increasing NAD+/NADH levels and LKB1 deacetylation in endothelial cells.	NAD	83-87	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	49-53
35188710-2	2022	Nevertheless, due to intrinsic properties of NAD + e.g., high polarity and associated poor cell passage, these PTMs are difficult to characterize in cells.	NAD	45-50	parathymosin	Homo sapiens	111-115
35440550-5	2022	Purified Edc3 forms assemblies, promoted by the presence of RNA and NADH and the addition of purified Sbp1, but not the RGG-deletion mutant, leads to significantly decreased Edc3 assemblies.	NAD	68-72	enhancer of mRNA decapping 3	Homo sapiens	9-13
35493328-8	2022	Unexpectedly, ZIKV infection led to a rapid SARM1-independent reduction in NAD+.	NAD	75-79	sterile alpha and TIR motif containing 1	Homo sapiens	44-49
35397003-0	2022	Alpha-SYNUCLEINOPATHY reduces NMNAT3 protein levels and neurite formation that can be rescued by targeting the NAD+ pathway.	NAD	111-115	nicotinamide nucleotide adenylyltransferase 3	Homo sapiens	30-36
35235889-4	2022	The enzyme kinetic assay confirmed that C25 inhibited PHGDH in a nicotinamide adenine dinucleotide (NAD+) competitive manner.	NAD	65-98	phosphoglycerate dehydrogenase	Homo sapiens	54-59
35235889-4	2022	The enzyme kinetic assay confirmed that C25 inhibited PHGDH in a nicotinamide adenine dinucleotide (NAD+) competitive manner.	NAD	100-104	phosphoglycerate dehydrogenase	Homo sapiens	54-59
35137552-0	2022	NAD+ ameliorates endotoxin-induced acute kidney injury in a sirtuin1-dependent manner via GSK-3beta/Nrf2 signalling pathway.	NAD	0-4	glycogen synthase kinase 3 alpha	Homo sapiens	90-99
35134563-6	2022	ATP and NADH, derivatives of adenosine, inhibit insulin signaling inside cells by downregulation of activities of AMPK and SIRT1, respectively.	NAD	8-12	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	114-118
35172823-1	2022	PURPOSES: In addition to its role in cellular progression and cancer, SIRT6, a member of nicotinamide adenine dinucleotide (NAD+)-dependent class III deacylase sirtuin family, serves a variety of roles in the body"s immune system.	NAD	89-122	sirtuin 6	Homo sapiens	70-75
35172823-1	2022	PURPOSES: In addition to its role in cellular progression and cancer, SIRT6, a member of nicotinamide adenine dinucleotide (NAD+)-dependent class III deacylase sirtuin family, serves a variety of roles in the body"s immune system.	NAD	124-128	sirtuin 6	Homo sapiens	70-75
35168992-7	2022	The glucose- induced high NADH/NAD+ ratio upregulates the hypoxia-inducible factor-1 gene, which stimulates not only the glucose transporter-1 gene, but also many profibrotic genes like TGFbeta, VEGF, PAI-1 and CTGF, all known to be involved in the development of peritoneal fibrosis.	NAD	26-30	transforming growth factor alpha	Homo sapiens	186-193
35168992-7	2022	The glucose- induced high NADH/NAD+ ratio upregulates the hypoxia-inducible factor-1 gene, which stimulates not only the glucose transporter-1 gene, but also many profibrotic genes like TGFbeta, VEGF, PAI-1 and CTGF, all known to be involved in the development of peritoneal fibrosis.	NAD	26-30	cellular communication network factor 2	Homo sapiens	211-215
35168992-7	2022	The glucose- induced high NADH/NAD+ ratio upregulates the hypoxia-inducible factor-1 gene, which stimulates not only the glucose transporter-1 gene, but also many profibrotic genes like TGFbeta, VEGF, PAI-1 and CTGF, all known to be involved in the development of peritoneal fibrosis.	NAD	31-35	transforming growth factor alpha	Homo sapiens	186-193
35168992-7	2022	The glucose- induced high NADH/NAD+ ratio upregulates the hypoxia-inducible factor-1 gene, which stimulates not only the glucose transporter-1 gene, but also many profibrotic genes like TGFbeta, VEGF, PAI-1 and CTGF, all known to be involved in the development of peritoneal fibrosis.	NAD	31-35	cellular communication network factor 2	Homo sapiens	211-215
2214362-1	1990	The present study has demonstrated that H2O2-dependent NADH oxidation activity in aged transparent and senile cataractous human lenses is due to a glutathione redox cycle which consists of reduced glutathione, oxidized glutathione, glutathione peroxidase and glutathione reductase.	NAD	55-59	glutathione-disulfide reductase	Homo sapiens	259-280
33777213-1	2021	Nicotinamide phosphoribosyltransferase (NAMPT) is a critical rate-limiting enzyme involved in NAD synthesis that has been shown to contribute to the progression of liver cancer.	NAD	94-97	nicotinamide phosphoribosyltransferase	Homo sapiens	0-38
33777213-1	2021	Nicotinamide phosphoribosyltransferase (NAMPT) is a critical rate-limiting enzyme involved in NAD synthesis that has been shown to contribute to the progression of liver cancer.	NAD	94-97	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
2295642-4	1990	Both effects of butanol were blocked by an inhibitor of ADH, 4-methylpyrazole, consistent with the hypothesis that elevation of the NADH redox state by butanol inhibited H2O2 production via NAD+-requiring peroxisomal beta-oxidation, leading indirectly to diminished rates of catalase-dependent methanol uptake.	NAD	132-136	alcohol dehydrogenase 1C (class I), gamma polypeptide	Rattus norvegicus	56-59
33763084-2	2021	In response to T cell activation or extracellular NAD+ or ATP-mediated gating of the P2X7 ion channel ARTC2.2 is shed from the cell surface as a soluble enzyme.	NAD	50-54	ADP-ribosyltransferase 2a	Mus musculus	102-107
2295642-4	1990	Both effects of butanol were blocked by an inhibitor of ADH, 4-methylpyrazole, consistent with the hypothesis that elevation of the NADH redox state by butanol inhibited H2O2 production via NAD+-requiring peroxisomal beta-oxidation, leading indirectly to diminished rates of catalase-dependent methanol uptake.	NAD	190-194	alcohol dehydrogenase 1C (class I), gamma polypeptide	Rattus norvegicus	56-59
2184312-5	1990	Mutagenesis experiments using TTCE in the diploid D7 strain of Saccharomyces cerevisiae (from stationary growth phase) as a biological test system, showed a significant enhancement of mitotic gene conversion and reverse point mutation frequencies when using NADPH plus NADH in the medium.	NAD	269-273	2,4-dienoyl CoA reductase 1, mitochondrial	Mus musculus	258-263
33800266-1	2021	Sirtuin 6 (SIRT6) is a NAD+-dependent nuclear deacylase and mono-ADP-ribosylase with a wide spectrum of substrates.	NAD	23-26	sirtuin 6	Homo sapiens	0-9
33800266-1	2021	Sirtuin 6 (SIRT6) is a NAD+-dependent nuclear deacylase and mono-ADP-ribosylase with a wide spectrum of substrates.	NAD	23-26	sirtuin 6	Homo sapiens	11-16
33798699-3	2021	A novel strategy to boost NAD+ is to activate nicotinamide phosphoribosyltransferase (NAMPT), the putative rate-limiting step in the NAD+ salvage pathway.	NAD	26-30	nicotinamide phosphoribosyltransferase	Homo sapiens	46-84
27065803-8	2016	The ERbeta specific agonist DPN (10 pM) also significantly decreased the frequency of miniature postsynaptic currents (mPSCs) in GnRH neurons.	NAD	28-31	estrogen receptor 2 (beta)	Mus musculus	4-10
33798699-3	2021	A novel strategy to boost NAD+ is to activate nicotinamide phosphoribosyltransferase (NAMPT), the putative rate-limiting step in the NAD+ salvage pathway.	NAD	26-30	nicotinamide phosphoribosyltransferase	Homo sapiens	86-91
33798699-3	2021	A novel strategy to boost NAD+ is to activate nicotinamide phosphoribosyltransferase (NAMPT), the putative rate-limiting step in the NAD+ salvage pathway.	NAD	133-137	nicotinamide phosphoribosyltransferase	Homo sapiens	46-84
26389889-1	2015	Nicotinamide phosphoribosyltransferase (NAMPT) has crucial roles for myocardial development, cardiomyocyte energy metabolism and cell death/survival by regulating NAD+-dependent sirtuin-1 (SIRT1) deacetylase.	NAD	163-167	nicotinamide phosphoribosyltransferase	Homo sapiens	0-38
26389889-1	2015	Nicotinamide phosphoribosyltransferase (NAMPT) has crucial roles for myocardial development, cardiomyocyte energy metabolism and cell death/survival by regulating NAD+-dependent sirtuin-1 (SIRT1) deacetylase.	NAD	163-167	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
33798699-3	2021	A novel strategy to boost NAD+ is to activate nicotinamide phosphoribosyltransferase (NAMPT), the putative rate-limiting step in the NAD+ salvage pathway.	NAD	133-137	nicotinamide phosphoribosyltransferase	Homo sapiens	86-91
33798699-4	2021	We previously showed that NAMPT activators increase NAD+ levels in vitro and in vivo.	NAD	52-56	nicotinamide phosphoribosyltransferase	Homo sapiens	26-31
33771896-5	2021	Mechanistically, cisplatin inhibited expression of the NAD+ biosynthesis rate-limiting enzyme nicotinamide phosphoribosyl transferase (Nampt).	NAD	55-59	nicotinamide phosphoribosyltransferase	Homo sapiens	94-133
34843934-10	2022	Moreover, compared with M3 and M5 groups, the higher NAD+/NADH ratio in the liver of M1 group activated SIRT1, which stimulated the AMPK signaling associated pathways by up-regulating the LKB1 gene.	NAD	53-57	protein kinase AMP-activated catalytic subunit alpha 1	Sus scrofa	132-136
34843934-10	2022	Moreover, compared with M3 and M5 groups, the higher NAD+/NADH ratio in the liver of M1 group activated SIRT1, which stimulated the AMPK signaling associated pathways by up-regulating the LKB1 gene.	NAD	58-62	protein kinase AMP-activated catalytic subunit alpha 1	Sus scrofa	132-136
33771896-5	2021	Mechanistically, cisplatin inhibited expression of the NAD+ biosynthesis rate-limiting enzyme nicotinamide phosphoribosyl transferase (Nampt).	NAD	55-59	nicotinamide phosphoribosyltransferase	Homo sapiens	135-140
33771896-7	2021	Taken together, our findings suggest that aberrant Nampt-mediated NAD+ metabolic pathways may be a key contributor in cisplatin-induced neurogenic impairments, thus causally leading to memory dysfunction.	NAD	66-70	nicotinamide phosphoribosyltransferase	Homo sapiens	51-56
31427442-5	2019	Intracellular NAD+ was manipulated by nicotinamide riboside and the NAMPT inhibitor FK866.	NAD	14-18	nicotinamide phosphoribosyltransferase	Homo sapiens	68-73
34807408-4	2022	The brain cortex of HtrA2Hetero mice had increased superoxide dismutase (SOD) activity; lower levels of malondialdehyde (MDA); higher expressions of mitochondrial unfolded protein response (mtUPR)-related proteins, NADH dehydrogenase (ubiquinone) iron-sulfur protein 7 (Ndufs7), and uncoupling protein 2 (UCP2) proteins; more mitochondrial fission; higher levels of ATP and mtDNA copies; elevated sirtuin 3 (SIRT3) activity; and increased NAD+/NADH ratio.	NAD	439-443	HtrA serine peptidase 2	Mus musculus	20-25
21492230-1	2011	The purpose of the study was to determine in human malignant lymphomas the expression patterns of nicotinamide phosphoribosyltransferase (NAMPT) and nicotinic acid phosphoribosyltransferase (NAPRT), the primary, rate-limiting enzymes in the synthesis of NAD+.	NAD	254-258	nicotinamide phosphoribosyltransferase	Homo sapiens	98-136
34807408-4	2022	The brain cortex of HtrA2Hetero mice had increased superoxide dismutase (SOD) activity; lower levels of malondialdehyde (MDA); higher expressions of mitochondrial unfolded protein response (mtUPR)-related proteins, NADH dehydrogenase (ubiquinone) iron-sulfur protein 7 (Ndufs7), and uncoupling protein 2 (UCP2) proteins; more mitochondrial fission; higher levels of ATP and mtDNA copies; elevated sirtuin 3 (SIRT3) activity; and increased NAD+/NADH ratio.	NAD	444-448	HtrA serine peptidase 2	Mus musculus	20-25
34708329-1	2022	Silent information regulator 6 (SIRT6) is a mammalian homolog of the nicotinamide adenine dinucleotide (NAD)-dependent deacetylase sirtuin family.	NAD	69-102	sirtuin 6	Homo sapiens	0-30
34708329-1	2022	Silent information regulator 6 (SIRT6) is a mammalian homolog of the nicotinamide adenine dinucleotide (NAD)-dependent deacetylase sirtuin family.	NAD	69-102	sirtuin 6	Homo sapiens	32-37
34708329-1	2022	Silent information regulator 6 (SIRT6) is a mammalian homolog of the nicotinamide adenine dinucleotide (NAD)-dependent deacetylase sirtuin family.	NAD	104-107	sirtuin 6	Homo sapiens	0-30
34708329-1	2022	Silent information regulator 6 (SIRT6) is a mammalian homolog of the nicotinamide adenine dinucleotide (NAD)-dependent deacetylase sirtuin family.	NAD	104-107	sirtuin 6	Homo sapiens	32-37
34871777-10	2022	We also reveal a metabolic commonality between aged and diabetic beta cells: hyperactive glycolysis through increased expression of Nmnat2, a cytosolic NAD-synthesizing enzyme.	NAD	152-155	nicotinamide nucleotide adenylyltransferase 2	Mus musculus	132-138
34937015-0	2022	Highly sensitive voltammetric determination of NADH based on N-CQDs decorated SnO2/ionic liquid/carbon paste electrode.	NAD	47-51	strawberry notch homolog 1	Homo sapiens	78-81
34950960-1	2021	SIRT6 is an NAD+ dependent deacetylase that belongs to the mammalian sirtuin family.	NAD	12-15	sirtuin 6	Homo sapiens	0-5
34987507-8	2021	In contrast, restoration of NAD+ level by supplementation with nicotinamide mononucleotide abrogated the FK866-mediated caspase-1 cleavage.	NAD	28-32	caspase 1	Mus musculus	120-129
34948292-8	2021	Treatment-related changes in NAD+ levels correlated with shifts in nicotinamide N-methyltransferase (NNMT) expression.	NAD	29-33	nicotinamide N-methyltransferase	Homo sapiens	67-99
34948292-0	2021	Alterations in Kynurenine and NAD+ Salvage Pathways during the Successful Treatment of Inflammatory Bowel Disease Suggest HCAR3 and NNMT as Potential Drug Targets.	NAD	30-34	nicotinamide N-methyltransferase	Homo sapiens	132-136
34948292-8	2021	Treatment-related changes in NAD+ levels correlated with shifts in nicotinamide N-methyltransferase (NNMT) expression.	NAD	29-33	nicotinamide N-methyltransferase	Homo sapiens	101-105
34906231-1	2021	BACKGROUND: Silent information regulator 6 (SIRT6) is a mammalian homolog of the nicotinamide adenine dinucleotide (NAD)-dependent deacetylase sirtuin family.	NAD	81-114	sirtuin 6	Homo sapiens	12-42
34959937-9	2021	Also, TGPN and PNY stimulated NAD-dependent deacetylase sirtuin-1(SIRT1), peroxisome proliferator-activated receptor gamma coactivator-1 alpha (PGC-1alpha), nuclear respiratory factor 1,2, mitochondrial transcription factor A, along with mitochondrial DNA content via SIRT1/PGC-1alpha signaling.	NAD	30-33	peroxisome proliferative activated receptor, gamma, coactivator 1 alpha	Mus musculus	74-142
34959937-9	2021	Also, TGPN and PNY stimulated NAD-dependent deacetylase sirtuin-1(SIRT1), peroxisome proliferator-activated receptor gamma coactivator-1 alpha (PGC-1alpha), nuclear respiratory factor 1,2, mitochondrial transcription factor A, along with mitochondrial DNA content via SIRT1/PGC-1alpha signaling.	NAD	30-33	peroxisome proliferative activated receptor, gamma, coactivator 1 alpha	Mus musculus	144-154
34959937-9	2021	Also, TGPN and PNY stimulated NAD-dependent deacetylase sirtuin-1(SIRT1), peroxisome proliferator-activated receptor gamma coactivator-1 alpha (PGC-1alpha), nuclear respiratory factor 1,2, mitochondrial transcription factor A, along with mitochondrial DNA content via SIRT1/PGC-1alpha signaling.	NAD	30-33	peroxisome proliferative activated receptor, gamma, coactivator 1 alpha	Mus musculus	274-284
34866305-1	2021	The enzyme nicotinamide mononucleotide adenylyltransferase (NMNAT) catalyzes a reaction central to all known NAD biosynthetic routes.	NAD	109-112	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	60-65
35242812-14	2021	Transcriptomics-aided metabolic modeling provides a functional method for evaluating these changes and understanding downstream changes in NAD metabolism and aryl hydrocarbon receptor (AhR) signaling, with enhanced NAD metabolism in M. fascicularis and stronger AhR signaling in M. mulatta.	NAD	139-142	aryl hydrocarbon receptor	Macaca fascicularis	262-265
35242812-14	2021	Transcriptomics-aided metabolic modeling provides a functional method for evaluating these changes and understanding downstream changes in NAD metabolism and aryl hydrocarbon receptor (AhR) signaling, with enhanced NAD metabolism in M. fascicularis and stronger AhR signaling in M. mulatta.	NAD	215-218	aryl hydrocarbon receptor	Macaca fascicularis	158-183
35242812-14	2021	Transcriptomics-aided metabolic modeling provides a functional method for evaluating these changes and understanding downstream changes in NAD metabolism and aryl hydrocarbon receptor (AhR) signaling, with enhanced NAD metabolism in M. fascicularis and stronger AhR signaling in M. mulatta.	NAD	215-218	aryl hydrocarbon receptor	Macaca fascicularis	185-188
34997967-0	2022	NADH/NAD+ binding and linked tetrameric assembly of the oncogenic transcription factors CtBP1 and CtBP2.	NAD	0-4	C-terminal binding protein 1	Homo sapiens	88-93
34997967-0	2022	NADH/NAD+ binding and linked tetrameric assembly of the oncogenic transcription factors CtBP1 and CtBP2.	NAD	5-9	C-terminal binding protein 1	Homo sapiens	88-93
34906231-1	2021	BACKGROUND: Silent information regulator 6 (SIRT6) is a mammalian homolog of the nicotinamide adenine dinucleotide (NAD)-dependent deacetylase sirtuin family.	NAD	81-114	sirtuin 6	Homo sapiens	44-49
34906231-1	2021	BACKGROUND: Silent information regulator 6 (SIRT6) is a mammalian homolog of the nicotinamide adenine dinucleotide (NAD)-dependent deacetylase sirtuin family.	NAD	116-119	sirtuin 6	Homo sapiens	12-42
34906231-1	2021	BACKGROUND: Silent information regulator 6 (SIRT6) is a mammalian homolog of the nicotinamide adenine dinucleotide (NAD)-dependent deacetylase sirtuin family.	NAD	116-119	sirtuin 6	Homo sapiens	44-49
34871367-5	2021	These NAD+-consuming enzymes include PARPs, sirtuins, CD38, and SARM1.	NAD	6-10	sterile alpha and TIR motif containing 1	Homo sapiens	64-69
35008954-1	2022	AGC1/Aralar/Slc25a12 is the mitochondrial carrier of aspartate-glutamate, the regulatory component of the NADH malate-aspartate shuttle (MAS) that transfers cytosolic redox power to neuronal mitochondria.	NAD	106-110	solute carrier family 25 member 12	Homo sapiens	0-4
35008954-1	2022	AGC1/Aralar/Slc25a12 is the mitochondrial carrier of aspartate-glutamate, the regulatory component of the NADH malate-aspartate shuttle (MAS) that transfers cytosolic redox power to neuronal mitochondria.	NAD	106-110	solute carrier family 25 member 12	Homo sapiens	5-11
35008954-1	2022	AGC1/Aralar/Slc25a12 is the mitochondrial carrier of aspartate-glutamate, the regulatory component of the NADH malate-aspartate shuttle (MAS) that transfers cytosolic redox power to neuronal mitochondria.	NAD	106-110	solute carrier family 25 member 12	Homo sapiens	12-20
34793269-5	2021	RESULTS: In this study, we found that NADH:ubiquinone oxidoreductase subunit A6 (Ndufa6) participates in the regulation of adipogenic differentiation.	NAD	38-42	NADH:ubiquinone oxidoreductase subunit A6	Mus musculus	81-87
34880125-2	2022	NAD+-dependent 15-hydroxyprostaglandin dehydrogenase (15-PGDH) has been shown to inhibit CCA cell growth in vitro and in xenograft models.	NAD	0-3	hydroxyprostaglandin dehydrogenase 15 (NAD)	Mus musculus	54-61
33605178-1	2021	Nicotinamide riboside (NR), as a dietary supplement, can be converted to nicotinamide adenine dinucleotide (NAD+) in cells to support mitochondrial energy metabolism.	NAD	73-106	nervous	Mus musculus	23-25
34870595-2	2021	Axon degeneration in injury and disease is promoted by activation of the nicotinamide adenine dinucleotide (NAD)-consuming enzyme SARM1.	NAD	73-106	sterile alpha and TIR motif containing 1	Homo sapiens	130-135
33605178-1	2021	Nicotinamide riboside (NR), as a dietary supplement, can be converted to nicotinamide adenine dinucleotide (NAD+) in cells to support mitochondrial energy metabolism.	NAD	108-112	nervous	Mus musculus	23-25
34213829-1	2021	SARM1, an executioner in axon degeneration, is an autoinhibitory NAD-consuming enzyme, composed of multiple domains.	NAD	65-68	sterile alpha and TIR motif containing 1	Homo sapiens	0-5
34322899-6	2021	Inhibition of NAD+ producing enzyme Nicotinamide phosphoribosyl transferase (NAMPT) increased ciliary length and frequency in CCA cells and in SIRT1 overexpressed H69 cells.	NAD	14-18	nicotinamide phosphoribosyltransferase	Homo sapiens	36-75
34322899-6	2021	Inhibition of NAD+ producing enzyme Nicotinamide phosphoribosyl transferase (NAMPT) increased ciliary length and frequency in CCA cells and in SIRT1 overexpressed H69 cells.	NAD	14-18	nicotinamide phosphoribosyltransferase	Homo sapiens	77-82
34748530-0	2021	NAMPT-derived NAD+ fuels PARP1 to promote skin inflammation through parthanatos cell death.	NAD	14-18	nicotinamide phosphoribosyltransferase	Homo sapiens	0-5
34748530-6	2021	In conclusion, hyperactivation of PARP1 in response to ROS-induced DNA damage, fueled by NAMPT-derived NAD+, mediates skin inflammation through parthanatos cell death.	NAD	103-107	nicotinamide phosphoribosyltransferase	Homo sapiens	89-94
34787870-1	2021	OBJECTIVE: SIRT6 is an NAD-dependent histone deacetylase known to regulate aging, inflammation and energy metabolism, and might play an important role in atherosclerosis.	NAD	23-26	sirtuin 6	Homo sapiens	11-16
34835340-0	2021	Ultrasensitive Detection of SARS-CoV-2 Spike Proteins Using the Thio-NAD Cycling Reaction: A Preliminary Study before Clinical Trials.	NAD	69-72	surface glycoprotein	Severe acute respiratory syndrome coronavirus 2	39-44
34644262-6	2021	The further assays demonstrate that Nmnat2 activates AMPK by up-regulating the ratio of NAD+/NADH, moreover AMPK agonist AICAR can also increase ADAM10 activity and reduces Abeta1-40/1-42.	NAD	88-92	nicotinamide nucleotide adenylyltransferase 2	Mus musculus	36-42
34644262-6	2021	The further assays demonstrate that Nmnat2 activates AMPK by up-regulating the ratio of NAD+/NADH, moreover AMPK agonist AICAR can also increase ADAM10 activity and reduces Abeta1-40/1-42.	NAD	93-97	nicotinamide nucleotide adenylyltransferase 2	Mus musculus	36-42
34553901-4	2021	A metal-free heterojunction of pyromellitic diimide/g-C3N4 (PDI/CN) with an excellent visible light response (lambda < 660 nm) is fabricated for achieving a photoenzymatic catalytic cascade system, which efficiently regenerates nicotinamide adenine dinucleotide (NADH) and selectively reduces CO2 to formic acid (HCOOH).	NAD	228-261	prolyl 4-hydroxylase subunit beta	Homo sapiens	60-66
34553901-4	2021	A metal-free heterojunction of pyromellitic diimide/g-C3N4 (PDI/CN) with an excellent visible light response (lambda < 660 nm) is fabricated for achieving a photoenzymatic catalytic cascade system, which efficiently regenerates nicotinamide adenine dinucleotide (NADH) and selectively reduces CO2 to formic acid (HCOOH).	NAD	263-267	prolyl 4-hydroxylase subunit beta	Homo sapiens	60-66
34553901-5	2021	The highest NADH yield of the PDI/CN hybrid achieved is 75%, and the HCOOH generation rate achieved is 1.269 mmol g-1 h-1 with nearly 100% selectivity, which is much higher than those of the reported materials.	NAD	12-16	prolyl 4-hydroxylase subunit beta	Homo sapiens	30-36
34509469-7	2021	Decreasing tissue NAD+ concentrations have been ascribed to an imbalance between biosynthesis and consumption of the dinucleotide, resulting from, for instance, reduced levels of the rate limiting enzyme NAMPT along with an increased activation state of the NAD+-consuming enzymes PARPs and CD38.	NAD	18-22	nicotinamide phosphoribosyltransferase	Homo sapiens	204-209
34641449-5	2021	Our models suggest similarities in the ways that PGE2 and SW033291 interact with key residues in the 15-PGDH-NAD+ complex.	NAD	109-113	hydroxyprostaglandin dehydrogenase 15 (NAD)	Mus musculus	101-108
34548492-0	2021	NAD+ augmentation with nicotinamide riboside improves lymphoid potential of Atm-/- and old mice HSCs.	NAD	0-4	ataxia telangiectasia mutated	Mus musculus	76-79
34603081-14	2021	In conclusion, NAD+ biosynthesis was significantly impaired in CKD, which may attribute to downregulation of QPRT and NMNAT 1/3.	NAD	15-19	quinolinate phosphoribosyltransferase	Rattus norvegicus	109-113
34576949-7	2021	AlDH activity increased significantly in the first 10 days by 70-170%, reflecting the effectiveness of the enzyme and NAD+ in utilizing toxic aldehydes at this stage of burn disease.	NAD	118-122	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	0-4
34076906-5	2021	Nicotinamide adenine dinucleotide (NAD+ ) was shown to increase the sensitivity of P2X7 receptors to eATP via ecto-ADP-ribosyltransferase 2 (ARTC2)-catalyzed ADP-ribosylation in peripheral immune cells.	NAD	0-33	ADP-ribosyltransferase 2a	Mus musculus	141-146
34076906-5	2021	Nicotinamide adenine dinucleotide (NAD+ ) was shown to increase the sensitivity of P2X7 receptors to eATP via ecto-ADP-ribosyltransferase 2 (ARTC2)-catalyzed ADP-ribosylation in peripheral immune cells.	NAD	35-39	ADP-ribosyltransferase 2a	Mus musculus	141-146
34302821-2	2021	These strategies include supplementing with NAD+ precursors, small molecule activation of NAD+ biosynthetic enzymes, and treatment with small molecule inhibitors of NAD+ consuming enzymes such as CD38, SARM1 or members of the PARP family.	NAD	165-169	sterile alpha and TIR motif containing 1	Homo sapiens	202-207
34076541-0	2021	EXPRESS: pH-Dependent Flavin Adenine Dinucleotide and Nicotinamide Adenine Dinucleotide Ultraviolet Resonance Raman (UVRR) Spectra at Intracellular Concentration.	NAD	54-87	phenylalanine hydroxylase	Homo sapiens	9-11
34130091-4	2021	In mammals, nicotinamide phosphoribosyltransferase (NAMPT) is the rate-limiting enzyme in the NAD+ salvage pathway and essential for NAD+ homeostasis.	NAD	94-98	nicotinamide phosphoribosyltransferase	Homo sapiens	12-50
34130091-4	2021	In mammals, nicotinamide phosphoribosyltransferase (NAMPT) is the rate-limiting enzyme in the NAD+ salvage pathway and essential for NAD+ homeostasis.	NAD	94-98	nicotinamide phosphoribosyltransferase	Homo sapiens	52-57
34130091-4	2021	In mammals, nicotinamide phosphoribosyltransferase (NAMPT) is the rate-limiting enzyme in the NAD+ salvage pathway and essential for NAD+ homeostasis.	NAD	133-137	nicotinamide phosphoribosyltransferase	Homo sapiens	12-50
34130091-4	2021	In mammals, nicotinamide phosphoribosyltransferase (NAMPT) is the rate-limiting enzyme in the NAD+ salvage pathway and essential for NAD+ homeostasis.	NAD	133-137	nicotinamide phosphoribosyltransferase	Homo sapiens	52-57
34130091-6	2021	Here, we show that NAMPT prevents NAD+ depletion in epidermal keratinocytes to protect against the mild-dose UVA and UVB (UVA/B)-induced proliferation defects.	NAD	34-38	nicotinamide phosphoribosyltransferase	Homo sapiens	19-24
2560924-3	1989	We have focused our attention on two chromatin enzymes: NMN-adenylyltransferase that catalyzes reversible synthesis of NAD+ utilizing ATP and NMN, and poly(ADP-ribose)polymerase that covalently modifies nucleosomal proteins through poly ADP-ribosylation reactions.	NAD	119-123	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	56-79
2817348-5	1989	By stoichiometric coupling of this reaction with diaphorase/iodonitro tetrazolium chloride (INT) the formed NADH converts INT to a formazan whereby the reaction is displaced in favor of phenylpyruvate.	NAD	108-112	dihydrolipoamide dehydrogenase	Homo sapiens	49-59
2588336-6	1989	The protective effect of the NAD+ against ALDH I and II inactivation by disulfiram and disulphides I, IV, VI-VIII and X is shown.	NAD	29-33	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	42-46
2471721-2	1989	The reaction principle is based on the oxidation of D-glucose, liberated by the disaccharidases, into D-gluconolactone and the production of NADH by glucose dehydrogenase.	NAD	141-145	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	149-170
2925614-0	1989	The nicotinamide adenine dinucleotide-binding site of chicken liver xanthine dehydrogenase.	NAD	4-37	xanthine dehydrogenase	Gallus gallus	68-90
2925614-2	1989	Affinity labeling of the NAD-binding site of chicken liver xanthine dehydrogenase by 5"-p-fluorosulfonylbenzoyladenosine (5"-FSBA) caused spectral perturbation around 450 nm in the same way as NAD.	NAD	25-28	xanthine dehydrogenase	Gallus gallus	59-81
2925614-2	1989	Affinity labeling of the NAD-binding site of chicken liver xanthine dehydrogenase by 5"-p-fluorosulfonylbenzoyladenosine (5"-FSBA) caused spectral perturbation around 450 nm in the same way as NAD.	NAD	193-196	xanthine dehydrogenase	Gallus gallus	59-81
2925614-3	1989	Reductive titration with xanthine of native xanthine dehydrogenase in the presence of NAD showed that redox potentials of the FAD/FADH.	NAD	86-89	xanthine dehydrogenase	Gallus gallus	44-66
2925614-6	1989	These results provide further evidence that binding of NAD to chicken liver xanthine dehydrogenase modulates the reactivity of the enzyme by shifting the redox potential of FAD.	NAD	55-58	xanthine dehydrogenase	Gallus gallus	76-98
2930578-9	1989	Inhibition of ALDH activity measured in the mitochondrial plus microsomal fractions of rat liver also required NADH and was prevented by glutathione and heat treatment of the microsomes.	NAD	111-115	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	14-18
2910350-1	1989	Time-resolved fluorescence studies on the emission of NADH bound to porcine heart mitochondrial malate dehydrogenase [S)-malate:NAD+ oxidoreductase, EC 1.1.1.37), in the presence and absence of saturating levels of hydroxymalonate, were carried out.	NAD	54-58	hydroxysteroid 17-beta dehydrogenase 6	Homo sapiens	133-147
2644223-0	1989	Roles of glycerol and glycerol-3-phosphate dehydrogenase (NAD+) in acquired osmotolerance of Saccharomyces cerevisiae.	NAD	58-62	glycerol-3-phosphate dehydrogenase	Saccharomyces cerevisiae S288C	22-56
3166459-0	1988	Rapid reaction studies on the reduction and oxidation of chicken liver xanthine dehydrogenase by the xanthine/urate and NAD/NADH couples.	NAD	120-123	xanthine dehydrogenase	Gallus gallus	71-93
3166459-0	1988	Rapid reaction studies on the reduction and oxidation of chicken liver xanthine dehydrogenase by the xanthine/urate and NAD/NADH couples.	NAD	124-128	xanthine dehydrogenase	Gallus gallus	71-93
3166459-1	1988	Chicken liver xanthine dehydrogenase can be partially reduced by either xanthine or NADH.	NAD	84-88	xanthine dehydrogenase	Gallus gallus	14-36
3166459-5	1988	Oxidation of fully (6-electron) reduced xanthine dehydrogenase by either urate or NAD is monophasic and dependent on the oxidant concentration.	NAD	82-85	xanthine dehydrogenase	Gallus gallus	40-62
2853168-6	1988	After separation of the bile acids, NADH was produced by use of immobilized 3 alpha-hydroxysteroid dehydrogenase column and then determined fluorimetrically (gamma em = 460 nm, gamma ex = 350 nm).	NAD	36-40	aldo-keto reductase family 1 member C3	Homo sapiens	76-112
34130091-9	2021	Moreover, the NAMPT inhibitor abrogated the sirtuin-1 (SIRT1)-mediated deacetylation of p53 and significantly inhibited the proliferation of UVA/B-irradiated cells, suggesting that the NAMPT-NAD+-SIRT1 axis regulates p53 functions upon UVA/B stress.	NAD	191-195	nicotinamide phosphoribosyltransferase	Homo sapiens	14-19
34130091-9	2021	Moreover, the NAMPT inhibitor abrogated the sirtuin-1 (SIRT1)-mediated deacetylation of p53 and significantly inhibited the proliferation of UVA/B-irradiated cells, suggesting that the NAMPT-NAD+-SIRT1 axis regulates p53 functions upon UVA/B stress.	NAD	191-195	nicotinamide phosphoribosyltransferase	Homo sapiens	185-190
34870595-2	2021	Axon degeneration in injury and disease is promoted by activation of the nicotinamide adenine dinucleotide (NAD)-consuming enzyme SARM1.	NAD	108-111	sterile alpha and TIR motif containing 1	Homo sapiens	130-135
33605178-6	2021	Oral administration of NR/RESms for 8 hours significantly elevated NAD+ levels in serum (169.88 nM versus 30.93 nM in the NR group, p < .01; and 66.89 nM in the NR + RES group, p < .05), and enhanced NAD+ abundance in multiple organs in mice, exhibiting an improved oral NAD+ bioavailability.	NAD	67-71	nervous	Mus musculus	23-25
33605178-6	2021	Oral administration of NR/RESms for 8 hours significantly elevated NAD+ levels in serum (169.88 nM versus 30.93 nM in the NR group, p < .01; and 66.89 nM in the NR + RES group, p < .05), and enhanced NAD+ abundance in multiple organs in mice, exhibiting an improved oral NAD+ bioavailability.	NAD	67-71	nervous	Mus musculus	122-124
33605178-6	2021	Oral administration of NR/RESms for 8 hours significantly elevated NAD+ levels in serum (169.88 nM versus 30.93 nM in the NR group, p < .01; and 66.89 nM in the NR + RES group, p < .05), and enhanced NAD+ abundance in multiple organs in mice, exhibiting an improved oral NAD+ bioavailability.	NAD	67-71	nervous	Mus musculus	161-163
33605178-6	2021	Oral administration of NR/RESms for 8 hours significantly elevated NAD+ levels in serum (169.88 nM versus 30.93 nM in the NR group, p < .01; and 66.89 nM in the NR + RES group, p < .05), and enhanced NAD+ abundance in multiple organs in mice, exhibiting an improved oral NAD+ bioavailability.	NAD	200-204	nervous	Mus musculus	23-25
34330933-4	2021	The mitochondrial NAD+-dependent enzyme sirtuin 5 (SIRT5) is a key regulator of mitochondrial form and function, but its role in ischemic renal injury (IRI) is unknown.	NAD	18-22	sirtuin 5	Homo sapiens	40-49
33605178-6	2021	Oral administration of NR/RESms for 8 hours significantly elevated NAD+ levels in serum (169.88 nM versus 30.93 nM in the NR group, p < .01; and 66.89 nM in the NR + RES group, p < .05), and enhanced NAD+ abundance in multiple organs in mice, exhibiting an improved oral NAD+ bioavailability.	NAD	271-275	nervous	Mus musculus	23-25
34330933-4	2021	The mitochondrial NAD+-dependent enzyme sirtuin 5 (SIRT5) is a key regulator of mitochondrial form and function, but its role in ischemic renal injury (IRI) is unknown.	NAD	18-22	sirtuin 5	Homo sapiens	51-56
33605178-6	2021	Oral administration of NR/RESms for 8 hours significantly elevated NAD+ levels in serum (169.88 nM versus 30.93 nM in the NR group, p < .01; and 66.89 nM in the NR + RES group, p < .05), and enhanced NAD+ abundance in multiple organs in mice, exhibiting an improved oral NAD+ bioavailability.	NAD	271-275	nervous	Mus musculus	122-124
34356514-5	2021	MacroH2A1.1 and macroH2A1.2 isoforms differ only in a few amino acids and their ability to bind NAD-derived metabolites, a property allegedly conferring their different functions in vivo.	NAD	96-99	macroH2A.1 histone	Mus musculus	16-27
34752167-1	2021	Background: Nicotinamide phosphoribosyltransferase (NAMPT) catalyzes the rate-limiting step in the salvage pathway of mammalian nicotinamide adenine dinucleotide (NAD+) biosynthesis.	NAD	128-161	nicotinamide phosphoribosyltransferase	Homo sapiens	12-50
34752167-1	2021	Background: Nicotinamide phosphoribosyltransferase (NAMPT) catalyzes the rate-limiting step in the salvage pathway of mammalian nicotinamide adenine dinucleotide (NAD+) biosynthesis.	NAD	128-161	nicotinamide phosphoribosyltransferase	Homo sapiens	52-57
34752167-1	2021	Background: Nicotinamide phosphoribosyltransferase (NAMPT) catalyzes the rate-limiting step in the salvage pathway of mammalian nicotinamide adenine dinucleotide (NAD+) biosynthesis.	NAD	163-167	nicotinamide phosphoribosyltransferase	Homo sapiens	12-50
34239868-2	2021	Sirtuin protein 6 (SIRT6) is a nicotinamide adenine dinucleotide (NAD)-dependent deacetylase that plays important roles in cell differentiation.	NAD	31-64	sirtuin 6	Homo sapiens	0-17
34752167-1	2021	Background: Nicotinamide phosphoribosyltransferase (NAMPT) catalyzes the rate-limiting step in the salvage pathway of mammalian nicotinamide adenine dinucleotide (NAD+) biosynthesis.	NAD	163-167	nicotinamide phosphoribosyltransferase	Homo sapiens	52-57
34239868-2	2021	Sirtuin protein 6 (SIRT6) is a nicotinamide adenine dinucleotide (NAD)-dependent deacetylase that plays important roles in cell differentiation.	NAD	31-64	sirtuin 6	Homo sapiens	19-24
34239868-2	2021	Sirtuin protein 6 (SIRT6) is a nicotinamide adenine dinucleotide (NAD)-dependent deacetylase that plays important roles in cell differentiation.	NAD	66-69	sirtuin 6	Homo sapiens	0-17
34752167-2	2021	Through its NAD+-biosynthetic activity, NAMPT is able to regulate the development of hepatic steatosis and inflammation induced by diet or alcohol.	NAD	12-16	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
34239868-2	2021	Sirtuin protein 6 (SIRT6) is a nicotinamide adenine dinucleotide (NAD)-dependent deacetylase that plays important roles in cell differentiation.	NAD	66-69	sirtuin 6	Homo sapiens	19-24
34752167-4	2021	Purpose: To investigate the roles of NAMPT-mediated NAD+ biosynthesis in hepatic stellate cell (HSC) activation and liver fibrosis.	NAD	52-56	nicotinamide phosphoribosyltransferase	Homo sapiens	37-42
34752167-12	2021	Adenovirus-mediated NAMPT overexpression augments liver NAD+ levels, inhibits HSC activation and alleviates CCl4-induced liver fibrosis in mice.	NAD	56-60	nicotinamide phosphoribosyltransferase	Homo sapiens	20-25
34142751-0	2021	The new insight into extracellular NAD+ degradation-the contribution of CD38 and CD73 in calcific aortic valve disease.	NAD	35-39	5'-nucleotidase ecto	Homo sapiens	81-85
34605570-5	2021	Among the most significantly altered metabolites, we identified metabolites related with mitochondrial fatty acid elongation (MFAE) and mitochondrial beta-oxidation such as lauroyl-CoA, cholesterol, triglycerides, (S)-3-hydroxyhexadecanoyl-CoA, and NAD+ .	NAD	249-253	enoyl-CoA hydratase, short chain 1	Homo sapiens	89-102
34142751-4	2021	Human non-stenotic valves (n = 10) actively converted NAD+ and NMN via both CD73 and NAD+ -glycohydrolase (CD38) according to our analysis with RP-HPLC and immunofluorescence.	NAD	54-58	5'-nucleotidase ecto	Homo sapiens	76-80
34142751-5	2021	In stenotic valves (n = 50), due to reduced CD73 activity, NAD+ was degraded predominantly by CD38 and additionally by ALP and eNPP1.	NAD	59-63	5'-nucleotidase ecto	Homo sapiens	44-48
34605570-5	2021	Among the most significantly altered metabolites, we identified metabolites related with mitochondrial fatty acid elongation (MFAE) and mitochondrial beta-oxidation such as lauroyl-CoA, cholesterol, triglycerides, (S)-3-hydroxyhexadecanoyl-CoA, and NAD+ .	NAD	249-253	enoyl-CoA hydratase, short chain 1	Homo sapiens	136-149
34208136-2	2021	SARS-CoV-2 infection occurs through the interaction of the viral protein Spike with the angiotensin II receptor (ACE 2), leading to an increase of angiotensin II and activation of nicotinamide adenine dinucleotide phosphate oxidase2 (NOX2), resulting in the release of both reactive oxygen species (ROS) and inflammatory molecules.	NAD	180-213	surface glycoprotein	Severe acute respiratory syndrome coronavirus 2	73-78
34731617-0	2021	Temporal dynamics of base excision/single-strand break repair protein complex assembly/disassembly are modulated by the PARP/NAD+/SIRT6 axis.	NAD	125-129	sirtuin 6	Homo sapiens	130-135
34208136-2	2021	SARS-CoV-2 infection occurs through the interaction of the viral protein Spike with the angiotensin II receptor (ACE 2), leading to an increase of angiotensin II and activation of nicotinamide adenine dinucleotide phosphate oxidase2 (NOX2), resulting in the release of both reactive oxygen species (ROS) and inflammatory molecules.	NAD	180-213	angiotensin converting enzyme 2	Homo sapiens	113-118
34731617-6	2021	These findings highlight coordinated yet independent roles for PARP1, PARP2, and SIRT6 and their regulation by NAD+ bioavailability to facilitate BER.	NAD	111-115	sirtuin 6	Homo sapiens	81-86
34559251-0	2021	Aryl hydrocarbon receptor (AHR) functions in infectious and sterile inflammation and NAD+-dependent metabolic adaptation.	NAD	85-89	aryl hydrocarbon receptor	Homo sapiens	0-25
34559251-0	2021	Aryl hydrocarbon receptor (AHR) functions in infectious and sterile inflammation and NAD+-dependent metabolic adaptation.	NAD	85-89	aryl hydrocarbon receptor	Homo sapiens	27-30
34403688-2	2021	Recently, we elucidated the molecular mechanism of SARM1 activation, demonstrating that SARM1 is a metabolic sensor regulated by the levels of NAD+ and its precursor, nicotinamide mononucleotide (NMN), via their competitive binding to an allosteric site within the SARM1 N-terminal ARM domain.	NAD	143-147	sterile alpha and TIR motif containing 1	Homo sapiens	51-56
34199982-4	2021	Furthermore, the influence of the mitochondrial status on cytosolic NAD+ availability affecting the activity of cytosolic SIRT5 iso1 and iso4-in turn regulating cytosolic protein lysine succinylations-is presented.	NAD	68-72	sirtuin 5	Homo sapiens	122-127
34403688-2	2021	Recently, we elucidated the molecular mechanism of SARM1 activation, demonstrating that SARM1 is a metabolic sensor regulated by the levels of NAD+ and its precursor, nicotinamide mononucleotide (NMN), via their competitive binding to an allosteric site within the SARM1 N-terminal ARM domain.	NAD	143-147	sterile alpha and TIR motif containing 1	Homo sapiens	88-93
34403688-2	2021	Recently, we elucidated the molecular mechanism of SARM1 activation, demonstrating that SARM1 is a metabolic sensor regulated by the levels of NAD+ and its precursor, nicotinamide mononucleotide (NMN), via their competitive binding to an allosteric site within the SARM1 N-terminal ARM domain.	NAD	143-147	sterile alpha and TIR motif containing 1	Homo sapiens	265-270
34671164-7	2021	OspC3, but not its paralogues OspC1 and 2, covalently modified caspase-11/4; although it used the NAD+ donor, this modification was not ADP-ribosylation.	NAD	98-102	ospC3	Shigella flexneri	0-5
34068917-6	2021	In fact, research has mainly focused on inhibiting the key enzyme of the latter NAD production route, nicotinamide phosphoribosyltransferase (NAMPT), leading to the identification of numerous inhibitors, including FK866 and CHS-828.	NAD	80-83	nicotinamide phosphoribosyltransferase	Homo sapiens	102-140
34068917-6	2021	In fact, research has mainly focused on inhibiting the key enzyme of the latter NAD production route, nicotinamide phosphoribosyltransferase (NAMPT), leading to the identification of numerous inhibitors, including FK866 and CHS-828.	NAD	80-83	nicotinamide phosphoribosyltransferase	Homo sapiens	142-147
3047261-1	1988	Enzyme-amplified immunoassays have been adapted for electrochemical measurement, using an NAD+/NADH redox cycle coupled to an electrode via the active site of diaphorase.	NAD	90-94	dihydrolipoamide dehydrogenase	Homo sapiens	159-169
3346227-2	1988	Diphtheria toxin and Pseudomonas exotoxin A catalyze the transfer of an ADP-ribose residue from NAD to diphthamide, causing the inactivation of EF-2.	NAD	96-99	elongation factor 2	Cricetulus griseus	144-148
34696484-10	2021	DEGs detected between LPL and HPL groups were found to have significantly enriched regulation of signaling receptor activity, the response to toxic substances, nicotinamide adenine dinucleotide (NADH) dehydrogenase complex assembly, cytokine production, vesicle, and vacuole organization.	NAD	160-193	lipoprotein lipase	Capra hircus	22-25
35599556-4	2022	The average maximum RAF size is 275 reactions for a rich organic medium and 93 for a medium with a single organic cofactor, NAD.	NAD	124-127	zinc fingers and homeoboxes 2	Homo sapiens	20-23
34696484-10	2021	DEGs detected between LPL and HPL groups were found to have significantly enriched regulation of signaling receptor activity, the response to toxic substances, nicotinamide adenine dinucleotide (NADH) dehydrogenase complex assembly, cytokine production, vesicle, and vacuole organization.	NAD	195-199	lipoprotein lipase	Capra hircus	22-25
34639240-1	2021	Nicotinamide Phosphoribosyltransferase (Nampt)/Nicotinamide Adenine Dinucleotide (NAD) Axis Suppresses Atrial Fibrillation by Modulating the Calcium Handling Pathway.	NAD	47-80	nicotinamide phosphoribosyltransferase	Homo sapiens	0-38
35459935-3	2022	Here, we report the discovery and development of a class of potent activators (NATs) of nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme in the NAD salvage pathway.	NAD	168-171	nicotinamide phosphoribosyltransferase	Homo sapiens	88-126
35459935-3	2022	Here, we report the discovery and development of a class of potent activators (NATs) of nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme in the NAD salvage pathway.	NAD	168-171	nicotinamide phosphoribosyltransferase	Homo sapiens	128-133
35626746-2	2022	Here, we present several lines of evidence that in HL-1 cardiomyocytes, a forced, chemically induced reduction in the FBP2 dimer-tetramer ratio that imitates AMP and NAD+ action and restricts FBP2-mitochondria interaction, results in an increase in Tau phosphorylation, augmentation of FBP2-Tau and FBP2-MAP1B interactions, disturbance of tubulin network, marked reduction in the speed of mitochondrial trafficking and increase in mitophagy.	NAD	166-170	fructose-bisphosphatase 2	Homo sapiens	118-122
35628596-5	2022	RT-qPCR analysis revealed the upregulation of the expression of the NAD+ synthesis enzyme nicotinamide phosphoribosyltransferase (NAMPT).	NAD	68-72	nicotinamide phosphoribosyltransferase	Homo sapiens	90-128
35628596-5	2022	RT-qPCR analysis revealed the upregulation of the expression of the NAD+ synthesis enzyme nicotinamide phosphoribosyltransferase (NAMPT).	NAD	68-72	nicotinamide phosphoribosyltransferase	Homo sapiens	130-135
35491967-1	2022	Congenital nicotinamide adenine dinucleotide (NAD) deficiency disorders are associated with pathogenic variants in the genes NADSYN1, HAAO, and KYNU.	NAD	11-44	3-hydroxyanthranilate 3,4-dioxygenase	Homo sapiens	134-138
35488293-0	2022	Correction: Mesenchymal stromal cells attenuate alveolar type 2 cells senescence through regulating NAMPT-mediated NAD metabolism.	NAD	115-118	nicotinamide phosphoribosyltransferase	Homo sapiens	100-105
34639240-1	2021	Nicotinamide Phosphoribosyltransferase (Nampt)/Nicotinamide Adenine Dinucleotide (NAD) Axis Suppresses Atrial Fibrillation by Modulating the Calcium Handling Pathway.	NAD	47-80	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
34639240-1	2021	Nicotinamide Phosphoribosyltransferase (Nampt)/Nicotinamide Adenine Dinucleotide (NAD) Axis Suppresses Atrial Fibrillation by Modulating the Calcium Handling Pathway.	NAD	82-85	nicotinamide phosphoribosyltransferase	Homo sapiens	0-38
3292518-7	1988	Since the amino acid residues around FAD and NAD binding sites and at the reaction centers of the two enzymes are strongly conserved, the lipoamide dehydrogenase may catalyze the opposite reaction through a similar mechanism to that proposed for glutathione reductase.	NAD	45-48	glutathione-disulfide reductase	Homo sapiens	246-267
2827635-0	1987	The effect of rate limitation by cytochrome c on the redox state of the ubiquinone pool in reconstituted NADH: cytochrome c reductase.	NAD	105-109	LOC104968582	Bos taurus	33-45
34639240-1	2021	Nicotinamide Phosphoribosyltransferase (Nampt)/Nicotinamide Adenine Dinucleotide (NAD) Axis Suppresses Atrial Fibrillation by Modulating the Calcium Handling Pathway.	NAD	82-85	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
34455132-8	2021	In physical and chemical transection of axons, SARM1 was found to promotes axon degeneration by hydrolyzing NAD+.	NAD	108-112	sterile alpha and TIR motif containing 1	Homo sapiens	47-52
2827635-0	1987	The effect of rate limitation by cytochrome c on the redox state of the ubiquinone pool in reconstituted NADH: cytochrome c reductase.	NAD	105-109	LOC104968582	Bos taurus	111-123
2827635-4	1987	These conditions can be met by reconstituted NADH: cytochrome c reductase (Complex I-III from bovine heart) when electron flow is rate-limited by a low concentration of cytochrome c.	NAD	45-49	LOC104968582	Bos taurus	51-63
2827635-4	1987	These conditions can be met by reconstituted NADH: cytochrome c reductase (Complex I-III from bovine heart) when electron flow is rate-limited by a low concentration of cytochrome c.	NAD	45-49	LOC104968582	Bos taurus	169-181
34509469-2	2021	NAD+ is also important in cellular signalling as it is consumed by PARPs, SARM1, sirtuins and CD38.	NAD	0-4	sterile alpha and TIR motif containing 1	Homo sapiens	74-79
34253597-7	2021	Previously, we showed that mTOR regulator p21 activated kinase 4 (PAK4) and nicotinamide adenine dinucleotide biosynthesis enzyme nicotinamide phosphoribosyl transferase (NAMPT) were aberrantly expressed in PNET tissue and promoted everolimus resistance.	NAD	76-109	nicotinamide phosphoribosyltransferase	Homo sapiens	130-169
3444373-4	1987	AGMO activity was monitored at 340 nm by coupling the NADH redox reaction to the tetrahydropteridine cofactor of the rat liver microsomal enzyme.	NAD	54-58	alkylglycerol monooxygenase	Rattus norvegicus	0-4
3619922-1	1987	The activity of the pH 7.5 NADH-linked nitrate reductase isoform from soybean seedlings is termed inducible.	NAD	27-31	chalcone reductase CHR1	Glycine max	47-56
3109485-1	1987	Incorporation into rabbit liver microsomal membranes of detergent-solubilized cytochrome b5 stimulates NADH-supported electron flow to ferric cytochrome P-450, but impairs NADPH-dependent reduction of the pigment such as to make the rates of both reactions equivalent; yet, in the enriched preparations NADPH-driven N-oxidation of 4-chloroaniline proceeds at considerably higher rate than does the NADH-supported process.	NAD	103-107	cytochrome P-450	Oryctolagus cuniculus	142-158
3109485-2	1987	Analysis of transfer of the second electron to oxyferrous cytochrome P-450, as assessed by measuring substrate-induced reoxidation of ferrous cytochrome b5, reveals faster flow with NADH than with NADPH as the source of reducing equivalents.	NAD	182-186	cytochrome P-450	Oryctolagus cuniculus	58-74
3109485-4	1987	The NADH- and NADPH-supported pathway of N-oxidation in the cytochrome b5-supplemented microsomal fractions thus probably involves distinct forms of cytochrome P-450.	NAD	4-8	cytochrome P-450	Oryctolagus cuniculus	149-165
3475129-0	1987	Evidence for the existence of a tyrosyl residue in the nicotinamide adenine dinucleotide binding site of chicken liver xanthine dehydrogenase.	NAD	55-88	xanthine dehydrogenase	Gallus gallus	119-141
3475129-1	1987	Xanthine-NAD and NADH-methylene blue oxidoreductase activities of chicken liver xanthine dehydrogenase were inactivated by incubation with 5"-[p-(fluorosulfonyl)benzoyl]adenosine (5"-FSBA), an active site directed reagent for nucleotide binding sites.	NAD	9-12	xanthine dehydrogenase	Gallus gallus	80-102
3475129-7	1987	These results indicated that 5"-FSBA modified specifically the binding site for NAD of chicken liver xanthine dehydrogenase.	NAD	80-83	xanthine dehydrogenase	Gallus gallus	101-123
3036647-4	1987	The exon-intron organization of mouse LDH-A gene is compared with the organizations of other dehydrogenase genes, and the molecular evolution of the nicotinamide adenine dinucleotide binding domains is discussed.	NAD	149-182	lactate dehydrogenase A	Mus musculus	38-43
3593587-6	1987	Vmax values obtained were 0.86, 0.61, and 0.51 mumole NADH produced/min/mg of protein for KIV, KIC, and KMV, respectively, in the presence of excess amount of lipoamide oxidoreductase.	NAD	54-58	hydroxysteroid 17-beta dehydrogenase 6	Homo sapiens	169-183
3580021-2	1987	An addition of glutathione, dithiothreitol, nicotinic acid-amide-adenine-dinucleotide (NAD) or its reduced form (NADH) to the ALDH preparations preserved the enzyme activity; the above SH-reagents regenerated an already occurred loss of activity rapidly (within minutes) and almost completely.	NAD	113-117	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	126-130
2822347-10	1987	NAD kinase was inhibited by EDTA, sulfhydryl reagents, NADH but not by nicotinamide.	NAD	55-59	NAD kinase	Equus caballus	0-10
2822347-12	1987	The substantial phosphorylation of the intracellular NAD(H) pool noticed in stimulated granulocytes is probably due to enhanced NAD kinase activity and modulated by physiological concentrations of NADH.	NAD	53-59	NAD kinase	Equus caballus	128-138
2876727-2	1986	Membrane treatments and conditions of rebinding of F1 and OSCP were optimized to reconstitute efficient NADH- and ATP-dependent proton fluxes, ATP synthesis and oligomycin-sensitive ATPase activity.	NAD	104-108	ATP synthase subunit O, mitochondrial	Sus scrofa	58-62
2876727-6	1986	The rebinding of OSCP alone or F1 alone, does not modify the NADH-dependent proton flux, while the rebinding of both F1 and OSCP controls this flux, inducing an inhibition of the rate of NADH oxidation.	NAD	187-191	ATP synthase subunit O, mitochondrial	Sus scrofa	17-21
2876727-6	1986	The rebinding of OSCP alone or F1 alone, does not modify the NADH-dependent proton flux, while the rebinding of both F1 and OSCP controls this flux, inducing an inhibition of the rate of NADH oxidation.	NAD	187-191	ATP synthase subunit O, mitochondrial	Sus scrofa	124-128
3015030-4	1986	Elution of catalase beta was also obtained with NADH, NADP+, and ADP at higher concentration.	NAD	48-52	catalase	Bos taurus	11-19
2940338-1	1986	In mammalian peripheral organs, 3-hydroxyanthranilic acid oxygenase (3HAO), catalyzing the conversion of 3-hydroxyanthranilic acid to quinolinic acid, constitutes a link in the catabolic pathway of tryptophan to NAD.	NAD	212-215	3-hydroxyanthranilate 3,4-dioxygenase	Homo sapiens	32-67
2940338-1	1986	In mammalian peripheral organs, 3-hydroxyanthranilic acid oxygenase (3HAO), catalyzing the conversion of 3-hydroxyanthranilic acid to quinolinic acid, constitutes a link in the catabolic pathway of tryptophan to NAD.	NAD	212-215	3-hydroxyanthranilate 3,4-dioxygenase	Homo sapiens	69-73
16664862-8	1986	Blue Sepharose columns loaded with NR extract of urea-grown mutants and sequentially eluted with NADPH and NADH yielded a NADPH:NR peak only, while the wild-type yielded both NADPH: and NADH:NR peaks.	NAD	107-111	inducible nitrate reductase [NADH] 1	Glycine max	128-130
16664862-8	1986	Blue Sepharose columns loaded with NR extract of urea-grown mutants and sequentially eluted with NADPH and NADH yielded a NADPH:NR peak only, while the wild-type yielded both NADPH: and NADH:NR peaks.	NAD	107-111	inducible nitrate reductase [NADH] 1	Glycine max	128-130
3086121-5	1986	IAP, which inactivates Ni (the inhibitory GTP-binding regulatory protein of the adenylate cyclase system) catalyzed the incorporation of radioactivity from [32P]NAD into a 41 kDa peptide associated with the membranes.	NAD	161-164	Cd47 molecule	Rattus norvegicus	0-3
3512723-3	1986	First, NADP is dephosphorylated to produce NAD, which catalytically activates a specific redox-cycle involving the enzymes alcohol dehydrogenase and diaphorase.	NAD	7-10	dihydrolipoamide dehydrogenase	Homo sapiens	149-159
16664248-4	1985	Root pyridine nucleotide reductase mediated the transfer of electrons from either NADPH or NADH to cytochrome c via ferredoxin or the root electron carrier.	NAD	91-95	cytochrome c	Zea mays	99-111
4073832-3	1985	The ALDH3 isozymes show optimal activity with benzaldehyde and can use either NAD or NADP as cofactor.	NAD	78-81	aldehyde dehydrogenase 3 family member A1	Homo sapiens	4-9
35430611-9	2022	In conclusion, increased renal NNMT expression induces NAD + and methionine metabolism perturbation and contributes to renal fibrosis.	NAD	55-60	nicotinamide N-methyltransferase	Homo sapiens	31-35
35457169-8	2022	Recently, inhibition of the NAD+-dependent deac(et)ylase sirtuin 6 was demonstrated to delay the onset of experimental autoimmune encephalomyelitis, by dampening DC trafficking towards inflamed LNs.	NAD	28-31	sirtuin 6	Homo sapiens	57-66
35410407-0	2022	NAMPT-dependent NAD+ salvage is crucial for the decision between apoptotic and necrotic cell death under oxidative stress.	NAD	16-20	nicotinamide phosphoribosyltransferase	Homo sapiens	0-5
35410407-8	2022	NAD+ recovery was mediated by nicotinamide (NAM) phosphoribosyltransferase (NAMPT)-dependent synthesis via the NAD+ salvage pathway, which was suggested to be impaired only under strong H2O2 stimulation.	NAD	0-4	nicotinamide phosphoribosyltransferase	Homo sapiens	30-74
35410407-8	2022	NAD+ recovery was mediated by nicotinamide (NAM) phosphoribosyltransferase (NAMPT)-dependent synthesis via the NAD+ salvage pathway, which was suggested to be impaired only under strong H2O2 stimulation.	NAD	0-4	nicotinamide phosphoribosyltransferase	Homo sapiens	76-81
35410407-8	2022	NAD+ recovery was mediated by nicotinamide (NAM) phosphoribosyltransferase (NAMPT)-dependent synthesis via the NAD+ salvage pathway, which was suggested to be impaired only under strong H2O2 stimulation.	NAD	111-115	nicotinamide phosphoribosyltransferase	Homo sapiens	30-74
35410407-8	2022	NAD+ recovery was mediated by nicotinamide (NAM) phosphoribosyltransferase (NAMPT)-dependent synthesis via the NAD+ salvage pathway, which was suggested to be impaired only under strong H2O2 stimulation.	NAD	111-115	nicotinamide phosphoribosyltransferase	Homo sapiens	76-81
35410407-10	2022	Collectively, these findings suggest that NAD+ dynamics balanced by PARP1-dependent consumption and NAMPT-dependent production are important to determine the form of cell death activated under oxidative stress.	NAD	42-46	nicotinamide phosphoribosyltransferase	Homo sapiens	100-105
35218737-9	2022	In addition, we demonstrate the possibility of simultaneous detection of pHi and endogenous fluorescence of metabolic cofactor NADH, which provides a complementary insight into metabolic aspects of cancer.	NAD	127-131	glucose-6-phosphate isomerase 1	Mus musculus	73-76
35251333-14	2022	SIRT1 serves a role in the process of IVDD through Nampt/NAD+/SIRT1 pathway that regulates autophagy of nucleus pulposus cells.	NAD	57-61	nicotinamide phosphoribosyltransferase	Homo sapiens	51-56
35219878-1	2022	Nicotinamide phosphoribosyltransferase (NAMPT) possesses a vital role in mammalian cells due to its activity as a rate-limiting enzyme in the biosynthesis of nicotinamide adenine dinucleotide (NAD) from nicotinamide.	NAD	158-191	nicotinamide phosphoribosyltransferase	Homo sapiens	0-38
35219878-1	2022	Nicotinamide phosphoribosyltransferase (NAMPT) possesses a vital role in mammalian cells due to its activity as a rate-limiting enzyme in the biosynthesis of nicotinamide adenine dinucleotide (NAD) from nicotinamide.	NAD	158-191	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
35219878-1	2022	Nicotinamide phosphoribosyltransferase (NAMPT) possesses a vital role in mammalian cells due to its activity as a rate-limiting enzyme in the biosynthesis of nicotinamide adenine dinucleotide (NAD) from nicotinamide.	NAD	193-196	nicotinamide phosphoribosyltransferase	Homo sapiens	0-38
35219878-1	2022	Nicotinamide phosphoribosyltransferase (NAMPT) possesses a vital role in mammalian cells due to its activity as a rate-limiting enzyme in the biosynthesis of nicotinamide adenine dinucleotide (NAD) from nicotinamide.	NAD	193-196	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
35219878-3	2022	A common strategy that several tumor types adopt to sustain NAD synthesis is to over-express NAMPT.	NAD	60-63	nicotinamide phosphoribosyltransferase	Homo sapiens	93-98
35219878-6	2022	For all these reasons, NAMPT targeting has emerged as promising anti-cancer strategy to deplete NAD and impair cellular metabolism, but also to counteract the other NAMPT-related functions.	NAD	96-99	nicotinamide phosphoribosyltransferase	Homo sapiens	23-28
35137552-7	2022	Inhibition of SIRT1 blunted the protective effect of NAD+ and up-regulated the activity of glycogen synthase kinase-3beta (GSK-3beta) that was concomitant with mitigated Nrf2 nuclear accumulation, thereby exacerbates AKI.	NAD	53-57	glycogen synthase kinase 3 alpha	Homo sapiens	123-132
35063804-4	2022	Nampt-deficient macrophages exhibit reduced phagocytic activity due to insufficient NAD+ abundance, which is required to produce NADPH for the oxidative burst.	NAD	84-88	2,4-dienoyl CoA reductase 1, mitochondrial	Mus musculus	129-134
35298165-3	2022	Glucose dehydrogenase (GDH) with 18.13-fold higher activity than FDH was used for reconstructing a cofactor self-sufficient system, which was combined with the overexpression of the rate-limiting genes involved in NAD+ salvage metabolic flow to expand the available intracellular NAD(H) pool.	NAD	214-218	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	0-21
35298165-3	2022	Glucose dehydrogenase (GDH) with 18.13-fold higher activity than FDH was used for reconstructing a cofactor self-sufficient system, which was combined with the overexpression of the rate-limiting genes involved in NAD+ salvage metabolic flow to expand the available intracellular NAD(H) pool.	NAD	214-218	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	23-26
35298165-3	2022	Glucose dehydrogenase (GDH) with 18.13-fold higher activity than FDH was used for reconstructing a cofactor self-sufficient system, which was combined with the overexpression of the rate-limiting genes involved in NAD+ salvage metabolic flow to expand the available intracellular NAD(H) pool.	NAD	280-286	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	0-21
35298165-3	2022	Glucose dehydrogenase (GDH) with 18.13-fold higher activity than FDH was used for reconstructing a cofactor self-sufficient system, which was combined with the overexpression of the rate-limiting genes involved in NAD+ salvage metabolic flow to expand the available intracellular NAD(H) pool.	NAD	280-286	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	23-26
35408818-2	2022	In mammals, the mainly synthetic pathway of NAD+ is the salvage synthesis, a reaction catalyzed by nicotinamide mononucleotide adenylyltransferase (NAMPT) and nicotinamide mononucleotide adenylyltransferase (NMNATs) successively, converting nicotinamide (NAM) to nicotinamide mononucleotide (NMN) and NMN to NAD+, respectively.	NAD	44-48	nicotinamide phosphoribosyltransferase	Homo sapiens	148-153
35408818-2	2022	In mammals, the mainly synthetic pathway of NAD+ is the salvage synthesis, a reaction catalyzed by nicotinamide mononucleotide adenylyltransferase (NAMPT) and nicotinamide mononucleotide adenylyltransferase (NMNATs) successively, converting nicotinamide (NAM) to nicotinamide mononucleotide (NMN) and NMN to NAD+, respectively.	NAD	308-312	nicotinamide phosphoribosyltransferase	Homo sapiens	148-153
35408818-4	2022	Here our study found that the disruption of NAD+ anabolism homeostasis caused an elevation in both oxidative stress and fibronectin expression, along with a decrease in Sirt1 and an increase in both NF-kappaB P65 expression and acetylation, culminating in extracellular matrix deposition and globular fibrosis in DN.	NAD	44-48	RELA proto-oncogene, NF-kB subunit	Homo sapiens	199-212
35408818-5	2022	More importantly, through constitutively overexpressing NMNAT1 or NAMPT in human mesangial cells, we revealed NAD+ levels altered inversely with NMN levels in the context of DN and, further, their changes affect Sirt1/NF-kappaB P65, thus playing a crucial role in the pathogenesis of DN.	NAD	110-114	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	56-62
35408818-5	2022	More importantly, through constitutively overexpressing NMNAT1 or NAMPT in human mesangial cells, we revealed NAD+ levels altered inversely with NMN levels in the context of DN and, further, their changes affect Sirt1/NF-kappaB P65, thus playing a crucial role in the pathogenesis of DN.	NAD	110-114	nicotinamide phosphoribosyltransferase	Homo sapiens	66-71
35408818-5	2022	More importantly, through constitutively overexpressing NMNAT1 or NAMPT in human mesangial cells, we revealed NAD+ levels altered inversely with NMN levels in the context of DN and, further, their changes affect Sirt1/NF-kappaB P65, thus playing a crucial role in the pathogenesis of DN.	NAD	110-114	RELA proto-oncogene, NF-kB subunit	Homo sapiens	218-231
35272691-1	2022	BACKGROUND: Nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme in nicotinamide adenine dinucleotide (NAD) biosynthesis, is up-regulated in several cancers, including metastatic melanoma (MM).	NAD	88-121	nicotinamide phosphoribosyltransferase	Homo sapiens	12-50
35272691-1	2022	BACKGROUND: Nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme in nicotinamide adenine dinucleotide (NAD) biosynthesis, is up-regulated in several cancers, including metastatic melanoma (MM).	NAD	88-121	nicotinamide phosphoribosyltransferase	Homo sapiens	52-57
35272691-1	2022	BACKGROUND: Nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme in nicotinamide adenine dinucleotide (NAD) biosynthesis, is up-regulated in several cancers, including metastatic melanoma (MM).	NAD	123-126	nicotinamide phosphoribosyltransferase	Homo sapiens	12-50
35272691-1	2022	BACKGROUND: Nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme in nicotinamide adenine dinucleotide (NAD) biosynthesis, is up-regulated in several cancers, including metastatic melanoma (MM).	NAD	123-126	nicotinamide phosphoribosyltransferase	Homo sapiens	52-57
35195252-5	2022	Specifically, FoxOs regulate mitochondrial biogenesis by dampening NRF1-Tfam and c-Myc-Tfam cascades directly, and inhibiting NAD-Sirt1-Pgc1alpha cascade indirectly by inducing Hmox1 or repressing Fxn and Urod.	NAD	126-129	frataxin	Homo sapiens	197-200
35195252-5	2022	Specifically, FoxOs regulate mitochondrial biogenesis by dampening NRF1-Tfam and c-Myc-Tfam cascades directly, and inhibiting NAD-Sirt1-Pgc1alpha cascade indirectly by inducing Hmox1 or repressing Fxn and Urod.	NAD	126-129	uroporphyrinogen decarboxylase	Homo sapiens	205-209
35216232-10	2022	Both PACAP-38 and PACAP(6-38) treatments caused significant downregulation of NADH: ubiquinone oxidoreductase subunit B6 and upregulation of transient receptor potential cation channel, subfamily M, member 8.	NAD	78-82	adenylate cyclase activating polypeptide 1	Rattus norvegicus	18-23
35220131-14	2022	The label-free quantitative proteomic analysis predicted the crucial participation of NAD-dependent protein deacylase sirtuin-5 (SIRT5).	NAD	86-89	sirtuin 5	Mus musculus	118-127
35220131-14	2022	The label-free quantitative proteomic analysis predicted the crucial participation of NAD-dependent protein deacylase sirtuin-5 (SIRT5).	NAD	86-89	sirtuin 5	Mus musculus	129-134
34260721-0	2022	Inhibition of nicotinamide phosphoribosyltransferase, the rate-limiting enzyme of the nicotinamide adenine dinucleotide salvage pathway, to target glioma heterogeneity through mitochondrial oxidative stress.	NAD	86-119	nicotinamide phosphoribosyltransferase	Homo sapiens	14-52
34260721-2	2022	Tumor cells preferentially using nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme in the salvage pathway for synthesis of NAD, a critical cofactor for diverse biological processes including cellular redox reactions, energy metabolism and biosynthesis.	NAD	146-149	nicotinamide phosphoribosyltransferase	Homo sapiens	33-71
34260721-2	2022	Tumor cells preferentially using nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme in the salvage pathway for synthesis of NAD, a critical cofactor for diverse biological processes including cellular redox reactions, energy metabolism and biosynthesis.	NAD	146-149	nicotinamide phosphoribosyltransferase	Homo sapiens	73-78
34981121-0	2022	Overexpression of NMNAT3 improves mitochondrial function and enhances anti-oxidative stress of bone marrow mesenchymal stem cells via the NAD+-Sirt3 pathway.	NAD	138-142	nicotinamide nucleotide adenylyltransferase 3	Homo sapiens	18-24
34981121-6	2022	We increased the level of nicotinamide adenine dinucleotide (NAD+) by overexpressing NMNAT3 in BMSCs and found that it could significantly increase the activity of silent mating type information regulation 2 homolog 3 (Sirt3) and significantly decrease the acetylation levels of Sirt3-dependent deacetylation-related proteins isocitrate dehydrogenase 2 (Idh2) and Forkhead-box protein O3a (FOXO3a).	NAD	26-59	nicotinamide nucleotide adenylyltransferase 3	Homo sapiens	85-91
34981121-6	2022	We increased the level of nicotinamide adenine dinucleotide (NAD+) by overexpressing NMNAT3 in BMSCs and found that it could significantly increase the activity of silent mating type information regulation 2 homolog 3 (Sirt3) and significantly decrease the acetylation levels of Sirt3-dependent deacetylation-related proteins isocitrate dehydrogenase 2 (Idh2) and Forkhead-box protein O3a (FOXO3a).	NAD	61-65	nicotinamide nucleotide adenylyltransferase 3	Homo sapiens	85-91
34981121-7	2022	These findings show that NMNAT3 may increase the activity of Sirt3 by increasing NAD+ levels.	NAD	81-85	nicotinamide nucleotide adenylyltransferase 3	Homo sapiens	25-31
34981121-8	2022	Our results confirm that the NMNAT3-NAD+-Sirt3 axis is a potential mechanism for improving mitochondrial function and enhancing anti-oxidative stress of BMSCs.	NAD	36-40	nicotinamide nucleotide adenylyltransferase 3	Homo sapiens	29-35
16667103-6	1989	The enzyme was capable of accepting electrons from NADPH or NADH to reduce either ferricyanide, juglone, duroquinone, or cytochrome c, but did not transfer electrons to ascorbate free-radical or nitrate.	NAD	60-64	cytochrome c	Zea mays	121-133
2611200-5	1989	These trends in binding can be rationalized by considering the behavior of the analogues in the first two chemical steps of the mechanism: NAD+-mediated oxidation at C-5 and enolization at C-6 (the first part of the E1cB elimination of inorganic phosphate).	NAD	139-143	complement C6	Homo sapiens	189-192
18553714-6	1985	NADH regeneration activity based on malic acid production rate was 4.7 U/mg of the enzyme protein of the commercial diaphorase preparation.	NAD	0-4	dihydrolipoamide dehydrogenase	Homo sapiens	116-126
3994742-3	1985	In addition, the presence of NAD or NADH was necessary for cyanamide inhibition of the ALDH activity.	NAD	29-32	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	87-91
3994742-3	1985	In addition, the presence of NAD or NADH was necessary for cyanamide inhibition of the ALDH activity.	NAD	36-40	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	87-91
2981686-3	1985	At low NAD concentrations the enzyme can poly(ADP-ribosyl)ate histones H1 and H1, H2A, A2A, and H2B.	NAD	7-10	H2A clustered histone 18	Homo sapiens	82-85
2735948-4	1989	On the other hand, ALDH activity appears to be irreversibly inhibited when the incubation mixture contained ALDH, catalase, NAD+ and cyanamide.	NAD	124-128	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	19-23
34253597-7	2021	Previously, we showed that mTOR regulator p21 activated kinase 4 (PAK4) and nicotinamide adenine dinucleotide biosynthesis enzyme nicotinamide phosphoribosyl transferase (NAMPT) were aberrantly expressed in PNET tissue and promoted everolimus resistance.	NAD	76-109	nicotinamide phosphoribosyltransferase	Homo sapiens	171-176
6497899-3	1984	For the six rat strains, at millimolar propionaldehyde concentrations, NAD-dependent ALDH activity was associated primarily with mitochondria (51%) and microsomes (30%).	NAD	71-74	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	85-89
6497899-4	1984	At millimolar acetaldehyde concentrations, NAD-dependent ALDH was primarily mitochondrial (up to 80%).	NAD	43-46	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	57-61
34663976-4	2021	Concurrently, AMPK phosphorylates PHGDH-Ser55, selectively increasing PHGDH oxidation of malate into oxaloacetate, thus generating NADH.	NAD	131-135	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	14-18
6497899-5	1984	Less than 1% of total NAD-dependent aldehyde dehydrogenase was found in the cytosol.	NAD	22-25	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	36-58
6497899-7	1984	In CD-1 mouse liver, millimolar Km, NAD-dependent ALDH activity was found in mitochondria (60%), microsomes (23%) and cytosol (5%).	NAD	36-39	aldehyde dehydrogenase family 3, subfamily A1	Mus musculus	50-54
6497899-8	1984	In rabbit liver, millimolar Km, NAD-dependent ALDH was also distributed among mitochondria (36%), microsomes (19%) and cytosol (28%).	NAD	32-35	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	46-50
34663976-4	2021	Concurrently, AMPK phosphorylates PHGDH-Ser55, selectively increasing PHGDH oxidation of malate into oxaloacetate, thus generating NADH.	NAD	131-135	phosphoglycerate dehydrogenase	Homo sapiens	34-39
2735948-5	1989	Influence of catalase, NAD+ and cyanamide concentrations in the incubation mixtures on the ALDH activity were also established.	NAD	23-27	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	91-95
34663976-4	2021	Concurrently, AMPK phosphorylates PHGDH-Ser55, selectively increasing PHGDH oxidation of malate into oxaloacetate, thus generating NADH.	NAD	131-135	phosphoglycerate dehydrogenase	Homo sapiens	70-75
2735948-6	1989	The time course of the concentration of cyanamide in an incubation mixture when ALDH activity was inhibited by cyanamide in the presence of catalase and NAD+, was evaluated by HPLC.	NAD	153-157	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	80-84
34663976-5	2021	In the nucleus, the altered PHGDH activity restricts NAD+ level and compartmentally repressed NAD+-dependent PARP1 activity for poly(ADP-ribosyl)ation of c-Jun, thereby leading to impaired c-Jun transcriptional activity linked to cell growth inhibition.	NAD	53-57	phosphoglycerate dehydrogenase	Homo sapiens	28-33
34663976-5	2021	In the nucleus, the altered PHGDH activity restricts NAD+ level and compartmentally repressed NAD+-dependent PARP1 activity for poly(ADP-ribosyl)ation of c-Jun, thereby leading to impaired c-Jun transcriptional activity linked to cell growth inhibition.	NAD	94-97	phosphoglycerate dehydrogenase	Homo sapiens	28-33
2736323-3	1989	Spectrofluorometric detection of NADH, formed as the column eluate passed through a column of immobilized 3 alpha-hydroxysteroid dehydrogenase, enabled amounts less than 40 pmol to be quantified.	NAD	33-37	aldo-keto reductase family 1 member C3	Homo sapiens	106-142
34548590-3	2021	Microscale Thermophoresis analysis of the porcine heart MDH-CS complex revealed that substrates of the MDH and CS reactions, NAD+ and acetyl-CoA, enhance complex association while products of the reactions, NADH and citrate, weaken the affinity of the complex.	NAD	125-129	citrate synthase	Homo sapiens	60-62
34548590-3	2021	Microscale Thermophoresis analysis of the porcine heart MDH-CS complex revealed that substrates of the MDH and CS reactions, NAD+ and acetyl-CoA, enhance complex association while products of the reactions, NADH and citrate, weaken the affinity of the complex.	NAD	125-129	citrate synthase	Homo sapiens	111-113
34548590-3	2021	Microscale Thermophoresis analysis of the porcine heart MDH-CS complex revealed that substrates of the MDH and CS reactions, NAD+ and acetyl-CoA, enhance complex association while products of the reactions, NADH and citrate, weaken the affinity of the complex.	NAD	207-211	citrate synthase	Homo sapiens	60-62
2494990-6	1989	199, 585-597] [NADH: (acceptor) oxidoreductase, EC 1.6.99.3], a component of Complex I that contains the FMN.	NAD	15-19	hydroxysteroid 17-beta dehydrogenase 6	Homo sapiens	32-46
34500765-2	2021	Furthermore, all compounds were investigated in silico for their ability to inhibit mitochondrial NADH: ubiquinone oxidoreductase (complex I) by targeting the AMPK/mTOR signaling pathway and inhibiting hexokinase, a key glycolytic enzyme to prevent the Warburg effect in cancer cells.	NAD	98-102	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	159-163
34382917-8	2021	In comparison to normal cells, various cancer lines showed several fold-higher expression of NAMPT which is a rate-limiting enzyme in the main biosynthetic pathway for NAD+.	NAD	168-172	nicotinamide phosphoribosyltransferase	Homo sapiens	93-98
34183378-7	2021	Supplementing NMN as an NAD+ donor inhibited p65 acetylation, decreased p65 nuclear translocation, and restored cyp3a transcription in both HepG2 cells and mouse hepatocytes.	NAD	24-28	RELA proto-oncogene, NF-kB subunit	Homo sapiens	45-48
2610112-0	1989	Interconversion between NAD-dependent and O2-dependent types of rat liver xanthine dehydrogenase and difference in kinetic and redox properties between them.	NAD	24-27	xanthine dehydrogenase	Rattus norvegicus	74-96
34183378-7	2021	Supplementing NMN as an NAD+ donor inhibited p65 acetylation, decreased p65 nuclear translocation, and restored cyp3a transcription in both HepG2 cells and mouse hepatocytes.	NAD	24-28	RELA proto-oncogene, NF-kB subunit	Homo sapiens	72-75
34213345-1	2021	Sirtuin 6 (SIRT6) is an NAD+-dependent protein deacylase and mono-ADP-ribosyltransferase of the sirtuin family with a wide substrate specificity.	NAD	24-27	sirtuin 6	Homo sapiens	0-9
2851277-3	1988	Glucose 6-phosphatase activity is measured by following NADH formation at 340 nm.	NAD	56-60	glucose-6-phosphatase catalytic subunit 1	Homo sapiens	0-21
34213345-1	2021	Sirtuin 6 (SIRT6) is an NAD+-dependent protein deacylase and mono-ADP-ribosyltransferase of the sirtuin family with a wide substrate specificity.	NAD	24-27	sirtuin 6	Homo sapiens	11-16
34290089-0	2021	Nuclear NAD+ homeostasis governed by NMNAT1 prevents apoptosis of acute myeloid leukemia stem cells.	NAD	8-12	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	37-43
2973349-11	1988	The plasmin-catalyzed cleavage of the polypeptide of Mr 56,000-42,000 was greatly accelerated by the specific ligand NAD+.	NAD	117-121	plasminogen	Homo sapiens	4-11
34290089-3	2021	We integrated whole-genome CRISPR screening and pan-cancer genetic dependency mapping to identify NAMPT and NMNAT1 as AML dependencies governing NAD+ biosynthesis.	NAD	145-149	nicotinamide phosphoribosyltransferase	Homo sapiens	98-103
34290089-3	2021	We integrated whole-genome CRISPR screening and pan-cancer genetic dependency mapping to identify NAMPT and NMNAT1 as AML dependencies governing NAD+ biosynthesis.	NAD	145-149	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	108-114
3343508-9	1988	AlDH in upper GI tissues and in liver nodules shared three characteristics: a sharp localization; a preference for Bz and NADP compared to the aliphatic substrate acetaldehyde and NAD; and a high co-enzyme-independent activity in the presence of Bz.	NAD	122-125	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	0-4
34290089-4	2021	While both NAMPT and NMNAT1 were required for AML, the presence of NAD+ precursors bypassed the dependence of AML on NAMPT but not NMNAT1, pointing to NMNAT1 as a gatekeeper of NAD+ biosynthesis.	NAD	67-71	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	151-157
34290089-4	2021	While both NAMPT and NMNAT1 were required for AML, the presence of NAD+ precursors bypassed the dependence of AML on NAMPT but not NMNAT1, pointing to NMNAT1 as a gatekeeper of NAD+ biosynthesis.	NAD	177-181	nicotinamide phosphoribosyltransferase	Homo sapiens	11-16
34290089-4	2021	While both NAMPT and NMNAT1 were required for AML, the presence of NAD+ precursors bypassed the dependence of AML on NAMPT but not NMNAT1, pointing to NMNAT1 as a gatekeeper of NAD+ biosynthesis.	NAD	177-181	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	21-27
34290089-4	2021	While both NAMPT and NMNAT1 were required for AML, the presence of NAD+ precursors bypassed the dependence of AML on NAMPT but not NMNAT1, pointing to NMNAT1 as a gatekeeper of NAD+ biosynthesis.	NAD	177-181	nicotinamide phosphoribosyltransferase	Homo sapiens	117-122
34290089-4	2021	While both NAMPT and NMNAT1 were required for AML, the presence of NAD+ precursors bypassed the dependence of AML on NAMPT but not NMNAT1, pointing to NMNAT1 as a gatekeeper of NAD+ biosynthesis.	NAD	177-181	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	151-157
34290089-5	2021	Deletion of NMNAT1 reduced nuclear NAD+, activated p53, and increased venetoclax sensitivity.	NAD	35-39	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	12-18
3422556-8	1988	It was concluded that xanthine dehydrogenase requires a minimum mechanism of degree 1:1 for xanthine, 2:2 for NAD+, 1:1 for uric acid and 1:2 for NADH in the xanthine/NAD+ oxidoreductase reaction.	NAD	110-114	xanthine dehydrogenase	Gallus gallus	22-44
34290089-8	2021	Our findings identify NMNAT1 as a previously unidentified therapeutic target that maintains NAD+ for AML progression and chemoresistance.	NAD	92-96	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	22-28
3422556-8	1988	It was concluded that xanthine dehydrogenase requires a minimum mechanism of degree 1:1 for xanthine, 2:2 for NAD+, 1:1 for uric acid and 1:2 for NADH in the xanthine/NAD+ oxidoreductase reaction.	NAD	146-150	xanthine dehydrogenase	Gallus gallus	22-44
34229568-1	2021	Nicotinamide phosphoribosyltransferase (NAMPT) is a bottleneck enzyme that plays a key role in recycling nicotinamide to maintain the adequate NAD + level inside the cell.	NAD	143-148	nicotinamide phosphoribosyltransferase	Homo sapiens	0-38
3276524-3	1988	It is based on the PTS-catalysed formation of tetrahydrobiopterin from dihydroneopterin triphosphate in the presence of magnesium, sepiapterin reductase, NADPH, dihydropteridine reductase, and NADH, and fluorimetric measurement of the product as biopterin by high performance liquid chromatography (HPLC) after oxidation with iodine.	NAD	193-197	6-pyruvoyltetrahydropterin synthase	Homo sapiens	19-22
34229568-1	2021	Nicotinamide phosphoribosyltransferase (NAMPT) is a bottleneck enzyme that plays a key role in recycling nicotinamide to maintain the adequate NAD + level inside the cell.	NAD	143-148	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
3276524-3	1988	It is based on the PTS-catalysed formation of tetrahydrobiopterin from dihydroneopterin triphosphate in the presence of magnesium, sepiapterin reductase, NADPH, dihydropteridine reductase, and NADH, and fluorimetric measurement of the product as biopterin by high performance liquid chromatography (HPLC) after oxidation with iodine.	NAD	193-197	sepiapterin reductase	Homo sapiens	131-152
34096221-1	2021	Objective: Our study aimed to investigate function and mechanism of miR-373 in proliferation and apoptosis of pancreatic cancer (PC) cells by regulating NAD+-dependent histone deacetylase sirtulin 1 (SIRT1).	NAD	153-157	microRNA 373	Homo sapiens	68-75
2841681-4	1988	When soluble cytochrome c is added to the electron transport chain oxidizing NADH or succinate, no increase in 02 uptake is observed.	NAD	77-81	LOC104968582	Bos taurus	13-25
2841681-17	1988	The respiratory chain on the membranes of a cytochrome c-deficient mutant can reduce cytochrome aa3 using NADH as substrate in a manner similar to that of the wild type, although at somewhat lower rate, suggesting diffusional encounter of the large complexes within the membrane.	NAD	106-110	LOC104968582	Bos taurus	44-56
34202251-0	2021	Enhanced NAMPT-Mediated NAD Salvage Pathway Contributes to Psoriasis Pathogenesis by Amplifying Epithelial Auto-Inflammatory Circuits.	NAD	24-27	nicotinamide phosphoribosyltransferase	Homo sapiens	9-14
34202251-2	2021	NAMPT-mediated NAD salvage pathway has been recently described as an immunometabolic route having inflammatory function in several disorders, including arthritis and inflammatory bowel diseases.	NAD	15-18	nicotinamide phosphoribosyltransferase	Homo sapiens	0-5
34202251-4	2021	Here, we show that NAD content is enhanced in lesional skin of psoriatic patients and is associated to high NAMPT transcriptional levels.	NAD	19-22	nicotinamide phosphoribosyltransferase	Homo sapiens	108-113
2893631-1	1987	gamma-Glutamyl cyclotransferase activity is assayed in tissues by a colorimetric method using gamma-glutamyl alanine as a substrate coupled with alanine dehydrogenase from B. sphericus, to measure the formation of NADH.	NAD	214-218	gamma-glutamyl cyclotransferase	Rattus norvegicus	0-31
34202251-6	2021	We provide evidence that NAMPT-mediated NAD+ metabolism fuels the immune responses executed by resident skin cells in psoriatic skin.	NAD	40-44	nicotinamide phosphoribosyltransferase	Homo sapiens	25-30
34202251-8	2021	Furthermore, NAMPT-mediated NAD+ boosting synergizes with psoriasis-related cytokines in the upregulation of inflammatory chemokines important for neutrophil and Th1/Th17 cell recruitment.	NAD	28-32	nicotinamide phosphoribosyltransferase	Homo sapiens	13-18
34202251-10	2021	In conclusion, our results showed that NAMPT-mediated NAD salvage pathway contributes to psoriasis pathogenic processes by amplifying epithelial auto-inflammatory responses in psoriasis.	NAD	54-57	nicotinamide phosphoribosyltransferase	Homo sapiens	39-44
3632722-11	1987	Our results are consistent with the following model: hypoxia converts NAD-dependent xanthine dehydrogenase (XD) into the oxygen-dependent xanthine oxidase (XO).	NAD	70-73	xanthine dehydrogenase	Rattus norvegicus	84-106
34200964-5	2021	Nicotinamide phosphoribosyltransferase (NAMPT) is the rate-limiting enzyme in the classical salvage pathway for NAD+ synthesis, and NAMPT is overexpressed in OS.	NAD	112-116	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
3622513-7	1987	In contrast, single exchanges of these residues are the ones involved in the major allelic differences (beta 1 versus beta 2 and gamma 1 versus gamma 2), which affects the overall rate of alcohol oxidation since NADH dissociation is the rate-determining step.	NAD	212-216	potassium calcium-activated channel subfamily M regulatory beta subunit 2	Homo sapiens	118-124
3662051-1	1987	Investigations were carried out into the activity and localization of NADH-dependant diaphorase in boar spermatozoa.	NAD	70-74	dihydrolipoamide dehydrogenase	Homo sapiens	85-95
34103421-8	2021	We found that NAMPT inhibition reduced NAD+ concentrations below a critical threshold that resulted in depletion of adenine, which was the metabolic trigger that primed TNBC cells for apoptosis.	NAD	39-43	nicotinamide phosphoribosyltransferase	Homo sapiens	14-19
34073600-1	2021	The activity of nicotinamide N-methyltransferase (NNMT) is tightly linked to the maintenance of the nicotinamide adenine dinucleotide (NAD+) level.	NAD	100-133	nicotinamide N-methyltransferase	Homo sapiens	16-48
3593764-8	1987	All the rate constants involved in determining the Km and Kd of NADH (kcat, k1 and k-1) can be modified.	NAD	64-68	keratin 1	Homo sapiens	76-86
34073600-1	2021	The activity of nicotinamide N-methyltransferase (NNMT) is tightly linked to the maintenance of the nicotinamide adenine dinucleotide (NAD+) level.	NAD	100-133	nicotinamide N-methyltransferase	Homo sapiens	50-54
34073600-1	2021	The activity of nicotinamide N-methyltransferase (NNMT) is tightly linked to the maintenance of the nicotinamide adenine dinucleotide (NAD+) level.	NAD	135-139	nicotinamide N-methyltransferase	Homo sapiens	16-48
34073600-1	2021	The activity of nicotinamide N-methyltransferase (NNMT) is tightly linked to the maintenance of the nicotinamide adenine dinucleotide (NAD+) level.	NAD	135-139	nicotinamide N-methyltransferase	Homo sapiens	50-54
3564015-7	1987	The high-affinity mitochondrial, low-affinity cytosolic, and microsomal ALDH isozymes oxidized HX, displaying V/K values of 0.600, 0.058, and 0.058 nmol NADH formed/min/mg protein/mumol HX/liter, respectively.	NAD	153-157	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	72-76
34073600-3	2021	Enzymatic activity of NNMT is important for the prevention of NAM-mediated inhibition of NAD+-consuming enzymes poly-adenosine -diphosphate (ADP), ribose polymerases (PARPs), and sirtuins (SIRTs).	NAD	89-93	nicotinamide N-methyltransferase	Homo sapiens	22-26
34073600-4	2021	Inappropriately high expression and activity of NNMT, commonly present in various types of cancer, has the potential to disrupt NAD+ homeostasis and cellular methylation potential.	NAD	128-132	nicotinamide N-methyltransferase	Homo sapiens	48-52
34073600-5	2021	Largely overlooked, in the context of cancer, is the inhibitory effect of 2-PY on PARP-1 activity, which abrogates NNMT"s positive effect on cellular NAD+ flux by stalling liberation of NAM and reducing NAD+ synthesis in the salvage pathway.	NAD	150-154	nicotinamide N-methyltransferase	Homo sapiens	115-119
34073600-5	2021	Largely overlooked, in the context of cancer, is the inhibitory effect of 2-PY on PARP-1 activity, which abrogates NNMT"s positive effect on cellular NAD+ flux by stalling liberation of NAM and reducing NAD+ synthesis in the salvage pathway.	NAD	203-207	nicotinamide N-methyltransferase	Homo sapiens	115-119
34073600-6	2021	This review describes, and discusses, the mechanisms by which NNMT promotes NAD+ depletion and epigenetic reprogramming, leading to the development of metabolic plasticity, evasion of a major tumor suppressive process of cellular senescence, and acquisition of stem cell properties.	NAD	76-80	nicotinamide N-methyltransferase	Homo sapiens	62-66
35278642-1	2022	Sirtuin 6 (SIRT6) is a nicotinamide adenine dinucleotide (NAD+)-dependent enzyme.	NAD	23-56	sirtuin 6	Homo sapiens	0-9
35278642-1	2022	Sirtuin 6 (SIRT6) is a nicotinamide adenine dinucleotide (NAD+)-dependent enzyme.	NAD	23-56	sirtuin 6	Homo sapiens	11-16
35278642-1	2022	Sirtuin 6 (SIRT6) is a nicotinamide adenine dinucleotide (NAD+)-dependent enzyme.	NAD	58-62	sirtuin 6	Homo sapiens	0-9
35278642-1	2022	Sirtuin 6 (SIRT6) is a nicotinamide adenine dinucleotide (NAD+)-dependent enzyme.	NAD	58-62	sirtuin 6	Homo sapiens	11-16
35616339-8	2022	The circadian metabolite, NAD+ , serves as a crucial link connecting clock genes to sirtuin activity.	NAD	26-30	clock circadian regulator	Homo sapiens	69-74
6439557-3	1984	Treatment of oocyte membranes with islet activating protein (IAP) in the presence of [32P]NAD led to incorporation of radiolabel into a 41 000-dalton membrane protein.	NAD	90-93	islet amyloid polypeptide	Homo sapiens	61-64
35616339-9	2022	This is because, NAMPT which is a rate limiting enzyme in NAD+ biosynthesis is transcriptionally regulated by the clock genes and NAD+ in turn is a cofactor regulating the deacetylation activity of sirtuins.	NAD	58-62	nicotinamide phosphoribosyltransferase	Homo sapiens	17-22
35616339-9	2022	This is because, NAMPT which is a rate limiting enzyme in NAD+ biosynthesis is transcriptionally regulated by the clock genes and NAD+ in turn is a cofactor regulating the deacetylation activity of sirtuins.	NAD	58-62	clock circadian regulator	Homo sapiens	114-119
35616339-9	2022	This is because, NAMPT which is a rate limiting enzyme in NAD+ biosynthesis is transcriptionally regulated by the clock genes and NAD+ in turn is a cofactor regulating the deacetylation activity of sirtuins.	NAD	130-134	nicotinamide phosphoribosyltransferase	Homo sapiens	17-22
35616339-9	2022	This is because, NAMPT which is a rate limiting enzyme in NAD+ biosynthesis is transcriptionally regulated by the clock genes and NAD+ in turn is a cofactor regulating the deacetylation activity of sirtuins.	NAD	130-134	clock circadian regulator	Homo sapiens	114-119
6388629-1	1984	The reduction of benzaldehyde and p-nitrobenzaldehyde by NADH, catalyzed by horse liver alcohol dehydrogenase (LADH), has been found to be faster when NADH is bound to glyceraldehyde-3-phosphate dehydrogenase (GPDH) than with free NADH.	NAD	151-155	glyceraldehyde-3-phosphate dehydrogenase	Equus caballus	168-208
6388629-1	1984	The reduction of benzaldehyde and p-nitrobenzaldehyde by NADH, catalyzed by horse liver alcohol dehydrogenase (LADH), has been found to be faster when NADH is bound to glyceraldehyde-3-phosphate dehydrogenase (GPDH) than with free NADH.	NAD	151-155	glyceraldehyde-3-phosphate dehydrogenase	Equus caballus	210-214
35616339-11	2022	Thus, the Clock-NAD+-Sirtuin connection represents a novel "feedback loop" circuit that regulates the metabolic machinery.	NAD	16-20	clock circadian regulator	Homo sapiens	10-15
6388629-2	1984	The rate of reduction of aldehyde substrate with GPDH-NADH follows a Michaelian concentration dependence on GPDH-NADH.	NAD	54-58	glyceraldehyde-3-phosphate dehydrogenase	Equus caballus	49-53
6388629-2	1984	The rate of reduction of aldehyde substrate with GPDH-NADH follows a Michaelian concentration dependence on GPDH-NADH.	NAD	54-58	glyceraldehyde-3-phosphate dehydrogenase	Equus caballus	108-112
35616339-12	2022	The current review underpins the importance of NAD+ on the sirtuin and clock connection in preventing fatty liver disorder.	NAD	47-51	clock circadian regulator	Homo sapiens	71-76
6388629-2	1984	The rate of reduction of aldehyde substrate with GPDH-NADH follows a Michaelian concentration dependence on GPDH-NADH.	NAD	113-117	glyceraldehyde-3-phosphate dehydrogenase	Equus caballus	49-53
35596692-15	2022	The increased NAD-GDH (deaminating) and NADH-GDH (aminating) activities indicated that GDH was needed more for NH4 + detoxification.	NAD	14-17	glutamic dehydrogenase1	Zea mays	18-21
6388629-2	1984	The rate of reduction of aldehyde substrate with GPDH-NADH follows a Michaelian concentration dependence on GPDH-NADH.	NAD	113-117	glyceraldehyde-3-phosphate dehydrogenase	Equus caballus	108-112
6388629-3	1984	The reaction velocity is independent of GPDH concentration when [GPDH] greater than [NADH]total.	NAD	85-89	glyceraldehyde-3-phosphate dehydrogenase	Equus caballus	40-44
6388629-4	1984	The Km for GPDH-NADH is higher than that for free NADH.	NAD	16-20	glyceraldehyde-3-phosphate dehydrogenase	Equus caballus	11-15
6388629-4	1984	The Km for GPDH-NADH is higher than that for free NADH.	NAD	50-54	glyceraldehyde-3-phosphate dehydrogenase	Equus caballus	11-15
6388629-5	1984	The reaction velocities in the presence of excess GPDH over NADH cannot be accounted for on the basis of the free NADH concentration arising from dissociation of the GPDH-NADH complex.	NAD	60-64	glyceraldehyde-3-phosphate dehydrogenase	Equus caballus	50-54
6388629-5	1984	The reaction velocities in the presence of excess GPDH over NADH cannot be accounted for on the basis of the free NADH concentration arising from dissociation of the GPDH-NADH complex.	NAD	60-64	glyceraldehyde-3-phosphate dehydrogenase	Equus caballus	166-170
6388629-5	1984	The reaction velocities in the presence of excess GPDH over NADH cannot be accounted for on the basis of the free NADH concentration arising from dissociation of the GPDH-NADH complex.	NAD	114-118	glyceraldehyde-3-phosphate dehydrogenase	Equus caballus	50-54
6388629-5	1984	The reaction velocities in the presence of excess GPDH over NADH cannot be accounted for on the basis of the free NADH concentration arising from dissociation of the GPDH-NADH complex.	NAD	114-118	glyceraldehyde-3-phosphate dehydrogenase	Equus caballus	50-54
6388629-6	1984	These observations suggest that transfer of NADH from GPDH to LADH proceeds through the initial formation of a GPDH-NADH-LADH complex.	NAD	44-48	glyceraldehyde-3-phosphate dehydrogenase	Equus caballus	54-58
6388629-6	1984	These observations suggest that transfer of NADH from GPDH to LADH proceeds through the initial formation of a GPDH-NADH-LADH complex.	NAD	44-48	glyceraldehyde-3-phosphate dehydrogenase	Equus caballus	111-115
35596692-15	2022	The increased NAD-GDH (deaminating) and NADH-GDH (aminating) activities indicated that GDH was needed more for NH4 + detoxification.	NAD	14-17	glutamic dehydrogenase1	Zea mays	87-90
35596692-15	2022	The increased NAD-GDH (deaminating) and NADH-GDH (aminating) activities indicated that GDH was needed more for NH4 + detoxification.	NAD	40-44	glutamic dehydrogenase1	Zea mays	45-48
35596692-15	2022	The increased NAD-GDH (deaminating) and NADH-GDH (aminating) activities indicated that GDH was needed more for NH4 + detoxification.	NAD	40-44	glutamic dehydrogenase1	Zea mays	87-90
35176139-6	2022	Furthermore, the interaction of LDHA and eEF2 was dependent on NADH, a coenzyme of LDHA.	NAD	63-67	lactate dehydrogenase A	Mus musculus	32-36
6091559-6	1984	However, preincubation of SAH hydrolase with NAD+ results in a 25% activation of the enzyme.	NAD	45-49	acyl-CoA synthetase medium chain family member 3	Homo sapiens	26-29
6091559-10	1984	NAD+-reversible inactivation by cAMP and 2"-deoxyadenosine was also observed with the SAH hydrolase from rabbit erythrocytes.	NAD	0-4	acyl-CoA synthetase medium chain family member 3	Homo sapiens	86-89
6548741-0	1984	Effect of nicotinamide adenine dinucleotide on the oxidation-reduction potentials of lipoamide dehydrogenase from pig heart.	NAD	10-43	dihydrolipoamide dehydrogenase	Sus scrofa	85-108
6548741-1	1984	The effect of NAD+ on lipoamide dehydrogenase from pig heart was investigated physicochemically.	NAD	14-18	dihydrolipoamide dehydrogenase	Sus scrofa	22-45
6548741-2	1984	The observed and theoretical oxidation-reduction mid-point potentials for the oxidized lipoamide dehydrogenase (E)/two-electron-reduced lipoamide dehydrogenase (EH2) couple in the presence on NAD+ were -218 mV and -251 mV, respectively, at pH 6.0.	NAD	192-196	dihydrolipoamide dehydrogenase	Sus scrofa	87-110
6548741-2	1984	The observed and theoretical oxidation-reduction mid-point potentials for the oxidized lipoamide dehydrogenase (E)/two-electron-reduced lipoamide dehydrogenase (EH2) couple in the presence on NAD+ were -218 mV and -251 mV, respectively, at pH 6.0.	NAD	192-196	dihydrolipoamide dehydrogenase	Sus scrofa	136-159
6715329-4	1984	However, with respect to esterase activity, Mg2+ had a similar effect on both isozymes in that only the NADH-stimulated reaction was effected.	NAD	104-108	mucin 7, secreted	Homo sapiens	44-47
6715329-7	1984	With E1, where NADH release is the rate-determining step, Mg2+ inhibits by causing a tighter binding of NADH to the enzyme.	NAD	15-19	mucin 7, secreted	Homo sapiens	58-61
6715329-7	1984	With E1, where NADH release is the rate-determining step, Mg2+ inhibits by causing a tighter binding of NADH to the enzyme.	NAD	104-108	mucin 7, secreted	Homo sapiens	58-61
6201064-3	1984	recently reported that the NAD contents of CS fibroblasts were lower than those of normal fibroblasts, and that addition of NAD to the cellular growth medium rectified most of the abnormal responses of CS cells to uv-irradiation.	NAD	27-30	citrate synthase	Homo sapiens	43-45
6201064-3	1984	recently reported that the NAD contents of CS fibroblasts were lower than those of normal fibroblasts, and that addition of NAD to the cellular growth medium rectified most of the abnormal responses of CS cells to uv-irradiation.	NAD	124-127	citrate synthase	Homo sapiens	202-204
6200076-5	1984	NADH also inhibited the key enzyme of the salvage pathway, hypoxanthine-guanine-phosphoribosyltransferase, in cell-free extracts.	NAD	0-4	hypoxanthine-guanine phosphoribosyltransferase	Rattus norvegicus	59-105
6719320-0	1984	[Congenital deficiency of erythrocyte NADH-dependent methemoglobin reductase (diaphorase)].	NAD	38-42	dihydrolipoamide dehydrogenase	Homo sapiens	78-88
6196110-5	1983	During hepatocarcinogenesis, ALDH staining patterns in grossly normal liver range from normal-appearing to patterns of distinct, intense focal hepatocyte staining with propionaldehyde-NAD and/or benzaldehyde-NADP.	NAD	184-187	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	29-33
6196110-8	1983	Neoplasms with elevated ALDH activity with propionaldehyde-NAD and/or benzaldehyde-NADP, as well as with no detectable ALDH, have been observed.	NAD	59-62	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	24-28
6357355-3	1983	After insulin injection blood glucose fell from 6.85 mumol/ml to 0.45 mumol/ml at EEG isoelectricity and was accompanied by an oxidation of NADH+.	NAD	140-144	insulin	Felis catus	6-13
6882768-1	1983	The binding of NADH to uridine diphosphate glucose dehydrogenase has been examined by equilibrium dialysis.	NAD	15-19	glucose dehydrogenase	Bos taurus	43-64
16663088-6	1983	It was concluded that NADH to NAD(+) ratio could be the primary signal for coordination of fluxes through electron transport chain or malate dehydrogenase and NAD(+)-linked Krebs cycle dehydrogenases.	NAD	22-26	NAD-dependent malic enzyme 62 kDa isoform, mitochondrial	Solanum tuberosum	134-154
16663088-6	1983	It was concluded that NADH to NAD(+) ratio could be the primary signal for coordination of fluxes through electron transport chain or malate dehydrogenase and NAD(+)-linked Krebs cycle dehydrogenases.	NAD	30-36	NAD-dependent malic enzyme 62 kDa isoform, mitochondrial	Solanum tuberosum	134-154
16663088-6	1983	It was concluded that NADH to NAD(+) ratio could be the primary signal for coordination of fluxes through electron transport chain or malate dehydrogenase and NAD(+)-linked Krebs cycle dehydrogenases.	NAD	159-165	NAD-dependent malic enzyme 62 kDa isoform, mitochondrial	Solanum tuberosum	134-154
6838484-3	1983	Incidentally, the study indicated that the NADH-as well as the NADPH-dependent BLVR activities are due to one and the same enzyme and that, most probably, only one gene in the human genome codes for BLVR and the BLVR is a monomer in its functional configuration.	NAD	43-47	biliverdin reductase A	Homo sapiens	199-203
6838484-3	1983	Incidentally, the study indicated that the NADH-as well as the NADPH-dependent BLVR activities are due to one and the same enzyme and that, most probably, only one gene in the human genome codes for BLVR and the BLVR is a monomer in its functional configuration.	NAD	43-47	biliverdin reductase A	Homo sapiens	199-203
6839008-1	1983	The activities of pyruvate dehydrogenase and oxoglutarate dehydrogenase can be reliably measured by coupling the production of NADH to the reduction of added cytochrome c. Maximum activities required the addition of NADH-cytochrome c reductase activity prepared from rat heart mitochondria.	NAD	127-131	oxoglutarate dehydrogenase	Rattus norvegicus	45-71
6961918-5	1982	The complete protection afforded by NAD+ against the action of disulphiram suggests that the essential thiol group may be involved in binding of NAD+ to the xanthine oxidoreductase molecule.	NAD	36-40	xanthine dehydrogenase	Rattus norvegicus	157-180
6961918-5	1982	The complete protection afforded by NAD+ against the action of disulphiram suggests that the essential thiol group may be involved in binding of NAD+ to the xanthine oxidoreductase molecule.	NAD	145-149	xanthine dehydrogenase	Rattus norvegicus	157-180
7200979-4	1982	No ADP ribosylation occurred in the membranes prepared from intact C6 cells that had been incubated with IAP, suggesting that the IAP substrate had already been ADP-ribosylated by the intracellular NAD during incubation of the intact cells.	NAD	198-201	Cd47 molecule	Rattus norvegicus	130-133
6954534-1	1982	Extensive amino acid sequence homology has been found between nine tryptic peptides of pig heart lipoamide dehydrogenase (NADH:lipoamide oxidoreductase, EC 1.6.4.3] and the sequence of human erythrocyte glutathione reductase [NAD(P)H:glutathione oxidoreductase, EC 1.6.4.2].	NAD	122-125	dihydrolipoamide dehydrogenase	Sus scrofa	97-120
6954534-1	1982	Extensive amino acid sequence homology has been found between nine tryptic peptides of pig heart lipoamide dehydrogenase (NADH:lipoamide oxidoreductase, EC 1.6.4.3] and the sequence of human erythrocyte glutathione reductase [NAD(P)H:glutathione oxidoreductase, EC 1.6.4.2].	NAD	122-125	glutathione-disulfide reductase	Homo sapiens	203-224
7060551-10	1982	The structure of the NADPH domain is probably homologous with the NAD domain of lipoamide dehydrogenase and with the FAD domain of several proteins, but not with NADPH domains of known chain-fold in other proteins.	NAD	21-24	dihydrolipoamide dehydrogenase	Homo sapiens	80-103
7056565-2	1982	In this investigation we measured NAD+-dependent 15-hydroxyprostaglandin dehydrogenase (PGDH) activity in kidney tissue of male and female NZB/NZW F1 hybrid mice and in kidney tissue of male and female mice of other strains.	NAD	34-38	hydroxyprostaglandin dehydrogenase 15 (NAD)	Mus musculus	88-92
6290286-7	1982	Product inhibition studies on C. utilis NAD+ kinase suggest the mechanism of NAD+, ATP addition is best described as rapid equilibrium random with multiple binding of ADP to the free enzyme and the E X ATP and E X NAD+ complexes.	NAD	77-81	NAD kinase	Gallus gallus	40-51
6274398-2	1981	The doses required for 50% inhibition were 0.58 mol myxothiazol/mol cytochrome b for oxygen consumption of beef heart mitochondria, and 0.45 mol/mol cytochrome b for NADH oxidation by submitochondrial particles.	NAD	166-170	cytochrome b	Saccharomyces cerevisiae S288C	149-161
3109450-11	1987	Malate dehydrogenase from S. acidocaldarius utilizes both NADH and NADPH to reduce oxaloacetate.	NAD	58-62	ATZ20_RS08070	Sulfolobus acidocaldarius	0-20
3593260-2	1987	In the presence of NADH, lipoamide dehydrogenase reduces the nitro group of 4-nitropyridine and 4-nitropyridine N-oxide.	NAD	19-23	dihydrolipoamide dehydrogenase	Homo sapiens	25-48
3576723-1	1987	Lipoamide dehydrogenase (EC 1.6.4.3) from the ketoglutarate dehydrogenase complex of adrenals catalyzes the oxidation of NADH by lipoamide and quinone compounds according to the "ping-pong" scheme.	NAD	121-125	dihydrolipoamide dehydrogenase	Homo sapiens	0-23
3576723-6	1987	The patterns of NAD+ inhibition in the quinone reductase reaction differ from that of lipoamide reductase reaction.	NAD	16-20	dihydrolipoamide dehydrogenase	Homo sapiens	86-105
3541787-5	1986	CR1 was unique in being equally active with NADH as its cofactor.	NAD	44-48	complement C3b/C4b receptor 1 (Knops blood group)	Homo sapiens	0-3
3768396-1	1986	An endogenous inhibitor of the NAD+-dependent 15-hydroxyprostaglandin dehydrogenase was isolated from the 105,000 X g supernatant fraction of lungs of pregnant rabbits following DEAE chromatography.	NAD	31-35	carbonyl reductase [NADPH] 1	Oryctolagus cuniculus	46-83
3811968-4	1986	The activity of ALDH is not only preserved, but also significantly enhanced, when propionaldehyde, phenylacetaldehyde, benzaldehyde and D-glucuronolactone are used as substrates and NAD as the coenzyme.	NAD	182-185	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	16-20
3804697-5	1986	Fibroblast UDPGDH activity was regulated by the NAD/NADH ratio and it was also affected by modifications of extracellular matrix composition.	NAD	48-51	UDP-glucose 6-dehydrogenase	Homo sapiens	11-17
3804697-5	1986	Fibroblast UDPGDH activity was regulated by the NAD/NADH ratio and it was also affected by modifications of extracellular matrix composition.	NAD	52-56	UDP-glucose 6-dehydrogenase	Homo sapiens	11-17
3768318-1	1986	In the dark, arylazido-beta-alanylnicotinamide adenine dinucleotide (N3-NAD) can replace NAD as cofactor for D-(-)-beta-hydroxybutyrate dehydrogenase (BDH) purified from bovine heart mitochondria.	NAD	72-75	3-hydroxybutyrate dehydrogenase 1	Bos taurus	109-149
3768318-1	1986	In the dark, arylazido-beta-alanylnicotinamide adenine dinucleotide (N3-NAD) can replace NAD as cofactor for D-(-)-beta-hydroxybutyrate dehydrogenase (BDH) purified from bovine heart mitochondria.	NAD	72-75	3-hydroxybutyrate dehydrogenase 1	Bos taurus	151-154
3768318-3	1986	NAD(H) protects BDH against photolabeling and inhibition by N3-NAD [Yamaguchi, M., Chen, S., &amp; Hatefi, Y.	NAD	0-6	3-hydroxybutyrate dehydrogenase 1	Bos taurus	16-19
3732277-10	1986	Diaphorase was used to couple the oxidation of NADH to the production of duroquinol which acted as electron donor to nitrate reductase.	NAD	47-51	dihydrolipoamide dehydrogenase	Homo sapiens	0-10
3485044-5	1986	When hCG (5 IU) was administered sc and the follicles were isolated 3 h later, androstenedione synthesis was inhibited whether NADH or NADPH was added as cofactors.	NAD	127-131	chorionic gonadotropin subunit beta 5	Homo sapiens	5-8
3955788-1	1986	Approximately 90% of the NADPH- and NADH-dependent O-demethylation of p-nitroanisole (PNA) in the hepatic microsomal fraction from phenobarbital (PB)-treated rabbits and in the pulmonary microsomal fraction from untreated rabbits is catalyzed by the same isozyme of cytochrome P-450.	NAD	36-40	cytochrome P-450	Oryctolagus cuniculus	266-282
6456774-7	1981	Under limited fatty acid supply, the transfer to glucose oxidation gives rise to a region of the ATPase loads, where in the steady state levels of NADH and CoAsAc increase with load.	NAD	147-151	dynein axonemal heavy chain 8	Homo sapiens	97-103
35176139-6	2022	Furthermore, the interaction of LDHA and eEF2 was dependent on NADH, a coenzyme of LDHA.	NAD	63-67	lactate dehydrogenase A	Mus musculus	83-87
3955788-7	1986	For NADH-dependent metabolism of pNA, our results indicate that both electrons are transferred to cytochrome P-450 from cytochrome b5.	NAD	4-8	cytochrome P-450	Oryctolagus cuniculus	98-114
35176139-7	2022	NADH-competitive inhibitors of LDHA could release eEF2 from the LDHA pool, up-regulate translation and enhance MK maturation in vitro.	NAD	0-4	lactate dehydrogenase A	Mus musculus	31-35
7313516-0	1981	Decrease in the NADH2 absorbance in enzymatic blood glucose determination using the glucose dehydrogenase end point method.	NAD	16-21	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	84-105
35176139-7	2022	NADH-competitive inhibitors of LDHA could release eEF2 from the LDHA pool, up-regulate translation and enhance MK maturation in vitro.	NAD	0-4	lactate dehydrogenase A	Mus musculus	64-68
3754027-2	1986	Formate is oxidized by formate dehydrogenase producing NADH which reduces INT via diaphorase to a visible red-colored endpoint that can be measured on a spectrophotometer at 500 nm.	NAD	55-59	dihydrolipoamide dehydrogenase	Homo sapiens	82-92
35629916-3	2022	We also observed more conversion of RD to RK when the oxidized form of nicotinamide adenine dinucleotide (NAD+), a coenzyme of alcohol dehydrogenase (ADH), was added to human skin homogenates.	NAD	71-104	ribokinase	Homo sapiens	42-44
6452897-9	1981	Oxidation of NADH by submitochondrial particles resulted in a decrease of bound (14C)MABI-IF1; the effect was counteracted by antimycin.	NAD	13-17	ATP synthase inhibitory factor subunit 1	Homo sapiens	90-93
35629916-3	2022	We also observed more conversion of RD to RK when the oxidized form of nicotinamide adenine dinucleotide (NAD+), a coenzyme of alcohol dehydrogenase (ADH), was added to human skin homogenates.	NAD	106-110	ribokinase	Homo sapiens	42-44
7265115-4	1981	They can oxidize NADH into NAD+ through a nonenzymatic process, and, moreover, quinone from N2-methyl-9-hydroxyellipticine may undergo a nucleophilic attack, resulting in an irreversible binding of the drug to bovine serum albumin.	NAD	17-21	albumin	Mus musculus	217-230
35500221-8	2022	These data identify an IFNgamma-induced, NAMPT-dependent, NAD+ salvage pathway that is critical for IFNgamma activation of human monocytes.	NAD	58-62	nicotinamide phosphoribosyltransferase	Homo sapiens	41-46
4091279-2	1985	Enzymatic determination of D-erythrulose made use of the D-erythrulose reductase purified from beef or chicken liver, which catalyzes specifically the reduction of D-erythrulose with concomitant conversion of NADH to NAD+.	NAD	209-213	dicarbonyl and L-xylulose reductase	Gallus gallus	57-80
35430611-2	2022	Nicotinamide N-methyltransferase (NNMT), a nicotinamide (NAM) metabolizing enzyme, regulates both NAD + and methionine metabolism.	NAD	98-103	nicotinamide N-methyltransferase	Homo sapiens	0-32
4091279-2	1985	Enzymatic determination of D-erythrulose made use of the D-erythrulose reductase purified from beef or chicken liver, which catalyzes specifically the reduction of D-erythrulose with concomitant conversion of NADH to NAD+.	NAD	217-221	dicarbonyl and L-xylulose reductase	Gallus gallus	57-80
6460614-4	1981	While results confirm earlier reports on skeletal muscle properties and performance it was concluded that end point histochemistry could be reliably quantified and that an "oxidative" stain such as NADH-D correlates extremely well with VO2 max (r = 0.86, p less than 0.001) whereas correlations between % slow twitch fibres (Alkaline ATPase stain) and VO2 max were lower (r = 0.44, p less than 0.05).	NAD	198-202	dynein axonemal heavy chain 8	Homo sapiens	334-340
35430611-2	2022	Nicotinamide N-methyltransferase (NNMT), a nicotinamide (NAM) metabolizing enzyme, regulates both NAD + and methionine metabolism.	NAD	98-103	nicotinamide N-methyltransferase	Homo sapiens	34-38
35396381-2	2022	This led to the development of inhibitors of nicotinamide (NAM) phosphoribosyltransferase (NAMPT), the rate-limiting NAD+ biosynthesis enzyme from NAM.	NAD	117-121	nicotinamide phosphoribosyltransferase	Homo sapiens	45-89
7464825-0	1980	Effect of micromolar Ca2+ on NADH inhibition of bovine kidney alpha-ketoglutarate dehydrogenase complex and possible role of Ca2+ in signal amplification.	NAD	29-33	oxoglutarate dehydrogenase	Bos taurus	62-95
2995124-1	1985	Addition of NADH, but not NAD+ or NADPH, to rat liver plasma membranes resulted in the increase of their 5"-nucleotidase activity.	NAD	12-16	5' nucleotidase, ecto	Rattus norvegicus	105-120
2995124-2	1985	NADH-dependent activation of 5"-nucleotidase was significantly suppressed by atebrine, an inhibitor of NADH dehydrogenase of plasma membranes, and completely abolished by 2,4-dinitrophenol (2 X 10(-4)M) and Triton X-100 (2%).	NAD	0-4	5' nucleotidase, ecto	Rattus norvegicus	29-44
35396381-2	2022	This led to the development of inhibitors of nicotinamide (NAM) phosphoribosyltransferase (NAMPT), the rate-limiting NAD+ biosynthesis enzyme from NAM.	NAD	117-121	nicotinamide phosphoribosyltransferase	Homo sapiens	91-96
35218657-0	2022	Intestinal epithelial NAD + biosynthesis regulates GLP-1 production and postprandial glucose metabolism in mice.	NAD	22-27	glucagon	Mus musculus	51-56
2991914-7	1985	Since preincubation of HDP in NADH prevents its binding to ss DNA, both NADH and ss DNA may be binding at the same site.	NAD	30-34	heterogeneous nuclear ribonucleoprotein A1	Rattus norvegicus	23-26
7408894-0	1980	The binding of NADH to succinic semialdehyde dehydrogenase.	NAD	15-19	aldehyde dehydrogenase 5 family member A1	Sus scrofa	23-58
35218657-8	2022	Collectively, our study provides mechanistic and therapeutic insights into intestinal NAD + biology related to obesity-associated dysregulation of GLP-1 production and postprandial hyperglycemia.	NAD	86-91	glucagon	Mus musculus	147-152
2991914-7	1985	Since preincubation of HDP in NADH prevents its binding to ss DNA, both NADH and ss DNA may be binding at the same site.	NAD	72-76	heterogeneous nuclear ribonucleoprotein A1	Rattus norvegicus	23-26
35402885-1	2022	Nicotinamide phosphoribosyltransferase (NAMPT), alongside being a crucial enzyme in NAD synthesis, has been shown to be a secreted protein (eNAMPT), whose levels are increased in patients affected by immune-mediated disorders.	NAD	84-87	nicotinamide phosphoribosyltransferase	Homo sapiens	0-38
4034373-1	1985	Localization of NAD+-dependent (type I) 15-hydroxyprostaglandin dehydrogenase (15PGDH) in the rat kidney was examined using an ultramicro assay of the enzyme activity based on the enzymatic cycling method.	NAD	16-20	15-hydroxyprostaglandin dehydrogenase	Rattus norvegicus	79-85
4034373-6	1985	The kinetic analysis for renal 15PGDH of 3 week-old rats revealed that Km for PGE2 (8.4 microM) was lower than that for PGF2 alpha (22.6 microM) with constant NAD+, while Vmax for both was similar.	NAD	159-163	15-hydroxyprostaglandin dehydrogenase	Rattus norvegicus	31-37
4034373-8	1985	These data suggest that the rate-limiting factor of type I 15PGDH is the concentration of prostaglandins in the kidney rather than the concentration of NAD+.	NAD	152-156	15-hydroxyprostaglandin dehydrogenase	Rattus norvegicus	59-65
7468250-3	1980	Redox changes similar to State 3 to 4  transition (NAD+ reduction) were observed when mechanical activity was reduced by perfusing the hearts with 0.65 or 0.31 mM Cap2+, which was also substrate independent.	NAD	51-55	cyclase associated actin cytoskeleton regulatory protein 2	Rattus norvegicus	163-167
7468250-4	1980	At high Cap2+ (2.6--7.8 mM) increase of contractile activity and O2-consumption was accompanied by Cap2+ dependent NAD+ reduction in the presence of glucose.	NAD	115-119	cyclase associated actin cytoskeleton regulatory protein 2	Rattus norvegicus	8-12
7468250-4	1980	At high Cap2+ (2.6--7.8 mM) increase of contractile activity and O2-consumption was accompanied by Cap2+ dependent NAD+ reduction in the presence of glucose.	NAD	115-119	cyclase associated actin cytoskeleton regulatory protein 2	Rattus norvegicus	99-103
7468250-5	1980	Inhibition of glycolisis by pyruvate reversed the direction of NADH response (NADH oxidation following Cap2+ elevation).	NAD	63-67	cyclase associated actin cytoskeleton regulatory protein 2	Rattus norvegicus	103-107
7468250-5	1980	Inhibition of glycolisis by pyruvate reversed the direction of NADH response (NADH oxidation following Cap2+ elevation).	NAD	78-82	cyclase associated actin cytoskeleton regulatory protein 2	Rattus norvegicus	103-107
7468250-8	1980	The direction of NAD+/NADH redox state changes following Cap2+ elevation is grately influenced by the substrate  preferentially consumed by the heart.	NAD	17-21	cyclase associated actin cytoskeleton regulatory protein 2	Rattus norvegicus	57-61
7468250-8	1980	The direction of NAD+/NADH redox state changes following Cap2+ elevation is grately influenced by the substrate  preferentially consumed by the heart.	NAD	22-26	cyclase associated actin cytoskeleton regulatory protein 2	Rattus norvegicus	57-61
35402885-1	2022	Nicotinamide phosphoribosyltransferase (NAMPT), alongside being a crucial enzyme in NAD synthesis, has been shown to be a secreted protein (eNAMPT), whose levels are increased in patients affected by immune-mediated disorders.	NAD	84-87	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
35328428-5	2022	In addition, both NADH- and FAD-binding domains for oxidoreductase function are conserved in HlAIF-2.	NAD	18-22	uncharacterized protein LOC101207246	Cucumis sativus	52-66
121057-12	1979	The Km values of NADPH and NADH for the NADPH-cytochrome c reductase activity and those of cytochrome c for the activity of NADPH-cytochrome P-450 reductase were determined kinetically.	NAD	27-31	LOC104968582	Bos taurus	46-58
121057-12	1979	The Km values of NADPH and NADH for the NADPH-cytochrome c reductase activity and those of cytochrome c for the activity of NADPH-cytochrome P-450 reductase were determined kinetically.	NAD	27-31	cytochrome p450 oxidoreductase	Bos taurus	124-156
2579078-6	1985	Incubation of the supernatant fraction of mast cell homogenates with the active component of IAP caused the transfer of the ADP-ribosyl moiety of added [alpha-32P]NAD to a protein with Mr = 41,000.	NAD	163-166	islet amyloid polypeptide	Homo sapiens	93-96
4043713-4	1985	Twenty-four hours following a potentiating dose of ethanol and CCl4 an 81 and 57% decline in NAD+-dependent microsomal and mitochondrial ALDH activity was observed, respectively.	NAD	93-97	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	137-141
39757-11	1979	Incubation of mouse glutathione reductase in the presence of NADPH or NADH, but not NADP+ or NAD+, produced an almost complete inactivation.	NAD	70-74	glutathione reductase	Mus musculus	20-41
35241643-0	2022	miR-146a impedes the anti-aging effect of AMPK via NAMPT suppression and NAD+/SIRT inactivation.	NAD	73-77	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	42-46
37807-2	1979	Glutathione reductase activities, both with NADPH and NADH, were determined in basal and squamous cell epitheliomas, in verrucae seborrhoeicae and in human epidermis.	NAD	54-58	glutathione-disulfide reductase	Homo sapiens	0-21
6095915-3	1984	In the present study, two derivatives of NAD, spin-labeled either at N-6 or C-8 of the adenine ring, were found to be active as coenzyme.	NAD	41-44	homeobox C8	Homo sapiens	76-79
35241643-2	2022	AMP-activated protein kinase (AMPK) upregulates NAD+ synthesis and SIRT activity in a nicotinamide phosphoribosyltransferase (NAMPT)-dependent manner.	NAD	48-52	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	0-28
35241643-2	2022	AMP-activated protein kinase (AMPK) upregulates NAD+ synthesis and SIRT activity in a nicotinamide phosphoribosyltransferase (NAMPT)-dependent manner.	NAD	48-52	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	30-34
35241643-2	2022	AMP-activated protein kinase (AMPK) upregulates NAD+ synthesis and SIRT activity in a nicotinamide phosphoribosyltransferase (NAMPT)-dependent manner.	NAD	48-52	nicotinamide phosphoribosyltransferase	Homo sapiens	86-124
6149820-2	1984	The hepatic ALDH phenotype was determined at intervals over 280 days by histochemical analysis, total ALDH activity assays and gel electrophoresis, using propionaldehyde and NAD (P/NAD) to characterize normal liver ALDH activity or benzaldehyde and NADP (B/NADP) to determine tumor-associated ALDH activity.	NAD	181-185	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	12-16
454630-3	1979	Lipoyl dehydrogenase (NADH:lipoamide oxidereductase, EC 1.6.4.3), DT-diaphorase (NAD(P)H:(quinone-acceptor) oxidoreductase, EC 1.6.99.2) and liver microsomes could also catalyze the conversion of cis-3-(5-nitro-2-furyl)-2-(2-furyl)acrylamide to its trans isomer in the presence of an appropriate electron donor.	NAD	22-26	dihydrolipoamide dehydrogenase	Homo sapiens	0-20
35241643-2	2022	AMP-activated protein kinase (AMPK) upregulates NAD+ synthesis and SIRT activity in a nicotinamide phosphoribosyltransferase (NAMPT)-dependent manner.	NAD	48-52	nicotinamide phosphoribosyltransferase	Homo sapiens	126-131
6388629-0	1984	Direct transfer of reduced nicotinamide adenine dinucleotide from glyceraldehyde-3-phosphate dehydrogenase to liver alcohol dehydrogenase.	NAD	27-60	glyceraldehyde-3-phosphate dehydrogenase	Equus caballus	66-106
35241643-10	2022	These findings identified a novel cascade that negatively regulates the NAD+/SIRT pathway by suppressing miR-146a-mediated NAMPT downregulation.	NAD	72-76	nicotinamide phosphoribosyltransferase	Homo sapiens	123-128
6388629-1	1984	The reduction of benzaldehyde and p-nitrobenzaldehyde by NADH, catalyzed by horse liver alcohol dehydrogenase (LADH), has been found to be faster when NADH is bound to glyceraldehyde-3-phosphate dehydrogenase (GPDH) than with free NADH.	NAD	57-61	glyceraldehyde-3-phosphate dehydrogenase	Equus caballus	168-208
6388629-1	1984	The reduction of benzaldehyde and p-nitrobenzaldehyde by NADH, catalyzed by horse liver alcohol dehydrogenase (LADH), has been found to be faster when NADH is bound to glyceraldehyde-3-phosphate dehydrogenase (GPDH) than with free NADH.	NAD	57-61	glyceraldehyde-3-phosphate dehydrogenase	Equus caballus	210-214
35241643-12	2022	This mutual inhibitory relationship between miR-146a and AMPK enriches our understanding of the molecular connections between AMPK and SIRT and provides new insight into miRNA-mediated NAD+/SIRT regulation and an intervention point for the prevention of aging and age-related diseases.	NAD	185-189	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	57-61
6388629-1	1984	The reduction of benzaldehyde and p-nitrobenzaldehyde by NADH, catalyzed by horse liver alcohol dehydrogenase (LADH), has been found to be faster when NADH is bound to glyceraldehyde-3-phosphate dehydrogenase (GPDH) than with free NADH.	NAD	151-155	glyceraldehyde-3-phosphate dehydrogenase	Equus caballus	168-208
6388629-1	1984	The reduction of benzaldehyde and p-nitrobenzaldehyde by NADH, catalyzed by horse liver alcohol dehydrogenase (LADH), has been found to be faster when NADH is bound to glyceraldehyde-3-phosphate dehydrogenase (GPDH) than with free NADH.	NAD	151-155	glyceraldehyde-3-phosphate dehydrogenase	Equus caballus	210-214
37557-4	1979	With NAD+ as electron acceptor a different profile in the pKM xanthine plot is obtained for chicken liver xanthine dehydrogenase.	NAD	5-9	xanthine dehydrogenase	Gallus gallus	106-128
35203360-2	2022	Under normal physiological conditions, NAD+ consumption is matched by its synthesis primarily via the salvage pathway catalyzed by nicotinamide phosphoribosyltransferase (NAMPT).	NAD	39-43	nicotinamide phosphoribosyltransferase	Homo sapiens	131-169
35203360-2	2022	Under normal physiological conditions, NAD+ consumption is matched by its synthesis primarily via the salvage pathway catalyzed by nicotinamide phosphoribosyltransferase (NAMPT).	NAD	39-43	nicotinamide phosphoribosyltransferase	Homo sapiens	171-176
689031-7	1978	NAD+ immobilized on agarose through the C-8 of the adenine ring is a superior substrate compared with NAD+ linked to agarose via its periodate-oxidized ribose moieties.	NAD	0-4	homeobox C8	Homo sapiens	40-43
35256952-1	2022	SIRT6 belongs to the conserved NAD+-dependent deacetylase superfamily and mediates multiple biological and pathological processes.	NAD	31-34	sirtuin 6	Homo sapiens	0-5
6086348-14	1984	Comparing electron flow rates of succinate:cytochrome c oxidoreductase and NADH:cytochrome c oxidoreductase in cob- mutants and two revertants provides evidence that ubiquinone does not constitute a homogeneous pool, suggested by the dissimilar interaction of both dehydrogenases with the bc1 segment.	NAD	75-79	cytochrome b	Saccharomyces cerevisiae S288C	111-114
6539095-13	1984	The results indicate that the NADH: (acceptor) oxidoreductase could be identified as a ferric Lb reductase.	NAD	30-34	chalcone reductase CHR1	Glycine max	52-61
35198877-0	2022	SARM1 is a multi-functional NAD(P)ase with prominent base exchange activity, all regulated bymultiple physiologically relevant NAD metabolites.	NAD	127-130	sterile alpha and TIR motif containing 1	Homo sapiens	0-5
35198877-5	2022	All SARM1 activities, including base exchange at neutral pH, are activated by an increased NMN:NAD ratio, at physiological levels of both metabolites.	NAD	95-98	sterile alpha and TIR motif containing 1	Homo sapiens	4-9
6546954-5	1984	Under physiological conditions, lipoamide dehydrogenase and glutathione reductase act in opposite directions, passing reducing equivalents to NAD+ or from NADPH (respectively), and two key substitutions near the redox centre could be associated with this difference in function.	NAD	142-146	dihydrolipoamide dehydrogenase	Homo sapiens	32-55
2479640-6	1989	bFGF caused a small reduction in steady state NAD-dependent ADP-ribosylation and had no detectable effects on the steady-state levels of the Gi alpha (alpha subunit of the inhibitory G protein) 1, 2, and 3, visualized with specific antibodies in these cells.	NAD	46-49	fibroblast growth factor 2	Rattus norvegicus	0-4
6546954-5	1984	Under physiological conditions, lipoamide dehydrogenase and glutathione reductase act in opposite directions, passing reducing equivalents to NAD+ or from NADPH (respectively), and two key substitutions near the redox centre could be associated with this difference in function.	NAD	142-146	glutathione-disulfide reductase	Homo sapiens	60-81
6698026-12	1984	A cytochrome of type b with an absorption maximum at 559 nm accumulates during starvation only in queuine-lacking cells; it might be a component of an NAD-independent lactic acid oxidoreductase as is cytochrome b 557 in yeast and be responsible for the reduced level of lactate in cells lacking queuine in tRNA.	NAD	151-154	cytochrome b	Saccharomyces cerevisiae S288C	200-212
2806555-1	1989	Formaldehyde dehydrogenase (EC 1.2.1.1) is a widely occurring enzyme which catalyzes the oxidation of S-hydroxymethylglutathione, formed from formaldehyde and glutathione, into S-formyglutathione in the presence of NAD.	NAD	215-218	alcohol dehydrogenase 5 (class III), chi polypeptide	Homo sapiens	0-26
6378467-0	1984	Activities of NAD+-dependent aldehyde dehydrogenase and alcohol dehydrogenase in the liver of spontaneously hypertensive rats in the process of development.	NAD	14-17	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	29-51
6378467-1	1984	The difference in the basal activities of NAD+-dependent aldehyde dehydrogenase (ALDH) and alcohol dehydrogenase (ADH) was investigated in the liver of age-matched spontaneously hypertensive (SH) and normotensive Wistar Kyoto (WK) rats.	NAD	42-45	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	57-79
6378467-1	1984	The difference in the basal activities of NAD+-dependent aldehyde dehydrogenase (ALDH) and alcohol dehydrogenase (ADH) was investigated in the liver of age-matched spontaneously hypertensive (SH) and normotensive Wistar Kyoto (WK) rats.	NAD	42-45	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	81-85
2806555-3	1989	Formaldehyde dehydrogenase was found to be able at high pH values to catalyze the NAD-dependent oxidation of long-chain aliphatic alcohols like n-octanol and 12-hydroxydodecanoate but ethanol was used only at very high substrate concentrations and pyrazole was not inhibitory.	NAD	82-85	alcohol dehydrogenase 5 (class III), chi polypeptide	Homo sapiens	0-26
6586086-1	1984	Several NAD(P)+-dependent hydroxysteroid dehydrogenases, namely 3 alpha-hydroxysteroid dehydrogenase, beta-hydroxysteroid dehydrogenase, 7 alpha-hydroxysteroid dehydrogenase, and 12 alpha-hydroxysteroid dehydrogenase were separately immobilized on nylon tubes for the continuous-flow automated assay of hydroxysteroids.	NAD	8-12	aldo-keto reductase family 1 member C3	Homo sapiens	64-100
2777772-0	1989	Differences in environment of FAD between NAD-dependent and O2-dependent types of rat liver xanthine dehydrogenase shown by active site probe study.	NAD	42-45	xanthine dehydrogenase	Rattus norvegicus	92-114
6088199-0	1984	[NAD-H-dependent activation of the 5"-nucleotidase of the plasma membranes in the rat liver].	NAD	1-6	5' nucleotidase, ecto	Rattus norvegicus	35-50
2549869-3	1989	Physiologically, this reaction occurs at a relatively low rate, because the native form of the enzyme is xanthine dehydrogenase (XD) which produces NADH instead of O2-.	NAD	148-152	xanthine dehydrogenase	Rattus norvegicus	105-127
2531616-1	1989	An addition of the inhibitor protein (IF1) to submitochondrial particles (SMP) essentially free of endogenous IF1 (AS-SMP) results in a synchroneous inhibition of ATP hydrolysis and ATP-dependent reduction of NAD+ by succinate without any effect on the oxidative phosphorylation rate.	NAD	209-213	ATP synthase inhibitory factor subunit 1	Homo sapiens	38-41
2531616-1	1989	An addition of the inhibitor protein (IF1) to submitochondrial particles (SMP) essentially free of endogenous IF1 (AS-SMP) results in a synchroneous inhibition of ATP hydrolysis and ATP-dependent reduction of NAD+ by succinate without any effect on the oxidative phosphorylation rate.	NAD	209-213	ATP synthase inhibitory factor subunit 1	Homo sapiens	110-113
2722858-0	1989	Differences in redox and kinetic properties between NAD-dependent and O2-dependent types of rat liver xanthine dehydrogenase.	NAD	52-55	xanthine dehydrogenase	Rattus norvegicus	102-124
2722858-1	1989	Reductive titrations of a NAD-dependent type (type-D) and an O2-dependent type (type-O) of rat liver xanthine dehydrogenase showed that only the type-D enzyme formed a pronounced stable FAD semiquinone (FADH*).	NAD	26-29	xanthine dehydrogenase	Rattus norvegicus	101-123
2500152-6	1989	Aldose reductase utilized both NADPH and NADH as coenzyme, whereas aldehyde reductase utilized only NADPH.	NAD	41-45	aldo-keto reductase family 1 member B1	Rattus norvegicus	0-16
2736782-0	1989	Determination of NADH2-ferricyanide oxidoreductase (cytochrome b5 reductase, diaphorase) activity of human erythrocytes by an analysis of the time-dependence of NADH2 oxidation.	NAD	17-22	dihydrolipoamide dehydrogenase	Homo sapiens	77-87
2736782-1	1989	The time-dependence of the reaction of human erythrocyte diaphorase activity has been studied by the use of NADH2 and ferricyanide as substrates.	NAD	108-113	dihydrolipoamide dehydrogenase	Homo sapiens	57-67
2736782-3	1989	These findings indicate that human erythrocyte diaphorase has a Km value for NADH2 by far higher than, and for ferricyanide by far lower than, the concentration of the substrates used, i.e. 0.1 and 0.2 mmol/l, respectively.	NAD	77-82	dihydrolipoamide dehydrogenase	Homo sapiens	47-57
2736782-5	1989	Diaphorase activity was found to be 7.29 +/- 3.69 1 SD mumol NADH2 oxidized/ml packed cells per min, at 25 degrees C, and pH 7.00.	NAD	61-66	dihydrolipoamide dehydrogenase	Homo sapiens	0-10
2537814-5	1989	NADPH instead of NADH was the preferred electron donor of this lipoamide dehydrogenase.	NAD	17-21	dihydrolipoamide dehydrogenase	Homo sapiens	63-86
2692433-0	1989	Structure of xanthine dehydrogenase from chicken and rat liver: chemical modification of NAD binding site with 5"-FSBA.	NAD	89-92	xanthine dehydrogenase	Gallus gallus	13-35
2755909-7	1989	The activity of ALDH was found to be induced by PB in the liver and the intestinal mucosa, when measured with NAD and propionaldehyde (P/NAD) or phenylacetaldehyde (Ph/NAD).	NAD	110-113	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	16-20
2755909-7	1989	The activity of ALDH was found to be induced by PB in the liver and the intestinal mucosa, when measured with NAD and propionaldehyde (P/NAD) or phenylacetaldehyde (Ph/NAD).	NAD	137-140	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	16-20
2755909-7	1989	The activity of ALDH was found to be induced by PB in the liver and the intestinal mucosa, when measured with NAD and propionaldehyde (P/NAD) or phenylacetaldehyde (Ph/NAD).	NAD	137-140	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	16-20
3178232-7	1988	Gel filtration of GDH in the presence of GTP with NADH rendered a subunimeric tripeptide, largely independent of ionic strength or GDH concentration.	NAD	50-54	glucose dehydrogenase	Bos taurus	18-21
3350116-2	1988	The enzyme has been separated from the endoplasmic reticulum using Triton X-114 and further purified using NAD to release glucose dehydrogenase from a NADP-linked sepharose column.	NAD	107-110	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	122-143
2970751-6	1988	The presence of this enzyme activity in the sarcoplasmic reticulum should be taken into consideration when planning experiments with vanadate, especially when measuring ATPase activity through NADH oxidation with coupled enzymatic assay.	NAD	193-197	dynein axonemal heavy chain 8	Homo sapiens	169-175
3691517-3	1987	ALDH activity was measured in a microbiochemical assay using the oil-well technique with luminometric determination of NADH.	NAD	119-123	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	0-4
657494-3	1978	Bile acids are converted to 3-oxo bile acids with 3alpha-hydroxysteroid dehydrogenase (EC 1.1.1.50) with concomitant reduction of NAD+ to NADH.	NAD	130-134	aldo-keto reductase family 1 member C3	Homo sapiens	50-85
657494-3	1978	Bile acids are converted to 3-oxo bile acids with 3alpha-hydroxysteroid dehydrogenase (EC 1.1.1.50) with concomitant reduction of NAD+ to NADH.	NAD	138-142	aldo-keto reductase family 1 member C3	Homo sapiens	50-85
3319289-1	1987	This method for the specific determination of methanol in serum is based on the following two reactions: (formula; see text) Alcohol oxidase is not specific: it converts all lower alcohols to their corresponding aldehydes; however, formaldehyde dehydrogenase is specific and thus the transformation of NAD+ to NADH (which is used to monitor the reaction) proceeds only if methanol is originally present in the sample.	NAD	302-306	alcohol dehydrogenase 5 (class III), chi polypeptide	Homo sapiens	232-258
657494-4	1978	The hydrogen in the generated NADH is transferred by diaphorase (EC 1.6.4.3) to resazurin to yield resorfin, the fluorophore.	NAD	30-34	dihydrolipoamide dehydrogenase	Homo sapiens	53-63
3319289-1	1987	This method for the specific determination of methanol in serum is based on the following two reactions: (formula; see text) Alcohol oxidase is not specific: it converts all lower alcohols to their corresponding aldehydes; however, formaldehyde dehydrogenase is specific and thus the transformation of NAD+ to NADH (which is used to monitor the reaction) proceeds only if methanol is originally present in the sample.	NAD	310-314	alcohol dehydrogenase 5 (class III), chi polypeptide	Homo sapiens	232-258
16660377-2	1978	The effect of cyanide and ferrocyanide was not due to elimination of cytochrome oxidase interference but resulted from the stimulation of NADH-dependent reduction of Cyt c.	NAD	138-142	cytochrome c	Zea mays	166-171
2889718-1	1987	Glutamic acid 553 of Pseudomonas aeruginosa exotoxin A (ETA) has been identified by photoaffinity labeling as a residue within the NAD binding site (S.F.	NAD	131-134	endothelin receptor type A	Mus musculus	56-59
219869-8	1978	Reversal of electron transport with formation of NADH by succinate in the presence of rotenone and ATP was, concentration dependently, improved by MPG.	NAD	49-53	N-methylpurine-DNA glycosylase	Rattus norvegicus	147-150
6688532-0	1983	Proton nuclear magnetic resonance investigation of the mechanism of flavin C-4a adduct formation induced by oxidized nicotinamide adenine dinucleotide binding to monoalkylated pig heart lipoamide dehydrogenase.	NAD	117-150	dihydrolipoamide dehydrogenase	Sus scrofa	186-209
6688532-1	1983	The active center thiol of monoalkylated pig heart lipoamide dehydrogenase, EHR, is induced to form an adduct to the enzyme-bound flavin adenine dinucleotide (FAD) at the C-4a position upon binding oxidized nicotinamide adenine dinucleotide (NAD+) [Thorpe, C., &amp; Williams, C. H., Jr. (1976) J. Biol.	NAD	207-240	dihydrolipoamide dehydrogenase	Sus scrofa	51-74
6688532-1	1983	The active center thiol of monoalkylated pig heart lipoamide dehydrogenase, EHR, is induced to form an adduct to the enzyme-bound flavin adenine dinucleotide (FAD) at the C-4a position upon binding oxidized nicotinamide adenine dinucleotide (NAD+) [Thorpe, C., &amp; Williams, C. H., Jr. (1976) J. Biol.	NAD	242-246	dihydrolipoamide dehydrogenase	Sus scrofa	51-74
3666295-5	1987	260, 3902-3905) that NADH-semidehydroascorbate reductase and ascorbate participate in an electron transport pathway (ETP) supplying reducing equivalents from NADH to cytochrome P-450scc.	NAD	21-25	cholesterol side-chain cleavage enzyme, mitochondrial	Bos taurus	166-185
6612739-9	1983	Mitochondria contained an ALDH enzyme with lower affinity (Km of 7.3 mM with NAD+) for malondialdehyde.	NAD	77-81	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	26-30
198506-2	1977	By use of a 3alpha-hydroxysteroid dehydrogenase, oxidation of bile acids with NAD is completed in 200 seconds with the observed NADH fluorescence being proportional to the concentration of serum bile acids.	NAD	78-81	aldo-keto reductase family 1 member C3	Homo sapiens	12-47
198506-2	1977	By use of a 3alpha-hydroxysteroid dehydrogenase, oxidation of bile acids with NAD is completed in 200 seconds with the observed NADH fluorescence being proportional to the concentration of serum bile acids.	NAD	128-132	aldo-keto reductase family 1 member C3	Homo sapiens	12-47
3666295-5	1987	260, 3902-3905) that NADH-semidehydroascorbate reductase and ascorbate participate in an electron transport pathway (ETP) supplying reducing equivalents from NADH to cytochrome P-450scc.	NAD	158-162	cholesterol side-chain cleavage enzyme, mitochondrial	Bos taurus	166-185
3028490-4	1987	Glutathione reductase (EC 1.6.4.2) in the presence of NADPH and oxidised glutathione, and dihydrolipoamide dehydrogenase (EC 1.8.1.4) with NADH and lipoamide, are found to accelerate the radical decay by reducing the quinone or semiquinone.	NAD	139-143	glutathione-disulfide reductase	Homo sapiens	0-21
14154-1	1977	The catalytic mechanism of the phosphoglycerate dehydrogenase reaction in both directions was investigated by studying: (a) pre-steady state transients in reduced coenzyme appearance or disappearance or disappearance and in protein fluorescence; (b) deuterium isotope effects on the transients and on the steady state reactions; and (c) the partial reaction between the enzyme-NADH complex and hydroxypyruvate-P.	NAD	377-381	phosphoglycerate dehydrogenase	Homo sapiens	31-61
6575778-15	1983	Furthermore, preliminary inhibition studies with the NAD+-linked PGDH system indicate that this enzyme is not only inhibited by NADH, but also by NADPH, a property not previously reported for NAD+-linked PGDH derived from other tissues.	NAD	53-57	15-hydroxyprostaglandin dehydrogenase	Rattus norvegicus	65-69
6575778-15	1983	Furthermore, preliminary inhibition studies with the NAD+-linked PGDH system indicate that this enzyme is not only inhibited by NADH, but also by NADPH, a property not previously reported for NAD+-linked PGDH derived from other tissues.	NAD	53-57	15-hydroxyprostaglandin dehydrogenase	Rattus norvegicus	204-208
6575778-15	1983	Furthermore, preliminary inhibition studies with the NAD+-linked PGDH system indicate that this enzyme is not only inhibited by NADH, but also by NADPH, a property not previously reported for NAD+-linked PGDH derived from other tissues.	NAD	128-132	15-hydroxyprostaglandin dehydrogenase	Rattus norvegicus	65-69
6575778-15	1983	Furthermore, preliminary inhibition studies with the NAD+-linked PGDH system indicate that this enzyme is not only inhibited by NADH, but also by NADPH, a property not previously reported for NAD+-linked PGDH derived from other tissues.	NAD	128-132	15-hydroxyprostaglandin dehydrogenase	Rattus norvegicus	204-208
6575778-15	1983	Furthermore, preliminary inhibition studies with the NAD+-linked PGDH system indicate that this enzyme is not only inhibited by NADH, but also by NADPH, a property not previously reported for NAD+-linked PGDH derived from other tissues.	NAD	192-196	15-hydroxyprostaglandin dehydrogenase	Rattus norvegicus	65-69
6575778-15	1983	Furthermore, preliminary inhibition studies with the NAD+-linked PGDH system indicate that this enzyme is not only inhibited by NADH, but also by NADPH, a property not previously reported for NAD+-linked PGDH derived from other tissues.	NAD	192-196	15-hydroxyprostaglandin dehydrogenase	Rattus norvegicus	204-208
3813560-8	1987	Glucokinase was assayed either by allowing glucose 6-phosphate to accumulate over 10 min (discontinuous assay) or by coupling the formation of glucose 6-phosphate with its oxidation by Leuconostoc mesenteroides glucose 6-phosphate dehydrogenase and NAD (continuous assay).	NAD	249-252	glucokinase	Rattus norvegicus	0-11
3025205-0	1987	The role of nicotinamide adenine dinucleotide in the inhibition of bovine liver S-adenosylhomocysteine hydrolase by neplanocin A.	NAD	12-45	adenosylhomocysteinase	Bos taurus	80-112
6340103-4	1983	By using a third enzyme, lipoamide dehydrogenase (NADH:lipoamide oxidoreductase, EC 1.6.4.3), which was also coupled to the same beads and which competes with lactate dehydrogenase for the NADH produced by alcohol dehydrogenase, the effect of site-to-site directed immobilization was studied.	NAD	50-54	dihydrolipoamide dehydrogenase	Homo sapiens	25-48
6340103-4	1983	By using a third enzyme, lipoamide dehydrogenase (NADH:lipoamide oxidoreductase, EC 1.6.4.3), which was also coupled to the same beads and which competes with lactate dehydrogenase for the NADH produced by alcohol dehydrogenase, the effect of site-to-site directed immobilization was studied.	NAD	50-54	hydroxysteroid 17-beta dehydrogenase 6	Homo sapiens	65-79
2835176-5	1987	In mutant devoid of core protein I, cytochrome b was found to be reducible by NADH but not by succinate, suggesting two different electron transfer pathways inside comples III from each substrate to cytochrome b heme(s).	NAD	78-82	cytochrome b	Saccharomyces cerevisiae S288C	36-48
6304829-4	1983	Thus, the redox potential span from NADH to cytochrome c, delta Eh, varied with the energy demand such that delta Eh and delta G(ATP)c changed in the same direction.	NAD	36-40	cytochrome c	Oryctolagus cuniculus	44-56
6340090-2	1983	The method uses antibody competitive binding of free and NAD labeled insulin.	NAD	57-60	INS	Equus caballus	69-76
3093302-5	1986	The inhibition of aldose reductase by sorbinil tends to normalize the redox state of the nicotinamide nucleotides, reimposing the NADPH limitation on the PPP and increasing the availability of NAD+ for the glycolytic route.	NAD	193-197	aldo-keto reductase family 1 member B1	Rattus norvegicus	18-34
7115343-6	1982	When membranes from horse neutrophils were incubated anaerobically with either NADH or NADPH the cytochrome b became reduced.	NAD	79-83	cytochrome b	Equus caballus	97-109
6280769-3	1982	The improved resolution of composite spectra consisting of freely tumbling and immobilized components is demonstrated in ternary complexes of the spin-labeled NAD+ derivatives with lactate dehydrogenase (L-lactate:NAD+ oxidoreductase, EC 1.1.1.27) and oxalate.	NAD	159-163	hydroxysteroid 17-beta dehydrogenase 6	Homo sapiens	219-233
2871926-4	1986	The first NAD+- and NADP+-dependent ALDH-positive enzyme-altered foci were also seen at 9 weeks.	NAD	10-14	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	36-40
7108552-2	1982	Kinetic studies suggested the presence of several forms of NAD-dependent aldehyde dehydrogenase (ALDH) in rat brain.	NAD	59-62	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	73-95
7108552-2	1982	Kinetic studies suggested the presence of several forms of NAD-dependent aldehyde dehydrogenase (ALDH) in rat brain.	NAD	59-62	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	97-101
7128914-2	1982	An enzyme system is present in mouse hepatic microsomes which is capable of reducing NAD+ and NADP+ and, consequently, of reducing cytochrome b5 in the absence of other externally added cofactors.	NAD	85-89	cytochrome b5 type A (microsomal)	Mus musculus	131-144
7173489-0	1982	Regulation of coenzyme utilization by bovine liver glutamate dehydrogenase: investigations using thionicotinamide analogues of NAD and NADP in a dual wavelength assay.	NAD	127-130	glutamate dehydrogenase 1, mitochondrial	Bos taurus	51-74
7173489-2	1982	The coenzyme preference of bovine liver glutamate dehydrogenase (GDH) was probed using dual wavelength spectroscopy and pairing the thionicotinamide analogues, S-NAD or S-NADP (which have absorbance maxima at 400 nm), with the natural coenzymes, NADP or NAD.	NAD	160-165	glutamate dehydrogenase 1, mitochondrial	Bos taurus	40-63
7173489-2	1982	The coenzyme preference of bovine liver glutamate dehydrogenase (GDH) was probed using dual wavelength spectroscopy and pairing the thionicotinamide analogues, S-NAD or S-NADP (which have absorbance maxima at 400 nm), with the natural coenzymes, NADP or NAD.	NAD	160-165	glutamate dehydrogenase 1, mitochondrial	Bos taurus	65-68
7173489-2	1982	The coenzyme preference of bovine liver glutamate dehydrogenase (GDH) was probed using dual wavelength spectroscopy and pairing the thionicotinamide analogues, S-NAD or S-NADP (which have absorbance maxima at 400 nm), with the natural coenzymes, NADP or NAD.	NAD	162-165	glutamate dehydrogenase 1, mitochondrial	Bos taurus	40-63
7173489-2	1982	The coenzyme preference of bovine liver glutamate dehydrogenase (GDH) was probed using dual wavelength spectroscopy and pairing the thionicotinamide analogues, S-NAD or S-NADP (which have absorbance maxima at 400 nm), with the natural coenzymes, NADP or NAD.	NAD	162-165	glutamate dehydrogenase 1, mitochondrial	Bos taurus	65-68
7173489-4	1982	S-NAD and S-NADP were found to be good alternate substrates for GDH: the apparent Km"s for the thioderivatives were similar to those of the corresponding natural coenzymes, the apparent Km"s for glutamate were unaltered by the substitution of the thioderivatives, and the effects of inhibitors and activators on S-NAD or S-NADP kinetics were qualitatively the same as those found for NAD or NADP, respectively.	NAD	0-5	glutamate dehydrogenase 1, mitochondrial	Bos taurus	64-67
7173489-4	1982	S-NAD and S-NADP were found to be good alternate substrates for GDH: the apparent Km"s for the thioderivatives were similar to those of the corresponding natural coenzymes, the apparent Km"s for glutamate were unaltered by the substitution of the thioderivatives, and the effects of inhibitors and activators on S-NAD or S-NADP kinetics were qualitatively the same as those found for NAD or NADP, respectively.	NAD	10-15	glutamate dehydrogenase 1, mitochondrial	Bos taurus	64-67
7173489-4	1982	S-NAD and S-NADP were found to be good alternate substrates for GDH: the apparent Km"s for the thioderivatives were similar to those of the corresponding natural coenzymes, the apparent Km"s for glutamate were unaltered by the substitution of the thioderivatives, and the effects of inhibitors and activators on S-NAD or S-NADP kinetics were qualitatively the same as those found for NAD or NADP, respectively.	NAD	2-5	glutamate dehydrogenase 1, mitochondrial	Bos taurus	64-67
7173489-9	1982	Activators and inhibitors of the GDH reaction also showed differential effects upon the NAD vs NADP linked reaction rates in the dual wavelength assay.	NAD	88-91	glutamate dehydrogenase 1, mitochondrial	Bos taurus	33-36
7131097-5	1982	As kynurenine 3-hydroxylase is reported to be a rate-limiting enzyme in the tryptophan-NAD pathway in rats, branched chain amino acids, branched chain alpha-keto acids and several other keto acids were tested for their effects on kynurenine 3-hydroxylase activity in the mitochondrial outer membrane fraction prepared from rat liver.	NAD	87-90	kynurenine 3-monooxygenase	Rattus norvegicus	3-27
6952874-0	1981	Effect of NADH on hypoxanthine hydroxylation by native NAD+-dependent xanthine oxidoreductase of rat liver, and the possible biological role of this effect.	NAD	10-14	xanthine dehydrogenase	Rattus norvegicus	70-93
6952874-0	1981	Effect of NADH on hypoxanthine hydroxylation by native NAD+-dependent xanthine oxidoreductase of rat liver, and the possible biological role of this effect.	NAD	55-59	xanthine dehydrogenase	Rattus norvegicus	70-93
6952874-1	1981	The course of the reaction sequence hypoxanthine leads to xanthine leads to uric acid, catalysed by the NAD+-dependent activity of xanthine oxidoreductase, was investigated under conditions either of immediate oxidation of the NADH formed or of NADH accumulation.	NAD	104-108	xanthine dehydrogenase	Rattus norvegicus	131-154
6952874-1	1981	The course of the reaction sequence hypoxanthine leads to xanthine leads to uric acid, catalysed by the NAD+-dependent activity of xanthine oxidoreductase, was investigated under conditions either of immediate oxidation of the NADH formed or of NADH accumulation.	NAD	227-231	xanthine dehydrogenase	Rattus norvegicus	131-154
6952874-1	1981	The course of the reaction sequence hypoxanthine leads to xanthine leads to uric acid, catalysed by the NAD+-dependent activity of xanthine oxidoreductase, was investigated under conditions either of immediate oxidation of the NADH formed or of NADH accumulation.	NAD	245-249	xanthine dehydrogenase	Rattus norvegicus	131-154
6952874-2	1981	The enzymic preparation was obtained from rat liver, and purified 75-fold (as compared with the 25000 g supernatant) on a 5"-AMP-Sepharose 4B column; in this preparation the NAD+-dependent activity accounted for 100% of total xanthine oxidoreductase activity.	NAD	174-178	xanthine dehydrogenase	Rattus norvegicus	226-249
6952874-6	1981	The inhibition of the Xanthine oxidoreductase NAD+-dependent activity by NADH is discussed as a possible factor in the regulation of IMP biosynthesis by the "de novo" pathway or (from unchanged hypoxanthine) by ther salvage pathway.	NAD	46-50	xanthine dehydrogenase	Rattus norvegicus	22-45
6952874-6	1981	The inhibition of the Xanthine oxidoreductase NAD+-dependent activity by NADH is discussed as a possible factor in the regulation of IMP biosynthesis by the "de novo" pathway or (from unchanged hypoxanthine) by ther salvage pathway.	NAD	73-77	xanthine dehydrogenase	Rattus norvegicus	22-45
7464825-1	1980	NADH inhibition of bovine kidney alpha-ketoglutarate dehydrogenase complex was compared at 10 microM free Ca2+ or in the absence of Ca2+ (i.e., less than 1.0 nM free Ca2+).	NAD	0-4	oxoglutarate dehydrogenase	Bos taurus	33-66
7464825-6	1980	This indicates that the overall reaction catalyzed by the alpha-ketoglutarate dehydrogenase complex is required to elicit the effect of Ca2+ on NADH inhibition.	NAD	144-148	oxoglutarate dehydrogenase	Bos taurus	58-91
7464825-7	1980	At a fixed alpha-ketoglutarate concentration (50 microM), removal of Ca2+ reduced the activity of the alpha-ketoglutarate dehydrogenase complex by 8.5-fold (due to an increase in S0.5 for alpha-ketoglutarate) and, in the presence of different NADH:NAD+ ratios, decreased the activity of the complex by 50 to 100-fold.	NAD	243-247	oxoglutarate dehydrogenase	Bos taurus	102-135
7464825-7	1980	At a fixed alpha-ketoglutarate concentration (50 microM), removal of Ca2+ reduced the activity of the alpha-ketoglutarate dehydrogenase complex by 8.5-fold (due to an increase in S0.5 for alpha-ketoglutarate) and, in the presence of different NADH:NAD+ ratios, decreased the activity of the complex by 50 to 100-fold.	NAD	248-252	oxoglutarate dehydrogenase	Bos taurus	102-135
6157422-2	1980	All four Nad-binding domains of the tetrameric apoglyceraldehyde-phosphate dehydrogenase (D-glyceraldehyde 3-phosphate:NAD+ oxidoreductase (phosphorylating), EC 1.2.1.12) displayed identical affinities (Kd = 4.8 x 10(-5) M) towards the chromophore of Blue Dextran.	NAD	9-12	hydroxysteroid 17-beta dehydrogenase 6	Homo sapiens	124-138
7390994-0	1980	NADH- and NADPH-dependent reconstituted p-nitroanisole O-demethylation system containing cytochrome P-450 with high affinity for cytochrome b5.	NAD	0-4	cytochrome P-450	Oryctolagus cuniculus	89-105
15462070-8	1980	These results suggest that the breakdown of NAD occurs in human skin via ADPR to AMP and ribose-5"-phosphate by sequential action of NADase and ADPR-PPase.	NAD	44-47	nudix hydrolase 9	Homo sapiens	144-154
500014-2	1979	In binding experiments on Blue Sepharose CL-6B (an affinity gel for nucleotide-specific enzymes) it is observed that ATP citrate lyase recognizes ATP and CoA as well as ADP, 3"-AMP, and NADP, but not 5"-AMP, NAD, or adenosine.	NAD	186-189	ATP citrate lyase	Rattus norvegicus	117-134
292645-3	1979	The pellet also possesses NADH-cytochrome c reductase activity which is inhibited by anti-cytochrome b5 gamma-globulin, indicating the presence of cytochrome b5 reductase.	NAD	26-30	cytochrome b5 type A (microsomal)	Mus musculus	90-103
507807-0	1979	Purification of lipoamide dehydrogenase from Ascaris muscle mitochondria and its relationship to NADH:NAD+ transhydrogenase activity.	NAD	97-101	dihydrolipoamide dehydrogenase	Homo sapiens	16-39
221463-2	1979	The phenylalanine-dependent, phenylalanine hydroxylase-catalyzed reaction in the presence of the pyrimidine is largely, but not completely, uncoupled; the ratio of DPNH oxidized to tyrosine formed is about 20 to 1.	NAD	164-168	phenylalanine hydroxylase	Homo sapiens	29-54
232638-0	1979	Xanthine oxidoreductase inhibition by NADH as a regulatory factor of purine metabolism.	NAD	38-42	xanthine dehydrogenase	Homo sapiens	0-23
738913-4	1978	Generally, a high diffusion rate of reduced electron carriers (PMS and MB) from the section into the incubation medium (PVA) leads to a loss of reduction equivalents, particularly in the demonstration of NAD- or NADP-dependent dehydrogenases (LDH, G-6-PDH) with lower TNBT concentrations.	NAD	204-207	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	248-255
207876-1	1978	Organic pyrophosphates such as UppA and NAD are formed when a solution containing a nucleotide, a nucleoside 5"-polyphosphate, Mg2+ and imidazole are allowed to dry out.	NAD	40-43	mucin 7, secreted	Homo sapiens	127-130
13132-1	1977	The NADH-dependent stearoyl CoA desaturase of hepatic microsomes (EC 1.14.99.5) is an enzyme system consisting of cytochrome b5 reductase (EC 1.6.2.2), cytochrome b5, and the terminal desaturase.	NAD	4-8	cytochrome b5 type A	Gallus gallus	114-127
13132-1	1977	The NADH-dependent stearoyl CoA desaturase of hepatic microsomes (EC 1.14.99.5) is an enzyme system consisting of cytochrome b5 reductase (EC 1.6.2.2), cytochrome b5, and the terminal desaturase.	NAD	4-8	cytochrome b5 type A	Gallus gallus	152-165
16659756-9	1976	Under the latter condition, in vitro NR activity was appreciable (19 mumol NO(2) (-) [g fresh weight, hr](-1)) suggesting that enzyme level per se was not the limiting factor and that reductant energy might be limiting.The addition of NADH to the in vivo NR assay medium did not stimulate NR activity, although it was not established that NADH entered the tissue.	NAD	235-239	inducible nitrate reductase [NADH] 1	Glycine max	37-39
16659756-9	1976	Under the latter condition, in vitro NR activity was appreciable (19 mumol NO(2) (-) [g fresh weight, hr](-1)) suggesting that enzyme level per se was not the limiting factor and that reductant energy might be limiting.The addition of NADH to the in vivo NR assay medium did not stimulate NR activity, although it was not established that NADH entered the tissue.	NAD	339-343	inducible nitrate reductase [NADH] 1	Glycine max	37-39
3527172-7	1986	These results suggest that the essential thiol of BDH is located at its nucleotide-binding site, and agree with our previous observation that NAD and NADH protect BDH against inhibition by thiol modifiers.	NAD	142-145	3-hydroxybutyrate dehydrogenase 1	Bos taurus	50-53
259500-5	1978	A stereospecific assay was used to measure D-lactate in human plasma; it involved the spectrophotometric analysis of NADH at 340 nm catalysed by D-lactate dehydrogenase (D-lactate:NAD+ oxidoreductase; EC 1.1.1.28) from Lactobacillus leichmannii.	NAD	117-121	hydroxysteroid 17-beta dehydrogenase 6	Homo sapiens	185-199
3527172-7	1986	These results suggest that the essential thiol of BDH is located at its nucleotide-binding site, and agree with our previous observation that NAD and NADH protect BDH against inhibition by thiol modifiers.	NAD	142-145	3-hydroxybutyrate dehydrogenase 1	Bos taurus	163-166
3527172-7	1986	These results suggest that the essential thiol of BDH is located at its nucleotide-binding site, and agree with our previous observation that NAD and NADH protect BDH against inhibition by thiol modifiers.	NAD	150-154	3-hydroxybutyrate dehydrogenase 1	Bos taurus	50-53
3527172-7	1986	These results suggest that the essential thiol of BDH is located at its nucleotide-binding site, and agree with our previous observation that NAD and NADH protect BDH against inhibition by thiol modifiers.	NAD	150-154	3-hydroxybutyrate dehydrogenase 1	Bos taurus	163-166
3954355-1	1986	A NAD-dependent 15-hydroxyprostaglandin dehydrogenase (PGDH) was purified to a specific activity of over 25,000 nmol NADH formed/min/mg protein with 50 microM prostaglandin E1 as substrate from the lungs of 28-day-old pregnant rabbits.	NAD	2-5	carbonyl reductase [NADPH] 1	Oryctolagus cuniculus	16-53
334589-1	1977	The pancreatic islets show a remarkably high activity of L-3-hydroxy-acyl CoA dehydrogenase, an enzyme which operates in the fatty acid cycle by catalyzing the NAD+ oxidation of some of the degradation products.	NAD	160-164	enoyl-CoA hydratase and 3-hydroxyacyl CoA dehydrogenase	Homo sapiens	57-91
3954355-1	1986	A NAD-dependent 15-hydroxyprostaglandin dehydrogenase (PGDH) was purified to a specific activity of over 25,000 nmol NADH formed/min/mg protein with 50 microM prostaglandin E1 as substrate from the lungs of 28-day-old pregnant rabbits.	NAD	117-121	carbonyl reductase [NADPH] 1	Oryctolagus cuniculus	16-53
196615-17	1977	The inverse relationship between protein level in the diet and liver quinolinate phosphoribosyltransferase activity, the rate-limiting enzyme of the tryptophan-NAD pathway suggests that the efficiency of conversion of tryptophan to NAD is related to protein level in the diet, the efficiency decreasing with an increase in the level of dietary protein.	NAD	160-163	quinolinate phosphoribosyltransferase	Rattus norvegicus	69-106
3003181-2	1986	Objectives of this study were first, to determine if liver cancers in vinyl chloride-treated rats also expressed this AlDH phenotype, and second, to quantitate the NAD- and NADP-dependent AlDH activity for the substrates Bz and acetaldehyde (Ac) in the cancers and surrounding tissue.	NAD	164-167	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	188-192
196615-17	1977	The inverse relationship between protein level in the diet and liver quinolinate phosphoribosyltransferase activity, the rate-limiting enzyme of the tryptophan-NAD pathway suggests that the efficiency of conversion of tryptophan to NAD is related to protein level in the diet, the efficiency decreasing with an increase in the level of dietary protein.	NAD	232-235	quinolinate phosphoribosyltransferase	Rattus norvegicus	69-106
20083-0	1977	The involvement of cytochrome P-450 in the NADH-dependent O-demethylation of p-nitroanisole in phenobarbital-treated rabbit liver microsomes.	NAD	43-47	cytochrome P-450	Oryctolagus cuniculus	19-35
4074780-5	1985	In parallel, with a rise in pH the steady-state concentration of the oxy-complex of cytochrome P-450 increases, while the synergism of NADPH and NADH action in the H2O2 formation reaction is replaced by competition.	NAD	145-149	cytochrome P-450	Oryctolagus cuniculus	84-100
16659756-12	1976	Increased NR activities from the various additives were attributed to production of NADH.	NAD	84-88	inducible nitrate reductase [NADH] 1	Glycine max	10-12
3834063-4	1985	In the system containing MV or FAD, other one-electron reducing flavoenzymes such as nicotinamide adenine dinucleotide (reduced form) (NADH) dehydrogenase, lipoamide dehydrogenase and glutathione reductase with an appropriate electron donor, could replace XO.	NAD	85-118	glutathione-disulfide reductase	Homo sapiens	184-205
6467-10	1976	464-472; Elsevier Scientific Publishing Co., Amsterdam) that the role of NAD+ in the NADH-lipoamide reductase reaction catalyzed by lipoamide dehydrogenase is to prevent accumulation of inactive 4-electron reduced enzyme by simple reversal of the reduction of 2-electron reduced enzyme by NADH.	NAD	73-77	dihydrolipoamide dehydrogenase	Sus scrofa	132-155
6467-10	1976	464-472; Elsevier Scientific Publishing Co., Amsterdam) that the role of NAD+ in the NADH-lipoamide reductase reaction catalyzed by lipoamide dehydrogenase is to prevent accumulation of inactive 4-electron reduced enzyme by simple reversal of the reduction of 2-electron reduced enzyme by NADH.	NAD	85-89	dihydrolipoamide dehydrogenase	Sus scrofa	132-155
945314-3	1976	Follicular 3-PGDH was characterized using a sensitive fluorometric assay with NADH as a co-substrate.	NAD	78-82	phosphoglycerate dehydrogenase	Homo sapiens	11-17
3000462-5	1985	Cytochrome c stimulated the increase of NADH oxidation in mitochondria of normal and ischemic myocardium by the factors of 3.5 and 3.4, respectively.	NAD	40-44	cytochrome c	Oryctolagus cuniculus	0-12
176939-0	1976	Purification and properties of the NAD+-dependent (type D) and O2-dependent (type O) forms of rat liver xanthine dehydrogenase.	NAD	35-39	xanthine dehydrogenase	Rattus norvegicus	104-126
176940-0	1976	The mechanism of conversion of rat liver xanthine dehydrogenase from an NAD+-dependent form (type D) to an O2-dependent form (type O).	NAD	72-76	xanthine dehydrogenase	Rattus norvegicus	41-63
4073474-4	1985	In cat brain, the resulting underestimation of the MAO activity was prevented by the addition of nicotinamide adenine dinucleotide (10(-3) M) in the incubation medium or by allowing a 2-h period between the end of incubation and the LIEC extraction procedure.	NAD	97-130	monoamine oxidase A	Rattus norvegicus	51-54
187502-0	1976	Turkey liver xanthine dehydrogenase: effects of methanol on the enzyme-catalysed oxidation of reduced nicotinamide-adenine dinucleotide.	NAD	102-135	xanthine dehydrogenase/oxidase	Meleagris gallopavo	13-35
2981281-2	1985	Pretreatment of membranes with islet-activating protein (IAP) in the presence of NAD caused an increase in IC50 and nH values for clonidine compared with control membranes in the absence of GTP, the addition of which was without effect.	NAD	81-84	Cd47 molecule	Rattus norvegicus	31-55
1023336-9	1976	Under our experimental conditions, UDP-glucose 4"-epimerase present in the cells epimerizes UDP-galactose (added in the incubation mixture) to UDP-glucose which can bo oxidized by the excess of UDP-glucose dehydrogenase to UDP-glucuronic acid with a consequent NADH formation.	NAD	261-265	UDP-galactose-4-epimerase	Homo sapiens	35-59
1023336-9	1976	Under our experimental conditions, UDP-glucose 4"-epimerase present in the cells epimerizes UDP-galactose (added in the incubation mixture) to UDP-glucose which can bo oxidized by the excess of UDP-glucose dehydrogenase to UDP-glucuronic acid with a consequent NADH formation.	NAD	261-265	UDP-glucose 6-dehydrogenase	Homo sapiens	194-219
240770-9	1975	Both NADH and NADPH inhibited glucose dehydrogenase when the corresponding oxidized coenzymes were used (Ki values: 8.0 x 10(-5)M by NADH and 9.1 x 10(-5)M by NADPH), while only NADPH inhibited cytoplasmic glucose 6-phosphate dehydrogenase (Ki: 2.4 x 10(-5)M).	NAD	5-9	glucose-6-phosphate dehydrogenase	Rattus norvegicus	206-239
11093-12	1976	Uteroglobin incubated in the presence or absence of cofactors (NADH and NADPH) with or without dithiothreitol did not metabolize progesterone.	NAD	63-67	uteroglobin	Oryctolagus cuniculus	0-11
8143-7	1976	It was concluded from the results of purification, electrofocusing and inhibition studies that glutathione reductase is a single enzyme which used both NADPH and NADH as hydrogen donors.	NAD	162-166	glutathione-disulfide reductase	Homo sapiens	95-116
2981281-2	1985	Pretreatment of membranes with islet-activating protein (IAP) in the presence of NAD caused an increase in IC50 and nH values for clonidine compared with control membranes in the absence of GTP, the addition of which was without effect.	NAD	81-84	Cd47 molecule	Rattus norvegicus	57-60
2985983-3	1985	The normally latent glycerophosphate dehydrogenase (NAD+ linked), it is proposed, is an intraglycosomal enzyme having no membrane association, but bound to the core by weak ionic linkages.	NAD	52-56	glycerol-3-phosphate dehydrogenase 1	Homo sapiens	20-50
185137-1	1976	The stereochemistry of the hydrogen transfer to NAD catalyzed by ribitol dehydrogenase (ribitol:NAD 2-oxidoreductase, EC 1.1.1.56) from Klebsiella pneumoniae and D-mannitol-1-phosphate dehydrogenase (D-mannitol-1-phosphate:NAD 2-oxidoreductase, EC 1.1.1.17) from Escherichia coli was investigated.	NAD	48-51	hydroxysteroid 17-beta dehydrogenase 6	Homo sapiens	102-116
185137-1	1976	The stereochemistry of the hydrogen transfer to NAD catalyzed by ribitol dehydrogenase (ribitol:NAD 2-oxidoreductase, EC 1.1.1.56) from Klebsiella pneumoniae and D-mannitol-1-phosphate dehydrogenase (D-mannitol-1-phosphate:NAD 2-oxidoreductase, EC 1.1.1.17) from Escherichia coli was investigated.	NAD	48-51	hydroxysteroid 17-beta dehydrogenase 6	Homo sapiens	229-243
3893464-3	1985	beta 2 beta 2-Bern has a higher specific activity and a lower pH-optimum, has a higher kM for NAD+, is less susceptible to inactivation by iodoacetate, and cannot be activated with chloride ions.	NAD	94-98	potassium calcium-activated channel subfamily M regulatory beta subunit 2	Homo sapiens	0-6
962863-2	1976	The turkey liver xanthine dehydrogenase-catalysed oxidation of NADH by Methylene Blue, by ferricyanide or by O2 is not dependent on the integrity of the active-centre persulphide groups.	NAD	63-67	xanthine dehydrogenase/oxidase	Meleagris gallopavo	17-39
173299-1	1975	Citrate synthase from two typical facultative methylotrophs, but not from four obligate methylotrophs or from two restricted facultative methylotrophs, is inhibited by 0.1 mM-NADH.	NAD	175-179	citrate synthase	Homo sapiens	0-16
3893464-3	1985	beta 2 beta 2-Bern has a higher specific activity and a lower pH-optimum, has a higher kM for NAD+, is less susceptible to inactivation by iodoacetate, and cannot be activated with chloride ions.	NAD	94-98	potassium calcium-activated channel subfamily M regulatory beta subunit 2	Homo sapiens	7-13
235382-4	1975	Erythrocyte and plasma NADH-GR and NADPH-GR activities in 100 healthy blood donors, and 85 cord blood samples and plasma NADH-GR and NADPH-GR levels in patients with various disease conditions are given.	NAD	23-27	glutathione-disulfide reductase	Homo sapiens	28-30
185674-2	1976	An obvious difference between the changes in NAD+ and NADH in the various models of hypertension, was established: Thus in NaC1 hypertension a high level of the coenzymes in the kidneys and in the vessel wall was found, while the liver coenzyme content was in normal ranges.	NAD	45-49	nucleus accumbens associated 1	Rattus norvegicus	123-127
185674-2	1976	An obvious difference between the changes in NAD+ and NADH in the various models of hypertension, was established: Thus in NaC1 hypertension a high level of the coenzymes in the kidneys and in the vessel wall was found, while the liver coenzyme content was in normal ranges.	NAD	54-58	nucleus accumbens associated 1	Rattus norvegicus	123-127
3893464-7	1985	This exchange, which is identical to that reported for the beta 2-Oriental chain, alters the binding of the pyrophosphate group of the coenzyme NAD(H), and also that of iodoacetate, thus explaining the observed differences between beta 2 beta 2-Bern and beta 1 beta 1.	NAD	144-150	potassium calcium-activated channel subfamily M regulatory beta subunit 2	Homo sapiens	59-65
3893464-7	1985	This exchange, which is identical to that reported for the beta 2-Oriental chain, alters the binding of the pyrophosphate group of the coenzyme NAD(H), and also that of iodoacetate, thus explaining the observed differences between beta 2 beta 2-Bern and beta 1 beta 1.	NAD	144-150	potassium calcium-activated channel subfamily M regulatory beta subunit 2	Homo sapiens	231-237
3893464-7	1985	This exchange, which is identical to that reported for the beta 2-Oriental chain, alters the binding of the pyrophosphate group of the coenzyme NAD(H), and also that of iodoacetate, thus explaining the observed differences between beta 2 beta 2-Bern and beta 1 beta 1.	NAD	144-150	potassium calcium-activated channel subfamily M regulatory beta subunit 2	Homo sapiens	231-237
4370440-0	1974	The clinical-chemical application of the NADH test for the determination of diamine oxidase activity in human pregnancy.	NAD	41-45	amine oxidase copper containing 1	Homo sapiens	76-91
3966800-2	1985	Measurements of oxygen consumption revealed that the electron transport system was capable of reoxidizing ALDH-generated NADH much faster than it was produced and hence was not rate-limiting for aldehyde metabolism.	NAD	121-125	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	106-110
16658848-0	1974	Specificity for nicotinamide adenine dinucleotide by nitrate reductase from leaves.	NAD	16-49	chalcone reductase CHR1	Glycine max	61-70
16658848-1	1974	Preliminary work revealed that nitrate reductase in crude extracts prepared from leaves of certain corn genotypes as well as soybeans could utilize NADPH as well as NADH as the electron donor.	NAD	165-169	chalcone reductase CHR1	Glycine max	39-48
236788-3	1975	Cytochrome P-450-dependent mixed function oxidases in the membranes comprised both an NADPH-dependent system and an NADH-dependent system.	NAD	116-120	cytochrome P-450	Oryctolagus cuniculus	0-16
164204-9	1975	One major difference in the binding behavior of NAD+ and epsilonNAD+ seems to be present in the muscle glyceraldehyde-3-phosphate dehydrogenase.	NAD	48-52	glyceraldehyde-3-phosphate dehydrogenase	Equus caballus	103-143
3885259-6	1985	Km and Ki values for NAD are 7.4 and 90 microM for beta 1 beta 1, 180 and 340 microM for beta 2 beta 2 and 490 and 1300 microM for beta Ind beta Ind.	NAD	21-24	potassium calcium-activated channel subfamily M regulatory beta subunit 2	Homo sapiens	89-95
237890-0	1975	Kinetic study by pulse radiolysis of the lactate dehydrogenase-catalyzed chain oxidation of nicotinamide adenine dinucleotide by HO2 and O2-RADICALS.	NAD	92-125	heme oxygenase 2	Homo sapiens	129-132
237890-1	1975	The lactate dehydrogenase-catalyzed chain oxidation of NADH (LDH-NADH) by the superoxide radicals, HO2 and O2, has been studied with pulse radiolysis in the pH range between 4.5 and 9.0.	NAD	55-59	heme oxygenase 2	Homo sapiens	99-102
237890-1	1975	The lactate dehydrogenase-catalyzed chain oxidation of NADH (LDH-NADH) by the superoxide radicals, HO2 and O2, has been studied with pulse radiolysis in the pH range between 4.5 and 9.0.	NAD	65-69	heme oxygenase 2	Homo sapiens	99-102
237890-2	1975	The rate constants for the oxidation of the LDH-NADH by HO2 and O2 determined at 23 degrees are 1.2 times 10-6 M(-1) s(-1) and 3.6 times 10-4 M(-1) s(-1), respectively.	NAD	48-52	heme oxygenase 2	Homo sapiens	56-59
4361531-0	1973	Comparison of the 14-C-putrescine assay with the NADH test for the determination of diamine oxidase: description of a standard procedure with a high precision and an improved accuracy.	NAD	49-53	amine oxidase copper containing 1	Homo sapiens	84-99
4349663-9	1973	Results suggest that ethanol inhibited alpha-ketoglutarate dehydrogenase in the mitochondria of hepatocytes by elevating the mitochondrial NADH:NAD ratio.	NAD	139-143	oxoglutarate dehydrogenase	Rattus norvegicus	39-72
4349663-9	1973	Results suggest that ethanol inhibited alpha-ketoglutarate dehydrogenase in the mitochondria of hepatocytes by elevating the mitochondrial NADH:NAD ratio.	NAD	139-142	oxoglutarate dehydrogenase	Rattus norvegicus	39-72
4114435-3	1972	Thus, in a single coupled system neuraminidase releases N-acetylneuraminic acid, which is cleaved to N-acetyl-D-mannosamine and pyruvic acid; finally, pyruvate is reduced to lactate as reduced nicotinamide adenine dinucleotide is oxidized.	NAD	193-226	neuraminidase 1	Homo sapiens	33-46
3885259-6	1985	Km and Ki values for NAD are 7.4 and 90 microM for beta 1 beta 1, 180 and 340 microM for beta 2 beta 2 and 490 and 1300 microM for beta Ind beta Ind.	NAD	21-24	potassium calcium-activated channel subfamily M regulatory beta subunit 2	Homo sapiens	96-102
6091764-1	1984	Two spin-labeled analogues of NAD+ were synthesized with an 15N and perdeuterated nitroxide radical, 4-amino-2,2,6,6-[2H17, 15N]tetramethylpiperidone-1-oxyl, which was attached to either the C-6 or C-8 position of the purine ring.	NAD	30-34	complement C6	Homo sapiens	191-194
4391601-0	1969	NAD-dependent cytochrome b5 reduction in liver microsomes of mice.	NAD	0-3	cytochrome b5 type A (microsomal)	Mus musculus	14-27
16658412-5	1973	On the assumption of a drop in NAD/NADH ratio, as found by other workers in wheat leaves, the reverse crossover between triose phosphates and 3-phospholglycerate was attributed to inhibition of glyceraldehyde 3-phosphate dehydrogenase.	NAD	31-34	glyceraldehyde-3-phosphate dehydrogenase 1, cytosolic	Triticum aestivum	194-234
16658412-5	1973	On the assumption of a drop in NAD/NADH ratio, as found by other workers in wheat leaves, the reverse crossover between triose phosphates and 3-phospholglycerate was attributed to inhibition of glyceraldehyde 3-phosphate dehydrogenase.	NAD	35-39	glyceraldehyde-3-phosphate dehydrogenase 1, cytosolic	Triticum aestivum	194-234
6091764-1	1984	Two spin-labeled analogues of NAD+ were synthesized with an 15N and perdeuterated nitroxide radical, 4-amino-2,2,6,6-[2H17, 15N]tetramethylpiperidone-1-oxyl, which was attached to either the C-6 or C-8 position of the purine ring.	NAD	30-34	homeobox C8	Homo sapiens	198-201
6091764-4	1984	The enhanced spectral resolution obtained with (2H17, 15N)spin-labeled-NAD+ analogues has facilitated simulation of the EPR lineshape of the nucleotide bound to lactate dehydrogenase (L-lactate:NAD+ oxidoreductase, EC 1.1.1.27).	NAD	71-75	hydroxysteroid 17-beta dehydrogenase 6	Homo sapiens	199-213
6091764-7	1984	By contrast, the spin label on the membrane-bound enzyme, D-beta-hydroxybutyrate dehydrogenase (D-beta-hydroxybutyrate:NAD+ oxidoreductase, EC 1.1.1.30), is completely immobilized and exhibits two distinct spectral components for spin-labeled NAD+, which appear to differ in the polarity of the environment of the nitroxide.	NAD	119-123	hydroxysteroid 17-beta dehydrogenase 6	Homo sapiens	124-138
21488412-2	1972	Fe3+ is reduced to Fez+ by NADH formed when lactate is oxidized to pyruvate.	NAD	27-31	FEZ family zinc finger 1	Homo sapiens	19-22
5379109-7	1969	Still a third pathway for NADH oxidation is dependent on the addition of cytochrome c and is insensitive to antimycin A.	NAD	26-30	cytochrome c	Zea mays	73-85
16663876-5	1984	In roots, ammonium and glutamine produced an increase in GDH-NADH activity whereas the same metabolites were inhibitory of this activity in leaves.	NAD	61-65	glutamic dehydrogenase1	Zea mays	57-60
4388687-7	1968	The enzyme is a dehydrogenase, unable to utilize oxygen, NAD, NADP, flavines or menadione as electron acceptors, but able to utilize phenazine methosulphate, ferricyanide, cytochrome c or brilliant cresyl blue.	NAD	57-60	MEXAM1_RS21720	Methylobacterium extorquens AM1	16-29
13996531-0	1963	A new NAD-dependent spectral species of lipoamide dehydrogenase.	NAD	6-9	dihydrolipoamide dehydrogenase	Homo sapiens	40-63
6329192-0	1984	NAD: guanidino group specific mono ADP-ribosyltransferase activity in skeletal muscle.	NAD	0-3	ecto-ADP-ribosyltransferase 3	Oryctolagus cuniculus	30-57
33888598-2	2021	Mitochondrial NADP(H) production depends on the phosphorylation of NAD(H) by NAD kinase 2 (NADK2).	NAD	67-73	NAD kinase 2, mitochondrial	Homo sapiens	77-89
33888598-2	2021	Mitochondrial NADP(H) production depends on the phosphorylation of NAD(H) by NAD kinase 2 (NADK2).	NAD	67-73	NAD kinase 2, mitochondrial	Homo sapiens	91-96
4381999-7	1966	The 3-alpha-hydroxysteroid dehydrogenase involved functioned with either NADH or NADPH as hydrogen donor.	NAD	73-77	aldo-keto reductase family 1 member C3	Homo sapiens	4-40
4380255-0	1966	[NADPH- and NADH-specific glutathione reductase (GSSGR) activity in the serum and muscles of patients with muscular dystrophy (Erb)].	NAD	12-16	estrogen receptor 2	Homo sapiens	127-130
6374651-5	1984	The histidine/arginine-47 mutational replacement corresponds to a position that binds the pyrophosphate group of the coenzyme NAD(H); this explains the functional differences between the beta 1 beta 1 and beta 2 beta 2 isozymes, including both a lower pH optimum and higher turnover number of beta 2 beta 2, which is likely to be the mutant form.	NAD	126-132	potassium calcium-activated channel subfamily M regulatory beta subunit 2	Homo sapiens	205-211
14333553-9	1965	Growth hormone increased the concentrations and total amounts of NAD(+) and NADH but significantly decreased the concentrations and total amounts of NADP(+) and NADPH.	NAD	65-71	gonadotropin releasing hormone receptor	Rattus norvegicus	0-14
14333553-9	1965	Growth hormone increased the concentrations and total amounts of NAD(+) and NADH but significantly decreased the concentrations and total amounts of NADP(+) and NADPH.	NAD	76-80	gonadotropin releasing hormone receptor	Rattus norvegicus	0-14
34054807-7	2021	The production of lactate and NAD+/NADH ratio were elevated 5 days after BAFF priming.	NAD	30-34	tumor necrosis factor (ligand) superfamily, member 13b	Mus musculus	73-77
34054807-7	2021	The production of lactate and NAD+/NADH ratio were elevated 5 days after BAFF priming.	NAD	35-39	tumor necrosis factor (ligand) superfamily, member 13b	Mus musculus	73-77
6374651-5	1984	The histidine/arginine-47 mutational replacement corresponds to a position that binds the pyrophosphate group of the coenzyme NAD(H); this explains the functional differences between the beta 1 beta 1 and beta 2 beta 2 isozymes, including both a lower pH optimum and higher turnover number of beta 2 beta 2, which is likely to be the mutant form.	NAD	126-132	potassium calcium-activated channel subfamily M regulatory beta subunit 2	Homo sapiens	212-218
33982328-0	2021	TFB2M activates aerobic glycolysis in hepatocellular carcinoma cells through the NAD+ /SIRT3/HIF-1alpha signaling.	NAD	81-85	transcription factor B2, mitochondrial	Homo sapiens	0-5
33982328-9	2021	Mechanistically, TFB2M regulates the up-regulation of glycolytic genes and down-regulation of PGC-1alpha mainly through NAD+ /SIRT3/HIF-1alpha signaling.	NAD	120-124	transcription factor B2, mitochondrial	Homo sapiens	17-22
33976173-3	2021	Here, we identify NAMPT, the rate limiting enzyme in NAD salvage synthesis, as a target of STAT1 during cellular activation by interferon gamma, an important driver of macrophage polarization and antitumor responses.	NAD	53-56	nicotinamide phosphoribosyltransferase	Homo sapiens	18-23
33862368-7	2021	Increase in expression levels of proteins related to oxidative phosphorylation such as NADH:ubiquinone oxidoreductase core subunit V1 (Ndufv1) was observed in LXRbeta-knockdown Dami cells.	NAD	87-91	nuclear receptor subfamily 1 group H member 3	Homo sapiens	159-166
6374651-5	1984	The histidine/arginine-47 mutational replacement corresponds to a position that binds the pyrophosphate group of the coenzyme NAD(H); this explains the functional differences between the beta 1 beta 1 and beta 2 beta 2 isozymes, including both a lower pH optimum and higher turnover number of beta 2 beta 2, which is likely to be the mutant form.	NAD	126-132	potassium calcium-activated channel subfamily M regulatory beta subunit 2	Homo sapiens	212-218
6374651-5	1984	The histidine/arginine-47 mutational replacement corresponds to a position that binds the pyrophosphate group of the coenzyme NAD(H); this explains the functional differences between the beta 1 beta 1 and beta 2 beta 2 isozymes, including both a lower pH optimum and higher turnover number of beta 2 beta 2, which is likely to be the mutant form.	NAD	126-132	potassium calcium-activated channel subfamily M regulatory beta subunit 2	Homo sapiens	212-218
6425280-5	1984	Maximum stimulation was dependent on the concentration of NAD+ used in the assay; an increase in Km value of NAD+ was observed to parallel the increase in maximal velocity with increasing Mg2+ concentration, indicating that alterations in the catalytic properties of the E2 isozyme occur in the presence of Mg2+.	NAD	58-62	mucin 7, secreted	Homo sapiens	188-191
33675899-13	2021	SIGNIFICANCE: NMN could attenuate cardiac fibrosis in vivo and fibroblast activation in vitro by suppressing oxidative stress and Smad3 acetylation in a NAD+/SIRT1-dependent manner.	NAD	153-157	SMAD family member 3	Mus musculus	130-135
33957971-0	2021	MiR-34a suppression targets Nampt to ameliorate bone marrow mesenchymal stem cell senescence by regulating NAD+-Sirt1 pathway.	NAD	107-111	microRNA 34a	Homo sapiens	0-7
33957971-0	2021	MiR-34a suppression targets Nampt to ameliorate bone marrow mesenchymal stem cell senescence by regulating NAD+-Sirt1 pathway.	NAD	107-111	nicotinamide phosphoribosyltransferase	Homo sapiens	28-33
33957971-7	2021	The underlying regulatory mechanism of miR-34a targeting Nampt in MSC senescence was further explored by measuring intracellular NAD+ content, NAD+/NADH ratio and Sirt1 activity.	NAD	129-133	microRNA 34a	Homo sapiens	39-46
33957971-7	2021	The underlying regulatory mechanism of miR-34a targeting Nampt in MSC senescence was further explored by measuring intracellular NAD+ content, NAD+/NADH ratio and Sirt1 activity.	NAD	129-133	nicotinamide phosphoribosyltransferase	Homo sapiens	57-62
33957971-7	2021	The underlying regulatory mechanism of miR-34a targeting Nampt in MSC senescence was further explored by measuring intracellular NAD+ content, NAD+/NADH ratio and Sirt1 activity.	NAD	143-147	microRNA 34a	Homo sapiens	39-46
33957971-7	2021	The underlying regulatory mechanism of miR-34a targeting Nampt in MSC senescence was further explored by measuring intracellular NAD+ content, NAD+/NADH ratio and Sirt1 activity.	NAD	143-147	nicotinamide phosphoribosyltransferase	Homo sapiens	57-62
6425280-5	1984	Maximum stimulation was dependent on the concentration of NAD+ used in the assay; an increase in Km value of NAD+ was observed to parallel the increase in maximal velocity with increasing Mg2+ concentration, indicating that alterations in the catalytic properties of the E2 isozyme occur in the presence of Mg2+.	NAD	58-62	mucin 7, secreted	Homo sapiens	307-310
33957971-7	2021	The underlying regulatory mechanism of miR-34a targeting Nampt in MSC senescence was further explored by measuring intracellular NAD+ content, NAD+/NADH ratio and Sirt1 activity.	NAD	148-152	microRNA 34a	Homo sapiens	39-46
33957971-7	2021	The underlying regulatory mechanism of miR-34a targeting Nampt in MSC senescence was further explored by measuring intracellular NAD+ content, NAD+/NADH ratio and Sirt1 activity.	NAD	148-152	nicotinamide phosphoribosyltransferase	Homo sapiens	57-62
33957971-12	2021	In addition, miR-34a repletion resulted in prominent reductions in Nampt expression levels, NAD+ content, NAD+/NADH ratio, and Sirt1 activity, whereas anti-miR-34a treatment exerted the opposite effects.	NAD	92-96	microRNA 34a	Homo sapiens	13-20
34029951-0	2021	Notoginsenoside R1 activates the NAMPT-NAD+-SIRT1 cascade to promote postischemic angiogenesis by modulating Notch signaling.	NAD	39-43	nicotinamide phosphoribosyltransferase	Homo sapiens	33-38
34029951-14	2021	The promotion of R1 on angiogenesis were associated with the NAMPT-NAD+-SIRT1 cascade and Notch/VEGFR-2 signaling pathway, which was partially eliminated by inhibitors of NAMPT and SIRT1.	NAD	67-71	nicotinamide phosphoribosyltransferase	Homo sapiens	61-66
33957971-12	2021	In addition, miR-34a repletion resulted in prominent reductions in Nampt expression levels, NAD+ content, NAD+/NADH ratio, and Sirt1 activity, whereas anti-miR-34a treatment exerted the opposite effects.	NAD	106-110	microRNA 34a	Homo sapiens	13-20
6425280-5	1984	Maximum stimulation was dependent on the concentration of NAD+ used in the assay; an increase in Km value of NAD+ was observed to parallel the increase in maximal velocity with increasing Mg2+ concentration, indicating that alterations in the catalytic properties of the E2 isozyme occur in the presence of Mg2+.	NAD	109-113	mucin 7, secreted	Homo sapiens	188-191
34029951-14	2021	The promotion of R1 on angiogenesis were associated with the NAMPT-NAD+-SIRT1 cascade and Notch/VEGFR-2 signaling pathway, which was partially eliminated by inhibitors of NAMPT and SIRT1.	NAD	67-71	nicotinamide phosphoribosyltransferase	Homo sapiens	171-176
34029951-15	2021	We demonstrated that R1 promotes post-stroke angiogenesis via activating NAMPT-NAD+-SIRT1 cascade.	NAD	79-83	nicotinamide phosphoribosyltransferase	Homo sapiens	73-78
6425280-5	1984	Maximum stimulation was dependent on the concentration of NAD+ used in the assay; an increase in Km value of NAD+ was observed to parallel the increase in maximal velocity with increasing Mg2+ concentration, indicating that alterations in the catalytic properties of the E2 isozyme occur in the presence of Mg2+.	NAD	109-113	mucin 7, secreted	Homo sapiens	307-310
33928788-12	2021	Conclusions:Nampt-mediated production of NAD+ protects against oxidative stress in part through the NADPH-dependent reducing system, thereby alleviating the development of diabetic cardiomyopathy in response to HFD consumption.	NAD	41-45	2,4-dienoyl CoA reductase 1, mitochondrial	Mus musculus	100-105
33887438-1	2021	Nicotinamide phosphoribosyltransferase (NAMPT) catalyzes the rate-limiting step of the NAD+ salvage pathway.	NAD	87-91	nicotinamide phosphoribosyltransferase	Homo sapiens	0-38
33887438-1	2021	Nicotinamide phosphoribosyltransferase (NAMPT) catalyzes the rate-limiting step of the NAD+ salvage pathway.	NAD	87-91	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
33887438-2	2021	Since NAD+ plays a pivotal role in many biological processes including metabolism and aging, activation of NAMPT is an attractive therapeutic target for treatment of diverse array of diseases.	NAD	6-10	nicotinamide phosphoribosyltransferase	Homo sapiens	107-112
33920726-4	2021	Sirtuin 6 (SIRT6) is an NAD+ dependent histone deacetylase enzyme and a unique Sirtuin family member.	NAD	24-27	sirtuin 6	Homo sapiens	0-9
33921788-1	2021	The human enzyme D-3-phosphoglycerate dehydrogenase (hPHGDH) catalyzes the reversible dehydrogenation of 3-phosphoglycerate (3PG) into 3-phosphohydroxypyruvate (PHP) using the NAD+/NADH redox cofactor, the first step in the phosphorylated pathway producing L-serine.	NAD	176-180	phosphoglycerate dehydrogenase	Homo sapiens	17-51
33921788-1	2021	The human enzyme D-3-phosphoglycerate dehydrogenase (hPHGDH) catalyzes the reversible dehydrogenation of 3-phosphoglycerate (3PG) into 3-phosphohydroxypyruvate (PHP) using the NAD+/NADH redox cofactor, the first step in the phosphorylated pathway producing L-serine.	NAD	176-180	phosphoglycerate dehydrogenase	Homo sapiens	53-59
33921788-1	2021	The human enzyme D-3-phosphoglycerate dehydrogenase (hPHGDH) catalyzes the reversible dehydrogenation of 3-phosphoglycerate (3PG) into 3-phosphohydroxypyruvate (PHP) using the NAD+/NADH redox cofactor, the first step in the phosphorylated pathway producing L-serine.	NAD	181-185	phosphoglycerate dehydrogenase	Homo sapiens	17-51
33921788-1	2021	The human enzyme D-3-phosphoglycerate dehydrogenase (hPHGDH) catalyzes the reversible dehydrogenation of 3-phosphoglycerate (3PG) into 3-phosphohydroxypyruvate (PHP) using the NAD+/NADH redox cofactor, the first step in the phosphorylated pathway producing L-serine.	NAD	181-185	phosphoglycerate dehydrogenase	Homo sapiens	53-59
33912035-8	2021	Consequently, dezocine treatment inhibited NAMPT enzyme activity, resulting in cellular NAD abolishment.	NAD	88-91	nicotinamide phosphoribosyltransferase	Homo sapiens	43-48
33831359-0	2021	An NAD+/NMN balancing act by SARM1 and NMNAT2 controls axonal degeneration.	NAD	3-7	sterile alpha and TIR motif containing 1	Homo sapiens	29-34
33831359-3	2021	(2021) reveal a key regulatory mechanism that controls SARM1"s enzymatic activity, providing insight into how NAD+ biosynthesis by the NMNAT2 enzyme protects axons, and a new therapeutic path to tune SARM1 activity.	NAD	110-114	sterile alpha and TIR motif containing 1	Homo sapiens	55-60
33831359-3	2021	(2021) reveal a key regulatory mechanism that controls SARM1"s enzymatic activity, providing insight into how NAD+ biosynthesis by the NMNAT2 enzyme protects axons, and a new therapeutic path to tune SARM1 activity.	NAD	110-114	sterile alpha and TIR motif containing 1	Homo sapiens	200-205
33599110-0	2021	FGF21 promotes ischaemic angiogenesis and endothelial progenitor cells function under diabetic conditions in an AMPK/NAD+-dependent manner.	NAD	117-121	fibroblast growth factor 21	Mus musculus	0-5
33599110-6	2021	The in vitro results revealed that FGF21 directly prevented EPC damage induced by high glucose, and the mechanistic studies demonstrated that nicotinamide adenine dinucleotide (NAD+ ) was dramatically decreased in EPCs challenged with high glucose, whereas FGF21 treatment significantly increased NAD+ content in an AMPK-dependent manner, resulting in improved angiogenic capability of EPCs.	NAD	142-175	fibroblast growth factor 21	Mus musculus	257-262
33599110-6	2021	The in vitro results revealed that FGF21 directly prevented EPC damage induced by high glucose, and the mechanistic studies demonstrated that nicotinamide adenine dinucleotide (NAD+ ) was dramatically decreased in EPCs challenged with high glucose, whereas FGF21 treatment significantly increased NAD+ content in an AMPK-dependent manner, resulting in improved angiogenic capability of EPCs.	NAD	177-181	fibroblast growth factor 21	Mus musculus	35-40
33599110-6	2021	The in vitro results revealed that FGF21 directly prevented EPC damage induced by high glucose, and the mechanistic studies demonstrated that nicotinamide adenine dinucleotide (NAD+ ) was dramatically decreased in EPCs challenged with high glucose, whereas FGF21 treatment significantly increased NAD+ content in an AMPK-dependent manner, resulting in improved angiogenic capability of EPCs.	NAD	177-181	fibroblast growth factor 21	Mus musculus	257-262
33599110-7	2021	These results indicate that FGF21 promotes ischaemic angiogenesis and the angiogenic ability of EPCs under diabetic conditions by activating the AMPK/NAD+ pathway.	NAD	150-154	fibroblast growth factor 21	Mus musculus	28-33
33597293-0	2021	NAD+ depletion by type I interferon signaling sensitizes pancreatic cancer cells to NAMPT inhibition.	NAD	0-4	nicotinamide phosphoribosyltransferase	Homo sapiens	84-89
33597293-5	2021	Nicotinamide phosphoribosyltransferase (NAMPT) is the rate-limiting enzyme in the NAD salvage pathway, a dominant source of NAD in cancer cells.	NAD	82-85	nicotinamide phosphoribosyltransferase	Homo sapiens	0-38
33597293-5	2021	Nicotinamide phosphoribosyltransferase (NAMPT) is the rate-limiting enzyme in the NAD salvage pathway, a dominant source of NAD in cancer cells.	NAD	82-85	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
33597293-5	2021	Nicotinamide phosphoribosyltransferase (NAMPT) is the rate-limiting enzyme in the NAD salvage pathway, a dominant source of NAD in cancer cells.	NAD	124-127	nicotinamide phosphoribosyltransferase	Homo sapiens	0-38
33597293-5	2021	Nicotinamide phosphoribosyltransferase (NAMPT) is the rate-limiting enzyme in the NAD salvage pathway, a dominant source of NAD in cancer cells.	NAD	124-127	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
33597293-6	2021	We found that IFN-induced NAD consumption increased dependence upon NAMPT for its role in recycling NAM to salvage NAD pools, thus sensitizing PDAC cells to pharmacologic NAMPT inhibition.	NAD	26-29	nicotinamide phosphoribosyltransferase	Homo sapiens	68-73
33597293-6	2021	We found that IFN-induced NAD consumption increased dependence upon NAMPT for its role in recycling NAM to salvage NAD pools, thus sensitizing PDAC cells to pharmacologic NAMPT inhibition.	NAD	26-29	nicotinamide phosphoribosyltransferase	Homo sapiens	171-176
33597293-6	2021	We found that IFN-induced NAD consumption increased dependence upon NAMPT for its role in recycling NAM to salvage NAD pools, thus sensitizing PDAC cells to pharmacologic NAMPT inhibition.	NAD	115-118	nicotinamide phosphoribosyltransferase	Homo sapiens	68-73
33606677-4	2021	The underlying mechanism involves increases in the cellular nicotinamide adenine dinucleotide (NAD+) pool-potentially via the salvage pathway and induction of nicotinamide phosphoribosyltransferase (NAMPT) along with augmentation of glucose-induced ATP levels.	NAD	95-99	nicotinamide phosphoribosyltransferase	Homo sapiens	159-197
33606677-4	2021	The underlying mechanism involves increases in the cellular nicotinamide adenine dinucleotide (NAD+) pool-potentially via the salvage pathway and induction of nicotinamide phosphoribosyltransferase (NAMPT) along with augmentation of glucose-induced ATP levels.	NAD	95-99	nicotinamide phosphoribosyltransferase	Homo sapiens	199-204
33744645-2	2021	Nicotinamide riboside (NR), a NAD+ precursor, restores cellular NAD+ levels.	NAD	30-34	nervous	Mus musculus	23-25
33744645-2	2021	Nicotinamide riboside (NR), a NAD+ precursor, restores cellular NAD+ levels.	NAD	64-68	nervous	Mus musculus	23-25
33744645-5	2021	RESULTS: NR increased total NAD+ in muscle tissue (NR3 P = 0.01; NR6 P = 0.004, both versus PLB), enhanced treadmill endurance and open-field activity, and prevented decline in grip strength.	NAD	28-32	nervous	Mus musculus	9-11
33546767-1	2021	BACKGROUND: Nicotinamide phosphoribosyltransferase (NAMPT) regulates cellular functions through the protein deacetylation activity of nicotinamide adenine dinucleotide (NAD+)-dependent sirtuins (SIRTs).	NAD	134-167	nicotinamide phosphoribosyltransferase	Homo sapiens	52-57
33546767-1	2021	BACKGROUND: Nicotinamide phosphoribosyltransferase (NAMPT) regulates cellular functions through the protein deacetylation activity of nicotinamide adenine dinucleotide (NAD+)-dependent sirtuins (SIRTs).	NAD	169-173	nicotinamide phosphoribosyltransferase	Homo sapiens	12-50
33546767-1	2021	BACKGROUND: Nicotinamide phosphoribosyltransferase (NAMPT) regulates cellular functions through the protein deacetylation activity of nicotinamide adenine dinucleotide (NAD+)-dependent sirtuins (SIRTs).	NAD	169-173	nicotinamide phosphoribosyltransferase	Homo sapiens	52-57
33619381-4	2021	Here, we show that the NAD+-dependent histone deacetylase sirtuin 6 is a robust tumour suppressor in SCC, acting as a modulator of glycolysis in these tumours.	NAD	23-26	sirtuin 6	Homo sapiens	58-67
33524397-2	2021	We have previously shown that NAD(H) promotes the assembly of similar tetramers from either human CtBP1 and CtBP2 and that CtBP2 tetramer destabilizing mutants are defective for oncogenic activity.	NAD	30-36	C-terminal binding protein 1	Homo sapiens	98-103
33503805-6	2021	In the presence of the selective inhibitor for SRC-family kinases PP2, the effects of DPN and PPT on transmigration and soft agar colony formation assays were decreased.	NAD	86-89	neuropeptide Y receptor Y6 (pseudogene)	Homo sapiens	66-69
33441761-6	2021	Further studies on cytochrome b5 (CYB5), an alternative NADH-dependent electron donor indicated particularly strong support of CYP2C8-dependent amodiaquine N-deethylation by CYB5 and this was confirmed by genetic CYB5 single- and POR/CYB5 double-knockout.	NAD	56-60	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	127-133
33058282-6	2021	Kinetic studies revealed that PHGDH uses NADH as a coenzyme to reduce phosphohydroxypyruvate.	NAD	41-45	D-3-phosphoglycerate dehydrogenase	Bombyx mori	30-35
33290962-9	2021	Treatment with NAD + also inhibited the expressions of NLRP3 and modulated the differentiation of Th1 and Th17 cells, reduced the expressions of the pro-inflammatory factors IL-1beta, IL-2, IL-18, IFN-gamma and IL-17, and increased the expression of anti-inflammatory IL-10.	NAD	15-20	interleukin 18	Mus musculus	190-195
33920726-4	2021	Sirtuin 6 (SIRT6) is an NAD+ dependent histone deacetylase enzyme and a unique Sirtuin family member.	NAD	24-27	sirtuin 6	Homo sapiens	11-16
33754169-3	2021	Therefore, it is important to investigate the response of NAD+-dependent FDH against both temperature and H2O2, to understand the defense mechanisms, and to increase its stability under oxidative stress conditions.	NAD	58-62	3-ketoacyl-CoA synthase 10-like	Gossypium hirsutum	73-76
33754169-4	2021	In the present study, we characterized the oxidative and thermal stability of NAD+-dependent FDH isolated from cotton, Gossypium hirsutum (GhFDH), by investigating the effect of Met/Leu substitutions in the positions of 225, 234, and 243.	NAD	78-82	3-ketoacyl-CoA synthase 10-like	Gossypium hirsutum	93-96
33754169-4	2021	In the present study, we characterized the oxidative and thermal stability of NAD+-dependent FDH isolated from cotton, Gossypium hirsutum (GhFDH), by investigating the effect of Met/Leu substitutions in the positions of 225, 234, and 243.	NAD	78-82	3-ketoacyl-CoA synthase 10-like	Gossypium hirsutum	139-144
33388853-2	2021	Sirtuins (SIRTs) are nuclear, cytoplasmic and mitochondrial histone deacetylases that influence the circadian clock with clock-controlled oscillatory protein, NAMPT, and its metabolite NAD+.	NAD	185-189	clock circadian regulator	Homo sapiens	110-115
33388853-4	2021	This review focuses on SIRT1, an NAD+-dependent class III histone deacetylase which counterbalances the intrinsic histone acetyltransferase activity of one of the clock genes, CLOCK.	NAD	33-36	clock circadian regulator	Homo sapiens	163-168
33388853-4	2021	This review focuses on SIRT1, an NAD+-dependent class III histone deacetylase which counterbalances the intrinsic histone acetyltransferase activity of one of the clock genes, CLOCK.	NAD	33-36	clock circadian regulator	Homo sapiens	176-181
33508415-8	2021	The alignment of proteins showed that these proteins are conserved in the same regions at ten positions in COX and CYTB proteins while at twelve locations in NADH.	NAD	158-162	CYTB	Fasciola hepatica	115-119
33508415-9	2021	Three-dimensional structure of COX, CYTB, and NADH proteins were compared and showed differences in additional conserved and binding sites in COX and CYTB proteins as compared to NADH in three species of Fasciola.	NAD	46-50	CYTB	Fasciola hepatica	150-154
33453420-3	2021	Nicotinamide N-methyltransferase (NNMT) is a metabolic enzyme that catalyzes the methylation of nicotinamide (NAM) using the universal methyl donor S-adenosyl methionine (SAM), directly linking one-carbon metabolism with a cell"s methylation balance and nicotinamide adenine dinucleotide (NAD+) levels.	NAD	254-287	nicotinamide N-methyltransferase	Homo sapiens	0-32
33453420-3	2021	Nicotinamide N-methyltransferase (NNMT) is a metabolic enzyme that catalyzes the methylation of nicotinamide (NAM) using the universal methyl donor S-adenosyl methionine (SAM), directly linking one-carbon metabolism with a cell"s methylation balance and nicotinamide adenine dinucleotide (NAD+) levels.	NAD	254-287	nicotinamide N-methyltransferase	Homo sapiens	34-38
33453420-3	2021	Nicotinamide N-methyltransferase (NNMT) is a metabolic enzyme that catalyzes the methylation of nicotinamide (NAM) using the universal methyl donor S-adenosyl methionine (SAM), directly linking one-carbon metabolism with a cell"s methylation balance and nicotinamide adenine dinucleotide (NAD+) levels.	NAD	289-293	nicotinamide N-methyltransferase	Homo sapiens	0-32
33453420-3	2021	Nicotinamide N-methyltransferase (NNMT) is a metabolic enzyme that catalyzes the methylation of nicotinamide (NAM) using the universal methyl donor S-adenosyl methionine (SAM), directly linking one-carbon metabolism with a cell"s methylation balance and nicotinamide adenine dinucleotide (NAD+) levels.	NAD	289-293	nicotinamide N-methyltransferase	Homo sapiens	34-38
32971159-17	2021	Moreover, compared with PPT (ERalpha agonist) and DPN (ERbeta agonist), G1 could significantly increase the expression of A20.	NAD	50-53	TNF alpha induced protein 3	Homo sapiens	122-125
33453800-6	2021	After reaction with NTR accompanied by NADH as an electron donor, the nitro group in the RCO-NTR probe can be reduced and then the RCOH fluorophore can be released through rearrangement and elimination, leading to the enhancement of fluorescence signal.	NAD	39-43	neurotensin receptor 1	Homo sapiens	20-23
33453800-6	2021	After reaction with NTR accompanied by NADH as an electron donor, the nitro group in the RCO-NTR probe can be reduced and then the RCOH fluorophore can be released through rearrangement and elimination, leading to the enhancement of fluorescence signal.	NAD	39-43	neurotensin receptor 1	Homo sapiens	93-96
33038343-4	2021	In this review, we summarize the contribution of NAD+ metabolism to inflammation, with special emphasis in the major NAD+ biosynthetic enzyme, nicotinamide phosphoribosyl transferase (NAMPT), and the NAD+-consuming enzyme, poly(ADP-ribose) polymerase (PARP).	NAD	49-53	nicotinamide phosphoribosyltransferase	Homo sapiens	143-182
33038343-4	2021	In this review, we summarize the contribution of NAD+ metabolism to inflammation, with special emphasis in the major NAD+ biosynthetic enzyme, nicotinamide phosphoribosyl transferase (NAMPT), and the NAD+-consuming enzyme, poly(ADP-ribose) polymerase (PARP).	NAD	49-53	nicotinamide phosphoribosyltransferase	Homo sapiens	184-189
33129841-7	2021	Axon degeneration following both vincristine and bortezomib is mediated by a phylogenetically ancient, genetically encoded axon destruction program that leads to the activation of the Toll-like receptor adaptor SARM1 (sterile alpha and TIR motif containing protein 1) and local decrease of nicotinamide dinucleotide (NAD+).	NAD	317-321	sterile alpha and TIR motif containing 1	Homo sapiens	211-216
33501899-5	2021	Offspring were protected from these deleterious effects by concurrent maternal administration of the NAD+-modulating agent P7C3-A20, which crossed the placenta to access the embryonic brain.	NAD	101-105	tumor necrosis factor, alpha-induced protein 3	Mus musculus	128-131
33509912-2	2021	Tpt1 performs a two-step reaction in which: (i) the 2"-PO4 attacks NAD+ to form an RNA-2"-phospho-(ADP-ribose) intermediate; and (ii) transesterification of the ADP-ribose O2"" to the RNA 2"-phosphodiester yields 2"-OH RNA and ADP-ribose-1"",2""-cyclic phosphate.	NAD	67-71	tRNA 2'-phosphotransferase	Saccharomyces cerevisiae S288C	0-4
33509912-5	2021	All four pathogen Tpt1s were active in vivo in complementing a lethal Saccharomyces cerevisiae tpt1  mutation and in vitro in NAD+-dependent conversion of a 2"-PO4 to a 2"-OH.	NAD	126-130	tRNA 2'-phosphotransferase	Saccharomyces cerevisiae S288C	18-22
33509912-6	2021	The fungal Tpt1s utilized nicotinamide hypoxanthine dinucleotide as a substrate in lieu of NAD+, albeit with much lower affinity, whereas nicotinic acid adenine dinucleotide was ineffective.	NAD	91-95	tRNA 2'-phosphotransferase	Saccharomyces cerevisiae S288C	11-15
33479917-3	2021	Exposure of rat primary astrocytes to NAD or cADPR elicited an increase in mitochondrial calcium through ryanodine receptor (RyR) in the endoplasmic reticulum (ER).	NAD	38-41	ryanodine receptor 2	Rattus norvegicus	105-123
33479917-3	2021	Exposure of rat primary astrocytes to NAD or cADPR elicited an increase in mitochondrial calcium through ryanodine receptor (RyR) in the endoplasmic reticulum (ER).	NAD	38-41	ryanodine receptor 2	Rattus norvegicus	125-128
33407464-6	2021	Finally, the space-time yield of L-tle catalyzing by GDH-R3-LeuDH whole cells could achieve 2136 g/L/day in a 200 mL scale system under the optimal catalysis conditions (pH 9.0, 30  C, 0.4 mM of NAD+ and 500 mM of a substrate including trimethylpyruvic acid and glucose).	NAD	195-199	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	53-56
32882659-4	2021	Molecular docking simulation revealed that phytic acid, NADH interacted with His170, Ala34, Arg38, Ser73, Arg31, Lys174, Gln176, Asn175, Arg75; Gln176, Asn175, Phe221, Lys174, Gly173, Ser167, Phe172, Gly169, His170 in peroxidase, respectively and blocked substrates into catalytic reactions.	NAD	56-60	activity regulated cytoskeleton associated protein	Homo sapiens	106-111
32541922-1	2021	Sirtuin 6 (SIRT6), a member of the sirtuin family, is a nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase that is involved in various physiological and pathological processes.	NAD	91-94	sirtuin 6	Homo sapiens	11-16
32789757-6	2021	Both, XO and XDH, catalyse the conversion of hypoxanthine via xanthine to uric acid, the former by using oxygen forming superoxide and hydrogen peroxide and the latter NAD+.	NAD	168-172	xanthine dehydrogenase	Homo sapiens	13-16
32527186-7	2021	The activity-based assay uses an alpha-NAD+, anomer of beta-NAD+, which is accepted as a substrate by MacroD1, MacroD2, and ARH3 due to its resemblance to the protein-linked ADP-ribose.	NAD	55-64	mono-ADP ribosylhydrolase 1	Homo sapiens	102-109
33759784-6	2021	It displayed typical FMO activities as demonstrated by oxygenating benzydamine, tamoxifen, and thioanisole, drug-related compounds known to be also accepted by human FMO1, and both NADH and NADPH cofactors could act as electron donors, a feature only described for the FMO1 paralogs.	NAD	181-185	flavin containing dimethylaniline monoxygenase 1	Homo sapiens	269-273
33326785-4	2020	Reduced NADH is not available for NAD+-dependent enzymatic reactions involving glyceraldehyde 3-phosphate dehydrogenase (GAPDH) and 3-phosphoglycerate dehydrogenase (PGDH).	NAD	8-12	phosphoglycerate dehydrogenase	Homo sapiens	132-164
33326785-4	2020	Reduced NADH is not available for NAD+-dependent enzymatic reactions involving glyceraldehyde 3-phosphate dehydrogenase (GAPDH) and 3-phosphoglycerate dehydrogenase (PGDH).	NAD	8-12	phosphoglycerate dehydrogenase	Homo sapiens	166-170
33146386-6	2020	Supplementation of NAD+ also reduced YAP1 phosphorylation, suggesting that the loss of cellular NAD+ caused by PARP-1 activation after oxidative treatment is responsible for the phosphorylation of YAP1.	NAD	19-23	Yes1 associated transcriptional regulator	Homo sapiens	37-41
33146386-6	2020	Supplementation of NAD+ also reduced YAP1 phosphorylation, suggesting that the loss of cellular NAD+ caused by PARP-1 activation after oxidative treatment is responsible for the phosphorylation of YAP1.	NAD	19-23	Yes1 associated transcriptional regulator	Homo sapiens	197-201
33146386-6	2020	Supplementation of NAD+ also reduced YAP1 phosphorylation, suggesting that the loss of cellular NAD+ caused by PARP-1 activation after oxidative treatment is responsible for the phosphorylation of YAP1.	NAD	96-100	Yes1 associated transcriptional regulator	Homo sapiens	197-201
33146386-8	2020	Since, NAD+ supplementation reduced the phosphorylation of some AMPK substrates, we hypothesized that the loss of cellular NAD+ after PARP-1 activation may induce an energy stress that activates AMPK.	NAD	7-11	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	64-68
33146386-8	2020	Since, NAD+ supplementation reduced the phosphorylation of some AMPK substrates, we hypothesized that the loss of cellular NAD+ after PARP-1 activation may induce an energy stress that activates AMPK.	NAD	7-11	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	195-199
33146386-8	2020	Since, NAD+ supplementation reduced the phosphorylation of some AMPK substrates, we hypothesized that the loss of cellular NAD+ after PARP-1 activation may induce an energy stress that activates AMPK.	NAD	123-127	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	64-68
33146386-8	2020	Since, NAD+ supplementation reduced the phosphorylation of some AMPK substrates, we hypothesized that the loss of cellular NAD+ after PARP-1 activation may induce an energy stress that activates AMPK.	NAD	123-127	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	195-199
33146386-9	2020	In summary, we showed a new crucial role of PARP-1 in the response to oxidative stress in which PARP-1 activation reduced cell viability by promoting the phosphorylation and degradation of YAP1 through a mechanism that involves the depletion of NAD+.	NAD	245-249	Yes1 associated transcriptional regulator	Homo sapiens	189-193
33297334-5	2020	Here, we show that the binding of NADH to the 26S PC inhibits the ATP-dependent and ubiquitin-independent degradation of the structured ODC enzyme.	NAD	34-38	ornithine decarboxylase 1	Homo sapiens	136-139
33297334-8	2020	These results indicate that in vitro, physiological concentrations of NADH can alter the processivity of ATP-dependent 26S PC substrates such as ODC and, more importantly, the NADH-stabilized 26S PCs promote the efficient degradation of many IDPs.	NAD	70-74	ornithine decarboxylase 1	Homo sapiens	145-148
33038659-5	2020	SIRT1 that is an NAD+-dependent deacetylase positively regulates circadian clock and telomere homeostasis.	NAD	17-20	clock circadian regulator	Homo sapiens	75-80
33330464-6	2020	NAD+ is mainly synthesized from salvage pathway mediated by two enzymes, Nampt and Nmnat.	NAD	0-4	nicotinamide phosphoribosyltransferase	Homo sapiens	73-78
33330464-6	2020	NAD+ is mainly synthesized from salvage pathway mediated by two enzymes, Nampt and Nmnat.	NAD	0-4	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	83-88
33262783-6	2020	Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses suggested that PPP1R14B-AS1 strongly participated in regulating cell aerobic respiration processes, such as mitochondrial electron respiration chain and NADH dehydrogenation processes.	NAD	231-235	protein phosphatase 1 regulatory inhibitor subunit 14B	Homo sapiens	93-101
33262783-6	2020	Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses suggested that PPP1R14B-AS1 strongly participated in regulating cell aerobic respiration processes, such as mitochondrial electron respiration chain and NADH dehydrogenation processes.	NAD	231-235	prostaglandin D2 receptor	Homo sapiens	102-105
32740958-2	2021	Citrin is a component of the malate-aspartate nicotinamide adenine dinucleotide hydrogen (NADH) shuttle, an essential shuttle for hepatic glycolysis.	NAD	90-94	solute carrier family 25 member 13	Homo sapiens	0-6
32740958-6	2021	Hepatocytes with citrin deficiency cannot use glucose and fatty acids as energy sources due to defects in the NADH shuttle and downregulation of peroxisome proliferator-activated receptor alpha (PPARalpha), respectively.	NAD	110-114	solute carrier family 25 member 13	Homo sapiens	17-23
33053398-12	2021	Furthermore, in DM mice, NAD+ and its precursors nicotinamide mononucleotide and nicotinamide riboside also facilitated corneal epithelial and nerve regeneration, accompanied with the recovered expression of SIRT1 and phosphorylated EGFR, AKT, and ERK1/2 in epithelium and corneal sensitivity.	NAD	25-29	mitogen-activated protein kinase 3	Mus musculus	248-254
33051211-6	2020	We further demonstrate that infection with MHV induces a severe attack on host cell NAD+ and NADP+ Finally, we show that NAMPT activation, NAM, and NR dramatically decrease the replication of an MHV that is sensitive to PARP activity.	NAD	84-88	nicotinamide phosphoribosyltransferase	Homo sapiens	121-126
6425280-6	1984	The presteady state burst of NADH product was observed to decrease in the presence of Mg2+, suggesting that the rate-limiting step of the dehydrogenase reaction is altered by Mg2+.	NAD	29-33	mucin 7, secreted	Homo sapiens	86-89
6425280-6	1984	The presteady state burst of NADH product was observed to decrease in the presence of Mg2+, suggesting that the rate-limiting step of the dehydrogenase reaction is altered by Mg2+.	NAD	29-33	mucin 7, secreted	Homo sapiens	175-178
6712738-6	1984	Evidence is presented and discussed that suggests that NADH-dependent vitamin K-reductase may be inhibited in the anticoagulant effect of warfarin and may be altered as a result of expression of the warfarin-resistance gene in HS rats.	NAD	55-59	vitamin K epoxide reductase complex, subunit 1	Rattus norvegicus	199-218
33325526-7	2020	The X-ray crystal structure of the catalytically inactive AldA C302A mutant in complex with IAA and NAD+ showed the cofactor adopting a conformation that differs from the previously reported structure of AldA.	NAD	100-104	aldolase, fructose-bisphosphate A	Homo sapiens	58-62
33325526-7	2020	The X-ray crystal structure of the catalytically inactive AldA C302A mutant in complex with IAA and NAD+ showed the cofactor adopting a conformation that differs from the previously reported structure of AldA.	NAD	100-104	aldolase, fructose-bisphosphate A	Homo sapiens	204-208
33325526-8	2020	These structures suggest that NAD+ undergoes a conformational change during the AldA reaction mechanism similar to that reported for human ALDH.	NAD	30-34	aldolase, fructose-bisphosphate A	Homo sapiens	80-84
33163999-5	2020	Assay conditions such as incubation time and temperature were optimised resulting in a 3 min assay at 37  C in the presence of 10 mM NAD+ and 20 mM sorbitol co-substrates, enabling NADH electro oxidation (linear range 0.25-5 mM, sensitivity 9.17 muC cm-2 mM-1 in undiluted milk).	NAD	181-185	MUC	Bos taurus	246-249
6319381-3	1984	The cAMP-dependent protein kinase of CYR3 mutant cells, which has a high K alpha value for cAMP in the phosphorylation reaction, required a high cAMP concentration for the inactivation of NAD-dependent glutamate dehydrogenase.	NAD	188-191	Ras family GTPase RAS2	Saccharomyces cerevisiae S288C	37-41
6648970-2	1983	This method contains two coupling enzymes of UDP-galactose-4-epimerase and UDP-glucose dehydrogenase, and conversion of NAD to NADH.	NAD	120-123	UDP-galactose-4-epimerase	Homo sapiens	45-70
33107823-1	2020	Leber congenital amaurosis type nine is an autosomal recessive retinopathy caused by mutations of the NAD+ synthesis enzyme NMNAT1.	NAD	102-106	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	124-130
6648970-2	1983	This method contains two coupling enzymes of UDP-galactose-4-epimerase and UDP-glucose dehydrogenase, and conversion of NAD to NADH.	NAD	127-131	UDP-galactose-4-epimerase	Homo sapiens	45-70
6311045-2	1983	The liberated lactose is hydrolyzed with beta-galactosidase, and the released galactose is oxidized with galactose dehydrogenase and NAD+; finally, the NADH produced is measured by fluorometry (excitation at 340 nm and analysis of emitted light at 465 nm).	NAD	152-156	galactosidase beta 1	Homo sapiens	41-59
33087354-0	2020	MCART1/SLC25A51 is required for mitochondrial NAD transport.	NAD	46-49	solute carrier family 25 member 51	Homo sapiens	0-6
33087354-0	2020	MCART1/SLC25A51 is required for mitochondrial NAD transport.	NAD	46-49	solute carrier family 25 member 51	Homo sapiens	7-15
33087354-4	2020	MCART1-null cells have large decreases in TCA cycle flux, mitochondrial respiration, ETC complex I activity, and mitochondrial levels of NAD+ and NADH.	NAD	137-141	solute carrier family 25 member 51	Homo sapiens	0-6
33087354-4	2020	MCART1-null cells have large decreases in TCA cycle flux, mitochondrial respiration, ETC complex I activity, and mitochondrial levels of NAD+ and NADH.	NAD	146-150	solute carrier family 25 member 51	Homo sapiens	0-6
33087354-5	2020	Isolated mitochondria from cells lacking or overexpressing MCART1 have greatly decreased or increased NAD uptake in vitro, respectively.	NAD	102-105	solute carrier family 25 member 51	Homo sapiens	59-65
33087354-7	2020	Thus, we propose that MCART1 is the long sought mitochondrial transporter for NAD in human cells.	NAD	78-81	solute carrier family 25 member 51	Homo sapiens	22-28
32840960-7	2020	Loss of complex I was associated with disturbed NAD+ metabolism with increased UCP2 expression and reduced phosphorylated SirT1.	NAD	48-52	uncoupling protein 2	Homo sapiens	79-83
32828421-3	2020	SARM1 promotes neurodegeneration by catalyzing the hydrolysis of NAD+ to form a mixture of ADPR and cADPR.	NAD	65-69	sterile alpha and TIR motif containing 1	Homo sapiens	0-5
33326496-1	2020	The ability of CD38 and CD157 to utilize nicotinamide adenine dinucleotide (NAD) has received much attention because the aging-induced elevation of CD38 expression plays a role in the senescence-related decline in NAD levels.	NAD	41-74	bone marrow stromal cell antigen 1	Mus musculus	24-29
33326496-1	2020	The ability of CD38 and CD157 to utilize nicotinamide adenine dinucleotide (NAD) has received much attention because the aging-induced elevation of CD38 expression plays a role in the senescence-related decline in NAD levels.	NAD	76-79	bone marrow stromal cell antigen 1	Mus musculus	24-29
33326496-1	2020	The ability of CD38 and CD157 to utilize nicotinamide adenine dinucleotide (NAD) has received much attention because the aging-induced elevation of CD38 expression plays a role in the senescence-related decline in NAD levels.	NAD	214-217	bone marrow stromal cell antigen 1	Mus musculus	24-29
33326496-9	2020	We discuss the distinct differences in aging effects from the perspective of inhibition of NAD metabolism in CD157 and CD38 KO mice, which may contribute to differential behavioral changes during aging.	NAD	91-94	bone marrow stromal cell antigen 1	Mus musculus	109-114
33414897-3	2020	NAD+ is reduced with age at a cellular, tissue, and organismal level due to inflammation, defect in NAMPT-mediated NAD+ biosynthesis, and the PARP-mediated NAD+ depletion.	NAD	0-4	nicotinamide phosphoribosyltransferase	Homo sapiens	100-105
33414897-3	2020	NAD+ is reduced with age at a cellular, tissue, and organismal level due to inflammation, defect in NAMPT-mediated NAD+ biosynthesis, and the PARP-mediated NAD+ depletion.	NAD	115-119	nicotinamide phosphoribosyltransferase	Homo sapiens	100-105
33414897-3	2020	NAD+ is reduced with age at a cellular, tissue, and organismal level due to inflammation, defect in NAMPT-mediated NAD+ biosynthesis, and the PARP-mediated NAD+ depletion.	NAD	115-119	nicotinamide phosphoribosyltransferase	Homo sapiens	100-105
33096031-5	2020	Xanthine dehydrogenase converted the hypoxanthine to uric acid and yielded two molecules of NADH, which in turn reduced Fe3+ to Fe2+ (mediated by 1-methoxy-5-ethylphenazinium ethylsulfate).	NAD	92-96	xanthine dehydrogenase	Homo sapiens	0-22
6575778-2	1983	To clarify its role, the basic kinetics of 15-hydroxyprostaglandin dehydrogenase (PGDH) from rat skin were investigated with either NAD+ of NADP+ as co-substrate.	NAD	132-136	15-hydroxyprostaglandin dehydrogenase	Rattus norvegicus	82-86
6575778-13	1983	These results show that skin contains NAD+- and NADP+-dependent PGDH.	NAD	38-42	15-hydroxyprostaglandin dehydrogenase	Rattus norvegicus	64-68
6346125-3	1983	NAD-dependent ADH and ALDH were present in various rodents and were both species and strain-dependent.	NAD	0-3	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	22-26
33053563-0	2020	The NAD+-mediated self-inhibition mechanism of pro-neurodegenerative Sarm1.	NAD	4-8	sterile alpha and TIR motif containing 1	Homo sapiens	69-74
33053563-7	2020	Disruption of the NAD+-binding site or the ARM-TIR interaction caused the constitutively-active Sarm1 leading to axonal degeneration.	NAD	18-22	sterile alpha and TIR motif containing 1	Homo sapiens	96-101
6346125-10	1983	The results indicate the presence of NAD-dependent ADH and ALDH in male and female genital systems, which can be altered by pharmacologic interventions.	NAD	37-40	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	59-63
32983978-8	2020	These results indicate that in the absence of CA IX, reduction of pHi disrupts LDHA activity and hinders the cellular capacity to regenerate NAD+ and secrete protons to the extracellular space.	NAD	141-145	glucose-6-phosphate isomerase	Homo sapiens	66-69
6346128-10	1983	The results indicate the presence of NAD-dependent ALDH in various subcellular fractions of the female genital system which may be important in the gonadal metabolic detoxification of ethanol derived acetaldehyde.	NAD	37-40	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	51-55
33324653-1	2020	Proteins from the poly(ADP-ribose) polymerase (PARP) family, such as PARP1 and PARP2, use NAD+ as a substrate to catalyze the synthesis of polymeric chains consisting of ADP-ribose units covalently attached to an acceptor molecule.	NAD	90-94	poly(ADP-ribose) polymerase	Arabidopsis thaliana	18-45
6404248-3	1983	On electrophoresis in a starch gel containing NAD or NADH, of purified AdhS which consists of the three Adh forms S-5, S-4, and S-3, five enzymatically active zones appear.	NAD	46-49	l(3)87Db	Drosophila melanogaster	114-117
33324653-1	2020	Proteins from the poly(ADP-ribose) polymerase (PARP) family, such as PARP1 and PARP2, use NAD+ as a substrate to catalyze the synthesis of polymeric chains consisting of ADP-ribose units covalently attached to an acceptor molecule.	NAD	90-94	poly(ADP-ribose) polymerase	Arabidopsis thaliana	47-51
33324653-1	2020	Proteins from the poly(ADP-ribose) polymerase (PARP) family, such as PARP1 and PARP2, use NAD+ as a substrate to catalyze the synthesis of polymeric chains consisting of ADP-ribose units covalently attached to an acceptor molecule.	NAD	90-94	poly(ADP-ribose) polymerase	Arabidopsis thaliana	79-84
6404248-3	1983	On electrophoresis in a starch gel containing NAD or NADH, of purified AdhS which consists of the three Adh forms S-5, S-4, and S-3, five enzymatically active zones appear.	NAD	46-49	Regulatory particle triple-A ATPase 2	Drosophila melanogaster	119-122
6404248-3	1983	On electrophoresis in a starch gel containing NAD or NADH, of purified AdhS which consists of the three Adh forms S-5, S-4, and S-3, five enzymatically active zones appear.	NAD	46-49	Ribosomal protein S3	Drosophila melanogaster	128-131
6404248-3	1983	On electrophoresis in a starch gel containing NAD or NADH, of purified AdhS which consists of the three Adh forms S-5, S-4, and S-3, five enzymatically active zones appear.	NAD	53-57	l(3)87Db	Drosophila melanogaster	114-117
32878777-1	2020	BACKGROUND/AIM: Nicotinamide phosphoribosyl-transferase (NAMPT) is a rate-limiting enzyme in the pathway synthesizing nicotinamide adenine dinucleotide (NAD (+)) from nicotinamide (NAM).	NAD	118-151	nicotinamide phosphoribosyltransferase	Homo sapiens	16-55
6404248-3	1983	On electrophoresis in a starch gel containing NAD or NADH, of purified AdhS which consists of the three Adh forms S-5, S-4, and S-3, five enzymatically active zones appear.	NAD	53-57	Regulatory particle triple-A ATPase 2	Drosophila melanogaster	119-122
32878777-1	2020	BACKGROUND/AIM: Nicotinamide phosphoribosyl-transferase (NAMPT) is a rate-limiting enzyme in the pathway synthesizing nicotinamide adenine dinucleotide (NAD (+)) from nicotinamide (NAM).	NAD	118-151	nicotinamide phosphoribosyltransferase	Homo sapiens	57-62
32878777-1	2020	BACKGROUND/AIM: Nicotinamide phosphoribosyl-transferase (NAMPT) is a rate-limiting enzyme in the pathway synthesizing nicotinamide adenine dinucleotide (NAD (+)) from nicotinamide (NAM).	NAD	153-160	nicotinamide phosphoribosyltransferase	Homo sapiens	16-55
33182523-4	2020	Intracellularly, visfatin/iNAMPT plays a regulatory role in NAD+ biosynthesis and thereby affects many NAD-dependent proteins such as sirtuins, PARPs, MARTs and CD38/157.	NAD	60-64	nicotinamide phosphoribosyltransferase	Homo sapiens	17-25
6404248-3	1983	On electrophoresis in a starch gel containing NAD or NADH, of purified AdhS which consists of the three Adh forms S-5, S-4, and S-3, five enzymatically active zones appear.	NAD	53-57	Ribosomal protein S3	Drosophila melanogaster	128-131
33182523-4	2020	Intracellularly, visfatin/iNAMPT plays a regulatory role in NAD+ biosynthesis and thereby affects many NAD-dependent proteins such as sirtuins, PARPs, MARTs and CD38/157.	NAD	60-63	nicotinamide phosphoribosyltransferase	Homo sapiens	17-25
32878777-1	2020	BACKGROUND/AIM: Nicotinamide phosphoribosyl-transferase (NAMPT) is a rate-limiting enzyme in the pathway synthesizing nicotinamide adenine dinucleotide (NAD (+)) from nicotinamide (NAM).	NAD	153-160	nicotinamide phosphoribosyltransferase	Homo sapiens	57-62
6295757-4	1982	With this assay, it appeared that the reaction catalysed by NMN adenylyltransferase proceeded with a rapid, early "burst" of NAD before steady-state velocities were established.	NAD	125-128	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	60-83
32618367-0	2020	Glycolysis, via NADH-dependent dimerisation of CtBPs, regulates hypoxia-induced expression of CAIX and stem-like breast cancer cell survival.	NAD	16-20	carbonic anhydrase 9	Homo sapiens	94-98
6961918-0	1982	Involvement of a single thiol group in the conversion of the NAD+-dependent activity of rat liver xanthine oxidoreductase to the O2-dependent activity.	NAD	61-65	xanthine dehydrogenase	Rattus norvegicus	98-121
32228195-3	2020	Nicotinamide adenine dinucleotide-dependent deacetylase sirtuin-1 (SIRT1)/forkhead box O3 (FOXO3a) signaling is critical for maintaining neuronal function and regulation of the apoptotic pathway.	NAD	0-33	forkhead box O3	Rattus norvegicus	74-89
32228195-3	2020	Nicotinamide adenine dinucleotide-dependent deacetylase sirtuin-1 (SIRT1)/forkhead box O3 (FOXO3a) signaling is critical for maintaining neuronal function and regulation of the apoptotic pathway.	NAD	0-33	forkhead box O3	Rattus norvegicus	91-97
6293814-6	1982	HMG 1 and HMG 2 were found to be ADP-ribosylated, the reaction being dependent on NAD concentration and time.	NAD	82-85	high mobility group box 1	Bos taurus	0-5
32533184-0	2020	An Alu-mediated duplication in NMNAT1, involved in NAD biosynthesis, causes a novel syndrome, SHILCA, affecting multiple tissues and organs.	NAD	51-54	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	31-37
6289905-1	1982	Two derivatives of NAD+ spin-labeled at N6 or C-8 of the adenine ring have been shown previously to be active coenzymes of glyceraldehyde-3-phosphate dehydrogenase (D-glyceraldehyde-3-phosphate: NAD+ oxidoreductase (phosphorylating), EC 1.2.1.12).	NAD	19-23	homeobox C8	Homo sapiens	46-49
6289905-1	1982	Two derivatives of NAD+ spin-labeled at N6 or C-8 of the adenine ring have been shown previously to be active coenzymes of glyceraldehyde-3-phosphate dehydrogenase (D-glyceraldehyde-3-phosphate: NAD+ oxidoreductase (phosphorylating), EC 1.2.1.12).	NAD	19-23	hydroxysteroid 17-beta dehydrogenase 6	Homo sapiens	200-214
32236974-2	2020	Sirtuin 6 (SIRT6) is a NAD-dependent protein deacetylase encoded by the SIRT6 gene.	NAD	23-26	sirtuin 6	Homo sapiens	0-9
32236974-2	2020	Sirtuin 6 (SIRT6) is a NAD-dependent protein deacetylase encoded by the SIRT6 gene.	NAD	23-26	sirtuin 6	Homo sapiens	11-16
6289905-5	1982	After reduction of enzyme-bound NAD+ spin-labeled at C-8 to the corresponding NADH derivative, the additional peaks due to this spin-spin interaction disappear, which implies that the distance between the two radicals increases.	NAD	32-36	homeobox C8	Homo sapiens	53-56
32236974-2	2020	Sirtuin 6 (SIRT6) is a NAD-dependent protein deacetylase encoded by the SIRT6 gene.	NAD	23-26	sirtuin 6	Homo sapiens	72-77
6289905-5	1982	After reduction of enzyme-bound NAD+ spin-labeled at C-8 to the corresponding NADH derivative, the additional peaks due to this spin-spin interaction disappear, which implies that the distance between the two radicals increases.	NAD	78-82	homeobox C8	Homo sapiens	53-56
6289905-16	1982	The N6 derivative of NAD+ also shows spin-spin interaction; however, only data for the C-8 derivatives are shown in detail.	NAD	21-25	homeobox C8	Homo sapiens	87-90
16662475-6	1982	The FMNH(2)-linked nitrate reductase activity was about 40% of NADH-linked activity.	NAD	63-67	chalcone reductase CHR1	Glycine max	27-36
32779442-1	2020	Objective: Nicotinamide phosphoribosyltransferase (NAMPT), which is responsible for biosynthesis of nicotinamide adenine dinucleotide (NAD), has a regulatory role in cellular metabolism and thus, might be implicated in non-alcoholic fatty liver disease (NAFLD).	NAD	100-133	nicotinamide phosphoribosyltransferase	Homo sapiens	11-49
32779442-1	2020	Objective: Nicotinamide phosphoribosyltransferase (NAMPT), which is responsible for biosynthesis of nicotinamide adenine dinucleotide (NAD), has a regulatory role in cellular metabolism and thus, might be implicated in non-alcoholic fatty liver disease (NAFLD).	NAD	100-133	nicotinamide phosphoribosyltransferase	Homo sapiens	51-56
32779442-1	2020	Objective: Nicotinamide phosphoribosyltransferase (NAMPT), which is responsible for biosynthesis of nicotinamide adenine dinucleotide (NAD), has a regulatory role in cellular metabolism and thus, might be implicated in non-alcoholic fatty liver disease (NAFLD).	NAD	135-138	nicotinamide phosphoribosyltransferase	Homo sapiens	11-49
32779442-1	2020	Objective: Nicotinamide phosphoribosyltransferase (NAMPT), which is responsible for biosynthesis of nicotinamide adenine dinucleotide (NAD), has a regulatory role in cellular metabolism and thus, might be implicated in non-alcoholic fatty liver disease (NAFLD).	NAD	135-138	nicotinamide phosphoribosyltransferase	Homo sapiens	51-56
32779442-2	2020	This study aimed to show how NAMPT down-regulation in liver cells influences lipid metabolism and sirtiun 1 (SIRT1), as the main NAD-dependent deacetylase enzyme.	NAD	129-132	nicotinamide phosphoribosyltransferase	Homo sapiens	29-34
6216130-3	1982	The experiments reported here demonstrate that low concentrations of n-octylamine, in the presence of limiting quantities of NAD+, cause an increased level of cytochrome b5 reduction by mouse hepatic microsomes and also delays its reoxidation.	NAD	125-129	cytochrome b5 type A (microsomal)	Mus musculus	159-172
7326683-8	1981	Thereby the blockage of glyceraldehyde-3-phosphate-dehydrogenase (GAPDH) by high NADH/NAD-ratios in ischaemic myocardium should be moderated, and ATP production by anaerobic glycolysis stimulated.	NAD	81-85	glyceraldehyde-3-phosphate dehydrogenase	Canis lupus familiaris	24-64
32519817-4	2020	We further demonstrated that the NAD-dependent protein deacetylase, SIRT7, and the FOXO4 transcription factor acted as endogenous brakes for GLS1 expression, which are inhibited by TGF-beta.	NAD	33-36	transforming growth factor alpha	Homo sapiens	181-189
31974433-3	2020	Nicotinamide adenine dinucleotide (NAD) is an essential co-factor in energy metabolism and is constantly replenished by nicotinamide phosphoribosyl-transferase (Nampt), the rate-limiting enzyme in the NAD salvage pathway.	NAD	0-33	nicotinamide phosphoribosyltransferase	Homo sapiens	120-159
31974433-3	2020	Nicotinamide adenine dinucleotide (NAD) is an essential co-factor in energy metabolism and is constantly replenished by nicotinamide phosphoribosyl-transferase (Nampt), the rate-limiting enzyme in the NAD salvage pathway.	NAD	0-33	nicotinamide phosphoribosyltransferase	Homo sapiens	161-166
31974433-3	2020	Nicotinamide adenine dinucleotide (NAD) is an essential co-factor in energy metabolism and is constantly replenished by nicotinamide phosphoribosyl-transferase (Nampt), the rate-limiting enzyme in the NAD salvage pathway.	NAD	35-38	nicotinamide phosphoribosyltransferase	Homo sapiens	120-159
7326683-8	1981	Thereby the blockage of glyceraldehyde-3-phosphate-dehydrogenase (GAPDH) by high NADH/NAD-ratios in ischaemic myocardium should be moderated, and ATP production by anaerobic glycolysis stimulated.	NAD	81-85	glyceraldehyde-3-phosphate dehydrogenase	Canis lupus familiaris	66-71
31974433-3	2020	Nicotinamide adenine dinucleotide (NAD) is an essential co-factor in energy metabolism and is constantly replenished by nicotinamide phosphoribosyl-transferase (Nampt), the rate-limiting enzyme in the NAD salvage pathway.	NAD	35-38	nicotinamide phosphoribosyltransferase	Homo sapiens	161-166
7326683-8	1981	Thereby the blockage of glyceraldehyde-3-phosphate-dehydrogenase (GAPDH) by high NADH/NAD-ratios in ischaemic myocardium should be moderated, and ATP production by anaerobic glycolysis stimulated.	NAD	86-90	glyceraldehyde-3-phosphate dehydrogenase	Canis lupus familiaris	24-64
31974433-3	2020	Nicotinamide adenine dinucleotide (NAD) is an essential co-factor in energy metabolism and is constantly replenished by nicotinamide phosphoribosyl-transferase (Nampt), the rate-limiting enzyme in the NAD salvage pathway.	NAD	201-204	nicotinamide phosphoribosyltransferase	Homo sapiens	120-159
31974433-3	2020	Nicotinamide adenine dinucleotide (NAD) is an essential co-factor in energy metabolism and is constantly replenished by nicotinamide phosphoribosyl-transferase (Nampt), the rate-limiting enzyme in the NAD salvage pathway.	NAD	201-204	nicotinamide phosphoribosyltransferase	Homo sapiens	161-166
7326683-8	1981	Thereby the blockage of glyceraldehyde-3-phosphate-dehydrogenase (GAPDH) by high NADH/NAD-ratios in ischaemic myocardium should be moderated, and ATP production by anaerobic glycolysis stimulated.	NAD	86-90	glyceraldehyde-3-phosphate dehydrogenase	Canis lupus familiaris	66-71
6895053-2	1981	Bile acids are converted to 3-oxo bile acids with 3 alpha-hydroxysteroid dehydrogenase (EC 1.1.1.50) with concomitant reduction of NAD+ to NADH.	NAD	131-135	aldo-keto reductase family 1 member C3	Homo sapiens	50-86
31865509-3	2020	Prior studies have focused on the regulatory K+ transport and NAD-binding (KTN) domain in the C-terminus of the thylakoid carrier KEA3 but the localization of this domain remains unclear.	NAD	62-65	K+ efflux antiporter 3	Arabidopsis thaliana	130-134
32630078-19	2020	NADH inhibited in a dose-response manner the binding of SA to GAPA1, validating our data.	NAD	0-4	glyceraldehyde 3-phosphate dehydrogenase A subunit	Arabidopsis thaliana	62-67
6895053-2	1981	Bile acids are converted to 3-oxo bile acids with 3 alpha-hydroxysteroid dehydrogenase (EC 1.1.1.50) with concomitant reduction of NAD+ to NADH.	NAD	139-143	aldo-keto reductase family 1 member C3	Homo sapiens	50-86
6895053-3	1981	The hydrogen in the NADH generated is transferred by diaphorase (EC 1.6.4.3) to nitrotetrazolium blue to yield diformazan 540 nm).	NAD	20-24	dihydrolipoamide dehydrogenase	Homo sapiens	53-63
7248931-3	1981	The specific activity of nicotinamide adenine dinucleotide-dependent 15-hydroxyprostaglandin dehydrogenase in hydatidiform mole tissue (0 to 1.2 nmol 15-ketoprostaglandin E2 formed x min-1 x mg-1 cytosolic protein) and in choriocarcinoma cells (1.0 nmol 15-ketoprostaglandin E2 x min-1 x mg-1 protein) was strikingly less than that found in normal placental tissue [11.4 +/- 2.3 (S.E.)	NAD	25-58	mucin 5B, oligomeric mucus/gel-forming	Homo sapiens	191-195
32595600-5	2020	NAMPT is the rate-limiting enzyme of the NAD+ salvage pathway and its expression is under the control of the circadian clock.	NAD	41-45	nicotinamide phosphoribosyltransferase	Homo sapiens	0-5
7248931-3	1981	The specific activity of nicotinamide adenine dinucleotide-dependent 15-hydroxyprostaglandin dehydrogenase in hydatidiform mole tissue (0 to 1.2 nmol 15-ketoprostaglandin E2 formed x min-1 x mg-1 cytosolic protein) and in choriocarcinoma cells (1.0 nmol 15-ketoprostaglandin E2 x min-1 x mg-1 protein) was strikingly less than that found in normal placental tissue [11.4 +/- 2.3 (S.E.)	NAD	25-58	mucin 5B, oligomeric mucus/gel-forming	Homo sapiens	288-292
32595600-6	2020	NAD+ produced from NAMPT can modulate the circadian clock, demonstrating bidirectional interactions between circadian and metabolic pathways.	NAD	0-4	nicotinamide phosphoribosyltransferase	Homo sapiens	19-24
6894547-0	1981	Inhibition of bovine kidney alpha-ketoglutarate dehydrogenase complex by reduced nicotinamide adenine dinucleotide in the presence or absence of calcium ion and effect of adenosine 5"-diphosphate on reduced nicotinamide adenine dinucleotide inhibition.	NAD	81-114	oxoglutarate dehydrogenase	Bos taurus	28-61
32471290-4	2020	Recent investigations show the importance of nicotinamide adenine dinucleotide (NAD+) and its producing enzyme nicotinic acid mononucleotide transferase 2 (Nmnat2) for neurodegeneration as well as for the preservation of health of the neuronal cells.	NAD	45-78	nicotinamide nucleotide adenylyltransferase 2	Mus musculus	156-162
6894547-1	1981	Micromolar Ca2+ markedly reduces NADH inhibition of bovine kidney alpha-ketoglutarate dehydrogenase complex [Lawlis, V. B., &amp; Roche, T. E. (1980) Mol.	NAD	33-37	oxoglutarate dehydrogenase	Bos taurus	66-99
32471290-4	2020	Recent investigations show the importance of nicotinamide adenine dinucleotide (NAD+) and its producing enzyme nicotinic acid mononucleotide transferase 2 (Nmnat2) for neurodegeneration as well as for the preservation of health of the neuronal cells.	NAD	80-84	nicotinamide nucleotide adenylyltransferase 2	Mus musculus	156-162
7193456-11	1980	The Km for NAD+ is 0.7 mM for both the complex and the lipoamide dehydrogenase.	NAD	11-15	dihydrolipoamide dehydrogenase	Homo sapiens	55-78
32392755-4	2020	Here we report that expression level of the nuclear NAD synthesis enzyme, nicotinamide mononucleotide adenylyltransferase-1 (NMNAT1), increases in U-2OS cells upon exposure to DNA damaging agents, suggesting the involvement of the enzyme in the DNA damage response.	NAD	52-55	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	74-123
32392755-4	2020	Here we report that expression level of the nuclear NAD synthesis enzyme, nicotinamide mononucleotide adenylyltransferase-1 (NMNAT1), increases in U-2OS cells upon exposure to DNA damaging agents, suggesting the involvement of the enzyme in the DNA damage response.	NAD	52-55	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	125-131
32392755-7	2020	Activation of the DNA damage sensor enzyme poly(ADP-ribose) polymerase 1 (PARP1), a major consumer of NAD+ in the nucleus, was fully blocked by NMNAT1 inactivation, leading to increased DNA damage (phospho-H2AX foci).	NAD	102-106	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	144-150
7193456-13	1980	The lipoamide dehydrogenase is inhibited by NADH and NADPH competitively with NAD+, with Ki values of 80 and 90 microM respectively.	NAD	44-48	dihydrolipoamide dehydrogenase	Homo sapiens	4-27
7193456-13	1980	The lipoamide dehydrogenase is inhibited by NADH and NADPH competitively with NAD+, with Ki values of 80 and 90 microM respectively.	NAD	78-82	dihydrolipoamide dehydrogenase	Homo sapiens	4-27
7002807-1	1980	The distribution of (newly found) NAD-dependent aldehyde dehydrogenase (ALDH) was determined in the rat testis and epididymis as a function of age.	NAD	34-37	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	48-70
32369778-7	2020	Interestingly, muscle citrate synthase activity levels (i.e., mitochondrial density) increased in MA participants from Pre to Post (+183%, p<0.001), and this increase was significantly associated with increases in muscle NAD+ (r2=0.592, p=0.001).	NAD	221-225	citrate synthase	Homo sapiens	22-38
31912134-7	2020	Expression of mitochondrial bifunctional NAD-dependent methylene-tetrahydrofolate dehydrogenase/methenyl-tetrahydrofolate cyclohydrolase (Mthfd2) was significantly enriched in PP and liver of P, intermediate in F liver, and much lower in liver of N and J, relative to PP.	NAD	41-44	methylenetetrahydrofolate dehydrogenase (NADP+ dependent) 2, methenyltetrahydrofolate cyclohydrolase	Rattus norvegicus	138-144
7002807-1	1980	The distribution of (newly found) NAD-dependent aldehyde dehydrogenase (ALDH) was determined in the rat testis and epididymis as a function of age.	NAD	34-37	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	72-76
6445762-4	1980	Simple as it is, the model can explain the following properties of carbohydrate metabolism: a drastic rise of the rate of glucose consumption during transition to a higher level of ATPase load; stabilization of ATP and an increase of the steady state rates of glycolysis and oxidation of cytoplasmic NADH by the H-transporting shuttles and of pyruvate in the Krebs cycle with increasing rate of the ATPase load; activation of glycolysis and a decrease of the rate of oxidative phosphorylation following an inhibition of the H-transporting shuttles.	NAD	300-304	dynein axonemal heavy chain 8	Homo sapiens	181-187
32209328-13	2020	CONCLUSIONS: NAD+ precursors differentially regulate NaV1.5 via multiple mechanisms.	NAD	13-17	neuron navigator 1	Mus musculus	53-57
32697331-3	2020	The CYB5R3 gene encodes cytochrome b5 reductase 3, which converts methemoglobin to hemoglobin through oxidation of NADH.	NAD	115-119	cytochrome b5 reductase 3	Homo sapiens	4-10
32697331-3	2020	The CYB5R3 gene encodes cytochrome b5 reductase 3, which converts methemoglobin to hemoglobin through oxidation of NADH.	NAD	115-119	cytochrome b5 reductase 3	Homo sapiens	24-49
6445762-4	1980	Simple as it is, the model can explain the following properties of carbohydrate metabolism: a drastic rise of the rate of glucose consumption during transition to a higher level of ATPase load; stabilization of ATP and an increase of the steady state rates of glycolysis and oxidation of cytoplasmic NADH by the H-transporting shuttles and of pyruvate in the Krebs cycle with increasing rate of the ATPase load; activation of glycolysis and a decrease of the rate of oxidative phosphorylation following an inhibition of the H-transporting shuttles.	NAD	300-304	dynein axonemal heavy chain 8	Homo sapiens	399-405
16661245-0	1980	Development of NAD(P)H: and NADH:Nitrate Reductase Activities in Soybean Cotyledons.	NAD	28-32	chalcone reductase CHR1	Glycine max	41-50
32270032-3	2020	Here, we showed that NAD+-dependent class III HDAC sirtuin 1 (Sirt1) is highly expressed in resting B cells and down-regulated by stimuli inducing AID.	NAD	21-25	activation induced cytidine deaminase	Homo sapiens	147-150
16661245-9	1980	When 5- to 8-day-old cotyledons were extracted and purified, further elution of the blue-Sepharose with KNO(3), subsequent to the NADPH elution, yielded an NR fraction most active with NADH.	NAD	185-189	inducible nitrate reductase [NADH] 1	Glycine max	156-158
32270032-4	2020	B cell Sirt1 down-regulation, deprivation of NAD+ cofactor, or genetic Sirt1 deletion reduced deacetylation of Aicda promoter histones, Dnmt1, and nuclear factor-kappaB (NF-kappaB) p65 and increased AID expression.	NAD	45-49	activation induced cytidine deaminase	Homo sapiens	111-116
16661245-10	1980	Assays of this fraction with different nitrate concentrations revealed that this NR had a higher nitrate affinity and was similar to the NADH:NR of soybean leaves.	NAD	137-141	inducible nitrate reductase [NADH] 1	Glycine max	81-83
16661245-12	1980	The analysis of these fractions prepared from the extracts of older cotyledons indicated that residual NAD(P)H:NR contaminated the NADH:NR.	NAD	131-135	inducible nitrate reductase [NADH] 1	Glycine max	111-113
31932306-4	2020	The synthesis of UDP-glucuronic acid can alter the NAD+:NADH ratio via the enzyme UDP-glucose dehydrogenase, which oxidizes the alcohol group at C6 to the COO- group.	NAD	51-54	UDP-glucose 6-dehydrogenase	Homo sapiens	82-107
16661245-12	1980	The analysis of these fractions prepared from the extracts of older cotyledons indicated that residual NAD(P)H:NR contaminated the NADH:NR.	NAD	131-135	inducible nitrate reductase [NADH] 1	Glycine max	136-138
31932306-4	2020	The synthesis of UDP-glucuronic acid can alter the NAD+:NADH ratio via the enzyme UDP-glucose dehydrogenase, which oxidizes the alcohol group at C6 to the COO- group.	NAD	56-60	UDP-glucose 6-dehydrogenase	Homo sapiens	82-107
31932306-5	2020	Here, we show that HAS2 expression can be modulated by sirtuin 1 (SIRT1), the master metabolic sensor of the cell, belonging to the class of NAD+-dependent deacetylases.	NAD	141-144	hyaluronan synthase 2	Homo sapiens	19-23
16661245-14	1980	It was concluded that NADH:NR was most active in young cotyledons and that as the cotyledons aged the NAD(P)H:NR became more active.	NAD	22-26	inducible nitrate reductase [NADH] 1	Glycine max	27-29
31988240-0	2020	A nicotinamide phosphoribosyltransferase-GAPDH interaction sustains the stress-induced NMN/NAD+ salvage pathway in the nucleus.	NAD	91-94	nicotinamide phosphoribosyltransferase	Homo sapiens	2-40
16661245-14	1980	It was concluded that NADH:NR was most active in young cotyledons and that as the cotyledons aged the NAD(P)H:NR became more active.	NAD	22-26	inducible nitrate reductase [NADH] 1	Glycine max	110-112
31988240-3	2020	The nicotinamide salvage pathway, constituted by nicotinamide mononucleotide adenylyltransferase (NMNAT) and nicotinamide phosphoribosyltransferase (NAMPT), mainly replenishes NAD+ in eukaryotes.	NAD	176-179	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	49-96
6782807-4	1980	In the developing and adult rat kidney the activity of NAD-PGDH was localized predominantly to medullary rays and inner cortex.	NAD	55-58	15-hydroxyprostaglandin dehydrogenase	Rattus norvegicus	59-63
31988240-3	2020	The nicotinamide salvage pathway, constituted by nicotinamide mononucleotide adenylyltransferase (NMNAT) and nicotinamide phosphoribosyltransferase (NAMPT), mainly replenishes NAD+ in eukaryotes.	NAD	176-179	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	98-103
31988240-3	2020	The nicotinamide salvage pathway, constituted by nicotinamide mononucleotide adenylyltransferase (NMNAT) and nicotinamide phosphoribosyltransferase (NAMPT), mainly replenishes NAD+ in eukaryotes.	NAD	176-179	nicotinamide phosphoribosyltransferase	Homo sapiens	109-147
31988240-3	2020	The nicotinamide salvage pathway, constituted by nicotinamide mononucleotide adenylyltransferase (NMNAT) and nicotinamide phosphoribosyltransferase (NAMPT), mainly replenishes NAD+ in eukaryotes.	NAD	176-179	nicotinamide phosphoribosyltransferase	Homo sapiens	149-154
7468251-4	1980	NADH-oxidation was antagonized by excess Cap2+ in the presence of glucose only.	NAD	0-4	cyclase associated actin cytoskeleton regulatory protein 2	Rattus norvegicus	41-45
32130883-4	2020	Bacteria confer resistance to inhibitors of NAMPT, the rate-limiting enzyme in the amidated NAD salvage pathway, in cancer cells and xenograft tumors.	NAD	92-95	nicotinamide phosphoribosyltransferase	Homo sapiens	44-49
6967287-2	1980	The enzyme activity is visually estimated by to reduction of NAD+ (non fluorescent) to NADH (fluorescent) in a coupled reaction with uridine diphosphate glucose dehydrogenase.	NAD	61-65	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	153-174
6967287-2	1980	The enzyme activity is visually estimated by to reduction of NAD+ (non fluorescent) to NADH (fluorescent) in a coupled reaction with uridine diphosphate glucose dehydrogenase.	NAD	87-91	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	153-174
6250824-4	1980	About 30% of the bound NAD+ could be reduced with rabbit muscle lactae dehydrogenase, yeast alcohol dehydrogenase and Bacillus subtilis alanine dehydrogenase; 84% of the bound ADP was phosphorylated with rabbit muscle creatine kinase.	NAD	23-27	creatine kinase M-type	Oryctolagus cuniculus	211-233
31987812-6	2020	Though treatment of cells with MPP+ also increased pAMPK levels, but, SIRT1 and PGC1alpha levels decreased substantially, possibly due to the block in the mitochondrial electron transport chain and reduced NAD/NADH levels.	NAD	206-209	peroxisome proliferative activated receptor, gamma, coactivator 1 alpha	Mus musculus	80-89
31987812-6	2020	Though treatment of cells with MPP+ also increased pAMPK levels, but, SIRT1 and PGC1alpha levels decreased substantially, possibly due to the block in the mitochondrial electron transport chain and reduced NAD/NADH levels.	NAD	210-214	peroxisome proliferative activated receptor, gamma, coactivator 1 alpha	Mus musculus	80-89
32042007-9	2020	Furthermore, treatment with FK866, a selective inhibitor of the NAD+ salvage pathway enzyme nicotinamide phosphoribosyltransferase (NAMPT), synergizes with MMS to induce cytotoxicity and Aag-/- cells are resistant to this combination FK866 and MMS treatment.	NAD	64-67	nicotinamide phosphoribosyltransferase	Homo sapiens	92-130
32042007-9	2020	Furthermore, treatment with FK866, a selective inhibitor of the NAD+ salvage pathway enzyme nicotinamide phosphoribosyltransferase (NAMPT), synergizes with MMS to induce cytotoxicity and Aag-/- cells are resistant to this combination FK866 and MMS treatment.	NAD	64-67	nicotinamide phosphoribosyltransferase	Homo sapiens	132-137
6988213-5	1980	Immobilization of NADH onto this copolymer was accomplished in three steps, namely, alkylation of NAD at N-1, reduction of the nicotinamide moiety with dithionite and Dimroth rearrangement of the alkyl linkage from the N-1 to the C-6 amino position.	NAD	18-22	complement C6	Homo sapiens	230-233
31732790-5	2020	Dimerisation is essential for the NAD-biosynthetic capacity of NAMPT.	NAD	34-37	nicotinamide phosphoribosyltransferase	Homo sapiens	63-68
6988213-5	1980	Immobilization of NADH onto this copolymer was accomplished in three steps, namely, alkylation of NAD at N-1, reduction of the nicotinamide moiety with dithionite and Dimroth rearrangement of the alkyl linkage from the N-1 to the C-6 amino position.	NAD	18-21	complement C6	Homo sapiens	230-233
6988213-7	1980	Using this copolymer, immobilization of NADH through the adenine C-6 amino position was accomplished in a single step.	NAD	40-44	complement C6	Homo sapiens	65-68
32015410-3	2020	Moreover, the levels of NADP+, NADPH, NAD+, and NADH were significantly decreased in the brown adipose tissue (BAT) of the HFD-fed IDH2KO animals, accompanied by decreased mitochondrial function and reduced expression of key genes involved in mitochondrial biogenesis, energy expenditure, and ROS resolution.	NAD	24-27	isocitrate dehydrogenase 2 (NADP+), mitochondrial	Mus musculus	131-135
226134-10	1979	It was decreased in particles treated to remove the inhibitor protein, either by prior energisation of the particles with NADH, or by addition of aurovertin, which competes with the inhibitor protein for the ATPase.	NAD	122-126	dynein axonemal heavy chain 8	Homo sapiens	208-214
32015410-3	2020	Moreover, the levels of NADP+, NADPH, NAD+, and NADH were significantly decreased in the brown adipose tissue (BAT) of the HFD-fed IDH2KO animals, accompanied by decreased mitochondrial function and reduced expression of key genes involved in mitochondrial biogenesis, energy expenditure, and ROS resolution.	NAD	48-52	isocitrate dehydrogenase 2 (NADP+), mitochondrial	Mus musculus	131-135
31710095-7	2020	Protein levels of nicotinamide phosphoribosyltransferase (NAMPT), an essential NAD+ biosynthetic enzyme in skeletal muscle, decreased 14% with NR.	NAD	79-82	nicotinamide phosphoribosyltransferase	Homo sapiens	18-56
31710095-7	2020	Protein levels of nicotinamide phosphoribosyltransferase (NAMPT), an essential NAD+ biosynthetic enzyme in skeletal muscle, decreased 14% with NR.	NAD	79-82	nicotinamide phosphoribosyltransferase	Homo sapiens	58-63
445827-1	1979	We describe a multi-point method for the determination of the serum enzyme activity 5"-nucleotidase by means of an NADH sensor reaction.	NAD	115-119	5'-nucleotidase ecto	Homo sapiens	84-99
30556496-7	2020	Although the tertiary structure of BVR and its complex with NAD+ was determined more than 10 years ago, the catalytic residues and the reaction mechanism of BVR remain unknown.	NAD	60-64	biliverdin reductase A	Homo sapiens	35-38
37797-2	1979	The method employs the enzyme glucose dehydrogenase in the presence of mutarotase, with nicotinamide adenine dinucleotide as hydrogen acceptor.	NAD	88-121	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	30-51
31691304-7	2020	Importantly, genetic deficiencies in several metabolite repair enzymes lead to "inborn errors of metabolite repair", such as L-2-hydroxyglutaric aciduria, D-2-hydroxyglutaric aciduria, "ubiquitous glucose-6-phosphatase" (G6PC3) deficiency, the neutropenia present in Glycogen Storage Disease type Ib or defects in the enzymes that repair the hydrated forms of NADH or NADPH.	NAD	360-364	glucose-6-phosphatase catalytic subunit 1	Homo sapiens	197-218
121007-4	1979	Citrate synthase of both organisms showed low sensitivity to 2-oxoglutarate, NADH and ATP.	NAD	77-81	citrate synthase	Homo sapiens	0-16
31678070-9	2020	Increased lipid accumulation and reduced NAD+ and SIRT1 activity were observed in Phgdh-knockout MEF and primary hepatocytes incubated with free fatty acids; these effects were reversed by overexpression of Phgdh.	NAD	41-44	phosphoglycerate dehydrogenase	Homo sapiens	82-87
31678070-9	2020	Increased lipid accumulation and reduced NAD+ and SIRT1 activity were observed in Phgdh-knockout MEF and primary hepatocytes incubated with free fatty acids; these effects were reversed by overexpression of Phgdh.	NAD	41-44	phosphoglycerate dehydrogenase	Homo sapiens	207-212
210449-1	1978	In the presence of ATP and a cytosolic factor, cholera toxin fragment A1 catalyzes the transfer of ADP-ribose from NAD to a number of soluble and membrane-bound proteins of the pigeon erythrocyte.	NAD	115-118	ATPase phospholipid transporting 8A2	Homo sapiens	19-72
201613-3	1977	Like 5-methylphenazinium methyl sulfate (PMS), it mediates electron transfer between NADH and various electron acceptors such as tetrazolium dyes or the electrode of an enzymic electric cell, and yet it does not deteriorate upon storage under scattered light in normal laboratories.	NAD	85-89	proline rich protein BstNI subfamily 1	Homo sapiens	41-44
31881755-10	2019	We point out new roles of CD38 and CD157 during neuronal development and aging in relation to nicotinamide adenine dinucleotide+ levels in embryonic and adult nervous systems.	NAD	94-127	bone marrow stromal cell antigen 1	Mus musculus	35-40
201613-4	1977	The rate of reduction of 1-methoxyPMS coupled to the reoxidation of NADH produced by the lactate dehydrogenase reaction, was even faster than that of PMS.	NAD	68-72	proline rich protein BstNI subfamily 1	Homo sapiens	34-37
31875550-0	2019	Decapping Enzyme NUDT12 Partners with BLMH for Cytoplasmic Surveillance of NAD-Capped RNAs.	NAD	75-78	nudix hydrolase 12	Homo sapiens	17-23
199007-6	1977	A distinct correlation was discovered between the intensity of the reactions for Al.,P.,ATP-ase and NADH2 t.r.	NAD	100-105	dynein axonemal heavy chain 8	Homo sapiens	88-95
21484-3	1977	The activity of NADP-dependent glutathione reductase was increased under effect of ADP; at the same time, the activity of NAD-dependent glutathione reductase did not depend on the diphosphate effect.	NAD	16-19	glutathione-disulfide reductase	Homo sapiens	31-52
31844103-1	2019	Mammalian Sirtuin 6 (Sirt6) is an NAD+-dependent protein deacylase regulating metabolism and chromatin homeostasis.	NAD	34-37	sirtuin 6	Homo sapiens	10-19
31844103-1	2019	Mammalian Sirtuin 6 (Sirt6) is an NAD+-dependent protein deacylase regulating metabolism and chromatin homeostasis.	NAD	34-37	sirtuin 6	Homo sapiens	21-26
21484-3	1977	The activity of NADP-dependent glutathione reductase was increased under effect of ADP; at the same time, the activity of NAD-dependent glutathione reductase did not depend on the diphosphate effect.	NAD	16-19	glutathione-disulfide reductase	Homo sapiens	136-157
888410-2	1977	The method is based on the property of alcohol dehydrogenase (from horse liver tissue) to catalyze the reduction of fatty-aromatic aldehydes (products of the MAO reaction) to appropriate alcohols in presence of NADH2 excess.	NAD	211-216	monoamine oxidase A	Rattus norvegicus	158-161
31993108-3	2019	Nicotinamide phosphoribosyltransferase (NAMPT) is an important rate-limiting enzyme found throughout the body that converts the intracellular pool of nicotinamide adenine dinucleotide (NAD) into nicotinamide mononucleotide (NMN).	NAD	150-183	nicotinamide phosphoribosyltransferase	Homo sapiens	0-38
31993108-3	2019	Nicotinamide phosphoribosyltransferase (NAMPT) is an important rate-limiting enzyme found throughout the body that converts the intracellular pool of nicotinamide adenine dinucleotide (NAD) into nicotinamide mononucleotide (NMN).	NAD	150-183	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
31993108-3	2019	Nicotinamide phosphoribosyltransferase (NAMPT) is an important rate-limiting enzyme found throughout the body that converts the intracellular pool of nicotinamide adenine dinucleotide (NAD) into nicotinamide mononucleotide (NMN).	NAD	185-188	nicotinamide phosphoribosyltransferase	Homo sapiens	0-38
31993108-3	2019	Nicotinamide phosphoribosyltransferase (NAMPT) is an important rate-limiting enzyme found throughout the body that converts the intracellular pool of nicotinamide adenine dinucleotide (NAD) into nicotinamide mononucleotide (NMN).	NAD	185-188	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
33046741-6	2020	Our results demonstrated that shorter and stricter reaction time was critical to approach the initial rate of NAD+-dependent desuccinylation activity in crude cell lysate systems, as compared to the desuccinylation reaction of purified His-SIRT5.	NAD	110-114	sirtuin 5	Homo sapiens	240-245
31598701-5	2019	Pyruvate represses histone gene expression by inducing the expression of NAD+ biosynthesis enzyme, nicotinamide phosphoribosyltransferase (NAMPT) via myocyte enhancer factor 2C (MEF2C), which then increases NAD+ levels and activates the histone deacetylase activity of SIRT1.	NAD	207-210	nicotinamide phosphoribosyltransferase	Homo sapiens	139-144
831800-7	1977	It is concluded that the rate of uptake of transferrin-bound iron by immature erythroid cells is dependent on the intracellular concentration of ATP but is independent of the NADH concentration.	NAD	175-179	serotransferrin	Oryctolagus cuniculus	43-54
30582964-5	2019	The results indicated cluster genes related to NAD+ biosynthesis (including NAMPT), DNA repair, and ATP-binding cassette transporters were differentially altered in these cells.	NAD	47-51	nicotinamide phosphoribosyltransferase	Homo sapiens	76-81
188354-0	1977	NADH-coupled spectrophotometric assy of diamine oxidase.	NAD	0-4	amine oxidase copper containing 1	Homo sapiens	40-55
31649033-4	2019	Notably, GSNO reductase (GSNOR, Adh5) accounts for most NADH-dependent GSNOR activity, whereas NADPH-dependent GSNOR activity is largely unaccounted for (CBR1 mediates a minor portion).	NAD	56-60	alcohol dehydrogenase 5 (class III), chi polypeptide	Homo sapiens	9-23
31649033-4	2019	Notably, GSNO reductase (GSNOR, Adh5) accounts for most NADH-dependent GSNOR activity, whereas NADPH-dependent GSNOR activity is largely unaccounted for (CBR1 mediates a minor portion).	NAD	56-60	alcohol dehydrogenase 5 (class III), chi polypeptide	Homo sapiens	25-30
12171-10	1976	Titration of the adrenodoxin reductase-adrenodoxin complex with the physiologic reductant, NADPH, was followed by EPR and visible spectra, and yielded an order of reduction of the components identical with that seen when NADH was used as reductant.	NAD	221-225	ferredoxin reductase	Homo sapiens	17-38
31649033-4	2019	Notably, GSNO reductase (GSNOR, Adh5) accounts for most NADH-dependent GSNOR activity, whereas NADPH-dependent GSNOR activity is largely unaccounted for (CBR1 mediates a minor portion).	NAD	56-60	alcohol dehydrogenase 5 (class III), chi polypeptide	Homo sapiens	32-36
31649033-4	2019	Notably, GSNO reductase (GSNOR, Adh5) accounts for most NADH-dependent GSNOR activity, whereas NADPH-dependent GSNOR activity is largely unaccounted for (CBR1 mediates a minor portion).	NAD	56-60	alcohol dehydrogenase 5 (class III), chi polypeptide	Homo sapiens	71-76
6475-9	1976	Titration of adrenodoxin reductase with NADH, instead of NADPH, provides a curved titration plot rather than the sharp break seen with NADPH, and permits calculation of a potential for the AR/ARH2 couple of -0.291 V, close to that of NAD(P)H (-0.316 V).	NAD	40-44	ferredoxin reductase	Homo sapiens	13-34
4794-3	1976	In agreement with published data, the 15-hydroxyprostaglandin dehydrogenase(s) derived from the kidney cortex were found to degrade all prostaglandins examined (PGE, PGF, PGA) in the presence of added cofactor NAD.	NAD	210-213	carbonyl reductase [NADPH] 1	Oryctolagus cuniculus	38-75
31754102-4	2019	WRN regulates transcription of a key NAD+ biosynthetic enzyme nicotinamide nucleotide adenylyltransferase 1 (NMNAT1).	NAD	37-41	WRN RecQ like helicase	Homo sapiens	0-3
31754102-4	2019	WRN regulates transcription of a key NAD+ biosynthetic enzyme nicotinamide nucleotide adenylyltransferase 1 (NMNAT1).	NAD	37-41	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	62-107
31754102-4	2019	WRN regulates transcription of a key NAD+ biosynthetic enzyme nicotinamide nucleotide adenylyltransferase 1 (NMNAT1).	NAD	37-41	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	109-115
31754102-5	2019	NAD+ repletion restores NAD+ metabolic profiles and improves mitochondrial quality through DCT-1 and ULK-1-dependent mitophagy.	NAD	0-4	unc-51 like autophagy activating kinase 1	Homo sapiens	101-106
180230-2	1976	Glucose is oxidized to gluconic acid and NAD is reduced to NADH in the presence of glucose dehydrogenase.	NAD	41-44	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	83-104
31456414-6	2019	Expression patterns of NAD+ biosynthetic enzymes were then biochemically studied in isolated organelles, revealing expression of NAMPT in all three cellular compartments, while NAPRT was predominantly cytosolic and mitochondrial, and NRK mitochondrial and nuclear.	NAD	23-27	nicotinamide phosphoribosyltransferase	Homo sapiens	129-134
180230-2	1976	Glucose is oxidized to gluconic acid and NAD is reduced to NADH in the presence of glucose dehydrogenase.	NAD	59-63	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	83-104
173299-0	1975	Regulation of citrate synthase activity in methylotrophs by reduced nicotinamide-adenine dinucleotide, adenine nucleotides and 2-oxoglutarate.	NAD	68-101	citrate synthase	Homo sapiens	14-30
1125255-7	1975	Reduction of alpha-lipoic cid with NADH by lipoyl dehydrogenase was activated by NAD, but that of asparagusic acid by asparagusate dehydrogenase was inactivated by NAD.	NAD	35-39	dihydrolipoamide dehydrogenase	Homo sapiens	43-63
31803365-1	2019	APO866 is a small molecule drug that specifically inhibits nicotinamide phosphoribosyltransferase (NAMPT), a key enzyme involved in nicotinamide adenine dinucleotide (NAD) biosynthesis from the natural precursor nicotinamide.	NAD	132-165	nicotinamide phosphoribosyltransferase	Homo sapiens	59-97
31803365-1	2019	APO866 is a small molecule drug that specifically inhibits nicotinamide phosphoribosyltransferase (NAMPT), a key enzyme involved in nicotinamide adenine dinucleotide (NAD) biosynthesis from the natural precursor nicotinamide.	NAD	132-165	nicotinamide phosphoribosyltransferase	Homo sapiens	99-104
31803365-1	2019	APO866 is a small molecule drug that specifically inhibits nicotinamide phosphoribosyltransferase (NAMPT), a key enzyme involved in nicotinamide adenine dinucleotide (NAD) biosynthesis from the natural precursor nicotinamide.	NAD	167-170	nicotinamide phosphoribosyltransferase	Homo sapiens	59-97
31803365-1	2019	APO866 is a small molecule drug that specifically inhibits nicotinamide phosphoribosyltransferase (NAMPT), a key enzyme involved in nicotinamide adenine dinucleotide (NAD) biosynthesis from the natural precursor nicotinamide.	NAD	167-170	nicotinamide phosphoribosyltransferase	Homo sapiens	99-104
1125255-7	1975	Reduction of alpha-lipoic cid with NADH by lipoyl dehydrogenase was activated by NAD, but that of asparagusic acid by asparagusate dehydrogenase was inactivated by NAD.	NAD	35-38	dihydrolipoamide dehydrogenase	Homo sapiens	43-63
31628926-4	2019	Nicotinamide phosphoribosyltransferase (NAMPT), which is a rate-limiting enzyme for NAD+ synthesis in the salvage pathway, was shown to be overexpressed in many types of cancer cells.	NAD	84-88	nicotinamide phosphoribosyltransferase	Homo sapiens	0-38
1125255-7	1975	Reduction of alpha-lipoic cid with NADH by lipoyl dehydrogenase was activated by NAD, but that of asparagusic acid by asparagusate dehydrogenase was inactivated by NAD.	NAD	81-84	dihydrolipoamide dehydrogenase	Homo sapiens	43-63
31628926-4	2019	Nicotinamide phosphoribosyltransferase (NAMPT), which is a rate-limiting enzyme for NAD+ synthesis in the salvage pathway, was shown to be overexpressed in many types of cancer cells.	NAD	84-88	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
31628926-5	2019	The NAMPT inhibitor FK866 significantly depletes NAD+ and subsequently suppresses cancer cell proliferation.	NAD	49-53	nicotinamide phosphoribosyltransferase	Homo sapiens	4-9
165834-2	1975	Lipoamide dehydrogenase NADH: lipoamide oxidoreductase, (EC 1.6.4.3) from pig heart has been separated into two sets of isoenzymes by chromatography on lipoyl- and NAD+-derivatized Sepharose-4B matrices.	NAD	164-168	dihydrolipoamide dehydrogenase	Sus scrofa	0-23
31465774-0	2019	Functions of aryl hydrocarbon receptor (AHR) and CD38 in NAD metabolism and nonalcoholic steatohepatitis (NASH).	NAD	57-60	aryl hydrocarbon receptor	Homo sapiens	13-38
31465774-0	2019	Functions of aryl hydrocarbon receptor (AHR) and CD38 in NAD metabolism and nonalcoholic steatohepatitis (NASH).	NAD	57-60	aryl hydrocarbon receptor	Homo sapiens	40-43
31465774-1	2019	Aryl hydrocarbon receptor (AHR), identified in studies of dioxin toxicity, has been characterized as ligand-activated transcription factor involved in diverse functions including microbial defense, cell proliferation, immunity and NAD metabolism.	NAD	231-234	aryl hydrocarbon receptor	Homo sapiens	0-25
235983-10	1975	The addition of succinate, NADH or ascorbate/N,N,N"-N"-tetramethyl-p-phenylenediamine as electron donor induced high ATPase activity in the presence of low concentrations of uncouplers.	NAD	27-31	dynein axonemal heavy chain 8	Homo sapiens	117-123
31465774-1	2019	Aryl hydrocarbon receptor (AHR), identified in studies of dioxin toxicity, has been characterized as ligand-activated transcription factor involved in diverse functions including microbial defense, cell proliferation, immunity and NAD metabolism.	NAD	231-234	aryl hydrocarbon receptor	Homo sapiens	27-30
31465774-2	2019	AHR targets of the latter function are PARPs/ARTs and CD38 that are regulating glucose and lipid metabolism via NAD-dependent sirtuins.	NAD	112-115	aryl hydrocarbon receptor	Homo sapiens	0-3
4377102-0	1974	The binding of oxidized and reduced nicotinamide--adenine dinucleotides to bovine liver uridine diphosphate glucose dehydrogenase.	NAD	36-71	glucose dehydrogenase	Bos taurus	108-129
31665043-3	2019	Successful attempts to rescue CI function by introducing an exogenous NADH dehydrogenase, such as the NDI1 from Saccharomyces cerevisiae (ScNDI1), have been reported although with drawbacks related to competition with CI.	NAD	70-74	NADH-ubiquinone reductase (H(+)-translocating) NDI1	Saccharomyces cerevisiae S288C	102-106
31636635-2	2019	There, high extracellular levels of nucleotides, mainly NAD+ and ATP, are catabolized by different ectonucleotidases, which can be divided in two families according to substrate specificity: on one side those that metabolize NAD+, including CD38, CD157, and CD203a; on the other, those that convert ATP, namely CD39 (and other ENTPDases) and CD73.	NAD	56-60	5'-nucleotidase ecto	Homo sapiens	342-346
4350136-0	1972	Study of the interaction of  -glycerophosphate dehydrogenase and NAD-H by the methods of circular dichroism and fluorimetry.	NAD	65-70	glycerol-3-phosphate dehydrogenase 1	Homo sapiens	30-60
31636635-2	2019	There, high extracellular levels of nucleotides, mainly NAD+ and ATP, are catabolized by different ectonucleotidases, which can be divided in two families according to substrate specificity: on one side those that metabolize NAD+, including CD38, CD157, and CD203a; on the other, those that convert ATP, namely CD39 (and other ENTPDases) and CD73.	NAD	225-229	5'-nucleotidase ecto	Homo sapiens	342-346
4339465-0	1972	Inhibition of rat citrate synthase by acetoacetyl CoA and NADH.	NAD	58-62	citrate synthase	Rattus norvegicus	18-34
4320681-1	1970	The enzymatic technique using 3alpha-hydroxysteroid dehydrogenase for determining bile acids in blood has been modified by measuring the reduced nicotinamide adenine dinucleotide fluorimetrically.	NAD	145-178	aldo-keto reductase family 1 member C3	Homo sapiens	30-65
31104322-0	2019	An integrative bioinformatics pipeline to demonstrate the alteration of the interaction between the ALDH2*2 allele with NAD+ and Disulfiram.	NAD	120-124	aldehyde dehydrogenase 2 family member	Homo sapiens	100-105
31104322-5	2019	In this study, we aimed to test the known inactive allele ALDH2*2, to validate the use of our extensive computational pipeline (in silico tools, molecular modeling, and molecular docking) for testing the interaction between the ALDH2*2 allele, NAD+, and Disulfiram.	NAD	244-248	aldehyde dehydrogenase 2 family member	Homo sapiens	58-63
31104322-5	2019	In this study, we aimed to test the known inactive allele ALDH2*2, to validate the use of our extensive computational pipeline (in silico tools, molecular modeling, and molecular docking) for testing the interaction between the ALDH2*2 allele, NAD+, and Disulfiram.	NAD	244-248	aldehyde dehydrogenase 2 family member	Homo sapiens	228-233
30607371-7	2018	Nicotinamide phosphoribosyltransferase (NAMPT) inhibition induced NAD + depletion and resulted in equilibration of metabolites upstream of glyceraldehyde phosphate dehydrogenase (GAPDH).	NAD	66-71	nicotinamide phosphoribosyltransferase	Homo sapiens	0-38
4388010-4	1969	gamma-Glutamylcysteine synthetase is subject to feedback inhibition by GSH, and is also inhibited by NADH, and to a lesser extent by NAD(+) and NADPH.	NAD	101-105	glutamate-cysteine ligase catalytic subunit	Homo sapiens	0-33
30607371-7	2018	Nicotinamide phosphoribosyltransferase (NAMPT) inhibition induced NAD + depletion and resulted in equilibration of metabolites upstream of glyceraldehyde phosphate dehydrogenase (GAPDH).	NAD	66-71	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
4388010-4	1969	gamma-Glutamylcysteine synthetase is subject to feedback inhibition by GSH, and is also inhibited by NADH, and to a lesser extent by NAD(+) and NADPH.	NAD	133-139	glutamate-cysteine ligase catalytic subunit	Homo sapiens	0-33
4284825-0	1965	A kinetic study of the lipoamide dehydrogenase-NADH-dye reaction.	NAD	47-51	dihydrolipoamide dehydrogenase	Homo sapiens	23-46
31347251-3	2019	UV/Vis, resonance-Raman, and transient-absorption spectroscopy have been employed to characterize the catalytically competent intermediate [(tbbpy)2 RuII (tpphz)RhI Cp*] of [(tbbpy)2 Ru(tpphz)Rh(Cp*)Cl]Cl(PF6 )2 (Ru(tpphz)RhCp*), a photocatalyst for the hydrogenation of nicotinamide (NAD-analogue) and proton reduction, generated by electrochemical and chemical reduction.	NAD	285-288	sperm associated antigen 17	Homo sapiens	205-208
32990599-5	2020	COX6B2, but not its somatic isoform COX6B1, enhances activity of complex IV, increasing oxidative phosphorylation (OXPHOS) and NAD+ generation.	NAD	127-131	cytochrome c oxidase subunit 6B2	Homo sapiens	0-6
13981232-0	1963	The use of deuterated DPNH mixtures as an aid in establishing dehydrogenase mechanism.	NAD	22-26	activation induced cytidine deaminase	Homo sapiens	42-45
32828286-7	2020	The preference of NADP+ over NAD+ was significantly subjected by a pair of Ser37 and Arg38, whose manners were similar to other Gfo/Idh/MocA members.	NAD	29-33	dedicator of cytokinesis 3	Homo sapiens	136-140
33957971-12	2021	In addition, miR-34a repletion resulted in prominent reductions in Nampt expression levels, NAD+ content, NAD+/NADH ratio, and Sirt1 activity, whereas anti-miR-34a treatment exerted the opposite effects.	NAD	111-115	microRNA 34a	Homo sapiens	13-20
32651204-4	2020	In this study, based on the genetic manipulation and biochemical assay, we characterized XanH as an indispensable FAD-dependent halogenase (FDH) for the biosynthesis of 1 XanH was found to be a bifunctional protein capable of flavin reduction and chlorination, and exclusively used the reduced nicotinamide adenine dinucleotide (NADH).	NAD	294-327	alcohol dehydrogenase 5 (class III), chi polypeptide	Homo sapiens	114-138
32651204-4	2020	In this study, based on the genetic manipulation and biochemical assay, we characterized XanH as an indispensable FAD-dependent halogenase (FDH) for the biosynthesis of 1 XanH was found to be a bifunctional protein capable of flavin reduction and chlorination, and exclusively used the reduced nicotinamide adenine dinucleotide (NADH).	NAD	294-327	alcohol dehydrogenase 5 (class III), chi polypeptide	Homo sapiens	140-143
32651204-4	2020	In this study, based on the genetic manipulation and biochemical assay, we characterized XanH as an indispensable FAD-dependent halogenase (FDH) for the biosynthesis of 1 XanH was found to be a bifunctional protein capable of flavin reduction and chlorination, and exclusively used the reduced nicotinamide adenine dinucleotide (NADH).	NAD	329-333	alcohol dehydrogenase 5 (class III), chi polypeptide	Homo sapiens	114-138
32651204-4	2020	In this study, based on the genetic manipulation and biochemical assay, we characterized XanH as an indispensable FAD-dependent halogenase (FDH) for the biosynthesis of 1 XanH was found to be a bifunctional protein capable of flavin reduction and chlorination, and exclusively used the reduced nicotinamide adenine dinucleotide (NADH).	NAD	329-333	alcohol dehydrogenase 5 (class III), chi polypeptide	Homo sapiens	140-143
33957971-14	2021	CONCLUSION: This study identifies a significant role of miR-34a playing in MSC replicative senescence and natural senescence via targeting Nampt and further mediating by NAD+-Sirt1 pathway, carrying great implications for optimal strategies for MSC therapeutic applications.	NAD	170-174	microRNA 34a	Homo sapiens	56-63
32037512-12	2021	CONCLUSIONS AND IMPLICATIONS: The NAD+ boosting agent P7C3-A20 alleviates NAFLD through stimulating FGF21 and FGF1 in an LKB1/AMPK/CRTC2-dependent manner and shaping gut microbiota.	NAD	34-37	fibroblast growth factor 21	Mus musculus	100-105
32037512-12	2021	CONCLUSIONS AND IMPLICATIONS: The NAD+ boosting agent P7C3-A20 alleviates NAFLD through stimulating FGF21 and FGF1 in an LKB1/AMPK/CRTC2-dependent manner and shaping gut microbiota.	NAD	34-37	CREB regulated transcription coactivator 2	Mus musculus	131-136
31873757-0	2020	Extracellular signal-regulated kinase 1/2 regulates NAD metabolism during acute kidney injury through microRNA-34a-mediated NAMPT expression.	NAD	52-55	mitogen-activated protein kinase 3	Mus musculus	0-39
33946543-3	2021	NAD+ and AMP stabilize an inactive T-state of Fbp2 and thus, affect these interactions.	NAD	0-4	fructose-bisphosphatase 2	Homo sapiens	46-50
31873757-3	2020	In this study, ERK1/2 regulation of cellular nicotinamide adenine dinucleotide (NAD) and PGC-1alpha were explored.	NAD	45-78	mitogen-activated protein kinase 3	Mus musculus	15-21
31873757-3	2020	In this study, ERK1/2 regulation of cellular nicotinamide adenine dinucleotide (NAD) and PGC-1alpha were explored.	NAD	80-83	mitogen-activated protein kinase 3	Mus musculus	15-21
31873757-4	2020	Inhibition of ERK1/2 activation during AKI in mice using the MEK1/2 inhibitor, trametinib, attenuated renal cortical oxidized NAD (NAD+) depletion.	NAD	126-129	mitogen-activated protein kinase 3	Mus musculus	14-20
31873757-4	2020	Inhibition of ERK1/2 activation during AKI in mice using the MEK1/2 inhibitor, trametinib, attenuated renal cortical oxidized NAD (NAD+) depletion.	NAD	126-129	mitogen-activated protein kinase kinase 1	Mus musculus	61-67
31873757-4	2020	Inhibition of ERK1/2 activation during AKI in mice using the MEK1/2 inhibitor, trametinib, attenuated renal cortical oxidized NAD (NAD+) depletion.	NAD	131-134	mitogen-activated protein kinase 3	Mus musculus	14-20
31873757-4	2020	Inhibition of ERK1/2 activation during AKI in mice using the MEK1/2 inhibitor, trametinib, attenuated renal cortical oxidized NAD (NAD+) depletion.	NAD	131-134	mitogen-activated protein kinase kinase 1	Mus musculus	61-67
31873757-5	2020	The rate-limiting NAD biosynthesis salvage enzyme, NAMPT, decreased following AKI, and this decrease was prevented by ERK1/2 inhibition.	NAD	18-21	mitogen-activated protein kinase 3	Mus musculus	118-124
34046646-2	2021	The expression of nicotinamide phosphoribosyltransferase (NAMPT) is regulated in a circadian manner by the core clock mechanism and NAD+-dependent sirtuins, producing the circadian oscillation of NAD+.	NAD	132-136	nicotinamide phosphoribosyltransferase	Homo sapiens	18-56
31873757-8	2020	In addition, ERK1/2 activation increased acetylated PGC-1alpha, the less active form, whereas inhibition of ERK1/2 activation prevented an increase in acetylated PGC-1alpha after AKI through SIRT1 and NAD+ attenuation.	NAD	201-204	mitogen-activated protein kinase 3	Mus musculus	108-114
31873757-8	2020	In addition, ERK1/2 activation increased acetylated PGC-1alpha, the less active form, whereas inhibition of ERK1/2 activation prevented an increase in acetylated PGC-1alpha after AKI through SIRT1 and NAD+ attenuation.	NAD	201-204	peroxisome proliferative activated receptor, gamma, coactivator 1 alpha	Mus musculus	162-172
31873757-9	2020	These results implicate IR-induced ERK1/2 activation as an important contributor to the downregulation of both PGC-1alpha and NAD+ pathways that ultimately decrease cellular metabolism and renal function.	NAD	126-129	mitogen-activated protein kinase 3	Mus musculus	35-41
31873757-10	2020	Inhibition of ERK1/2 activation prior to the initiation of IR injury attenuated decreases in PGC-1alpha and NAD+ and prevented kidney dysfunction.	NAD	108-111	mitogen-activated protein kinase 3	Mus musculus	14-20
32846968-1	2020	The stress-inducible and senescence-associated tumor suppressor SIRT4, a member of the family of mitochondrial sirtuins (SIRT3, SIRT4, and SIRT5), regulates bioenergetics and metabolism via NAD+-dependent enzymatic activities.	NAD	190-194	sirtuin 5	Homo sapiens	139-144
34046646-2	2021	The expression of nicotinamide phosphoribosyltransferase (NAMPT) is regulated in a circadian manner by the core clock mechanism and NAD+-dependent sirtuins, producing the circadian oscillation of NAD+.	NAD	132-136	nicotinamide phosphoribosyltransferase	Homo sapiens	58-63
34046646-2	2021	The expression of nicotinamide phosphoribosyltransferase (NAMPT) is regulated in a circadian manner by the core clock mechanism and NAD+-dependent sirtuins, producing the circadian oscillation of NAD+.	NAD	196-200	nicotinamide phosphoribosyltransferase	Homo sapiens	18-56
34046646-2	2021	The expression of nicotinamide phosphoribosyltransferase (NAMPT) is regulated in a circadian manner by the core clock mechanism and NAD+-dependent sirtuins, producing the circadian oscillation of NAD+.	NAD	196-200	nicotinamide phosphoribosyltransferase	Homo sapiens	58-63
33918226-6	2021	Among NAD+ biosynthesis pathways in mammals, the NAD+ salvage pathway is the dominant pathway in most of tissues, and NAMPT is the rate limiting enzyme of this pathway.	NAD	6-10	nicotinamide phosphoribosyltransferase	Homo sapiens	118-123
32574562-4	2020	We generated a mouse that conditionally expresses the yeast NADH dehydrogenase (NDI1), a single enzyme that can replace the NAD+ regeneration capability of the 45-subunit mammalian mitochondrial complex I without proton pumping.	NAD	124-128	NADH-ubiquinone reductase (H(+)-translocating) NDI1	Saccharomyces cerevisiae S288C	80-84
32755591-5	2020	Notably, the mutants cannot be further activated by the endogenous activator nicotinamide mononucleotide (NMN), and active SARM1 is product inhibited by Nicotinamide (NAM), highlighting SARM1"s functional dependence on key metabolites in the NAD salvage pathway.	NAD	242-245	sterile alpha and TIR motif containing 1	Homo sapiens	123-128
32533606-3	2020	We recently reported that the overexpression of NAMPT, which is the rate-limiting enzyme in mammalian NAD+ salvage pathway, delays replicative senescence in vitro.	NAD	102-106	nicotinamide phosphoribosyltransferase	Homo sapiens	48-53
33918226-7	2021	However, only a few activators of NAMPT, which are supposed to increase NAD+, have been developed so far.	NAD	72-76	nicotinamide phosphoribosyltransferase	Homo sapiens	34-39
33349973-1	2021	Nicotinamide phosphoribosyltransferase (NAMPT) is a rate-limiting enzyme for nicotinamide adenine dinucleotide (NAD) synthesis and is involved in cancer cell proliferation through regulation of energy production pathways.	NAD	77-110	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
32651404-1	2020	The enzyme nicotidamide-N-methyltransferase (NNMT) regulates adipose tissue energy expenditure through increasing nicotinamide adenosine dinucleotide (NAD+) content.	NAD	151-155	nicotinamide N-methyltransferase	Homo sapiens	11-43
33349973-1	2021	Nicotinamide phosphoribosyltransferase (NAMPT) is a rate-limiting enzyme for nicotinamide adenine dinucleotide (NAD) synthesis and is involved in cancer cell proliferation through regulation of energy production pathways.	NAD	112-115	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
32651404-1	2020	The enzyme nicotidamide-N-methyltransferase (NNMT) regulates adipose tissue energy expenditure through increasing nicotinamide adenosine dinucleotide (NAD+) content.	NAD	151-155	nicotinamide N-methyltransferase	Homo sapiens	45-49
33522796-2	2021	Nicotinamide phosphoribosyltransferase (NAMPT) is a rate-limiting enzyme in NAD+ biosynthesis.	NAD	76-80	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
33522796-3	2021	Thus, boosting NAD+ level via an increase in NAMPT levels is an attractive approach for countering the effects of aging and metabolic disease.	NAD	15-19	nicotinamide phosphoribosyltransferase	Homo sapiens	45-50
32775493-2	2020	Although the causative gene, NMNAT1, plays an essential role in nuclear nicotinamide adenine dinucleotide (NAD)+ metabolism in tissues throughout the body, NMNAT1-associated disease is isolated to the retina.	NAD	72-105	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	29-35
32775493-2	2020	Although the causative gene, NMNAT1, plays an essential role in nuclear nicotinamide adenine dinucleotide (NAD)+ metabolism in tissues throughout the body, NMNAT1-associated disease is isolated to the retina.	NAD	72-105	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	156-162
32775493-2	2020	Although the causative gene, NMNAT1, plays an essential role in nuclear nicotinamide adenine dinucleotide (NAD)+ metabolism in tissues throughout the body, NMNAT1-associated disease is isolated to the retina.	NAD	107-110	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	29-35
33562281-5	2021	Moreover, exogenous NAD+ reduced senescence-associated-beta-galactosidase activity, and downregulated poly (ADP-ribose) polymerase 1 expression.	NAD	20-24	galactosidase beta 1	Homo sapiens	55-73
32775493-2	2020	Although the causative gene, NMNAT1, plays an essential role in nuclear nicotinamide adenine dinucleotide (NAD)+ metabolism in tissues throughout the body, NMNAT1-associated disease is isolated to the retina.	NAD	107-110	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	156-162
33546767-1	2021	BACKGROUND: Nicotinamide phosphoribosyltransferase (NAMPT) regulates cellular functions through the protein deacetylation activity of nicotinamide adenine dinucleotide (NAD+)-dependent sirtuins (SIRTs).	NAD	134-167	nicotinamide phosphoribosyltransferase	Homo sapiens	12-50
33181191-10	2021	PAK1 knockdown disrupted the NAD+/NADH and NADP+/NADPH ratios, and elevated ROS.	NAD	29-33	p21 (RAC1) activated kinase 1	Homo sapiens	0-4
32332106-9	2020	Results obtained from the glycerol condition indicate that the internal NADH:ubiquinone oxidoreductase Ndi1 is part of an electron transport chain supercomplex.	NAD	72-76	NADH-ubiquinone reductase (H(+)-translocating) NDI1	Saccharomyces cerevisiae S288C	103-107
32371575-6	2020	Moreover, we report a novel drug combination in which nicotinamide phosphoribosyltransferase (NAMPT) inhibition, which blocks production of the PHGDH substrate NAD+, synergized with NCT-503 to abolish ES cell proliferation and tumor growth.	NAD	160-164	nicotinamide phosphoribosyltransferase	Homo sapiens	54-92
33181191-10	2021	PAK1 knockdown disrupted the NAD+/NADH and NADP+/NADPH ratios, and elevated ROS.	NAD	34-38	p21 (RAC1) activated kinase 1	Homo sapiens	0-4
32371575-6	2020	Moreover, we report a novel drug combination in which nicotinamide phosphoribosyltransferase (NAMPT) inhibition, which blocks production of the PHGDH substrate NAD+, synergized with NCT-503 to abolish ES cell proliferation and tumor growth.	NAD	160-164	nicotinamide phosphoribosyltransferase	Homo sapiens	94-99
33468661-2	2021	In healthy neurons, SARM1 is autoinhibited and, upon injury autoinhibition is relieved, activating the SARM1 enzyme to deplete NAD+ and induce axon degeneration.	NAD	127-131	sterile alpha and TIR motif containing 1	Homo sapiens	20-25
32371575-6	2020	Moreover, we report a novel drug combination in which nicotinamide phosphoribosyltransferase (NAMPT) inhibition, which blocks production of the PHGDH substrate NAD+, synergized with NCT-503 to abolish ES cell proliferation and tumor growth.	NAD	160-164	phosphoglycerate dehydrogenase	Homo sapiens	144-149
31278906-2	2019	SARM1 activity depends on the integrity of the protein"s SAM domains, as well as on the enzymatic conversion of NAD+ to ADPR (ADP Ribose) products by the SARM1"s TIR domain.	NAD	112-116	sterile alpha and TIR motif containing 1	Homo sapiens	0-5
31278906-2	2019	SARM1 activity depends on the integrity of the protein"s SAM domains, as well as on the enzymatic conversion of NAD+ to ADPR (ADP Ribose) products by the SARM1"s TIR domain.	NAD	112-116	sterile alpha and TIR motif containing 1	Homo sapiens	154-159
31278893-11	2019	Utilizing co-immunoprecipitation method, we found that NAD administration promoted the Sirt5 and SDH-a interaction and decreased the succinylation level of SDH-a.	NAD	55-58	succinate dehydrogenase complex flavoprotein subunit A	Rattus norvegicus	97-102
33468661-2	2021	In healthy neurons, SARM1 is autoinhibited and, upon injury autoinhibition is relieved, activating the SARM1 enzyme to deplete NAD+ and induce axon degeneration.	NAD	127-131	sterile alpha and TIR motif containing 1	Homo sapiens	103-108
31278893-11	2019	Utilizing co-immunoprecipitation method, we found that NAD administration promoted the Sirt5 and SDH-a interaction and decreased the succinylation level of SDH-a.	NAD	55-58	succinate dehydrogenase complex flavoprotein subunit A	Rattus norvegicus	156-161
33468661-6	2021	Mutation of residues in full-length SARM1 within the region encompassed by the peptide led to loss of autoinhibition, rendering SARM1 constitutively active and inducing spontaneous NAD+ and axon loss.	NAD	181-185	sterile alpha and TIR motif containing 1	Homo sapiens	36-41
31278893-12	2019	These results implied that exogenous NAD administration promoted Sirt5-mediated SDH-a desuccinylation and decreased the activity of SDH-a, which attenuated the succinate accumulation during ischemia and its depleting rate during reperfusion and finally alleviated reactive oxygen species generation.	NAD	37-40	succinate dehydrogenase complex flavoprotein subunit A	Rattus norvegicus	80-85
33356147-3	2021	We herein show that starting from O-phospho-l-Ser (OPS) and l-Glu precursors, CmnB catalyzes the condensation reaction to generate a metabolite intermediate N-(1-amino-1-carboxyl-2-ethyl)glutamic acid (ACEGA), which undergoes NAD+-dependent oxidative hydrolysis by CmnK to generate l-Dap.	NAD	226-229	death associated protein	Homo sapiens	284-287
31278893-12	2019	These results implied that exogenous NAD administration promoted Sirt5-mediated SDH-a desuccinylation and decreased the activity of SDH-a, which attenuated the succinate accumulation during ischemia and its depleting rate during reperfusion and finally alleviated reactive oxygen species generation.	NAD	37-40	succinate dehydrogenase complex flavoprotein subunit A	Rattus norvegicus	132-137
31439792-1	2019	SARM1 (sterile alpha and TIR motif containing 1) is responsible for depletion of nicotinamide adenine dinucleotide in its oxidized form (NAD+) during Wallerian degeneration associated with neuropathies.	NAD	81-114	sterile alpha and TIR motif containing 1	Homo sapiens	0-5
31439792-1	2019	SARM1 (sterile alpha and TIR motif containing 1) is responsible for depletion of nicotinamide adenine dinucleotide in its oxidized form (NAD+) during Wallerian degeneration associated with neuropathies.	NAD	81-114	sterile alpha and TIR motif containing 1	Homo sapiens	7-47
31439792-1	2019	SARM1 (sterile alpha and TIR motif containing 1) is responsible for depletion of nicotinamide adenine dinucleotide in its oxidized form (NAD+) during Wallerian degeneration associated with neuropathies.	NAD	137-141	sterile alpha and TIR motif containing 1	Homo sapiens	0-5
33440786-4	2021	In this review, we provide an overview of the current knowledge of NAD+ metabolism, highlighting the functional liaison with mono(ADP-ribosyl)ating enzymes, such as the well-known ARTD10 (also named PARP10), SIRT6, and SIRT7.	NAD	67-71	sirtuin 6	Homo sapiens	208-213
31439792-1	2019	SARM1 (sterile alpha and TIR motif containing 1) is responsible for depletion of nicotinamide adenine dinucleotide in its oxidized form (NAD+) during Wallerian degeneration associated with neuropathies.	NAD	137-141	sterile alpha and TIR motif containing 1	Homo sapiens	7-47
31439793-3	2019	Both cell death induction and NAD+ cleavage activity of plant TIR domains require known self-association interfaces and a putative catalytic glutamic acid that is conserved in both bacterial TIR NAD+-cleaving enzymes (NADases) and the mammalian SARM1 (sterile alpha and TIR motif containing 1) NADase.	NAD	30-34	sterile alpha and TIR motif containing 1	Homo sapiens	245-250
31439793-3	2019	Both cell death induction and NAD+ cleavage activity of plant TIR domains require known self-association interfaces and a putative catalytic glutamic acid that is conserved in both bacterial TIR NAD+-cleaving enzymes (NADases) and the mammalian SARM1 (sterile alpha and TIR motif containing 1) NADase.	NAD	195-199	sterile alpha and TIR motif containing 1	Homo sapiens	245-250
33171124-3	2021	Here, we find nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme of the NAD+ biogenesis, drives interferon gamma (IFNgamma)-induced PD-L1 expression in multiple types of tumors and governs tumor immune evasion in a CD8+ T cell-dependent manner.	NAD	94-98	nicotinamide phosphoribosyltransferase	Homo sapiens	14-52
31456942-1	2019	Sirtuin 5 (SIRT5), a mitochondrial class III NAD-dependent deacetylase, plays controversial roles in tumorigenesis and chemoresistance.	NAD	45-48	sirtuin 5	Homo sapiens	0-9
31456942-1	2019	Sirtuin 5 (SIRT5), a mitochondrial class III NAD-dependent deacetylase, plays controversial roles in tumorigenesis and chemoresistance.	NAD	45-48	sirtuin 5	Homo sapiens	11-16
33171124-3	2021	Here, we find nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme of the NAD+ biogenesis, drives interferon gamma (IFNgamma)-induced PD-L1 expression in multiple types of tumors and governs tumor immune evasion in a CD8+ T cell-dependent manner.	NAD	94-98	nicotinamide phosphoribosyltransferase	Homo sapiens	54-59
31391079-0	2019	NAD+ improves neuromuscular development in a zebrafish model of FKRP-associated dystroglycanopathy.	NAD	0-4	fukutin related protein	Danio rerio	64-68
32541922-1	2021	Sirtuin 6 (SIRT6), a member of the sirtuin family, is a nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase that is involved in various physiological and pathological processes.	NAD	56-89	sirtuin 6	Homo sapiens	0-9
31391079-6	2019	RESULTS: We found that NAD+ supplementation prior to muscle development improved muscle structure, myotendinous junction structure, and muscle function in fkrp morphants.	NAD	23-27	fukutin related protein	Danio rerio	155-159
32541922-1	2021	Sirtuin 6 (SIRT6), a member of the sirtuin family, is a nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase that is involved in various physiological and pathological processes.	NAD	56-89	sirtuin 6	Homo sapiens	11-16
32541922-1	2021	Sirtuin 6 (SIRT6), a member of the sirtuin family, is a nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase that is involved in various physiological and pathological processes.	NAD	91-94	sirtuin 6	Homo sapiens	0-9
31448236-0	2019	NAMPT and NAPRT, Key Enzymes in NAD Salvage Synthesis Pathway, Are of Negative Prognostic Value in Colorectal Cancer.	NAD	32-35	nicotinamide phosphoribosyltransferase	Homo sapiens	0-5
31448236-2	2019	Nicotinamide phosphoribosyltransferase (NAMPT) and nicotinate phosphoribosyltransferase (NAPRT) are key enzymes for NAD salvage biosynthesis pathway, which reciprocally synthesize NAD to supply the main source of NAD biosythesis.	NAD	116-119	nicotinamide phosphoribosyltransferase	Homo sapiens	0-38
32712045-12	2021	CONCLUSION: SG significantly alleviated NAFLD in HFD-induced obese mice with increasing the hepatic NAD + levels and upregulating the NRK1/NAD+/SIRT1 pathway.	NAD	139-143	nicotinamide riboside kinase 1	Mus musculus	134-138
31448236-2	2019	Nicotinamide phosphoribosyltransferase (NAMPT) and nicotinate phosphoribosyltransferase (NAPRT) are key enzymes for NAD salvage biosynthesis pathway, which reciprocally synthesize NAD to supply the main source of NAD biosythesis.	NAD	116-119	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
31448236-2	2019	Nicotinamide phosphoribosyltransferase (NAMPT) and nicotinate phosphoribosyltransferase (NAPRT) are key enzymes for NAD salvage biosynthesis pathway, which reciprocally synthesize NAD to supply the main source of NAD biosythesis.	NAD	180-183	nicotinamide phosphoribosyltransferase	Homo sapiens	0-38
31448236-2	2019	Nicotinamide phosphoribosyltransferase (NAMPT) and nicotinate phosphoribosyltransferase (NAPRT) are key enzymes for NAD salvage biosynthesis pathway, which reciprocally synthesize NAD to supply the main source of NAD biosythesis.	NAD	180-183	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
31448236-2	2019	Nicotinamide phosphoribosyltransferase (NAMPT) and nicotinate phosphoribosyltransferase (NAPRT) are key enzymes for NAD salvage biosynthesis pathway, which reciprocally synthesize NAD to supply the main source of NAD biosythesis.	NAD	180-183	nicotinamide phosphoribosyltransferase	Homo sapiens	0-38
31448236-2	2019	Nicotinamide phosphoribosyltransferase (NAMPT) and nicotinate phosphoribosyltransferase (NAPRT) are key enzymes for NAD salvage biosynthesis pathway, which reciprocally synthesize NAD to supply the main source of NAD biosythesis.	NAD	180-183	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
33290962-8	2021	In addition, NAD + increased the expressions of the autophagy-related proteins LC3-II/I and Beclin 1, and reduced the expression of p62.	NAD	13-18	sequestosome 1	Mus musculus	132-135
33419372-3	2020	Herein, we demonstrated that the nicotinamide adenine dinucleotide (NAD)-biosynthetic enzyme nicotinamide phosphoribosyltransferase (NAMPT) is a driving factor in BRAFi resistance development.	NAD	33-66	nicotinamide phosphoribosyltransferase	Homo sapiens	93-131
31341085-5	2019	Our results reveal an unexpected coevolution and kinetic interplay between NNMT and NamPT that enables extensive NAD signaling.	NAD	113-116	nicotinamide N-methyltransferase	Homo sapiens	75-79
31341085-5	2019	Our results reveal an unexpected coevolution and kinetic interplay between NNMT and NamPT that enables extensive NAD signaling.	NAD	113-116	nicotinamide phosphoribosyltransferase	Homo sapiens	84-89
30453040-3	2019	As a family of NAD+ dependent protein modifying enzymes, sirtuins (SIRT1-SIRT7) have multiple catalytic functions such as deacetylase, desuccinylase, demalonylase, demyristoylase, depalmitoylase, and/or mono-ADP-ribosyltransferase.	NAD	15-18	ADP-ribosyltransferase 3 (inactive)	Homo sapiens	203-230
33419372-3	2020	Herein, we demonstrated that the nicotinamide adenine dinucleotide (NAD)-biosynthetic enzyme nicotinamide phosphoribosyltransferase (NAMPT) is a driving factor in BRAFi resistance development.	NAD	33-66	nicotinamide phosphoribosyltransferase	Homo sapiens	133-138
33419372-3	2020	Herein, we demonstrated that the nicotinamide adenine dinucleotide (NAD)-biosynthetic enzyme nicotinamide phosphoribosyltransferase (NAMPT) is a driving factor in BRAFi resistance development.	NAD	68-71	nicotinamide phosphoribosyltransferase	Homo sapiens	93-131
33419372-3	2020	Herein, we demonstrated that the nicotinamide adenine dinucleotide (NAD)-biosynthetic enzyme nicotinamide phosphoribosyltransferase (NAMPT) is a driving factor in BRAFi resistance development.	NAD	68-71	nicotinamide phosphoribosyltransferase	Homo sapiens	133-138
31189734-1	2019	UDP-glucose dehydrogenase (UGDH), an oxidoreductase, catalyzes the NAD+-dependent four-electron oxidation of UDP-glucose to UDP-glucuronic acid.	NAD	67-71	UDP-glucose 6-dehydrogenase	Homo sapiens	0-25
32818702-6	2020	In addition, we observed that Wnt3a exacerbated hypoxia-induced mitochondrial dysfunction and cytosolic release of cytochrome C. Furthermore, we found that Sirt3, a mitochondrial NAD+-dependent deacetylase that modulates mitochondrial metabolism and homeostasis, was negatively regulated by Wnt3a.	NAD	179-182	Wnt family member 3A	Rattus norvegicus	30-35
31189734-1	2019	UDP-glucose dehydrogenase (UGDH), an oxidoreductase, catalyzes the NAD+-dependent four-electron oxidation of UDP-glucose to UDP-glucuronic acid.	NAD	67-71	UDP-glucose 6-dehydrogenase	Homo sapiens	27-31
31189734-1	2019	UDP-glucose dehydrogenase (UGDH), an oxidoreductase, catalyzes the NAD+-dependent four-electron oxidation of UDP-glucose to UDP-glucuronic acid.	NAD	67-71	hydroxysteroid 17-beta dehydrogenase 6	Homo sapiens	37-51
30909324-0	2019	NMNAT2-mediated NAD+ generation is essential for quality control of aged oocytes.	NAD	16-20	nicotinamide nucleotide adenylyltransferase 2	Mus musculus	0-6
32818702-6	2020	In addition, we observed that Wnt3a exacerbated hypoxia-induced mitochondrial dysfunction and cytosolic release of cytochrome C. Furthermore, we found that Sirt3, a mitochondrial NAD+-dependent deacetylase that modulates mitochondrial metabolism and homeostasis, was negatively regulated by Wnt3a.	NAD	179-182	Wnt family member 3A	Rattus norvegicus	291-296
30909324-6	2019	To sum up, our data indicate a role for NMNAT2 in controlling redox homeostasis during oocyte maturation and uncover that NMNAT2- NAD+ -SIRT1 is an important pathway mediating the effects of maternal age on oocyte developmental competence.	NAD	130-134	nicotinamide nucleotide adenylyltransferase 2	Mus musculus	122-128
33103371-1	2020	Sirtuin 5 (SIRT5) is a NAD+ -dependent class III protein deacetylase, and its role in prostate cancer has not yet been reported.	NAD	23-26	sirtuin 5	Homo sapiens	0-9
30951610-1	2019	This chemoenzymatic procedure describes a strategy for the preparation of 4"-thioribose nicotinamide adenine dinucleotide (S-NAD+ ), including chemical synthesis of nicotinamide 4"-riboside (S-NR), recombinant expression and purification of two NAD+ biosynthesis enzymes nicotinamide riboside kinase (NRK) and nicotinamide mononucleotide adenylyltransferase (NMNAT), and enzymatic synthesis of S-NAD+ .	NAD	123-129	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	310-357
30951610-1	2019	This chemoenzymatic procedure describes a strategy for the preparation of 4"-thioribose nicotinamide adenine dinucleotide (S-NAD+ ), including chemical synthesis of nicotinamide 4"-riboside (S-NR), recombinant expression and purification of two NAD+ biosynthesis enzymes nicotinamide riboside kinase (NRK) and nicotinamide mononucleotide adenylyltransferase (NMNAT), and enzymatic synthesis of S-NAD+ .	NAD	123-129	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	359-364
30951610-3	2019	In the second basic protocol, experimental methods are detailed for the production of recombinant human NRK1 and NMNAT1 to catalyze conversion of S-NR to S-NAD+ .	NAD	156-160	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	113-119
33103371-1	2020	Sirtuin 5 (SIRT5) is a NAD+ -dependent class III protein deacetylase, and its role in prostate cancer has not yet been reported.	NAD	23-26	sirtuin 5	Homo sapiens	11-16
31140365-5	2019	Conversely, increasing NAD+ levels by supplementation or genetic manipulation, which may benefit tissue homeostasis, also may worsen SASP and encourage tumorigenesis at least in mouse models of cancer.	NAD	23-27	aspartic peptidase, retroviral-like 1	Mus musculus	133-137
32906142-0	2020	SLC25A51 is a mammalian mitochondrial NAD+ transporter.	NAD	38-41	solute carrier family 25 member 51	Homo sapiens	0-8
30975903-1	2019	Nicotinamide phosphoribosyltransferase (NAMPT) is located in both the nucleus and cytoplasm and has multiple biological functions including catalyzing the rate-limiting step in NAD synthesis.	NAD	177-180	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
30975903-12	2019	These results suggest that NAMPT is transported into the nucleus where it presumably increases NAD synthesis required for cell proliferation.	NAD	95-98	nicotinamide phosphoribosyltransferase	Homo sapiens	27-32
30779909-0	2019	Aryl hydrocarbon receptor (AHR) functions in NAD+ metabolism, myelopoiesis and obesity.	NAD	45-49	aryl hydrocarbon receptor	Homo sapiens	0-25
30779909-0	2019	Aryl hydrocarbon receptor (AHR) functions in NAD+ metabolism, myelopoiesis and obesity.	NAD	45-49	aryl hydrocarbon receptor	Homo sapiens	27-30
30885568-3	2019	In this paper, we developed inhibitors of nicotinamide adenine dinucleotide-dependent deacetylase isoform 2 of Sirtuin protein (SIRT2), based on HPH-1Trt/HPH-2Trt, and aimed to generate new anti-cancer drugs.	NAD	42-75	polyhomeotic homolog 1	Homo sapiens	145-150
30050056-4	2019	p300 activity toward p53 is negatively regulated by the NAD-dependent deacetylase SIRT1, which deacetylates p53 preventing its transcriptional activation and the induction of p53-dependent apoptosis.	NAD	56-59	E1A binding protein p300	Homo sapiens	0-4
30915433-4	2019	However, the external NADH dehydrogenases (Nde1/2) and the L-glycerol 3-phosphate shuttle (composed of Gpd1/2 and Gut2), both coupled to the respiratory chain, are known to contribute to cytosolic NAD+ regeneration during growth on non-fermentable carbon sources.	NAD	197-201	glycerol-3-phosphate dehydrogenase	Saccharomyces cerevisiae S288C	114-118
30708027-1	2019	The human SLC25A13 gene encodes the liver type aspartate/glutamate carrier isoform 2 (AGC2, commonly named as citrin), which plays a key role in the main NADH-shuttle of human hepatocyte.	NAD	154-158	solute carrier family 25 member 13	Homo sapiens	10-18
30708027-1	2019	The human SLC25A13 gene encodes the liver type aspartate/glutamate carrier isoform 2 (AGC2, commonly named as citrin), which plays a key role in the main NADH-shuttle of human hepatocyte.	NAD	154-158	solute carrier family 25 member 13	Homo sapiens	110-116
31807629-1	2019	As a nicotinamide adenine dinucleotide (NAD)-dependent histone deacetylase and ADP ribosyl transferase, the silent information regulator 7 (Sirtuin 7, SIRT7) plays a crucial role in regulating the differentiation of adipocytes and myoblasts, lipid metabolism, glucose metabolism, and cellular growth in mammals.	NAD	5-38	NAD-dependent protein deacetylase sirtuin-7	Ovis aries	140-149
31807629-1	2019	As a nicotinamide adenine dinucleotide (NAD)-dependent histone deacetylase and ADP ribosyl transferase, the silent information regulator 7 (Sirtuin 7, SIRT7) plays a crucial role in regulating the differentiation of adipocytes and myoblasts, lipid metabolism, glucose metabolism, and cellular growth in mammals.	NAD	5-38	NAD-dependent protein deacetylase sirtuin-7	Ovis aries	151-156
31807629-1	2019	As a nicotinamide adenine dinucleotide (NAD)-dependent histone deacetylase and ADP ribosyl transferase, the silent information regulator 7 (Sirtuin 7, SIRT7) plays a crucial role in regulating the differentiation of adipocytes and myoblasts, lipid metabolism, glucose metabolism, and cellular growth in mammals.	NAD	40-43	NAD-dependent protein deacetylase sirtuin-7	Ovis aries	140-149
31807629-1	2019	As a nicotinamide adenine dinucleotide (NAD)-dependent histone deacetylase and ADP ribosyl transferase, the silent information regulator 7 (Sirtuin 7, SIRT7) plays a crucial role in regulating the differentiation of adipocytes and myoblasts, lipid metabolism, glucose metabolism, and cellular growth in mammals.	NAD	40-43	NAD-dependent protein deacetylase sirtuin-7	Ovis aries	151-156
30695683-3	2019	Western blotting respectively assayed protein expression of LC3I, LC3II, Beclin-1, Autophagy-related protein 7 (Atg7), Autophagy-related protein 3 (Atg3), NAD-dependent deacetylase sirtuin-3 (SIRT3) and major histocompatibility complex class I chain-related gene A (MICA).	NAD	155-158	MHC class I polypeptide-related sequence A	Homo sapiens	266-270
30952715-2	2019	Nicotinamide phosphoribosyl transferase (NAMPT) catalyzes the rate-limiting step of nicotinamide adenine dinucleotide synthesis and is increased in multiple tumor types.	NAD	84-117	nicotinamide phosphoribosyltransferase	Homo sapiens	0-39
30952715-2	2019	Nicotinamide phosphoribosyl transferase (NAMPT) catalyzes the rate-limiting step of nicotinamide adenine dinucleotide synthesis and is increased in multiple tumor types.	NAD	84-117	nicotinamide phosphoribosyltransferase	Homo sapiens	41-46
30777922-2	2019	High extracellular ATP concentrations or NAD-mediated P2RX7 ribosylation by the enzyme ARTC2.2 can induce P2RX7 pore formation and cell death.	NAD	41-44	ADP-ribosyltransferase 2a	Mus musculus	87-92
30777922-3	2019	Because both ATP and NAD are released during tissue preparation for analysis, cell death through these pathways may compromise the analysis of iNKT and CD8+ TRM Indeed, ARTC2.2 blockade enhanced recovery of viable liver iNKT and TRM The expression of ARTC2.2 and P2RX7 on distinct iNKT subsets and TRM is unclear, however, as is the impact of recovery from other nonlymphoid sites.	NAD	21-24	ADP-ribosyltransferase 2a	Mus musculus	169-174
30858618-2	2019	Macrophages stimulated with lipopolysaccharide increase their expression of nicotinamide phosphoribosyltransferase (NAMPT), a key enzyme in NAD+ salvage, and loss of NAMPT activity alters their inflammatory potential.	NAD	140-144	nicotinamide phosphoribosyltransferase	Homo sapiens	76-114
30858618-2	2019	Macrophages stimulated with lipopolysaccharide increase their expression of nicotinamide phosphoribosyltransferase (NAMPT), a key enzyme in NAD+ salvage, and loss of NAMPT activity alters their inflammatory potential.	NAD	140-144	nicotinamide phosphoribosyltransferase	Homo sapiens	116-121
30629785-9	2019	NAD+ /NADH ratio and autophagic flux, which are key factors for mitochondrial function, were higher in hCPC-1%, but hCPC-21% were highly dependent on BNIP3/NIX-mediated mitophagy to maintain mitochondrial function.	NAD	0-4	BCL2 interacting protein 3 like	Homo sapiens	156-159
30700550-7	2019	Direct complex I inhibition with rotenone mimicked the restrictive effects of CDK1 inhibition on mitochondrial respiration, NADH turnover, ATP/ADP, and calcium influx.	NAD	124-128	cyclin-dependent kinase 1	Mus musculus	78-82
30875389-0	2019	Quantitative analysis of the effects of nicotinamide phosphoribosyltransferase induction on the rates of NAD+ synthesis and breakdown in mammalian cells using stable isotope-labeling combined with mass spectrometry.	NAD	105-109	nicotinamide phosphoribosyltransferase	Homo sapiens	40-78
30875389-1	2019	NAD+ is mainly synthesized from nicotinamide (Nam) by the rate-limiting enzyme Nam phosphoribosyltransferase (Nampt) and degraded to Nam by NAD+-degrading enzymes in mammals.	NAD	0-4	nicotinamide phosphoribosyltransferase	Homo sapiens	79-108
30875389-1	2019	NAD+ is mainly synthesized from nicotinamide (Nam) by the rate-limiting enzyme Nam phosphoribosyltransferase (Nampt) and degraded to Nam by NAD+-degrading enzymes in mammals.	NAD	0-4	nicotinamide phosphoribosyltransferase	Homo sapiens	110-115
30875389-3	2019	Although increased expression of Nampt might be a promising intervention for healthy aging, forced expression of Nampt gene, inducing more than 10-fold increases in the enzyme protein level, has been reported to elevate NAD+ levels only 40-60% in mammalian cells.	NAD	220-224	nicotinamide phosphoribosyltransferase	Homo sapiens	113-118
30875389-5	2019	Here we show that Nampt is inhibited in cells and that enhanced expression of Nampt activates NAD+ breakdown.	NAD	94-98	nicotinamide phosphoribosyltransferase	Homo sapiens	78-83
30875389-8	2019	RS was much smaller than the total Nampt activity, indicating that NAD+ synthesis from Nam in the cells is suppressed.	NAD	67-71	nicotinamide phosphoribosyltransferase	Homo sapiens	35-40
30875389-9	2019	Forced expression of Nampt leading to 6-fold increase in total Nampt activity induced only a 1.6-fold increase in cellular NAD+ concentration.	NAD	123-127	nicotinamide phosphoribosyltransferase	Homo sapiens	21-26
30707389-2	2019	RESULTS: To alter NADH levels in lager yeast, the native FDH1 (YOR388C) encoding NAD+-dependent formate dehydrogenase was overexpressed in the yeast strain M14, yielding strain M-FDH1.	NAD	18-22	formate dehydrogenase (NAD+)	Saccharomyces cerevisiae S288C	57-61
30707389-2	2019	RESULTS: To alter NADH levels in lager yeast, the native FDH1 (YOR388C) encoding NAD+-dependent formate dehydrogenase was overexpressed in the yeast strain M14, yielding strain M-FDH1.	NAD	81-85	formate dehydrogenase (NAD+)	Saccharomyces cerevisiae S288C	57-61
30707389-2	2019	RESULTS: To alter NADH levels in lager yeast, the native FDH1 (YOR388C) encoding NAD+-dependent formate dehydrogenase was overexpressed in the yeast strain M14, yielding strain M-FDH1.	NAD	81-85	formate dehydrogenase (NAD+)	Saccharomyces cerevisiae S288C	179-183
30707389-3	2019	This led to a simultaneous increase of NADH availability and NADH/NAD+ ratio in the M-FDH1 strain during fermentation.	NAD	39-43	formate dehydrogenase (NAD+)	Saccharomyces cerevisiae S288C	86-90
30707389-3	2019	This led to a simultaneous increase of NADH availability and NADH/NAD+ ratio in the M-FDH1 strain during fermentation.	NAD	61-65	formate dehydrogenase (NAD+)	Saccharomyces cerevisiae S288C	86-90
30707389-3	2019	This led to a simultaneous increase of NADH availability and NADH/NAD+ ratio in the M-FDH1 strain during fermentation.	NAD	66-70	formate dehydrogenase (NAD+)	Saccharomyces cerevisiae S288C	86-90
32439659-6	2020	Blocking tumor necrosis factor-alpha signaling or preventing senescence with nicotinamide adenine dinucleotide precursors partially rescues premature aging in mice with Tfam-deficient T cells.	NAD	77-110	transcription factor A, mitochondrial	Mus musculus	169-173
32544883-6	2020	Collectively, this study revealed potential roles of miR-9 and miR-29a as contributors to DPN development through the SHH signaling pathway by binding to ISL1.	NAD	90-93	microRNA 29a	Rattus norvegicus	63-70
32383848-3	2020	Superoxide dismutase (SOD) and catalase (CAT) were chosen as scavengers and covalently encapsulated into silica nanoreactors, together with glucose dehydrogenase (GDH) which simultaneously should produce the coenzyme nicotinamide adenine dinucleotide (NADH, reduced form).	NAD	217-250	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	140-161
32383848-3	2020	Superoxide dismutase (SOD) and catalase (CAT) were chosen as scavengers and covalently encapsulated into silica nanoreactors, together with glucose dehydrogenase (GDH) which simultaneously should produce the coenzyme nicotinamide adenine dinucleotide (NADH, reduced form).	NAD	217-250	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	163-166
32383848-3	2020	Superoxide dismutase (SOD) and catalase (CAT) were chosen as scavengers and covalently encapsulated into silica nanoreactors, together with glucose dehydrogenase (GDH) which simultaneously should produce the coenzyme nicotinamide adenine dinucleotide (NADH, reduced form).	NAD	252-256	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	140-161
32383848-3	2020	Superoxide dismutase (SOD) and catalase (CAT) were chosen as scavengers and covalently encapsulated into silica nanoreactors, together with glucose dehydrogenase (GDH) which simultaneously should produce the coenzyme nicotinamide adenine dinucleotide (NADH, reduced form).	NAD	252-256	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	163-166
32383848-4	2020	By the enzymatic reactions of SOD and CAT, the interior of silica nanoreactors becomes a "ROS safe zone" to protect the glucose-dependent NADH production of co-encapsulated GDH.	NAD	138-142	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	173-176
32335094-1	2020	AIMS: Citrin is an aspartate/glutamate carrier that composes the malate-aspartate reduced nicotinamide adenine dinucleotide (NADH) shuttle in the liver.	NAD	90-123	solute carrier family 25 member 13	Homo sapiens	6-12
32335094-1	2020	AIMS: Citrin is an aspartate/glutamate carrier that composes the malate-aspartate reduced nicotinamide adenine dinucleotide (NADH) shuttle in the liver.	NAD	125-129	solute carrier family 25 member 13	Homo sapiens	6-12
32300965-3	2020	However, age-related DNA damage and increased SASP activate PARP-1 and CD38, the enzymes competing with SIRTs for NAD+.	NAD	114-118	aspartic peptidase, retroviral-like 1	Mus musculus	46-50
32428862-5	2020	SLC37A2 deletion reprograms macrophages to a hyper-glycolytic process and accelerates LPS-induced inflammatory cytokine production, which partially depends on nicotinamide adenine dinucleotide (NAD+) biosynthesis.	NAD	159-192	solute carrier family 37 (glycerol-3-phosphate transporter), member 2	Mus musculus	0-7
32428862-5	2020	SLC37A2 deletion reprograms macrophages to a hyper-glycolytic process and accelerates LPS-induced inflammatory cytokine production, which partially depends on nicotinamide adenine dinucleotide (NAD+) biosynthesis.	NAD	194-198	solute carrier family 37 (glycerol-3-phosphate transporter), member 2	Mus musculus	0-7
32477131-5	2020	In the many cells in which the salvage pathway is predominant, NAMPT, therefore, represents an important controller of intracellular NAD concentrations, and as a consequence of energy metabolism.	NAD	133-136	nicotinamide phosphoribosyltransferase	Homo sapiens	63-68
32454935-7	2020	Herein, we discuss important findings in the field of NAD+ metabolism, with particular emphasis on the importance of the NAD+ biosynthesizing enzyme NAMPT, the related metabolism of NAD+ in the retina, and the consequences of NAMPT and NAD+ deficiency or depletion in this tissue in aging and disease.	NAD	54-58	nicotinamide phosphoribosyltransferase	Homo sapiens	149-154
32454935-7	2020	Herein, we discuss important findings in the field of NAD+ metabolism, with particular emphasis on the importance of the NAD+ biosynthesizing enzyme NAMPT, the related metabolism of NAD+ in the retina, and the consequences of NAMPT and NAD+ deficiency or depletion in this tissue in aging and disease.	NAD	54-58	nicotinamide phosphoribosyltransferase	Homo sapiens	226-231
32454935-7	2020	Herein, we discuss important findings in the field of NAD+ metabolism, with particular emphasis on the importance of the NAD+ biosynthesizing enzyme NAMPT, the related metabolism of NAD+ in the retina, and the consequences of NAMPT and NAD+ deficiency or depletion in this tissue in aging and disease.	NAD	121-125	nicotinamide phosphoribosyltransferase	Homo sapiens	149-154
32454935-7	2020	Herein, we discuss important findings in the field of NAD+ metabolism, with particular emphasis on the importance of the NAD+ biosynthesizing enzyme NAMPT, the related metabolism of NAD+ in the retina, and the consequences of NAMPT and NAD+ deficiency or depletion in this tissue in aging and disease.	NAD	121-125	nicotinamide phosphoribosyltransferase	Homo sapiens	149-154
32169417-2	2020	Recently, evidence has been obtained that AHR is involved in NAD+ and energy homeostasis in cooperation with NAD+-consuming enzymes including CD38, TiPARP and sirtuins.	NAD	61-65	aryl hydrocarbon receptor	Homo sapiens	42-45
32169417-2	2020	Recently, evidence has been obtained that AHR is involved in NAD+ and energy homeostasis in cooperation with NAD+-consuming enzymes including CD38, TiPARP and sirtuins.	NAD	109-113	aryl hydrocarbon receptor	Homo sapiens	42-45
32014438-7	2020	In addition, we found altered expression of enzymes involved in NAD+ synthesis (NAMPT and NMNAT2) and decreased SIRT6 expression in the spinal cord of ALS patients, suggesting deficits of this neuroprotective pathway in the human pathology.	NAD	64-68	nicotinamide phosphoribosyltransferase	Homo sapiens	80-85
32232843-0	2020	ddhCTP produced by the radical-SAM activity of RSAD2 (viperin) inhibits the NAD+ -dependent activity of enzymes to modulate metabolism.	NAD	76-80	radical S-adenosyl methionine domain containing 2	Homo sapiens	47-52
32232843-0	2020	ddhCTP produced by the radical-SAM activity of RSAD2 (viperin) inhibits the NAD+ -dependent activity of enzymes to modulate metabolism.	NAD	76-80	radical S-adenosyl methionine domain containing 2	Homo sapiens	54-61
32003519-4	2020	Concurrent with this metabolic remodeling, NAD+ increases hESC pluripotent marker expression and proliferation, inhibits BMP4-induced differentiation and reduces global H3K27me3, plausibly inducing an intermediate naive-to-primed bivalent metabolism and pluripotent state.	NAD	43-46	bone morphogenetic protein 4	Homo sapiens	121-125
32301489-0	2020	NAD+ Attenuates Experimental Autoimmune Encephalomyelitis through Inducing of CD11b+ gr-1+ Myeloid-Derived Suppressor Cells.	NAD	0-4	lymphocyte antigen 6 complex, locus G	Mus musculus	85-89
32301489-9	2020	Western blot showed that NAD+ treatment up-regulated the expression of p-STAT6 and SIRT1.	NAD	25-29	signal transducer and activator of transcription 6	Mus musculus	73-78
32301489-11	2020	In addition, NAD+ treatment could increase the numbers of CD11b+ gr-1+ MDSCs and the expression of Arginase-1.	NAD	13-17	lymphocyte antigen 6 complex, locus G	Mus musculus	65-69
32301489-11	2020	In addition, NAD+ treatment could increase the numbers of CD11b+ gr-1+ MDSCs and the expression of Arginase-1.	NAD	13-17	arginase, liver	Mus musculus	99-109
32301489-13	2020	CONCLUSIONS: The present study demonstrated that NAD+ treatment may induce the CD11b+ gr-1+ MDSCs to attenuate EAE via activating the phosphorylation of STAT6 expression.	NAD	49-53	lymphocyte antigen 6 complex, locus G	Mus musculus	86-90
32301489-13	2020	CONCLUSIONS: The present study demonstrated that NAD+ treatment may induce the CD11b+ gr-1+ MDSCs to attenuate EAE via activating the phosphorylation of STAT6 expression.	NAD	49-53	signal transducer and activator of transcription 6	Mus musculus	153-158
32483423-2	2020	Sirtuin6 (SIRT6) is a conserved nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase that is widely pathologically downregulated in CRC, but its pharmacological effect in CRC remains undefined due to the lack of small-molecule SIRT6 activators.	NAD	32-65	sirtuin 6	Homo sapiens	0-8
32483423-2	2020	Sirtuin6 (SIRT6) is a conserved nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase that is widely pathologically downregulated in CRC, but its pharmacological effect in CRC remains undefined due to the lack of small-molecule SIRT6 activators.	NAD	32-65	sirtuin 6	Homo sapiens	10-15
32483423-2	2020	Sirtuin6 (SIRT6) is a conserved nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase that is widely pathologically downregulated in CRC, but its pharmacological effect in CRC remains undefined due to the lack of small-molecule SIRT6 activators.	NAD	67-70	sirtuin 6	Homo sapiens	0-8
32483423-2	2020	Sirtuin6 (SIRT6) is a conserved nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase that is widely pathologically downregulated in CRC, but its pharmacological effect in CRC remains undefined due to the lack of small-molecule SIRT6 activators.	NAD	67-70	sirtuin 6	Homo sapiens	10-15
32059949-7	2020	Nudt12 also bound RNAs with 5" NAD+ caps more tightly than those with NADH or m7G cap.	NAD	28-34	nudix hydrolase 12	Homo sapiens	0-6
32283646-1	2020	Sirtuin 6 (SIRT6) is an NAD+-dependent deacetylase with a significant role in 20% of all cancers, such as colon cancers and rectal adenocarcinoma.	NAD	24-27	sirtuin 6	Homo sapiens	0-9
32283646-1	2020	Sirtuin 6 (SIRT6) is an NAD+-dependent deacetylase with a significant role in 20% of all cancers, such as colon cancers and rectal adenocarcinoma.	NAD	24-27	sirtuin 6	Homo sapiens	11-16
30685480-7	2019	Hepatic microsomal fractions were also utilised in incubations with ellipticine and DNA in the presence of NADPH, cofactor for POR, and NADH, cofactor for Cyb5 reductase (Cyb5R), to examine ellipticine-DNA adduct formation.	NAD	136-140	cytochrome b5 type A (microsomal)	Mus musculus	155-159
29295624-7	2019	The NAD+ deficiency in the diseases and aging results from not only poly(ADP-ribose) polymerase-1 (PARP-1) activation but also decreased nicotinamide phosphoribosyltransferase (Nampt) activity and increased CD38 activity.	NAD	4-8	nicotinamide phosphoribosyltransferase	Homo sapiens	137-175
30670969-3	2018	The present study identified SIRT6, an important subtype of NAD+ dependent class III histone deacetylase, to be a negative regulator of NFATc4 in cardiomyocyte hypertrophy.	NAD	60-64	sirtuin 6	Homo sapiens	29-34
32906142-4	2020	Loss of SLC25A51 decreases mitochondrial-but not whole-cell-NAD+ content, impairs mitochondrial respiration, and blocks the uptake of NAD+ into isolated mitochondria.	NAD	60-64	solute carrier family 25 member 51	Homo sapiens	8-16
32308774-8	2020	Results: We found that the concomitant activation of the NAD+-dependent deacetylase SIRT1 and the PI3K/AKT signaling pathway converge to increase the presence of deacetylated and phosphorylated FOXO3a, a transcription factor, in the nucleus.	NAD	57-60	forkhead box O3	Rattus norvegicus	194-200
32906142-4	2020	Loss of SLC25A51 decreases mitochondrial-but not whole-cell-NAD+ content, impairs mitochondrial respiration, and blocks the uptake of NAD+ into isolated mitochondria.	NAD	134-138	solute carrier family 25 member 51	Homo sapiens	8-16
32906142-5	2020	Conversely, overexpression of SLC25A51 or SLC25A52 (a nearly identical paralogue of SLC25A51) increases mitochondrial NAD+ levels and restores NAD+ uptake into yeast mitochondria lacking endogenous NAD+ transporters.	NAD	118-122	solute carrier family 25 member 51	Homo sapiens	30-38
32906142-5	2020	Conversely, overexpression of SLC25A51 or SLC25A52 (a nearly identical paralogue of SLC25A51) increases mitochondrial NAD+ levels and restores NAD+ uptake into yeast mitochondria lacking endogenous NAD+ transporters.	NAD	118-122	solute carrier family 25 member 51	Homo sapiens	84-92
32694608-0	2020	NRH salvage and conversion to NAD+ requires NRH kinase activity by adenosine kinase.	NAD	30-34	adenosine kinase	Mus musculus	67-83
32906142-5	2020	Conversely, overexpression of SLC25A51 or SLC25A52 (a nearly identical paralogue of SLC25A51) increases mitochondrial NAD+ levels and restores NAD+ uptake into yeast mitochondria lacking endogenous NAD+ transporters.	NAD	143-147	solute carrier family 25 member 51	Homo sapiens	30-38
32694608-2	2020	Here, we show that NRH can be converted into NAD+ via a salvage pathway in which adenosine kinase (ADK, also known as AK) acts as an NRH kinase.	NAD	45-49	adenosine kinase	Mus musculus	81-97
32906142-5	2020	Conversely, overexpression of SLC25A51 or SLC25A52 (a nearly identical paralogue of SLC25A51) increases mitochondrial NAD+ levels and restores NAD+ uptake into yeast mitochondria lacking endogenous NAD+ transporters.	NAD	143-147	solute carrier family 25 member 51	Homo sapiens	84-92
32694608-2	2020	Here, we show that NRH can be converted into NAD+ via a salvage pathway in which adenosine kinase (ADK, also known as AK) acts as an NRH kinase.	NAD	45-49	adenosine kinase	Mus musculus	99-102
32906142-6	2020	Together, these findings identify SLC25A51 as a mammalian transporter capable of importing NAD+ into mitochondria.	NAD	91-95	solute carrier family 25 member 51	Homo sapiens	34-42
33262325-0	2020	Epistasis-driven identification of SLC25A51 as a regulator of human mitochondrial NAD import.	NAD	82-85	solute carrier family 25 member 51	Homo sapiens	35-43
30588784-6	2020	We were able to validate the underexpression of the mitochondrial complex subunits NADH:Ubiquinone Oxidoreductase Core Subunit S1 (NDUFS1) and ubiquinol-cytochrome C reductase core protein 2 (UQCRC2), as well as the underexpression of the testis-specific sodium/potassium-transporting ATPase subunit alpha-4 (ATP1A4) in the NSTC group.	NAD	83-87	ubiquinol-cytochrome c reductase core protein 2	Homo sapiens	192-198
30588784-6	2020	We were able to validate the underexpression of the mitochondrial complex subunits NADH:Ubiquinone Oxidoreductase Core Subunit S1 (NDUFS1) and ubiquinol-cytochrome C reductase core protein 2 (UQCRC2), as well as the underexpression of the testis-specific sodium/potassium-transporting ATPase subunit alpha-4 (ATP1A4) in the NSTC group.	NAD	83-87	ATPase Na+/K+ transporting subunit alpha 4	Homo sapiens	309-315
33262325-5	2020	Through a combination of metabolomics, genomics and genetics approaches, we demonstrate a role for SLC25A51 as enabler of mitochondrial import of NAD, showcasing the potential of genetic interaction-driven functional gene deorphanization.	NAD	146-149	solute carrier family 25 member 51	Homo sapiens	99-107
32049506-6	2020	Finally, we show that the SARM1 hydrolyzes NAD+ via an ordered uni-bi reaction in which nicotinamide is released prior to ADPR.	NAD	43-47	sterile alpha and TIR motif containing 1	Homo sapiens	26-31
32996222-8	2020	Inhibition of ABA synthesis rescued the stomatal phenotype in mutants deficient in intracellular NAD+ transport, whereas exogenous NAD+ feeding of aba-2 and ost1 seedlings, impaired in ABA synthesis and ABA signaling respectively, did not impact stomatal number, placing NAD upstream of ABA.	NAD	131-135	Protein kinase superfamily protein	Arabidopsis thaliana	157-161
31935360-4	2020	The aim was to investigate whether the PGR5 (pgr5) and the type I NADH dehydrogenase (NDH-1) (ndho) systems protect PSI from excess electron stress and whether these systems help plants to cope with the consequences of PSI photoinhibition.	NAD	66-70	NADH dehydrogenase subunit 1	Arabidopsis thaliana	86-91
31740269-5	2020	Here, we show that disruption of mitochondrial membrane potential leads to axonal NMNAT2 depletion in mouse sympathetic neurons, increasing the substrate-to-product ratio (NMN/NAD) of this NAD-synthesising enzyme, a metabolic fingerprint of Wallerian degeneration.	NAD	176-179	nicotinamide nucleotide adenylyltransferase 2	Mus musculus	82-88
31740269-5	2020	Here, we show that disruption of mitochondrial membrane potential leads to axonal NMNAT2 depletion in mouse sympathetic neurons, increasing the substrate-to-product ratio (NMN/NAD) of this NAD-synthesising enzyme, a metabolic fingerprint of Wallerian degeneration.	NAD	189-192	nicotinamide nucleotide adenylyltransferase 2	Mus musculus	82-88
31059816-4	2020	Nicotinamide phosphoribosyltransferase (NAMPT) is the most important NAD+ biosynthetic enzyme in mammalian cells and a direct target of the BRAF oncogenic signaling pathway.	NAD	69-73	nicotinamide phosphoribosyltransferase	Homo sapiens	0-38
31059816-4	2020	Nicotinamide phosphoribosyltransferase (NAMPT) is the most important NAD+ biosynthetic enzyme in mammalian cells and a direct target of the BRAF oncogenic signaling pathway.	NAD	69-73	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
31059816-6	2020	Here we review current knowledge on how oncogenic signaling reprograms metabolism in BRAF-mutated melanoma, and discuss how NAMPT/NAD+ axis contributes to these processes.	NAD	130-134	nicotinamide phosphoribosyltransferase	Homo sapiens	124-129
32005247-2	2020	Nicotinamide phosphoribosyltransferase (NAMPT), which converts nicotinamide into NAD+, is the rate-limiting enzyme in the NAD+ salvage pathway.	NAD	81-84	nicotinamide phosphoribosyltransferase	Homo sapiens	0-38
32005247-2	2020	Nicotinamide phosphoribosyltransferase (NAMPT), which converts nicotinamide into NAD+, is the rate-limiting enzyme in the NAD+ salvage pathway.	NAD	81-84	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
32005247-2	2020	Nicotinamide phosphoribosyltransferase (NAMPT), which converts nicotinamide into NAD+, is the rate-limiting enzyme in the NAD+ salvage pathway.	NAD	122-125	nicotinamide phosphoribosyltransferase	Homo sapiens	0-38
32005247-2	2020	Nicotinamide phosphoribosyltransferase (NAMPT), which converts nicotinamide into NAD+, is the rate-limiting enzyme in the NAD+ salvage pathway.	NAD	122-125	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
31947613-6	2020	Since Fbp2 oligomerization state and thus, its role is regulated by AMP and NAD+-crucial indicators of cellular metabolic conditions-we hypothesize that the Hif1alpha-dependent regulation of the metabolism in cancer is modulated through Fbp2, a sensor of the energy and redox state of a cell.	NAD	76-79	fructose-bisphosphatase 2	Homo sapiens	6-10
31936863-13	2020	ATCAY has therefore been excluded as a candidate gene for eNAD/EDM.	NAD	58-62	ATCAY kinesin light chain interacting caytaxin	Equus caballus	0-5
31676226-7	2020	We found that 8mg/kg DPN (ERbeta-specific agonist) replacement therapy (3 weeks) to the ovariectomized (OVX) mice significantly reduced ischemia injury and alleviated microglia and astrocyte activation, and markedly inhibited the expression of NF-kappaB and proinflammatory cytokines (TNF-alpha, IL-1beta, and IL-6).	NAD	21-24	estrogen receptor 2 (beta)	Mus musculus	26-32
33180391-3	2020	No previous studies had evaluated the relationship between CD40 rs1883832 polymorphism and DN/DPN.	NAD	94-97	CD40 molecule	Homo sapiens	59-63
31462712-1	2020	Citrin, encoded by SLC25A13 gene, is an inner mitochondrial transporter that is part of the malate-aspartate shuttle, which regulates the NAD+/NADH ratio between the cytosol and mitochondria.	NAD	138-142	solute carrier family 25 member 13	Homo sapiens	0-6
31462712-1	2020	Citrin, encoded by SLC25A13 gene, is an inner mitochondrial transporter that is part of the malate-aspartate shuttle, which regulates the NAD+/NADH ratio between the cytosol and mitochondria.	NAD	138-142	solute carrier family 25 member 13	Homo sapiens	19-27
31462712-1	2020	Citrin, encoded by SLC25A13 gene, is an inner mitochondrial transporter that is part of the malate-aspartate shuttle, which regulates the NAD+/NADH ratio between the cytosol and mitochondria.	NAD	143-147	solute carrier family 25 member 13	Homo sapiens	0-6
31462712-1	2020	Citrin, encoded by SLC25A13 gene, is an inner mitochondrial transporter that is part of the malate-aspartate shuttle, which regulates the NAD+/NADH ratio between the cytosol and mitochondria.	NAD	143-147	solute carrier family 25 member 13	Homo sapiens	19-27
31462712-3	2020	The association of citrin with glycolysis and NAD+/NADH ratio led us to hypothesize that it may play a role in carcinogenesis.	NAD	51-55	solute carrier family 25 member 13	Homo sapiens	19-25
31462712-4	2020	Indeed, we find that citrin is upregulated in multiple cancer types and is essential for supplementing NAD+ for glycolysis and NADH for oxidative phosphorylation.	NAD	103-107	solute carrier family 25 member 13	Homo sapiens	21-27
31462712-4	2020	Indeed, we find that citrin is upregulated in multiple cancer types and is essential for supplementing NAD+ for glycolysis and NADH for oxidative phosphorylation.	NAD	127-131	solute carrier family 25 member 13	Homo sapiens	21-27
31888244-6	2019	However, in astrocytes IDH1R132H led to elevated expression of the NAD-synthesizing enzyme nicotinamide phosphoribosyltransferase (NAMPT).	NAD	67-70	nicotinamide phosphoribosyltransferase	Homo sapiens	131-136
31888308-6	2019	This arsenate resistance system was potentially linked to two genes: orf69, encoding an organoarsenical efflux major facilitator superfamily (MFS) transporter-like protein related to ArsJ, and orf70, encoding nicotinamide adenine dinucleotide (NAD)-dependent glyceraldehyde-3-phosphate dehydrogenase.	NAD	209-242	hypothetical protein	Escherichia coli	193-198
31888308-6	2019	This arsenate resistance system was potentially linked to two genes: orf69, encoding an organoarsenical efflux major facilitator superfamily (MFS) transporter-like protein related to ArsJ, and orf70, encoding nicotinamide adenine dinucleotide (NAD)-dependent glyceraldehyde-3-phosphate dehydrogenase.	NAD	244-247	hypothetical protein	Escherichia coli	193-198
31843902-3	2019	Here, we report that SIRT5, a mitochondrial NAD+-dependent lysine deacylase, plays a key role in stabilizing GLS.	NAD	44-47	sirtuin 5	Homo sapiens	21-26
31614144-4	2019	NAD+ biosynthesis via nicotinamide phosphoribosyltransferase (NAMPT) modulates Sirtuin 1 activity.	NAD	0-3	nicotinamide phosphoribosyltransferase	Homo sapiens	62-67
31614144-5	2019	Here, we examined the expression and effects of inhibiting NAMPT, a rate-limiting enzyme in NAD+ biosynthesis, in ATL cells.	NAD	92-95	nicotinamide phosphoribosyltransferase	Homo sapiens	59-64
31598701-0	2019	Exogenous pyruvate represses histone gene expression and inhibits cancer cell proliferation via the NAMPT-NAD+-SIRT1 pathway.	NAD	106-109	nicotinamide phosphoribosyltransferase	Homo sapiens	100-105
31598701-5	2019	Pyruvate represses histone gene expression by inducing the expression of NAD+ biosynthesis enzyme, nicotinamide phosphoribosyltransferase (NAMPT) via myocyte enhancer factor 2C (MEF2C), which then increases NAD+ levels and activates the histone deacetylase activity of SIRT1.	NAD	73-76	nicotinamide phosphoribosyltransferase	Homo sapiens	99-137
31598701-5	2019	Pyruvate represses histone gene expression by inducing the expression of NAD+ biosynthesis enzyme, nicotinamide phosphoribosyltransferase (NAMPT) via myocyte enhancer factor 2C (MEF2C), which then increases NAD+ levels and activates the histone deacetylase activity of SIRT1.	NAD	73-76	nicotinamide phosphoribosyltransferase	Homo sapiens	139-144
31598701-5	2019	Pyruvate represses histone gene expression by inducing the expression of NAD+ biosynthesis enzyme, nicotinamide phosphoribosyltransferase (NAMPT) via myocyte enhancer factor 2C (MEF2C), which then increases NAD+ levels and activates the histone deacetylase activity of SIRT1.	NAD	207-210	nicotinamide phosphoribosyltransferase	Homo sapiens	99-137
31810909-1	2019	BACKGROUND/AIM: Nicotinamide phosphoribosyltransferase (NAMPT), a key enzyme in the NAD+ biosynthetic pathway, is a drug target of potent anticancer candidates, including FK866 and other reported NAMPT inhibitors.	NAD	84-87	nicotinamide phosphoribosyltransferase	Homo sapiens	16-54
31810909-1	2019	BACKGROUND/AIM: Nicotinamide phosphoribosyltransferase (NAMPT), a key enzyme in the NAD+ biosynthetic pathway, is a drug target of potent anticancer candidates, including FK866 and other reported NAMPT inhibitors.	NAD	84-87	nicotinamide phosphoribosyltransferase	Homo sapiens	56-61
31810909-1	2019	BACKGROUND/AIM: Nicotinamide phosphoribosyltransferase (NAMPT), a key enzyme in the NAD+ biosynthetic pathway, is a drug target of potent anticancer candidates, including FK866 and other reported NAMPT inhibitors.	NAD	84-87	nicotinamide phosphoribosyltransferase	Homo sapiens	196-201
30996287-1	2019	Poly (ADP-ribose) polymerase (PARP)-1 and PARP-2 regulate the function of various DNA-interacting proteins by transferring ADP-ribose emerging from catalytic cleavage of cellular beta-NAD+.	NAD	179-188	poly (ADP-ribose) polymerase family, member 2	Mus musculus	42-48
31626975-0	2019	NAD+ repletion inhibits the endothelial-to-mesenchymal transition induced by TGF-beta in endothelial cells through improving mitochondrial unfolded protein response.	NAD	0-3	transforming growth factor, beta 1	Mus musculus	77-85
31626975-4	2019	NAD + precursor nicotinamide riboside (NR) could attenuate TGF-beta1-induced EndMT and improve the levels of mtUPR.	NAD	0-3	transforming growth factor, beta 1	Mus musculus	59-68
30009951-1	2019	SIRT2 has been shown to possess NAD+-dependent deacetylase and desuccinylase enzymatic activities, it also regulates metabolism homeostasis in mammals.	NAD	32-36	sirtuin 2	Bos taurus	0-5
30655890-1	2019	SIRT6, is a member of the NAD-dependent sirtuin family of enzymes, and has been reported as a novel tumor suppressor gene or oncogene, dependent on the type of cancer.	NAD	26-29	sirtuin 6	Homo sapiens	0-5
30427660-7	2018	In murine mesentery venules, the intravenous administration of 2.5 mg/kg of tPA-DPNs resolves almost 90% of the blood clots, whereas a similar dose of free tPA successfully recanalizes only about 40% of the treated vessels.	NAD	80-84	plasminogen activator, tissue	Mus musculus	76-79
30427660-8	2018	At about 1/10 of the clinical dose (1.0 mg/kg), tPA-DPNs still effectively dissolve 70% of the clots, whereas free tPA works efficiently only on 16% of the vessels.	NAD	52-56	plasminogen activator, tissue	Mus musculus	48-51
30427660-9	2018	In vivo, discoidal tPA-DPNs outperform the lytic activity of 200 nm spherical tPA-coated nanoconstructs in terms of both percentage of successful recanalization events and clot area reduction.	NAD	23-27	plasminogen activator, tissue	Mus musculus	19-22
30619878-5	2018	PGDH catalyzes the first step in the pathway by converting d-3-phosphoglycerate (PGA), an intermediate in glycolysis, to phosphohydroxypyruvate (PHP) concomitant with the reduction of NAD+.	NAD	184-188	phosphoglycerate dehydrogenase	Homo sapiens	0-4
33292758-3	2020	We previously described that loss-of-aspartate glutamate carrier 1 (SLC25A12 or AGC1), an important component of the malate-aspartate shuttle, impairs cytosolic aspartate levels, NAD+/NADH ratio, mitochondrial respiration, and tumor growth.	NAD	179-183	solute carrier family 25 member 12	Homo sapiens	68-76
31553812-0	2019	Subcellular NAMPT-mediated NAD+ salvage pathways and their roles in bioenergetics and neuronal protection after ischemic injury.	NAD	27-31	nicotinamide phosphoribosyltransferase	Homo sapiens	12-17
33292758-3	2020	We previously described that loss-of-aspartate glutamate carrier 1 (SLC25A12 or AGC1), an important component of the malate-aspartate shuttle, impairs cytosolic aspartate levels, NAD+/NADH ratio, mitochondrial respiration, and tumor growth.	NAD	179-183	solute carrier family 25 member 12	Homo sapiens	80-84
31553812-2	2019	In mammalian cells, NAD+ is predominantly synthesized through the salvage pathway, where nicotinamide phosphoribosyltransferase (NAMPT) is the rate-limiting enzyme.	NAD	20-24	nicotinamide phosphoribosyltransferase	Homo sapiens	89-127
33292758-3	2020	We previously described that loss-of-aspartate glutamate carrier 1 (SLC25A12 or AGC1), an important component of the malate-aspartate shuttle, impairs cytosolic aspartate levels, NAD+/NADH ratio, mitochondrial respiration, and tumor growth.	NAD	184-188	solute carrier family 25 member 12	Homo sapiens	68-76
31553812-2	2019	In mammalian cells, NAD+ is predominantly synthesized through the salvage pathway, where nicotinamide phosphoribosyltransferase (NAMPT) is the rate-limiting enzyme.	NAD	20-24	nicotinamide phosphoribosyltransferase	Homo sapiens	129-134
33292758-3	2020	We previously described that loss-of-aspartate glutamate carrier 1 (SLC25A12 or AGC1), an important component of the malate-aspartate shuttle, impairs cytosolic aspartate levels, NAD+/NADH ratio, mitochondrial respiration, and tumor growth.	NAD	184-188	solute carrier family 25 member 12	Homo sapiens	80-84
33230181-5	2020	Interestingly, hyper-succinylated proteins are distributed across cellular compartments, and many are known targets of the (NAD+)-dependent desuccinylase SIRT5.	NAD	124-127	sirtuin 5	Homo sapiens	154-159
31562200-3	2019	NAMPT inhibition elicits depletion of total cellular NAD+ levels and ultimately cytotoxicity via depletion of cellular ATP levels.	NAD	53-57	nicotinamide phosphoribosyltransferase	Homo sapiens	0-5
33185189-1	2020	SARM1 an executor of axonal degeneration, displays NADase activity that depletes the key cellular metabolite, NAD+, in response to nerve injury.	NAD	110-114	sterile alpha and TIR motif containing 1	Homo sapiens	0-5
31456414-4	2019	RESULTS: FK866, a specific inhibitor of nicotinamide phosphoribosyltransferase (NAMPT), the main NAD+-producing enzyme in MM cells, was used to monitor NAD+ depletion kinetics at the subcellular level in biosensor-transduced A375 cells.	NAD	97-101	nicotinamide phosphoribosyltransferase	Homo sapiens	40-78
31456414-4	2019	RESULTS: FK866, a specific inhibitor of nicotinamide phosphoribosyltransferase (NAMPT), the main NAD+-producing enzyme in MM cells, was used to monitor NAD+ depletion kinetics at the subcellular level in biosensor-transduced A375 cells.	NAD	97-101	nicotinamide phosphoribosyltransferase	Homo sapiens	80-85
31456414-4	2019	RESULTS: FK866, a specific inhibitor of nicotinamide phosphoribosyltransferase (NAMPT), the main NAD+-producing enzyme in MM cells, was used to monitor NAD+ depletion kinetics at the subcellular level in biosensor-transduced A375 cells.	NAD	152-156	nicotinamide phosphoribosyltransferase	Homo sapiens	40-78
31456414-4	2019	RESULTS: FK866, a specific inhibitor of nicotinamide phosphoribosyltransferase (NAMPT), the main NAD+-producing enzyme in MM cells, was used to monitor NAD+ depletion kinetics at the subcellular level in biosensor-transduced A375 cells.	NAD	152-156	nicotinamide phosphoribosyltransferase	Homo sapiens	80-85
33185189-5	2020	This inactive conformation is stabilized by binding of SARM1"s own substrate NAD+ in an allosteric location, away from the catalytic sites.	NAD	77-81	sterile alpha and TIR motif containing 1	Homo sapiens	55-60
33185189-7	2020	We propose that the reduction of cellular NAD+ concentration contributes to the disassembly of SARM1"s peripheral ring, which allows formation of active NADase domain dimers, thereby further depleting NAD+ to cause an energetic catastrophe and cell death.	NAD	42-46	sterile alpha and TIR motif containing 1	Homo sapiens	95-100
31705020-3	2019	Metabolic analysis showed that lipid peroxidation by reactive oxygen species led to spontaneous production of 4-hydroxynonenal, which was converted to fatty acids with NADH production by ALDH3A1, resulting in further fatty acid oxidation.	NAD	168-172	aldehyde dehydrogenase 3 family member A1	Homo sapiens	187-194
31681271-4	2019	Low dose endotoxin triggered nicotinamide phosphoribosyltransferase (NAMPT)-dependent NAD salvage activity to adapt pro-inflammation.	NAD	86-89	nicotinamide phosphoribosyltransferase	Homo sapiens	29-67
31681271-4	2019	Low dose endotoxin triggered nicotinamide phosphoribosyltransferase (NAMPT)-dependent NAD salvage activity to adapt pro-inflammation.	NAD	86-89	nicotinamide phosphoribosyltransferase	Homo sapiens	69-74
31681271-5	2019	In contrast, high dose endotoxin drove a shift of NAD synthesis pathway from early NAMPT-dependent NAD salvage to late indoleamine 2,3-dioxygenase-1 (IDO1)-dependent NAD de novo biosynthesis, leading to persistent immune suppression.	NAD	50-53	nicotinamide phosphoribosyltransferase	Homo sapiens	83-88
31681271-5	2019	In contrast, high dose endotoxin drove a shift of NAD synthesis pathway from early NAMPT-dependent NAD salvage to late indoleamine 2,3-dioxygenase-1 (IDO1)-dependent NAD de novo biosynthesis, leading to persistent immune suppression.	NAD	99-102	nicotinamide phosphoribosyltransferase	Homo sapiens	83-88
31681271-5	2019	In contrast, high dose endotoxin drove a shift of NAD synthesis pathway from early NAMPT-dependent NAD salvage to late indoleamine 2,3-dioxygenase-1 (IDO1)-dependent NAD de novo biosynthesis, leading to persistent immune suppression.	NAD	99-102	nicotinamide phosphoribosyltransferase	Homo sapiens	83-88
31681271-8	2019	Thus, NAMPT-NAD-SIRT1 axis adapts pro-inflammation, but IDO1-NAD-SIRT1-RelB axis sustains endotoxin tolerance during acute inflammatory response.	NAD	12-15	nicotinamide phosphoribosyltransferase	Homo sapiens	6-11
31353811-3	2019	Recent studies suggest that NAD+ /NADH ratio may play a critical role in cellular senescence by regulating sirtuins, PARP-1, and PGC-1alpha.	NAD	28-32	peroxisome proliferative activated receptor, gamma, coactivator 1 alpha	Mus musculus	129-139
31353811-3	2019	Recent studies suggest that NAD+ /NADH ratio may play a critical role in cellular senescence by regulating sirtuins, PARP-1, and PGC-1alpha.	NAD	34-38	peroxisome proliferative activated receptor, gamma, coactivator 1 alpha	Mus musculus	129-139
31353811-6	2019	We elucidated that the reduction of cellular NAD+ during the aging process was an important contributor for ARHL; it facilitated oxidative stress and pro-inflammatory responses in the cochlear tissue through regulating sirtuins that alter various signaling pathways, such as NF-kappaB, p53, and IDH2.	NAD	45-49	isocitrate dehydrogenase 2 (NADP+), mitochondrial	Mus musculus	295-299
31136762-1	2019	The three nicotinamide mononucleotide adenylyltransferase (NMNAT) family members synthesize the electron carrier nicotinamide adenine dinucleotide (NAD+) and are essential for cellular metabolism.	NAD	113-146	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	10-57
31136762-1	2019	The three nicotinamide mononucleotide adenylyltransferase (NMNAT) family members synthesize the electron carrier nicotinamide adenine dinucleotide (NAD+) and are essential for cellular metabolism.	NAD	113-146	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	59-64
31136762-1	2019	The three nicotinamide mononucleotide adenylyltransferase (NMNAT) family members synthesize the electron carrier nicotinamide adenine dinucleotide (NAD+) and are essential for cellular metabolism.	NAD	148-152	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	10-57
31136762-1	2019	The three nicotinamide mononucleotide adenylyltransferase (NMNAT) family members synthesize the electron carrier nicotinamide adenine dinucleotide (NAD+) and are essential for cellular metabolism.	NAD	148-152	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	59-64
30901096-6	2019	Further experiments confirmed that MRPS5 promoted the production of nicotinamide adenine dinucleotide (NAD+ ), which is necessary for enhanced mitochondrial function in liver CSCs.	NAD	68-101	mitochondrial ribosomal protein S5	Homo sapiens	35-40
30901096-6	2019	Further experiments confirmed that MRPS5 promoted the production of nicotinamide adenine dinucleotide (NAD+ ), which is necessary for enhanced mitochondrial function in liver CSCs.	NAD	103-107	mitochondrial ribosomal protein S5	Homo sapiens	35-40
30901096-8	2019	Mechanistically, the acetylation status of MRPS5 is directly regulated by NAD+ dependent deacetylase sirtuin-1 (SIRT1), which is abundant in liver CSCs and decreased during differentiation.	NAD	74-77	mitochondrial ribosomal protein S5	Homo sapiens	43-48
30901096-9	2019	Deacetylated MRPS5 locates in mitochondria to promote the function complex-I and the generation of NAD+ to enhance mitochondrial respiration.	NAD	99-103	mitochondrial ribosomal protein S5	Homo sapiens	13-18
31409698-4	2019	Disruption of AtNDB2 expression via T-DNA insertion led to a 90% decrease of external NADH oxidation in isolated mitochondria.	NAD	86-90	NAD(P)H dehydrogenase B2	Arabidopsis thaliana	14-20
31541116-3	2019	We have previously shown that NR kinase 1 (NRK1) is rate-limiting and essential for NR-induced NAD+ synthesis in hepatic cells.	NAD	95-98	nicotinamide riboside kinase 1	Mus musculus	30-41
31541116-3	2019	We have previously shown that NR kinase 1 (NRK1) is rate-limiting and essential for NR-induced NAD+ synthesis in hepatic cells.	NAD	95-98	nicotinamide riboside kinase 1	Mus musculus	43-47
31365252-3	2019	Herein, we report the discovery of BI-4916, a prodrug of the co-factor nicotinamide adenine dinucleotide (NADH/NAD+)-competitive PHGDH inhibitor BI-4924, which has shown high selectivity against the majority of other dehydrogenase targets.	NAD	71-104	phosphoglycerate dehydrogenase	Homo sapiens	129-134
31365252-3	2019	Herein, we report the discovery of BI-4916, a prodrug of the co-factor nicotinamide adenine dinucleotide (NADH/NAD+)-competitive PHGDH inhibitor BI-4924, which has shown high selectivity against the majority of other dehydrogenase targets.	NAD	106-110	phosphoglycerate dehydrogenase	Homo sapiens	129-134
31365252-3	2019	Herein, we report the discovery of BI-4916, a prodrug of the co-factor nicotinamide adenine dinucleotide (NADH/NAD+)-competitive PHGDH inhibitor BI-4924, which has shown high selectivity against the majority of other dehydrogenase targets.	NAD	111-115	phosphoglycerate dehydrogenase	Homo sapiens	129-134
31514314-1	2019	Aspartate-Glutamate Carrier 1 (AGC1) deficiency is a rare neurological disease caused by mutations in the solute carrier family 25, member 12 (SLC25A12) gene, encoding for the mitochondrial aspartate-glutamate carrier isoform 1 (AGC1), a component of the malate-aspartate NADH shuttle (MAS), expressed in excitable tissues only.	NAD	272-276	solute carrier family 25 member 12	Homo sapiens	106-141
31514314-1	2019	Aspartate-Glutamate Carrier 1 (AGC1) deficiency is a rare neurological disease caused by mutations in the solute carrier family 25, member 12 (SLC25A12) gene, encoding for the mitochondrial aspartate-glutamate carrier isoform 1 (AGC1), a component of the malate-aspartate NADH shuttle (MAS), expressed in excitable tissues only.	NAD	272-276	solute carrier family 25 member 12	Homo sapiens	143-151
31514314-1	2019	Aspartate-Glutamate Carrier 1 (AGC1) deficiency is a rare neurological disease caused by mutations in the solute carrier family 25, member 12 (SLC25A12) gene, encoding for the mitochondrial aspartate-glutamate carrier isoform 1 (AGC1), a component of the malate-aspartate NADH shuttle (MAS), expressed in excitable tissues only.	NAD	272-276	solute carrier family 25 member 12	Homo sapiens	31-35
31233753-4	2019	In network data, the most significant targets of tyrosyl-DNA phosphodiesterase-1 (TDP1), aldehyde dehydrogenase 1 family member A-1 (ALDH1A1), muscleblind like splicing regulator 1 (MBNL1), aldehyde dehydrogenase-2 (ALDH2), and nicotinamide adenine dinucleotide (HPGD) were screened and defined in anti-CRC effects exerted by puerarin.	NAD	228-261	tyrosyl-DNA phosphodiesterase 1	Homo sapiens	49-80
31233753-4	2019	In network data, the most significant targets of tyrosyl-DNA phosphodiesterase-1 (TDP1), aldehyde dehydrogenase 1 family member A-1 (ALDH1A1), muscleblind like splicing regulator 1 (MBNL1), aldehyde dehydrogenase-2 (ALDH2), and nicotinamide adenine dinucleotide (HPGD) were screened and defined in anti-CRC effects exerted by puerarin.	NAD	228-261	tyrosyl-DNA phosphodiesterase 1	Homo sapiens	82-86
31233753-4	2019	In network data, the most significant targets of tyrosyl-DNA phosphodiesterase-1 (TDP1), aldehyde dehydrogenase 1 family member A-1 (ALDH1A1), muscleblind like splicing regulator 1 (MBNL1), aldehyde dehydrogenase-2 (ALDH2), and nicotinamide adenine dinucleotide (HPGD) were screened and defined in anti-CRC effects exerted by puerarin.	NAD	228-261	muscleblind like splicing regulator 1	Homo sapiens	143-180
31269239-1	2019	Nicotinamide phosphoribosyltransferase (NAMPT) is the key enzyme of the salvage pathway of nicotinamide adenine dinucleotide synthesis.	NAD	91-124	nicotinamide phosphoribosyltransferase	Homo sapiens	0-38
31269239-1	2019	Nicotinamide phosphoribosyltransferase (NAMPT) is the key enzyme of the salvage pathway of nicotinamide adenine dinucleotide synthesis.	NAD	91-124	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
31611752-1	2019	Nicotinamide phosphoribosyltransferase (NAMPT), a rate-limiting enzyme involved in nicotinamide adenine dinucleotide (NAD) salvage pathway, is overexpressed in many human malignancies such as breast cancer.	NAD	83-116	nicotinamide phosphoribosyltransferase	Homo sapiens	0-38
31611752-1	2019	Nicotinamide phosphoribosyltransferase (NAMPT), a rate-limiting enzyme involved in nicotinamide adenine dinucleotide (NAD) salvage pathway, is overexpressed in many human malignancies such as breast cancer.	NAD	83-116	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
31611752-1	2019	Nicotinamide phosphoribosyltransferase (NAMPT), a rate-limiting enzyme involved in nicotinamide adenine dinucleotide (NAD) salvage pathway, is overexpressed in many human malignancies such as breast cancer.	NAD	118-121	nicotinamide phosphoribosyltransferase	Homo sapiens	0-38
31611752-1	2019	Nicotinamide phosphoribosyltransferase (NAMPT), a rate-limiting enzyme involved in nicotinamide adenine dinucleotide (NAD) salvage pathway, is overexpressed in many human malignancies such as breast cancer.	NAD	118-121	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
31611752-9	2019	Our results revealed that the 3"-UTR of NAMPT was a direct target of miR-381 and its up-regulation decreased NAMPT gene and protein expression, leading to a notable reduction in intracellular NAD and subsequently cell survival and induction of apoptosis.	NAD	192-195	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
31611752-9	2019	Our results revealed that the 3"-UTR of NAMPT was a direct target of miR-381 and its up-regulation decreased NAMPT gene and protein expression, leading to a notable reduction in intracellular NAD and subsequently cell survival and induction of apoptosis.	NAD	192-195	nicotinamide phosphoribosyltransferase	Homo sapiens	109-114
31447857-6	2019	AMP-activated kinase (AMPK), which mediates anti-inflammatory effects of IL-10, and nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme of the NAD+ salvage pathway, which is under the control of AMPK, were also required for P2Y11 receptor expression.	NAD	164-168	nicotinamide phosphoribosyltransferase	Homo sapiens	84-122
31447857-6	2019	AMP-activated kinase (AMPK), which mediates anti-inflammatory effects of IL-10, and nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme of the NAD+ salvage pathway, which is under the control of AMPK, were also required for P2Y11 receptor expression.	NAD	164-168	nicotinamide phosphoribosyltransferase	Homo sapiens	124-129
31447857-9	2019	In conclusion, our data indicate that an AMPK-NAMPT-NAD+ signaling axis promotes P2Y11 receptor expression during M2 polarization of human macrophages in response to IL-10.	NAD	52-56	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	41-45
31447857-9	2019	In conclusion, our data indicate that an AMPK-NAMPT-NAD+ signaling axis promotes P2Y11 receptor expression during M2 polarization of human macrophages in response to IL-10.	NAD	52-56	nicotinamide phosphoribosyltransferase	Homo sapiens	46-51
31173250-7	2019	GO analysis revealed that the downregulated DEGs were mainly enriched in "detoxification of copper ion" [biological process, (BP)], "oxidoreductase activity, acting on CH-OH group of donors, NAD or NADP as acceptor" [molecular function, (MF)] and "brush border" [cellular component, (CC)].	NAD	191-194	hydroxysteroid 17-beta dehydrogenase 6	Homo sapiens	132-147
31324777-0	2019	Boosting NAD+ with a small molecule that activates NAMPT.	NAD	9-13	nicotinamide phosphoribosyltransferase	Homo sapiens	51-56
31324777-2	2019	One approach is activation of nicotinamide phosphoribosyltransferase (NAMPT) to increase production of nicotinamide mononucleotide (NMN), the predominant NAD+ precursor in mammalian cells.	NAD	154-158	nicotinamide phosphoribosyltransferase	Homo sapiens	30-68
31324777-2	2019	One approach is activation of nicotinamide phosphoribosyltransferase (NAMPT) to increase production of nicotinamide mononucleotide (NMN), the predominant NAD+ precursor in mammalian cells.	NAD	154-158	nicotinamide phosphoribosyltransferase	Homo sapiens	70-75
31324019-2	2019	Here, we report that machilin A (MA), which acts as a competitive inhibitor by blocking the nicotinamide adenine dinucleotide (NAD) binding site of LDHA, suppresses growth of cancer cells and lactate production in various cancer cell types, including colon, breast, lung, and liver cancers.	NAD	92-125	lactate dehydrogenase A	Mus musculus	148-152
31324019-2	2019	Here, we report that machilin A (MA), which acts as a competitive inhibitor by blocking the nicotinamide adenine dinucleotide (NAD) binding site of LDHA, suppresses growth of cancer cells and lactate production in various cancer cell types, including colon, breast, lung, and liver cancers.	NAD	127-130	lactate dehydrogenase A	Mus musculus	148-152
30969017-5	2019	High-producing cell lines bear unique mutations in nicotinamide adenine dinucleotide (NADH) dehydrogenase (ND2 and ND4) and in peroxisomal acyl-CoA synthetase (ACSL4), involved in lipid metabolism.	NAD	51-84	NADH dehydrogenase subunit 2	Cricetulus griseus	107-110
30969017-5	2019	High-producing cell lines bear unique mutations in nicotinamide adenine dinucleotide (NADH) dehydrogenase (ND2 and ND4) and in peroxisomal acyl-CoA synthetase (ACSL4), involved in lipid metabolism.	NAD	86-90	NADH dehydrogenase subunit 2	Cricetulus griseus	107-110
31207144-3	2019	In skeletal muscle, NAD+ is mainly generated by the NAD+ salvage pathway in which nicotinamide phosphoribosyltransferase (NAMPT) is rate-limiting.	NAD	20-24	nicotinamide phosphoribosyltransferase	Homo sapiens	82-120
31207144-3	2019	In skeletal muscle, NAD+ is mainly generated by the NAD+ salvage pathway in which nicotinamide phosphoribosyltransferase (NAMPT) is rate-limiting.	NAD	20-24	nicotinamide phosphoribosyltransferase	Homo sapiens	122-127
31207144-3	2019	In skeletal muscle, NAD+ is mainly generated by the NAD+ salvage pathway in which nicotinamide phosphoribosyltransferase (NAMPT) is rate-limiting.	NAD	52-56	nicotinamide phosphoribosyltransferase	Homo sapiens	82-120
31207144-3	2019	In skeletal muscle, NAD+ is mainly generated by the NAD+ salvage pathway in which nicotinamide phosphoribosyltransferase (NAMPT) is rate-limiting.	NAD	52-56	nicotinamide phosphoribosyltransferase	Homo sapiens	122-127
31005557-4	2019	Sirtuin 6 (SIRT6), a nicotinamide adenine dinucleotide (NAD)-dependent deacetylase, has been proved to prevent fibrosis in the liver, renal and myocardial tissues.	NAD	21-54	sirtuin 6	Homo sapiens	0-9
31005557-4	2019	Sirtuin 6 (SIRT6), a nicotinamide adenine dinucleotide (NAD)-dependent deacetylase, has been proved to prevent fibrosis in the liver, renal and myocardial tissues.	NAD	21-54	sirtuin 6	Homo sapiens	11-16
31005557-4	2019	Sirtuin 6 (SIRT6), a nicotinamide adenine dinucleotide (NAD)-dependent deacetylase, has been proved to prevent fibrosis in the liver, renal and myocardial tissues.	NAD	56-59	sirtuin 6	Homo sapiens	0-9
31005557-4	2019	Sirtuin 6 (SIRT6), a nicotinamide adenine dinucleotide (NAD)-dependent deacetylase, has been proved to prevent fibrosis in the liver, renal and myocardial tissues.	NAD	56-59	sirtuin 6	Homo sapiens	11-16
31151734-1	2019	Various nutritional signals are transduced by two epigenetic pathways: NAD-dependent sirtuin Sirt1 (NAD+-Sirt1) deacetylase and flavin adenine dinucleotide-dependent lysine-specific demethylase 1 (FAD-LSD1).	NAD	71-74	presenilin 1	Homo sapiens	197-205
30948509-8	2019	Studies to identify its biochemical mechanism of action showed that it does not inhibit NAD+ consumption, suggesting that it acts as a biochemical precursor to NAD+ Cell lysates possess an ATP-dependent kinase activity that efficiently converts NRH to the compound NMNH, but independent of Nrk1 or Nrk2.	NAD	160-164	nicotinamide riboside kinase 2	Homo sapiens	298-302
31016551-4	2019	These cells co-express P2X7 and ADP-ribosyltransferase ARTC2, permitting gating of P2X7 by NAD+-dependent ADP-ribosylation without the need to add exogenous ATP.	NAD	91-95	ADP-ribosyltransferase 2a	Mus musculus	55-60
31214171-1	2019	CD38 (Cluster of Differentiation 38) is a multifunctional ecto-enzyme that metabolizes NAD+ and mediates nicotinamide dinucleotide (NAD+) and extracellular nucleotide homeostasis as well as intracellular calcium.	NAD	87-91	tripartite motif containing 33	Homo sapiens	58-62
31214171-1	2019	CD38 (Cluster of Differentiation 38) is a multifunctional ecto-enzyme that metabolizes NAD+ and mediates nicotinamide dinucleotide (NAD+) and extracellular nucleotide homeostasis as well as intracellular calcium.	NAD	105-130	tripartite motif containing 33	Homo sapiens	58-62
31214171-1	2019	CD38 (Cluster of Differentiation 38) is a multifunctional ecto-enzyme that metabolizes NAD+ and mediates nicotinamide dinucleotide (NAD+) and extracellular nucleotide homeostasis as well as intracellular calcium.	NAD	132-136	tripartite motif containing 33	Homo sapiens	58-62
31214171-4	2019	Of greatest significance is the role of CD38 as an ecto-enzyme capable of modulating extracellular NAD+ precursor availability: 1 to bacteria unable to perform de novo synthesis of NAD+; and 2 in aged parenchyma impacted by the accumulation of immune cells during the process of "inflammaging".	NAD	99-103	tripartite motif containing 33	Homo sapiens	51-55
31214171-4	2019	Of greatest significance is the role of CD38 as an ecto-enzyme capable of modulating extracellular NAD+ precursor availability: 1 to bacteria unable to perform de novo synthesis of NAD+; and 2 in aged parenchyma impacted by the accumulation of immune cells during the process of "inflammaging".	NAD	181-185	tripartite motif containing 33	Homo sapiens	51-55
30715743-2	2019	Owing to a defect in the NADH-shuttle, citrin deficiency impairs hepatic glycolysis and de novo lipogenesis leading to hepatic energy deficit.	NAD	25-29	solute carrier family 25 member 13	Homo sapiens	39-45
31019297-8	2019	Dependence on another rate-limiting enzyme of the NAD synthesis pathway, NAMPT, as a result of enhancer remodelling is subject to resistance by NMRK1-dependent synthesis of NAD.	NAD	50-53	nicotinamide phosphoribosyltransferase	Homo sapiens	73-78
31019297-8	2019	Dependence on another rate-limiting enzyme of the NAD synthesis pathway, NAMPT, as a result of enhancer remodelling is subject to resistance by NMRK1-dependent synthesis of NAD.	NAD	173-176	nicotinamide phosphoribosyltransferase	Homo sapiens	73-78
31179339-3	2019	This study evaluated the effects of BSF on podocyte injury in vivo and in vitro and explored the possible involvement of the nicotinamide adenine dinucleotide phosphate-oxidase-4/reactive oxygen species- (NOX-4/ROS-) activated p38 pathway.	NAD	125-158	NADPH oxidase 4	Homo sapiens	205-210
30858618-7	2019	In this setting, increased NAMPT expression allowed the maintenance of NAD+ pools sufficient for glyceraldehyde-3-phosphate dehydrogenase activity and Warburg metabolism.	NAD	71-75	nicotinamide phosphoribosyltransferase	Homo sapiens	27-32
30885209-8	2019	RESULTS: Our work demonstrates that GFPT2 is transcriptionally upregulated by NF-kappaB and repressed by the NAD+-dependent deacetylase SIRT6.	NAD	109-113	sirtuin 6	Homo sapiens	136-141
30870143-5	2019	PGC1alpha not only counteracted this effect but also raised basal mitophagy, as did the downstream mediator nicotinamide adenine dinucleotide (NAD+).	NAD	108-141	peroxisome proliferative activated receptor, gamma, coactivator 1 alpha	Mus musculus	0-9
30870143-5	2019	PGC1alpha not only counteracted this effect but also raised basal mitophagy, as did the downstream mediator nicotinamide adenine dinucleotide (NAD+).	NAD	143-147	peroxisome proliferative activated receptor, gamma, coactivator 1 alpha	Mus musculus	0-9
30205735-0	2019	CERKL regulates autophagy via the NAD-dependent deacetylase SIRT1.	NAD	34-37	ceramide kinase like	Homo sapiens	0-5
30841449-8	2019	Conversely, AMPK depletion significantly abolishes the effects of physcion (a selective small-molecule 6PGD inhibitor) in decreasing NADPH/NAD + ratio, growth and survival, confirming the role of AMPK as the relevant upstream activator with 6PGD inhibition in HCC cells.	NAD	139-144	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	12-16
30514106-1	2019	Nicotinamide phosphoribosyltransferase (NAMPT) is the rate-limiting enzyme in the NAD+ salvage pathway from nicotinamide.	NAD	82-86	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
30514106-2	2019	By controlling the biosynthesis of NAD+, NAMPT regulates the activity of NAD+-converting enzymes, such as CD38, poly-ADP-ribose polymerases, and sirtuins (SIRTs).	NAD	35-39	nicotinamide phosphoribosyltransferase	Homo sapiens	41-46
30514106-2	2019	By controlling the biosynthesis of NAD+, NAMPT regulates the activity of NAD+-converting enzymes, such as CD38, poly-ADP-ribose polymerases, and sirtuins (SIRTs).	NAD	73-77	nicotinamide phosphoribosyltransferase	Homo sapiens	41-46
30514106-6	2019	In SIRT6-overexpressing cells, NAD(H) levels were up-regulated, as a consequence of NAMPT activation.	NAD	31-37	sirtuin 6	Homo sapiens	3-8
30514106-6	2019	In SIRT6-overexpressing cells, NAD(H) levels were up-regulated, as a consequence of NAMPT activation.	NAD	31-37	nicotinamide phosphoribosyltransferase	Homo sapiens	84-89
30778219-5	2019	Here, we show that nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme of the NAD+ salvage pathway, governs the proinflammatory SASP independent of senescence-associated growth arrest.	NAD	99-103	nicotinamide phosphoribosyltransferase	Homo sapiens	19-57
30778219-5	2019	Here, we show that nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme of the NAD+ salvage pathway, governs the proinflammatory SASP independent of senescence-associated growth arrest.	NAD	99-103	nicotinamide phosphoribosyltransferase	Homo sapiens	59-64
30778219-7	2019	The HMGA-NAMPT-NAD+ signalling axis promotes the proinflammatory SASP by enhancing glycolysis and mitochondrial respiration.	NAD	15-19	nicotinamide phosphoribosyltransferase	Homo sapiens	9-14
30778219-8	2019	HMGA proteins and NAMPT promote the proinflammatory SASP through NAD+-mediated suppression of AMPK kinase, which suppresses the p53-mediated inhibition of p38 MAPK to enhance NF-kappaB activity.	NAD	65-69	nicotinamide phosphoribosyltransferase	Homo sapiens	18-23
30588060-7	2018	Citrin is aspartate/glutamate transporter in mitochondria, a component of malate-aspartate nicotinamide adenine dinucleotide hydrogen shuttle, and is essential for the hepatic glycolysis.	NAD	91-124	solute carrier family 25 member 13	Homo sapiens	0-6
30631755-6	2018	In fact, nicotinamide phosphoribosyltransferase (Nampt), a rate-limiting enzyme for NAD synthesis in mammalian cells, is frequently amplified in several cancer cells.	NAD	84-87	nicotinamide phosphoribosyltransferase	Homo sapiens	9-47
30631755-6	2018	In fact, nicotinamide phosphoribosyltransferase (Nampt), a rate-limiting enzyme for NAD synthesis in mammalian cells, is frequently amplified in several cancer cells.	NAD	84-87	nicotinamide phosphoribosyltransferase	Homo sapiens	49-54
30631755-7	2018	In addition, Nampt-specific inhibitors significantly deplete NAD levels and subsequently suppress cancer cell proliferation through inhibition of energy production pathways, such as glycolysis, tricarboxylic acid (TCA) cycle, and oxidative phosphorylation.	NAD	61-64	nicotinamide phosphoribosyltransferase	Homo sapiens	13-18
30571167-8	2018	Mechanistically, Sin1 T86 phosphorylation amplifies mTORC2-mediated downstream signals; it is also required for alphaIIbbeta3-mediated outside-in signaling and plays a role in generating hypoxia/reactive oxygen species through NAD+/Sirt3 (sirtuin 3)/SOD2 (superoxide dismutase 2) pathway.	NAD	227-231	mitogen-activated protein kinase associated protein 1	Mus musculus	17-21
30571167-8	2018	Mechanistically, Sin1 T86 phosphorylation amplifies mTORC2-mediated downstream signals; it is also required for alphaIIbbeta3-mediated outside-in signaling and plays a role in generating hypoxia/reactive oxygen species through NAD+/Sirt3 (sirtuin 3)/SOD2 (superoxide dismutase 2) pathway.	NAD	227-231	CREB regulated transcription coactivator 2	Mus musculus	52-58
30446247-10	2018	RESULT(S): In Clpp-knockout oocytes compared with WT, FAD tau1 and tau2 were longer and I was higher, NADH tau2 was longer, and F was lower.	NAD	102-106	caseinolytic mitochondrial matrix peptidase proteolytic subunit	Mus musculus	14-18
30585266-0	2018	The intracellular NADH level regulates atrophic nonunion pathogenesis through the CtBP2-p300-Runx2 transcriptional complex.	NAD	18-22	E1A binding protein p300	Homo sapiens	88-92
30585266-5	2018	The lower NADH level in atrophic nonunion tissues disrupted CtBP2 dimerization and enhanced the blockage of the accessibility of the p300-Runx2 complex to the promoters of a series of bone-related target genes, such as OSC, ALPL, COL1A1, IBSP, SPP1 and MMP13.	NAD	10-14	E1A binding protein p300	Homo sapiens	133-137
30585266-5	2018	The lower NADH level in atrophic nonunion tissues disrupted CtBP2 dimerization and enhanced the blockage of the accessibility of the p300-Runx2 complex to the promoters of a series of bone-related target genes, such as OSC, ALPL, COL1A1, IBSP, SPP1 and MMP13.	NAD	10-14	alkaline phosphatase, biomineralization associated	Homo sapiens	224-228
30585266-7	2018	In conclusion, our study revealed that NADH levels determine the expression of bone formation and development of related genes through affecting the dissociation or binding of CtBP2 to the p300-Runx2 complex.	NAD	39-43	E1A binding protein p300	Homo sapiens	189-193
30585266-8	2018	These results represent a conserved mechanism, by which CtBP2 serves as a NADH-dependent repressor of the p300-Runx2 transcriptional complex and thus affects bone formation.	NAD	74-78	E1A binding protein p300	Homo sapiens	106-110
30179595-5	2018	NAD (a selective 5-HT1A antagonist) was microinjected into the CA1 region of the hippocampus at the doses of 2.5 and 5 mug/1 mul.	NAD	0-3	5-hydroxytryptamine receptor 1A	Rattus norvegicus	17-23
30055417-3	2018	With the catalysis of 3alpha-hydroxysteroid dehydrogenase (3alpha-HSD), 3alpha-bile acids reacted specifically with nicotinamide adenine dinucleotide (NAD+).	NAD	116-149	aldo-keto reductase family 1 member C3	Homo sapiens	22-57
30055417-3	2018	With the catalysis of 3alpha-hydroxysteroid dehydrogenase (3alpha-HSD), 3alpha-bile acids reacted specifically with nicotinamide adenine dinucleotide (NAD+).	NAD	116-149	aldo-keto reductase family 1 member C3	Homo sapiens	59-69
30055417-3	2018	With the catalysis of 3alpha-hydroxysteroid dehydrogenase (3alpha-HSD), 3alpha-bile acids reacted specifically with nicotinamide adenine dinucleotide (NAD+).	NAD	151-155	aldo-keto reductase family 1 member C3	Homo sapiens	22-57
30055417-3	2018	With the catalysis of 3alpha-hydroxysteroid dehydrogenase (3alpha-HSD), 3alpha-bile acids reacted specifically with nicotinamide adenine dinucleotide (NAD+).	NAD	151-155	aldo-keto reductase family 1 member C3	Homo sapiens	59-69
30309019-1	2018	Cytochrome b5 reductase 3 (CYB5R3) is a membrane-bound NADH-dependent redox enzyme anchored to the mitochondrial outer membrane, endoplasmic reticulum, and plasma membrane.	NAD	55-59	cytochrome b5 reductase 3	Homo sapiens	0-25
30309019-1	2018	Cytochrome b5 reductase 3 (CYB5R3) is a membrane-bound NADH-dependent redox enzyme anchored to the mitochondrial outer membrane, endoplasmic reticulum, and plasma membrane.	NAD	55-59	cytochrome b5 reductase 3	Homo sapiens	27-33
29886033-2	2018	Nicotinamide phosphoribosyltransferase (NAMPT) functions as a key enzyme in the salvage pathway of NAD biosynthesis.	NAD	99-102	nicotinamide phosphoribosyltransferase	Homo sapiens	0-38
29886033-2	2018	Nicotinamide phosphoribosyltransferase (NAMPT) functions as a key enzyme in the salvage pathway of NAD biosynthesis.	NAD	99-102	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
29886033-3	2018	Cancer cells have higher rate of NAD consumption and therefore NAMPT is essential for their survival.	NAD	33-36	nicotinamide phosphoribosyltransferase	Homo sapiens	63-68
29886033-11	2018	miR-206 reduced NAMPT expression at the protein level, leading to a significant decrease in the intracellular NAD level and subsequent decline in cell survival and induction of apoptosis.	NAD	110-113	nicotinamide phosphoribosyltransferase	Homo sapiens	16-21
29886033-12	2018	Targeting of NAMPT-mediated NAD salvage pathway by miR-206 might provide a new insight in the possible molecular mechanism of breast cancer cell growth regulation.	NAD	28-31	nicotinamide phosphoribosyltransferase	Homo sapiens	13-18
28877980-1	2018	OBJECTIVE: Nicotinamide phosphoribosyltransferase (NAMPT, also referred to as pre-B cell colony-enhancing factor or visfatin) is critically required for the maintenance of cellular nicotinamide adenine dinucleotide (NAD) supply catalysing the rate-limiting step of the NAD salvage pathway.	NAD	269-272	nicotinamide phosphoribosyltransferase	Homo sapiens	51-56
28877980-1	2018	OBJECTIVE: Nicotinamide phosphoribosyltransferase (NAMPT, also referred to as pre-B cell colony-enhancing factor or visfatin) is critically required for the maintenance of cellular nicotinamide adenine dinucleotide (NAD) supply catalysing the rate-limiting step of the NAD salvage pathway.	NAD	269-272	nicotinamide phosphoribosyltransferase	Homo sapiens	116-124
28877980-2	2018	NAMPT is strongly upregulated in inflammation including IBD and counteracts an increased cellular NAD turnover mediated by NAD-depleting enzymes.	NAD	98-101	nicotinamide phosphoribosyltransferase	Homo sapiens	0-5
28877980-2	2018	NAMPT is strongly upregulated in inflammation including IBD and counteracts an increased cellular NAD turnover mediated by NAD-depleting enzymes.	NAD	123-126	nicotinamide phosphoribosyltransferase	Homo sapiens	0-5
28877980-8	2018	FK866 potently inhibited NAMPT activity as demonstrated by reduced mucosal NAD, resulting in reduced abundances and activities of NAD-dependent enzymes including PARP1, Sirt6 and CD38, reduced nuclear factor kappa B activation, and decreased cellular infiltration by inflammatory monocytes, macrophages and activated T cells.	NAD	75-78	nicotinamide phosphoribosyltransferase	Homo sapiens	25-30
28877980-8	2018	FK866 potently inhibited NAMPT activity as demonstrated by reduced mucosal NAD, resulting in reduced abundances and activities of NAD-dependent enzymes including PARP1, Sirt6 and CD38, reduced nuclear factor kappa B activation, and decreased cellular infiltration by inflammatory monocytes, macrophages and activated T cells.	NAD	130-133	nicotinamide phosphoribosyltransferase	Homo sapiens	25-30
30007118-5	2018	SUMMARY: Background Platelets from patients with X-linked chronic granulomatous disease or mice deficient in nicotinamide adenine dinucleotide (phosphate) (NAD(P)H) oxidase isoform NOX2 exhibit diminished reactive oxygen species (ROS) generation and platelet activation.	NAD	109-142	cytochrome b-245, beta polypeptide	Mus musculus	181-185
30158377-3	2018	Nicotinamide phosphate transferase (NAMPT) is the rate limiting enzyme in the synthesis of NAD, but extracellular NAMPT shows the characteristics of cytokines/adipokines, suggesting that it may be a link between metabolism and inflammation.	NAD	91-94	nicotinamide phosphoribosyltransferase	Homo sapiens	0-34
30158377-3	2018	Nicotinamide phosphate transferase (NAMPT) is the rate limiting enzyme in the synthesis of NAD, but extracellular NAMPT shows the characteristics of cytokines/adipokines, suggesting that it may be a link between metabolism and inflammation.	NAD	91-94	nicotinamide phosphoribosyltransferase	Homo sapiens	36-41
30158377-6	2018	The results showed that the expression of the NAMPT/NAD+/Sirt1 signaling pathway was up-regulated in the peripheral blood of patients with ACS.	NAD	52-56	nicotinamide phosphoribosyltransferase	Homo sapiens	46-51
30158377-10	2018	Our findings suggested that NAMPT is involved in the pathogenesis of atherosclerosis; the increased expression of eNAMPT in ACS patients may play a protective role by the up regulation of the NAMPT/NAD+/Sirt1 signaling pathway.	NAD	198-202	nicotinamide phosphoribosyltransferase	Homo sapiens	28-33
30158377-10	2018	Our findings suggested that NAMPT is involved in the pathogenesis of atherosclerosis; the increased expression of eNAMPT in ACS patients may play a protective role by the up regulation of the NAMPT/NAD+/Sirt1 signaling pathway.	NAD	198-202	nicotinamide phosphoribosyltransferase	Homo sapiens	115-120
30096284-3	2018	We found that ERalpha and/or ERbeta activation using their agonists (0.5 mg/kg E2, PPT or DPN) ameliorate memory impairment in the Morris water maze (MWM) and Y-maze tests and suppress apoptosis as evidenced by decreased caspase-3 activity and increased ratio of Bcl-2/Bax.	NAD	90-93	estrogen receptor 2 (beta)	Mus musculus	29-35
30166529-2	2018	NMNAT1 is a nuclear enzyme essential for nicotinamide adenine dinucleotide (NAD) biosynthesis pathways, but the mechanisms underlying the LCA pathology and whether NMNAT1 has a role in normal retinal development remain unclear.	NAD	41-74	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	0-6
30166529-2	2018	NMNAT1 is a nuclear enzyme essential for nicotinamide adenine dinucleotide (NAD) biosynthesis pathways, but the mechanisms underlying the LCA pathology and whether NMNAT1 has a role in normal retinal development remain unclear.	NAD	76-79	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	0-6
30166529-5	2018	Decreased intracellular NAD content was observed and the addition of NAD to the culture medium attenuated sh-Nmnat1-induced apoptosis.	NAD	69-72	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	109-115
29935245-0	2018	Oxyresveratrol stimulates mucin production in an NAD+-dependent manner in human intestinal goblet cells.	NAD	49-53	LOC100508689	Homo sapiens	26-31
30038627-1	2018	On murine T cells, GPI-anchored ADP-ribosyltransferase 2.2 (ARTC2.2) ADP-ribosylates the P2X7 ion channel at arginine 125 in response to nicotinamide adenine dinucleotide (NAD+) released during cell preparation.	NAD	137-170	ADP-ribosyltransferase 2a	Mus musculus	60-65
30038627-1	2018	On murine T cells, GPI-anchored ADP-ribosyltransferase 2.2 (ARTC2.2) ADP-ribosylates the P2X7 ion channel at arginine 125 in response to nicotinamide adenine dinucleotide (NAD+) released during cell preparation.	NAD	172-176	ADP-ribosyltransferase 2a	Mus musculus	60-65
29526705-3	2018	Nicotinamide adenine dinucleotide (phosphate) (NADPH) oxidase 4 (NOX4) is one of the major enzymes responsible for intracellular ROS production during the inflammatory process.	NAD	0-33	NADPH oxidase 4	Homo sapiens	65-69
29700119-4	2018	Here, multi-angle light scattering (MALS) data established the NAD+- and NADH-dependent assembly of CtBP1 and CtBP2 into tetramers.	NAD	63-67	C-terminal binding protein 1	Homo sapiens	100-105
29700119-4	2018	Here, multi-angle light scattering (MALS) data established the NAD+- and NADH-dependent assembly of CtBP1 and CtBP2 into tetramers.	NAD	73-77	C-terminal binding protein 1	Homo sapiens	100-105
29700119-5	2018	An examination of subunit interactions within CtBP1 and CtBP2 crystal lattices revealed that both share a very similar tetrameric arrangement resulting from assembly of two dimeric pairs, with specific interactions probably being sensitive to NAD(H) binding.	NAD	243-249	C-terminal binding protein 1	Homo sapiens	46-51
29700119-8	2018	The crystal structure of a subtle destabilizing mutant suggested that small structural perturbations of the hinge region linking the substrate- and NAD-binding domains are sufficient to weaken the CtBP1 tetramer.	NAD	148-151	C-terminal binding protein 1	Homo sapiens	197-202
29874584-6	2018	Human neurons require nicotinamide phosphoribosyltransferase (NAMPT) to maintain the NAD+ pool and utilize NRK1 to synthesize NAD+ from NAD+ precursors.	NAD	85-89	nicotinamide phosphoribosyltransferase	Homo sapiens	22-60
29874584-6	2018	Human neurons require nicotinamide phosphoribosyltransferase (NAMPT) to maintain the NAD+ pool and utilize NRK1 to synthesize NAD+ from NAD+ precursors.	NAD	85-89	nicotinamide phosphoribosyltransferase	Homo sapiens	62-67
29874586-5	2018	Furthermore, we identify SIRT6, a NAD+-dependent histone deacetylase, as a corepressor of ATF4 transcriptional activity.	NAD	34-37	sirtuin 6	Homo sapiens	25-30
29678570-3	2018	Here we sought to identify the roles of nicotinamide riboside kinase 1 (NRK1) plays in regulating hepatic NAD+ biosynthesis and lipid metabolism.	NAD	106-110	nicotinamide riboside kinase 1	Mus musculus	40-70
29678570-3	2018	Here we sought to identify the roles of nicotinamide riboside kinase 1 (NRK1) plays in regulating hepatic NAD+ biosynthesis and lipid metabolism.	NAD	106-110	nicotinamide riboside kinase 1	Mus musculus	72-76
29678570-4	2018	Using adenovirus mediated gene transduction to overexpress or knockdown NRK1 in mouse liver, we have demonstrated that NRK1 is critical for maintaining hepatic NAD+ levels and triglyceride content.	NAD	160-164	nicotinamide riboside kinase 1	Mus musculus	72-76
29678570-4	2018	Using adenovirus mediated gene transduction to overexpress or knockdown NRK1 in mouse liver, we have demonstrated that NRK1 is critical for maintaining hepatic NAD+ levels and triglyceride content.	NAD	160-164	nicotinamide riboside kinase 1	Mus musculus	119-123
29603199-10	2018	Furthermore, deacetylation of CypD at Lys residue by sirtuin 3 (SIRT3) caused its dissociation from ANT, contributing to an increase in mPT threshold in NAD+ -pretreated animals.	NAD	153-157	peptidylprolyl isomerase F	Rattus norvegicus	30-34
29653431-1	2018	NAMPT (Nicotinamide phosphoribosyltransferase) catalyses the rate-limiting step in the NAD biosynthesis from nicotinamide and thereby regulates the activity of NAD-dependent enzymes.	NAD	87-90	nicotinamide phosphoribosyltransferase	Homo sapiens	0-5
29653431-1	2018	NAMPT (Nicotinamide phosphoribosyltransferase) catalyses the rate-limiting step in the NAD biosynthesis from nicotinamide and thereby regulates the activity of NAD-dependent enzymes.	NAD	87-90	nicotinamide phosphoribosyltransferase	Homo sapiens	7-45
29653431-1	2018	NAMPT (Nicotinamide phosphoribosyltransferase) catalyses the rate-limiting step in the NAD biosynthesis from nicotinamide and thereby regulates the activity of NAD-dependent enzymes.	NAD	160-163	nicotinamide phosphoribosyltransferase	Homo sapiens	0-5
29653431-1	2018	NAMPT (Nicotinamide phosphoribosyltransferase) catalyses the rate-limiting step in the NAD biosynthesis from nicotinamide and thereby regulates the activity of NAD-dependent enzymes.	NAD	160-163	nicotinamide phosphoribosyltransferase	Homo sapiens	7-45
29748257-4	2018	Adipogenic signaling rapidly induces cytoplasmic NMNAT-2, which competes with nuclear NMNAT-1 for the common substrate, nicotinamide mononucleotide, leading to a precipitous reduction in nuclear NAD+ levels.	NAD	195-199	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	86-93
29748257-5	2018	This inhibits the catalytic activity of poly[adenosine diphosphate (ADP)-ribose] polymerase-1 (PARP-1), a NAD+-dependent enzyme that represses adipogenic transcription by ADP-ribosylating the adipogenic transcription factor C/EBPbeta.	NAD	106-110	CCAAT enhancer binding protein beta	Homo sapiens	224-233
29739976-3	2018	However, KARI with a preference for NADH is desirable in industrial applications including anaerobic fermentation for the production of branched-chain amino acids or biofuels.	NAD	36-40	ATZ20_RS01865	Sulfolobus acidocaldarius	9-13
29739976-6	2018	Sac-KARI has very high affinity for NADPH and NADH, with K M values of 0.4 muM for NADPH and 6.0 muM for NADH, suggesting that both are good cofactors at low concentrations although NADPH is favoured over NADH.	NAD	46-50	ATZ20_RS01865	Sulfolobus acidocaldarius	4-8
29739976-6	2018	Sac-KARI has very high affinity for NADPH and NADH, with K M values of 0.4 muM for NADPH and 6.0 muM for NADH, suggesting that both are good cofactors at low concentrations although NADPH is favoured over NADH.	NAD	105-109	ATZ20_RS01865	Sulfolobus acidocaldarius	4-8
29739976-6	2018	Sac-KARI has very high affinity for NADPH and NADH, with K M values of 0.4 muM for NADPH and 6.0 muM for NADH, suggesting that both are good cofactors at low concentrations although NADPH is favoured over NADH.	NAD	105-109	ATZ20_RS01865	Sulfolobus acidocaldarius	4-8
28194019-9	2018	Furthermore, IL-25 improved the mitochondrial respiratory capacity and oxygen consumption rate of macrophages and produced more NAD+/NADH and ATP.	NAD	128-132	interleukin 25	Mus musculus	13-18
28194019-9	2018	Furthermore, IL-25 improved the mitochondrial respiratory capacity and oxygen consumption rate of macrophages and produced more NAD+/NADH and ATP.	NAD	133-137	interleukin 25	Mus musculus	13-18
29512698-1	2018	Sirtuin 6 (SIRT6) is a member of the nicotinamide adenine dinucleotide positivity-dependent class III deacetylase sirtuin family.	NAD	37-70	sirtuin 6	Homo sapiens	0-9
29512698-1	2018	Sirtuin 6 (SIRT6) is a member of the nicotinamide adenine dinucleotide positivity-dependent class III deacetylase sirtuin family.	NAD	37-70	sirtuin 6	Homo sapiens	11-16
29363378-1	2018	Objective To explore the prognostic significance of nicotinamide adenine dinucleotide (NAD)-dependent protein deacetylase sirtuin-6 (SIRT6), encoded by the sirtuin 6 ( SIRT6) gene, in a population of Chinese Han patients with non-small cell lung cancer (NSCLC).	NAD	87-90	sirtuin 6	Homo sapiens	133-138
29363378-1	2018	Objective To explore the prognostic significance of nicotinamide adenine dinucleotide (NAD)-dependent protein deacetylase sirtuin-6 (SIRT6), encoded by the sirtuin 6 ( SIRT6) gene, in a population of Chinese Han patients with non-small cell lung cancer (NSCLC).	NAD	87-90	sirtuin 6	Homo sapiens	156-165
29363378-1	2018	Objective To explore the prognostic significance of nicotinamide adenine dinucleotide (NAD)-dependent protein deacetylase sirtuin-6 (SIRT6), encoded by the sirtuin 6 ( SIRT6) gene, in a population of Chinese Han patients with non-small cell lung cancer (NSCLC).	NAD	87-90	sirtuin 6	Homo sapiens	168-173
29420256-5	2018	Despite a 68% reduction in cellular NAD levels in NAMPT-deficient cells, no change in expression or activity of dihydrofolate reductase was observed and uptake of MTX was not significantly altered.	NAD	36-39	nicotinamide phosphoribosyltransferase	Homo sapiens	50-55
29769837-3	2018	Alternatively, ADO can be generated starting from NAD+, which is metabolized by the concerted action of CD38, CD203a/PC-1, and CD73.	NAD	50-54	5'-nucleotidase ecto	Homo sapiens	127-131
29329057-9	2018	CORT-treated rats showed degenerated mitochondrial functions represented by decreased adenosine triphosphate production, decreased nicotinamide adenine dinucleotide+ content, and decreased activity of nicotinamide phosphoribosyltransferase.	NAD	131-165	cortistatin	Rattus norvegicus	0-4
28707979-2	2018	SIRT5 is one of the seven members of the nicotinamide adenine dinucleotide-dependent sirtuin family of lysine deacetylases.	NAD	41-74	sirtuin 5	Homo sapiens	0-5
29541451-1	2018	Background: Inhibitors of nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme in NAD+ biosynthesis from nicotinamide, exhibit anticancer effects in preclinical models.	NAD	102-106	nicotinamide phosphoribosyltransferase	Homo sapiens	26-64
29541451-1	2018	Background: Inhibitors of nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme in NAD+ biosynthesis from nicotinamide, exhibit anticancer effects in preclinical models.	NAD	102-106	nicotinamide phosphoribosyltransferase	Homo sapiens	66-71
29511198-0	2018	Author Correction: Rev1 contributes to proper mitochondrial function via the PARP-NAD+-SIRT1-PGC1alpha axis.	NAD	82-86	collagen type XI alpha 2 chain	Homo sapiens	77-81
29203587-6	2018	Therapeutic approaches.Results: NAMPT, the rate-limiting enzyme responsible for the highest source of physiologic NAD biosynthesis, increases tumorigenic properties and induces cancer stem cell-like properties through pathways that control stem cell signaling, thus enriching the cancer-initiating cell (CIC) population.	NAD	114-117	nicotinamide phosphoribosyltransferase	Homo sapiens	32-37
29567766-1	2018	In BRAFV600E melanoma cells, a global metabolomic analysis discloses a decrease in nicotinamide adenine dinucleotide (NAD+) levels upon PLX4032 treatment that is conveyed by a STAT5 inhibition and a transcriptional regulation of the nicotinamide phosphoribosyltransferase (NAMPT) gene.	NAD	118-122	nicotinamide phosphoribosyltransferase	Homo sapiens	233-271
29567766-1	2018	In BRAFV600E melanoma cells, a global metabolomic analysis discloses a decrease in nicotinamide adenine dinucleotide (NAD+) levels upon PLX4032 treatment that is conveyed by a STAT5 inhibition and a transcriptional regulation of the nicotinamide phosphoribosyltransferase (NAMPT) gene.	NAD	118-122	nicotinamide phosphoribosyltransferase	Homo sapiens	273-278
29567766-4	2018	Therefore, NAMPT, the key enzyme in the NAD+ salvage pathway, appears as a rational target in targeted therapy-resistant melanoma cells and a key player in phenotypic plasticity of melanoma cells.	NAD	40-44	nicotinamide phosphoribosyltransferase	Homo sapiens	11-16
29568399-3	2018	C-terminal binding protein 1 (CTBP1) is a co-repressor of tumor suppressor genes that is activated by low NAD+/NADH ratio.	NAD	106-110	C-terminal binding protein 1	Homo sapiens	0-28
29568399-3	2018	C-terminal binding protein 1 (CTBP1) is a co-repressor of tumor suppressor genes that is activated by low NAD+/NADH ratio.	NAD	106-110	C-terminal binding protein 1	Homo sapiens	30-35
29568399-3	2018	C-terminal binding protein 1 (CTBP1) is a co-repressor of tumor suppressor genes that is activated by low NAD+/NADH ratio.	NAD	111-115	C-terminal binding protein 1	Homo sapiens	0-28
29568399-3	2018	C-terminal binding protein 1 (CTBP1) is a co-repressor of tumor suppressor genes that is activated by low NAD+/NADH ratio.	NAD	111-115	C-terminal binding protein 1	Homo sapiens	30-35
30794635-1	2019	Nicotinamide phosphoribosyltransferase (NAMPT) is a rate-limiting enzyme in mammalian nicotinamide adenine dinucleotide (NAD)+ biosynthesis.	NAD	86-119	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
30794635-1	2019	Nicotinamide phosphoribosyltransferase (NAMPT) is a rate-limiting enzyme in mammalian nicotinamide adenine dinucleotide (NAD)+ biosynthesis.	NAD	121-124	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
30794635-2	2019	Through its NAD+-biosynthetic activity, NAMPT influences the activity of NAD+-dependent enzymes, such as sirtuins.	NAD	12-16	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
30794635-2	2019	Through its NAD+-biosynthetic activity, NAMPT influences the activity of NAD+-dependent enzymes, such as sirtuins.	NAD	73-77	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
30794635-6	2019	We next demonstrate that hepatocytes infected with Ad-NAMPT adenovirus exhibit significantly elevated intracellular NAD+ levels and decreased ethanol-induced triglyceride (TG) accumulation.	NAD	116-120	nicotinamide phosphoribosyltransferase	Homo sapiens	54-59
30759120-1	2019	Sirtuin 5 (SIRT5) is a member of the NAD+-dependent sirtuin family of protein deacylase that catalyzes removal of post-translational modifications, such as succinylation, malonylation, and glutarylation on lysine residues.	NAD	37-40	sirtuin 5	Mus musculus	0-9
30759120-1	2019	Sirtuin 5 (SIRT5) is a member of the NAD+-dependent sirtuin family of protein deacylase that catalyzes removal of post-translational modifications, such as succinylation, malonylation, and glutarylation on lysine residues.	NAD	37-40	sirtuin 5	Mus musculus	11-16
30759120-2	2019	In light of the SIRT5"s roles in regulating mitochondrion function, we show here that SIRT5 deficiency leads to suppression of mitochondrial NADH oxidation and inhibition of ATP synthase activity.	NAD	141-145	sirtuin 5	Mus musculus	16-21
30759120-2	2019	In light of the SIRT5"s roles in regulating mitochondrion function, we show here that SIRT5 deficiency leads to suppression of mitochondrial NADH oxidation and inhibition of ATP synthase activity.	NAD	141-145	sirtuin 5	Mus musculus	86-91
33185189-7	2020	We propose that the reduction of cellular NAD+ concentration contributes to the disassembly of SARM1"s peripheral ring, which allows formation of active NADase domain dimers, thereby further depleting NAD+ to cause an energetic catastrophe and cell death.	NAD	201-205	sterile alpha and TIR motif containing 1	Homo sapiens	95-100
33149812-0	2020	Notoginseng Leaf Triterpenes Ameliorates OGD/R-Induced Neuronal Injury via SIRT1/2/3-Foxo3a-MnSOD/PGC-1alpha Signaling Pathways Mediated by the NAMPT-NAD Pathway.	NAD	150-153	nicotinamide phosphoribosyltransferase	Homo sapiens	144-149
30457689-4	2019	Here, we showed that the NAD(H) pool size and NAD+ /NADH ratio both increased during colorectal cancer (CRC) progression due to activation of the NAD+ salvage pathway mediated by nicotinamide phosphoribosyltransferase (NAMPT).	NAD	46-50	nicotinamide phosphoribosyltransferase	Homo sapiens	179-217
30457689-4	2019	Here, we showed that the NAD(H) pool size and NAD+ /NADH ratio both increased during colorectal cancer (CRC) progression due to activation of the NAD+ salvage pathway mediated by nicotinamide phosphoribosyltransferase (NAMPT).	NAD	52-56	nicotinamide phosphoribosyltransferase	Homo sapiens	179-217
30457689-4	2019	Here, we showed that the NAD(H) pool size and NAD+ /NADH ratio both increased during colorectal cancer (CRC) progression due to activation of the NAD+ salvage pathway mediated by nicotinamide phosphoribosyltransferase (NAMPT).	NAD	146-150	nicotinamide phosphoribosyltransferase	Homo sapiens	179-217
30457689-4	2019	Here, we showed that the NAD(H) pool size and NAD+ /NADH ratio both increased during colorectal cancer (CRC) progression due to activation of the NAD+ salvage pathway mediated by nicotinamide phosphoribosyltransferase (NAMPT).	NAD	146-150	nicotinamide phosphoribosyltransferase	Homo sapiens	219-224
30457689-8	2019	Collectively, our results suggest that NAMPT-mediated upregulation of the NAD(H) pool protects cancer cells against detrimental oxidative stress and that detecting NADH fluorescence by TPEF microscopy could be a potential method for monitoring CRC progression.	NAD	164-168	nicotinamide phosphoribosyltransferase	Homo sapiens	39-44
30668112-2	2019	While this step is classically considered to be catalyzed by an NAD-dependent dehydrogenase (e.g., PHGDH in mammals), evidence has shown that in Pseudomonas, Escherichia coli, and Saccharomyces cerevisiae, the PHGDH homologues act as transhydrogenases.	NAD	64-67	phosphoglycerate dehydrogenase	Homo sapiens	99-104
30668112-2	2019	While this step is classically considered to be catalyzed by an NAD-dependent dehydrogenase (e.g., PHGDH in mammals), evidence has shown that in Pseudomonas, Escherichia coli, and Saccharomyces cerevisiae, the PHGDH homologues act as transhydrogenases.	NAD	64-67	phosphoglycerate dehydrogenase	Homo sapiens	210-215
30679956-9	2019	To further characterize the benefit of methanol as the carbon source, extra NADH from methanol oxidation was engineered to generate NADPH to improve lysine biosynthesis by expression of the POS5 gene from Saccharomyces cerevisiae, which resulted in a twofold improvement of lysine production.	NAD	76-80	NADH kinase	Saccharomyces cerevisiae S288C	190-194
30455381-8	2019	Specifically, CFZ treatment reduced the expression of nicotinamide phosphoribosyltransferase (NAMPT), thus limiting IDH2 activation through the NAD+-dependent deacetylase SIRT3.	NAD	144-148	nicotinamide phosphoribosyltransferase	Homo sapiens	54-92
30455381-8	2019	Specifically, CFZ treatment reduced the expression of nicotinamide phosphoribosyltransferase (NAMPT), thus limiting IDH2 activation through the NAD+-dependent deacetylase SIRT3.	NAD	144-148	nicotinamide phosphoribosyltransferase	Homo sapiens	94-99
30201537-3	2019	We found that ERalpha and/or ERbeta activation using their agonists (0.5 mg/kg E2, PPT or DPN) ameliorate memory impairment in the Morris water maze and Y-maze tests, increase hippocampal neurogenesis and prevent hippocampal apoptotic responses.	NAD	90-93	estrogen receptor 2 (beta)	Mus musculus	29-35
31131364-4	2019	We find that Slc12a8 is highly expressed and regulated by NAD+ in the murine small intestine.	NAD	58-62	solute carrier family 12 (potassium/chloride transporters), member 8	Mus musculus	13-20
31131364-7	2019	Slc12a8 deficiency significantly decreases NAD+ levels in the jejunum and ileum, which is associated with reduced NMN uptake as traced by doubly labeled isotopic NMN.	NAD	43-47	solute carrier family 12 (potassium/chloride transporters), member 8	Mus musculus	0-7
31131364-8	2019	Finally, we observe that Slc12a8 expression is upregulated in the aged murine ileum, which contributes to the maintenance of ileal NAD+ levels.	NAD	131-135	solute carrier family 12 (potassium/chloride transporters), member 8	Mus musculus	25-32
31131364-9	2019	Our work identifies the first NMN transporter and demonstrates that Slc12a8 has a critical role in regulating intestinal NAD+ metabolism.	NAD	121-125	solute carrier family 12 (potassium/chloride transporters), member 8	Mus musculus	68-75
30427660-10	2018	The conjugation of tPA with preserved lytic activity, the deformability and blood circulating time of DPNs together with the faster blood clot dissolution would make tPA-DPNs a promising nanotool for enhancing both potency and safety of thrombolytic therapies.	NAD	102-106	plasminogen activator, tissue	Mus musculus	19-22
30427660-10	2018	The conjugation of tPA with preserved lytic activity, the deformability and blood circulating time of DPNs together with the faster blood clot dissolution would make tPA-DPNs a promising nanotool for enhancing both potency and safety of thrombolytic therapies.	NAD	102-106	plasminogen activator, tissue	Mus musculus	166-169
30333228-0	2018	c-Jun N-terminal kinase (JNK)-mediated phosphorylation of SARM1 regulates NAD+ cleavage activity to inhibit mitochondrial respiration.	NAD	74-78	sterile alpha and TIR motif containing 1	Homo sapiens	58-63
30333228-4	2018	Here, we report that NAD+ cleavage activity of SARM1 is regulated by its own phosphorylation at serine 548.	NAD	21-25	sterile alpha and TIR motif containing 1	Homo sapiens	47-52
30333228-5	2018	The phosphorylation of SARM1 was mediated by c-jun N-terminal kinase (JNK) under oxidative stress conditions, resulting in inhibition of mitochondrial respiration concomitant with enhanced activity of NAD+ cleavage.	NAD	201-205	sterile alpha and TIR motif containing 1	Homo sapiens	23-28
29080400-8	2018	We propose that using AMPK activators such as 5-aminoimidazole-4-carboxamide ribonucleotide, A769662, metformin, and oxidized nicotinamide adenine dinucleotide (NAD+) are practical ways to be employed for achieving better optimized results in stem cell-based transplantation therapies.	NAD	126-159	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	22-26
29080400-8	2018	We propose that using AMPK activators such as 5-aminoimidazole-4-carboxamide ribonucleotide, A769662, metformin, and oxidized nicotinamide adenine dinucleotide (NAD+) are practical ways to be employed for achieving better optimized results in stem cell-based transplantation therapies.	NAD	161-165	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	22-26
30404003-5	2018	NAD treatment also improved ATP production in MTDPS3-null rats and in hepatocyte-like cells that were deficient in ribonucleoside-diphosphate reductase subunit M2B (RRM2B), suggesting that it could be broadly effective.	NAD	0-3	ribonucleotide reductase regulatory TP53 inducible subunit M2B	Rattus norvegicus	115-163
30404003-5	2018	NAD treatment also improved ATP production in MTDPS3-null rats and in hepatocyte-like cells that were deficient in ribonucleoside-diphosphate reductase subunit M2B (RRM2B), suggesting that it could be broadly effective.	NAD	0-3	ribonucleotide reductase regulatory TP53 inducible subunit M2B	Rattus norvegicus	165-170
30179604-8	2018	Exogenous NAD suppressed NPY and AgRP transcriptional activity, which was mediated by SIRT1 and FOXO1.	NAD	10-13	neuropeptide Y	Mus musculus	25-28
29261292-10	2018	The primary finding of this work is that mono- versus multi-HAAs address different molecular targets, and the results are generally consistent with a model in which monoHAAs activate the PDC through GAPDH inhibition-mediated disruption in cellular metabolites, including altering ATP-to-ADP and NADH-to-NAD ratios.	NAD	295-299	glyceraldehyde-3-phosphate dehydrogenase	Cricetulus griseus	199-204
29261292-10	2018	The primary finding of this work is that mono- versus multi-HAAs address different molecular targets, and the results are generally consistent with a model in which monoHAAs activate the PDC through GAPDH inhibition-mediated disruption in cellular metabolites, including altering ATP-to-ADP and NADH-to-NAD ratios.	NAD	295-298	glyceraldehyde-3-phosphate dehydrogenase	Cricetulus griseus	199-204
29721988-2	2018	We recently demonstrated that both rod and cone photoreceptors rely on NAMPT-mediated NAD+ biosynthesis to meet their energetic requirements.	NAD	86-90	nicotinamide phosphoribosyltransferase	Homo sapiens	71-76
29333085-7	2018	Results: We were able to identify a significant down-expression of mitochondrial encoded NADH: ubiquinone oxidoreductase core subunit 6 (MT-ND6) in men with KS.	NAD	89-93	mitochondrially encoded NADH dehydrogenase 6	Homo sapiens	137-143
32991157-5	2020	SIRT5 is a mitochondria-localized enzyme belonging to a family of NAD+-dependent histone deacetylases.	NAD	66-69	sirtuin 5	Homo sapiens	0-5
33046741-3	2020	Sirtuins have been shown to possess NAD+-dependent desuccinylation activity in vitro and in vivo, among which the desuccinylation activity of SIRT5 is most extensively studied.	NAD	36-40	sirtuin 5	Homo sapiens	142-147
29115436-1	2018	Sirtuin 5 (SIRT5) is a member of the NAD+-dependent class III protein deacetylases.	NAD	37-40	sirtuin 5	Homo sapiens	0-9
29115436-1	2018	Sirtuin 5 (SIRT5) is a member of the NAD+-dependent class III protein deacetylases.	NAD	37-40	sirtuin 5	Homo sapiens	11-16
32721181-7	2020	New evidence indicates that NAMPT/NAD metabolism can direct both innate immune cell effector functions and the homeostatic robustness, in both cancer and infection.	NAD	34-37	nicotinamide phosphoribosyltransferase	Homo sapiens	28-33
29464059-7	2018	Finally, we perform analysis of SDHC synthetic lethality with lactate dehydrogenase A (LDHA) and pyruvate carboxylase (PCX), which are important for regeneration of NAD+ and aspartate biosynthesis, respectively.	NAD	165-169	lactate dehydrogenase A	Mus musculus	62-85
29464059-7	2018	Finally, we perform analysis of SDHC synthetic lethality with lactate dehydrogenase A (LDHA) and pyruvate carboxylase (PCX), which are important for regeneration of NAD+ and aspartate biosynthesis, respectively.	NAD	165-169	lactate dehydrogenase A	Mus musculus	87-91
29464059-7	2018	Finally, we perform analysis of SDHC synthetic lethality with lactate dehydrogenase A (LDHA) and pyruvate carboxylase (PCX), which are important for regeneration of NAD+ and aspartate biosynthesis, respectively.	NAD	165-169	pyruvate carboxylase	Mus musculus	97-117
29464059-7	2018	Finally, we perform analysis of SDHC synthetic lethality with lactate dehydrogenase A (LDHA) and pyruvate carboxylase (PCX), which are important for regeneration of NAD+ and aspartate biosynthesis, respectively.	NAD	165-169	pyruvate carboxylase	Mus musculus	119-122
32721181-8	2020	Moreover, a bidirectional relationship exists between the metabolism of NAD and the protective role that angiotensin converting enzyme 2, the COVID-19 receptor, can play against hyperinflammation.	NAD	72-75	angiotensin converting enzyme 2	Homo sapiens	105-136
32717224-1	2020	Aldehyde dehydrogenase 9A1 (ALDH9A1) is a human enzyme that catalyzes the NAD+-dependent oxidation of the carnitine precursor 4-trimethylaminobutyraldehyde to 4-N-trimethylaminobutyrate.	NAD	74-78	aldehyde dehydrogenase 9 family member A1	Homo sapiens	0-26
29185343-5	2017	Moreover, we observed that PQQ treatment induces deacetylation of the peroxisome proliferator-activated receptor-gamma-coactivator 1alpha (PGC-1alpha) and facilitates its nuclear translocation and target gene expression but does not affect its protein levels, implying increased activity of the NAD+-dependent protein deacetylase sirtuin 1 (SIRT1).	NAD	295-298	peroxisome proliferative activated receptor, gamma, coactivator 1 alpha	Mus musculus	70-137
29185343-5	2017	Moreover, we observed that PQQ treatment induces deacetylation of the peroxisome proliferator-activated receptor-gamma-coactivator 1alpha (PGC-1alpha) and facilitates its nuclear translocation and target gene expression but does not affect its protein levels, implying increased activity of the NAD+-dependent protein deacetylase sirtuin 1 (SIRT1).	NAD	295-298	peroxisome proliferative activated receptor, gamma, coactivator 1 alpha	Mus musculus	139-149
29220653-10	2017	Our data show that the NAD+-metabolite and nucleic acid PAR triggers ALC1 to drive chromatin relaxation.	NAD	23-27	chromodomain helicase DNA binding protein 1 like	Homo sapiens	69-73
32717224-1	2020	Aldehyde dehydrogenase 9A1 (ALDH9A1) is a human enzyme that catalyzes the NAD+-dependent oxidation of the carnitine precursor 4-trimethylaminobutyraldehyde to 4-N-trimethylaminobutyrate.	NAD	74-78	aldehyde dehydrogenase 9 family member A1	Homo sapiens	28-35
32717224-4	2020	Two crystal structures of ALDH9A1 are reported, including the first of the enzyme complexed with NAD+.	NAD	97-101	aldehyde dehydrogenase 9 family member A1	Homo sapiens	26-33
33100963-9	2020	Furthermore, treatment with DPN increased p-GSK-3beta expression in NSPCs exposed to ketamine.	NAD	28-31	glycogen synthase kinase 3 alpha	Homo sapiens	44-53
32645646-2	2020	An aryl piperazine compound 3a (RTC1) has been described as a promoter of glucose uptake, in part through a cellular mechanism that involves inhibition of NADH:ubiquinone oxidoreductase.	NAD	155-159	RNA 3'-terminal phosphate cyclase	Homo sapiens	32-36
30356033-5	2018	Moreover, blockage of the cellular NADH level with the glycolysis inhibitor 2-Deoxy-D-Glucose (2-DG) rescued MPC1 and MPC2 expression.	NAD	35-39	mitochondrial pyruvate carrier 1	Mus musculus	109-113
30356033-5	2018	Moreover, blockage of the cellular NADH level with the glycolysis inhibitor 2-Deoxy-D-Glucose (2-DG) rescued MPC1 and MPC2 expression.	NAD	35-39	mitochondrial pyruvate carrier 2	Mus musculus	118-122
30356033-8	2018	Consequently, restoring MPC1 and MPC2 in human tumor cells decreases free NADH and inhibits melanoma cell proliferation and migration.	NAD	74-78	mitochondrial pyruvate carrier 1	Mus musculus	24-28
32645646-3	2020	We report herein the synthesis of 41 derivatives of 3a (RTC1) and a systematic structure-activity-relationship study where a number of compounds were shown to effectively stimulate glucose uptake in vitro and inhibit NADH:ubiquinone oxidoreductase.	NAD	217-221	RNA 3'-terminal phosphate cyclase	Homo sapiens	56-60
30356033-8	2018	Consequently, restoring MPC1 and MPC2 in human tumor cells decreases free NADH and inhibits melanoma cell proliferation and migration.	NAD	74-78	mitochondrial pyruvate carrier 2	Mus musculus	33-37
30356033-9	2018	CONCLUSIONS Our data indicate that MPC1 and MPC2 are principal mediators that link CtBP1-mediated transcription regulation to NADH production.	NAD	126-130	mitochondrial pyruvate carrier 1	Mus musculus	35-39
32645646-4	2020	The hit compound 3a (RTC1) remained the most efficacious with a 2.57 fold increase in glucose uptake compared to vehicle control and micromolar inhibition of NADH:ubiquinone oxidoreductase (IC50 = 27 muM).	NAD	158-162	RNA 3'-terminal phosphate cyclase	Homo sapiens	21-25
30356033-9	2018	CONCLUSIONS Our data indicate that MPC1 and MPC2 are principal mediators that link CtBP1-mediated transcription regulation to NADH production.	NAD	126-130	mitochondrial pyruvate carrier 2	Mus musculus	44-48
32905773-6	2020	RNA sequencing (RNA-seq) identifies Me2, encoding the mitochondrial NAD-dependent isoform of malic enzyme, as being specifically upregulated during osteoblast differentiation.	NAD	68-71	malic enzyme 2, NAD(+)-dependent, mitochondrial	Mus musculus	36-39
32883024-6	2020	We have previously shown that cytosolic NADH production supported by aldehyde dehydrogenase (ALDH) is critical for supplying ATP through oxidative phosphorylation (OxPhos) in cancer cell mitochondria.	NAD	40-44	aldehyde dehydrogenase family 3, subfamily A1	Mus musculus	69-91
30353243-4	2018	When CMCs were grown in 17.5 mM glucose, CMCdb/db cells showed &gt; twofold higher glycolytic activity and a threefold higher expression of Pfkfb3 compared with CMCWT cells; however, culture of CMCdb/db cells in 5.5 mM glucose led to metabolic remodeling characterized by normalization of metabolism, a higher NAD+/NADH ratio, and a sixfold upregulation of Sirt1.	NAD	310-314	cerebral malaria susceptibility in CBA/N	Mus musculus	5-9
30353243-4	2018	When CMCs were grown in 17.5 mM glucose, CMCdb/db cells showed &gt; twofold higher glycolytic activity and a threefold higher expression of Pfkfb3 compared with CMCWT cells; however, culture of CMCdb/db cells in 5.5 mM glucose led to metabolic remodeling characterized by normalization of metabolism, a higher NAD+/NADH ratio, and a sixfold upregulation of Sirt1.	NAD	315-319	cerebral malaria susceptibility in CBA/N	Mus musculus	5-9
32883024-6	2020	We have previously shown that cytosolic NADH production supported by aldehyde dehydrogenase (ALDH) is critical for supplying ATP through oxidative phosphorylation (OxPhos) in cancer cell mitochondria.	NAD	40-44	aldehyde dehydrogenase family 3, subfamily A1	Mus musculus	93-97
33087267-4	2020	These signaling enzymes include nicotinamide adenine dinucleotide (NAD+) dependent poly(ADP-ribose) polymerases (PARP1, PARP2) and class III deacetylases (SIRT1, SIRT6) that comprise a key PARP-NAD-SIRT axis to facilitate the regulation and coordination of BER in the mammalian cell.	NAD	32-65	sirtuin 6	Homo sapiens	162-167
30257945-1	2018	Axon degeneration, a hallmark of chemotherapy-induced peripheral neuropathy (CIPN), is thought to be caused by a loss of the essential metabolite nicotinamide adenine dinucleotide (NAD+) via the prodegenerative protein SARM1.	NAD	146-179	sterile alpha and TIR motif containing 1	Homo sapiens	219-224
30257945-1	2018	Axon degeneration, a hallmark of chemotherapy-induced peripheral neuropathy (CIPN), is thought to be caused by a loss of the essential metabolite nicotinamide adenine dinucleotide (NAD+) via the prodegenerative protein SARM1.	NAD	181-185	sterile alpha and TIR motif containing 1	Homo sapiens	219-224
33087267-4	2020	These signaling enzymes include nicotinamide adenine dinucleotide (NAD+) dependent poly(ADP-ribose) polymerases (PARP1, PARP2) and class III deacetylases (SIRT1, SIRT6) that comprise a key PARP-NAD-SIRT axis to facilitate the regulation and coordination of BER in the mammalian cell.	NAD	67-71	sirtuin 6	Homo sapiens	162-167
33015038-4	2020	Sirtuin 3 (SIRT3) is the major mitochondrial nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase, which deacetylates two critical lysine residues (lysine 68 and lysine 122) on SOD2 and promotes its antioxidative activity.	NAD	45-78	superoxide dismutase 2	Homo sapiens	187-191
28877980-1	2018	OBJECTIVE: Nicotinamide phosphoribosyltransferase (NAMPT, also referred to as pre-B cell colony-enhancing factor or visfatin) is critically required for the maintenance of cellular nicotinamide adenine dinucleotide (NAD) supply catalysing the rate-limiting step of the NAD salvage pathway.	NAD	181-214	nicotinamide phosphoribosyltransferase	Homo sapiens	51-56
28877980-1	2018	OBJECTIVE: Nicotinamide phosphoribosyltransferase (NAMPT, also referred to as pre-B cell colony-enhancing factor or visfatin) is critically required for the maintenance of cellular nicotinamide adenine dinucleotide (NAD) supply catalysing the rate-limiting step of the NAD salvage pathway.	NAD	181-214	nicotinamide phosphoribosyltransferase	Homo sapiens	116-124
28877980-1	2018	OBJECTIVE: Nicotinamide phosphoribosyltransferase (NAMPT, also referred to as pre-B cell colony-enhancing factor or visfatin) is critically required for the maintenance of cellular nicotinamide adenine dinucleotide (NAD) supply catalysing the rate-limiting step of the NAD salvage pathway.	NAD	216-219	nicotinamide phosphoribosyltransferase	Homo sapiens	51-56
33015038-4	2020	Sirtuin 3 (SIRT3) is the major mitochondrial nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase, which deacetylates two critical lysine residues (lysine 68 and lysine 122) on SOD2 and promotes its antioxidative activity.	NAD	80-83	superoxide dismutase 2	Homo sapiens	187-191
28877980-1	2018	OBJECTIVE: Nicotinamide phosphoribosyltransferase (NAMPT, also referred to as pre-B cell colony-enhancing factor or visfatin) is critically required for the maintenance of cellular nicotinamide adenine dinucleotide (NAD) supply catalysing the rate-limiting step of the NAD salvage pathway.	NAD	216-219	nicotinamide phosphoribosyltransferase	Homo sapiens	116-124
32807821-6	2020	We found that the inhibition or depletion of nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme in the NAD+ salvage biosynthesis pathway, mimicked CDA deficiency, resulting in a decrease in basal PARP-1 activity, regardless of NAD+ levels.	NAD	125-129	nicotinamide phosphoribosyltransferase	Homo sapiens	45-83
32807821-6	2020	We found that the inhibition or depletion of nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme in the NAD+ salvage biosynthesis pathway, mimicked CDA deficiency, resulting in a decrease in basal PARP-1 activity, regardless of NAD+ levels.	NAD	125-129	nicotinamide phosphoribosyltransferase	Homo sapiens	85-90
32807821-6	2020	We found that the inhibition or depletion of nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme in the NAD+ salvage biosynthesis pathway, mimicked CDA deficiency, resulting in a decrease in basal PARP-1 activity, regardless of NAD+ levels.	NAD	249-253	nicotinamide phosphoribosyltransferase	Homo sapiens	85-90
32518153-1	2020	Sirtuin 6 (SIRT6) is a nuclear NAD+-dependent deacetylase of histone H3 that regulates genome stability and gene expression.	NAD	31-34	sirtuin 6	Homo sapiens	0-9
30250535-7	2018	Through bioinformatics, we identified 487 target genes predicted from miR-320a, that were mostly enriched in the bone morphogenetic protein signaling pathway, nicotinamide adenine dinucleotide pathway and de novo ceramide biosynthetic pathway.	NAD	159-192	microRNA 320a	Homo sapiens	70-78
30250025-1	2018	Sirtuin 6 (SIRT6) is a member of the NAD+-dependent class III deacetylase sirtuin family, which plays a key role in cancer by controlling transcription, genome stability, telomere integrity, DNA repair, and autophagy.	NAD	37-41	sirtuin 6	Homo sapiens	0-9
30250025-1	2018	Sirtuin 6 (SIRT6) is a member of the NAD+-dependent class III deacetylase sirtuin family, which plays a key role in cancer by controlling transcription, genome stability, telomere integrity, DNA repair, and autophagy.	NAD	37-41	sirtuin 6	Homo sapiens	11-16
32518153-1	2020	Sirtuin 6 (SIRT6) is a nuclear NAD+-dependent deacetylase of histone H3 that regulates genome stability and gene expression.	NAD	31-34	sirtuin 6	Homo sapiens	11-16
29886046-10	2018	Although additional investigation is needed, our findings raise the possibility that the pathomechanism of COX deficiency and possibly also in other OXPHOS defects, include nuclear DNA damage resulting from nicotinamide adenine dinucleotide (NAD+) deficit combined with a replicative state, rather than oxidative stress and energy depletion.	NAD	207-240	cytochrome c oxidase subunit 8A	Homo sapiens	107-110
32535108-7	2020	(ii) Energy, NAD+ and lipid metabolism: In obese individuals AHR is involved in either generation or inhibition of fatty liver and associated hepatitis.	NAD	13-17	aryl hydrocarbon receptor	Homo sapiens	61-64
29886046-10	2018	Although additional investigation is needed, our findings raise the possibility that the pathomechanism of COX deficiency and possibly also in other OXPHOS defects, include nuclear DNA damage resulting from nicotinamide adenine dinucleotide (NAD+) deficit combined with a replicative state, rather than oxidative stress and energy depletion.	NAD	242-246	cytochrome c oxidase subunit 8A	Homo sapiens	107-110
33045951-2	2020	Zn2+ is a differential regulator of the mitochondrial enzyme lipoamide dehydrogenase (LADH) at physiological concentrations (Ka = 0.1 microM free zinc), inhibiting lipoamide and accelerating NADH dehydrogenase activities.	NAD	191-195	dihydrolipoamide dehydrogenase	Sus scrofa	61-84
29651749-1	2018	Citrin, encoded by SLC25A13, constitutes the malate-aspartate shuttle, the main NADH-shuttle in the liver.	NAD	80-84	solute carrier family 25 member 13	Homo sapiens	0-6
29651749-1	2018	Citrin, encoded by SLC25A13, constitutes the malate-aspartate shuttle, the main NADH-shuttle in the liver.	NAD	80-84	solute carrier family 25 member 13	Homo sapiens	19-27
33045951-2	2020	Zn2+ is a differential regulator of the mitochondrial enzyme lipoamide dehydrogenase (LADH) at physiological concentrations (Ka = 0.1 microM free zinc), inhibiting lipoamide and accelerating NADH dehydrogenase activities.	NAD	191-195	dihydrolipoamide dehydrogenase	Sus scrofa	86-90
30031171-1	2018	Nicotinamide phosphoribosyltransferase (NAMPT) is the bottleneck enzyme of the NAD salvage pathway and thereby is a controller of intracellular NAD concentrations.	NAD	79-82	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
30031171-1	2018	Nicotinamide phosphoribosyltransferase (NAMPT) is the bottleneck enzyme of the NAD salvage pathway and thereby is a controller of intracellular NAD concentrations.	NAD	144-147	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
33045951-7	2020	This implies that the two-electron reduced form of LADH, prevalent at low NADH levels, is a poor two-electron donor compared to the four-electron reduced or Zn2+-modified reduced LADH forms.	NAD	74-78	dihydrolipoamide dehydrogenase	Sus scrofa	51-55
32311648-0	2020	The SARM1 axon degeneration pathway: control of the NAD+ metabolome regulates axon survival in health and disease.	NAD	52-56	sterile alpha and TIR motif containing 1	Homo sapiens	4-9
30157431-0	2018	The NAD+ Salvage Pathway Supports PHGDH-Driven Serine Biosynthesis.	NAD	4-8	phosphoglycerate dehydrogenase	Homo sapiens	34-39
30157431-2	2018	Here, we find that inhibiting the NAD+ salvage pathway depletes serine biosynthesis from glucose by impeding the NAD+-dependent protein, 3-phosphoglycerate dehydrogenase (PHGDH).	NAD	34-38	phosphoglycerate dehydrogenase	Homo sapiens	137-169
30157431-2	2018	Here, we find that inhibiting the NAD+ salvage pathway depletes serine biosynthesis from glucose by impeding the NAD+-dependent protein, 3-phosphoglycerate dehydrogenase (PHGDH).	NAD	34-38	phosphoglycerate dehydrogenase	Homo sapiens	171-176
30157431-2	2018	Here, we find that inhibiting the NAD+ salvage pathway depletes serine biosynthesis from glucose by impeding the NAD+-dependent protein, 3-phosphoglycerate dehydrogenase (PHGDH).	NAD	113-117	phosphoglycerate dehydrogenase	Homo sapiens	137-169
32761799-1	2020	Apocynin has been widely used in vivo as a Nox2-contaninig nicotinamide adenine dinucleotide phosphate oxidase inhibitor.	NAD	59-92	cytochrome b-245, beta polypeptide	Mus musculus	43-47
30157431-2	2018	Here, we find that inhibiting the NAD+ salvage pathway depletes serine biosynthesis from glucose by impeding the NAD+-dependent protein, 3-phosphoglycerate dehydrogenase (PHGDH).	NAD	113-117	phosphoglycerate dehydrogenase	Homo sapiens	171-176
30157431-4	2018	Further, we find that PHGDH protein levels and those of the rate-limiting enzyme of NAD+ salvage, NAMPT, correlate in ER-negative, basal-like breast cancers.	NAD	84-88	nicotinamide phosphoribosyltransferase	Homo sapiens	98-103
30157431-5	2018	Although NAD+ salvage pathway inhibitors are actively being pursued in cancer treatment, their efficacy has been poor, and our findings suggest that they may be effective for PHGDH-dependent cancers.	NAD	9-13	phosphoglycerate dehydrogenase	Homo sapiens	175-180
30147639-5	2018	The high atom-efficiency was exemplified by the conversion of 75 mM of rac-2-phenylpropanal with 0.03 mol% of HLADH in the presence of ~0.013 eq. of oxidized nicotinamide adenine dinucleotide (NAD+), yielding 28.1 mM of (S)-2-phenylpropanol in 96% ee and 26.5 mM of (S)-2-phenylpropionic acid in 89% ee, in 73% overall conversion.	NAD	158-191	Rac family small GTPase 2	Equus caballus	71-76
30147639-5	2018	The high atom-efficiency was exemplified by the conversion of 75 mM of rac-2-phenylpropanal with 0.03 mol% of HLADH in the presence of ~0.013 eq. of oxidized nicotinamide adenine dinucleotide (NAD+), yielding 28.1 mM of (S)-2-phenylpropanol in 96% ee and 26.5 mM of (S)-2-phenylpropionic acid in 89% ee, in 73% overall conversion.	NAD	193-197	Rac family small GTPase 2	Equus caballus	71-76
28625351-2	2017	The tolerance mechanisms involved in the strain might have existed through the upregulation of genes involved in NAD(H)/NADP(H) cofactors generations (ALD6, ZWF1, GND1), membrane robustness for efflux pump (YOR1, PDR5, TPO3) and cation/polyamine transport (TPO3).	NAD	113-119	ATP-binding cassette transporter YOR1	Saccharomyces cerevisiae S288C	207-211
29178516-3	2017	Nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme in mammalian NAD+ salvage pathway, has shown a protective effect on cellular senescence of human primary cells.	NAD	86-90	nicotinamide phosphoribosyltransferase	Homo sapiens	0-38
29178516-3	2017	Nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme in mammalian NAD+ salvage pathway, has shown a protective effect on cellular senescence of human primary cells.	NAD	86-90	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
32432673-1	2020	We recently reported the presence of nicotinamide adenine dinucleotide (NAD)-capped RNAs in mammalian cells and a role for DXO and the Nudix hydrolase Nudt12 in decapping NAD-capped RNAs (deNADding) in cells.	NAD	37-70	nudix hydrolase 12	Homo sapiens	151-157
29187201-6	2017	METHODS: A two-hybrid chimera interacting system allowed to identify Sirt1, a NAD+ dependent type III histone deacetylase, as a novel Smad2 interactor.	NAD	78-81	SMAD family member 2	Homo sapiens	134-139
32432673-1	2020	We recently reported the presence of nicotinamide adenine dinucleotide (NAD)-capped RNAs in mammalian cells and a role for DXO and the Nudix hydrolase Nudt12 in decapping NAD-capped RNAs (deNADding) in cells.	NAD	72-75	nudix hydrolase 12	Homo sapiens	151-157
28650465-0	2017	MCU-dependent mitochondrial Ca2+ inhibits NAD+/SIRT3/SOD2 pathway to promote ROS production and metastasis of HCC cells.	NAD	42-46	superoxide dismutase 2	Homo sapiens	53-57
29996103-3	2018	Here, we show that NAD+ depletion by TNT activates RIPK3 and MLKL, key mediators of necroptosis.	NAD	19-23	mixed lineage kinase domain like pseudokinase	Homo sapiens	61-65
32432673-1	2020	We recently reported the presence of nicotinamide adenine dinucleotide (NAD)-capped RNAs in mammalian cells and a role for DXO and the Nudix hydrolase Nudt12 in decapping NAD-capped RNAs (deNADding) in cells.	NAD	171-174	nudix hydrolase 12	Homo sapiens	151-157
29996103-7	2018	Surprisingly, NAD+ depletion itself was sufficient to trigger necroptosis in a RIPK3- and MLKL-dependent manner by inhibiting the NAD+ salvage pathway in THP-1 cells or by TNT expression in Jurkat T cells.	NAD	14-18	mixed lineage kinase domain like pseudokinase	Homo sapiens	90-94
29996103-7	2018	Surprisingly, NAD+ depletion itself was sufficient to trigger necroptosis in a RIPK3- and MLKL-dependent manner by inhibiting the NAD+ salvage pathway in THP-1 cells or by TNT expression in Jurkat T cells.	NAD	130-134	mixed lineage kinase domain like pseudokinase	Homo sapiens	90-94
32087251-2	2020	SARM1 is an injury-activated NAD+ cleavage enzyme, and this NADase activity is required for the pro-degenerative function of SARM1.	NAD	29-33	sterile alpha and TIR motif containing 1	Homo sapiens	0-5
29337590-6	2018	Inhibition of nicotinamide mononucleotide synthesis by FK866 (a selective NAMPT enzymatic inhibitor) failed to alter TNF-alpha-induced human lung EC apoptosis, suggesting that NAMPT-dependent NAD+ generation is unlikely to be involved in regulation of TNF-alpha-induced EC apoptosis.	NAD	192-196	nicotinamide phosphoribosyltransferase	Homo sapiens	176-181
29966233-1	2018	Sirtuin 6 (SIRT6) is a nicotinamide adenine dinucleotide+ (NAD+) dependent enzyme and stress response protein that has sparked the curiosity of many researchers in different branches of the biomedical sciences.	NAD	23-56	sirtuin 6	Homo sapiens	0-9
29966233-1	2018	Sirtuin 6 (SIRT6) is a nicotinamide adenine dinucleotide+ (NAD+) dependent enzyme and stress response protein that has sparked the curiosity of many researchers in different branches of the biomedical sciences.	NAD	23-56	sirtuin 6	Homo sapiens	11-16
29966233-1	2018	Sirtuin 6 (SIRT6) is a nicotinamide adenine dinucleotide+ (NAD+) dependent enzyme and stress response protein that has sparked the curiosity of many researchers in different branches of the biomedical sciences.	NAD	59-63	sirtuin 6	Homo sapiens	0-9
29966233-1	2018	Sirtuin 6 (SIRT6) is a nicotinamide adenine dinucleotide+ (NAD+) dependent enzyme and stress response protein that has sparked the curiosity of many researchers in different branches of the biomedical sciences.	NAD	59-63	sirtuin 6	Homo sapiens	11-16
29194485-3	2018	However, redox dependence of other NAD-dependent MDH isoforms have been less studied.	NAD	35-38	malate dehydrogenase	Arabidopsis thaliana	49-52
29905535-4	2018	NAD+ levels declined with age and correlated directly with decreased nicotinamide phosphoribosyltransferase (NAMPT) expression, increased expression of senescence markers (p16INK4a, p21Waf/Cip1, ApoJ, CTGF and beta-galactosidase) and significant reductions in SIRT1 expression and activity.	NAD	0-4	cellular communication network factor 2	Mus musculus	201-205
28756747-0	2018	NAMPT-Mediated NAD Biosynthesis as the Internal Timing Mechanism: In NAD+ World, Time Is Running in Its Own Way.	NAD	15-18	nicotinamide phosphoribosyltransferase	Homo sapiens	0-5
28756747-0	2018	NAMPT-Mediated NAD Biosynthesis as the Internal Timing Mechanism: In NAD+ World, Time Is Running in Its Own Way.	NAD	69-73	nicotinamide phosphoribosyltransferase	Homo sapiens	0-5
28756747-8	2018	Nicotinamide phosphoribosyltransferase (NAMPT)-mediated nicotinamide adenine dinucleotide (NAD+) levels, being regulated by the circadian clock, might be the missing link between aging, cell cycle control, DNA damage repair, cellular metabolism and the aging clock, which is responsible for the biological age of an organism.	NAD	56-89	nicotinamide phosphoribosyltransferase	Homo sapiens	0-38
28756747-8	2018	Nicotinamide phosphoribosyltransferase (NAMPT)-mediated nicotinamide adenine dinucleotide (NAD+) levels, being regulated by the circadian clock, might be the missing link between aging, cell cycle control, DNA damage repair, cellular metabolism and the aging clock, which is responsible for the biological age of an organism.	NAD	56-89	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
28756747-8	2018	Nicotinamide phosphoribosyltransferase (NAMPT)-mediated nicotinamide adenine dinucleotide (NAD+) levels, being regulated by the circadian clock, might be the missing link between aging, cell cycle control, DNA damage repair, cellular metabolism and the aging clock, which is responsible for the biological age of an organism.	NAD	91-95	nicotinamide phosphoribosyltransferase	Homo sapiens	0-38
28756747-8	2018	Nicotinamide phosphoribosyltransferase (NAMPT)-mediated nicotinamide adenine dinucleotide (NAD+) levels, being regulated by the circadian clock, might be the missing link between aging, cell cycle control, DNA damage repair, cellular metabolism and the aging clock, which is responsible for the biological age of an organism.	NAD	91-95	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
29977153-8	2018	However, re-expression of CD38 in the knockdown clones reversed the effect on Sirt1/NF-kappaB/TLR2 signaling, which is NAD-dependent.	NAD	119-122	toll-like receptor 2	Mus musculus	94-98
29330025-2	2018	Intracellular Nampt plays an important role in cellular bioenergetics and metabolism, particularly NAD biosynthesis.	NAD	99-102	nicotinamide phosphoribosyltransferase	Homo sapiens	14-19
29478906-2	2018	Suppression of nicotinamide salvage by nicotinamide phosphoribosyl transferase (NAMPT) inhibitors, however, gave inconclusive results in neoplastic patients because several metabolic routes circumvent the enzymatic block converging directly on nicotinamide mononucleotide adenylyl transferases (NMNATs) for NAD synthesis.	NAD	307-310	nicotinamide phosphoribosyltransferase	Homo sapiens	80-85
29478906-4	2018	Here, we report the identification of Vacor as a substrate metabolized by the consecutive action of NAMPT and NMNAT2 into the NAD analog Vacor adenine dinucleotide (VAD).	NAD	126-129	nicotinamide phosphoribosyltransferase	Homo sapiens	100-105
29447131-3	2018	Using unbiased proteomic and metabolic high-throughput profiling on a unique in-house-generated isogenic model of ERCC1 deficiency, we found marked metabolic rewiring of ERCC1-deficient populations, including decreased levels of the metabolite NAD+ and reduced expression of the rate-limiting NAD+ biosynthetic enzyme nicotinamide phosphoribosyltransferase (NAMPT).	NAD	244-248	nicotinamide phosphoribosyltransferase	Homo sapiens	318-356
29447131-3	2018	Using unbiased proteomic and metabolic high-throughput profiling on a unique in-house-generated isogenic model of ERCC1 deficiency, we found marked metabolic rewiring of ERCC1-deficient populations, including decreased levels of the metabolite NAD+ and reduced expression of the rate-limiting NAD+ biosynthetic enzyme nicotinamide phosphoribosyltransferase (NAMPT).	NAD	244-248	nicotinamide phosphoribosyltransferase	Homo sapiens	358-363
29363378-1	2018	Objective To explore the prognostic significance of nicotinamide adenine dinucleotide (NAD)-dependent protein deacetylase sirtuin-6 (SIRT6), encoded by the sirtuin 6 ( SIRT6) gene, in a population of Chinese Han patients with non-small cell lung cancer (NSCLC).	NAD	52-85	sirtuin 6	Homo sapiens	122-131
29363378-1	2018	Objective To explore the prognostic significance of nicotinamide adenine dinucleotide (NAD)-dependent protein deacetylase sirtuin-6 (SIRT6), encoded by the sirtuin 6 ( SIRT6) gene, in a population of Chinese Han patients with non-small cell lung cancer (NSCLC).	NAD	52-85	sirtuin 6	Homo sapiens	133-138
29363378-1	2018	Objective To explore the prognostic significance of nicotinamide adenine dinucleotide (NAD)-dependent protein deacetylase sirtuin-6 (SIRT6), encoded by the sirtuin 6 ( SIRT6) gene, in a population of Chinese Han patients with non-small cell lung cancer (NSCLC).	NAD	52-85	sirtuin 6	Homo sapiens	156-165
29363378-1	2018	Objective To explore the prognostic significance of nicotinamide adenine dinucleotide (NAD)-dependent protein deacetylase sirtuin-6 (SIRT6), encoded by the sirtuin 6 ( SIRT6) gene, in a population of Chinese Han patients with non-small cell lung cancer (NSCLC).	NAD	52-85	sirtuin 6	Homo sapiens	168-173
29363378-1	2018	Objective To explore the prognostic significance of nicotinamide adenine dinucleotide (NAD)-dependent protein deacetylase sirtuin-6 (SIRT6), encoded by the sirtuin 6 ( SIRT6) gene, in a population of Chinese Han patients with non-small cell lung cancer (NSCLC).	NAD	87-90	sirtuin 6	Homo sapiens	122-131
29269607-1	2018	Reactive oxygen species (ROS) generated by reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (Nox)1 mediate cellular signalings involved in normal physiological processes, and aberrant control of Nox1 has been implicated in the pathogenesis of various diseases.	NAD	51-84	NADPH oxidase 1	Homo sapiens	112-117
29269607-1	2018	Reactive oxygen species (ROS) generated by reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (Nox)1 mediate cellular signalings involved in normal physiological processes, and aberrant control of Nox1 has been implicated in the pathogenesis of various diseases.	NAD	51-84	NADPH oxidase 1	Homo sapiens	214-218
29285579-6	2018	The IDH1 activity between WT, R132H, and R132S transfectants was compared by measuring the production of NADH and NADPH.	NAD	105-109	isocitrate dehydrogenase [NADP] cytoplasmic	Canis lupus familiaris	4-8
29395922-4	2018	Upon axon injury, the SARM1 TIR domain cleaves nicotinamide adenine dinucleotide (NAD+), destroying this essential metabolic co-factor to trigger axon destruction [11, 12].	NAD	47-80	sterile alpha and TIR motif containing 1	Homo sapiens	22-27
29395922-4	2018	Upon axon injury, the SARM1 TIR domain cleaves nicotinamide adenine dinucleotide (NAD+), destroying this essential metabolic co-factor to trigger axon destruction [11, 12].	NAD	82-86	sterile alpha and TIR motif containing 1	Homo sapiens	22-27
29322283-5	2018	When the ratio of GA and GDH was 3:1, the NADH production rate of the whole-cell biocatalyst reached the highest level using starch as substrate, which was three times higher than that of mixture of free enzymes, indicating that the highly ordered spatial organization of enzymes would promote reactions, due to the ratio of enzymes and proximity effect.	NAD	42-46	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	25-28
29162772-7	2018	The IDH2 activity between cIDH2 WT and cIDH2 R174K transfectants was compared by measuring the production of NADH and NADPH.	NAD	109-113	isocitrate dehydrogenase (NADP(+)) 2	Canis lupus familiaris	4-8
30261504-4	2018	Nicotinamide phosphoribosyltransferase (Nampt) catalyzes the first step in the biosynthesis of nicotinamide adenine dinucleotide (NAD) and is known to be induced by IL-1beta.	NAD	95-128	nicotinamide phosphoribosyltransferase	Homo sapiens	0-38
30261504-4	2018	Nicotinamide phosphoribosyltransferase (Nampt) catalyzes the first step in the biosynthesis of nicotinamide adenine dinucleotide (NAD) and is known to be induced by IL-1beta.	NAD	95-128	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
30261504-4	2018	Nicotinamide phosphoribosyltransferase (Nampt) catalyzes the first step in the biosynthesis of nicotinamide adenine dinucleotide (NAD) and is known to be induced by IL-1beta.	NAD	130-133	nicotinamide phosphoribosyltransferase	Homo sapiens	0-38
30261504-4	2018	Nicotinamide phosphoribosyltransferase (Nampt) catalyzes the first step in the biosynthesis of nicotinamide adenine dinucleotide (NAD) and is known to be induced by IL-1beta.	NAD	130-133	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
30097878-1	2018	Mouse T cells express the toxin-related ecto-ADP-ribosyltransferase ARTC2 that catalyzes the posttranslational ADP-ribosylation of cell surface proteins by transferring the ADP-ribose group of its substrate nicotinamide adenine dinucleotide (NAD+) to arginine residues of its target proteins.	NAD	207-240	ADP-ribosyltransferase 2a	Mus musculus	68-73
30097878-1	2018	Mouse T cells express the toxin-related ecto-ADP-ribosyltransferase ARTC2 that catalyzes the posttranslational ADP-ribosylation of cell surface proteins by transferring the ADP-ribose group of its substrate nicotinamide adenine dinucleotide (NAD+) to arginine residues of its target proteins.	NAD	242-246	ADP-ribosyltransferase 2a	Mus musculus	68-73
30097878-4	2018	Previous studies have shown that the ARTC2 substrate NAD+ is released during T cell preparation.	NAD	53-57	ADP-ribosyltransferase 2a	Mus musculus	37-42
29185343-8	2017	Our results suggest that PQQ-inducible mitochondrial biogenesis can be attributed to activation of the SIRT1/PGC-1alpha signaling pathway by enhancing cellular NAD+ formation.	NAD	160-164	peroxisome proliferative activated receptor, gamma, coactivator 1 alpha	Mus musculus	109-119
28916476-7	2017	NAD+ supplementation prevented ATP depletion and cell death, while treatment with a PARP inhibitor, olaparib, preserved NAD+ and ATP levels but led to increased DNA double-strand breakage and did not prevent ascorbate-induced cell death.	NAD	120-124	collagen type XI alpha 2 chain	Homo sapiens	84-88
28916476-8	2017	These data indicate that in cells with an intact PARP-associated DNA repair system, ascorbate-induced cell death is caused by NAD+ and ATP depletion, while in the absence of PARP activation ascorbate-induced cell death still occurs but is a consequence of ROS-induced DNA damage.	NAD	126-130	collagen type XI alpha 2 chain	Homo sapiens	49-53
29044328-4	2018	The cascade reaction to reduce carbon dioxide into methanol has been explored by the authors, using, sequentially, alcohol dehydrogenase (ADH), formaldehyde dehydrogenase (FalDH), and formate dehydrogenase (FDH), powered by NAD+/NADH and glutamate dehydrogenase (GDH) as the co-enzyme regenerating system.	NAD	224-228	alcohol dehydrogenase 5 (class III), chi polypeptide	Homo sapiens	172-177
29044328-4	2018	The cascade reaction to reduce carbon dioxide into methanol has been explored by the authors, using, sequentially, alcohol dehydrogenase (ADH), formaldehyde dehydrogenase (FalDH), and formate dehydrogenase (FDH), powered by NAD+/NADH and glutamate dehydrogenase (GDH) as the co-enzyme regenerating system.	NAD	229-233	alcohol dehydrogenase 5 (class III), chi polypeptide	Homo sapiens	172-177
28137513-1	2017	3alpha-Hydroxysteroid dehydrogenase/carbonyl reductase (3alpha-HSD/CR) catalyzes the oxidation of androsterone with NAD+ to form androstanedione and NADH with the rate limiting step being the release of NADH.	NAD	116-120	aldo-keto reductase family 1 member C3	Homo sapiens	0-35
28137513-1	2017	3alpha-Hydroxysteroid dehydrogenase/carbonyl reductase (3alpha-HSD/CR) catalyzes the oxidation of androsterone with NAD+ to form androstanedione and NADH with the rate limiting step being the release of NADH.	NAD	149-153	aldo-keto reductase family 1 member C3	Homo sapiens	0-35
28137513-1	2017	3alpha-Hydroxysteroid dehydrogenase/carbonyl reductase (3alpha-HSD/CR) catalyzes the oxidation of androsterone with NAD+ to form androstanedione and NADH with the rate limiting step being the release of NADH.	NAD	203-207	aldo-keto reductase family 1 member C3	Homo sapiens	0-35
29042923-8	2017	Inversely, ERalpha-knocked down osteoblasts were treated with ERbeta agonist 2,3-bis(4-hydroxyphenyl)-propionitrile (DPN) to activate ERbeta.	NAD	117-120	estrogen receptor 2	Homo sapiens	62-68
29042923-8	2017	Inversely, ERalpha-knocked down osteoblasts were treated with ERbeta agonist 2,3-bis(4-hydroxyphenyl)-propionitrile (DPN) to activate ERbeta.	NAD	117-120	estrogen receptor 2	Homo sapiens	134-140
29042923-11	2017	Treatment with ERbeta agonist DPN significantly rescued the effects of downregulation of ERalpha on cell viability (P&lt;0.01).	NAD	30-33	estrogen receptor 2	Homo sapiens	15-21
28756225-0	2017	Identification of novel resistance mechanisms to NAMPT inhibition via the de novo NAD+ biosynthesis pathway and NAMPT mutation.	NAD	82-86	nicotinamide phosphoribosyltransferase	Homo sapiens	49-54
28756225-2	2017	The rate limiting step within the NAD+ salvage pathway required for converting nicotinamide to NAD+ is catalyzed by nicotinamide phosphoribosyltransferase (NAMPT).	NAD	34-38	nicotinamide phosphoribosyltransferase	Homo sapiens	116-154
28756225-2	2017	The rate limiting step within the NAD+ salvage pathway required for converting nicotinamide to NAD+ is catalyzed by nicotinamide phosphoribosyltransferase (NAMPT).	NAD	34-38	nicotinamide phosphoribosyltransferase	Homo sapiens	156-161
28939871-7	2017	The acute vasodilatory effects of 17beta-estradiol (non-specific estrogen receptor (ER) agonist), PPT (ERalpha-specific agonist) and DPN (ERbeta-specific agonist) on resistance arteries were attenuated by aging and the menopause.	NAD	133-136	estrogen receptor 2	Homo sapiens	138-144
28877739-9	2017	The ERbeta selective agonist DPN and low physiological concentrations of the soy-derived phytoestrogens genistein, daidzein, and s-equol also decreased sensitivity of D283 Med cells to cisplatin.	NAD	29-32	estrogen receptor 2	Homo sapiens	4-10
28883796-6	2017	Emerging roles of NQO1 include its function as an efficient intracellular generator of NAD+ for enzymes including PARP and sirtuins which has gained particular attention with respect to metabolic syndrome.	NAD	87-91	collagen type XI alpha 2 chain	Homo sapiens	114-118
29029387-9	2017	Our findings suggest that CTCF PARylation is underpinned by a cellular metabolic context engendered by regulation of the beta-NAD+ salvage pathway in which NMNAT-1 acts as a rheostat to control localized beta-NAD+ synthesis at CTCF/PARP-1 complexes.	NAD	121-130	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	156-163
29029387-9	2017	Our findings suggest that CTCF PARylation is underpinned by a cellular metabolic context engendered by regulation of the beta-NAD+ salvage pathway in which NMNAT-1 acts as a rheostat to control localized beta-NAD+ synthesis at CTCF/PARP-1 complexes.	NAD	204-213	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	156-163
28615457-4	2017	Here, we comprehensively analyze nucleotide binding to wild-type and mutant AMPK protein complexes by quantitative competition assays and by hydrogen-deuterium exchange MS. We also demonstrate that NADPH, in addition to the known AMPK ligand NADH, directly and competitively binds AMPK at the AMP-sensing CBS3 site.	NAD	242-246	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	76-80
28617502-1	2017	Diaphorase and a benzylpropylviologen redox polymer were combined to create a bioelectrode that can both oxidize NADH and reduce NAD+.	NAD	113-117	dihydrolipoamide dehydrogenase	Homo sapiens	0-10
28617502-1	2017	Diaphorase and a benzylpropylviologen redox polymer were combined to create a bioelectrode that can both oxidize NADH and reduce NAD+.	NAD	129-133	dihydrolipoamide dehydrogenase	Homo sapiens	0-10
28507103-1	2017	In the last decade, substantial efforts have been made to identify NAD+ biosynthesis inhibitors, specifically against nicotinamide phosphoribosyltransferase (NAMPT), as preclinical studies indicate their potential efficacy as cancer drugs.	NAD	67-71	nicotinamide phosphoribosyltransferase	Homo sapiens	118-156
28507103-1	2017	In the last decade, substantial efforts have been made to identify NAD+ biosynthesis inhibitors, specifically against nicotinamide phosphoribosyltransferase (NAMPT), as preclinical studies indicate their potential efficacy as cancer drugs.	NAD	67-71	nicotinamide phosphoribosyltransferase	Homo sapiens	158-163
28507103-2	2017	However, the clinical activity of NAMPT inhibitors has proven limited, suggesting that alternative NAD+ production routes exploited by tumors confer resistance.	NAD	99-103	nicotinamide phosphoribosyltransferase	Homo sapiens	34-39
28507103-4	2017	Both NAPRT and NAMPT increased intracellular NAD+ levels.	NAD	45-49	nicotinamide phosphoribosyltransferase	Homo sapiens	15-20
28381791-3	2017	RBPH elevated the expression levels of gamma-glutamylcysteine synthetase (gamma-GCS), which constitutes the rate-limiting enzyme of GSH synthesis, and of another two enzymes, hemeoxygenase-1 (HO-1) and reduced nicotinamide adenine dinucleotide (phosphate): quinone oxidoreductase 1 (NQO1).	NAD	210-243	glutamate-cysteine ligase catalytic subunit	Homo sapiens	74-83
28363952-3	2017	CD73 on EPDCs extensively generated adenosine from both extracellular ATP and NAD.	NAD	78-81	5' nucleotidase, ecto	Rattus norvegicus	0-4
28429368-1	2017	ARALAR/AGC1 (aspartate-glutamate mitochondrial carrier 1) is an important component of the NADH malate-aspartate shuttle (MAS).	NAD	91-95	solute carrier family 25 member 12	Homo sapiens	0-6
27766571-7	2017	Strong correlation has been proved between the expression levels of HDAC4 and SIRT6 (r = 0.722 in full cohort and r = 0.794 in AML), that confirms the recently suggested cooperation between NAD+-independent and NAD+-dependent HDAC enzymes in leukemia.	NAD	190-194	sirtuin 6	Homo sapiens	78-83
27766571-7	2017	Strong correlation has been proved between the expression levels of HDAC4 and SIRT6 (r = 0.722 in full cohort and r = 0.794 in AML), that confirms the recently suggested cooperation between NAD+-independent and NAD+-dependent HDAC enzymes in leukemia.	NAD	211-215	sirtuin 6	Homo sapiens	78-83
29156703-4	2017	Our previous study showed the importance of NAMPT in maintaining NAD levels in pancreatic ductal adenocarcinoma cells (PDAC), and that the NAMPT inhibitor FK866 decreased pancreatic cancer growth.	NAD	65-68	nicotinamide phosphoribosyltransferase	Homo sapiens	44-49
28445802-0	2017	NMNAT: It"s an NAD+ synthase...	NAD	15-18	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	0-5
28445802-6	2017	New mechanistic studies have challenged the role of NMNAT-catalyzed NAD+ production in delaying Wallerian degeneration and have specified new mechanisms of NMNAT"s chaperone function critical for neuronal health.	NAD	68-72	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	52-57
27519885-3	2017	Similar to dietary restriction, mice overexpressing the NAD+ dependent protein deacylase SIRT6 (MOSES) live longer and have reduced IGF-1 levels.	NAD	56-59	insulin-like growth factor 1	Mus musculus	132-137
28450888-5	2017	RESULTS: GPD2 encodes one of two S. cerevisiae isoenzymes of NAD+-dependent glycerol-3-phosphate dehydrogenase (G3PDH).	NAD	61-64	glycerol-3-phosphate dehydrogenase	Saccharomyces cerevisiae S288C	76-110
28450888-5	2017	RESULTS: GPD2 encodes one of two S. cerevisiae isoenzymes of NAD+-dependent glycerol-3-phosphate dehydrogenase (G3PDH).	NAD	61-64	glycerol-3-phosphate dehydrogenase	Saccharomyces cerevisiae S288C	112-117
32087251-2	2020	SARM1 is an injury-activated NAD+ cleavage enzyme, and this NADase activity is required for the pro-degenerative function of SARM1.	NAD	29-33	sterile alpha and TIR motif containing 1	Homo sapiens	125-130
32087251-3	2020	At present, SARM1 function is assayed by either analysis of axonal loss, which is far downstream of SARM1 enzymatic activity, or via NAD+ levels, which are regulated by many competing pathways.	NAD	133-137	sterile alpha and TIR motif containing 1	Homo sapiens	12-17
32087251-4	2020	Here we explored the utility of measuring cADPR, a product of SARM1-dependent cleavage of NAD+, as an in cell and in vivo biomarker of SARM1 enzymatic activity.	NAD	90-94	sterile alpha and TIR motif containing 1	Homo sapiens	62-67
32573651-12	2020	An update is also provided on other key NAD+ research including perturbation of the NAD+ salvage enzyme NAMPT in the context of the tumour microenvironment (TME), methodology to study subcellular NAD+ dynamics in real-time and the regulation of differentiation by competing NAD+ pools.	NAD	40-44	nicotinamide phosphoribosyltransferase	Homo sapiens	104-109
32573651-12	2020	An update is also provided on other key NAD+ research including perturbation of the NAD+ salvage enzyme NAMPT in the context of the tumour microenvironment (TME), methodology to study subcellular NAD+ dynamics in real-time and the regulation of differentiation by competing NAD+ pools.	NAD	84-88	nicotinamide phosphoribosyltransferase	Homo sapiens	104-109
32573651-12	2020	An update is also provided on other key NAD+ research including perturbation of the NAD+ salvage enzyme NAMPT in the context of the tumour microenvironment (TME), methodology to study subcellular NAD+ dynamics in real-time and the regulation of differentiation by competing NAD+ pools.	NAD	84-88	nicotinamide phosphoribosyltransferase	Homo sapiens	104-109
32573651-12	2020	An update is also provided on other key NAD+ research including perturbation of the NAD+ salvage enzyme NAMPT in the context of the tumour microenvironment (TME), methodology to study subcellular NAD+ dynamics in real-time and the regulation of differentiation by competing NAD+ pools.	NAD	84-88	nicotinamide phosphoribosyltransferase	Homo sapiens	104-109
32572044-5	2020	Here, we show that CD157 knockout mice have low levels of circulating OT in cerebrospinal fluid, which can be corrected by the oral administration of nicotinamide riboside, a recently discovered vitamin precursor of nicotinamide adenine dinucleotide (NAD).	NAD	216-249	bone marrow stromal cell antigen 1	Mus musculus	19-24
32572044-5	2020	Here, we show that CD157 knockout mice have low levels of circulating OT in cerebrospinal fluid, which can be corrected by the oral administration of nicotinamide riboside, a recently discovered vitamin precursor of nicotinamide adenine dinucleotide (NAD).	NAD	251-254	bone marrow stromal cell antigen 1	Mus musculus	19-24
32572044-6	2020	NAD is the substrate for the CD157- and CD38-dependent production of cADPR.	NAD	0-3	bone marrow stromal cell antigen 1	Mus musculus	29-34
32555317-5	2020	Moreover, SLC25A11 is essential for ATP generation in cancers as it regulates NADH transportation from the cytoplasm to mitochondria.	NAD	78-82	solute carrier family 25 member 11	Homo sapiens	10-18
32492972-4	2020	Silencing of Fbp2 expression or simultaneous inhibition and tetramerization of the enzyme with a synthetic effector mimicking the action of physiological inhibitors (NAD+ and AMP) abolishes Camk2 autoactivation and blocks formation of the early phase of LTP and expression of the late phase LTP markers.	NAD	166-170	fructose-bisphosphatase 2	Homo sapiens	13-17
32492972-4	2020	Silencing of Fbp2 expression or simultaneous inhibition and tetramerization of the enzyme with a synthetic effector mimicking the action of physiological inhibitors (NAD+ and AMP) abolishes Camk2 autoactivation and blocks formation of the early phase of LTP and expression of the late phase LTP markers.	NAD	166-170	calcium/calmodulin dependent protein kinase II beta	Homo sapiens	190-195
32492972-6	2020	We therefore hypothesize that this NAD+-level-dependent increase of the Fbp2 dimer/tetramer ratio might be a crucial mechanism in which astrocyte-neuron lactate shuttle stimulates LTP formation.	NAD	35-39	fructose-bisphosphatase 2	Homo sapiens	72-76
32278117-3	2020	This study aims to identify changes of specific components of NAD+/SIRTs system in white adipose tissue (WAT) and brown adipose tissue (BAT) of mice upon energy imbalance, focusing on key enzymes in NAD+ salvage (Nampt, Nmnat1, Nrk1), clearance (Nnmt, Aox1, Cyp2e1) and consumption pathways (Sirt1, Sirt2, Sirt3, Sirt6, Parp1).	NAD	62-66	nicotinamide riboside kinase 1	Mus musculus	228-232
32278117-3	2020	This study aims to identify changes of specific components of NAD+/SIRTs system in white adipose tissue (WAT) and brown adipose tissue (BAT) of mice upon energy imbalance, focusing on key enzymes in NAD+ salvage (Nampt, Nmnat1, Nrk1), clearance (Nnmt, Aox1, Cyp2e1) and consumption pathways (Sirt1, Sirt2, Sirt3, Sirt6, Parp1).	NAD	199-203	nicotinamide riboside kinase 1	Mus musculus	228-232
32286819-6	2020	Diaphorase (DH) was immobilized by a cobaltocene-modified poly(allylamine) redox polymer on the electrode surface (DH/Cc-PAA bioelectrode) to achieve effective bioelectrocatalytic NADH regeneration.	NAD	180-184	dihydrolipoamide dehydrogenase	Homo sapiens	0-10
32156684-8	2020	In vitro assays confirmed that human FMO1 catalyzes the conversion of hypotaurine to taurine utilizing either NADPH or NADH as co-factor.	NAD	119-123	flavin containing dimethylaniline monoxygenase 1	Homo sapiens	37-41
31950503-2	2020	NAMPT, a rate-limiting enzyme in the NAD salvage pathway, is a potential therapeutic target in OVC.	NAD	37-40	nicotinamide phosphoribosyltransferase	Homo sapiens	0-5
32212192-1	2020	Mitochondrial aconitase (Aco2) catalyzes the conversion of citrate to isocitrate in the TCA cycle, which produces NADH and FADH2, driving synthesis of ATP through OXPHOS.	NAD	114-118	aconitase 2, mitochondrial	Mus musculus	25-29
32569553-2	2020	Here, we investigated the functional diversity of homologs of L-threonic acid dehydrogenase (ThrDH; UniProt ID: Q0KBC7), an enzyme composed of two NAD-binding domains (PF14833 and PF03446).	NAD	147-150	ARAD_RS06005	Agrobacterium radiobacter K84	78-91
32209328-3	2020	Previous studies have shown that increased cellular NAD+ and NAD+/NADH ratio increase INa through suppression of mitochondrial reactive oxygen species and PKC-mediated NaV1.5 phosphorylation.	NAD	52-56	neuron navigator 1	Homo sapiens	168-172
32209328-3	2020	Previous studies have shown that increased cellular NAD+ and NAD+/NADH ratio increase INa through suppression of mitochondrial reactive oxygen species and PKC-mediated NaV1.5 phosphorylation.	NAD	61-65	neuron navigator 1	Homo sapiens	168-172
32209328-3	2020	Previous studies have shown that increased cellular NAD+ and NAD+/NADH ratio increase INa through suppression of mitochondrial reactive oxygen species and PKC-mediated NaV1.5 phosphorylation.	NAD	66-70	neuron navigator 1	Homo sapiens	168-172
32235053-6	2021	Overall, our FLIM study combined with confocal fluorescence imaging visualizes the absorption of the mutant Htt protein aggregates which results in a distinct NADH fluorescence lifetime between control cells and acceptor cells.	NAD	159-163	huntingtin	Homo sapiens	108-111
28585087-1	2017	We previously demonstrated the role of Kvbeta1.1 subunit of voltage-activated potassium channel in heart for its sensory roles in detecting changes in NADH/NAD and modulation of ion channel.	NAD	151-155	potassium voltage-gated channel, shaker-related subfamily, beta member 1	Mus musculus	39-48
28585087-1	2017	We previously demonstrated the role of Kvbeta1.1 subunit of voltage-activated potassium channel in heart for its sensory roles in detecting changes in NADH/NAD and modulation of ion channel.	NAD	151-154	potassium voltage-gated channel, shaker-related subfamily, beta member 1	Mus musculus	39-48
32266141-1	2020	Nicotinamide phosphoribosyltransferase (NAMPT) and nicotinate phosphoribosyltransferase (NAPRT) are two intracellular enzymes that catalyze the first step in the biosynthesis of NAD from nicotinamide and nicotinic acid, respectively.	NAD	178-181	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
29054982-1	2017	NAMPT, an enzyme essential for NAD+ biosynthesis, has been extensively studied as an anticancer target for developing potential novel therapeutics.	NAD	31-35	nicotinamide phosphoribosyltransferase	Homo sapiens	0-5
32049506-3	2020	Recently, SARM1 was shown to promote neurodegeneration via its ability to hydrolyze NAD+, forming nicotinamide and ADP ribose (ADPR).	NAD	84-88	sterile alpha and TIR motif containing 1	Homo sapiens	10-15
32111066-3	2020	Targeting nicotinamide phosphoribosyltransferase (NAMPT), a rate limiting enzyme of the NAD salvage pathway, affects the NAD and NADPH pool.	NAD	88-91	nicotinamide phosphoribosyltransferase	Homo sapiens	10-48
29262655-5	2017	PHGDH catalyzes the NAD+-dependent conversion of 3-phosphoglycerate to phosphohydroxypyruvate, which is the first step in the de novo synthesis pathway of serine, a critical amino acid for protein and nucleic acid biosynthesis.	NAD	20-24	phosphoglycerate dehydrogenase	Homo sapiens	0-5
32111066-3	2020	Targeting nicotinamide phosphoribosyltransferase (NAMPT), a rate limiting enzyme of the NAD salvage pathway, affects the NAD and NADPH pool.	NAD	88-91	nicotinamide phosphoribosyltransferase	Homo sapiens	50-55
32111066-3	2020	Targeting nicotinamide phosphoribosyltransferase (NAMPT), a rate limiting enzyme of the NAD salvage pathway, affects the NAD and NADPH pool.	NAD	121-124	nicotinamide phosphoribosyltransferase	Homo sapiens	10-48
32111066-3	2020	Targeting nicotinamide phosphoribosyltransferase (NAMPT), a rate limiting enzyme of the NAD salvage pathway, affects the NAD and NADPH pool.	NAD	121-124	nicotinamide phosphoribosyltransferase	Homo sapiens	50-55
32015132-3	2020	Biallelic loss-of-function variants in HAAO or KYNU, two genes of the nicotinamide adenine dinucleotide (NAD) synthesis pathway, are causative of congenital malformation and miscarriage in humans and mice.	NAD	70-103	3-hydroxyanthranilate 3,4-dioxygenase	Homo sapiens	39-43
28919418-5	2017	Pharmacological and genetic inhibition of NAMPT decreased NAD+ levels and melanoma cell proliferation capacity, and NAMPT knockdown induced apoptosis through the activity of the tumor suppressor p53.	NAD	58-62	nicotinamide phosphoribosyltransferase	Homo sapiens	42-47
32015132-3	2020	Biallelic loss-of-function variants in HAAO or KYNU, two genes of the nicotinamide adenine dinucleotide (NAD) synthesis pathway, are causative of congenital malformation and miscarriage in humans and mice.	NAD	105-108	3-hydroxyanthranilate 3,4-dioxygenase	Homo sapiens	39-43
31862297-5	2020	A high-resolution NMR structure of human VDAC-1 with bound NADH, combined with molecular dynamics simulation show that beta-NADH binding reduces the pore conductance sterically without triggering a structural change.	NAD	59-63	voltage dependent anion channel 1	Homo sapiens	41-47
28958848-1	2017	The NAD+-dependent deacetylase SIRT6 is an emerging cancer drug target, whose inhibition sensitizes cancer cells to chemo-radiotherapy and has pro-differentiating effects.	NAD	4-8	sirtuin 6	Homo sapiens	31-36
31862297-5	2020	A high-resolution NMR structure of human VDAC-1 with bound NADH, combined with molecular dynamics simulation show that beta-NADH binding reduces the pore conductance sterically without triggering a structural change.	NAD	119-128	voltage dependent anion channel 1	Homo sapiens	41-47
31671075-6	2020	Recombinant SDR9C7 catalyzed NAD+-dependent dehydrogenation of linoleate 9,10-trans-epoxy-11E-13-alcohol to the corresponding 13-ketone, while ichthyosis mutants were inactive.	NAD	29-33	4short chain dehydrogenase/reductase family 9C, member 7	Mus musculus	12-18
28955611-4	2017	Meanwhile, NAD+-regenerating enzymes GPD1 (glycerol-3-phosphate dehydrogenase) was expressed; however, the results showed 3-HP was significantly decreased from 56.73-4 mM, and malic acid was obviously increased.	NAD	11-15	glycerol-3-phosphate dehydrogenase 1	Homo sapiens	37-41
28970491-6	2017	We conclude that replication stress via Rev1-deficiency contributes to metabolic stress caused by compromized mitochondrial function via the PARP-NAD+-SIRT1-PGC1alpha axis.	NAD	146-150	peroxisome proliferative activated receptor, gamma, coactivator 1 alpha	Mus musculus	157-166
31816398-1	2020	Mitochondria plays a key role in regulating cell death process under stress conditions and it has been indicated that NAMPT overexpression promotes cell survival under genotoxic stress by maintaining mitochondrial NAD+ level.	NAD	214-217	nicotinamide phosphoribosyltransferase	Homo sapiens	118-123
28756225-2	2017	The rate limiting step within the NAD+ salvage pathway required for converting nicotinamide to NAD+ is catalyzed by nicotinamide phosphoribosyltransferase (NAMPT).	NAD	95-99	nicotinamide phosphoribosyltransferase	Homo sapiens	116-154
28756225-2	2017	The rate limiting step within the NAD+ salvage pathway required for converting nicotinamide to NAD+ is catalyzed by nicotinamide phosphoribosyltransferase (NAMPT).	NAD	95-99	nicotinamide phosphoribosyltransferase	Homo sapiens	156-161
31816398-2	2020	NAMPT is a rate-limiting enzyme for NAD+ production in mammalian cells and it was suggested that NAMPT and NMNAT3 are responsible for mitochondrial NAD+ production to maintain mitochondrial NAD+ pool.	NAD	36-39	nicotinamide phosphoribosyltransferase	Homo sapiens	0-5
28756225-3	2017	Targeting NAMPT has been investigated as an anti-cancer strategy, and several highly selective small molecule inhibitors have been found to potently inhibit NAMPT in cancer cells, resulting in NAD+ depletion and cytotoxicity.	NAD	193-197	nicotinamide phosphoribosyltransferase	Homo sapiens	10-15
28756225-3	2017	Targeting NAMPT has been investigated as an anti-cancer strategy, and several highly selective small molecule inhibitors have been found to potently inhibit NAMPT in cancer cells, resulting in NAD+ depletion and cytotoxicity.	NAD	193-197	nicotinamide phosphoribosyltransferase	Homo sapiens	157-162
28756225-7	2017	The combination of upregulation of the NAD+ de novo synthesis pathway through QPRT over-expression and NAMPT mutation confers resistance to GMX1778, but the cells are only partially resistant to next-generation NAMPT inhibitors.	NAD	39-43	nicotinamide phosphoribosyltransferase	Homo sapiens	103-108
28756225-7	2017	The combination of upregulation of the NAD+ de novo synthesis pathway through QPRT over-expression and NAMPT mutation confers resistance to GMX1778, but the cells are only partially resistant to next-generation NAMPT inhibitors.	NAD	39-43	nicotinamide phosphoribosyltransferase	Homo sapiens	211-216
31816398-2	2020	NAMPT is a rate-limiting enzyme for NAD+ production in mammalian cells and it was suggested that NAMPT and NMNAT3 are responsible for mitochondrial NAD+ production to maintain mitochondrial NAD+ pool.	NAD	36-39	nicotinamide phosphoribosyltransferase	Homo sapiens	97-102
31816398-2	2020	NAMPT is a rate-limiting enzyme for NAD+ production in mammalian cells and it was suggested that NAMPT and NMNAT3 are responsible for mitochondrial NAD+ production to maintain mitochondrial NAD+ pool.	NAD	36-39	nicotinamide nucleotide adenylyltransferase 3	Homo sapiens	107-113
31816398-2	2020	NAMPT is a rate-limiting enzyme for NAD+ production in mammalian cells and it was suggested that NAMPT and NMNAT3 are responsible for mitochondrial NAD+ production to maintain mitochondrial NAD+ pool.	NAD	148-151	nicotinamide phosphoribosyltransferase	Homo sapiens	0-5
31816398-2	2020	NAMPT is a rate-limiting enzyme for NAD+ production in mammalian cells and it was suggested that NAMPT and NMNAT3 are responsible for mitochondrial NAD+ production to maintain mitochondrial NAD+ pool.	NAD	148-151	nicotinamide phosphoribosyltransferase	Homo sapiens	97-102
31816398-2	2020	NAMPT is a rate-limiting enzyme for NAD+ production in mammalian cells and it was suggested that NAMPT and NMNAT3 are responsible for mitochondrial NAD+ production to maintain mitochondrial NAD+ pool.	NAD	148-151	nicotinamide nucleotide adenylyltransferase 3	Homo sapiens	107-113
28935892-6	2017	Changes in the NADH:NAD+ ratio regulate CtBP binding to the acetyltransferase p300, and regulate binding of p300 and the transcription factor NF-kappaB to pro-inflammatory gene promoters.	NAD	15-19	E1A binding protein p300	Homo sapiens	78-82
31816398-2	2020	NAMPT is a rate-limiting enzyme for NAD+ production in mammalian cells and it was suggested that NAMPT and NMNAT3 are responsible for mitochondrial NAD+ production to maintain mitochondrial NAD+ pool.	NAD	148-151	nicotinamide phosphoribosyltransferase	Homo sapiens	0-5
28935892-6	2017	Changes in the NADH:NAD+ ratio regulate CtBP binding to the acetyltransferase p300, and regulate binding of p300 and the transcription factor NF-kappaB to pro-inflammatory gene promoters.	NAD	15-19	E1A binding protein p300	Homo sapiens	108-112
31816398-2	2020	NAMPT is a rate-limiting enzyme for NAD+ production in mammalian cells and it was suggested that NAMPT and NMNAT3 are responsible for mitochondrial NAD+ production to maintain mitochondrial NAD+ pool.	NAD	148-151	nicotinamide phosphoribosyltransferase	Homo sapiens	97-102
31816398-2	2020	NAMPT is a rate-limiting enzyme for NAD+ production in mammalian cells and it was suggested that NAMPT and NMNAT3 are responsible for mitochondrial NAD+ production to maintain mitochondrial NAD+ pool.	NAD	148-151	nicotinamide nucleotide adenylyltransferase 3	Homo sapiens	107-113
31816398-3	2020	However, subsequent studies suggested mitochondrial may lack the NAMPT-NMANT3 pathway to maintain NAD+ level.	NAD	98-101	nicotinamide phosphoribosyltransferase	Homo sapiens	65-70
28728845-6	2017	Here, we determined the first crystal structures of NahB in the absence and presence of NAD+ and 2,3-dihydroxybiphenyl (2,3-DB).	NAD	88-92	nahB	Pseudomonas sp. MC1	52-56
31816398-4	2020	Therefore, how NAMPT overexpression rescues mitochondrial NAD+ content to promote cell survival in response to genotoxic stress remains elusive.	NAD	58-61	nicotinamide phosphoribosyltransferase	Homo sapiens	15-20
31816398-6	2020	Mitochondrial content and membrane potential were significantly reduced in response to H2O2 treatment, whereas activated NRF2-PPARalpha/AMPKalpha pathway by NAMPT overexpression rescued the mitochondrial membrane potential and content, suggesting that maintained mitochondrial content and integrity by NAMPT overexpression might be one of the key mechanisms to maintain mitochondrial NAD+ level and subsequently dictate cell survival under oxidative stress.	NAD	384-387	nicotinamide phosphoribosyltransferase	Homo sapiens	157-162
31822559-6	2020	Using this novel activator, we conducted biochemical and kinetic analyses revealing that SIRT6 is activated via acceleration of a catalytic step occurring after substrate binding but before NAD+ cleavage.	NAD	190-193	sirtuin 6	Homo sapiens	89-94
28854367-7	2017	Our study suggests that the NAMPT-mediated NAD+ biosynthesis pathway is a potential therapeutic target for degenerative MN diseases.	NAD	43-47	nicotinamide phosphoribosyltransferase	Homo sapiens	28-33
31995750-5	2020	The activation of TTP by Sirt1-dependent deacetylation, in response to increased NAD+ levels, suppresses the acute inflammatory response and decreases Rheb expression, inhibits mTORC1, and induces autophagolysosomes for bacterial clearance.	NAD	81-84	ZFP36 ring finger protein	Homo sapiens	18-21
31959836-3	2020	The ecto-5"-nucleotidase CD73, an ectoenzyme highly expressed in cancer, is suggested to regulate intracellular NAD+ levels by processing NAD+ and its bio-precursor, nicotinamide mononucleotide (NMN), from tumor microenvironments, thereby enhancing tumor DNA repair capacity and chemotherapy resistance.	NAD	112-115	5'-nucleotidase ecto	Homo sapiens	4-24
31959836-3	2020	The ecto-5"-nucleotidase CD73, an ectoenzyme highly expressed in cancer, is suggested to regulate intracellular NAD+ levels by processing NAD+ and its bio-precursor, nicotinamide mononucleotide (NMN), from tumor microenvironments, thereby enhancing tumor DNA repair capacity and chemotherapy resistance.	NAD	112-115	5'-nucleotidase ecto	Homo sapiens	25-29
31959836-3	2020	The ecto-5"-nucleotidase CD73, an ectoenzyme highly expressed in cancer, is suggested to regulate intracellular NAD+ levels by processing NAD+ and its bio-precursor, nicotinamide mononucleotide (NMN), from tumor microenvironments, thereby enhancing tumor DNA repair capacity and chemotherapy resistance.	NAD	138-141	5'-nucleotidase ecto	Homo sapiens	4-24
31959836-3	2020	The ecto-5"-nucleotidase CD73, an ectoenzyme highly expressed in cancer, is suggested to regulate intracellular NAD+ levels by processing NAD+ and its bio-precursor, nicotinamide mononucleotide (NMN), from tumor microenvironments, thereby enhancing tumor DNA repair capacity and chemotherapy resistance.	NAD	138-141	5'-nucleotidase ecto	Homo sapiens	25-29
31959836-4	2020	We therefore investigated whether expression of CD73 impacts intracellular NAD+ content and NAD+-dependent DNA repair capacity.	NAD	75-78	5'-nucleotidase ecto	Homo sapiens	48-52
31959836-4	2020	We therefore investigated whether expression of CD73 impacts intracellular NAD+ content and NAD+-dependent DNA repair capacity.	NAD	92-95	5'-nucleotidase ecto	Homo sapiens	48-52
31959836-8	2020	In opposition to its proposed role in extracellular NAD+ bioprocessing, we found that recombinant human CD73 only poorly processes NMN but not NAD+.	NAD	52-55	5'-nucleotidase ecto	Homo sapiens	104-108
31959836-8	2020	In opposition to its proposed role in extracellular NAD+ bioprocessing, we found that recombinant human CD73 only poorly processes NMN but not NAD+.	NAD	143-146	5'-nucleotidase ecto	Homo sapiens	104-108
31959836-9	2020	A positive correlation between CD73 expression and intracellular NAD+ content could not be made as CD73 knockout human cells were efficient in generating intracellular NAD+ when supplemented with NAD+ or NMN.	NAD	168-171	5'-nucleotidase ecto	Homo sapiens	99-103
31959836-9	2020	A positive correlation between CD73 expression and intracellular NAD+ content could not be made as CD73 knockout human cells were efficient in generating intracellular NAD+ when supplemented with NAD+ or NMN.	NAD	168-171	5'-nucleotidase ecto	Homo sapiens	99-103
32010616-3	2019	This dependence may be exploited therapeutically through pharmacological targeting of NAMPT, the rate-limiting enzyme in the NAD+ salvage pathway.	NAD	125-128	nicotinamide phosphoribosyltransferase	Homo sapiens	86-91
29245920-2	2017	NAMPT, a rate-limiting enzyme that boosts the nicotinamide adenine dinucleotide (NAD) regeneration in the salvage pathway, is commonly expressed in these tumors.	NAD	46-79	nicotinamide phosphoribosyltransferase	Homo sapiens	0-5
29245920-2	2017	NAMPT, a rate-limiting enzyme that boosts the nicotinamide adenine dinucleotide (NAD) regeneration in the salvage pathway, is commonly expressed in these tumors.	NAD	81-84	nicotinamide phosphoribosyltransferase	Homo sapiens	0-5
28817657-4	2017	Ferredoxin-NADP reductase, present in bacteria in genus Azotobacter, is an important enzyme for NADH/NAD+ equilibrium regulation in hydrogen production.	NAD	96-100	ferredoxin reductase	Homo sapiens	0-25
28817657-4	2017	Ferredoxin-NADP reductase, present in bacteria in genus Azotobacter, is an important enzyme for NADH/NAD+ equilibrium regulation in hydrogen production.	NAD	101-105	ferredoxin reductase	Homo sapiens	0-25
28845527-0	2017	Extracellular NAMPT/visfatin causes p53 deacetylation via NAD production and SIRT1 activation in breast cancer cells.	NAD	58-61	nicotinamide phosphoribosyltransferase	Homo sapiens	14-19
28845527-0	2017	Extracellular NAMPT/visfatin causes p53 deacetylation via NAD production and SIRT1 activation in breast cancer cells.	NAD	58-61	nicotinamide phosphoribosyltransferase	Homo sapiens	20-28
28845527-2	2017	In this study, we investigated the NAD-producing ability of visfatin and its relationship with SIRT1 (silent information regulator 2) and p53 to clarify the role of visfatin in breast cancer.	NAD	35-38	nicotinamide phosphoribosyltransferase	Homo sapiens	60-68
28845527-7	2017	Visfatin increased both extracellular and intracellular NAD concentrations.	NAD	56-59	nicotinamide phosphoribosyltransferase	Homo sapiens	0-8
28845527-10	2017	In conclusion, the results show that extracellular visfatin produces NAD that causes upregulation of SIRT1 activity and p53 deacetylation.	NAD	69-72	nicotinamide phosphoribosyltransferase	Homo sapiens	51-59
28743869-7	2017	Constitutive expression of the NMNAT gene, which encodes a rate-limiting enzyme for NAD biosynthesis, resulted in enhanced disease resistance in Arabidopsis.	NAD	84-87	nicotinate/nicotinamide mononucleotide adenyltransferase	Arabidopsis thaliana	31-36
28668830-2	2017	Nicotinamide phosphoribosyltransferase (Nampt) catalyzes the rate-limiting step of NAD+ synthesis and its expression is increased in several tumors.	NAD	83-87	nicotinamide phosphoribosyltransferase	Homo sapiens	0-38
32010616-8	2019	Combining NAMPT inhibitors with other therapies that target NAD+-dependent processes or selecting tumors with specific vulnerabilities that can be co-targeted with NAMPT inhibitors may represent opportunities to exploit the multiple functions of this enzyme for greater therapeutic benefit.	NAD	60-63	nicotinamide phosphoribosyltransferase	Homo sapiens	10-15
31812668-6	2020	We also demonstrate that mutant p53 induces the expression of Sirtuin3 (SIRT3), a major mitochondrial NAD+-dependent deacetylase, stimulating MnSOD deacetylation and enzymatic activity.	NAD	102-105	superoxide dismutase 2	Homo sapiens	142-147
27783203-2	2017	As a target for oncology, NAMPT is particularly attractive, because it catalyzes the rate-limiting step in the salvage pathway to generate nicotinamide adenine dinucleotide (NAD), a universal energy- and signal-carrying molecule involved in cellular energy metabolism and many homeostatic functions.	NAD	139-172	nicotinamide phosphoribosyltransferase	Homo sapiens	26-31
32009900-0	2019	Astrocytes and Microglia Are Resistant to NAD+-Mediated Cell Death Along the ARTC2/P2X7 Axis.	NAD	42-45	ADP-ribosyltransferase 2a	Mus musculus	77-82
27783203-2	2017	As a target for oncology, NAMPT is particularly attractive, because it catalyzes the rate-limiting step in the salvage pathway to generate nicotinamide adenine dinucleotide (NAD), a universal energy- and signal-carrying molecule involved in cellular energy metabolism and many homeostatic functions.	NAD	174-177	nicotinamide phosphoribosyltransferase	Homo sapiens	26-31
27783203-3	2017	Inhibition of NAMPT generally results in NAD depletion, followed by ATP reduction and loss of cell viability.	NAD	41-44	nicotinamide phosphoribosyltransferase	Homo sapiens	14-19
32009900-1	2019	ADP-ribosylation of the P2X7k splice variant on mouse T cells by Ecto-ADP-ribosyltransferase ARTC2.2 in response to its substrate extracellular nicotinamide adenine dinucleotide (NAD+) triggers cell death.	NAD	144-177	ADP-ribosyltransferase 2a	Mus musculus	93-98
27783203-8	2017	This toxicity was mitigated in vitro by co-administration of nicotinic acid (NA), which can enable NAD production through the NAMPT-independent pathway; however, this resulted in only partial mitigation in in vivo studies.	NAD	99-102	nicotinamide phosphoribosyltransferase	Homo sapiens	126-131
32009900-1	2019	ADP-ribosylation of the P2X7k splice variant on mouse T cells by Ecto-ADP-ribosyltransferase ARTC2.2 in response to its substrate extracellular nicotinamide adenine dinucleotide (NAD+) triggers cell death.	NAD	179-182	ADP-ribosyltransferase 2a	Mus musculus	93-98
32009900-2	2019	Since NAD+ is released as a danger signal during tissue damage, this NAD+-induced cell death (NICD) may impact the survival of other cell populations co-expressing P2X7 and of one of the ARTC2 isoforms (ARTC2.1, ARTC2.2).	NAD	6-9	ADP-ribosyltransferase 2a	Mus musculus	187-192
32009900-2	2019	Since NAD+ is released as a danger signal during tissue damage, this NAD+-induced cell death (NICD) may impact the survival of other cell populations co-expressing P2X7 and of one of the ARTC2 isoforms (ARTC2.1, ARTC2.2).	NAD	6-9	ADP-ribosyltransferase 2a	Mus musculus	203-208
32009900-2	2019	Since NAD+ is released as a danger signal during tissue damage, this NAD+-induced cell death (NICD) may impact the survival of other cell populations co-expressing P2X7 and of one of the ARTC2 isoforms (ARTC2.1, ARTC2.2).	NAD	69-72	ADP-ribosyltransferase 2a	Mus musculus	187-192
28461090-5	2017	By screening the expression and function of NAD+ dependent type III deacetylase Sirtuin family members, we found that SIRT5 and SIRT1/2 had opposite expression patterns and functions in macrophages.	NAD	44-48	sirtuin 5	Homo sapiens	118-123
32009900-2	2019	Since NAD+ is released as a danger signal during tissue damage, this NAD+-induced cell death (NICD) may impact the survival of other cell populations co-expressing P2X7 and of one of the ARTC2 isoforms (ARTC2.1, ARTC2.2).	NAD	69-72	ADP-ribosyltransferase 2a	Mus musculus	203-208
32009900-5	2019	We found that astrocytes and microglia strongly upregulate cell surface levels of ARTC2.1 and ADP-ribosylation of cell surface proteins in response to treatment with lipopolysaccharide (LPS) and the mitogen-activated protein kinase kinase (MEK) 1 and 2 inhibitor U0126, but do not respond to extracellular NAD+ with P2X7 activation and induction of cell death.	NAD	306-309	mitogen-activated protein kinase kinase 1	Mus musculus	199-252
31919382-2	2020	Most NAD+ in mammalian cells is synthesized via the NAD+ salvage pathway, where nicotinamide phosphoribosyltransferase (NAMPT) is the rate-limiting enzyme, converting nicotinamide into nicotinamide mononucleotide (NMN).	NAD	5-9	nicotinamide phosphoribosyltransferase	Homo sapiens	80-118
31919382-2	2020	Most NAD+ in mammalian cells is synthesized via the NAD+ salvage pathway, where nicotinamide phosphoribosyltransferase (NAMPT) is the rate-limiting enzyme, converting nicotinamide into nicotinamide mononucleotide (NMN).	NAD	5-9	nicotinamide phosphoribosyltransferase	Homo sapiens	120-125
31919382-2	2020	Most NAD+ in mammalian cells is synthesized via the NAD+ salvage pathway, where nicotinamide phosphoribosyltransferase (NAMPT) is the rate-limiting enzyme, converting nicotinamide into nicotinamide mononucleotide (NMN).	NAD	52-56	nicotinamide phosphoribosyltransferase	Homo sapiens	80-118
31919382-2	2020	Most NAD+ in mammalian cells is synthesized via the NAD+ salvage pathway, where nicotinamide phosphoribosyltransferase (NAMPT) is the rate-limiting enzyme, converting nicotinamide into nicotinamide mononucleotide (NMN).	NAD	52-56	nicotinamide phosphoribosyltransferase	Homo sapiens	120-125
31818629-1	2020	Nicotinamide phosphoribosyltransferase (NAMPT) catalyzes the condensation of nicotinamide (NAM) with 5-phosphoribosyl-1-prophosphate (PRPP) to yield nicotinamide mononucleotide (NMN), a rate limiting enzyme in a mammalian salvage pathway of nicotinamide adenine dinucleotide (NAD+) synthesis.	NAD	241-274	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
31818629-1	2020	Nicotinamide phosphoribosyltransferase (NAMPT) catalyzes the condensation of nicotinamide (NAM) with 5-phosphoribosyl-1-prophosphate (PRPP) to yield nicotinamide mononucleotide (NMN), a rate limiting enzyme in a mammalian salvage pathway of nicotinamide adenine dinucleotide (NAD+) synthesis.	NAD	276-279	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
31818629-3	2020	NAMPT is found to be upregulated in various types of cancer, and given its importance in the NAD+ salvage pathway, NAMPT is considered as an attractive target for the development of new cancer therapies.	NAD	93-96	nicotinamide phosphoribosyltransferase	Homo sapiens	0-5
31818629-3	2020	NAMPT is found to be upregulated in various types of cancer, and given its importance in the NAD+ salvage pathway, NAMPT is considered as an attractive target for the development of new cancer therapies.	NAD	93-96	nicotinamide phosphoribosyltransferase	Homo sapiens	115-120
31898286-0	2020	alpha-Mangostin reduced the viability of A594 cells in vitro by provoking ROS production through downregulation of NAMPT/NAD.	NAD	121-124	nicotinamide phosphoribosyltransferase	Homo sapiens	115-120
31898286-8	2020	All these phenomena were synchronized with escalated oxidative stress and downregulation of nicotinamide phosphoribosyltransferase/nicotinamide adenine dinucleotide (NAMPT/NAD).	NAD	131-164	nicotinamide phosphoribosyltransferase	Homo sapiens	166-171
31595469-3	2020	GSNOR, which has been identified as a key component of S-nitrosothiols catabolism, catalyzes an irreversible decomposition of abundant intracellular S-nitrosothiol, S-nitrosoglutathione (GSNO) to oxidized glutathione using reduced NADH cofactor.	NAD	231-235	alcohol dehydrogenase 5 (class III), chi polypeptide	Homo sapiens	0-5
31604073-7	2020	Importantly, treatment with ER beta agonist DPN (5 nM) significantly decreased the inhibitory effect of a PTEN knockdown on tamoxifen response of both cell lines (p&lt;0.05).	NAD	44-47	estrogen receptor 2	Homo sapiens	28-35
31599159-3	2019	Here, we report that ARH1, ARH3 and macrodomain proteins i.e. MacroD1, MacroD2, C6orf130 (TARG1), Af1521, hydrolyzed alpha-NAD+ but not beta-NAD+.	NAD	117-126	mono-ADP ribosylhydrolase 1	Homo sapiens	62-69
31804482-3	2019	Aurora-A-mediated phosphorylation of LDHB serine 162 significantly increases its activity in reducing pyruvate to lactate, which efficiently promotes NAD+ regeneration, glycolytic flux, lactate production and bio-synthesis with glycolytic intermediates.	NAD	150-153	aurora kinase A	Homo sapiens	0-8
31748226-8	2019	Mitigation of drug-induced cytotoxicity and basal mitochondrial respiration with exogenous application of nicotinamide mononucleotide (NMN) or exacerbation of these phenotypes when blocking nicotinamide adenine dinucleotide (NAD+) production via nicotinamide phosphoribosyltransferase (NAMPT) inhibition demonstrated that metabolic catastrophe drives the combination-induced cytotoxicity.	NAD	190-223	nicotinamide phosphoribosyltransferase	Homo sapiens	246-284
31748226-8	2019	Mitigation of drug-induced cytotoxicity and basal mitochondrial respiration with exogenous application of nicotinamide mononucleotide (NMN) or exacerbation of these phenotypes when blocking nicotinamide adenine dinucleotide (NAD+) production via nicotinamide phosphoribosyltransferase (NAMPT) inhibition demonstrated that metabolic catastrophe drives the combination-induced cytotoxicity.	NAD	190-223	nicotinamide phosphoribosyltransferase	Homo sapiens	286-291
31752261-0	2019	NAD Analogs in Aid of Chemical Biology and Medicinal Chemistry.	NAD	0-3	activation induced cytidine deaminase	Homo sapiens	15-18
31752261-6	2019	Synthetic NAD analogs are invaluable molecular tools to detect, monitor, structurally investigate, and modulate activity of NAD-related enzymes and biological processes in order to aid their deeper understanding.	NAD	10-13	activation induced cytidine deaminase	Homo sapiens	181-184
31752261-6	2019	Synthetic NAD analogs are invaluable molecular tools to detect, monitor, structurally investigate, and modulate activity of NAD-related enzymes and biological processes in order to aid their deeper understanding.	NAD	124-127	activation induced cytidine deaminase	Homo sapiens	181-184
31730022-9	2019	The NMNAT-3 enzyme, which catalyzes an important step in the biosynthesis of NAD+ from adenosine triphosphate, was also upregulated in RA iPSCs.	NAD	77-81	nicotinamide nucleotide adenylyltransferase 3	Homo sapiens	4-11
31675930-1	2019	BACKGROUND: Nicotinamide phosphoribosyltransferase (NAMPT) enzyme acts as the major enzyme in the nicotinamide adenine dinucleotide (NAD) synthesis salvage pathway.	NAD	98-131	nicotinamide phosphoribosyltransferase	Homo sapiens	12-50
31675930-1	2019	BACKGROUND: Nicotinamide phosphoribosyltransferase (NAMPT) enzyme acts as the major enzyme in the nicotinamide adenine dinucleotide (NAD) synthesis salvage pathway.	NAD	98-131	nicotinamide phosphoribosyltransferase	Homo sapiens	52-57
31675930-1	2019	BACKGROUND: Nicotinamide phosphoribosyltransferase (NAMPT) enzyme acts as the major enzyme in the nicotinamide adenine dinucleotide (NAD) synthesis salvage pathway.	NAD	133-136	nicotinamide phosphoribosyltransferase	Homo sapiens	12-50
31675930-1	2019	BACKGROUND: Nicotinamide phosphoribosyltransferase (NAMPT) enzyme acts as the major enzyme in the nicotinamide adenine dinucleotide (NAD) synthesis salvage pathway.	NAD	133-136	nicotinamide phosphoribosyltransferase	Homo sapiens	52-57
31228464-5	2019	Discussed AHR functions include chemical and microbial defense, organ development, modulation of immunity and inflammation, reproduction, and NAD+-dependent energy metabolism.	NAD	142-146	aryl hydrocarbon receptor	Homo sapiens	10-13
31575956-7	2019	Antioxidant enzymes transcriptionally regulated by Nrf2 and involved in GSH, NADPH, and NADH generation were significantly lower including PRX1 and PRX3, GPX4, GSTP1, GCLC, and MTHFD2.	NAD	88-92	glutamate-cysteine ligase catalytic subunit	Homo sapiens	167-171
31327531-4	2019	Using X-ray crystallography, we show that the indole amides bind the NAD+ pocket of PHGDH.	NAD	69-73	phosphoglycerate dehydrogenase	Homo sapiens	84-89
31463593-5	2019	Furthermore, our in vitro reconstitution experiments with Dph1-Dph2 mutants suggested that the Dph1 cluster serves a catalytic role, while the Dph2 cluster facilitates the reduction of the Dph1 cluster by the physiological reducing system Dph3/Cbr1/NADH.	NAD	249-253	diphthamide biosynthesis 2	Homo sapiens	63-67
31463593-5	2019	Furthermore, our in vitro reconstitution experiments with Dph1-Dph2 mutants suggested that the Dph1 cluster serves a catalytic role, while the Dph2 cluster facilitates the reduction of the Dph1 cluster by the physiological reducing system Dph3/Cbr1/NADH.	NAD	249-253	diphthamide biosynthesis 2	Homo sapiens	143-147
31426748-2	2019	Poly (ADP-ribose) polymerase (PARP) catalyzes PARylation by consecutively adding ADP-ribose moieties from NAD+ to the amino acid receptor residues on target proteins.	NAD	106-110	poly(ADP-ribose) polymerase	Arabidopsis thaliana	0-28
31426748-7	2019	Domain swapping and point mutation assays indicated that AtPARP3 has lost NAD+-binding capability and is inactive.	NAD	74-78	poly ADP-ribose polymerase 3	Arabidopsis thaliana	57-64
31391079-16	2019	In contrast, NAD+ supplementation improves NMJ morphology in fkrp morphants but not dag1 morphants.	NAD	13-17	fukutin related protein	Danio rerio	61-65
30605226-1	2019	Sirtuin-1 (Sirt1), a member of the NAD-dependent sirtuin family of histone/protein deacetylases (HDAC), is an important target for immunotherapy due to its role in deacetylating the transcription factors Foxp3 and thymic retinoid acid receptor related orphan receptor gamma (RORgammat).	NAD	35-38	forkhead box P3	Homo sapiens	204-209
28468779-2	2017	Nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme for NAD+ salvage from nicotinamide, has been investigated as a target for anticancer therapy.	NAD	77-81	nicotinamide phosphoribosyltransferase	Homo sapiens	0-38
28468779-2	2017	Nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme for NAD+ salvage from nicotinamide, has been investigated as a target for anticancer therapy.	NAD	77-81	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
28468779-6	2017	Careful characterization of the kinetics of NAMPT inhibition in vivo allowed us to optimize dosing to produce sufficient NAD+ depletion over time that resulted in efficacy in an HCT116 xenograft model.	NAD	121-125	nicotinamide phosphoribosyltransferase	Homo sapiens	44-49
31257865-0	2019	The Zebrafish Cytochrome b5/Cytochrome b5 Reductase/NADH System Efficiently Reduces Cytoglobins 1 and 2: Conserved Activity of Cytochrome b5/Cytochrome b5 Reductases during Vertebrate Evolution.	NAD	52-56	cytoglobin 1	Danio rerio	84-103
28416194-4	2017	We report that the Treg transcription factor Foxp3 reprograms T cell metabolism by suppressing Myc and glycolysis, enhancing oxidative phosphorylation, and increasing nicotinamide adenine dinucleotide oxidation.	NAD	167-200	forkhead box P3	Homo sapiens	45-50
31287140-5	2019	The ubiquitin-independent proteasome pathway regulates the stability of Polbeta in the cytosol via interaction between Polbeta and NAD(P)H quinone dehydrogenase 1 (NQO1) in an NADH-dependent manner.	NAD	176-180	DNA polymerase beta	Homo sapiens	72-79
28978015-5	2017	We also found that the ectopic expression of ALDH1A1 decreased the intracellular NAD+/NADH ratio, while knockout of ALDH1A1 increased the NAD+/NADH ratio.	NAD	143-147	aldehyde dehydrogenase family 1, subfamily A1	Mus musculus	45-52
31287140-5	2019	The ubiquitin-independent proteasome pathway regulates the stability of Polbeta in the cytosol via interaction between Polbeta and NAD(P)H quinone dehydrogenase 1 (NQO1) in an NADH-dependent manner.	NAD	176-180	DNA polymerase beta	Homo sapiens	119-126
28978015-5	2017	We also found that the ectopic expression of ALDH1A1 decreased the intracellular NAD+/NADH ratio, while knockout of ALDH1A1 increased the NAD+/NADH ratio.	NAD	143-147	aldehyde dehydrogenase family 1, subfamily A1	Mus musculus	116-123
28978015-8	2017	Collectively, these results suggest that this newly characterized GSH/DHLA-dependent NAD+-reduction activity of ALDH1A1 can decrease cellular NAD+/NADH ratio and promote tumor growth.	NAD	85-89	aldehyde dehydrogenase family 1, subfamily A1	Mus musculus	112-119
31282472-4	2019	The structural characterization of a construct comprising the naturally fused CS and b5R domains with bound FAD and NAD+ (PDB entry 6mv1) or NADP+ (PDB entry 6mv2) is now reported.	NAD	116-120	cytochrome b5 reductase 3	Homo sapiens	85-88
28978015-8	2017	Collectively, these results suggest that this newly characterized GSH/DHLA-dependent NAD+-reduction activity of ALDH1A1 can decrease cellular NAD+/NADH ratio and promote tumor growth.	NAD	142-146	aldehyde dehydrogenase family 1, subfamily A1	Mus musculus	112-119
28978015-8	2017	Collectively, these results suggest that this newly characterized GSH/DHLA-dependent NAD+-reduction activity of ALDH1A1 can decrease cellular NAD+/NADH ratio and promote tumor growth.	NAD	147-151	aldehyde dehydrogenase family 1, subfamily A1	Mus musculus	112-119
29723660-2	2019	SIRT1, a NAD+-dependent protein deacetylase, deacetylates the p65 of NF-kappaB and shows protective effects in kidney disorders.	NAD	9-12	RELA proto-oncogene, NF-kB subunit	Homo sapiens	62-65
31073968-6	2019	PA reduced the total amount of NAD+ in neurons that caused an increase in p65 K310 acetylation due to inhibition of SIRT1 activity and low protein content.	NAD	31-35	RELA proto-oncogene, NF-kB subunit	Homo sapiens	74-77
28295415-1	2017	Nicotinamide adenine dinucleotide (NAD+ ) biosynthetic pathway, mediated by nicotinamide phosphoribosyltransferase (NAMPT), a key NAD+ biosynthetic enzyme, plays a pivotal role in controlling many biological processes, such as metabolism, circadian rhythm, inflammation, and aging.	NAD	0-33	nicotinamide phosphoribosyltransferase	Homo sapiens	76-114
31333804-1	2019	SIRT5 belongs to a family of NAD+-dependent lysine deacetylases called sirtuins.	NAD	29-33	sirtuin 5	Homo sapiens	0-5
28295415-1	2017	Nicotinamide adenine dinucleotide (NAD+ ) biosynthetic pathway, mediated by nicotinamide phosphoribosyltransferase (NAMPT), a key NAD+ biosynthetic enzyme, plays a pivotal role in controlling many biological processes, such as metabolism, circadian rhythm, inflammation, and aging.	NAD	0-33	nicotinamide phosphoribosyltransferase	Homo sapiens	116-121
28295415-1	2017	Nicotinamide adenine dinucleotide (NAD+ ) biosynthetic pathway, mediated by nicotinamide phosphoribosyltransferase (NAMPT), a key NAD+ biosynthetic enzyme, plays a pivotal role in controlling many biological processes, such as metabolism, circadian rhythm, inflammation, and aging.	NAD	35-39	nicotinamide phosphoribosyltransferase	Homo sapiens	76-114
28295415-1	2017	Nicotinamide adenine dinucleotide (NAD+ ) biosynthetic pathway, mediated by nicotinamide phosphoribosyltransferase (NAMPT), a key NAD+ biosynthetic enzyme, plays a pivotal role in controlling many biological processes, such as metabolism, circadian rhythm, inflammation, and aging.	NAD	35-39	nicotinamide phosphoribosyltransferase	Homo sapiens	116-121
28295415-1	2017	Nicotinamide adenine dinucleotide (NAD+ ) biosynthetic pathway, mediated by nicotinamide phosphoribosyltransferase (NAMPT), a key NAD+ biosynthetic enzyme, plays a pivotal role in controlling many biological processes, such as metabolism, circadian rhythm, inflammation, and aging.	NAD	130-134	nicotinamide phosphoribosyltransferase	Homo sapiens	76-114
28295415-1	2017	Nicotinamide adenine dinucleotide (NAD+ ) biosynthetic pathway, mediated by nicotinamide phosphoribosyltransferase (NAMPT), a key NAD+ biosynthetic enzyme, plays a pivotal role in controlling many biological processes, such as metabolism, circadian rhythm, inflammation, and aging.	NAD	130-134	nicotinamide phosphoribosyltransferase	Homo sapiens	116-121
28295415-2	2017	Over the past decade, NAMPT-mediated NAD+ biosynthesis, together with its key downstream mediator, namely the NAD+ -dependent protein deacetylase SIRT1, has been demonstrated to regulate glucose and lipid metabolism in a tissue-dependent manner.	NAD	37-41	nicotinamide phosphoribosyltransferase	Homo sapiens	22-27
28295415-2	2017	Over the past decade, NAMPT-mediated NAD+ biosynthesis, together with its key downstream mediator, namely the NAD+ -dependent protein deacetylase SIRT1, has been demonstrated to regulate glucose and lipid metabolism in a tissue-dependent manner.	NAD	37-40	nicotinamide phosphoribosyltransferase	Homo sapiens	22-27
28295415-4	2017	This review will focus on the importance of adipose tissue NAMPT-mediated NAD+ biosynthesis and SIRT1 in the pathophysiology of obesity and insulin resistance.	NAD	74-78	nicotinamide phosphoribosyltransferase	Homo sapiens	59-64
30841754-4	2019	We now show that increasing total NAD+ content in astrocytes leads to the activation of the transcription factor nuclear factor, erythroid-derived 2, like 2 (Nfe2l2 or Nrf2) and up-regulation of the antioxidant proteins heme oxygenase 1 (HO-1) and sulfiredoxin 1 (SRXN1).	NAD	34-38	sulfiredoxin 1	Homo sapiens	248-262
30841754-4	2019	We now show that increasing total NAD+ content in astrocytes leads to the activation of the transcription factor nuclear factor, erythroid-derived 2, like 2 (Nfe2l2 or Nrf2) and up-regulation of the antioxidant proteins heme oxygenase 1 (HO-1) and sulfiredoxin 1 (SRXN1).	NAD	34-38	sulfiredoxin 1	Homo sapiens	264-269
31101919-4	2019	Disruption of the Nudt12 gene stabilizes transfected NAD-capped RNA in cells, and its endogenous NAD-capped mRNA targets are enriched in those encoding proteins involved in cellular energetics.	NAD	53-56	nudix hydrolase 12	Homo sapiens	18-24
28202489-2	2017	Nicotinamide phosphoribosyltransferase (NAMPT) is a cytozyme that regulates intracellular nicotinamide adenine dinucleotide levels and cellular redox state, regulates histone deacetylases, promotes cell proliferation, and inhibits apoptosis.	NAD	90-123	nicotinamide phosphoribosyltransferase	Homo sapiens	0-38
28202489-2	2017	Nicotinamide phosphoribosyltransferase (NAMPT) is a cytozyme that regulates intracellular nicotinamide adenine dinucleotide levels and cellular redox state, regulates histone deacetylases, promotes cell proliferation, and inhibits apoptosis.	NAD	90-123	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
31101919-4	2019	Disruption of the Nudt12 gene stabilizes transfected NAD-capped RNA in cells, and its endogenous NAD-capped mRNA targets are enriched in those encoding proteins involved in cellular energetics.	NAD	97-100	nudix hydrolase 12	Homo sapiens	18-24
28355567-4	2017	SIRT6 is a member of the evolutionarily conserved sirtuin family of nicotinamide adenine dinucleotide (NAD)+-dependent protein deacetylases.	NAD	68-101	sirtuin 6	Homo sapiens	0-5
31101919-5	2019	Furthermore, exposure of cells to nutrient or environmental stress manifests changes in NAD-capped RNA levels that are selectively responsive to Nudt12 or DXO, respectively, indicating an association of deNADding to cellular metabolism.	NAD	88-91	nudix hydrolase 12	Homo sapiens	145-151
31128467-1	2019	SARM1, an NAD-utilizing enzyme, regulates axonal degeneration.	NAD	10-13	sterile alpha and TIR motif containing 1	Homo sapiens	0-5
28219011-1	2017	Aldehyde dehydrogenase 2 (ALDH2), one of 19 ALDH superfamily members, catalyzes the NAD+-dependent oxidation of aldehydes to their respective carboxylic acids.	NAD	84-88	aldehyde dehydrogenase 2 family member	Homo sapiens	0-24
28219011-1	2017	Aldehyde dehydrogenase 2 (ALDH2), one of 19 ALDH superfamily members, catalyzes the NAD+-dependent oxidation of aldehydes to their respective carboxylic acids.	NAD	84-88	aldehyde dehydrogenase 2 family member	Homo sapiens	26-31
31128467-2	2019	We show that CZ-48, a cell-permeant mimetic of NMN, activated SARM1 in vitro and in cellulo to cyclize NAD and produce a Ca2+ messenger, cADPR, with similar efficiency as NMN.	NAD	103-106	sterile alpha and TIR motif containing 1	Homo sapiens	62-67
28248093-6	2017	Furthermore, HPLC-MS/MS and computational modeling elucidate a potential role for acetyl-Lys369 on ALDH2 in perturbing normal beta-nicotinamide adenine dinucleotide (NAD+) cofactor binding.	NAD	126-164	aldehyde dehydrogenase 2 family member	Homo sapiens	99-104
28248093-6	2017	Furthermore, HPLC-MS/MS and computational modeling elucidate a potential role for acetyl-Lys369 on ALDH2 in perturbing normal beta-nicotinamide adenine dinucleotide (NAD+) cofactor binding.	NAD	166-170	aldehyde dehydrogenase 2 family member	Homo sapiens	99-104
31128467-7	2019	Both catalyzed similar set of reactions, but SARM1 had much higher NAD-cyclizing activity, making it more efficient in elevating cADPR.	NAD	67-70	sterile alpha and TIR motif containing 1	Homo sapiens	45-50
28262487-1	2017	Axons require the axonal NAD-synthesizing enzyme NMNAT2 to survive.	NAD	25-28	nicotinamide nucleotide adenylyltransferase 2	Mus musculus	49-55
31128467-9	2019	In SARM1-overexpressing cells, CZ-48 elevated cADPR, depleted NAD and ATP, and induced non-apoptotic death.	NAD	62-65	sterile alpha and TIR motif containing 1	Homo sapiens	3-8
28262487-3	2017	We have previously proposed that axonal NMNAT2 primarily promotes axon survival by maintaining low levels of its substrate NMN rather than generating NAD; however, this is still debated.	NAD	150-153	nicotinamide nucleotide adenylyltransferase 2	Mus musculus	40-46
30801870-9	2019	ABSTRACT: Nicotinamide adenine dinucleotide phosphate (NADPH) oxidases (Nox), comprise seven family members (Nox1-Nox5 and dual oxidase 1 and 2) and are major producers of reactive oxygen species in mammalian cells.	NAD	10-43	NADPH oxidase 1	Homo sapiens	109-113
28373875-2	2017	One set of ectoenzymes-CD39, CD38, CD203a, and CD73-leads to the generation of adenosine (ADO) by metabolizing ATP and NAD+.	NAD	119-123	5'-nucleotidase ecto	Homo sapiens	47-51
28232723-6	2017	Furthermore, we show that elevated NOX4 activity accelerates oxidation of NADH and supports increased glycolysis by generating NAD+, a substrate for GAPDH-mediated glycolytic reaction, promoting PDAC cell growth.	NAD	74-78	NADPH oxidase 4	Homo sapiens	35-39
30801870-9	2019	ABSTRACT: Nicotinamide adenine dinucleotide phosphate (NADPH) oxidases (Nox), comprise seven family members (Nox1-Nox5 and dual oxidase 1 and 2) and are major producers of reactive oxygen species in mammalian cells.	NAD	10-43	dual oxidase 1	Homo sapiens	123-143
28232723-6	2017	Furthermore, we show that elevated NOX4 activity accelerates oxidation of NADH and supports increased glycolysis by generating NAD+, a substrate for GAPDH-mediated glycolytic reaction, promoting PDAC cell growth.	NAD	127-131	NADPH oxidase 4	Homo sapiens	35-39
31338216-2	2019	Nicotinamide phosphoribosyltransferase (NAMPT) is the rate-limiting enzyme for nicotinamide adenine dinucleotide (NAD) salvage synthesis in mammals, thereby influencing NAD-dependent enzymes and constituting a strong endogenous defence system against various stresses.	NAD	79-112	nicotinamide phosphoribosyltransferase	Homo sapiens	0-38
28042046-5	2017	With subsequent characterization, we successfully identified PHGDH non-NAD+-competing allosteric inhibitors that attenuate its enzyme activity, selectively inhibit de novo serine synthesis in cancer cells, and reduce tumor growth in vivo.	NAD	71-75	phosphoglycerate dehydrogenase	Homo sapiens	61-66
28095293-1	2017	Injury-induced (Wallerian) axonal degeneration is regulated via the opposing actions of pro-degenerative factors such as SARM1 and a MAPK signal and pro-survival factors, the most important of which is the NAD+ biosynthetic enzyme NMNAT2 that inhibits activation of the SARM1 pathway.	NAD	206-210	sterile alpha and TIR motif containing 1	Homo sapiens	121-126
31338216-2	2019	Nicotinamide phosphoribosyltransferase (NAMPT) is the rate-limiting enzyme for nicotinamide adenine dinucleotide (NAD) salvage synthesis in mammals, thereby influencing NAD-dependent enzymes and constituting a strong endogenous defence system against various stresses.	NAD	79-112	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
31338216-2	2019	Nicotinamide phosphoribosyltransferase (NAMPT) is the rate-limiting enzyme for nicotinamide adenine dinucleotide (NAD) salvage synthesis in mammals, thereby influencing NAD-dependent enzymes and constituting a strong endogenous defence system against various stresses.	NAD	114-117	nicotinamide phosphoribosyltransferase	Homo sapiens	0-38
31338216-2	2019	Nicotinamide phosphoribosyltransferase (NAMPT) is the rate-limiting enzyme for nicotinamide adenine dinucleotide (NAD) salvage synthesis in mammals, thereby influencing NAD-dependent enzymes and constituting a strong endogenous defence system against various stresses.	NAD	114-117	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
31338216-2	2019	Nicotinamide phosphoribosyltransferase (NAMPT) is the rate-limiting enzyme for nicotinamide adenine dinucleotide (NAD) salvage synthesis in mammals, thereby influencing NAD-dependent enzymes and constituting a strong endogenous defence system against various stresses.	NAD	169-172	nicotinamide phosphoribosyltransferase	Homo sapiens	0-38
28095293-1	2017	Injury-induced (Wallerian) axonal degeneration is regulated via the opposing actions of pro-degenerative factors such as SARM1 and a MAPK signal and pro-survival factors, the most important of which is the NAD+ biosynthetic enzyme NMNAT2 that inhibits activation of the SARM1 pathway.	NAD	206-210	sterile alpha and TIR motif containing 1	Homo sapiens	270-275
31338216-2	2019	Nicotinamide phosphoribosyltransferase (NAMPT) is the rate-limiting enzyme for nicotinamide adenine dinucleotide (NAD) salvage synthesis in mammals, thereby influencing NAD-dependent enzymes and constituting a strong endogenous defence system against various stresses.	NAD	169-172	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
30484004-7	2019	The levels of nicotinamide phosphoribosyltransferase (NAMPT) were reduced in fibroblast-like synoviocytes by MAN both in vivo and in vitro, which was accompanied with a decline in nicotinamide adenine dinucleotide (NAD) production.	NAD	180-213	nicotinamide phosphoribosyltransferase	Homo sapiens	14-52
27388719-6	2017	We further clarified that NAD-dependent deacetylase SIRT1, a direct target of miR-34, is decreased by the treatment with AU-1.	NAD	26-29	microRNA 34a	Homo sapiens	78-84
30484004-7	2019	The levels of nicotinamide phosphoribosyltransferase (NAMPT) were reduced in fibroblast-like synoviocytes by MAN both in vivo and in vitro, which was accompanied with a decline in nicotinamide adenine dinucleotide (NAD) production.	NAD	180-213	nicotinamide phosphoribosyltransferase	Homo sapiens	54-59
30484004-7	2019	The levels of nicotinamide phosphoribosyltransferase (NAMPT) were reduced in fibroblast-like synoviocytes by MAN both in vivo and in vitro, which was accompanied with a decline in nicotinamide adenine dinucleotide (NAD) production.	NAD	215-218	nicotinamide phosphoribosyltransferase	Homo sapiens	14-52
27930300-3	2016	Here, we report nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting step in NAD+ synthesis, is highly expressed in glioblastoma tumors and patient-derived glioblastoma stem-like cells (GSCs).	NAD	90-94	nicotinamide phosphoribosyltransferase	Homo sapiens	16-54
27930300-3	2016	Here, we report nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting step in NAD+ synthesis, is highly expressed in glioblastoma tumors and patient-derived glioblastoma stem-like cells (GSCs).	NAD	90-94	nicotinamide phosphoribosyltransferase	Homo sapiens	56-61
30484004-7	2019	The levels of nicotinamide phosphoribosyltransferase (NAMPT) were reduced in fibroblast-like synoviocytes by MAN both in vivo and in vitro, which was accompanied with a decline in nicotinamide adenine dinucleotide (NAD) production.	NAD	215-218	nicotinamide phosphoribosyltransferase	Homo sapiens	54-59
27930300-5	2016	Pharmacological and genetic inhibition of NAMPT decreased NAD+ levels and GSC self-renewal capacity, and NAMPT knockdown inhibited the in vivo tumorigenicity of GSCs.	NAD	58-62	nicotinamide phosphoribosyltransferase	Homo sapiens	42-47
30860478-4	2019	First, adenine depletion promotes transcriptional upregulation of the de novo NAD+ biosynthesis genes by a mechanism requiring the key-purine intermediates ZMP/SZMP and the Bas1/Pho2 transcription factors.	NAD	78-82	Bas1p	Saccharomyces cerevisiae S288C	173-177
27930300-6	2016	Regulatory network analysis of RNA sequencing data using GSCs treated with NAMPT inhibitor identified transcription factor E2F2 as the center of a transcriptional hub in the NAD+-dependent network.	NAD	174-178	nicotinamide phosphoribosyltransferase	Homo sapiens	75-80
30796188-6	2019	Interaction of Mtln with NADH-dependent cytochrome b5 reductase stimulates complex I functioning most likely by providing a favorable lipid composition of the membrane.	NAD	25-29	cytochrome b5 type A (microsomal)	Mus musculus	40-53
27287071-1	2016	PURPOSE: Nicotinamide phosphoribosyltransferase (Nampt) regulates intracellular NAD+ pool and is highly expressed in a number of malignancies.	NAD	80-84	nicotinamide phosphoribosyltransferase	Homo sapiens	9-47
27287071-1	2016	PURPOSE: Nicotinamide phosphoribosyltransferase (Nampt) regulates intracellular NAD+ pool and is highly expressed in a number of malignancies.	NAD	80-84	nicotinamide phosphoribosyltransferase	Homo sapiens	49-54
27287071-2	2016	FK866, a selective inhibitor of Nampt, depletes intracellular NAD+ levels, thereby blocking cellular metabolism and triggering sensitization to other drugs and cell death.	NAD	62-66	nicotinamide phosphoribosyltransferase	Homo sapiens	32-37
30856230-1	2019	BACKGROUND: Nicotinamide phosphoribosyltransferase (NAMPT) plays a key role in the biosynthesis of nicotinamide adenine dinucleotide (NAD+), which is a vital cofactor in redox reactions and a substrate for NAD+ consuming enzymes including CD38, PARPs and sirtuins.	NAD	99-132	nicotinamide phosphoribosyltransferase	Homo sapiens	12-50
27761584-4	2016	Within the niche, NAD+ is able to activate a discontinuous adenosinergic pathway that relies upon CD38, CD203a, and CD73 or TRACP, according to the environmental pH.	NAD	18-22	5'-nucleotidase ecto	Homo sapiens	116-120
30856230-1	2019	BACKGROUND: Nicotinamide phosphoribosyltransferase (NAMPT) plays a key role in the biosynthesis of nicotinamide adenine dinucleotide (NAD+), which is a vital cofactor in redox reactions and a substrate for NAD+ consuming enzymes including CD38, PARPs and sirtuins.	NAD	99-132	nicotinamide phosphoribosyltransferase	Homo sapiens	52-57
30856230-1	2019	BACKGROUND: Nicotinamide phosphoribosyltransferase (NAMPT) plays a key role in the biosynthesis of nicotinamide adenine dinucleotide (NAD+), which is a vital cofactor in redox reactions and a substrate for NAD+ consuming enzymes including CD38, PARPs and sirtuins.	NAD	134-138	nicotinamide phosphoribosyltransferase	Homo sapiens	12-50
30856230-1	2019	BACKGROUND: Nicotinamide phosphoribosyltransferase (NAMPT) plays a key role in the biosynthesis of nicotinamide adenine dinucleotide (NAD+), which is a vital cofactor in redox reactions and a substrate for NAD+ consuming enzymes including CD38, PARPs and sirtuins.	NAD	134-138	nicotinamide phosphoribosyltransferase	Homo sapiens	52-57
27236139-6	2016	Since bile acids do not show electrochemical signals, they were converted to 3-ketosteroids by 3-alpha-hydroxysteroid dehydrogenase (3alpha-HSD) in the presence of nicotinamide adenine dinucleotide (NAD(+)), which was reduced to NADH.	NAD	164-197	aldo-keto reductase family 1 member C3	Homo sapiens	95-131
27236139-6	2016	Since bile acids do not show electrochemical signals, they were converted to 3-ketosteroids by 3-alpha-hydroxysteroid dehydrogenase (3alpha-HSD) in the presence of nicotinamide adenine dinucleotide (NAD(+)), which was reduced to NADH.	NAD	164-197	aldo-keto reductase family 1 member C3	Homo sapiens	133-143
27236139-6	2016	Since bile acids do not show electrochemical signals, they were converted to 3-ketosteroids by 3-alpha-hydroxysteroid dehydrogenase (3alpha-HSD) in the presence of nicotinamide adenine dinucleotide (NAD(+)), which was reduced to NADH.	NAD	199-205	aldo-keto reductase family 1 member C3	Homo sapiens	133-143
30856230-1	2019	BACKGROUND: Nicotinamide phosphoribosyltransferase (NAMPT) plays a key role in the biosynthesis of nicotinamide adenine dinucleotide (NAD+), which is a vital cofactor in redox reactions and a substrate for NAD+ consuming enzymes including CD38, PARPs and sirtuins.	NAD	206-210	nicotinamide phosphoribosyltransferase	Homo sapiens	12-50
30856230-1	2019	BACKGROUND: Nicotinamide phosphoribosyltransferase (NAMPT) plays a key role in the biosynthesis of nicotinamide adenine dinucleotide (NAD+), which is a vital cofactor in redox reactions and a substrate for NAD+ consuming enzymes including CD38, PARPs and sirtuins.	NAD	206-210	nicotinamide phosphoribosyltransferase	Homo sapiens	52-57
30633870-9	2019	SARM has been shown to deplete NAD+ by possessing intrinsic NADase activity in the TIR domain of the protein.	NAD	31-35	sterile alpha and TIR motif containing 1	Homo sapiens	0-4
27236139-6	2016	Since bile acids do not show electrochemical signals, they were converted to 3-ketosteroids by 3-alpha-hydroxysteroid dehydrogenase (3alpha-HSD) in the presence of nicotinamide adenine dinucleotide (NAD(+)), which was reduced to NADH.	NAD	229-233	aldo-keto reductase family 1 member C3	Homo sapiens	95-131
30633870-11	2019	It is thought that this activity of SARM is normally switched off by the axo-protective activities of NMNAT2 which maintain low levels of the NAD+ precursor NMN.	NAD	142-146	sterile alpha and TIR motif containing 1	Homo sapiens	36-40
27236139-6	2016	Since bile acids do not show electrochemical signals, they were converted to 3-ketosteroids by 3-alpha-hydroxysteroid dehydrogenase (3alpha-HSD) in the presence of nicotinamide adenine dinucleotide (NAD(+)), which was reduced to NADH.	NAD	229-233	aldo-keto reductase family 1 member C3	Homo sapiens	133-143
30692102-2	2019	Nicotinamide phosphoribosyltransferase (NAMPT) is involved in the generation of NAD+ and a potential therapeutic target in AML.	NAD	80-84	nicotinamide phosphoribosyltransferase	Homo sapiens	0-38
27751850-2	2016	Although the detailed mechanism of cell intoxication by BEC remains to be defined, BECa shows both NAD+-glycohydrolase and actin ADP-ribosyltransferase activities in the presence of NAD+.	NAD	99-103	becA	Clostridium perfringens	83-87
30692102-2	2019	Nicotinamide phosphoribosyltransferase (NAMPT) is involved in the generation of NAD+ and a potential therapeutic target in AML.	NAD	80-84	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
27751850-3	2016	In this study, we determined the first crystal structure of BECa in its apo-state and in complex with NADH.	NAD	102-106	becA	Clostridium perfringens	60-64
30755786-7	2019	Inhibition of PARP-mediated NAD+ depletion partially protected cells from death.	NAD	28-32	collagen type XI alpha 2 chain	Homo sapiens	14-18
27751850-5	2016	We present a detailed picture of interactions between BECa and NADH, including bound water molecules located near the C1"-N glycosidic bond of NADH and the catalytically important ADP-ribosylating turn-turn (ARTT) loop.	NAD	63-67	becA	Clostridium perfringens	54-58
27751850-5	2016	We present a detailed picture of interactions between BECa and NADH, including bound water molecules located near the C1"-N glycosidic bond of NADH and the catalytically important ADP-ribosylating turn-turn (ARTT) loop.	NAD	143-147	becA	Clostridium perfringens	54-58
30670978-1	2018	The present study examined whether angiotensin II (Ang II) mediates the pressor effect through nicotinamide adenine dinucleotide phosphate (NADPH) oxidase-derived reactive oxygen species (ROS)-mitogen-activated protein kinase (MAPK) signaling in the glutamatergic neurons of the rostral ventrolateral medulla (RVLM) in stress-induced hypertensive rats (SIHR).	NAD	95-128	mitogen activated protein kinase 3	Rattus norvegicus	227-231
27754828-4	2016	NAMPT is a key enzyme involved in nicotinamide adenine dinucleotide salvage pathway, and it is frequently overexpressed in human cancers.	NAD	34-67	nicotinamide phosphoribosyltransferase	Homo sapiens	0-5
29958894-3	2019	Among the host responses to the release of ATP, NAD+ and related small molecules is their breakdown on behalf of a panel of leukocyte ectonucleotidases - CD38, CD39, CD73, CD157, CD203a and CD203c -, whose activities are concatenated to form two nucleotide-catabolizing channels defined as the canonical and non-canonical adenosinergic pathways.	NAD	48-52	5'-nucleotidase ecto	Homo sapiens	166-170
30367518-4	2019	When the bovine GDH crystal structures were minimized to prepare for further computational analysis, unusually large deviations were found at the allosteric NADH binding site due to chemical sequence errors.	NAD	157-161	glutamate dehydrogenase 1, mitochondrial	Bos taurus	16-19
27681750-3	2016	Nicotinamide phosphoribosyltransferase (NAMPT) is not only a key enzyme for the nicotinamide adenine dinucleotide salvage pathway, but also a cytokine participating in cell survival, metabolism, and longevity, with a broad effect on cellular functions in physiology and pathology.	NAD	80-113	nicotinamide phosphoribosyltransferase	Homo sapiens	0-38
27681750-3	2016	Nicotinamide phosphoribosyltransferase (NAMPT) is not only a key enzyme for the nicotinamide adenine dinucleotide salvage pathway, but also a cytokine participating in cell survival, metabolism, and longevity, with a broad effect on cellular functions in physiology and pathology.	NAD	80-113	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
30574122-1	2018	The mammalian Sirtuins (SIRT1-7) are an evolutionarily conserved family of NAD+-dependent deacylase and mono-ADP-ribosyltransferase.	NAD	75-78	ADP-ribosyltransferase 3 (inactive)	Homo sapiens	104-131
27733253-4	2016	Glycerol-3-phosphate dehydrogenase 1 (GPD1), an NAD+/NADH-dependent enzyme present in the cytosol, catalyzes the reversible conversion of glycerol-3-phosphate (G3P) to dihydroxyacetone phosphate (DHAP).	NAD	48-52	glycerol-3-phosphate dehydrogenase 1 (soluble)	Mus musculus	0-36
27733253-4	2016	Glycerol-3-phosphate dehydrogenase 1 (GPD1), an NAD+/NADH-dependent enzyme present in the cytosol, catalyzes the reversible conversion of glycerol-3-phosphate (G3P) to dihydroxyacetone phosphate (DHAP).	NAD	48-52	glycerol-3-phosphate dehydrogenase 1 (soluble)	Mus musculus	38-42
27733253-4	2016	Glycerol-3-phosphate dehydrogenase 1 (GPD1), an NAD+/NADH-dependent enzyme present in the cytosol, catalyzes the reversible conversion of glycerol-3-phosphate (G3P) to dihydroxyacetone phosphate (DHAP).	NAD	53-57	glycerol-3-phosphate dehydrogenase 1 (soluble)	Mus musculus	0-36
27733253-4	2016	Glycerol-3-phosphate dehydrogenase 1 (GPD1), an NAD+/NADH-dependent enzyme present in the cytosol, catalyzes the reversible conversion of glycerol-3-phosphate (G3P) to dihydroxyacetone phosphate (DHAP).	NAD	53-57	glycerol-3-phosphate dehydrogenase 1 (soluble)	Mus musculus	38-42
27767101-1	2016	Sirtuin-1 (SIRT1) and SIRT6, NAD+-dependent Class III protein deacetylases, are putative anti-aging enzymes, down-regulated in patients with chronic obstructive pulmonary disease (COPD), which is characterized by the accelerated ageing of the lung and associated with increased oxidative stress.	NAD	29-32	sirtuin 6	Homo sapiens	22-27
27759041-4	2016	By interacting with nicotinamide phosphoribosyltransferase (NAMPT), a protein involved in NAD biosynthesis, PCNA coordinates glycolysis and survival, especially in HL-60R cells.	NAD	90-93	nicotinamide phosphoribosyltransferase	Homo sapiens	20-58
27759041-4	2016	By interacting with nicotinamide phosphoribosyltransferase (NAMPT), a protein involved in NAD biosynthesis, PCNA coordinates glycolysis and survival, especially in HL-60R cells.	NAD	90-93	nicotinamide phosphoribosyltransferase	Homo sapiens	60-65
27798264-7	2016	In combination, these studies suggest that the replenishment of NAD+ may benefit patients with muscular dystrophies or other neuromuscular degenerative conditions characterized by the PARP/NNMT gene expression signatures.	NAD	64-68	nicotinamide N-methyltransferase	Homo sapiens	189-193
27493223-0	2016	Human serine racemase is allosterically modulated by NADH and reduced nicotinamide derivatives.	NAD	53-57	serine racemase	Homo sapiens	6-21
27493223-4	2016	Following the recent observation that nicotinamide adenine dinucleotide (reduced form) (NADH) inhibits serine racemase, here we show that the inhibition is partial, with an IC50 of 246 +- 63 muM, several-fold higher than NADH intracellular concentrations.	NAD	38-71	serine racemase	Homo sapiens	103-118
27493223-4	2016	Following the recent observation that nicotinamide adenine dinucleotide (reduced form) (NADH) inhibits serine racemase, here we show that the inhibition is partial, with an IC50 of 246 +- 63 muM, several-fold higher than NADH intracellular concentrations.	NAD	88-92	serine racemase	Homo sapiens	103-118
27493223-4	2016	Following the recent observation that nicotinamide adenine dinucleotide (reduced form) (NADH) inhibits serine racemase, here we show that the inhibition is partial, with an IC50 of 246 +- 63 muM, several-fold higher than NADH intracellular concentrations.	NAD	221-225	serine racemase	Homo sapiens	103-118
27493223-6	2016	NADH also reduces the weak activity of human serine racemase in the absence of ATP, indicating an additional ATP-independent inhibition mechanism.	NAD	0-4	serine racemase	Homo sapiens	45-60
27562971-2	2016	Here, we test the hypothesis that metabolic reprogramming to aerobic glycolysis is a critical adaptation of fibroblasts in the hypertensive vessel wall that drives proliferative and proinflammatory activation through a mechanism involving increased activity of the NADH-sensitive transcriptional corepressor C-terminal binding protein 1 (CtBP1).	NAD	265-269	C-terminal binding protein 1	Homo sapiens	308-336
27562971-2	2016	Here, we test the hypothesis that metabolic reprogramming to aerobic glycolysis is a critical adaptation of fibroblasts in the hypertensive vessel wall that drives proliferative and proinflammatory activation through a mechanism involving increased activity of the NADH-sensitive transcriptional corepressor C-terminal binding protein 1 (CtBP1).	NAD	265-269	C-terminal binding protein 1	Homo sapiens	338-343
27562971-7	2016	Expression of the NADH sensor CtBP1 was increased in vivo and in vitro in fibroblasts within the pulmonary adventitia of humans with idiopathic pulmonary arterial hypertension and animals with PH and cultured PH-Fibs, respectively.	NAD	18-22	C-terminal binding protein 1	Homo sapiens	30-35
27562971-8	2016	Decreasing NADH pharmacologically with MTOB or genetically blocking CtBP1 with siRNA upregulated the cyclin-dependent genes (p15 and p21) and proapoptotic regulators (NOXA and PERP), attenuated proliferation, corrected the glycolytic reprogramming phenotype of PH-Fibs, and augmented transcription of the anti-inflammatory gene HMOX1.	NAD	11-15	C-terminal binding protein 1	Homo sapiens	68-73
27711204-2	2016	NAMPT, nicotinamide phosphoribosyltransferase, which converts nicotinamide (NAM) to nicotinamide mononucleotide (NMN), the immediate precursor of NAD, is an attractive therapeutic target as inhibition of NAMPT reduces cellular NAD levels and inhibits tumor growth in vivo.	NAD	146-149	nicotinamide phosphoribosyltransferase	Homo sapiens	0-5
27711204-2	2016	NAMPT, nicotinamide phosphoribosyltransferase, which converts nicotinamide (NAM) to nicotinamide mononucleotide (NMN), the immediate precursor of NAD, is an attractive therapeutic target as inhibition of NAMPT reduces cellular NAD levels and inhibits tumor growth in vivo.	NAD	146-149	nicotinamide phosphoribosyltransferase	Homo sapiens	204-209
27711204-2	2016	NAMPT, nicotinamide phosphoribosyltransferase, which converts nicotinamide (NAM) to nicotinamide mononucleotide (NMN), the immediate precursor of NAD, is an attractive therapeutic target as inhibition of NAMPT reduces cellular NAD levels and inhibits tumor growth in vivo.	NAD	227-230	nicotinamide phosphoribosyltransferase	Homo sapiens	0-5
27711204-2	2016	NAMPT, nicotinamide phosphoribosyltransferase, which converts nicotinamide (NAM) to nicotinamide mononucleotide (NMN), the immediate precursor of NAD, is an attractive therapeutic target as inhibition of NAMPT reduces cellular NAD levels and inhibits tumor growth in vivo.	NAD	227-230	nicotinamide phosphoribosyltransferase	Homo sapiens	204-209
27711204-10	2016	Our data reveals that cell lines show heterogeneous response to NAD depletion and that the underlying molecular and genetic framework in cells can influence the metabolic response to NAMPT inhibition.	NAD	64-67	nicotinamide phosphoribosyltransferase	Homo sapiens	183-188
27521998-6	2016	The results showed that Alda-1 dramatically modifies the properties of ALDH2, the Km for NAD+ decreased by 2.4-fold, and the catalytic efficiency increased 4.4-fold; however, the Km for the aldehyde increased 8.6-fold, thus, diminishing the catalytic efficiency.	NAD	89-93	aldehyde dehydrogenase 2 family member	Homo sapiens	71-76
27521998-9	2016	Finally, NADH inhibition patterns indicated that Alda-1 induced a change in the sequence of substrates entry and products release, in agreement with the proposal of both substrates entering ALDH2 by the NAD+ entrance site.	NAD	203-207	aldehyde dehydrogenase 2 family member	Homo sapiens	190-195
27580341-1	2016	The salicylaldehyde dehydrogenase (NahF) catalyzes the oxidation of salicylaldehyde to salicylate using NAD(+) as a cofactor, the last reaction of the upper degradation pathway of naphthalene in Pseudomonas putida G7.	NAD	104-110	salicyladehyde dehydrogenase	Pseudomonas putida	35-39
27734991-5	2016	Nicotinamide adenine dinucleotide hydrogen phosphate-diaphorase (NADPH-d) method showed neuronal somata in the intermediolateral column (IML), central cervical nucleus (CCN), laminae I, II, III, IV, V, VI, VII, VIII and X, besides dense presence of nerve fibers in laminae II and IX.	NAD	0-33	cytochrome c oxidase subunit 8A	Homo sapiens	211-215
27469140-12	2016	Furthermore, both isoflurane treatment and overexpression of TREK1 significantly decreased NADH.	NAD	91-95	potassium two pore domain channel subfamily K member 2	Rattus norvegicus	61-66
29568346-8	2018	A structure-guided fragment growing approach was applied to the PHGDH binders from the initial screen, yielding greater understanding of the binding site and suggesting routes to achieve higher affinity NAD-competitive inhibitors.	NAD	203-206	phosphoglycerate dehydrogenase	Homo sapiens	64-69
27186719-1	2016	INTRODUCTION: Nicotinamide phosphoribosyltransferase (Nampt) is the rate-limiting enzyme that catalyzes the first step in the mammalian nicotinamide adenine dinucleotide (NAD) salvage pathway.	NAD	136-169	nicotinamide phosphoribosyltransferase	Homo sapiens	14-52
27186719-1	2016	INTRODUCTION: Nicotinamide phosphoribosyltransferase (Nampt) is the rate-limiting enzyme that catalyzes the first step in the mammalian nicotinamide adenine dinucleotide (NAD) salvage pathway.	NAD	136-169	nicotinamide phosphoribosyltransferase	Homo sapiens	54-59
27186719-1	2016	INTRODUCTION: Nicotinamide phosphoribosyltransferase (Nampt) is the rate-limiting enzyme that catalyzes the first step in the mammalian nicotinamide adenine dinucleotide (NAD) salvage pathway.	NAD	171-174	nicotinamide phosphoribosyltransferase	Homo sapiens	14-52
27186719-1	2016	INTRODUCTION: Nicotinamide phosphoribosyltransferase (Nampt) is the rate-limiting enzyme that catalyzes the first step in the mammalian nicotinamide adenine dinucleotide (NAD) salvage pathway.	NAD	171-174	nicotinamide phosphoribosyltransferase	Homo sapiens	54-59
27186719-2	2016	Aberrant NAD metabolism was associated with oncogenic signal transduction, suggesting the critical roles of Nampt in tumorigenesis and metastasis.	NAD	9-12	nicotinamide phosphoribosyltransferase	Homo sapiens	108-113
27394173-4	2016	During reverse electron transfer (RET) from NADH, purified Ogdh generated ~3-3.5x more O2( -)/H2O2 in comparison to Pdh when metabolizing 0.5-10microM NADH.	NAD	44-48	oxoglutarate dehydrogenase	Homo sapiens	59-63
27307252-2	2016	UDP-glucose dehydrogenase (UGDH) catalyzes the NAD(+)-dependent oxidation of UDP-glucose to UDP-glucuronate, an essential precursor for androgen inactivation by the prostate glucuronidation enzymes UGT2B15 and UGT2B17.	NAD	47-53	UDP-glucose 6-dehydrogenase	Homo sapiens	0-25
27307252-2	2016	UDP-glucose dehydrogenase (UGDH) catalyzes the NAD(+)-dependent oxidation of UDP-glucose to UDP-glucuronate, an essential precursor for androgen inactivation by the prostate glucuronidation enzymes UGT2B15 and UGT2B17.	NAD	47-53	UDP-glucose 6-dehydrogenase	Homo sapiens	27-31
29869077-2	2018	As the members of the nicotinamide adenine dinucleotide-dependent family of histone deacetylases, class I sirtuin genes (including SIRT1, SIRT2 and SIRT3) play crucial roles in regulating lipid metabolism, cellular growth and metabolism, suggesting that they are potential candidate genes affecting body measurement traits in animals.	NAD	22-55	sirtuin 2	Bos taurus	138-143
27435822-1	2016	Sirtuin 5 (SIRT5) is a mitochondrial-localized NAD(+)-dependent lysine desuccinylase and a major regulator of the mitochondrial succinylome.	NAD	47-53	sirtuin 5	Mus musculus	0-9
27435822-1	2016	Sirtuin 5 (SIRT5) is a mitochondrial-localized NAD(+)-dependent lysine desuccinylase and a major regulator of the mitochondrial succinylome.	NAD	47-53	sirtuin 5	Mus musculus	11-16
29470999-9	2018	More importantly, although treatment with NAD+ resulted in decreased MHC II expression on CD11c+ cells, MC-mediated CD4+ T-cell differentiation rendered mice resistant to administration of lethal doses of L monocytogenes.	NAD	42-46	integrin subunit alpha X	Homo sapiens	90-95
27107935-2	2016	17beta-estradiol and the ERbeta-selective agonist DPN, but not the ERalpha-selective agonist PPT, increased the incorporation of [methyl-(3)H]thymidine and the expression of Cyclin D2, suggesting that ERbeta mediates the proliferative effect of estrogen on PC-3 cells.	NAD	50-53	estrogen receptor 2	Homo sapiens	25-31
27107935-2	2016	17beta-estradiol and the ERbeta-selective agonist DPN, but not the ERalpha-selective agonist PPT, increased the incorporation of [methyl-(3)H]thymidine and the expression of Cyclin D2, suggesting that ERbeta mediates the proliferative effect of estrogen on PC-3 cells.	NAD	50-53	estrogen receptor 2	Homo sapiens	201-207
30546461-2	2018	Nicotinamide phosphoribosyltransferase (NAMPT), the key enzyme in the nicotinamide-adenine dinucleotide (NAD+)-mediated pathway for the activation of silent information regulator 1 (SIRT1), serves a key function in HCC cell invasion and metastasis.	NAD	70-103	nicotinamide phosphoribosyltransferase	Homo sapiens	0-38
27107935-3	2016	In addition, upregulation of Cyclin D2 and incorporation of [methyl-(3)H]thymidine induced by 17beta-estradiol and DPN were blocked by the ERbeta-selective antagonist PHTPP in PC-3 cells.	NAD	115-118	estrogen receptor 2	Homo sapiens	139-145
27404390-5	2016	During ethanol metabolism, a low NAD(+)/NADH ratio repressed NAD-dependent deacetylase sirtuin 1 (SIRT1) activity, concomitantly resulting in increased acetylated PPARgamma with high transcriptional activity.	NAD	40-44	peroxisome proliferator activated receptor gamma	Mus musculus	163-172
30546461-2	2018	Nicotinamide phosphoribosyltransferase (NAMPT), the key enzyme in the nicotinamide-adenine dinucleotide (NAD+)-mediated pathway for the activation of silent information regulator 1 (SIRT1), serves a key function in HCC cell invasion and metastasis.	NAD	70-103	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
27404390-5	2016	During ethanol metabolism, a low NAD(+)/NADH ratio repressed NAD-dependent deacetylase sirtuin 1 (SIRT1) activity, concomitantly resulting in increased acetylated PPARgamma with high transcriptional activity.	NAD	33-36	peroxisome proliferator activated receptor gamma	Mus musculus	163-172
30546461-2	2018	Nicotinamide phosphoribosyltransferase (NAMPT), the key enzyme in the nicotinamide-adenine dinucleotide (NAD+)-mediated pathway for the activation of silent information regulator 1 (SIRT1), serves a key function in HCC cell invasion and metastasis.	NAD	105-109	nicotinamide phosphoribosyltransferase	Homo sapiens	0-38
27181414-4	2016	My research and others" suggest that the SIRT1-liver kinase B1-AMPK cascade creates positive feedback through nicotinamide adenine dinucleotide synthesis to help cells cope with metabolic stress.	NAD	110-143	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	63-67
30546461-2	2018	Nicotinamide phosphoribosyltransferase (NAMPT), the key enzyme in the nicotinamide-adenine dinucleotide (NAD+)-mediated pathway for the activation of silent information regulator 1 (SIRT1), serves a key function in HCC cell invasion and metastasis.	NAD	105-109	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
30546461-7	2018	Furthermore, FK866 inhibited the SIRT1-mediated EMT, invasion and migration of HCC cells by decreasing the expression of the NAMPT/NAD+ pathway.	NAD	131-135	nicotinamide phosphoribosyltransferase	Homo sapiens	125-130
30546461-8	2018	Taken together, the results of the present study suggest that FK866 may be an effective drug targeting HCC metastasis and invasion, and that the NAMPT/NAD+/SIRT1 pathway may be a potential therapeutic target for HCC.	NAD	151-155	nicotinamide phosphoribosyltransferase	Homo sapiens	145-150
30515162-1	2018	Sirtuin 5 (SIRT5) is a member of the family of NAD+-dependent lysine/histone deacetylases.	NAD	47-50	sirtuin 5	Mus musculus	0-9
27224875-1	2016	Inhibition of nicotinamide phosphoribosyltransferase (NAMPT) has the potential to directly limit NAD production in cancer cells and is an effective strategy for cancer treatment.	NAD	97-100	nicotinamide phosphoribosyltransferase	Homo sapiens	14-52
27224875-1	2016	Inhibition of nicotinamide phosphoribosyltransferase (NAMPT) has the potential to directly limit NAD production in cancer cells and is an effective strategy for cancer treatment.	NAD	97-100	nicotinamide phosphoribosyltransferase	Homo sapiens	54-59
30515162-1	2018	Sirtuin 5 (SIRT5) is a member of the family of NAD+-dependent lysine/histone deacetylases.	NAD	47-50	sirtuin 5	Mus musculus	11-16
27274101-7	2016	Level of mitochondrial NAD- and FAD-dependent oxidative pathways is decreased, however efficiency of phosphorylation is increased after Hif3alpha siRNA treatment.	NAD	23-26	hypoxia inducible factor 3 subunit alpha	Rattus norvegicus	136-145
29549647-6	2018	Recent findings suggest an essential implication of the NAD+-producing enzyme Nmnat2 in neurodegeneration as well as maintenance of healthy axons.	NAD	56-60	nicotinamide nucleotide adenylyltransferase 2	Mus musculus	78-84
26836485-5	2016	Di-E-GSSG was a very poor substrate for glutathione reductase, but we discovered that the molecule was an excellent substrate for glutaredoxin in a coupled assay system with GSH, nicotinamide adenine dinucleotide phosphate (NADPH), and glutathione reductase or with lipoamide, NADH, and lipoamide dehydrogenase.	NAD	277-281	glutaredoxin	Homo sapiens	130-142
30405740-10	2018	MAN induced declines of both HMGB1/TLR4/p-p65 and TNF-alpha were substantially reversed by cotreatment with nicotinamide mononucleotide or NAD.	NAD	139-142	high mobility group box 1	Homo sapiens	29-34
30058122-2	2018	The nicotinamide adenine dinucleotide phosphate (NADPH) oxidase subunit 4 (NOX4), a substrate of NADPH that can generate H2 O2 reactive oxygen species, has been reported to be highly expressed in gastrointestinal tumors.	NAD	4-37	NADPH oxidase 4	Homo sapiens	75-79
26586573-3	2016	Our data show that pharmacological inhibition or knockdown of nicotinamide phosphoribosyltransferase (NAMPT), a rate-limiting enzyme in the NAD(+) salvage pathway, enhances autophagy and decreases survival of cancer cells in a p53-independent manner.	NAD	140-146	nicotinamide phosphoribosyltransferase	Homo sapiens	62-100
26586573-3	2016	Our data show that pharmacological inhibition or knockdown of nicotinamide phosphoribosyltransferase (NAMPT), a rate-limiting enzyme in the NAD(+) salvage pathway, enhances autophagy and decreases survival of cancer cells in a p53-independent manner.	NAD	140-146	nicotinamide phosphoribosyltransferase	Homo sapiens	102-107
29980616-4	2018	In the present study, cellular NAD levels were decreased by overexpression of CD38, a NAD hydrolase, or by treating cells with FK866, an inhibitor of nicotinamide phosphoribosyltransferase (NAMPT).	NAD	31-34	nicotinamide phosphoribosyltransferase	Homo sapiens	150-188
29980616-4	2018	In the present study, cellular NAD levels were decreased by overexpression of CD38, a NAD hydrolase, or by treating cells with FK866, an inhibitor of nicotinamide phosphoribosyltransferase (NAMPT).	NAD	31-34	nicotinamide phosphoribosyltransferase	Homo sapiens	190-195
30148963-2	2018	Aberrantly increased NNMT activity results in the depletion of SAM, nicotinamide (NAM), and nicotinamide adenine dinucleotide (NAD+); NAM is required for NAD+ biosynthesis.	NAD	92-125	nicotinamide N-methyltransferase	Homo sapiens	21-25
26982719-0	2016	PGC1alpha drives NAD biosynthesis linking oxidative metabolism to renal protection.	NAD	17-20	peroxisome proliferative activated receptor, gamma, coactivator 1 alpha	Mus musculus	0-9
26982719-3	2016	Here we show that the mitochondrial biogenesis regulator, PGC1alpha, is a pivotal determinant of renal recovery from injury by regulating nicotinamide adenine dinucleotide (NAD) biosynthesis.	NAD	138-171	peroxisome proliferative activated receptor, gamma, coactivator 1 alpha	Mus musculus	58-67
26982719-3	2016	Here we show that the mitochondrial biogenesis regulator, PGC1alpha, is a pivotal determinant of renal recovery from injury by regulating nicotinamide adenine dinucleotide (NAD) biosynthesis.	NAD	173-176	peroxisome proliferative activated receptor, gamma, coactivator 1 alpha	Mus musculus	58-67
26982719-7	2016	PGC1alpha coordinately upregulates the enzymes that synthesize NAD de novo from amino acids whereas PGC1alpha deficiency or AKI attenuates the de novo pathway.	NAD	63-66	peroxisome proliferative activated receptor, gamma, coactivator 1 alpha	Mus musculus	0-9
26982719-12	2016	Given the importance of mitochondrial health in ageing and the function of metabolically active organs, the results implicate NAM and NAD as key effectors for achieving PGC1alpha-dependent stress resistance.	NAD	134-137	peroxisome proliferative activated receptor, gamma, coactivator 1 alpha	Mus musculus	169-178
30148963-2	2018	Aberrantly increased NNMT activity results in the depletion of SAM, nicotinamide (NAM), and nicotinamide adenine dinucleotide (NAD+); NAM is required for NAD+ biosynthesis.	NAD	127-131	nicotinamide N-methyltransferase	Homo sapiens	21-25
30148963-2	2018	Aberrantly increased NNMT activity results in the depletion of SAM, nicotinamide (NAM), and nicotinamide adenine dinucleotide (NAD+); NAM is required for NAD+ biosynthesis.	NAD	154-158	nicotinamide N-methyltransferase	Homo sapiens	21-25
30148963-5	2018	Because of its impact on epigenetic states and NAD+ levels, NNMT is implicated in cancer, neurodegenerative diseases, and metabolic diseases, making it an appealing target for therapeutic intervention.	NAD	47-51	nicotinamide N-methyltransferase	Homo sapiens	60-64
30252897-10	2018	Incubation of ADH with NAD+ or NADH prevented inhibition of the enzyme by H2O2 or DEA/NO.	NAD	23-27	alcohol dehydrogenase 1	Arabidopsis thaliana	14-17
26769382-3	2016	Using different pharmacological and knockout mice models, we demonstrated that lactate regulates Fgf21 expression through a NADH/NAD-independent pathway, but requires active p38-MAPK (mitogen activated protein kinase) signalling.	NAD	124-128	fibroblast growth factor 21	Mus musculus	97-102
26769382-3	2016	Using different pharmacological and knockout mice models, we demonstrated that lactate regulates Fgf21 expression through a NADH/NAD-independent pathway, but requires active p38-MAPK (mitogen activated protein kinase) signalling.	NAD	124-127	fibroblast growth factor 21	Mus musculus	97-102
26742628-5	2016	Furthermore, the ERalpha-selective agonist PPT selectively increased the expression of ERbeta and the ERbeta-selective agonist DPN increased ERalpha levels.	NAD	127-130	estrogen receptor 2	Homo sapiens	102-108
30252897-10	2018	Incubation of ADH with NAD+ or NADH prevented inhibition of the enzyme by H2O2 or DEA/NO.	NAD	31-35	alcohol dehydrogenase 1	Arabidopsis thaliana	14-17
29663373-2	2018	NAMPT (nicotinamide phosphoribosyl transferase), which catalyzes the rate-limiting step in the NAD+ salvage pathway, increases during in vitro osteogenic differentiation and inhibits RANKL-induced osteoclast differentiation.	NAD	95-99	TNF superfamily member 11	Rattus norvegicus	183-188
26891996-5	2016	In astrocytes, 2.5-20 nM 17beta-estradiol (E2) or 10 nM DPN (ERbeta agonist) not 10 nM PPT (ERalpha agonist), significantly increased GFAP expression.	NAD	56-59	estrogen receptor 2 (beta)	Mus musculus	61-67
29884622-0	2018	Two-step mechanism and step-arrest mutants of Runella slithyformis NAD+-dependent tRNA 2"-phosphotransferase Tpt1.	NAD	67-71	tRNA 2'-phosphotransferase	Saccharomyces cerevisiae S288C	109-113
26620563-4	2016	Furthermore, CerS1, -2, and -6 are hyperacetylated in the mitochondria of SIRT3-null mice, and SIRT3 directly deacetylates the ceramide synthases in a NAD(+)-dependent manner that increases enzyme activity.	NAD	151-157	ceramide synthase 1	Mus musculus	13-18
29636359-3	2018	Alteration in mitochondrial function resulted in strengthened NAD+ metabolism, here considered as a key mechanism of chemoresistance, particularly, of succinate dehydrogenase subunit B (SDHB)-mutated cluster I PCPGs via the PARP1/BER DNA repair pathway.	NAD	62-66	succinate dehydrogenase complex, subunit B, iron sulfur (Ip)	Mus musculus	151-184
26658104-3	2016	Recently, we demonstrated that CD73 enables the utilization of extracellular NAD+/nicotinamide mononucleotide (NMN) by converting them to Nicotinamide riboside (NR), which can cross the plasmamembrane and fuel intracellular NAD+ biosynthesis in human cells.	NAD	77-81	5'-nucleotidase ecto	Homo sapiens	31-35
26658104-3	2016	Recently, we demonstrated that CD73 enables the utilization of extracellular NAD+/nicotinamide mononucleotide (NMN) by converting them to Nicotinamide riboside (NR), which can cross the plasmamembrane and fuel intracellular NAD+ biosynthesis in human cells.	NAD	224-228	5'-nucleotidase ecto	Homo sapiens	31-35
28097126-2	2016	Nicotinamide phosphoribosyltransferase (NAMPT) is a rate-limiting enzyme in the biosynthesis of nicotinamide adenine dinucleotide and has a crucial role in cancer cell metabolism.	NAD	96-129	nicotinamide phosphoribosyltransferase	Homo sapiens	0-38
28097126-2	2016	Nicotinamide phosphoribosyltransferase (NAMPT) is a rate-limiting enzyme in the biosynthesis of nicotinamide adenine dinucleotide and has a crucial role in cancer cell metabolism.	NAD	96-129	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
26574954-5	2016	RESULTS: SIRT1, SIRT3, SIRT5, NAMPT, NMNAT2, NMNAT3, and NRK1 expressions were significantly down-regulated and the activity of main cellular NAD(+) consumers, PARPs, trended to be higher in the SAT of heavier co-twins of body mass index-discordant pairs.	NAD	142-148	sirtuin 5	Homo sapiens	23-28
29636359-3	2018	Alteration in mitochondrial function resulted in strengthened NAD+ metabolism, here considered as a key mechanism of chemoresistance, particularly, of succinate dehydrogenase subunit B (SDHB)-mutated cluster I PCPGs via the PARP1/BER DNA repair pathway.	NAD	62-66	succinate dehydrogenase complex, subunit B, iron sulfur (Ip)	Mus musculus	186-190
30038627-6	2018	Injection of the ARTC2.2-blocking nanobody s+16a 30 min prior to organ harvesting effectively prevented ADP-ribosylation of P2X7 during cell preparation and thereby prevented NAD-induced cell death of the isolated Trm upon subsequent incubation at 37 C. Consequently, preserving Trm vitality by s+16a injection enabled a highly sensitive in vitro cytokine expression profile analyses of FACS sorted liver Trm.	NAD	175-178	ADP-ribosyltransferase 2a	Mus musculus	17-22
30038627-6	2018	Injection of the ARTC2.2-blocking nanobody s+16a 30 min prior to organ harvesting effectively prevented ADP-ribosylation of P2X7 during cell preparation and thereby prevented NAD-induced cell death of the isolated Trm upon subsequent incubation at 37 C. Consequently, preserving Trm vitality by s+16a injection enabled a highly sensitive in vitro cytokine expression profile analyses of FACS sorted liver Trm.	NAD	175-178	acyl-CoA synthetase long-chain family member 1	Mus musculus	387-391
26574954-5	2016	RESULTS: SIRT1, SIRT3, SIRT5, NAMPT, NMNAT2, NMNAT3, and NRK1 expressions were significantly down-regulated and the activity of main cellular NAD(+) consumers, PARPs, trended to be higher in the SAT of heavier co-twins of body mass index-discordant pairs.	NAD	142-148	nicotinamide phosphoribosyltransferase	Homo sapiens	30-35
29294080-3	2018	We have previously found that cancer cells preferentially utilize cytosolic NADH supplied by aldehyde dehydrogenase (ALDH) for ATP production through oxidative phosphorylation (OxPhos).	NAD	76-80	aldehyde dehydrogenase family 3, subfamily A1	Mus musculus	93-115
26574954-5	2016	RESULTS: SIRT1, SIRT3, SIRT5, NAMPT, NMNAT2, NMNAT3, and NRK1 expressions were significantly down-regulated and the activity of main cellular NAD(+) consumers, PARPs, trended to be higher in the SAT of heavier co-twins of body mass index-discordant pairs.	NAD	142-148	nicotinamide nucleotide adenylyltransferase 3	Homo sapiens	45-51
29294080-3	2018	We have previously found that cancer cells preferentially utilize cytosolic NADH supplied by aldehyde dehydrogenase (ALDH) for ATP production through oxidative phosphorylation (OxPhos).	NAD	76-80	aldehyde dehydrogenase family 3, subfamily A1	Mus musculus	117-121
25384549-0	2016	NaDC3 Induces Premature Cellular Senescence by Promoting Transport of Krebs Cycle Intermediates, Increasing NADH, and Exacerbating Oxidative Damage.	NAD	108-112	solute carrier family 13 member 3	Homo sapiens	0-5
29678570-6	2018	However, adenoviral delivery of NRK1 in these diet- and age-induced mice elevates hepatic NAD+ levels, reduces hepatic steatosis, and improves glucose tolerance and insulin sensitivity.	NAD	90-94	nicotinamide riboside kinase 1	Mus musculus	32-36
29477240-3	2018	SIRT1 encodes an NAD-dependent deacetylase that modifies the activity of key transcriptional regulators affected in diabetic kidneys, including NF-kappaB, STAT3, p53, FOXO4, and PGC1-alpha.	NAD	17-20	peroxisome proliferative activated receptor, gamma, coactivator 1 alpha	Mus musculus	178-188
29650151-1	2018	The flavoprotein l-aspartate oxidase (LASPO) is the first enzyme of the de novo biosynthetic pathway of NAD+ in plants.	NAD	104-108	L-aspartate oxidase	Arabidopsis thaliana	17-36
27386154-3	2016	One of these is visfatin, a nicotinamide phosphoribosyltransferase involved in nicotinamide dinucleotide synthesis, which is known to participate in the synthesis of insulin by pancreatic beta cells.	NAD	79-104	nicotinamide phosphoribosyltransferase	Homo sapiens	16-24
29650151-1	2018	The flavoprotein l-aspartate oxidase (LASPO) is the first enzyme of the de novo biosynthetic pathway of NAD+ in plants.	NAD	104-108	L-aspartate oxidase	Arabidopsis thaliana	38-43
26611738-5	2015	Cells transfected with b5R exhibited significantly higher levels of the NAD(+)/NADH ratio, consistent with increased levels of b5R activity.	NAD	72-78	cytochrome b5 reductase 3	Homo sapiens	23-26
29650151-2	2018	Although LASPO is considered pivotal to maintain NAD+ homeostasis, it has not been hitherto characterized in plants.	NAD	49-53	L-aspartate oxidase	Arabidopsis thaliana	9-14
26611738-5	2015	Cells transfected with b5R exhibited significantly higher levels of the NAD(+)/NADH ratio, consistent with increased levels of b5R activity.	NAD	79-83	cytochrome b5 reductase 3	Homo sapiens	23-26
29650151-7	2018	LASPO optimal pH and temperature, as well as plastidial pyridine nucleotide concentrations may contribute to an increased NAD+ production in planta.	NAD	122-126	L-aspartate oxidase	Arabidopsis thaliana	0-5
29650151-8	2018	Moreover, in Arabidopsis thaliana AtLASPO gene expression exhibited a clear correlation between LASPO activity and NAD+ levels, thus demonstrating that plant LASPO catalyzes a key metabolic step of NAD+ synthesis.	NAD	115-119	L-aspartate oxidase	Arabidopsis thaliana	36-41
29650151-8	2018	Moreover, in Arabidopsis thaliana AtLASPO gene expression exhibited a clear correlation between LASPO activity and NAD+ levels, thus demonstrating that plant LASPO catalyzes a key metabolic step of NAD+ synthesis.	NAD	115-119	L-aspartate oxidase	Arabidopsis thaliana	96-101
29650151-8	2018	Moreover, in Arabidopsis thaliana AtLASPO gene expression exhibited a clear correlation between LASPO activity and NAD+ levels, thus demonstrating that plant LASPO catalyzes a key metabolic step of NAD+ synthesis.	NAD	198-202	L-aspartate oxidase	Arabidopsis thaliana	36-41
29650151-8	2018	Moreover, in Arabidopsis thaliana AtLASPO gene expression exhibited a clear correlation between LASPO activity and NAD+ levels, thus demonstrating that plant LASPO catalyzes a key metabolic step of NAD+ synthesis.	NAD	198-202	L-aspartate oxidase	Arabidopsis thaliana	96-101
29868045-3	2018	However, mitochondrial counterparts are NAD-dependent proteins (mNAD-ME) lacking OAD activity, which can be structured as homo- and hetero-oligomers of two different subunits.	NAD	40-43	malic enzyme 2, NAD(+)-dependent, mitochondrial	Mus musculus	64-71
29550483-9	2018	GR24 upregulated SIRT1 and enhanced the production of NAD+, an essential SIRT1 substrate.	NAD	54-58	taste receptor, type 2, member 124	Mus musculus	0-4
29642888-3	2018	RESULTS: A new metabolic module was established here, in which, permease Gap1p for L-phenylalanine transportation, catalytic enzymes Aro8p, Aro10p and Adh2p in Ehrlich pathway respectively responsible for transamination, decarboxylation and reduction were assembled, besides, glutamate dehydrogenase Gdh2p was harbored for re-supplying another substrate 2-oxoglutarate, relieving product glutamate repression and regenerating cofactor NADH.	NAD	435-439	phenylpyruvate decarboxylase ARO10	Saccharomyces cerevisiae S288C	140-146
29721178-2	2018	Nicotinamide phosphoribosyltransferase (NAMPT) is a key enzyme in NAD biosynthesis.	NAD	66-69	nicotinamide phosphoribosyltransferase	Homo sapiens	0-38
29721178-2	2018	Nicotinamide phosphoribosyltransferase (NAMPT) is a key enzyme in NAD biosynthesis.	NAD	66-69	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
28514875-1	2018	Nicotinamide Phosphoribosyltransferase (NAMPT) is a rate-limiting enzyme in the biosynthesis of NAD.	NAD	96-99	nicotinamide phosphoribosyltransferase	Homo sapiens	0-38
28514875-1	2018	Nicotinamide Phosphoribosyltransferase (NAMPT) is a rate-limiting enzyme in the biosynthesis of NAD.	NAD	96-99	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
28514875-3	2018	The perturbation of these intracellular processes is more sensitive and highly dependent on NAMPT to maintain the required NAD levels.	NAD	123-126	nicotinamide phosphoribosyltransferase	Homo sapiens	92-97
29442983-11	2018	Furthermore, when the strains were exposed to formaldehyde stress, NADH levels increased for strains overexpressing ALD6 and decreased for dominant negative strains.	NAD	67-71	aldehyde dehydrogenase (NADP(+)) ALD6	Saccharomyces cerevisiae S288C	116-120
29494135-3	2018	To easily assay it in the direction of l-serine synthesis, it can be coupled to the next enzyme in the pathway, phosphoserine aminotransferase (PSAT), with the activity monitored by the conversion of NAD+ to NADH by PGDH.	NAD	200-204	phosphoserine aminotransferase 1	Homo sapiens	112-142
29494135-3	2018	To easily assay it in the direction of l-serine synthesis, it can be coupled to the next enzyme in the pathway, phosphoserine aminotransferase (PSAT), with the activity monitored by the conversion of NAD+ to NADH by PGDH.	NAD	200-204	phosphoserine aminotransferase 1	Homo sapiens	144-148
29494135-3	2018	To easily assay it in the direction of l-serine synthesis, it can be coupled to the next enzyme in the pathway, phosphoserine aminotransferase (PSAT), with the activity monitored by the conversion of NAD+ to NADH by PGDH.	NAD	200-204	phosphoglycerate dehydrogenase	Homo sapiens	216-220
29494135-3	2018	To easily assay it in the direction of l-serine synthesis, it can be coupled to the next enzyme in the pathway, phosphoserine aminotransferase (PSAT), with the activity monitored by the conversion of NAD+ to NADH by PGDH.	NAD	208-212	phosphoserine aminotransferase 1	Homo sapiens	112-142
29494135-3	2018	To easily assay it in the direction of l-serine synthesis, it can be coupled to the next enzyme in the pathway, phosphoserine aminotransferase (PSAT), with the activity monitored by the conversion of NAD+ to NADH by PGDH.	NAD	208-212	phosphoserine aminotransferase 1	Homo sapiens	144-148
29494135-3	2018	To easily assay it in the direction of l-serine synthesis, it can be coupled to the next enzyme in the pathway, phosphoserine aminotransferase (PSAT), with the activity monitored by the conversion of NAD+ to NADH by PGDH.	NAD	208-212	phosphoglycerate dehydrogenase	Homo sapiens	216-220
29494135-4	2018	However, when PGDHs from several different species were coupled to PSAT, it was found that one of them, ecPGDH, conserves the coenzyme in the production of l-serine by utilizing an intrinsic cycle of NAD+/NADH interconversion coupled with the conversion of alpha-ketoglutarate (alphaKG) to alpha-hydroxyglutarate.	NAD	200-204	phosphoserine aminotransferase 1	Homo sapiens	67-71
29494135-4	2018	However, when PGDHs from several different species were coupled to PSAT, it was found that one of them, ecPGDH, conserves the coenzyme in the production of l-serine by utilizing an intrinsic cycle of NAD+/NADH interconversion coupled with the conversion of alpha-ketoglutarate (alphaKG) to alpha-hydroxyglutarate.	NAD	205-209	phosphoserine aminotransferase 1	Homo sapiens	67-71
29514063-3	2018	Three protein deacylases, SIRT3, SIRT4, and SIRT5, reside in the mitochondria and remove these modifications from targeted proteins in an NAD+-dependent manner.	NAD	138-142	sirtuin 5	Homo sapiens	44-49
29341930-7	2018	In PC-3 cells, ERbeta-selective agonist DPN decreased the expression of N-cadherin.	NAD	40-43	estrogen receptor 2	Homo sapiens	15-21
29341930-8	2018	DPN-induced downregulation of N-cadherin was blocked by pretreatment with the ERbeta-selective antagonist (PHTPP), indicating that ERbeta1 is the upstream receptor regulating the expression of N-cadherin.	NAD	0-3	estrogen receptor 2	Homo sapiens	78-84
29309612-8	2018	Conversely, treatment with BRAFi or MEK inhibitors decreased NAMPT expression and cellular NAD levels.	NAD	91-94	midkine	Mus musculus	36-39
28904384-5	2018	NAMPT is a rate-limiting enzyme in the salvage biosynthesis pathway of nicotinamide adenine dinucleotide (NAD) that plays a vital role in energy metabolism.	NAD	71-104	nicotinamide phosphoribosyltransferase	Homo sapiens	0-5
28904384-5	2018	NAMPT is a rate-limiting enzyme in the salvage biosynthesis pathway of nicotinamide adenine dinucleotide (NAD) that plays a vital role in energy metabolism.	NAD	106-109	nicotinamide phosphoribosyltransferase	Homo sapiens	0-5
28904384-9	2018	Moreover, we have found that the extreme susceptibility of B-ALL cells to NAMPT inhibition is related to the reduced cellular NAD+ reserve.	NAD	126-130	nicotinamide phosphoribosyltransferase	Homo sapiens	74-79
29309995-6	2018	17beta-estradiol, G-1, PPT, or ERbeta agonist DPN was infused directly into the medial amygdala of ovariectomized female mice.	NAD	46-49	estrogen receptor 2 (beta)	Mus musculus	31-37
29463777-6	2018	Overexpression of NT5C3A increased the abundance of NAD+ and the activation of the sirtuins SIRT1 and SIRT6, which are NAD+-dependent deacetylases.	NAD	52-56	5'-nucleotidase, cytosolic IIIA	Homo sapiens	18-24
29463777-6	2018	Overexpression of NT5C3A increased the abundance of NAD+ and the activation of the sirtuins SIRT1 and SIRT6, which are NAD+-dependent deacetylases.	NAD	52-55	5'-nucleotidase, cytosolic IIIA	Homo sapiens	18-24
28976891-1	2018	The mitochondrial F1FO-ATPase is uncompetitively inhibited by NAD+ only when the natural cofactor Mg2+ is replaced by Ca2+, a mode putatively involved in cell death.	NAD	62-66	mucin 7, secreted	Homo sapiens	98-101
29416562-9	2018	Additional deletion of GPD2, which encodes an isoenzyme of NAD+-dependent glycerol-3-phosphate dehydrogenase, combined with overexpression of the structural genes for enzymes of the non-oxidative pentose-phosphate pathway, yielded a CO2-reducing strain that grew at the same rate as a non-engineered reference strain in anaerobic bioreactor batch cultures, while exhibiting a 86% lower glycerol yield and a 15% higher ethanol yield.	NAD	59-63	glycerol-3-phosphate dehydrogenase	Saccharomyces cerevisiae S288C	74-108
26470683-5	2015	Furthermore, the coexpression of S. cerevisiae ZWF1 and ACS1 genes in the DWM strain increased intracellular concentrations of NADPH and NADH and improved maximum xylitol productivity by 17%, relative to that for the DWM strain.	NAD	137-141	acetate--CoA ligase 1	Saccharomyces cerevisiae S288C	56-60
26542945-1	2015	BACKGROUND: Nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme in NAD(+) biosynthesis from nicotinamide, is one of the major factors regulating cancer cells metabolism and is considered a promising target for treating cancer.	NAD	88-94	nicotinamide phosphoribosyltransferase	Homo sapiens	12-50
26542945-1	2015	BACKGROUND: Nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme in NAD(+) biosynthesis from nicotinamide, is one of the major factors regulating cancer cells metabolism and is considered a promising target for treating cancer.	NAD	88-94	nicotinamide phosphoribosyltransferase	Homo sapiens	52-57
26542945-2	2015	The prototypical NAMPT inhibitor FK866 effectively lowers NAD(+) levels in cancer cells, reducing the activity of NAD(+)-dependent enzymes, lowering intracellular ATP, and promoting cell death.	NAD	58-64	nicotinamide phosphoribosyltransferase	Homo sapiens	17-22
26542945-2	2015	The prototypical NAMPT inhibitor FK866 effectively lowers NAD(+) levels in cancer cells, reducing the activity of NAD(+)-dependent enzymes, lowering intracellular ATP, and promoting cell death.	NAD	114-120	nicotinamide phosphoribosyltransferase	Homo sapiens	17-22
26542945-6	2015	Jurkat cells in which AMPK or LKB1 expression was silenced or in which a non-phosphorylatable EIF2A mutant was ectopically expressed showed enhanced sensitivity to the NAMPT inhibitor, confirming a key role for the LKB1-AMPK-EIF2A axis in cell fate determination in response to energetic stress via NAD(+) depletion.	NAD	299-305	nicotinamide phosphoribosyltransferase	Homo sapiens	168-173
26358657-1	2015	High plasma levels of nicotinamide phosphoribosyltransferase (NAMPT), traditionally considered an intracellular enzyme with a key role in NAD synthesis, have been reported in several oncological, inflammatory and metabolic diseases.	NAD	138-141	nicotinamide phosphoribosyltransferase	Homo sapiens	22-60
26358657-1	2015	High plasma levels of nicotinamide phosphoribosyltransferase (NAMPT), traditionally considered an intracellular enzyme with a key role in NAD synthesis, have been reported in several oncological, inflammatory and metabolic diseases.	NAD	138-141	nicotinamide phosphoribosyltransferase	Homo sapiens	62-67
25850461-1	2015	Nicotinamide phosphoribosyltransferase (NAMPT) is a rate limiting enzyme that plays an important role in the synthesis of nicotinamide adenine dinucleotide (NAD) via a salvage pathway.	NAD	122-155	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
25850461-1	2015	Nicotinamide phosphoribosyltransferase (NAMPT) is a rate limiting enzyme that plays an important role in the synthesis of nicotinamide adenine dinucleotide (NAD) via a salvage pathway.	NAD	157-160	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
25850461-2	2015	Along with a role in bioenergetics, NAMPT regulates the activity of proteins such as SIRT-1 that utilize NAD as a cofactor.	NAD	105-108	nicotinamide phosphoribosyltransferase	Homo sapiens	36-41
25850461-3	2015	As NAD metabolism is usually high in diseased conditions, it has been hypothesized and proven that NAMPT is over expressed in various cancers and inflammatory disorders.	NAD	3-6	nicotinamide phosphoribosyltransferase	Homo sapiens	99-104
29191657-5	2018	Furthermore, we showed that miR-761 putatively targeted three proteins, thyroid hormone receptor interactor 6 (TRIP6), lamin A/C (LMNA), and NAD-dependent protein deacetylase sirtuin-3 (SIRT3).	NAD	141-144	microRNA 761	Homo sapiens	28-35
29074724-3	2018	We demonstrate here that glucose deprivation or hypoxia results in the AMPK-mediated phosphorylation of phosphoribosyl pyrophosphate synthetase 1 (PRPS1) S180 and PRPS2 S183, leading to conversion of PRPS hexamers to monomers and thereby inhibiting PRPS1/2 activity, nucleotide synthesis, and nicotinamide adenine dinucleotide (NAD) production.	NAD	293-326	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	71-75
29074724-3	2018	We demonstrate here that glucose deprivation or hypoxia results in the AMPK-mediated phosphorylation of phosphoribosyl pyrophosphate synthetase 1 (PRPS1) S180 and PRPS2 S183, leading to conversion of PRPS hexamers to monomers and thereby inhibiting PRPS1/2 activity, nucleotide synthesis, and nicotinamide adenine dinucleotide (NAD) production.	NAD	328-331	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	71-75
29074724-6	2018	Our findings highlight the significance of recalibrating tumor cell metabolism by fine-tuning nucleotide and NAD synthesis in tumor growth.Significance: Our findings elucidate an instrumental function of AMPK in direct regulation of nucleic acid and NAD synthesis in tumor cells in response to energy stress.	NAD	109-112	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	204-208
29074724-6	2018	Our findings highlight the significance of recalibrating tumor cell metabolism by fine-tuning nucleotide and NAD synthesis in tumor growth.Significance: Our findings elucidate an instrumental function of AMPK in direct regulation of nucleic acid and NAD synthesis in tumor cells in response to energy stress.	NAD	250-253	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	204-208
29074724-7	2018	AMPK phosphorylates PRPS1/2, converts PRPS1/2 hexamers to monomers, and inhibits PRPS1/2 activity and subsequent nucleotide and NAD synthesis to maintain tumor cell growth and survival.	NAD	128-131	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	0-4
29275294-2	2018	2,3-Bis(4-hydroxyphenyl)-propionitrile (DPN) is a specific ERbeta agonist; the effects of neonatal DPN exposure on PF induction and gene expression in the mouse ovary were examined.	NAD	40-43	estrogen receptor 2 (beta)	Mus musculus	59-65
26089537-3	2015	BPZE1-DC induces CD4(+) and CD8(+) T lymphocytes to express 2 sets of ectoenzymes generating ADO: 1 set is part of the conventional CD39/CD73 pathway, which uses ATP as substrate, whereas the other is part of the CD38/CD203a/CD73 pathway and metabolizes NAD(+).	NAD	254-260	2-aminoethanethiol (cysteamine) dioxygenase	Mus musculus	93-96
25288139-6	2015	Specifically, deacetylation of histone 3 at lysine 9 (H3K9), through the coordinated action of the NAD+-dependent protein deacetylase sirtuin-6 (SIRT6) and nuclear factor kappa B (NFkappaB), sequesters GR expression leading to disinhibition of CRF.	NAD	99-103	sirtuin 6	Homo sapiens	134-143
25288139-6	2015	Specifically, deacetylation of histone 3 at lysine 9 (H3K9), through the coordinated action of the NAD+-dependent protein deacetylase sirtuin-6 (SIRT6) and nuclear factor kappa B (NFkappaB), sequesters GR expression leading to disinhibition of CRF.	NAD	99-103	sirtuin 6	Homo sapiens	145-150
29275294-5	2018	The gene expression of growth differentiation factor 9 (Gdf9), Mullerian-inhibiting substance, steroidogenic factor 1 (Sf1) and steroidogenic acute regulatory protein (Star) in the ovary was significantly increased in the mice neonatally exposed to 40 mug DPN compared to oil-treated mice.	NAD	256-259	splicing factor 1	Mus musculus	63-122
29275294-6	2018	CONCLUSION: Since SF1 is an important transcription factor of several genes involved in ovarian function, up-regulation of Sf1 expression by neonatal exposure to DPN, through ERbeta, might affect expression of Gdf9, Mis and Star, resulting in increased PFs in mouse ovary.	NAD	162-165	splicing factor 1	Mus musculus	18-21
29275294-6	2018	CONCLUSION: Since SF1 is an important transcription factor of several genes involved in ovarian function, up-regulation of Sf1 expression by neonatal exposure to DPN, through ERbeta, might affect expression of Gdf9, Mis and Star, resulting in increased PFs in mouse ovary.	NAD	162-165	splicing factor 1	Mus musculus	123-126
29275294-6	2018	CONCLUSION: Since SF1 is an important transcription factor of several genes involved in ovarian function, up-regulation of Sf1 expression by neonatal exposure to DPN, through ERbeta, might affect expression of Gdf9, Mis and Star, resulting in increased PFs in mouse ovary.	NAD	162-165	estrogen receptor 2 (beta)	Mus musculus	175-181
25952905-10	2015	Overall, these findings suggest that hepatic glycerol synthesis is cytosolic NADH/NAD(+) ratio-dependent and reveal a likely regulatory mechanism for hepatic glycerol synthesis following a high carbohydrate load in citrin-deficient patients.	NAD	77-81	solute carrier family 25 member 13	Homo sapiens	215-221
29275294-6	2018	CONCLUSION: Since SF1 is an important transcription factor of several genes involved in ovarian function, up-regulation of Sf1 expression by neonatal exposure to DPN, through ERbeta, might affect expression of Gdf9, Mis and Star, resulting in increased PFs in mouse ovary.	NAD	162-165	anti-Mullerian hormone	Mus musculus	216-219
25952905-10	2015	Overall, these findings suggest that hepatic glycerol synthesis is cytosolic NADH/NAD(+) ratio-dependent and reveal a likely regulatory mechanism for hepatic glycerol synthesis following a high carbohydrate load in citrin-deficient patients.	NAD	82-88	solute carrier family 25 member 13	Homo sapiens	215-221
28820953-3	2018	The current method for assaying ALDOA activity involves monitoring the consumption of NADH in vitro using absorbance or intrinsic fluorescence via a coupled enzymatic reaction.	NAD	86-90	aldolase, fructose-bisphosphate A	Homo sapiens	32-37
28820953-9	2018	In conclusion, we demonstrate that a traditional ALDOA assay can be transformed readily into a fluorescence-based assay utilizing a commercial NADH detection kit that is rapid, sensitive, inexpensive, and HTS friendly.	NAD	143-147	aldolase, fructose-bisphosphate A	Homo sapiens	49-54
26067270-1	2015	C3 exoenzyme is a mono-ADP-ribosyltransferase (ART) that catalyzes transfer of an ADP-ribose moiety from NAD(+) to Rho GTPases.	NAD	105-111	ADP-ribosyltransferase 3 (inactive)	Homo sapiens	18-45
28899971-4	2017	Xenograft experiments were performed to determine efficacy and in vivo mechanism.Results: Several promising candidates emerged, including the combination of small-molecule PARP and nicotinamide phosphoribosyltransferase (NAMPT) inhibitors, a rational combination as NAMPTis block the rate-limiting enzyme in the production of nicotinamide adenine dinucleotide (NAD+), a necessary substrate of PARP.	NAD	326-359	nicotinamide phosphoribosyltransferase	Homo sapiens	181-219
25908444-3	2015	SOD2 is activated by sirtuin 3 (SIRT3) through NAD(+)-dependent deacetylation.	NAD	47-53	superoxide dismutase 2	Homo sapiens	0-4
26056253-6	2015	Peritoneal CD49d(high)CD4(+) T cells were more resistant to irradiation and more sensitive to NAD-induced cell death than CD49d(low)CD4(+) T cells.	NAD	94-97	integrin alpha 4	Mus musculus	11-16
25829149-3	2015	NADH-dependent reduction of metHb in coelomic fluid suggested the coexistence of cytochrome b5 reductase (b5R) and cytochrome b5 with hemoglobin in the fluid and that these proteins were involved in physiological metHb reduction in the larvae.	NAD	0-4	cytochrome b5 reductase 3	Homo sapiens	106-109
26060246-0	2015	Regenerative Neurogenesis After Ischemic Stroke Promoted by Nicotinamide Phosphoribosyltransferase-Nicotinamide Adenine Dinucleotide Cascade.	NAD	99-132	nicotinamide phosphoribosyltransferase	Homo sapiens	60-98
26060246-2	2015	Nicotinamide phosphoribosyltransferase (Nampt) is the rate-limiting enzyme for mammalian NAD salvage synthesis and has been shown to protect against acute ischemic stroke.	NAD	89-92	nicotinamide phosphoribosyltransferase	Homo sapiens	0-38
26060246-2	2015	Nicotinamide phosphoribosyltransferase (Nampt) is the rate-limiting enzyme for mammalian NAD salvage synthesis and has been shown to protect against acute ischemic stroke.	NAD	89-92	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
26023773-3	2015	Mitotic repression of Pol I transcription correlates with transient nucleolar enrichment of the NAD(+)-dependent deacetylase SIRT1, which deacetylates another subunit of SL1, TAFI68.	NAD	96-102	DNA polymerase iota	Homo sapiens	22-27
25897714-5	2015	Here we provide a detailed kinetic and structural analysis that describes the interdependence of NAD(+)-binding and acyl-group selectivity for a diverse series of human Sirtuins, SIRT1-SIRT3 and SIRT6.	NAD	97-103	sirtuin 6	Homo sapiens	195-200
25323584-5	2015	Inhibitors of NMN-synthesising enzyme NAMPT confer robust morphological and functional protection of injured axons and synapses despite lowering NAD.	NAD	145-148	nicotinamide phosphoribosyltransferase	Homo sapiens	38-43
25757537-0	2015	Conformational Change Near the Redox Center of Dihydrolipoamide Dehydrogenase Induced by NAD(+) to Regulate the Enzyme Activity.	NAD	89-95	dihydrolipoamide dehydrogenase	Homo sapiens	47-77
25757537-1	2015	Dihydrolipoamide dehydrogenase (LipDH) transfers two electrons from dihydrolipoamide (DHL) to NAD(+) mediated by FAD.	NAD	94-100	dihydrolipoamide dehydrogenase	Homo sapiens	0-30
25603815-2	2015	By synthesizing nicotinamide adenine dinucleotide (NAD(+)), Nampt/PBEF/visfatin functions to maintain an energy supply that has critical roles in cell survival.	NAD	16-49	nicotinamide phosphoribosyltransferase	Homo sapiens	60-65
25603815-2	2015	By synthesizing nicotinamide adenine dinucleotide (NAD(+)), Nampt/PBEF/visfatin functions to maintain an energy supply that has critical roles in cell survival.	NAD	16-49	nicotinamide phosphoribosyltransferase	Homo sapiens	66-70
25603815-2	2015	By synthesizing nicotinamide adenine dinucleotide (NAD(+)), Nampt/PBEF/visfatin functions to maintain an energy supply that has critical roles in cell survival.	NAD	16-49	nicotinamide phosphoribosyltransferase	Homo sapiens	71-79
25603815-2	2015	By synthesizing nicotinamide adenine dinucleotide (NAD(+)), Nampt/PBEF/visfatin functions to maintain an energy supply that has critical roles in cell survival.	NAD	51-58	nicotinamide phosphoribosyltransferase	Homo sapiens	60-65
25603815-2	2015	By synthesizing nicotinamide adenine dinucleotide (NAD(+)), Nampt/PBEF/visfatin functions to maintain an energy supply that has critical roles in cell survival.	NAD	51-58	nicotinamide phosphoribosyltransferase	Homo sapiens	66-70
25603815-2	2015	By synthesizing nicotinamide adenine dinucleotide (NAD(+)), Nampt/PBEF/visfatin functions to maintain an energy supply that has critical roles in cell survival.	NAD	51-58	nicotinamide phosphoribosyltransferase	Homo sapiens	71-79
25652077-6	2015	This association is regulated by neuronal activity via modulation of cellular NAD/NADH levels and restrains the size of the CtBP1 pool available for nuclear import, thus contributing to the control of activity-dependent gene expression.	NAD	78-81	C-terminal binding protein 1	Homo sapiens	124-129
25652077-6	2015	This association is regulated by neuronal activity via modulation of cellular NAD/NADH levels and restrains the size of the CtBP1 pool available for nuclear import, thus contributing to the control of activity-dependent gene expression.	NAD	82-86	C-terminal binding protein 1	Homo sapiens	124-129
25876076-7	2015	This glucose effect on TNKS is mediated primarily by NAD+ since it is mirrored by the NAD+ precursor nicotinamide mononucleotide (NMN), and is blunted by the NAMPT inhibitor FK866.	NAD	53-57	nicotinamide phosphoribosyltransferase	Homo sapiens	158-163
25876076-9	2015	NAD+ flux analysis showed that glucose and nutrients, by increasing ATP, stimulate NAMPT-mediated NAD+ production to expand NAD+ stores.	NAD	0-4	nicotinamide phosphoribosyltransferase	Homo sapiens	83-88
25876076-9	2015	NAD+ flux analysis showed that glucose and nutrients, by increasing ATP, stimulate NAMPT-mediated NAD+ production to expand NAD+ stores.	NAD	98-102	nicotinamide phosphoribosyltransferase	Homo sapiens	83-88
25876076-9	2015	NAD+ flux analysis showed that glucose and nutrients, by increasing ATP, stimulate NAMPT-mediated NAD+ production to expand NAD+ stores.	NAD	98-102	nicotinamide phosphoribosyltransferase	Homo sapiens	83-88
25601988-7	2015	MeHg does not directly impair ALDH enzymatic activity, however MeHg depletes cytosolic levels of the ALDH cofactor NAD(+), which could contribute to impaired ALDH activity following exposure to MeHg.	NAD	115-121	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	101-105
28899971-4	2017	Xenograft experiments were performed to determine efficacy and in vivo mechanism.Results: Several promising candidates emerged, including the combination of small-molecule PARP and nicotinamide phosphoribosyltransferase (NAMPT) inhibitors, a rational combination as NAMPTis block the rate-limiting enzyme in the production of nicotinamide adenine dinucleotide (NAD+), a necessary substrate of PARP.	NAD	361-365	nicotinamide phosphoribosyltransferase	Homo sapiens	181-219
28806285-9	2017	Specimens were analyzed via quantitative polymerase chain reaction (qPCR) for mitochondrial DNA (mtDNA), via enzyme immunoassay for DNAse activity and via Western blot analysis for the ND6 subunit of the NADH: ubiquinone oxidoreductase, an N-formylated peptide.	NAD	204-208	mitochondrially encoded NADH dehydrogenase 6	Homo sapiens	185-188
28860121-1	2017	Nicotinamide phosphoribosyltransferase (NAMPT) and nicotinic acid phosphoribosyltransferase (NAPRT) are rate-limiting enzymes in the NAD+ synthesis pathway.	NAD	133-137	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
28860121-13	2017	In conclusion, this study identified NAMPT as a potential target for treatment of chondrosarcoma.Implications: Chondrosarcoma patients, especially those of high histologic grade with lower expression and hypermethylation of NAPRT, may benefit from inhibition of the NAD synthesis pathway.	NAD	266-269	nicotinamide phosphoribosyltransferase	Homo sapiens	37-42
29200830-9	2017	When treated with NR1, the cellular NAD+, NADPH and GSH concentrations increased, and the ratios of NAD+/NADH, NADPH/NADP+ and GSH/GSSG increased, similar to the control group.	NAD	36-40	glutamate ionotropic receptor NMDA type subunit 1	Rattus norvegicus	18-21
29200830-9	2017	When treated with NR1, the cellular NAD+, NADPH and GSH concentrations increased, and the ratios of NAD+/NADH, NADPH/NADP+ and GSH/GSSG increased, similar to the control group.	NAD	100-104	glutamate ionotropic receptor NMDA type subunit 1	Rattus norvegicus	18-21
29200830-9	2017	When treated with NR1, the cellular NAD+, NADPH and GSH concentrations increased, and the ratios of NAD+/NADH, NADPH/NADP+ and GSH/GSSG increased, similar to the control group.	NAD	105-109	glutamate ionotropic receptor NMDA type subunit 1	Rattus norvegicus	18-21
28812311-0	2017	NAD replenishment with nicotinamide mononucleotide protects blood-brain barrier integrity and attenuates delayed tissue plasminogen activator-induced haemorrhagic transformation after cerebral ischaemia.	NAD	0-3	plasminogen activator, tissue	Mus musculus	113-141
28812311-2	2017	Here, we determined whether nicotinamide mononucleotide (NMN), a key intermediate of nicotinamide adenine dinucleotide biosynthesis, affects tPA-induced haemorrhagic transformation.	NAD	85-118	plasminogen activator, tissue	Mus musculus	141-144
28631845-3	2017	Succinylation is sensitive to both increases and decreases of the NAD+ -dependent desuccinylase, SIRT5.	NAD	66-69	sirtuin 5	Homo sapiens	97-102
25541039-5	2015	SIRT5, which localizes in the mitochondrial matrix, is nicotinamide adenine dinucleotide (NAD(+))-dependent histone deacetylase.	NAD	55-88	sirtuin 5	Mus musculus	0-5
28850686-15	2017	MRNA expression of EMT markers was stimulated by ERalpha-specific agonist PPT and inhibited by ERbeta-specific agonist DPN.	NAD	119-122	estrogen receptor 2	Homo sapiens	95-101
25146190-7	2015	All these results suggest that up-regulation of Nampt play an important role in GR-extended lifespan of Hs68 cells by increasing the intracellular NAD(+) levels followed by activating SIRT1 activity in Hs68 cells.	NAD	147-153	nicotinamide phosphoribosyltransferase	Homo sapiens	48-53
25590809-1	2015	Nicotinamide phosphoribosyltransferase (NAMPT) inhibitors (e.g., FK866) target the most active pathway of NAD(+) synthesis in tumor cells, but lack tumor-selectivity for use as a single agent.	NAD	106-112	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
25590809-2	2015	Reducing NAD(+) pools by inhibiting NAMPT primed pancreatic ductal adenocarcinoma (PDA) cells for poly(ADP ribose) polymerase (PARP1)-dependent cell death induced by the targeted cancer therapeutic, beta-lapachone (beta-lap, ARQ761), independent of poly(ADP ribose) (PAR) accumulation.	NAD	9-15	nicotinamide phosphoribosyltransferase	Homo sapiens	36-41
28935892-6	2017	Changes in the NADH:NAD+ ratio regulate CtBP binding to the acetyltransferase p300, and regulate binding of p300 and the transcription factor NF-kappaB to pro-inflammatory gene promoters.	NAD	20-24	E1A binding protein p300	Homo sapiens	78-82
25404738-1	2015	We reported that NAD(+)-dependent SIRT1, RELB, and SIRT6 nuclear proteins in monocytes regulate a switch from the glycolysis-dependent acute inflammatory response to fatty acid oxidation-dependent sepsis adaptation.	NAD	17-23	sirtuin 6	Homo sapiens	51-56
28935892-6	2017	Changes in the NADH:NAD+ ratio regulate CtBP binding to the acetyltransferase p300, and regulate binding of p300 and the transcription factor NF-kappaB to pro-inflammatory gene promoters.	NAD	20-24	E1A binding protein p300	Homo sapiens	108-112
28501332-4	2017	Most importantly, combination of low concentration ATO with FK866 (a NAMPT inhibitor) exerted enhanced inhibitive effect on NAMPT protein and mRNA expressions, leading to synergistic cytotoxicity on cancer cells through increasing cell apoptosis and depleting intracellular nicotinamide adenine dinucleotide levels.	NAD	274-307	nicotinamide phosphoribosyltransferase	Homo sapiens	124-129
25529796-8	2015	Thus, the NAD(+)-dependent inhibition of SOD2 activity and ROS by SIRT1 provides a gatekeeper function to reduce PARK2-mediated mitophagy and aberrant cell survival.	NAD	10-16	superoxide dismutase 2	Homo sapiens	41-45
26558285-5	2015	Finally, low sirtuin-1 and sirtuin-3 gene expressions due to higher NADH/NAD in Cmah-null mice decreased Foxo-1 and MnSOD gene expression, suggesting that oxidative stress may result in mitochondrial dysfunction in Cmah-null mouse.	NAD	68-72	cytidine monophospho-N-acetylneuraminic acid hydroxylase	Mus musculus	215-219
26558285-5	2015	Finally, low sirtuin-1 and sirtuin-3 gene expressions due to higher NADH/NAD in Cmah-null mice decreased Foxo-1 and MnSOD gene expression, suggesting that oxidative stress may result in mitochondrial dysfunction in Cmah-null mouse.	NAD	68-71	cytidine monophospho-N-acetylneuraminic acid hydroxylase	Mus musculus	80-84
26558285-5	2015	Finally, low sirtuin-1 and sirtuin-3 gene expressions due to higher NADH/NAD in Cmah-null mice decreased Foxo-1 and MnSOD gene expression, suggesting that oxidative stress may result in mitochondrial dysfunction in Cmah-null mouse.	NAD	68-71	cytidine monophospho-N-acetylneuraminic acid hydroxylase	Mus musculus	215-219
25368373-1	2015	Nicotinamide phosphoribosyltransferase (NAMPT) is the rate-limiting enzyme in nicotinamide adenine dinucleotide biosynthesis.	NAD	78-111	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
25807436-1	2015	OBJECTIVE: SIRT6 belongs to the NAD+-dependent class III deacetylase sirtuin family.	NAD	32-36	sirtuin 6	Homo sapiens	11-16
25355314-4	2014	In all cell lines examined, NAD was rapidly depleted (average t1/2 of 8.1 h) following NAMPT inhibition.	NAD	28-31	nicotinamide phosphoribosyltransferase	Homo sapiens	87-92
25453901-3	2014	URI inhibits aryl hydrocarbon (AhR)- and estrogen receptor (ER)-mediated transcription of enzymes implicated in L-tryptophan/kynurenine/nicotinamide adenine dinucleotide (NAD(+)) metabolism, thereby causing DNA damage at early stages of tumorigenesis.	NAD	136-169	aryl hydrocarbon receptor	Homo sapiens	31-34
25453901-3	2014	URI inhibits aryl hydrocarbon (AhR)- and estrogen receptor (ER)-mediated transcription of enzymes implicated in L-tryptophan/kynurenine/nicotinamide adenine dinucleotide (NAD(+)) metabolism, thereby causing DNA damage at early stages of tumorigenesis.	NAD	171-177	aryl hydrocarbon receptor	Homo sapiens	31-34
28887543-2	2017	NAD + dependent Sirtuin 6 (SIRT6) is a glucose homeostasis regulator in animals and humans and its regulation at the molecular level is unknown.	NAD	0-5	sirtuin 6	Homo sapiens	16-25
25273830-3	2014	At Day 0.5 the gene expression level of PMA1 in AWRI R2 strain supplemented with 1.0 mg/mL PAs was decreased by around 54 % with a 50 % and a 56.5 % increase in the concentration of intracellular ATP and NADH/NAD(+) ratio, respectively, compared to that of control.	NAD	204-208	H(+)-exporting P2-type ATPase PMA1	Saccharomyces cerevisiae S288C	40-44
25273830-3	2014	At Day 0.5 the gene expression level of PMA1 in AWRI R2 strain supplemented with 1.0 mg/mL PAs was decreased by around 54 % with a 50 % and a 56.5 % increase in the concentration of intracellular ATP and NADH/NAD(+) ratio, respectively, compared to that of control.	NAD	209-215	H(+)-exporting P2-type ATPase PMA1	Saccharomyces cerevisiae S288C	40-44
25273830-4	2014	After the transient adaptation, the gene expression levels of PMA1 and HXT7 in PAs-treated cells were enhanced significantly accompanied by the decrease of ATP contents and NADH/NAD(+) ratio, which resulted in the high level of the activities of rate-limiting enzymes.	NAD	173-177	H(+)-exporting P2-type ATPase PMA1	Saccharomyces cerevisiae S288C	62-66
25273830-4	2014	After the transient adaptation, the gene expression levels of PMA1 and HXT7 in PAs-treated cells were enhanced significantly accompanied by the decrease of ATP contents and NADH/NAD(+) ratio, which resulted in the high level of the activities of rate-limiting enzymes.	NAD	173-177	hexose transporter HXT7	Saccharomyces cerevisiae S288C	71-75
25273830-4	2014	After the transient adaptation, the gene expression levels of PMA1 and HXT7 in PAs-treated cells were enhanced significantly accompanied by the decrease of ATP contents and NADH/NAD(+) ratio, which resulted in the high level of the activities of rate-limiting enzymes.	NAD	178-184	H(+)-exporting P2-type ATPase PMA1	Saccharomyces cerevisiae S288C	62-66
25273830-4	2014	After the transient adaptation, the gene expression levels of PMA1 and HXT7 in PAs-treated cells were enhanced significantly accompanied by the decrease of ATP contents and NADH/NAD(+) ratio, which resulted in the high level of the activities of rate-limiting enzymes.	NAD	178-184	hexose transporter HXT7	Saccharomyces cerevisiae S288C	71-75
25145669-0	2014	Synergy between the NAMPT inhibitor GMX1777(8) and pemetrexed in non-small cell lung cancer cells is mediated by PARP activation and enhanced NAD consumption.	NAD	142-145	nicotinamide phosphoribosyltransferase	Homo sapiens	20-25
28887543-2	2017	NAD + dependent Sirtuin 6 (SIRT6) is a glucose homeostasis regulator in animals and humans and its regulation at the molecular level is unknown.	NAD	0-5	sirtuin 6	Homo sapiens	27-32
28870901-1	2017	BACKGROUND/AIM: Nicotinamide phosphoribosyl transferase (Nampt) catalyses the rate-limiting step of the mammalian nicotinamide adenine dinucleotide (NAD) salvage pathway.	NAD	114-147	nicotinamide phosphoribosyltransferase	Homo sapiens	16-55
25145669-1	2014	GMX1778 and its prodrug GMX1777 represent a new class of cancer drugs that targets nicotinamide phosphoribosyltransferase (NAMPT) as a new strategy to interfere with biosynthesis of the key enzymatic cofactor NAD, which is critical for a number of cell functions, including DNA repair.	NAD	209-212	nicotinamide phosphoribosyltransferase	Homo sapiens	83-121
25145669-1	2014	GMX1778 and its prodrug GMX1777 represent a new class of cancer drugs that targets nicotinamide phosphoribosyltransferase (NAMPT) as a new strategy to interfere with biosynthesis of the key enzymatic cofactor NAD, which is critical for a number of cell functions, including DNA repair.	NAD	209-212	nicotinamide phosphoribosyltransferase	Homo sapiens	123-128
28870901-1	2017	BACKGROUND/AIM: Nicotinamide phosphoribosyl transferase (Nampt) catalyses the rate-limiting step of the mammalian nicotinamide adenine dinucleotide (NAD) salvage pathway.	NAD	114-147	nicotinamide phosphoribosyltransferase	Homo sapiens	57-62
25285661-1	2014	Inhibiting NAD biosynthesis by blocking the function of nicotinamide phosphoribosyl transferase (NAMPT) is an attractive therapeutic strategy for targeting tumor metabolism.	NAD	11-14	nicotinamide phosphoribosyltransferase	Homo sapiens	56-95
28870901-1	2017	BACKGROUND/AIM: Nicotinamide phosphoribosyl transferase (Nampt) catalyses the rate-limiting step of the mammalian nicotinamide adenine dinucleotide (NAD) salvage pathway.	NAD	149-152	nicotinamide phosphoribosyltransferase	Homo sapiens	16-55
25285661-1	2014	Inhibiting NAD biosynthesis by blocking the function of nicotinamide phosphoribosyl transferase (NAMPT) is an attractive therapeutic strategy for targeting tumor metabolism.	NAD	11-14	nicotinamide phosphoribosyltransferase	Homo sapiens	97-102
28870901-1	2017	BACKGROUND/AIM: Nicotinamide phosphoribosyl transferase (Nampt) catalyses the rate-limiting step of the mammalian nicotinamide adenine dinucleotide (NAD) salvage pathway.	NAD	149-152	nicotinamide phosphoribosyltransferase	Homo sapiens	57-62
28714034-2	2017	In eukaryotic cells, cellular NAD is mainly generated by the scavenge pathway in which nicotinamide phosphoribosyltransferase (NAMPT) catalyzes the formation of nicotinamide mononucleotide.	NAD	30-33	nicotinamide phosphoribosyltransferase	Homo sapiens	87-125
25108014-1	2014	Cardiac overexpression of locally acting muscle-restricted (m)IGF-1 and the consequent downstream activation of NAD(+)-dependent protein deacetylase sirtuin 1 (SIRT1) trigger potent cardiac antioxidative and antihypertrophic effects.	NAD	112-118	insulin-like growth factor 1	Mus musculus	62-67
24549054-4	2014	Mutations in GPD1 encoding glycerol-3-phosphate dehydrogenase that catalyzes the reversible redox reaction of dihydroxyacetone phosphate and NADH to glycerol-3-phosphate (G3P) and NAD(+) were identified.	NAD	180-186	glycerol-3-phosphate dehydrogenase 1	Homo sapiens	13-17
25250818-6	2014	miR-34a activity was validated by measuring the expression levels of one of its well described target: the NADH dependent sirtuin1 (SIRT1).	NAD	107-111	microRNA 34a	Homo sapiens	0-7
27493498-5	2014	By the opposite reaction, the 3-ketosteroid is reduced to a 3alpha-hydroxysteroid by 3alpha-HSD with a cofactor NADH.	NAD	112-116	aldo-keto reductase family 1 member C3	Homo sapiens	85-95
25188219-7	2014	Our data indicated that Sir2 and Pnc1, two enzymes that sequentially convert NAD+ to nicotinamide and then to nicotinic acid, are up-regulated by glucose restriction in rich media, and that Pnc1 alone is up-regulated in synthetic media while levels of all other enzymes are unchanged.	NAD	77-81	nicotinamidase	Saccharomyces cerevisiae S288C	33-37
25188219-7	2014	Our data indicated that Sir2 and Pnc1, two enzymes that sequentially convert NAD+ to nicotinamide and then to nicotinic acid, are up-regulated by glucose restriction in rich media, and that Pnc1 alone is up-regulated in synthetic media while levels of all other enzymes are unchanged.	NAD	77-81	nicotinamidase	Saccharomyces cerevisiae S288C	190-194
28714034-2	2017	In eukaryotic cells, cellular NAD is mainly generated by the scavenge pathway in which nicotinamide phosphoribosyltransferase (NAMPT) catalyzes the formation of nicotinamide mononucleotide.	NAD	30-33	nicotinamide phosphoribosyltransferase	Homo sapiens	127-132
28714034-4	2017	To explore the effects of NAMPT inhibition on cellular processes, cells were treated with 10 nM FK866, an NAMPT inhibitor, resulting in a decrease in the cellular NAD level, a lower growth rate, and enhanced susceptivity to oxidative stress as compared to the untreated cells.	NAD	163-166	nicotinamide phosphoribosyltransferase	Homo sapiens	106-111
28656307-1	2017	SIRT6, a member of NAD positivity-dependent class III deacetylase sirtuin family, played versatile roles in human cancers.	NAD	19-22	sirtuin 6	Homo sapiens	0-5
28708087-10	2017	In addition, AMPK-mediated increases in NAD+ in the second mechanism require several ATPs, which may not be available in many pathological conditions.	NAD	40-44	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	13-17
28706210-5	2017	The effect of E2 on aromatase expression was not imitated by oestrogen receptor (ER) alpha agonist PPT or the GPER agonist G1, but it was fully reproduced by DPN, a specific ligand of ERbeta.	NAD	158-161	estrogen receptor 2 (beta)	Mus musculus	184-190
28461337-9	2017	Pioglitazone or its analog NL-1 appears to inhibit the electron transfer activity of mitoNEET by forming a unique complex with mitoNEET and FMNH2 The results suggest that mitoNEET is a redox enzyme that may promote oxidation of NADH to facilitate enhanced glycolysis in the cytosol and that pioglitazone may regulate energy metabolism in mitochondria by inhibiting the electron transfer activity of mitoNEET.	NAD	228-232	neuroligin 1	Homo sapiens	27-31
24414799-2	2014	Nicotinamide phosphoribosyltransferase (Nampt) is a rate-limiting enzyme in the mammalian NAD(+) biosynthesis.	NAD	90-96	nicotinamide phosphoribosyltransferase	Homo sapiens	0-38
24414799-2	2014	Nicotinamide phosphoribosyltransferase (Nampt) is a rate-limiting enzyme in the mammalian NAD(+) biosynthesis.	NAD	90-96	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
24940578-4	2014	More importantly, the PLH-protected GDH exhibited excellent enzymatic activity for the oxidation of glucose accompanied by the reduction of NAD(+) to NADH.	NAD	140-146	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	36-39
24940578-4	2014	More importantly, the PLH-protected GDH exhibited excellent enzymatic activity for the oxidation of glucose accompanied by the reduction of NAD(+) to NADH.	NAD	150-154	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	36-39
24786309-3	2014	NAD(+) biosynthesis, particularly mediated by nicotinamide phosphoribosyltransferase (NAMPT), and SIRT1 function together to regulate metabolism and circadian rhythm.	NAD	0-6	nicotinamide phosphoribosyltransferase	Homo sapiens	46-84
24786309-3	2014	NAD(+) biosynthesis, particularly mediated by nicotinamide phosphoribosyltransferase (NAMPT), and SIRT1 function together to regulate metabolism and circadian rhythm.	NAD	0-6	nicotinamide phosphoribosyltransferase	Homo sapiens	86-91
24534575-3	2014	Coupling with GDH and hemin/G-quadruplex as NADH oxidase and HRP-mimicking DNAzyme, the cascade signal amplification was achieved by the following ways: in the presence of glucose and NAD(+) in the working buffer, GDH electrocatalyzed the oxidation of glucose with the production of NADH.	NAD	184-190	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	14-17
24534575-3	2014	Coupling with GDH and hemin/G-quadruplex as NADH oxidase and HRP-mimicking DNAzyme, the cascade signal amplification was achieved by the following ways: in the presence of glucose and NAD(+) in the working buffer, GDH electrocatalyzed the oxidation of glucose with the production of NADH.	NAD	184-190	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	214-217
24534575-3	2014	Coupling with GDH and hemin/G-quadruplex as NADH oxidase and HRP-mimicking DNAzyme, the cascade signal amplification was achieved by the following ways: in the presence of glucose and NAD(+) in the working buffer, GDH electrocatalyzed the oxidation of glucose with the production of NADH.	NAD	44-48	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	214-217
28356339-3	2017	Recently, cellular production of nicotinamide adenine dinucleotide (NAD+) via nicotinamide phosphoribosyltransferase (Nampt) has emerged as a mediator of cell vitality.	NAD	33-66	nicotinamide phosphoribosyltransferase	Homo sapiens	78-116
25197348-1	2014	SIRT6 is a member of the NAD(+)-dependent class III deacetylase sirtuin family.	NAD	25-31	sirtuin 6	Homo sapiens	0-5
28356339-3	2017	Recently, cellular production of nicotinamide adenine dinucleotide (NAD+) via nicotinamide phosphoribosyltransferase (Nampt) has emerged as a mediator of cell vitality.	NAD	33-66	nicotinamide phosphoribosyltransferase	Homo sapiens	118-123
28356339-3	2017	Recently, cellular production of nicotinamide adenine dinucleotide (NAD+) via nicotinamide phosphoribosyltransferase (Nampt) has emerged as a mediator of cell vitality.	NAD	68-72	nicotinamide phosphoribosyltransferase	Homo sapiens	78-116
28356339-3	2017	Recently, cellular production of nicotinamide adenine dinucleotide (NAD+) via nicotinamide phosphoribosyltransferase (Nampt) has emerged as a mediator of cell vitality.	NAD	68-72	nicotinamide phosphoribosyltransferase	Homo sapiens	118-123
28356339-5	2017	OBJECTIVES: To determine whether a Nampt-NAD+ control system exists within the aortic media and is required for aortic health.	NAD	41-45	nicotinamide phosphoribosyltransferase	Homo sapiens	35-40
28235644-1	2017	The mitochondrial aspartate-glutamate carrier isoform 1 (AGC1) catalyzes a Ca2+-stimulated export of aspartate to the cytosol in exchange for glutamate, and is a key component of the malate-aspartate shuttle which transfers NADH reducing equivalents from the cytosol to mitochondria.	NAD	224-228	solute carrier family 25 member 12	Homo sapiens	57-61
28752046-5	2017	RESULTS: Skeletal muscle cells primarily rely on nicotinamide phosphoribosyltransferase (NAMPT), NRK1, and NRK2 for salvage biosynthesis of NAD+.	NAD	140-144	nicotinamide riboside kinase 1	Mus musculus	97-101
28752046-6	2017	NAMPT inhibition depletes muscle NAD+ availability and can be rescued by NR and NMN as the preferred precursors for elevating muscle cell NAD+ in a pathway that depends on NRK1 and NRK2.	NAD	138-142	nicotinamide riboside kinase 1	Mus musculus	172-176
28752046-10	2017	CONCLUSIONS: These results identify skeletal muscle cells as requiring NAMPT to maintain NAD+ availability and reveal that NRK1 and 2 display overlapping function in salvage of exogenous NR and NMN to augment intracellular NAD+ availability.	NAD	223-227	nicotinamide riboside kinase 1	Mus musculus	123-133
28525742-5	2017	We show that the Dtx3L/Parp9 heterodimer mediates NAD+-dependent mono-ADP-ribosylation of ubiquitin, exclusively in the context of ubiquitin processing by E1 and E2 enzymes.	NAD	50-54	deltex E3 ubiquitin ligase 3L	Homo sapiens	17-22
28525742-11	2017	Dtx3L heterodimerization with Parp9 enables NAD+ and poly(ADP-ribose) regulation of E3 activity.	NAD	44-48	deltex E3 ubiquitin ligase 3L	Homo sapiens	0-5
28500115-2	2017	In GDH-based glucometers, glucose oxidation can be catalysed by different cofactors: nicotinamide adenine dinucleotide (GDH-NAD), flavin adenine dinucleotide (GDH-FAD), pyrroloquinolinequinone (GDH-PQQ) and mutant GDH-PQQ.	NAD	85-118	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	3-6
28500115-2	2017	In GDH-based glucometers, glucose oxidation can be catalysed by different cofactors: nicotinamide adenine dinucleotide (GDH-NAD), flavin adenine dinucleotide (GDH-FAD), pyrroloquinolinequinone (GDH-PQQ) and mutant GDH-PQQ.	NAD	85-118	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	120-123
28500115-2	2017	In GDH-based glucometers, glucose oxidation can be catalysed by different cofactors: nicotinamide adenine dinucleotide (GDH-NAD), flavin adenine dinucleotide (GDH-FAD), pyrroloquinolinequinone (GDH-PQQ) and mutant GDH-PQQ.	NAD	85-118	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	120-123
28500115-2	2017	In GDH-based glucometers, glucose oxidation can be catalysed by different cofactors: nicotinamide adenine dinucleotide (GDH-NAD), flavin adenine dinucleotide (GDH-FAD), pyrroloquinolinequinone (GDH-PQQ) and mutant GDH-PQQ.	NAD	85-118	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	120-123
28500115-2	2017	In GDH-based glucometers, glucose oxidation can be catalysed by different cofactors: nicotinamide adenine dinucleotide (GDH-NAD), flavin adenine dinucleotide (GDH-FAD), pyrroloquinolinequinone (GDH-PQQ) and mutant GDH-PQQ.	NAD	85-118	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	120-123
28500115-3	2017	GOD-based and GDH-NAD-based glucometers are substrate-specific and do not react with sugars other than glucose.	NAD	18-21	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	14-17
28978015-0	2017	Aldehyde dehydrogenase 1A1 increases NADH levels and promotes tumor growth via glutathione/dihydrolipoic acid-dependent NAD+ reduction.	NAD	37-41	aldehyde dehydrogenase family 1, subfamily A1	Mus musculus	0-26
28978015-0	2017	Aldehyde dehydrogenase 1A1 increases NADH levels and promotes tumor growth via glutathione/dihydrolipoic acid-dependent NAD+ reduction.	NAD	120-124	aldehyde dehydrogenase family 1, subfamily A1	Mus musculus	0-26
28978015-1	2017	Aldehyde dehydrogenase 1A1 (ALDH1A1) is a member of the aldehyde dehydrogenase superfamily that oxidizes aldehydes to their corresponding acids, reactions that are coupled to the reduction of NAD+ to NADH.	NAD	192-196	aldehyde dehydrogenase family 1, subfamily A1	Mus musculus	0-26
28978015-1	2017	Aldehyde dehydrogenase 1A1 (ALDH1A1) is a member of the aldehyde dehydrogenase superfamily that oxidizes aldehydes to their corresponding acids, reactions that are coupled to the reduction of NAD+ to NADH.	NAD	192-196	aldehyde dehydrogenase family 1, subfamily A1	Mus musculus	28-35
28978015-1	2017	Aldehyde dehydrogenase 1A1 (ALDH1A1) is a member of the aldehyde dehydrogenase superfamily that oxidizes aldehydes to their corresponding acids, reactions that are coupled to the reduction of NAD+ to NADH.	NAD	200-204	aldehyde dehydrogenase family 1, subfamily A1	Mus musculus	0-26
28978015-1	2017	Aldehyde dehydrogenase 1A1 (ALDH1A1) is a member of the aldehyde dehydrogenase superfamily that oxidizes aldehydes to their corresponding acids, reactions that are coupled to the reduction of NAD+ to NADH.	NAD	200-204	aldehyde dehydrogenase family 1, subfamily A1	Mus musculus	28-35
28978015-2	2017	We report here that ALDH1A1 can also use glutathione (GSH) and dihydrolipoic acid (DHLA) as electron donors to reduce NAD+ to NADH.	NAD	118-122	aldehyde dehydrogenase family 1, subfamily A1	Mus musculus	20-27
28978015-2	2017	We report here that ALDH1A1 can also use glutathione (GSH) and dihydrolipoic acid (DHLA) as electron donors to reduce NAD+ to NADH.	NAD	126-130	aldehyde dehydrogenase family 1, subfamily A1	Mus musculus	20-27
28978015-3	2017	The GSH/DHLA-dependent NAD+-reduction activity of ALDH1A1 is not affected by the aldehyde dehydrogenase inhibitor or by mutation of the residues in its aldehyde-binding pocket.	NAD	23-27	aldehyde dehydrogenase family 1, subfamily A1	Mus musculus	50-57
28978015-5	2017	We also found that the ectopic expression of ALDH1A1 decreased the intracellular NAD+/NADH ratio, while knockout of ALDH1A1 increased the NAD+/NADH ratio.	NAD	81-85	aldehyde dehydrogenase family 1, subfamily A1	Mus musculus	45-52
28978015-5	2017	We also found that the ectopic expression of ALDH1A1 decreased the intracellular NAD+/NADH ratio, while knockout of ALDH1A1 increased the NAD+/NADH ratio.	NAD	86-90	aldehyde dehydrogenase family 1, subfamily A1	Mus musculus	45-52
28978015-5	2017	We also found that the ectopic expression of ALDH1A1 decreased the intracellular NAD+/NADH ratio, while knockout of ALDH1A1 increased the NAD+/NADH ratio.	NAD	138-142	aldehyde dehydrogenase family 1, subfamily A1	Mus musculus	116-123
28423012-1	2017	The NAD+-dependent 15-hydroxyprostaglandin dehydrogenase (15-PGDH) catalyzes the oxidation of the 15(S)-hydroxyl group of prostaglandin E2 (PGE2), converting the pro-inflammatory PGE2 to the anti-inflammatory 15-keto-PGE2 (an endogenous ligand for peroxisome proliferator-activated receptor-gamma [PPAR-gamma]).	NAD	4-7	hydroxyprostaglandin dehydrogenase 15 (NAD)	Mus musculus	19-56
28423012-1	2017	The NAD+-dependent 15-hydroxyprostaglandin dehydrogenase (15-PGDH) catalyzes the oxidation of the 15(S)-hydroxyl group of prostaglandin E2 (PGE2), converting the pro-inflammatory PGE2 to the anti-inflammatory 15-keto-PGE2 (an endogenous ligand for peroxisome proliferator-activated receptor-gamma [PPAR-gamma]).	NAD	4-7	hydroxyprostaglandin dehydrogenase 15 (NAD)	Mus musculus	58-65
28423012-1	2017	The NAD+-dependent 15-hydroxyprostaglandin dehydrogenase (15-PGDH) catalyzes the oxidation of the 15(S)-hydroxyl group of prostaglandin E2 (PGE2), converting the pro-inflammatory PGE2 to the anti-inflammatory 15-keto-PGE2 (an endogenous ligand for peroxisome proliferator-activated receptor-gamma [PPAR-gamma]).	NAD	4-7	peroxisome proliferator activated receptor gamma	Mus musculus	248-296
28423012-1	2017	The NAD+-dependent 15-hydroxyprostaglandin dehydrogenase (15-PGDH) catalyzes the oxidation of the 15(S)-hydroxyl group of prostaglandin E2 (PGE2), converting the pro-inflammatory PGE2 to the anti-inflammatory 15-keto-PGE2 (an endogenous ligand for peroxisome proliferator-activated receptor-gamma [PPAR-gamma]).	NAD	4-7	peroxisome proliferator activated receptor gamma	Mus musculus	298-308
28160567-2	2017	EwS development is driven by a specific chromosomal translocation resulting in the generation of a chimeric EWS-ETS transcription factor, most frequently EWS-FLI1.Nicotinamide adenine dinucleotide (NAD) is a key metabolite of energy metabolism involved in cellular redox reactions, DNA repair, and in the maintenance of genomic stability.	NAD	163-196	EWS RNA binding protein 1	Homo sapiens	154-162
28167526-7	2017	The NatV Nudix hydrolase domain was also shown to be active, with preferred substrates of ADP-ribose, NAD+, and NADH.	NAD	102-106	NMN adenylyl tranferase	Vibrio phage KVP40	9-24
28167526-7	2017	The NatV Nudix hydrolase domain was also shown to be active, with preferred substrates of ADP-ribose, NAD+, and NADH.	NAD	112-116	NMN adenylyl tranferase	Vibrio phage KVP40	9-24
28108762-4	2017	Second, the soluble fumarate reductase from Saccharomyces cerevisiae was overexpressed to manipulate the anaerobic NADH/NAD+ ratio and ATP level.	NAD	115-119	fumarate reductase	Saccharomyces cerevisiae S288C	20-38
28108762-4	2017	Second, the soluble fumarate reductase from Saccharomyces cerevisiae was overexpressed to manipulate the anaerobic NADH/NAD+ ratio and ATP level.	NAD	120-124	fumarate reductase	Saccharomyces cerevisiae S288C	20-38
26442197-7	2014	SIRT6 is highly conserved NAD(+)-dependent lysine deacetylase and ADP-ribosyltransferase impacting longevity, metabolism, and cancer.	NAD	26-32	sirtuin 6	Homo sapiens	0-5
28334607-0	2017	The SARM1 Toll/Interleukin-1 Receptor Domain Possesses Intrinsic NAD+ Cleavage Activity that Promotes Pathological Axonal Degeneration.	NAD	65-69	sterile alpha and TIR motif containing 1	Homo sapiens	4-9
24757201-5	2014	Interestingly, miR-149 inhibits poly(ADP-ribose) polymerase-2 (PARP-2) and so increased cellular NAD(+) levels and SIRT-1 activity that subsequently increases mitochondrial function and biogenesis via PGC-1alpha activation.	NAD	97-103	poly (ADP-ribose) polymerase family, member 2	Mus musculus	32-61
24757201-5	2014	Interestingly, miR-149 inhibits poly(ADP-ribose) polymerase-2 (PARP-2) and so increased cellular NAD(+) levels and SIRT-1 activity that subsequently increases mitochondrial function and biogenesis via PGC-1alpha activation.	NAD	97-103	poly (ADP-ribose) polymerase family, member 2	Mus musculus	63-69
24757201-5	2014	Interestingly, miR-149 inhibits poly(ADP-ribose) polymerase-2 (PARP-2) and so increased cellular NAD(+) levels and SIRT-1 activity that subsequently increases mitochondrial function and biogenesis via PGC-1alpha activation.	NAD	97-103	peroxisome proliferative activated receptor, gamma, coactivator 1 alpha	Mus musculus	201-211
24375466-5	2014	Furthermore, lack of hepatocyte HMGB1 led to excessive poly(ADP-ribose)polymerase 1 activation, exhausting nicotinamide adenine dinucleotide and adenosine triphosphate stores, exacerbating mitochondrial instability and damage, and, consequently, leading to increased cell death.	NAD	107-140	high mobility group box 1	Mus musculus	32-37
24548601-1	2014	BACKGROUND: Together with p53, the NAD-dependent lysine deacetylase SIRT1 and the microRNA miR-34a form a feedback loop which self-regulates SIRT1 expression and modulates p53-dependent responses.	NAD	35-38	microRNA 34a	Homo sapiens	91-98
24603754-2	2014	Reversible conversion of NAD(+) and NADH cofactors was used to perform a XOR logic operation, while biocatalytic hydrolysis of p-nitrophenyl phosphate resulted in an Identity operation working in parallel.	NAD	25-31	xanthine dehydrogenase	Homo sapiens	73-76
24603754-2	2014	Reversible conversion of NAD(+) and NADH cofactors was used to perform a XOR logic operation, while biocatalytic hydrolysis of p-nitrophenyl phosphate resulted in an Identity operation working in parallel.	NAD	36-40	xanthine dehydrogenase	Homo sapiens	73-76
24113812-1	2014	A gene encoding an NADH-dependent short-chain dehydrogenase/reductase (gox2036) from Gluconobacter oxydans 621H was cloned and heterogeneously expressed in Escherichia coli.	NAD	19-23	acetoin reductase	Gluconobacter oxydans 621H	71-78
24515115-7	2014	Depending on the substrates present, the dominant sites of superoxide/H2O2 production at the level of NADH may be the OGDH and PDH complexes, but these activities may often be misattributed to complex I.	NAD	102-106	oxoglutarate dehydrogenase	Homo sapiens	118-122
24463048-9	2014	The cofactor specificity was shifted even further in favor of NADP(+), as the mutant ALDH3H1E149T/V178R/I200V uses NADP(+) with almost 7-fold higher catalytic efficiency compared to NAD(+).	NAD	182-188	aldehyde dehydrogenase 3I1	Arabidopsis thaliana	85-90
24513047-3	2014	The new system gained about 1200-fold cofactor specificity shift from NAD toward B-8 in terms of oxidative decarboxylation of l-malate.	NAD	70-73	NADH:ubiquinone oxidoreductase subunit A2	Homo sapiens	81-84
24412016-1	2014	BACKGROUND: APO866 is a highly specific inhibitor of nicotinamide phosphoribosyltransferase (NAMPT), inhibition of which reduces cellular NAD(+) levels.	NAD	138-144	nicotinamide phosphoribosyltransferase	Homo sapiens	53-91
24412016-1	2014	BACKGROUND: APO866 is a highly specific inhibitor of nicotinamide phosphoribosyltransferase (NAMPT), inhibition of which reduces cellular NAD(+) levels.	NAD	138-144	nicotinamide phosphoribosyltransferase	Homo sapiens	93-98
24438745-10	2014	Visfatin/NAMPT is also an intracellular enzyme acting as the rate-limiting enzyme of the generation of NAD.	NAD	103-106	nicotinamide phosphoribosyltransferase	Homo sapiens	0-8
24438745-10	2014	Visfatin/NAMPT is also an intracellular enzyme acting as the rate-limiting enzyme of the generation of NAD.	NAD	103-106	nicotinamide phosphoribosyltransferase	Homo sapiens	9-14
25483087-5	2014	CSCs demonstrated significant upregulation of CtBP1 and CtBP2 levels (mRNA and protein) and activity partly due to increased NADH/NAD ratio, as well as increased TCF/LEF transcriptional activity, compared to respective controls.	NAD	125-129	C-terminal binding protein 1	Homo sapiens	46-51
25483087-5	2014	CSCs demonstrated significant upregulation of CtBP1 and CtBP2 levels (mRNA and protein) and activity partly due to increased NADH/NAD ratio, as well as increased TCF/LEF transcriptional activity, compared to respective controls.	NAD	125-128	C-terminal binding protein 1	Homo sapiens	46-51
23968888-9	2014	Herein we show that upregulation of visfatin increased NAD levels in the remnant steatotic liver, whereas visfatin inhibition decreased them.	NAD	55-58	nicotinamide phosphoribosyltransferase	Homo sapiens	36-44
23968888-10	2014	These later observations suggest that visfatin may favour synthesis of NAD instead of DNA and induces alterations in amino acid metabolism-urea cycle and NO production, overall negatively affecting liver viability.	NAD	71-74	nicotinamide phosphoribosyltransferase	Homo sapiens	38-46
24198233-3	2014	These heterozygous plants show higher transcript levels of an alternative NAD(+)-regenerating enzyme, NADH-GOGAT, and, remarkably, improved growth when ammonium is the sole N-source.	NAD	74-80	NADH-dependent glutamate synthase 1	Arabidopsis thaliana	102-112
24616469-1	2014	Nicotinamide phosphoribosyltransferase (Nampt) is a rate-limiting enzyme for synthesis of nicotinamide adenine dinucleotide in mammalian cells.	NAD	90-123	nicotinamide phosphoribosyltransferase	Homo sapiens	0-38
24616469-1	2014	Nicotinamide phosphoribosyltransferase (Nampt) is a rate-limiting enzyme for synthesis of nicotinamide adenine dinucleotide in mammalian cells.	NAD	90-123	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
24360282-4	2013	We trace the cause to an alternate PGC-1alpha/beta-independent pathway of nuclear-mitochondrial communication that is induced by a decline in nuclear NAD(+) and the accumulation of HIF-1alpha under normoxic conditions, with parallels to Warburg reprogramming.	NAD	150-156	peroxisome proliferative activated receptor, gamma, coactivator 1 alpha	Mus musculus	35-45
23850783-4	2013	Significantly, the electrochemical signal was greatly enhanced based on cascade catalysis: firstly, GDH catalyzed the oxidation of glucose to gluconolactone with the concomitant generation of NADH in the presence of NAD(+).	NAD	192-196	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	100-103
23850783-4	2013	Significantly, the electrochemical signal was greatly enhanced based on cascade catalysis: firstly, GDH catalyzed the oxidation of glucose to gluconolactone with the concomitant generation of NADH in the presence of NAD(+).	NAD	216-222	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	100-103
24403854-1	2013	Nicotinamide adenine dinucleotide (NAD) is a metabolite essential for cell survival and generated de novo from tryptophan or recycled from nicotinamide (NAM) through the nicotinamide phosphoribosyltransferase (NAMPT)-dependent salvage pathway.	NAD	0-33	nicotinamide phosphoribosyltransferase	Homo sapiens	170-208
28334607-2	2017	SARM1 is the central executioner of the axonal degeneration pathway that culminates in depletion of axonal NAD+, yet the identity of the underlying NAD+-depleting enzyme(s) is unknown.	NAD	107-111	sterile alpha and TIR motif containing 1	Homo sapiens	0-5
24437277-4	2013	This review aims to summarize recent progress in elucidating the pathophysiological importance of clock genes, NAMPT-mediated NAD biosynthesis, and SIRT1, in the crosstalk between circadian rhythm and metabolism.	NAD	126-129	nicotinamide phosphoribosyltransferase	Homo sapiens	111-116
28334607-2	2017	SARM1 is the central executioner of the axonal degeneration pathway that culminates in depletion of axonal NAD+, yet the identity of the underlying NAD+-depleting enzyme(s) is unknown.	NAD	148-152	sterile alpha and TIR motif containing 1	Homo sapiens	0-5
28334607-3	2017	Here, in a series of experiments using purified proteins from mammalian cells, bacteria, and a cell-free protein translation system, we show that the SARM1-TIR domain itself has intrinsic NADase activity-cleaving NAD+ into ADP-ribose (ADPR), cyclic ADPR, and nicotinamide, with nicotinamide serving as a feedback inhibitor of the enzyme.	NAD	213-217	sterile alpha and TIR motif containing 1	Homo sapiens	150-155
28334607-4	2017	Using traumatic and vincristine-induced injury models in neurons, we demonstrate that the NADase activity of full-length SARM1 is required in axons to promote axonal NAD+ depletion and axonal degeneration after injury.	NAD	166-170	sterile alpha and TIR motif containing 1	Homo sapiens	121-126
27989687-7	2017	RESULTS: NADH enhanced PLD activity (1.6- +- 0.1-fold, P &lt;.01) and activated PKCdelta.	NAD	9-13	protein kinase C delta	Homo sapiens	80-88
23832307-8	2013	Here we present a diaphorase/lactate dehydrogenase NAD cycling assay optimized for hESCs, together with a mechanism-based, nonlinear regression models for the determination of NAD(+), NADH, and total NAD.	NAD	51-54	dihydrolipoamide dehydrogenase	Homo sapiens	18-28
27989687-12	2017	CONCLUSION: NADH activated PKCdelta by enhancing PLD activity.	NAD	12-16	protein kinase C delta	Homo sapiens	27-35
28382091-5	2017	In this study, we aimed to deplete the NAD+ content of MCF-7 cells, a model cell line for ER-positive breast cancer, by inhibiting NAMPT in order to evaluate downstream effects on p53 and its acetylation, p21 and Bcl-2-associated X protein (BAX) expression, and finally, apoptosis in MCF-7 breast cancer cells.	NAD	39-43	nicotinamide phosphoribosyltransferase	Homo sapiens	131-136
23831226-1	2013	NADH-Cytochrome b5 reductase (b5R), a flavoprotein consisting of NADH and flavin adenine dinucleotide (FAD) binding domains, catalyzes electron transfer from the two-electron carrier NADH to the one-electron carrier cytochrome b5 (Cb5).	NAD	0-4	cytochrome b5 reductase 3	Homo sapiens	30-33
27929719-3	2017	In a cross-species study, using primary rat neurons, the roundworm C. elegans, and a mouse model of A-T, we showed that loss of ATM induces mitochondrial dysfunction and compromised mitophagy due to NAD+ insufficiency.	NAD	199-203	ataxia telangiectasia mutated	Mus musculus	128-131
27929719-4	2017	Remarkably, NAD+ repletion mitigates both the DNA repair defect and mitochondrial dysfunction in ATM-deficient neurons.	NAD	12-16	ataxia telangiectasia mutated	Mus musculus	97-100
27806939-5	2017	Notably, both DHRS7C-Y191F and DHRS7C-K195Q cells also showed similar enlarged cellular morphology, suggesting that the NAD/NADH-dependent dehydrogenase catalytic core domain is pivotal for DHRS7C function.	NAD	120-123	dehydrogenase/reductase (SDR family) member 7C	Mus musculus	14-20
24223197-0	2013	Addition of exogenous NAD+ prevents mefloquine-induced neuroaxonal and hair cell degeneration through reduction of caspase-3-mediated apoptosis in cochlear organotypic cultures.	NAD	22-26	caspase 3	Rattus norvegicus	115-124
24013482-5	2013	For example, the activities of NAD(P)-dependent enzymes such as glyceraldehyde-3-phosphate dehydrogenase (G3PDH) in chloroplasts and isocitrate dehydrogenase (ICDH) in mitochondria were elevated, along with levels of pyridine nucleotides (nicotinamide coenzymes) [NAD(H) and NADP(H)] and activity of NAD kinase (NADP forming enzyme).	NAD	264-270	glyceraldehyde-3-phosphate dehydrogenase	Cucumis sativus	64-104
24013482-5	2013	For example, the activities of NAD(P)-dependent enzymes such as glyceraldehyde-3-phosphate dehydrogenase (G3PDH) in chloroplasts and isocitrate dehydrogenase (ICDH) in mitochondria were elevated, along with levels of pyridine nucleotides (nicotinamide coenzymes) [NAD(H) and NADP(H)] and activity of NAD kinase (NADP forming enzyme).	NAD	264-270	glyceraldehyde-3-phosphate dehydrogenase	Cucumis sativus	106-111
27806939-5	2017	Notably, both DHRS7C-Y191F and DHRS7C-K195Q cells also showed similar enlarged cellular morphology, suggesting that the NAD/NADH-dependent dehydrogenase catalytic core domain is pivotal for DHRS7C function.	NAD	120-123	dehydrogenase/reductase (SDR family) member 7C	Mus musculus	31-37
27806939-5	2017	Notably, both DHRS7C-Y191F and DHRS7C-K195Q cells also showed similar enlarged cellular morphology, suggesting that the NAD/NADH-dependent dehydrogenase catalytic core domain is pivotal for DHRS7C function.	NAD	120-123	dehydrogenase/reductase (SDR family) member 7C	Mus musculus	31-37
27806939-5	2017	Notably, both DHRS7C-Y191F and DHRS7C-K195Q cells also showed similar enlarged cellular morphology, suggesting that the NAD/NADH-dependent dehydrogenase catalytic core domain is pivotal for DHRS7C function.	NAD	124-128	dehydrogenase/reductase (SDR family) member 7C	Mus musculus	14-20
27576129-5	2017	Importantly, TGF-beta1 had a dose- and time-dependent upregulating effect on NADH activity and Nox4 gene expression in HDFs.	NAD	77-81	transforming growth factor, beta 1	Mus musculus	13-22
24155910-0	2013	Insight into molecular and functional properties of NMNAT3 reveals new hints of NAD homeostasis within human mitochondria.	NAD	80-83	nicotinamide nucleotide adenylyltransferase 3	Homo sapiens	52-58
24155910-1	2013	Among the enzymes involved in NAD homeostasis, nicotinamide mononucleotide adenylyltransferases (NMNAT1-3) are central to intracellular NAD formation.	NAD	30-33	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	97-103
28367271-5	2017	Expression levels of Beclin-1, Atg12-Atg5, LC3B-II, cleaved caspase 3, and Bax were upregulated in the I/R group and downregulated in the 75 mg/kg NAD+ group; p-mTOR, p-AKT, p62, and Bcl-2 were downregulated in the I/R group and upregulated in the 75 mg/kg NAD+ group.	NAD	147-151	beclin 1	Rattus norvegicus	21-29
25309947-9	2013	Nuclear translocation of NAD-dependent histone deacetylase SIRT1 and global chromatin silencing lead to hESC cardiac fate determination, while silencing of pluripotence-associated hsa-miR-302 family and drastic up-regulation of neuroectodermal Hox miRNA hsa-miR-10 family lead to hESC neural fate determination.	NAD	25-28	leukocyte immunoglobulin like receptor B2	Homo sapiens	258-264
28367271-5	2017	Expression levels of Beclin-1, Atg12-Atg5, LC3B-II, cleaved caspase 3, and Bax were upregulated in the I/R group and downregulated in the 75 mg/kg NAD+ group; p-mTOR, p-AKT, p62, and Bcl-2 were downregulated in the I/R group and upregulated in the 75 mg/kg NAD+ group.	NAD	257-261	beclin 1	Rattus norvegicus	21-29
27930300-6	2016	Regulatory network analysis of RNA sequencing data using GSCs treated with NAMPT inhibitor identified transcription factor E2F2 as the center of a transcriptional hub in the NAD+-dependent network.	NAD	174-178	E2F transcription factor 2	Homo sapiens	123-127
23747282-2	2013	The first assay is based on the reduction of Delta(1)-pyrroline-5-carboxylate (P5C), generated from ornithine by OAT, using human pyrroline 5-carboxylate reductase 1 (PYCR1), which results in the concomitant oxidation of NADH (nicotinamide adenine dinucleotide, reduced form) to NAD+ (nicotinamide adenine dinucleotide, oxidized form).	NAD	221-225	ornithine aminotransferase	Homo sapiens	113-116
23747282-2	2013	The first assay is based on the reduction of Delta(1)-pyrroline-5-carboxylate (P5C), generated from ornithine by OAT, using human pyrroline 5-carboxylate reductase 1 (PYCR1), which results in the concomitant oxidation of NADH (nicotinamide adenine dinucleotide, reduced form) to NAD+ (nicotinamide adenine dinucleotide, oxidized form).	NAD	227-260	ornithine aminotransferase	Homo sapiens	113-116
27930300-10	2016	The identification of a NAMPT-E2F2-ID axis establishes a link between NAD+ metabolism and a self-renewal transcriptional program in glioblastoma, with therapeutic implications for this formidable cancer.	NAD	70-74	nicotinamide phosphoribosyltransferase	Homo sapiens	24-29
27930300-10	2016	The identification of a NAMPT-E2F2-ID axis establishes a link between NAD+ metabolism and a self-renewal transcriptional program in glioblastoma, with therapeutic implications for this formidable cancer.	NAD	70-74	E2F transcription factor 2	Homo sapiens	30-34
26944347-3	2016	Results from cyclic voltammetric and FI amperometric measurements have revealed that GDH/ZnS-CdS/MWCNT/GCE is capable of signaling photoelectrocatalytic activity toward NADH when the surface of enzyme modified electrode was irradiated with a light source (250W Halogen lamp).	NAD	169-173	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	85-88
23848060-9	2013	PI3K or MEK1/2 inhibitor abrogated the infarct-sparing effect and inhibition of loss of NAD(+) induced by SpostC in young rats, respectively.	NAD	88-94	mitogen activated protein kinase kinase 1	Rattus norvegicus	8-14
27240865-8	2016	Promoter truncation of GPD1 and gene deletion of GPD2 coding for glycerol-3-phosphate dehydrogenase to produce surplus NADH also did not lead to improved acetate consumption.	NAD	119-123	glycerol-3-phosphate dehydrogenase	Saccharomyces cerevisiae S288C	65-99
27372904-4	2016	We performed co-immunoprecipitation experiments to examine whether VILIP-3 can interact with reduced nicotine adenine dinucleotide (NADH)-cytochrome b 5 reductase.	NAD	132-136	hippocalcin like 1	Homo sapiens	67-74
24003918-2	2013	SIRT1, the mammalian nicotinamide adenine dinucleotide (NAD)-dependent protein deacetylase, and nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting NAD biosynthetic enzyme, together comprise a novel systemic regulatory network, named the "NAD World", that orchestrates physiological responses to internal and external perturbations and maintains the robustness of the physiological system in mammals.	NAD	21-54	nicotinamide phosphoribosyltransferase	Homo sapiens	96-134
24003918-2	2013	SIRT1, the mammalian nicotinamide adenine dinucleotide (NAD)-dependent protein deacetylase, and nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting NAD biosynthetic enzyme, together comprise a novel systemic regulatory network, named the "NAD World", that orchestrates physiological responses to internal and external perturbations and maintains the robustness of the physiological system in mammals.	NAD	162-165	nicotinamide phosphoribosyltransferase	Homo sapiens	96-134
24003918-2	2013	SIRT1, the mammalian nicotinamide adenine dinucleotide (NAD)-dependent protein deacetylase, and nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting NAD biosynthetic enzyme, together comprise a novel systemic regulatory network, named the "NAD World", that orchestrates physiological responses to internal and external perturbations and maintains the robustness of the physiological system in mammals.	NAD	162-165	nicotinamide phosphoribosyltransferase	Homo sapiens	136-141
24003918-2	2013	SIRT1, the mammalian nicotinamide adenine dinucleotide (NAD)-dependent protein deacetylase, and nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting NAD biosynthetic enzyme, together comprise a novel systemic regulatory network, named the "NAD World", that orchestrates physiological responses to internal and external perturbations and maintains the robustness of the physiological system in mammals.	NAD	162-165	nicotinamide phosphoribosyltransferase	Homo sapiens	96-134
24003918-2	2013	SIRT1, the mammalian nicotinamide adenine dinucleotide (NAD)-dependent protein deacetylase, and nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting NAD biosynthetic enzyme, together comprise a novel systemic regulatory network, named the "NAD World", that orchestrates physiological responses to internal and external perturbations and maintains the robustness of the physiological system in mammals.	NAD	162-165	nicotinamide phosphoribosyltransferase	Homo sapiens	136-141
24003918-4	2013	In this article, we will summarize the physiological significance of SIRT1 and NAMPT-mediated NAD biosynthesis in metabolic regulation and discuss the ideas of functional hierarchy and frailty in determining the robustness of the system.	NAD	94-97	nicotinamide phosphoribosyltransferase	Homo sapiens	79-84
23804809-1	2013	NAMPT, also known as PBEF and visfatin, can act extracellularly as a cytokine-like molecule or intracellularly as a NAMPT, regulating NAD biosynthesis in the NAD salvage pathway.	NAD	134-137	nicotinamide phosphoribosyltransferase	Homo sapiens	0-5
23804809-1	2013	NAMPT, also known as PBEF and visfatin, can act extracellularly as a cytokine-like molecule or intracellularly as a NAMPT, regulating NAD biosynthesis in the NAD salvage pathway.	NAD	134-137	nicotinamide phosphoribosyltransferase	Homo sapiens	21-25
23804809-1	2013	NAMPT, also known as PBEF and visfatin, can act extracellularly as a cytokine-like molecule or intracellularly as a NAMPT, regulating NAD biosynthesis in the NAD salvage pathway.	NAD	134-137	nicotinamide phosphoribosyltransferase	Homo sapiens	30-38
23804809-1	2013	NAMPT, also known as PBEF and visfatin, can act extracellularly as a cytokine-like molecule or intracellularly as a NAMPT, regulating NAD biosynthesis in the NAD salvage pathway.	NAD	134-137	nicotinamide phosphoribosyltransferase	Homo sapiens	116-121
23804809-1	2013	NAMPT, also known as PBEF and visfatin, can act extracellularly as a cytokine-like molecule or intracellularly as a NAMPT, regulating NAD biosynthesis in the NAD salvage pathway.	NAD	158-161	nicotinamide phosphoribosyltransferase	Homo sapiens	0-5
23804809-1	2013	NAMPT, also known as PBEF and visfatin, can act extracellularly as a cytokine-like molecule or intracellularly as a NAMPT, regulating NAD biosynthesis in the NAD salvage pathway.	NAD	158-161	nicotinamide phosphoribosyltransferase	Homo sapiens	21-25
23804809-1	2013	NAMPT, also known as PBEF and visfatin, can act extracellularly as a cytokine-like molecule or intracellularly as a NAMPT, regulating NAD biosynthesis in the NAD salvage pathway.	NAD	158-161	nicotinamide phosphoribosyltransferase	Homo sapiens	30-38
23804809-1	2013	NAMPT, also known as PBEF and visfatin, can act extracellularly as a cytokine-like molecule or intracellularly as a NAMPT, regulating NAD biosynthesis in the NAD salvage pathway.	NAD	158-161	nicotinamide phosphoribosyltransferase	Homo sapiens	116-121
23799512-2	2013	The obtained Cu-MOF-MPC composites are used as electrocatalysts for the oxidation of NADH and reduction of H2O2 in neutral solution.	NAD	85-89	lysine acetyltransferase 8	Homo sapiens	16-19
23898059-1	2013	Nicotinamide phosphoribosyltransferase (NAMPT) catalyzes the rate-limiting step of nicotinamide adenine dinucleotide (NAD(+)) synthesis.	NAD	83-116	nicotinamide phosphoribosyltransferase	Homo sapiens	0-38
23898059-1	2013	Nicotinamide phosphoribosyltransferase (NAMPT) catalyzes the rate-limiting step of nicotinamide adenine dinucleotide (NAD(+)) synthesis.	NAD	83-116	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
23898059-1	2013	Nicotinamide phosphoribosyltransferase (NAMPT) catalyzes the rate-limiting step of nicotinamide adenine dinucleotide (NAD(+)) synthesis.	NAD	118-124	nicotinamide phosphoribosyltransferase	Homo sapiens	0-38
23898059-1	2013	Nicotinamide phosphoribosyltransferase (NAMPT) catalyzes the rate-limiting step of nicotinamide adenine dinucleotide (NAD(+)) synthesis.	NAD	118-124	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
23597856-0	2013	Poly(ADP-ribose) polymerase-1-induced NAD(+) depletion promotes nuclear factor-kappaB transcriptional activity by preventing p65 de-acetylation.	NAD	38-44	RELA proto-oncogene, NF-kB subunit	Homo sapiens	125-128
23603111-6	2013	DPN treatment of EAE animals resulted in phosphorylated ERbeta and activated the phosphatidylinositol 3-kinase (PI3K)/serine-threonine-specific protein kinase (Akt)/mammalian target of rapamycin (mTOR) signaling pathway, a pathway required for oligodendrocyte survival and axon myelination.	NAD	0-3	estrogen receptor 2	Homo sapiens	56-62
23887727-8	2013	AMPK can also modulate the circadian rhythms through nicotinamide adenine dinucleotide-dependent regulation of silent information regulator 1.	NAD	53-86	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	0-4
23339688-21	2013	Electrochemical and 13C NMR data for a series of N-alkylnicotinamides show that the 3.4 ppm downfield 13C-perturbation in GalE corresponds to an elevation of the NAD reduction potential by 150 mV.	NAD	162-165	UDP-galactose-4-epimerase	Homo sapiens	122-126
23339688-22	2013	These results account for the uridine nucleotide-dependence in the reduction of [GalE-NAD] by glucose or NaBH3CN.	NAD	86-89	UDP-galactose-4-epimerase	Homo sapiens	81-85
23339688-23	2013	Kinetics in the reduction of Tyr149Phe- and Lys153Met-GalE-NAD implicate Tyr149 and Lys153 in the nucleotide-dependent reduction of NAD.	NAD	59-62	UDP-galactose-4-epimerase	Homo sapiens	54-58
23339688-25	2013	In an O2-dependent reaction, [GalE-NADH] reduces the stable radical UDP-TEMPO with production of superoxide radical.	NAD	35-39	UDP-galactose-4-epimerase	Homo sapiens	30-34
23307072-2	2013	Altered expression of nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme of NAD(+)-salvage, accompanies the changes in NAD(H) during tumorigenesis.	NAD	98-104	nicotinamide phosphoribosyltransferase	Homo sapiens	22-60
23307072-2	2013	Altered expression of nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme of NAD(+)-salvage, accompanies the changes in NAD(H) during tumorigenesis.	NAD	98-104	nicotinamide phosphoribosyltransferase	Homo sapiens	62-67
23307072-2	2013	Altered expression of nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme of NAD(+)-salvage, accompanies the changes in NAD(H) during tumorigenesis.	NAD	141-147	nicotinamide phosphoribosyltransferase	Homo sapiens	22-60
23307072-2	2013	Altered expression of nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme of NAD(+)-salvage, accompanies the changes in NAD(H) during tumorigenesis.	NAD	141-147	nicotinamide phosphoribosyltransferase	Homo sapiens	62-67
23307072-3	2013	Here, we show by genetic and pharmacological inhibition of NAMPT in glioma cells that fluctuation in intracellular [NAD(H)] differentially affects cell growth and morphodynamics, with motility/invasion capacity showing the highest sensitivity to [NAD(H)] decrease.	NAD	116-122	nicotinamide phosphoribosyltransferase	Homo sapiens	59-64
23307072-3	2013	Here, we show by genetic and pharmacological inhibition of NAMPT in glioma cells that fluctuation in intracellular [NAD(H)] differentially affects cell growth and morphodynamics, with motility/invasion capacity showing the highest sensitivity to [NAD(H)] decrease.	NAD	247-253	nicotinamide phosphoribosyltransferase	Homo sapiens	59-64
23734016-5	2013	The generation of NAD can be coupled to a cycling assay using the enzymes alcohol dehydrogenase and diaphorase.	NAD	18-21	dihydrolipoamide dehydrogenase	Homo sapiens	100-110
23531116-2	2013	Pharmacological inhibition of nicotinamide phosphoribosyltransferase (NAMPT), the key enzyme in this biosynthetic pathway, almost invariably leads to intracellular NAD+ depletion and, when protracted, to ATP shortage and cell demise.	NAD	164-168	nicotinamide phosphoribosyltransferase	Homo sapiens	30-68
23531116-2	2013	Pharmacological inhibition of nicotinamide phosphoribosyltransferase (NAMPT), the key enzyme in this biosynthetic pathway, almost invariably leads to intracellular NAD+ depletion and, when protracted, to ATP shortage and cell demise.	NAD	164-168	nicotinamide phosphoribosyltransferase	Homo sapiens	70-75
23296366-5	2013	Other examples are the epimerase and the ATP-dependent dehydratase that repair hydrated forms of NADH and NADPH; ethylmalonyl-CoA decarboxylase, which eliminates an abnormal metabolite formed by acetyl-CoA carboxylase, an enzyme of fatty acid synthesis; L-pipecolate oxidase, which repairs a metabolite formed by a side activity of an enzyme of L-proline biosynthesis.	NAD	97-101	ethylmalonyl-CoA decarboxylase 1	Homo sapiens	113-143
23445365-6	2013	The binding of DMQn (n = 0 or 2) to GB1-hCLK-1 mediates reduction of the diiron center by nicotinamide adenine dinucleotide (NADH) and initiates O2 activation for subsequent DMQ hydroxylation.	NAD	90-123	CDC like kinase 1	Homo sapiens	40-46
23445365-6	2013	The binding of DMQn (n = 0 or 2) to GB1-hCLK-1 mediates reduction of the diiron center by nicotinamide adenine dinucleotide (NADH) and initiates O2 activation for subsequent DMQ hydroxylation.	NAD	125-129	CDC like kinase 1	Homo sapiens	40-46
23445365-7	2013	Deployment of DMQ to mediate reduction of the diiron center in GB1-hCLK-1 improves substrate specificity and diminishes consumption of NADH that is uncoupled from substrate oxidation.	NAD	135-139	CDC like kinase 1	Homo sapiens	67-73
23274177-2	2013	GSNOR catalyses the oxidation of HMGSH to S-formylglutathione using a catalytic zinc and NAD(+) as a coenzyme.	NAD	89-95	alcohol dehydrogenase class III	Solanum lycopersicum	0-5
23274177-12	2013	The crystal structures of the apoenzyme, of the enzyme in complex with NAD(+) and in complex with NADH, solved up to 1.9 A resolution, represent the first structures of a plant GSNOR.	NAD	71-77	alcohol dehydrogenase class III	Solanum lycopersicum	177-182
23274177-12	2013	The crystal structures of the apoenzyme, of the enzyme in complex with NAD(+) and in complex with NADH, solved up to 1.9 A resolution, represent the first structures of a plant GSNOR.	NAD	98-102	alcohol dehydrogenase class III	Solanum lycopersicum	177-182
23417421-9	2013	Furthermore, GHRH increased the phosphorylation of endothelial nitric oxide synthase and AMP-activated protein kinase and preserved postischemic nicotinamide adenine dinucleotide (NAD(+)) levels.	NAD	145-178	growth hormone releasing hormone	Rattus norvegicus	13-17
27372904-8	2016	These results suggest that VILIP-3, hippocalcin, and neurocalcin-delta provide a Ca2+-dependent modulation to the NADH-dependent microsomal electron transport.	NAD	114-118	hippocalcin like 1	Homo sapiens	27-34
23417421-9	2013	Furthermore, GHRH increased the phosphorylation of endothelial nitric oxide synthase and AMP-activated protein kinase and preserved postischemic nicotinamide adenine dinucleotide (NAD(+)) levels.	NAD	180-187	growth hormone releasing hormone	Rattus norvegicus	13-17
27372904-8	2016	These results suggest that VILIP-3, hippocalcin, and neurocalcin-delta provide a Ca2+-dependent modulation to the NADH-dependent microsomal electron transport.	NAD	114-118	neurocalcin delta	Homo sapiens	53-70
27694803-2	2016	Here, using a proteomic approach, we identified Saccharomyces cerevisiae cytochrome b5 reductase (Cbr1) as a NADH-dependent reductase for Dph3.	NAD	109-113	cytochrome-b5 reductase	Saccharomyces cerevisiae S288C	73-96
23866629-1	2013	Type-1recessive congenital methemoglobinemia (RCM) is a rare autosomal disease characterized by a deficiency of the soluble form of nicotineamide adenine dinucleotide (NADH)-cytochrome b5 reductase (b5R) and clinically manifests as cyanosis of skin and mucous membranes.	NAD	132-166	cytochrome b5 reductase 3	Homo sapiens	185-197
23866629-1	2013	Type-1recessive congenital methemoglobinemia (RCM) is a rare autosomal disease characterized by a deficiency of the soluble form of nicotineamide adenine dinucleotide (NADH)-cytochrome b5 reductase (b5R) and clinically manifests as cyanosis of skin and mucous membranes.	NAD	132-166	cytochrome b5 reductase 3	Homo sapiens	199-202
23866629-1	2013	Type-1recessive congenital methemoglobinemia (RCM) is a rare autosomal disease characterized by a deficiency of the soluble form of nicotineamide adenine dinucleotide (NADH)-cytochrome b5 reductase (b5R) and clinically manifests as cyanosis of skin and mucous membranes.	NAD	168-172	cytochrome b5 reductase 3	Homo sapiens	185-197
23866629-1	2013	Type-1recessive congenital methemoglobinemia (RCM) is a rare autosomal disease characterized by a deficiency of the soluble form of nicotineamide adenine dinucleotide (NADH)-cytochrome b5 reductase (b5R) and clinically manifests as cyanosis of skin and mucous membranes.	NAD	168-172	cytochrome b5 reductase 3	Homo sapiens	199-202
28003588-1	2016	Citrin deficiency, an inherited defect of the liver-type mitochondrial aspartate/glutamate carrier isoform (citrin), may cause impairment of glycolysis because of an increase in the cytosolic NADH/NAD+ ratio.	NAD	192-196	solute carrier family 25 member 13	Homo sapiens	108-114
23373462-2	2013	Human nicotinamide phosphoribosyltransferase (NAMPT) replenishes the NAD pool and controls the activities of sirtuins, mono- and poly-(ADP-ribose) polymerases, and NAD nucleosidase.	NAD	69-72	nicotinamide phosphoribosyltransferase	Homo sapiens	6-44
23373462-2	2013	Human nicotinamide phosphoribosyltransferase (NAMPT) replenishes the NAD pool and controls the activities of sirtuins, mono- and poly-(ADP-ribose) polymerases, and NAD nucleosidase.	NAD	69-72	nicotinamide phosphoribosyltransferase	Homo sapiens	46-51
28003588-1	2016	Citrin deficiency, an inherited defect of the liver-type mitochondrial aspartate/glutamate carrier isoform (citrin), may cause impairment of glycolysis because of an increase in the cytosolic NADH/NAD+ ratio.	NAD	197-201	solute carrier family 25 member 13	Homo sapiens	108-114
27655688-5	2016	Here, we show that both classical histone deacetylase HDAC1 and NAD+-dependent deacetylase SIRT1 regulate acetylation level of APE1 and acetylation of APE1 enhances its AP-endonuclease activity both in vitro and in cells.	NAD	64-67	apurinic/apyrimidinic endodeoxyribonuclease 1	Homo sapiens	127-131
23201774-2	2013	The aim of this study was to investigate whether SIRT6, a member of the sirtuin family of NAD(+)-dependent protein deacetylases/ADP-ribosyltransferases, protects endothelial cells from premature senescence and dysfunction, and if so which is its mode of action.	NAD	90-93	sirtuin 6	Homo sapiens	49-54
27655688-5	2016	Here, we show that both classical histone deacetylase HDAC1 and NAD+-dependent deacetylase SIRT1 regulate acetylation level of APE1 and acetylation of APE1 enhances its AP-endonuclease activity both in vitro and in cells.	NAD	64-67	apurinic/apyrimidinic endodeoxyribonuclease 1	Homo sapiens	151-155
27592202-6	2016	Regulation of the SIRT/NAD system was associated with early (SIRT4, SIRT7, NAPRT1 and NMNAT2) and late phases (NMNAT3, NMRK2, ABCA1 and CD38) of glucose intolerance.	NAD	23-26	nicotinamide nucleotide adenylyltransferase 2	Mus musculus	86-92
23053084-2	2013	In this study, construction of an efficient NADPH-regenerating system was attempted using direct phosphorylation of NADH by NADH kinase (Pos5p) from Saccharomyces cerevisiae for producing guanosine diphosphate (GDP)-L-fucose and epsilon-caprolactone in recombinant Escherichia coli.	NAD	116-120	NADH kinase	Saccharomyces cerevisiae S288C	137-142
23509928-2	2013	The aim of this study was to determine the effect of beta-NAD(+) on matrix metalloproteinase (MMP) expression on human gingival fibroblasts (hGF), the excess production of which leads to the matrix degradation associated with the pathological processes of periodontitis.	NAD	53-64	hepatocyte growth factor	Homo sapiens	141-144
23509928-7	2013	Transcripts of NAD(+)-metabolizing enzymes, such as NAD(+)-glycohydrolase, adenosine diphosphate (ADP)-ribosylcyclase, and ADP-ribosyltransferase, were expressed by hGF as assessed by RT-PCR.	NAD	15-21	hepatocyte growth factor	Homo sapiens	165-168
24222765-6	2013	The effects of E2, PPT (a potent ER alpha -selective agonist), and DPN (a potent ER beta -selective agonist) on modulation of metastatic phenotype were determined by using in vitro scratch wound assay and invasion assay.	NAD	67-70	estrogen receptor 2	Homo sapiens	81-88
27760313-5	2016	The model reproduces the dampened clock gene expression and NAD+ rhythms reported for mice on a high-fat diet and predicts that this effect may be pharmacologically rescued by timed REV-ERB agonist administration.	NAD	60-64	nuclear receptor subfamily 1, group D, member 2	Mus musculus	182-189
24146631-5	2013	Interestingly, a genetic assay suggests that Tdh3, an NAD(+)-binding protein, influences nuclear NAD(+) levels; we speculate that Tdh3 links nuclear Sir2 with NAD(+) from the cytoplasm.	NAD	54-60	glyceraldehyde-3-phosphate dehydrogenase (phosphorylating) TDH3	Saccharomyces cerevisiae S288C	45-49
27527516-6	2016	Enhanced resistance was also independent of the nicotinamide salvage pathway, which uses nicotinamide as a substrate to generate NAD+, and of a DNA damage-induced increase in the salvage enzyme Pnc1 Our data suggest a novel and unexpected function for nicotinamide that has broad implications for its use in the study of sirtuin biology across model systems.	NAD	129-133	nicotinamidase	Saccharomyces cerevisiae S288C	194-198
24146631-5	2013	Interestingly, a genetic assay suggests that Tdh3, an NAD(+)-binding protein, influences nuclear NAD(+) levels; we speculate that Tdh3 links nuclear Sir2 with NAD(+) from the cytoplasm.	NAD	97-103	glyceraldehyde-3-phosphate dehydrogenase (phosphorylating) TDH3	Saccharomyces cerevisiae S288C	45-49
24146631-5	2013	Interestingly, a genetic assay suggests that Tdh3, an NAD(+)-binding protein, influences nuclear NAD(+) levels; we speculate that Tdh3 links nuclear Sir2 with NAD(+) from the cytoplasm.	NAD	97-103	glyceraldehyde-3-phosphate dehydrogenase (phosphorylating) TDH3	Saccharomyces cerevisiae S288C	45-49
27790277-12	2016	CONCLUSION: Our results suggest that beta-lapachone can protect against bleomycin-induced lung inflammation and fibrosis in mice and TGF-beta1-induced EMT in vitro, by elevating the NAD+/NADH ratio through NQO1 activation.	NAD	182-186	transforming growth factor, beta 1	Mus musculus	133-142
23472183-2	2013	Malate can be synthesized from fumarate by the enzyme fumarase and further oxidized to oxaloacetate by malate dehydrogenase with the accompanying reduction of NAD.	NAD	159-162	putative fumarate hydratase, mitochondrial	Caenorhabditis elegans	54-62
27337995-3	2016	We have observed that p49/STRAP alters the intracellular NAD/NADH ratio and induces protein deacetylation.	NAD	57-60	serine/threonine kinase receptor associated protein	Homo sapiens	26-31
23383098-8	2013	In the actin-activated ATPase activity assay, the rate of NADH oxidation was higher in the wild-type myosin VIIA, indicating that the ATPase activity in the p.R668H mutant myosin VIIA was significantly destroyed.	NAD	58-62	dynein axonemal heavy chain 8	Homo sapiens	23-29
23383098-8	2013	In the actin-activated ATPase activity assay, the rate of NADH oxidation was higher in the wild-type myosin VIIA, indicating that the ATPase activity in the p.R668H mutant myosin VIIA was significantly destroyed.	NAD	58-62	dynein axonemal heavy chain 8	Homo sapiens	134-140
23995269-1	2013	The NAD-synthesising enzyme Nmnat2 is a critical survival factor for axons in vitro and in vivo.	NAD	4-7	nicotinamide nucleotide adenylyltransferase 2	Mus musculus	28-34
27337995-3	2016	We have observed that p49/STRAP alters the intracellular NAD/NADH ratio and induces protein deacetylation.	NAD	61-65	serine/threonine kinase receptor associated protein	Homo sapiens	26-31
27390344-6	2016	Furthermore, NAPRT1 downregulation, which we show occurs in all RCC cell lines tested, makes this tumor highly dependent on NAMPT for its NAD requirements, such that inhibition of NAMPT by KPT-9274 leads to decreased survival of these rapidly proliferating cells.	NAD	138-141	nicotinamide phosphoribosyltransferase	Homo sapiens	124-129
23132853-2	2012	We and others previously showed that ALC1 possesses a cryptic ATP-dependent nucleosome remodeling activity that is potently activated in the presence of PARP1 and NAD(+), its substrate for PAR synthesis.	NAD	163-169	chromodomain helicase DNA binding protein 1 like	Homo sapiens	37-41
23132853-3	2012	In this work, we dissected the mechanism by which PARP1 and NAD(+) activate ALC1 nucleosome remodeling.	NAD	60-66	chromodomain helicase DNA binding protein 1 like	Homo sapiens	76-80
23106432-1	2012	Human UDP-alpha-D-glucose dehydrogenase (hUGDH) catalyzes the NAD(+)-dependent oxidation of UDP-alpha-D-glucose (UDG) to produce UDP-alpha-D-glucuronic acid.	NAD	62-68	UDP-glucose 6-dehydrogenase	Homo sapiens	41-46
23079621-4	2012	Here we report that SIRT1, an NAD-dependent, class III deacetylase, forms a complex with RFX5.	NAD	30-33	regulatory factor X5	Homo sapiens	89-93
23079621-5	2012	Over-expression of SIRT1 or NAMPT, which synthesizes NAD+ to activate SIRT1, or treatment with the SIRT1 agonist resveratrol decreases RFX5 acetylation and disrupts repression of the COL1A2 promoter activity by RFX5.	NAD	53-57	nicotinamide phosphoribosyltransferase	Homo sapiens	28-33
22967499-7	2012	Addition of leucine to HFD correlated with increased expression of SIRT1 and NAMPT (nicotinamide phosphoribosyltransferase) as well as higher intracellular NAD(+) levels, which decreased acetylation of peroxisome proliferator-activated receptor-gamma coactivator 1alpha (PGC1alpha) and forkhead box O1 (FoxO1).	NAD	156-162	peroxisome proliferative activated receptor, gamma, coactivator 1 alpha	Mus musculus	202-269
22967499-7	2012	Addition of leucine to HFD correlated with increased expression of SIRT1 and NAMPT (nicotinamide phosphoribosyltransferase) as well as higher intracellular NAD(+) levels, which decreased acetylation of peroxisome proliferator-activated receptor-gamma coactivator 1alpha (PGC1alpha) and forkhead box O1 (FoxO1).	NAD	156-162	peroxisome proliferative activated receptor, gamma, coactivator 1 alpha	Mus musculus	271-280
23086143-2	2012	The yeast NDH-2 (Ndi1) oxidizes NADH on the matrix side and reduces ubiquinone to maintain mitochondrial NADH/NAD(+) homeostasis.	NAD	32-36	NADH-ubiquinone reductase (H(+)-translocating) NDI1	Saccharomyces cerevisiae S288C	17-21
23086143-2	2012	The yeast NDH-2 (Ndi1) oxidizes NADH on the matrix side and reduces ubiquinone to maintain mitochondrial NADH/NAD(+) homeostasis.	NAD	105-109	NADH-ubiquinone reductase (H(+)-translocating) NDI1	Saccharomyces cerevisiae S288C	17-21
23086143-2	2012	The yeast NDH-2 (Ndi1) oxidizes NADH on the matrix side and reduces ubiquinone to maintain mitochondrial NADH/NAD(+) homeostasis.	NAD	110-116	NADH-ubiquinone reductase (H(+)-translocating) NDI1	Saccharomyces cerevisiae S288C	17-21
23086143-5	2012	Here we solve the crystal structures of Ndi1 in its substrate-free, NADH-, ubiquinone- and NADH-ubiquinone-bound states, to help understand the catalytic mechanism of NDH-2s.	NAD	68-72	NADH-ubiquinone reductase (H(+)-translocating) NDI1	Saccharomyces cerevisiae S288C	40-44
23086143-8	2012	NADH and UQ(I) can bind to Ndi1 simultaneously to form a substrate-protein complex.	NAD	0-4	NADH-ubiquinone reductase (H(+)-translocating) NDI1	Saccharomyces cerevisiae S288C	27-31
26605631-1	2012	Formate dehydrogenase (FDH) catalyzes the oxidation of formic acid to carbon dioxide using nicotinamide adenine dinucleotide (NAD(+)) as a cofactor.	NAD	91-124	alcohol dehydrogenase 5 (class III), chi polypeptide	Homo sapiens	0-21
26605631-1	2012	Formate dehydrogenase (FDH) catalyzes the oxidation of formic acid to carbon dioxide using nicotinamide adenine dinucleotide (NAD(+)) as a cofactor.	NAD	91-124	alcohol dehydrogenase 5 (class III), chi polypeptide	Homo sapiens	23-26
26605631-1	2012	Formate dehydrogenase (FDH) catalyzes the oxidation of formic acid to carbon dioxide using nicotinamide adenine dinucleotide (NAD(+)) as a cofactor.	NAD	126-133	alcohol dehydrogenase 5 (class III), chi polypeptide	Homo sapiens	0-21
26605631-1	2012	Formate dehydrogenase (FDH) catalyzes the oxidation of formic acid to carbon dioxide using nicotinamide adenine dinucleotide (NAD(+)) as a cofactor.	NAD	126-133	alcohol dehydrogenase 5 (class III), chi polypeptide	Homo sapiens	23-26
23137106-2	2012	Telmisartan has been reported to function as a partial agonist of the peroxisome proliferator-activated receptor (PPAR) gamma, which is also targeted by the nicotinamide adenine dinucleotide (NAD)-dependent deacetylase (SIRT1).	NAD	157-190	peroxisome proliferator activated receptor gamma	Mus musculus	70-125
23137106-2	2012	Telmisartan has been reported to function as a partial agonist of the peroxisome proliferator-activated receptor (PPAR) gamma, which is also targeted by the nicotinamide adenine dinucleotide (NAD)-dependent deacetylase (SIRT1).	NAD	192-195	peroxisome proliferator activated receptor gamma	Mus musculus	70-125
22752181-4	2012	Two-dimensional SDS-polyacrylamide gel electrophoresis and subsequent peptide mass fingerprinting using matrix-assisted laser desorption and ionization time-of-flight mass spectrometry revealed that the 42 kDa protein was NAD-dependent sorbitol dehydrogenase (SDH).	NAD	222-225	sorbitol dehydrogenase	Rattus norvegicus	236-258
22752181-4	2012	Two-dimensional SDS-polyacrylamide gel electrophoresis and subsequent peptide mass fingerprinting using matrix-assisted laser desorption and ionization time-of-flight mass spectrometry revealed that the 42 kDa protein was NAD-dependent sorbitol dehydrogenase (SDH).	NAD	222-225	sorbitol dehydrogenase	Rattus norvegicus	260-263
22752181-7	2012	Pretreatment with the cofactor NAD, but not NADP or FAD, markedly prevented aggregation of SDH.	NAD	31-34	sorbitol dehydrogenase	Rattus norvegicus	91-94
22752181-8	2012	Such a protective effect of NAD on the aggregation of SDH caused by MeHg is discussed.	NAD	28-31	sorbitol dehydrogenase	Rattus norvegicus	54-57
24900427-0	2012	Inhibitors of the NAD(+)-Dependent Protein Desuccinylase and Demalonylase Sirt5.	NAD	18-24	sirtuin 5	Homo sapiens	74-79
22249251-7	2012	NQO1 protection of C/EBPalpha required binding of NADH with NQO1.	NAD	50-54	CCAAT/enhancer binding protein (C/EBP), alpha	Mus musculus	19-29
22613355-6	2012	Differential scanning fluorimetry revealed that p.K161N-hGALE was more stable than the wild-type protein and only changed stability in the presence of UDP-N-acetylglucosamine and NAD(+).	NAD	179-185	UDP-galactose-4-epimerase	Homo sapiens	56-61
22613355-8	2012	We postulate that p.K161N-hGALE causes its effects by abolishing an important interaction between the protein and the cofactor, whereas p.D175N-hGALE is predicted to remove a stabilizing salt bridge between the ends of two alpha-helices that contain residues that interact with NAD(+).	NAD	278-284	UDP-galactose-4-epimerase	Homo sapiens	26-31
22933245-3	2012	To better understand the mechanisms that determine the response to PARP inhibitors, we investigated whether enzymes involved in metabolism of the PARP substrate, beta-NAD(+) , might alter the response to a clinical PARP inhibitor.	NAD	162-173	collagen type XI alpha 2 chain	Homo sapiens	146-150
22933245-3	2012	To better understand the mechanisms that determine the response to PARP inhibitors, we investigated whether enzymes involved in metabolism of the PARP substrate, beta-NAD(+) , might alter the response to a clinical PARP inhibitor.	NAD	162-173	collagen type XI alpha 2 chain	Homo sapiens	146-150
22933245-5	2012	NAMPT is a rate-limiting enzyme involved in the generation of the PARP substrate beta-NAD(+)  and the suppression of beta-NAD(+)  levels by NAMPT inhibition most likely explains these observations.	NAD	81-92	nicotinamide phosphoribosyltransferase	Homo sapiens	0-5
22933245-5	2012	NAMPT is a rate-limiting enzyme involved in the generation of the PARP substrate beta-NAD(+)  and the suppression of beta-NAD(+)  levels by NAMPT inhibition most likely explains these observations.	NAD	81-92	collagen type XI alpha 2 chain	Homo sapiens	66-70
22933245-5	2012	NAMPT is a rate-limiting enzyme involved in the generation of the PARP substrate beta-NAD(+)  and the suppression of beta-NAD(+)  levels by NAMPT inhibition most likely explains these observations.	NAD	117-128	nicotinamide phosphoribosyltransferase	Homo sapiens	0-5
22933245-5	2012	NAMPT is a rate-limiting enzyme involved in the generation of the PARP substrate beta-NAD(+)  and the suppression of beta-NAD(+)  levels by NAMPT inhibition most likely explains these observations.	NAD	117-128	collagen type XI alpha 2 chain	Homo sapiens	66-70
22933245-5	2012	NAMPT is a rate-limiting enzyme involved in the generation of the PARP substrate beta-NAD(+)  and the suppression of beta-NAD(+)  levels by NAMPT inhibition most likely explains these observations.	NAD	117-128	nicotinamide phosphoribosyltransferase	Homo sapiens	140-145
22829200-11	2012	The lipid soluble antioxidant alpha-tocopherol can selectively protect SDH(var+) cells from oxidative damage, apoptosis resistance, and rebalance redox metabolites NAD/NADH.	NAD	164-167	serine dehydratase	Homo sapiens	71-74
22829200-11	2012	The lipid soluble antioxidant alpha-tocopherol can selectively protect SDH(var+) cells from oxidative damage, apoptosis resistance, and rebalance redox metabolites NAD/NADH.	NAD	168-172	serine dehydratase	Homo sapiens	71-74
22829588-2	2012	We hypothesized that NAD(+) would modulate the anti-inflammatory cytokine Transforming Growth Factor (TGF)-beta1.	NAD	21-27	transforming growth factor, beta 1	Mus musculus	74-112
22829588-3	2012	Indeed, NAD(+) led to increases in both active and latent cell-associated TGF-beta1 in RAW 264.7 mouse macrophages as well as in primary peritoneal macrophages isolated from both C3H/HeJ (TLR4-mutant) and C3H/HeOuJ (wild-type controls for C3H/HeJ) mice.	NAD	8-14	transforming growth factor, beta 1	Mus musculus	74-83
22829588-5	2012	Treatment of macrophages with the cADPR analog 3-deaza-cADPR or Ca(2+) ionophores recapitulated the effects of NAD(+) on TGF-beta1, whereas the cADPR antagonist 8-Br-cADPR, Ca(2+) chelation, and antagonism of L-type Ca(2+) channels suppressed these effects.	NAD	111-117	transforming growth factor, beta 1	Mus musculus	121-130
22829588-6	2012	The time and dose effects of NAD(+) on TGF-beta1 were complex and could be modeled both statistically and mathematically.	NAD	29-35	transforming growth factor, beta 1	Mus musculus	39-48
22829588-7	2012	Model-predicted levels of TGF-beta1 protein and mRNA were largely confirmed experimentally but also suggested the presence of other mechanisms of regulation of TGF-beta1 by NAD(+).	NAD	173-179	transforming growth factor, beta 1	Mus musculus	26-35
22842227-5	2012	NMNAT1 resides in the previously identified LCA9 locus and encodes the nuclear isoform of nicotinamide mononucleotide adenylyltransferase, a rate-limiting enzyme in nicotinamide adenine dinucleotide (NAD(+)) biosynthesis(4,5).	NAD	165-198	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	0-6
22842227-5	2012	NMNAT1 resides in the previously identified LCA9 locus and encodes the nuclear isoform of nicotinamide mononucleotide adenylyltransferase, a rate-limiting enzyme in nicotinamide adenine dinucleotide (NAD(+)) biosynthesis(4,5).	NAD	165-198	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	44-48
22842227-5	2012	NMNAT1 resides in the previously identified LCA9 locus and encodes the nuclear isoform of nicotinamide mononucleotide adenylyltransferase, a rate-limiting enzyme in nicotinamide adenine dinucleotide (NAD(+)) biosynthesis(4,5).	NAD	200-207	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	0-6
22842227-5	2012	NMNAT1 resides in the previously identified LCA9 locus and encodes the nuclear isoform of nicotinamide mononucleotide adenylyltransferase, a rate-limiting enzyme in nicotinamide adenine dinucleotide (NAD(+)) biosynthesis(4,5).	NAD	200-207	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	44-48
22842229-1	2012	In addition to its activity in nicotinamide adenine dinucleotide (NAD(+)) synthesis, the nuclear nicotinamide mononucleotide adenyltransferase NMNAT1 acts as a chaperone that protects against neuronal activity-induced degeneration.	NAD	31-64	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	143-149
22842229-1	2012	In addition to its activity in nicotinamide adenine dinucleotide (NAD(+)) synthesis, the nuclear nicotinamide mononucleotide adenyltransferase NMNAT1 acts as a chaperone that protects against neuronal activity-induced degeneration.	NAD	66-72	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	143-149
22842230-4	2012	Functional assays of the proteins encoded by the mutant alleles identified in our study showed that the mutations reduce the enzymatic activity of NMNAT1 in NAD biosynthesis and affect protein folding.	NAD	157-160	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	147-153
22497727-0	2012	In situ regeneration of NADH via lipoamide dehydrogenase-catalyzed electron transfer reaction evidenced by spectroelectrochemistry.	NAD	24-28	dihydrolipoamide dehydrogenase	Homo sapiens	33-56
22814755-7	2012	Respiration and growth rates in heterotrophic conditions were significantly altered in the double mutants investigated, suggesting that Nda1 plays a role in the oxidation of matrix NADH in the absence of complex I.	NAD	181-185	uncharacterized protein	Chlamydomonas reinhardtii	136-140
22733276-7	2012	Together with two-photon imaging of NAD(P)H and confocal imaging of lipoamide dehydrogenase (LipDH) autofluorescence, we show that the ETC predominantly draws electrons from LipDH/NADH-dependent Complex I rather than from ETF/FADH(2)-dependent ETF:CoQ oxidoreductase (ETF-QO).	NAD	180-184	dihydrolipoamide dehydrogenase	Homo sapiens	68-91
22733276-7	2012	Together with two-photon imaging of NAD(P)H and confocal imaging of lipoamide dehydrogenase (LipDH) autofluorescence, we show that the ETC predominantly draws electrons from LipDH/NADH-dependent Complex I rather than from ETF/FADH(2)-dependent ETF:CoQ oxidoreductase (ETF-QO).	NAD	180-184	dihydrolipoamide dehydrogenase	Homo sapiens	93-98
22733276-7	2012	Together with two-photon imaging of NAD(P)H and confocal imaging of lipoamide dehydrogenase (LipDH) autofluorescence, we show that the ETC predominantly draws electrons from LipDH/NADH-dependent Complex I rather than from ETF/FADH(2)-dependent ETF:CoQ oxidoreductase (ETF-QO).	NAD	180-184	dihydrolipoamide dehydrogenase	Homo sapiens	174-179
22648412-9	2012	Expression of mutant Htt results in decreased deacetylase activity of SIRT3 and further leads to reduction in cellular NAD(+) levels and mitochondrial biogenesis in cells.	NAD	119-125	huntingtin	Homo sapiens	21-24
22487558-1	2012	Arabidopsis mitochondria contain two NAD(+)-malic enzymes, NAD-ME1 and NAD-ME2.	NAD	37-43	NAD-dependent malic enzyme 2	Arabidopsis thaliana	71-78
22487558-9	2012	Together, the results indicate that the differential fumarate regulation of Arabidopsis NAD-MEs, which is further modulated by NAD(+) availability, is related to the gaining of an allosteric site for fumarate in NAD-ME1 and an active site-associated inhibition by this C(4)-organic acid in NAD-ME2.	NAD	127-133	NAD-dependent malic enzyme 2	Arabidopsis thaliana	290-297
22334709-1	2012	NMNAT-1 and PARP-1, two key enzymes in the NAD(+) metabolic pathway, localize to the nucleus where integration of their enzymatic activities has the potential to control a variety of nuclear processes.	NAD	43-49	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	0-7
22334709-3	2012	Specifically, we show that PARP-1 recruits NMNAT-1 to promoters where it produces NAD(+) to support PARP-1 catalytic activity, but also enhances the enzymatic activity of PARP-1 independently of NAD(+) production.	NAD	82-88	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	43-50
22334709-4	2012	Furthermore, using two-photon excitation microscopy, we show that NMNAT-1 catalyzes the production of NAD(+) in a nuclear pool that may be distinct from other cellular compartments.	NAD	102-108	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	66-73
22244860-3	2012	We investigated whether aspirin mitigates resistin-induced endothelial dysfunction via modulation of reactive oxygen species (ROS) generation and explored the role that AMP-activated protein kinase (AMPK), a negative regulator of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, plays in the suppressive effects of aspirin on resistin-induced endothelial dysfunction.	NAD	230-263	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	199-203
22257560-9	2012	The mRNA expression of all EPs and FP are downregulated by estradiol and the ERalpha specific agonist PPT, whereas the ERbeta specific agonist DPN downregulates only EP2 and EP4.	NAD	143-146	prostaglandin E receptor 4	Rattus norvegicus	174-177
22119381-1	2012	Nicotinamide phosphoribosyltransferase (NAMPT) is a key enzyme in the salvaging pathway for the synthesis of nicotinamide adenine dinucleotide (NAD) that is involved in cell metabolism and proliferation.	NAD	109-142	nicotinamide phosphoribosyltransferase	Homo sapiens	0-38
22119381-1	2012	Nicotinamide phosphoribosyltransferase (NAMPT) is a key enzyme in the salvaging pathway for the synthesis of nicotinamide adenine dinucleotide (NAD) that is involved in cell metabolism and proliferation.	NAD	109-142	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
22119381-1	2012	Nicotinamide phosphoribosyltransferase (NAMPT) is a key enzyme in the salvaging pathway for the synthesis of nicotinamide adenine dinucleotide (NAD) that is involved in cell metabolism and proliferation.	NAD	144-147	nicotinamide phosphoribosyltransferase	Homo sapiens	0-38
22119381-1	2012	Nicotinamide phosphoribosyltransferase (NAMPT) is a key enzyme in the salvaging pathway for the synthesis of nicotinamide adenine dinucleotide (NAD) that is involved in cell metabolism and proliferation.	NAD	144-147	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
22119381-2	2012	NAMPT is normally absent in astrocyte but highly expressed in glioblastoma, suggesting that it may promote cell survival through synthesizing more NAD.	NAD	147-150	nicotinamide phosphoribosyltransferase	Homo sapiens	0-5
21883939-5	2012	A critical source of endothelial ROS is a family of non-phagocytic nicotinamide adenine dinucleotide phosphate (NADPH) oxidases, including the prototypic Nox2-based NADPH oxidases, Nox1, Nox4 and Nox5.	NAD	67-100	NADPH oxidase 1	Homo sapiens	181-185
21883939-5	2012	A critical source of endothelial ROS is a family of non-phagocytic nicotinamide adenine dinucleotide phosphate (NADPH) oxidases, including the prototypic Nox2-based NADPH oxidases, Nox1, Nox4 and Nox5.	NAD	67-100	NADPH oxidase 4	Homo sapiens	187-191
23939409-7	2012	Relationships among PGC-1alpha and its downstream targets NRF1 and TFAM were very similar in PD and CTL and were related to mitochondrial NADH-driven electron flow.	NAD	138-142	nuclear respiratory factor 1	Homo sapiens	58-62
23028781-6	2012	In contrast, we find similar values for Sirt5 and Sirt3 for the intrinsic NAD(+) affinity as well as the apparent NAD(+) affinity in presence of peptide.	NAD	74-80	sirtuin 5	Homo sapiens	40-45
23028781-6	2012	In contrast, we find similar values for Sirt5 and Sirt3 for the intrinsic NAD(+) affinity as well as the apparent NAD(+) affinity in presence of peptide.	NAD	114-120	sirtuin 5	Homo sapiens	40-45
22013015-10	2011	GLP-1 decreases both the NAD(+)-to-NADH ratio and SirT1 expression in INS cells and isolated islets, thereby providing possible mechanisms by which GLP-1 could modulate SirT1 activity.	NAD	25-31	glucagon	Mus musculus	0-5
22013015-10	2011	GLP-1 decreases both the NAD(+)-to-NADH ratio and SirT1 expression in INS cells and isolated islets, thereby providing possible mechanisms by which GLP-1 could modulate SirT1 activity.	NAD	25-31	glucagon	Mus musculus	148-153
22013015-10	2011	GLP-1 decreases both the NAD(+)-to-NADH ratio and SirT1 expression in INS cells and isolated islets, thereby providing possible mechanisms by which GLP-1 could modulate SirT1 activity.	NAD	35-39	glucagon	Mus musculus	0-5
22013015-10	2011	GLP-1 decreases both the NAD(+)-to-NADH ratio and SirT1 expression in INS cells and isolated islets, thereby providing possible mechanisms by which GLP-1 could modulate SirT1 activity.	NAD	35-39	glucagon	Mus musculus	148-153
21743967-1	2011	Nicotinamide phosphoribosyltransferase (Nampt), an enzyme involved in the NAD+ salvage pathway, is over-expressed and important in the carcinogenesis in several types of cancers.	NAD	74-78	nicotinamide phosphoribosyltransferase	Homo sapiens	0-38
21743967-1	2011	Nicotinamide phosphoribosyltransferase (Nampt), an enzyme involved in the NAD+ salvage pathway, is over-expressed and important in the carcinogenesis in several types of cancers.	NAD	74-78	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
21982712-2	2011	One such pathway is mediated by nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme in mammalian NAD(+) biosynthesis, and the NAD(+)-dependent protein deacetylase SIRT1.	NAD	118-124	nicotinamide phosphoribosyltransferase	Homo sapiens	32-70
21982712-2	2011	One such pathway is mediated by nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme in mammalian NAD(+) biosynthesis, and the NAD(+)-dependent protein deacetylase SIRT1.	NAD	118-124	nicotinamide phosphoribosyltransferase	Homo sapiens	72-77
21982712-2	2011	One such pathway is mediated by nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme in mammalian NAD(+) biosynthesis, and the NAD(+)-dependent protein deacetylase SIRT1.	NAD	147-153	nicotinamide phosphoribosyltransferase	Homo sapiens	32-70
21982712-2	2011	One such pathway is mediated by nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme in mammalian NAD(+) biosynthesis, and the NAD(+)-dependent protein deacetylase SIRT1.	NAD	147-153	nicotinamide phosphoribosyltransferase	Homo sapiens	72-77
27648125-6	2016	We further found that the injection of NAD(+) can significantly decrease I/R-induced apoptotic damage in the heart: NAD(+) administration can both decrease the TUNEL signals, Bax, cleaved caspase-3 levels and increase the Bcl-XL levels in the rats that are subjected to myocardial I/R injury.	NAD	39-45	Bcl2-like 1	Rattus norvegicus	222-228
27648125-6	2016	We further found that the injection of NAD(+) can significantly decrease I/R-induced apoptotic damage in the heart: NAD(+) administration can both decrease the TUNEL signals, Bax, cleaved caspase-3 levels and increase the Bcl-XL levels in the rats that are subjected to myocardial I/R injury.	NAD	116-122	Bcl2-like 1	Rattus norvegicus	222-228
27394173-4	2016	During reverse electron transfer (RET) from NADH, purified Ogdh generated ~3-3.5x more O2( -)/H2O2 in comparison to Pdh when metabolizing 0.5-10microM NADH.	NAD	151-155	oxoglutarate dehydrogenase	Homo sapiens	59-63
32263141-2	2016	The nitro-benzyl substrate of HRCNs could be selectively reduced by NTR/NADH that was overexpressed under hypoxic conditions, while it was not responsive to reductive agents (GSH or DTT) commonly existing in biological systems.	NAD	72-76	neurotensin receptor 1	Homo sapiens	68-71
26568303-1	2016	Nicotinamide phosphoribosyltransferase (NAMPT) is a rate-limiting enzyme involved in NAD+ biosynthesis.	NAD	85-89	nicotinamide phosphoribosyltransferase	Homo sapiens	0-38
26568303-1	2016	Nicotinamide phosphoribosyltransferase (NAMPT) is a rate-limiting enzyme involved in NAD+ biosynthesis.	NAD	85-89	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
26568303-7	2016	Finally, we showed that NAMPT increased the pool of NAD+ that could be converted to NADPH through the pentose phosphate pathway and inhibited the depletion of reduced glutathione under glucose deprivation.	NAD	52-56	nicotinamide phosphoribosyltransferase	Homo sapiens	24-29
27128025-2	2016	Although intracellular NAMPT is a key enzyme in controlling NAD metabolism, eNAMPT has been reported to function as a cytokine, with many roles in physiology and pathology.	NAD	60-63	nicotinamide phosphoribosyltransferase	Homo sapiens	23-28
21739347-9	2011	RESULTS: We found that the Wld(S) gene is expressed in islets and protects beta cells against multiple low doses of STZ by increasing the NAD/NADH ratio, maintaining the ATP concentration, and reducing apoptosis.	NAD	138-141	wallerian degeneration	Mus musculus	27-30
21739347-9	2011	RESULTS: We found that the Wld(S) gene is expressed in islets and protects beta cells against multiple low doses of STZ by increasing the NAD/NADH ratio, maintaining the ATP concentration, and reducing apoptosis.	NAD	142-146	wallerian degeneration	Mus musculus	27-30
21605206-2	2011	Here, we analyzed how duplicated genes encoding quinolinate phosphoribosyltransferase (QPT), an enzyme involved in the synthesis of nicotinamide adenine dinucleotide (NAD) and the pyridine moiety of nicotine, are regulated by the jasmonate-responsive transcriptional factor ERF189 that functions critically for nicotine biosynthesis in tobacco (Nicotiana tabacum).	NAD	132-165	nicotinate-nucleotide pyrophosphorylase [carboxylating], chloroplastic-like	Nicotiana tabacum	48-85
21605206-2	2011	Here, we analyzed how duplicated genes encoding quinolinate phosphoribosyltransferase (QPT), an enzyme involved in the synthesis of nicotinamide adenine dinucleotide (NAD) and the pyridine moiety of nicotine, are regulated by the jasmonate-responsive transcriptional factor ERF189 that functions critically for nicotine biosynthesis in tobacco (Nicotiana tabacum).	NAD	132-165	nicotinate-nucleotide pyrophosphorylase [carboxylating], chloroplastic-like	Nicotiana tabacum	87-90
21605206-2	2011	Here, we analyzed how duplicated genes encoding quinolinate phosphoribosyltransferase (QPT), an enzyme involved in the synthesis of nicotinamide adenine dinucleotide (NAD) and the pyridine moiety of nicotine, are regulated by the jasmonate-responsive transcriptional factor ERF189 that functions critically for nicotine biosynthesis in tobacco (Nicotiana tabacum).	NAD	167-170	nicotinate-nucleotide pyrophosphorylase [carboxylating], chloroplastic-like	Nicotiana tabacum	48-85
21605206-2	2011	Here, we analyzed how duplicated genes encoding quinolinate phosphoribosyltransferase (QPT), an enzyme involved in the synthesis of nicotinamide adenine dinucleotide (NAD) and the pyridine moiety of nicotine, are regulated by the jasmonate-responsive transcriptional factor ERF189 that functions critically for nicotine biosynthesis in tobacco (Nicotiana tabacum).	NAD	167-170	nicotinate-nucleotide pyrophosphorylase [carboxylating], chloroplastic-like	Nicotiana tabacum	87-90
21730068-0	2011	Structural determinants of discrimination of NAD+ from NADH in yeast mitochondrial NADH kinase Pos5.	NAD	45-49	NADH kinase	Saccharomyces cerevisiae S288C	95-99
21730068-0	2011	Structural determinants of discrimination of NAD+ from NADH in yeast mitochondrial NADH kinase Pos5.	NAD	55-59	NADH kinase	Saccharomyces cerevisiae S288C	95-99
20964598-1	2011	In several cell types, a regulated efflux of NAD(+) across Connexin 43 hemichannels (Cx43 HC) can occur, and extracellular NAD(+) (NAD(+)(e)) affects cell-specific functions.	NAD	45-51	gap junction protein alpha 1	Homo sapiens	59-70
20964598-1	2011	In several cell types, a regulated efflux of NAD(+) across Connexin 43 hemichannels (Cx43 HC) can occur, and extracellular NAD(+) (NAD(+)(e)) affects cell-specific functions.	NAD	45-51	gap junction protein alpha 1	Homo sapiens	85-89
20964598-2	2011	We studied the capability of bone marrow-derived human mesenchymal stem cells (MSC) to release intracellular NAD(+) through Cx43 HC.	NAD	109-115	gap junction protein alpha 1	Homo sapiens	124-128
21477609-8	2011	An increase in ERbeta levels, with diminished ERalpha/ERbeta ratio, was observed in the tumors from mice treated with DPN/letrozole combination compared to single agents and control.	NAD	118-121	estrogen receptor 2 (beta)	Mus musculus	15-21
21477609-8	2011	An increase in ERbeta levels, with diminished ERalpha/ERbeta ratio, was observed in the tumors from mice treated with DPN/letrozole combination compared to single agents and control.	NAD	118-121	estrogen receptor 2 (beta)	Mus musculus	54-60
21504897-12	2011	When taken up into the organelles, NMN (together with ATP) serves as substrate of NMNAT3 to form NAD.	NAD	97-100	nicotinamide nucleotide adenylyltransferase 3	Homo sapiens	82-88
21504897-13	2011	NMNAT3 was conclusively localized to the mitochondrial matrix and is the only known enzyme of NAD synthesis residing within these organelles.	NAD	94-97	nicotinamide nucleotide adenylyltransferase 3	Homo sapiens	0-6
21256123-12	2011	In addition, hepatic cytosolic ALDH activity was induced by acrolein when 1mM NAD(+) was used as cofactor, suggesting an Aldh1a1-protective mechanism against acrolein toxicity in mice liver.	NAD	78-84	aldehyde dehydrogenase family 1, subfamily A1	Mus musculus	31-35
27282776-0	2016	Enhancement by GOSPEL protein of GAPDH aggregation induced by nitric oxide donor and its inhibition by NAD(.).	NAD	103-109	Rab interacting lysosomal protein like 1	Homo sapiens	15-21
21256123-12	2011	In addition, hepatic cytosolic ALDH activity was induced by acrolein when 1mM NAD(+) was used as cofactor, suggesting an Aldh1a1-protective mechanism against acrolein toxicity in mice liver.	NAD	78-84	aldehyde dehydrogenase family 1, subfamily A1	Mus musculus	121-128
27282776-5	2016	NAD(+) inhibited both GAPDH aggregation and co-aggregation with GOSPEL, a hitherto undescribed effect of the coenzyme against the consequences of oxidative stress.	NAD	0-6	Rab interacting lysosomal protein like 1	Homo sapiens	64-70
27059482-2	2016	In this study, xylose-converting ability of recombinant Saccharomyces cerevisiae SX6(MUT) expressing NADH-preferring xylose reductase mutant (R276H) and other xylose-metabolic enzymes, and deficient in aldehyde dehydrogenase 6 (Ald6p) were characterized at microaerobic conditions using various sugar mixtures.	NAD	101-105	aldehyde dehydrogenase (NADP(+)) ALD6	Saccharomyces cerevisiae S288C	228-233
21276436-5	2011	Cytotoxicity was attributed to increased NADH levels caused by CH(3)OH metabolism, catalyzed by ADH1, resulting in reductive stress, which reduced and released ferrous iron from Ferritin causing oxygen activation.	NAD	41-45	alcohol dehydrogenase 1C (class I), gamma polypeptide	Rattus norvegicus	96-100
27198584-1	2016	The enzyme UDP-glucose dehydrogenase (UGDH) catalyzes the reaction of UDP-glucose to UDP-glucuronate through two successive NAD(+)-dependent oxidation steps.	NAD	124-130	UDP-glucose 6-dehydrogenase	Homo sapiens	11-36
21589930-0	2011	Nrt1 and Tna1-independent export of NAD+ precursor vitamins promotes NAD+ homeostasis and allows engineering of vitamin production.	NAD	36-40	nicotinamide riboside transporter	Saccharomyces cerevisiae S288C	0-4
21589930-0	2011	Nrt1 and Tna1-independent export of NAD+ precursor vitamins promotes NAD+ homeostasis and allows engineering of vitamin production.	NAD	69-73	nicotinamide riboside transporter	Saccharomyces cerevisiae S288C	0-4
21398484-4	2011	In this work, we constructed a modified clostridial 1-butanol pathway in Escherichia coli to provide an irreversible reaction catalyzed by trans-enoyl-coenzyme A (CoA) reductase (Ter) and created NADH and acetyl-CoA driving forces to direct the flux.	NAD	196-200	Ter DNA replication terminus site binding protein	Escherichia coli	179-182
27198584-1	2016	The enzyme UDP-glucose dehydrogenase (UGDH) catalyzes the reaction of UDP-glucose to UDP-glucuronate through two successive NAD(+)-dependent oxidation steps.	NAD	124-130	UDP-glucose 6-dehydrogenase	Homo sapiens	38-42
21398484-6	2011	Without the NADH and acetyl-CoA driving forces, the Ter reaction alone only achieved about 1/10 the level of production.	NAD	12-16	Ter DNA replication terminus site binding protein	Escherichia coli	52-55
26987957-10	2016	Selective ERalpha receptor agonist, PPT, induced upregulation of both the protein level and activity of eN, while application of selective ERbeta receptor agonist, DPN, increased only the activity of eN.	NAD	164-167	5' nucleotidase, ecto	Rattus norvegicus	200-202
21166653-7	2011	Activity of ALDH3H1 was NAD+-dependent, whereas ALDH3I1 was able to use NAD+ and NADP+.	NAD	72-76	aldehyde dehydrogenase 3I1	Arabidopsis thaliana	48-55
20956937-1	2011	Nicotinamide phosphoribosyltransferase (NAMPT) is a rate-limiting enzyme in regenerating nicotinamide adenine dinucleotide (NAD(+)) from nicotinamide in mammals.	NAD	89-122	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
27258319-7	2016	We propose a model showing (i) how pyruvate derived from active glycolysis upon hypoxia is competitively used by the alanine aminotransferase/glutamate synthase cycle, leading to alanine accumulation and NAD+ regeneration.	NAD	204-208	glutamic--pyruvic transaminase	Homo sapiens	117-141
27258319-10	2016	Pyruvate produced by the reverse reaction of alanine aminotransferase is funneled to the TCA cycle, while deaminating glutamate dehydrogenase regenerates, reducing equivalent (NADH) and 2-oxoglutarate to maintain the cycle function.	NAD	176-180	glutamic--pyruvic transaminase	Homo sapiens	45-69
27078679-3	2016	In this study, we discuss these interference challenges and highlight the specific case of the diaphorase/resazurin system that can be coupled to enzymes utilizing NADH or NADPH.	NAD	164-168	dihydrolipoamide dehydrogenase	Homo sapiens	95-105
21339825-5	2011	Heterologous expression of Ndi1 in mammalian cells results in protein localization to the inner mitochondrial membrane which can function in parallel with endogenous complex I to oxidize NADH and pass electrons to ubiquinone.	NAD	187-191	NADH-ubiquinone reductase (H(+)-translocating) NDI1	Saccharomyces cerevisiae S288C	27-31
21339825-6	2011	Expression of Ndi1 in HL-1 cardiomyocytes and in neonatal rat ventricular myocytes protected the cells from simulated ischemia/reperfusion (sI/R), accompanied by lower ROS production, and preservation of ATP levels and NAD+/NADH ratios.	NAD	219-223	NADH-ubiquinone reductase (H(+)-translocating) NDI1	Saccharomyces cerevisiae S288C	14-18
21339825-6	2011	Expression of Ndi1 in HL-1 cardiomyocytes and in neonatal rat ventricular myocytes protected the cells from simulated ischemia/reperfusion (sI/R), accompanied by lower ROS production, and preservation of ATP levels and NAD+/NADH ratios.	NAD	224-228	NADH-ubiquinone reductase (H(+)-translocating) NDI1	Saccharomyces cerevisiae S288C	14-18
21068071-6	2011	Treatment of VSC4.1 motoneurons with PPT, DPN, or EST induced overexpression of ERalpha, ERbeta, or both, which contributed to neuroprotection by upregulating expression of anti-apoptotic proteins (p-AKT, p-CREB, Bcl-2, and p-Src).	NAD	42-45	estrogen receptor 2	Homo sapiens	89-95
26586573-0	2016	The NAD(+) salvage pathway modulates cancer cell viability via p73.	NAD	4-10	tumor protein p73	Homo sapiens	63-66
21068071-11	2011	Taken together, our data indicate that both ERalpha and ERbeta contribute to PPT, DPN, or EST-mediated neuroprotection with similar signaling profiles.	NAD	82-85	estrogen receptor 2	Homo sapiens	56-62
21738528-3	2011	In contrast, 30 min pretreatment with the selective ERbeta agonist, DPN, resulted in a dose-dependent neuroprotection following I/R, but was not protective following pMCAO.	NAD	68-71	estrogen receptor 2	Homo sapiens	52-58
26586573-2	2016	Here we show that the NAD(+) salvage pathway modulates cancer cell survival through the rarely mutated tumour suppressor p73.	NAD	22-28	tumor protein p73	Homo sapiens	121-124
26928119-0	2016	NAD(+) regulates Treg cell fate and promotes allograft survival via a systemic IL-10 production that is CD4(+) CD25(+) Foxp3(+) T cells independent.	NAD	0-6	interleukin 2 receptor subunit alpha	Homo sapiens	111-115
26928119-0	2016	NAD(+) regulates Treg cell fate and promotes allograft survival via a systemic IL-10 production that is CD4(+) CD25(+) Foxp3(+) T cells independent.	NAD	0-6	forkhead box P3	Homo sapiens	119-124
22179986-6	2011	A search for the histone deacetylase (HDAC) that counterbalanced CLOCK activity revealed that SIRT1, a nicotinamide adenine dinucleotide (NAD(+))-dependent HDAC, functions in a circadian manner.	NAD	103-136	clock circadian regulator	Homo sapiens	65-70
22179986-6	2011	A search for the histone deacetylase (HDAC) that counterbalanced CLOCK activity revealed that SIRT1, a nicotinamide adenine dinucleotide (NAD(+))-dependent HDAC, functions in a circadian manner.	NAD	138-145	clock circadian regulator	Homo sapiens	65-70
26928119-4	2016	Here, we investigated the impact of NAD(+) on the fate of CD4(+) CD25(+) Foxp3(+) Tregs in-depth, dissected their transcriptional signature profile and explored mechanisms underlying their conversion into IL-17A producing cells.	NAD	36-42	interleukin 2 receptor subunit alpha	Homo sapiens	65-69
26928119-4	2016	Here, we investigated the impact of NAD(+) on the fate of CD4(+) CD25(+) Foxp3(+) Tregs in-depth, dissected their transcriptional signature profile and explored mechanisms underlying their conversion into IL-17A producing cells.	NAD	36-42	forkhead box P3	Homo sapiens	73-78
26928119-5	2016	Our results demonstrate that NAD(+) promotes Treg conversion into Th17 cells in vitro and in vivo via CD25 cell surface marker.	NAD	29-35	interleukin 2 receptor subunit alpha	Homo sapiens	102-106
26928119-6	2016	Despite the reduced number of Tregs, known to promote homeostasis, and an increased number of pro-inflammatory Th17 cells, NAD(+) was able to promote an impressive allograft survival through a robust systemic IL-10 production that was CD4(+) CD25(+) Foxp3(+) independent.	NAD	123-129	interleukin 2 receptor subunit alpha	Homo sapiens	242-246
26928119-6	2016	Despite the reduced number of Tregs, known to promote homeostasis, and an increased number of pro-inflammatory Th17 cells, NAD(+) was able to promote an impressive allograft survival through a robust systemic IL-10 production that was CD4(+) CD25(+) Foxp3(+) independent.	NAD	123-129	forkhead box P3	Homo sapiens	250-255
21517775-4	2011	NMNAT is a key enzyme in all organisms catalyzing coupling of ATP and NMN or NaMN yielding NAD or NaAD, respectively.	NAD	91-94	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	0-5
21517776-0	2011	NMNAT expression and its relation to NAD metabolism.	NAD	37-40	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	0-5
26698328-7	2016	When cytochrome c was added, the supercomplex exhibited KCN-sensitive NADH oxidation; thus, the purified supercomplex was active.	NAD	70-74	LOC104968582	Bos taurus	5-17
21517776-1	2011	Nicotinamide mononucleotide adenylyltransferease (NMNAT), a rate-limiting enzyme present in all organisms, reversibly catalyzes the important step in the biosynthesis of NAD from ATP and NMN.	NAD	170-173	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	0-48
21517776-1	2011	Nicotinamide mononucleotide adenylyltransferease (NMNAT), a rate-limiting enzyme present in all organisms, reversibly catalyzes the important step in the biosynthesis of NAD from ATP and NMN.	NAD	170-173	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	50-55
21517776-5	2011	NMNAT also catalyzes the metabolic conversion of potent antitumor prodrugs like tiazofurin and benzamide riboside to their active forms which are analogs of NAD.	NAD	157-160	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	0-5
21517777-0	2011	NAMPT in regulated NAD biosynthesis and its pivotal role in human metabolism.	NAD	19-22	nicotinamide phosphoribosyltransferase	Homo sapiens	0-5
21517777-1	2011	Nicotinamide phosphoribosyltransferase (NAMPT) catalyzes the first reversible step in NAD biosynthesis and nicotinamide (NAM) salvage.	NAD	86-89	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
21517777-3	2011	NAMPT provides the mechanism to replenish the NAD pool in human metabolism.	NAD	46-49	nicotinamide phosphoribosyltransferase	Homo sapiens	0-5
26851003-1	2016	Nicotinamide phosphoribosyltransferase (NAMPT) catalyzes the rate-limiting step in NAD synthesis and is up-regulated in several human malignancies, including breast, colon, prostate, thyroid, gastric, and several hematopoietic malignancies.	NAD	83-86	nicotinamide phosphoribosyltransferase	Homo sapiens	0-38
21785227-6	2011	TRPM channels (TRPM2, TRPM4 and TRPM5) control insulin secretion levels by sensing intracellular Ca2+ increase, NAD metabolites, or hormone receptor activation.	NAD	112-115	transient receptor potential cation channel subfamily M member 5	Homo sapiens	32-37
26851003-1	2016	Nicotinamide phosphoribosyltransferase (NAMPT) catalyzes the rate-limiting step in NAD synthesis and is up-regulated in several human malignancies, including breast, colon, prostate, thyroid, gastric, and several hematopoietic malignancies.	NAD	83-86	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
26808812-5	2016	Adult NMNAT2+/- mice, which survive to adulthood, exhibited a 50% reduction of NMNAT2 protein levels in dorsal root ganglia relative to wildtype (WT) mice with no change in levels of other NMNAT isoforms (NMNAT1 or NMNAT3), NMNAT enzyme activity (i.e. NAD/NADH levels) or microtubule associated protein-2 (MAP2) or neurofilament protein levels.	NAD	252-255	nicotinamide nucleotide adenylyltransferase 2	Mus musculus	6-12
20981034-6	2011	A major source for cardiovascular, renal and neural ROS is a family of non-phagocytic nicotinamide adenine dinucleotide phosphate (NADPH) oxidases (Nox), including the prototypic Nox2 homolog-based NADPH oxidase, as well as other Noxes, such as Nox1 and Nox4.	NAD	86-119	NADPH oxidase 1	Homo sapiens	245-249
20981034-6	2011	A major source for cardiovascular, renal and neural ROS is a family of non-phagocytic nicotinamide adenine dinucleotide phosphate (NADPH) oxidases (Nox), including the prototypic Nox2 homolog-based NADPH oxidase, as well as other Noxes, such as Nox1 and Nox4.	NAD	86-119	NADPH oxidase 4	Homo sapiens	254-258
21031461-10	2011	These data suggest that high-glucose-induced PARP1 activation might play a role in glucose toxicity by down-regulating SIRT1 and AMPK activity through NAD depletion and resulting in insulin insensitivity.	NAD	151-154	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	129-133
26808812-5	2016	Adult NMNAT2+/- mice, which survive to adulthood, exhibited a 50% reduction of NMNAT2 protein levels in dorsal root ganglia relative to wildtype (WT) mice with no change in levels of other NMNAT isoforms (NMNAT1 or NMNAT3), NMNAT enzyme activity (i.e. NAD/NADH levels) or microtubule associated protein-2 (MAP2) or neurofilament protein levels.	NAD	256-260	nicotinamide nucleotide adenylyltransferase 2	Mus musculus	6-12
26658104-1	2016	Nicotinamide phosphoribosyltransferase (NAMPT) is a crucial enzyme in the biosynthesis of intracellular NAD+.	NAD	104-108	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
26658104-2	2016	NAMPT inhibitors have potent anticancer activity in several preclinical models by depleting NAD+ and ATP levels.	NAD	92-96	nicotinamide phosphoribosyltransferase	Homo sapiens	0-5
26729717-4	2016	We have also developed a new variant of the delitto perfetto methodology to place BDH1 under the control of the GAL1 promoter, resulting in a yeast strain that overexpresses butanediol dehydrogenase and formate dehydrogenase activities in the presence of galactose and regenerates NADH in the presence of formate.	NAD	281-285	galactokinase	Saccharomyces cerevisiae S288C	112-116
26678339-4	2015	Mutant IDH1 lowered NAD+ levels by downregulating the NAD+ salvage pathway enzyme nicotinate phosphoribosyltransferase (Naprt1), sensitizing to NAD+ depletion via concomitant nicotinamide phosphoribosyltransferase (NAMPT) inhibition.	NAD	20-24	nicotinamide phosphoribosyltransferase	Homo sapiens	175-213
26678339-4	2015	Mutant IDH1 lowered NAD+ levels by downregulating the NAD+ salvage pathway enzyme nicotinate phosphoribosyltransferase (Naprt1), sensitizing to NAD+ depletion via concomitant nicotinamide phosphoribosyltransferase (NAMPT) inhibition.	NAD	20-24	nicotinamide phosphoribosyltransferase	Homo sapiens	215-220
26678339-4	2015	Mutant IDH1 lowered NAD+ levels by downregulating the NAD+ salvage pathway enzyme nicotinate phosphoribosyltransferase (Naprt1), sensitizing to NAD+ depletion via concomitant nicotinamide phosphoribosyltransferase (NAMPT) inhibition.	NAD	54-58	nicotinamide phosphoribosyltransferase	Homo sapiens	175-213
26678339-4	2015	Mutant IDH1 lowered NAD+ levels by downregulating the NAD+ salvage pathway enzyme nicotinate phosphoribosyltransferase (Naprt1), sensitizing to NAD+ depletion via concomitant nicotinamide phosphoribosyltransferase (NAMPT) inhibition.	NAD	54-58	nicotinamide phosphoribosyltransferase	Homo sapiens	215-220
26678339-4	2015	Mutant IDH1 lowered NAD+ levels by downregulating the NAD+ salvage pathway enzyme nicotinate phosphoribosyltransferase (Naprt1), sensitizing to NAD+ depletion via concomitant nicotinamide phosphoribosyltransferase (NAMPT) inhibition.	NAD	54-58	nicotinamide phosphoribosyltransferase	Homo sapiens	175-213
26678339-4	2015	Mutant IDH1 lowered NAD+ levels by downregulating the NAD+ salvage pathway enzyme nicotinate phosphoribosyltransferase (Naprt1), sensitizing to NAD+ depletion via concomitant nicotinamide phosphoribosyltransferase (NAMPT) inhibition.	NAD	54-58	nicotinamide phosphoribosyltransferase	Homo sapiens	215-220
26678339-5	2015	NAD+ depletion activated the intracellular energy sensor AMPK, triggered autophagy, and resulted in cytotoxicity.	NAD	0-4	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	57-61
26482866-4	2015	Among 19 candidate enzymes involved in mammalian NAD metabolism, the mRNA expression level of nicotinamide n-methyltransferase (NNMT) was significantly increased in both the kidneys of FFA-albumin-overloaded mice and cultured PTCs stimulated with palmitate-albumin.	NAD	49-52	nicotinamide N-methyltransferase	Homo sapiens	94-126
26482866-4	2015	Among 19 candidate enzymes involved in mammalian NAD metabolism, the mRNA expression level of nicotinamide n-methyltransferase (NNMT) was significantly increased in both the kidneys of FFA-albumin-overloaded mice and cultured PTCs stimulated with palmitate-albumin.	NAD	49-52	nicotinamide N-methyltransferase	Homo sapiens	128-132
26388266-2	2015	Sirtuin5 (Sirt5) is a mitochondrial NAD(+)-dependent deacylase that catalyzes the removal of succinyl groups from proteins.	NAD	36-42	sirtuin 5	Mus musculus	0-8
26388266-2	2015	Sirtuin5 (Sirt5) is a mitochondrial NAD(+)-dependent deacylase that catalyzes the removal of succinyl groups from proteins.	NAD	36-42	sirtuin 5	Mus musculus	10-15
26428915-1	2015	The enzyme poly(ADP-ribose)polymerase (PARP) has a dual function being involved both in the poly(ADP-ribosyl)ation and being a constituent of the NAD(+) salvage pathway.	NAD	146-152	poly(ADP-ribose) polymerase	Arabidopsis thaliana	11-37
26428915-1	2015	The enzyme poly(ADP-ribose)polymerase (PARP) has a dual function being involved both in the poly(ADP-ribosyl)ation and being a constituent of the NAD(+) salvage pathway.	NAD	146-152	poly(ADP-ribose) polymerase	Arabidopsis thaliana	39-43
26230135-4	2015	Key intermediates of the proposed mechanism for the pathway leading to H2 are the porphyrin dye"s highly oxidizing singlet excited state (1)A* (E ~ +1.3 V vs NHE), its strongly reducing isobacteriochlorin analogue (E ~ +0.95 V), and the Co(I) form of C (E ~ -0.8 V), acting as catalyst for H2 formation.	NAD	237-242	solute carrier family 9 member C1	Homo sapiens	158-161
26276932-6	2015	We show the following: (i) Pex21p is required for peroxisomal import of Gpd1p as well as a key enzyme of the NAD(+) salvage pathway, Pnc1p; (ii) Pnc1p, a nicotinamidase without functional PTS2, is co-imported into peroxisomes by piggyback transport via Gpd1p.	NAD	109-115	Pex21p	Saccharomyces cerevisiae S288C	27-33
26276932-6	2015	We show the following: (i) Pex21p is required for peroxisomal import of Gpd1p as well as a key enzyme of the NAD(+) salvage pathway, Pnc1p; (ii) Pnc1p, a nicotinamidase without functional PTS2, is co-imported into peroxisomes by piggyback transport via Gpd1p.	NAD	109-115	nicotinamidase	Saccharomyces cerevisiae S288C	133-138
26276932-6	2015	We show the following: (i) Pex21p is required for peroxisomal import of Gpd1p as well as a key enzyme of the NAD(+) salvage pathway, Pnc1p; (ii) Pnc1p, a nicotinamidase without functional PTS2, is co-imported into peroxisomes by piggyback transport via Gpd1p.	NAD	109-115	nicotinamidase	Saccharomyces cerevisiae S288C	145-150
26466337-2	2015	However, alternative electron donors may exist such as cytochrome b5 reductase and cytochrome b5 (CBR and CYB5, respectively) via, which is NADH-dependent and are also anchored to the endoplasmic reticulum.	NAD	140-144	cytochrome-b5 reductase	Saccharomyces cerevisiae S288C	55-78
26466337-2	2015	However, alternative electron donors may exist such as cytochrome b5 reductase and cytochrome b5 (CBR and CYB5, respectively) via, which is NADH-dependent and are also anchored to the endoplasmic reticulum.	NAD	140-144	cytochrome-b5 reductase	Saccharomyces cerevisiae S288C	98-101
26462257-5	2015	ss-Lap is an NADPH:quinone oxidoreductase (NQO1)-bioactivatable drug that leads to NADPH depletion through high levels of reactive oxygen species (ROS) from the futile redox cycling of the drug and subsequently nicotinamide adenine dinucleotide (NAD)+ depletion through poly(ADP ribose) polymerase (PARP) hyperactivation.	NAD	211-244	leucine aminopeptidase 3	Rattus norvegicus	3-6
26462257-5	2015	ss-Lap is an NADPH:quinone oxidoreductase (NQO1)-bioactivatable drug that leads to NADPH depletion through high levels of reactive oxygen species (ROS) from the futile redox cycling of the drug and subsequently nicotinamide adenine dinucleotide (NAD)+ depletion through poly(ADP ribose) polymerase (PARP) hyperactivation.	NAD	13-16	leucine aminopeptidase 3	Rattus norvegicus	3-6
26462257-7	2015	As such, ss-lap treatment concurrent with inhibition of glutamine metabolism in mutant KRAS, NQO1 overexpressing PDA leads to massive redox imbalance, extensive DNA damage, rapid PARP-mediated NAD+ consumption, and PDA cell death-features not observed in NQO1-low, wild-type KRAS expressing cells.	NAD	193-197	leucine aminopeptidase 3	Rattus norvegicus	12-15
26177608-4	2015	Specifically, blocking nicotinamide adenine dinucleotide (NAD) biosynthesis via nicotinamide phosphoribosyltransferase (NAMPT) inhibition depletes cancer cells of the NAD needed for glycolysis.	NAD	23-56	nicotinamide phosphoribosyltransferase	Homo sapiens	80-118
21826208-1	2011	Nicotinamide (Nam) phosphoribosyltransferase (NAMPT) is the rate-limiting enzyme in mammalian NAD synthesis, catalyzing nicotinamide mononucleotide (NMN) formation from Nam and 5-phosphoribosyl 1-pyrophosphate (PRPP).	NAD	94-97	nicotinamide phosphoribosyltransferase	Homo sapiens	0-44
21826208-1	2011	Nicotinamide (Nam) phosphoribosyltransferase (NAMPT) is the rate-limiting enzyme in mammalian NAD synthesis, catalyzing nicotinamide mononucleotide (NMN) formation from Nam and 5-phosphoribosyl 1-pyrophosphate (PRPP).	NAD	94-97	nicotinamide phosphoribosyltransferase	Homo sapiens	46-51
26177608-4	2015	Specifically, blocking nicotinamide adenine dinucleotide (NAD) biosynthesis via nicotinamide phosphoribosyltransferase (NAMPT) inhibition depletes cancer cells of the NAD needed for glycolysis.	NAD	23-56	nicotinamide phosphoribosyltransferase	Homo sapiens	120-125
26177608-4	2015	Specifically, blocking nicotinamide adenine dinucleotide (NAD) biosynthesis via nicotinamide phosphoribosyltransferase (NAMPT) inhibition depletes cancer cells of the NAD needed for glycolysis.	NAD	58-61	nicotinamide phosphoribosyltransferase	Homo sapiens	80-118
20485294-1	2010	Pre-B-cell colony-enhancing factor (PBEF) (also known as nicotinamide phosphoribosyltransferase) is a rate-limiting enzyme in the salvage pathway for mammalian biosynthesis of nicotinamide adenine dinucleotide (NAD(+)).	NAD	176-209	nicotinamide phosphoribosyltransferase	Homo sapiens	0-34
20485294-1	2010	Pre-B-cell colony-enhancing factor (PBEF) (also known as nicotinamide phosphoribosyltransferase) is a rate-limiting enzyme in the salvage pathway for mammalian biosynthesis of nicotinamide adenine dinucleotide (NAD(+)).	NAD	176-209	nicotinamide phosphoribosyltransferase	Homo sapiens	36-40
26177608-4	2015	Specifically, blocking nicotinamide adenine dinucleotide (NAD) biosynthesis via nicotinamide phosphoribosyltransferase (NAMPT) inhibition depletes cancer cells of the NAD needed for glycolysis.	NAD	58-61	nicotinamide phosphoribosyltransferase	Homo sapiens	120-125
20485294-1	2010	Pre-B-cell colony-enhancing factor (PBEF) (also known as nicotinamide phosphoribosyltransferase) is a rate-limiting enzyme in the salvage pathway for mammalian biosynthesis of nicotinamide adenine dinucleotide (NAD(+)).	NAD	211-217	nicotinamide phosphoribosyltransferase	Homo sapiens	0-34
26177608-4	2015	Specifically, blocking nicotinamide adenine dinucleotide (NAD) biosynthesis via nicotinamide phosphoribosyltransferase (NAMPT) inhibition depletes cancer cells of the NAD needed for glycolysis.	NAD	167-170	nicotinamide phosphoribosyltransferase	Homo sapiens	80-118
20485294-1	2010	Pre-B-cell colony-enhancing factor (PBEF) (also known as nicotinamide phosphoribosyltransferase) is a rate-limiting enzyme in the salvage pathway for mammalian biosynthesis of nicotinamide adenine dinucleotide (NAD(+)).	NAD	211-217	nicotinamide phosphoribosyltransferase	Homo sapiens	36-40
26177608-4	2015	Specifically, blocking nicotinamide adenine dinucleotide (NAD) biosynthesis via nicotinamide phosphoribosyltransferase (NAMPT) inhibition depletes cancer cells of the NAD needed for glycolysis.	NAD	167-170	nicotinamide phosphoribosyltransferase	Homo sapiens	120-125
26310895-1	2015	The NAD(+)-dependent sirtuin SIRT6 is highly expressed in human breast, prostate, and skin cancer where it mediates resistance to cytotoxic agents and prevents differentiation.	NAD	4-10	sirtuin 6	Homo sapiens	29-34
20954240-1	2010	Nicotinamide mononucleotide adenylyltransferase (NMNAT) catalyzes the formation of NAD by means of nucleophilic attack by 5"-phosphoryl of NMN on the alpha-phosphoryl group of ATP.	NAD	83-86	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	0-47
20954240-1	2010	Nicotinamide mononucleotide adenylyltransferase (NMNAT) catalyzes the formation of NAD by means of nucleophilic attack by 5"-phosphoryl of NMN on the alpha-phosphoryl group of ATP.	NAD	83-86	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	49-54
26170451-6	2015	Using (32)P-labeled NAD(+) and immunoblotting, we also demonstrate that both subunits of the XPC-RAD23B are poly(ADP-ribosyl)ated by PARP1.	NAD	20-26	XPC complex subunit, DNA damage recognition and repair factor	Homo sapiens	93-96
20935547-2	2010	To achieve this goal, we have been studying mechanisms of mammalian aging and longevity, focusing on the physiological importance of the mammalian nicotinamide adenine dinucleotide (NAD)--dependent protein deacetylase SIRT1 and systemic NAD biosynthesis mediated by nicotinamide phosphoribosyltransferase for the regulation of metabolism and aging.	NAD	182-185	nicotinamide phosphoribosyltransferase	Homo sapiens	266-304
26332964-5	2015	Specifically, the nicotinamide adenine dinucleotide (NAD)(+) -dependent deacetylases SIRT1 and SIRT6 have been linked to circadian control of gene expression.	NAD	18-51	sirtuin 6	Homo sapiens	95-100
20724478-0	2010	Inhibition of nicotinamide phosphoribosyltransferase: cellular bioenergetics reveals a mitochondrial insensitive NAD pool.	NAD	113-116	nicotinamide phosphoribosyltransferase	Homo sapiens	14-52
20724478-1	2010	The NAD rescue pathway consists of two enzymatic steps operated by nicotinamide phosphoribosyltransferase (Nampt) and nicotinamide mononucleotide adenylyltransferases.	NAD	4-7	nicotinamide phosphoribosyltransferase	Homo sapiens	67-105
20724478-1	2010	The NAD rescue pathway consists of two enzymatic steps operated by nicotinamide phosphoribosyltransferase (Nampt) and nicotinamide mononucleotide adenylyltransferases.	NAD	4-7	nicotinamide phosphoribosyltransferase	Homo sapiens	107-112
20724478-3	2010	Yet, how Nampt inhibition affects NAD contents and bioenergetics is in part obscure.	NAD	34-37	nicotinamide phosphoribosyltransferase	Homo sapiens	9-14
20595677-1	2010	Sirtuins (silent information regulator 2 [Sir2] proteins) belong to an ancient family of evolutionary conserved nicotinamide adenine dinucleotide (NAD)(+)-dependent enzymes with deacetylase and/or mono-ADP-ribosyltransferase activity.	NAD	112-145	ADP-ribosyltransferase 3 (inactive)	Homo sapiens	197-224
20595677-1	2010	Sirtuins (silent information regulator 2 [Sir2] proteins) belong to an ancient family of evolutionary conserved nicotinamide adenine dinucleotide (NAD)(+)-dependent enzymes with deacetylase and/or mono-ADP-ribosyltransferase activity.	NAD	147-154	ADP-ribosyltransferase 3 (inactive)	Homo sapiens	197-224
20813124-9	2010	The NAD(+)/NADH ratio in WI38/hNaDC3 cells was also decreased.	NAD	4-10	solute carrier family 13 member 3	Homo sapiens	30-36
20813124-9	2010	The NAD(+)/NADH ratio in WI38/hNaDC3 cells was also decreased.	NAD	11-15	solute carrier family 13 member 3	Homo sapiens	30-36
20813124-10	2010	Further study found that enhanced intracellular NAD(+) level could attenuate the aging phenotypes induced by NaDC3.	NAD	48-54	solute carrier family 13 member 3	Homo sapiens	109-114
20813124-11	2010	Thus, NaDC3 promotes cellular senescence probably by inhibiting NAD(+)-dependent SIRT1.	NAD	64-70	solute carrier family 13 member 3	Homo sapiens	6-11
20528775-1	2010	The Arabidopsis thaliana genome contains two genes encoding NAD-MEs [NAD-dependent malic enzymes; NAD-ME1 (TAIR accession number At4G13560) and NAD-ME2 (TAIR accession number At4G00570)].	NAD	60-63	NAD-dependent malic enzyme 2	Arabidopsis thaliana	144-151
20528775-10	2010	The different kinetic mechanism of each NAD-ME entity suggests that, for a metabolic condition in which the mitochondrial NAD level is low and the L-malate level is high, the activity of NAD-ME2 and/or -MEH would be preferred over that of NAD-ME1.	NAD	40-43	NAD-dependent malic enzyme 2	Arabidopsis thaliana	187-194
20531298-6	2010	Recently, it became clear that the energy sensor, AMP-activated kinase (AMPK) translates the effects of energy stress into altered Sirt1 activity by regulating the intracellular level of its co-substrate nicotinamide adenine dinucleotide (NAD)(+).	NAD	204-237	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	50-70
20531298-6	2010	Recently, it became clear that the energy sensor, AMP-activated kinase (AMPK) translates the effects of energy stress into altered Sirt1 activity by regulating the intracellular level of its co-substrate nicotinamide adenine dinucleotide (NAD)(+).	NAD	204-237	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	72-76
20506278-3	2010	Nicotinamide phosphoribosyltransferase (Nampt) is a rate-limiting enzyme in the conversion of nicotinamide into NAD(+), which is crucial for SIRT1 activation.	NAD	112-118	nicotinamide phosphoribosyltransferase	Homo sapiens	0-38
20506278-3	2010	Nicotinamide phosphoribosyltransferase (Nampt) is a rate-limiting enzyme in the conversion of nicotinamide into NAD(+), which is crucial for SIRT1 activation.	NAD	112-118	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
20566368-7	2010	In yeast and human cells, Nrk2 phosphorylates Nicotinamide Riboside and generates NAD+ through an alternative salvage pathway.	NAD	82-86	nicotinamide riboside kinase 2	Homo sapiens	26-30
19583971-3	2010	Pre-B cell colony enhancing factor (PBEF)/nicotinamide phosphoribosyl transferase (NAMPT)/visfatin is a pleiotropic mediator acting as growth factor, cytokine and enzyme involved in energy and nicotinamide adenine dinucleotide (NAD) metabolism.	NAD	193-226	nicotinamide phosphoribosyltransferase	Homo sapiens	36-40
19583971-3	2010	Pre-B cell colony enhancing factor (PBEF)/nicotinamide phosphoribosyl transferase (NAMPT)/visfatin is a pleiotropic mediator acting as growth factor, cytokine and enzyme involved in energy and nicotinamide adenine dinucleotide (NAD) metabolism.	NAD	193-226	nicotinamide phosphoribosyltransferase	Homo sapiens	83-88
19583971-3	2010	Pre-B cell colony enhancing factor (PBEF)/nicotinamide phosphoribosyl transferase (NAMPT)/visfatin is a pleiotropic mediator acting as growth factor, cytokine and enzyme involved in energy and nicotinamide adenine dinucleotide (NAD) metabolism.	NAD	193-226	nicotinamide phosphoribosyltransferase	Homo sapiens	90-98
19583971-3	2010	Pre-B cell colony enhancing factor (PBEF)/nicotinamide phosphoribosyl transferase (NAMPT)/visfatin is a pleiotropic mediator acting as growth factor, cytokine and enzyme involved in energy and nicotinamide adenine dinucleotide (NAD) metabolism.	NAD	228-231	nicotinamide phosphoribosyltransferase	Homo sapiens	36-40
19583971-3	2010	Pre-B cell colony enhancing factor (PBEF)/nicotinamide phosphoribosyl transferase (NAMPT)/visfatin is a pleiotropic mediator acting as growth factor, cytokine and enzyme involved in energy and nicotinamide adenine dinucleotide (NAD) metabolism.	NAD	228-231	nicotinamide phosphoribosyltransferase	Homo sapiens	83-88
19583971-3	2010	Pre-B cell colony enhancing factor (PBEF)/nicotinamide phosphoribosyl transferase (NAMPT)/visfatin is a pleiotropic mediator acting as growth factor, cytokine and enzyme involved in energy and nicotinamide adenine dinucleotide (NAD) metabolism.	NAD	228-231	nicotinamide phosphoribosyltransferase	Homo sapiens	90-98
20590162-0	2010	Pnc1p supports increases in cellular NAD(H) levels in response to internal or external oxidative stress.	NAD	37-43	nicotinamidase	Saccharomyces cerevisiae S288C	0-5
20590162-3	2010	Similar transient increases in NAD(H) levels observed in the parental strain following addition of exogenous hydrogen peroxide were also attributable to Pnc1p.	NAD	31-37	nicotinamidase	Saccharomyces cerevisiae S288C	153-158
19897060-5	2010	More strikingly, we and others have discovered a novel circadian clock feedback loop in which both the rate-limiting enzyme in mammalian NAD biosynthesis, nicotinamide phosphoribosyltransferase (NAMPT), and NAD levels display circadian oscillations and modulate CLOCK:BMAL1-mediated circadian transcriptional regulation through SIRT1, demonstrating a new function of NAD as a "metabolic oscillator."	NAD	137-140	nicotinamide phosphoribosyltransferase	Homo sapiens	155-193
19897060-5	2010	More strikingly, we and others have discovered a novel circadian clock feedback loop in which both the rate-limiting enzyme in mammalian NAD biosynthesis, nicotinamide phosphoribosyltransferase (NAMPT), and NAD levels display circadian oscillations and modulate CLOCK:BMAL1-mediated circadian transcriptional regulation through SIRT1, demonstrating a new function of NAD as a "metabolic oscillator."	NAD	137-140	nicotinamide phosphoribosyltransferase	Homo sapiens	195-200
19897060-6	2010	These findings reveal a novel system dynamics of a recently proposed systemic regulatory network regulated by NAMPT-mediated NAD biosynthesis and SIRT1, namely, the NAD World.	NAD	125-128	nicotinamide phosphoribosyltransferase	Homo sapiens	110-115
19897060-6	2010	These findings reveal a novel system dynamics of a recently proposed systemic regulatory network regulated by NAMPT-mediated NAD biosynthesis and SIRT1, namely, the NAD World.	NAD	165-168	nicotinamide phosphoribosyltransferase	Homo sapiens	110-115
20591898-0	2010	Nicotinate/nicotinamide mononucleotide adenyltransferase-mediated regulation of NAD biosynthesis protects guard cells from reactive oxygen species in ABA-mediated stomatal movement in Arabidopsis.	NAD	80-83	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	0-56
20591898-10	2010	These results indicate that NAD biosynthesis is involved in protecting guard cells from ABA-induced local oxidative stress via the regulation of NMNAT activity.	NAD	28-31	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	145-150
20591898-11	2010	In this study, it is demonstrated that NMNAT is essential for the maintenance of NAD homeostasis enabling sustainable stomatal movement.	NAD	81-84	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	39-44
26332964-5	2015	Specifically, the nicotinamide adenine dinucleotide (NAD)(+) -dependent deacetylases SIRT1 and SIRT6 have been linked to circadian control of gene expression.	NAD	53-56	sirtuin 6	Homo sapiens	95-100
26235939-0	2015	Glutathione metabolism links FOXRED1 to NADH:ubiquinone oxidoreductase (complex I) deficiency: A hypothesis.	NAD	40-44	FAD dependent oxidoreductase domain containing 1	Homo sapiens	29-36
26235939-1	2015	FOXRED1 mutations result in complex I (NADH:ubiquinone oxidoreductase) deficiencies and Leigh syndrome (subacute necrotizing encephalomyelopathy).	NAD	39-43	FAD dependent oxidoreductase domain containing 1	Homo sapiens	0-7
25940138-4	2015	In the present study, we showed that overexpressed acyl-CoA-binding domain containing 3 (ACBD3), a Golgi-bound protein, significantly reduced cellular NAD(+) content via enhancing PARP1"s polymerase activity and enhancing auto-modification of the enzyme in a DNA damage-independent manner.	NAD	151-157	acyl-CoA binding domain containing 3	Homo sapiens	89-94
25940138-7	2015	Taken together, these findings suggest that ACBD3 has prominent impacts on cellular NAD(+) metabolism via regulating PARP1 activation-dependent auto-modification and thus cell metabolism and function.	NAD	84-90	acyl-CoA binding domain containing 3	Homo sapiens	44-49
26063178-1	2015	BACKGROUND: SIRT6, a member of the NAD(+)-dependent histone/protein deacetylase family, regulates genomic stability, metabolism, and lifespan.	NAD	35-39	sirtuin 6	Homo sapiens	12-17
26062589-1	2015	Citrin, encoded by SLC25A13, is a component of the malate-aspartate shuttle, which is the main NADH-transporting system in the liver.	NAD	95-99	solute carrier family 25 member 13	Homo sapiens	0-6
26062589-1	2015	Citrin, encoded by SLC25A13, is a component of the malate-aspartate shuttle, which is the main NADH-transporting system in the liver.	NAD	95-99	solute carrier family 25 member 13	Homo sapiens	19-27
25716654-4	2015	Analysis of downstream targets of the mutations in these two genes showed that the HNRNPA0 mutation affected expression patterns in the PI3 kinase and ERK/MAPK signaling pathways, while the WIF1 variant influenced expression of genes that play a role in NAD biosynthesis.	NAD	254-257	heterogeneous nuclear ribonucleoprotein A0	Homo sapiens	83-90
25498756-1	2015	BACKGROUND: Nicotinamide phosphoribosyltransferase (Nampt) is an enzyme involved in nicotinamide adenine dinucleotide biosynthesis.	NAD	84-117	nicotinamide phosphoribosyltransferase	Homo sapiens	12-50
25498756-1	2015	BACKGROUND: Nicotinamide phosphoribosyltransferase (Nampt) is an enzyme involved in nicotinamide adenine dinucleotide biosynthesis.	NAD	84-117	nicotinamide phosphoribosyltransferase	Homo sapiens	52-57
25890336-6	2015	Following initial validation, pathways that include NAD synthetase 1 (NADSYN1) and protein kinase B (AKT2) were hypothesized and experimentally tested to provide a mechanistic basis for AMPK regulation of cell migration and maintenance of cellular NAD(+) concentrations during catabolic processes.	NAD	248-254	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	186-190
25656579-1	2015	BACKGROUND: Nicotinamide phosphoribosyltransferase (NAMPT) is the key enzyme of the NAD salvage pathway starting from nicotinamide.	NAD	84-87	nicotinamide phosphoribosyltransferase	Homo sapiens	12-50
20620997-3	2010	Here we show that lack of nicotinamide adenine dinucleotide (NAD(+))-dependent deacetylase SIRT1 in pro-opiomelanocortin (POMC) neurons causes hypersensitivity to diet-induced obesity due to reduced energy expenditure.	NAD	26-59	pro-opiomelanocortin-alpha	Mus musculus	100-120
20620997-3	2010	Here we show that lack of nicotinamide adenine dinucleotide (NAD(+))-dependent deacetylase SIRT1 in pro-opiomelanocortin (POMC) neurons causes hypersensitivity to diet-induced obesity due to reduced energy expenditure.	NAD	26-59	pro-opiomelanocortin-alpha	Mus musculus	122-126
20620997-3	2010	Here we show that lack of nicotinamide adenine dinucleotide (NAD(+))-dependent deacetylase SIRT1 in pro-opiomelanocortin (POMC) neurons causes hypersensitivity to diet-induced obesity due to reduced energy expenditure.	NAD	61-68	pro-opiomelanocortin-alpha	Mus musculus	100-120
20620997-3	2010	Here we show that lack of nicotinamide adenine dinucleotide (NAD(+))-dependent deacetylase SIRT1 in pro-opiomelanocortin (POMC) neurons causes hypersensitivity to diet-induced obesity due to reduced energy expenditure.	NAD	61-68	pro-opiomelanocortin-alpha	Mus musculus	122-126
25656579-1	2015	BACKGROUND: Nicotinamide phosphoribosyltransferase (NAMPT) is the key enzyme of the NAD salvage pathway starting from nicotinamide.	NAD	84-87	nicotinamide phosphoribosyltransferase	Homo sapiens	52-57
25656579-11	2015	CONCLUSION: Taken together, these findings reveal an important role of the NAMPT-mediated NAD salvage pathway in the energy homeostasis of hepatocarcinoma cells and suggest NAMPT inhibition as a potential treatment option for HCC.	NAD	90-93	nicotinamide phosphoribosyltransferase	Homo sapiens	75-80
25656579-11	2015	CONCLUSION: Taken together, these findings reveal an important role of the NAMPT-mediated NAD salvage pathway in the energy homeostasis of hepatocarcinoma cells and suggest NAMPT inhibition as a potential treatment option for HCC.	NAD	90-93	nicotinamide phosphoribosyltransferase	Homo sapiens	173-178
25633578-3	2015	However, levels of Sir2 and Pnc1, two enzymes that sequentially convert NAD+ to nicotinic acid (NA), are up-regulated during CR.	NAD	72-76	nicotinamidase	Saccharomyces cerevisiae S288C	28-32
20085812-5	2010	On the other hand, sirtuin activity is regulated by NAD biosynthetic pathways, and nicotinamide phosphoribosyltransferase (NAMPT) plays a critical role in the regulation of mammalian sirtuin activity.	NAD	52-55	nicotinamide phosphoribosyltransferase	Homo sapiens	123-128
25590809-8	2015	Non-overlapping specificities of FK866 for PDA tumors that rely heavily on NAMPT-catalyzed NAD(+) synthesis and beta-lap for cancer cells with elevated NQO1 levels affords high tumor-selectivity.	NAD	91-97	nicotinamide phosphoribosyltransferase	Homo sapiens	75-80
21048875-4	2010	Study of the effects of NAD(+), NADH and NADPH at various concentrations in protecting against inactivation by 200 muM DTNB allowed determination of K(d) values for binding of these coenzymes to each protein, yielding surprising results.	NAD	24-30	dystrobrevin beta	Homo sapiens	119-123
26558285-5	2015	Finally, low sirtuin-1 and sirtuin-3 gene expressions due to higher NADH/NAD in Cmah-null mice decreased Foxo-1 and MnSOD gene expression, suggesting that oxidative stress may result in mitochondrial dysfunction in Cmah-null mouse.	NAD	68-72	cytidine monophospho-N-acetylneuraminic acid hydroxylase	Mus musculus	80-84
21048875-4	2010	Study of the effects of NAD(+), NADH and NADPH at various concentrations in protecting against inactivation by 200 muM DTNB allowed determination of K(d) values for binding of these coenzymes to each protein, yielding surprising results.	NAD	32-36	dystrobrevin beta	Homo sapiens	119-123
25048544-3	2015	In the presence of extracellular NAD(+), ARTC2.2 ADP-ribosylates several cell surface target proteins and thereby regulates their function.	NAD	33-39	ADP-ribosyltransferase 2a	Mus musculus	41-46
20421294-7	2010	Activation of AMPK by CA-alpha1 increases the SIRT1 activator NAD(+) content and SIRT1 expression in macrophages.	NAD	62-68	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	14-18
25048544-8	2015	This review will highlight the recent discoveries on the in vivo role of the ARTC2.2/P2X7 pathway triggered by the endogenous release of extracellular NAD(+), the relative sensitivity of lymphocytes subsets to this regulatory pathway and its pharmacological manipulation using camelid-derived ARTC2.2-blocking nanobodies.	NAD	151-157	ADP-ribosyltransferase 2a	Mus musculus	77-82
25814788-1	2015	Nampt/visfatin acts in both intracellular and extracellular compartments to regulate multiple biological roles, including NAD metabolism, cancer, inflammation, and senescence.	NAD	122-125	nicotinamide phosphoribosyltransferase	Homo sapiens	0-5
25814788-1	2015	Nampt/visfatin acts in both intracellular and extracellular compartments to regulate multiple biological roles, including NAD metabolism, cancer, inflammation, and senescence.	NAD	122-125	nicotinamide phosphoribosyltransferase	Homo sapiens	6-14
20457531-1	2010	Nicotinamide mononucleotide adenylyltransferase (NMNAT) catalyzes the formation of nicotinamide adenine dinucleotide (NAD).	NAD	83-116	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	0-47
24999994-7	2014	Electrodes modified with NG and NG/gold nanoparticals/formate dehydrogenase (NG/AuNPs/FDH) showed excellent analytical performance for the detection of NADH and formate.	NAD	152-156	alcohol dehydrogenase 5 (class III), chi polypeptide	Homo sapiens	86-89
20457531-1	2010	Nicotinamide mononucleotide adenylyltransferase (NMNAT) catalyzes the formation of nicotinamide adenine dinucleotide (NAD).	NAD	83-116	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	49-54
20606733-1	2010	Nicotinamide phosphoribosyltransferase (Nampt) catalyzes the rate-limiting step of nicotinamide adenine dinucleotide (NAD(+)) synthesis and is required for cell growth, survival, DNA replication and repair, and angiogenesis.	NAD	83-116	nicotinamide phosphoribosyltransferase	Homo sapiens	0-38
20606733-1	2010	Nicotinamide phosphoribosyltransferase (Nampt) catalyzes the rate-limiting step of nicotinamide adenine dinucleotide (NAD(+)) synthesis and is required for cell growth, survival, DNA replication and repair, and angiogenesis.	NAD	83-116	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
25486521-3	2014	NAMPT has been extensively studied over the past decade due to its role as a key regulator of nicotinamide adenine dinucleotide-consuming enzymes.	NAD	94-127	nicotinamide phosphoribosyltransferase	Homo sapiens	0-5
20606733-1	2010	Nicotinamide phosphoribosyltransferase (Nampt) catalyzes the rate-limiting step of nicotinamide adenine dinucleotide (NAD(+)) synthesis and is required for cell growth, survival, DNA replication and repair, and angiogenesis.	NAD	118-124	nicotinamide phosphoribosyltransferase	Homo sapiens	0-38
20606733-1	2010	Nicotinamide phosphoribosyltransferase (Nampt) catalyzes the rate-limiting step of nicotinamide adenine dinucleotide (NAD(+)) synthesis and is required for cell growth, survival, DNA replication and repair, and angiogenesis.	NAD	118-124	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
20388704-8	2010	We further demonstrate that the Golgi-associated NMNAT is palmitoylated at two adjacent cysteine residues of its isoform-specific domain and thereby anchored at the cytoplasmic surface, a potential mechanism to regulate the cytosolic NAD pool.	NAD	234-237	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	49-54
25331943-2	2014	However, concerns in this area were raised by observations that nicotinamide phosphoribosyltransferase (NAMPT), a key enzyme in mammalian NAD(+) biosynthesis, is frequently up-regulated in human malignancies, including breast cancer, suggesting possible protumorigenic effects for this protein.	NAD	138-144	nicotinamide phosphoribosyltransferase	Homo sapiens	64-102
25331943-2	2014	However, concerns in this area were raised by observations that nicotinamide phosphoribosyltransferase (NAMPT), a key enzyme in mammalian NAD(+) biosynthesis, is frequently up-regulated in human malignancies, including breast cancer, suggesting possible protumorigenic effects for this protein.	NAD	138-144	nicotinamide phosphoribosyltransferase	Homo sapiens	104-109
20299454-6	2010	The action of many global transcription factors such as ArcA, Fnr, CRP, and IHF commonly involved both NADH and ATP, whereas others responded to either ATP or NADH.	NAD	103-107	arginine deiminase	Escherichia coli	56-60
25331943-8	2014	These findings have implications for the design of therapeutic strategies exploiting NAD(+) biosynthesis via NAMPT in aging and cancer and also suggest the potential of anticancer agents designed to specifically neutralize extracellular NAMPT.	NAD	85-91	nicotinamide phosphoribosyltransferase	Homo sapiens	109-114
20299454-6	2010	The action of many global transcription factors such as ArcA, Fnr, CRP, and IHF commonly involved both NADH and ATP, whereas others responded to either ATP or NADH.	NAD	159-163	arginine deiminase	Escherichia coli	56-60
25331943-8	2014	These findings have implications for the design of therapeutic strategies exploiting NAD(+) biosynthesis via NAMPT in aging and cancer and also suggest the potential of anticancer agents designed to specifically neutralize extracellular NAMPT.	NAD	85-91	nicotinamide phosphoribosyltransferase	Homo sapiens	237-242
25429601-3	2014	CtBP1 and CtBP2 are closely related and act as transcriptional corepressors when activated by nicotinamide adenine dinucleotide binding to their dehydrogenase domains.	NAD	94-127	C-terminal binding protein 1	Homo sapiens	0-5
25301889-7	2014	The metabolomics pattern of cod1 mutants was also deeply altered, suggesting that alternative metabolic pathways compensated for the probable resulting restriction in NADH oxidation.	NAD	167-171	Pentatricopeptide repeat (PPR) superfamily protein	Arabidopsis thaliana	28-32
20435911-2	2010	In yeast, the single-subunit NADH dehydrogenase Ndi1 serves as a non-proton-translocating alternative enzyme that replaces complex I, bringing about the reoxidation of intramitochondrial NADH.	NAD	29-33	NADH-ubiquinone reductase (H(+)-translocating) NDI1	Saccharomyces cerevisiae S288C	48-52
20081535-7	2010	MEASUREMENTS AND MAIN RESULTS: Acetylcholine-induced endothelium-dependent relaxation decreased, whereas nicotinamide adenine dinucleotide-stimulated superoxide radical production in the aorta and aortic p22phox, p47phox, gp91phox, NOX1, and NOX4 mRNA concentrations increased in trauma-hemorrhaged rats vs. sham rats.	NAD	105-138	neutrophil cytosolic factor 1	Rattus norvegicus	213-220
20117162-3	2010	NAD synthesis activity of Wld(S) and Nmnats was shown to be responsible for their axon-protective function.	NAD	0-3	wallerian degeneration	Mus musculus	26-29
20117162-4	2010	The mitochondrial Nmnat3 and cytoplasm-localized mutants of Wld(S) and Nmnat1 have similar or even stronger effect than Wld(S) to delay axon degeneration, which suggest that increased mitochondrial or local NAD synthesis might contribute to the protective function of Wld(S) and Nmnats.	NAD	207-210	wallerian degeneration	Mus musculus	60-63
20117162-4	2010	The mitochondrial Nmnat3 and cytoplasm-localized mutants of Wld(S) and Nmnat1 have similar or even stronger effect than Wld(S) to delay axon degeneration, which suggest that increased mitochondrial or local NAD synthesis might contribute to the protective function of Wld(S) and Nmnats.	NAD	207-210	wallerian degeneration	Mus musculus	120-123
20117162-4	2010	The mitochondrial Nmnat3 and cytoplasm-localized mutants of Wld(S) and Nmnat1 have similar or even stronger effect than Wld(S) to delay axon degeneration, which suggest that increased mitochondrial or local NAD synthesis might contribute to the protective function of Wld(S) and Nmnats.	NAD	207-210	wallerian degeneration	Mus musculus	120-123
25387075-6	2014	Using different approaches including confocal imaging, mitochondrial DNA measurement and Western blot analysis of PGC-1 and NRF-1, we also found that NAD+ could significantly attenuate glutamate-induced mitochondrial fragmentation and the impairment of mitochondrial biogenesis.	NAD	150-154	nuclear respiratory factor 1	Homo sapiens	124-129
25263164-4	2014	We show that knockdown of NAMPT, the enzyme catalyzing the rate-limiting step of the NAD(+) salvage pathway, enhances metastatic aggressiveness in human breast cancer cells and involves modulation of integrin expression and function.	NAD	85-91	nicotinamide phosphoribosyltransferase	Homo sapiens	26-31
25263164-7	2014	NAMPT has been selected as a therapeutic target for cancer therapy based on the essential functions of this enzyme in NAD(+) metabolism, cellular redox, DNA repair and energy pathways.	NAD	118-124	nicotinamide phosphoribosyltransferase	Homo sapiens	0-5
25263164-8	2014	Notably, our results indicate that incomplete inhibition of NAMPT, which impedes NAD(+) metabolism but does not kill a tumor cell can alter its phenotype to be more aggressive and metastatic.	NAD	81-87	nicotinamide phosphoribosyltransferase	Homo sapiens	60-65
25277684-2	2014	Nicotinamide phosphoribosyltransferase (Nampt), a rate-limiting enzyme in the NAD+ salvage pathway, plays an important role in controlling the level of NAD+ and the activity of Sirt1 in the heart and the cardiomyocytes therein.	NAD	78-82	nicotinamide phosphoribosyltransferase	Homo sapiens	0-38
25277684-2	2014	Nicotinamide phosphoribosyltransferase (Nampt), a rate-limiting enzyme in the NAD+ salvage pathway, plays an important role in controlling the level of NAD+ and the activity of Sirt1 in the heart and the cardiomyocytes therein.	NAD	78-82	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
25277684-2	2014	Nicotinamide phosphoribosyltransferase (Nampt), a rate-limiting enzyme in the NAD+ salvage pathway, plays an important role in controlling the level of NAD+ and the activity of Sirt1 in the heart and the cardiomyocytes therein.	NAD	152-156	nicotinamide phosphoribosyltransferase	Homo sapiens	0-38
25277684-2	2014	Nicotinamide phosphoribosyltransferase (Nampt), a rate-limiting enzyme in the NAD+ salvage pathway, plays an important role in controlling the level of NAD+ and the activity of Sirt1 in the heart and the cardiomyocytes therein.	NAD	152-156	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
25401080-2	2014	High fluorescence levels were obtained in a glycerol 3-phosphate dehydrogenase double deletion strain (gpd1Deltagpd2Delta), which is deficient in the ability to regenerate NAD(+) via glycerol formation.	NAD	172-178	glycerol-3-phosphate dehydrogenase	Saccharomyces cerevisiae S288C	44-78
24450884-2	2014	CYB5R3 encodes for NADH-dependent redox enzyme that contributes to metabolic homeostasis and stress protection; however, how it is involved in the neurological pathology of RHM remains unknown.	NAD	19-23	cytochrome b5 reductase 3	Homo sapiens	0-6
24450884-4	2014	RESULTS: CYB5R3-deficient cells exhibited a decrease of the NAD(+)/NADH ratio, mitochondrial respiration rate, ATP production, and mitochondrial electron transport chain activities, which were associated with higher sensitivity to oxidative stress, and an increase in senescence-associated beta-galactosidase activity.	NAD	60-66	cytochrome b5 reductase 3	Homo sapiens	9-15
24450884-4	2014	RESULTS: CYB5R3-deficient cells exhibited a decrease of the NAD(+)/NADH ratio, mitochondrial respiration rate, ATP production, and mitochondrial electron transport chain activities, which were associated with higher sensitivity to oxidative stress, and an increase in senescence-associated beta-galactosidase activity.	NAD	67-71	cytochrome b5 reductase 3	Homo sapiens	9-15
24549054-4	2014	Mutations in GPD1 encoding glycerol-3-phosphate dehydrogenase that catalyzes the reversible redox reaction of dihydroxyacetone phosphate and NADH to glycerol-3-phosphate (G3P) and NAD(+) were identified.	NAD	141-145	glycerol-3-phosphate dehydrogenase 1	Homo sapiens	13-17
24945955-2	2014	In the present work, we evaluated the participation of VDAC1 and Cyb5R3 in the NADH-dependent activation of various redox cyclers in mitochondria.	NAD	79-83	voltage dependent anion channel 1	Homo sapiens	55-60
24945955-2	2014	In the present work, we evaluated the participation of VDAC1 and Cyb5R3 in the NADH-dependent activation of various redox cyclers in mitochondria.	NAD	79-83	cytochrome b5 reductase 3	Homo sapiens	65-71
25146220-1	2014	Nicotinamide phosphoribosyltransferase (NAMPT) is a rate-limiting enzyme in the salvage pathway of nicotinamide adenine dinucleotide biosynthesis.	NAD	99-132	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
24824603-9	2014	Xanthine dehydrogenase (XDH), which belongs to the family of xanthine oxidoreductases and preferentially reduces nicotinamide adenine dinucleotide (NAD(+)), was shown to contribute to the overall production of the 6TX intermediate as well as the final product 6TUA in the presence of NAD(+) in human liver cytosol.	NAD	113-146	xanthine dehydrogenase	Homo sapiens	0-22
20023106-3	2010	In a strain that was disabled in formate metabolism, we either overexpressed the native NAD(+)-dependent formate dehydrogenase in the cytosol or directed it into the mitochondria by fusing it with the mitochondrial signal sequence encoded by the CYB2 gene.	NAD	88-94	L-lactate dehydrogenase (cytochrome)	Saccharomyces cerevisiae S288C	246-250
19370397-9	2010	Expression of sod-3, a target gene of daf-16, and increased oxidative-stress resistance and adiposity were observed in response to NAD addition, indicating that NAD activated daf-16 in each phenotype.	NAD	131-134	Superoxide dismutase [Mn] 2, mitochondrial	Caenorhabditis elegans	14-19
19370397-9	2010	Expression of sod-3, a target gene of daf-16, and increased oxidative-stress resistance and adiposity were observed in response to NAD addition, indicating that NAD activated daf-16 in each phenotype.	NAD	161-164	Superoxide dismutase [Mn] 2, mitochondrial	Caenorhabditis elegans	14-19
20014039-1	2010	In this study, a novel glycerol-3-phosphate dehydrogenase (NAD(+)) (EC1.1.1.8) gene (PfGPD) was cloned from halotolerant yeast Pichia farinosa, using degenerate reverse transcription (RT)-PCR and rapid amplification of cDNA ends (RACE) methods.	NAD	59-65	glycerol-3-phosphate dehydrogenase	Saccharomyces cerevisiae S288C	23-57
19887595-1	2010	In mammals, nicotinamide phosphoribosyltransferase (NAMPT) is responsible for the first and rate-limiting step in the conversion of nicotinamide to nicotinamide adenine dinucleotide (NAD+).	NAD	148-181	nicotinamide phosphoribosyltransferase	Homo sapiens	12-50
19887595-1	2010	In mammals, nicotinamide phosphoribosyltransferase (NAMPT) is responsible for the first and rate-limiting step in the conversion of nicotinamide to nicotinamide adenine dinucleotide (NAD+).	NAD	148-181	nicotinamide phosphoribosyltransferase	Homo sapiens	52-57
19887595-1	2010	In mammals, nicotinamide phosphoribosyltransferase (NAMPT) is responsible for the first and rate-limiting step in the conversion of nicotinamide to nicotinamide adenine dinucleotide (NAD+).	NAD	183-187	nicotinamide phosphoribosyltransferase	Homo sapiens	12-50
19887595-1	2010	In mammals, nicotinamide phosphoribosyltransferase (NAMPT) is responsible for the first and rate-limiting step in the conversion of nicotinamide to nicotinamide adenine dinucleotide (NAD+).	NAD	183-187	nicotinamide phosphoribosyltransferase	Homo sapiens	52-57
19853671-1	2010	3alpha-Hydroxysteroid dehydrogenase/carbonyl reductase reversely catalyzes the oxidation of androsterone with NAD(+) to form androstanedione and NADH.	NAD	110-116	aldo-keto reductase family 1 member C3	Homo sapiens	0-35
19853671-1	2010	3alpha-Hydroxysteroid dehydrogenase/carbonyl reductase reversely catalyzes the oxidation of androsterone with NAD(+) to form androstanedione and NADH.	NAD	145-149	aldo-keto reductase family 1 member C3	Homo sapiens	0-35
24824603-9	2014	Xanthine dehydrogenase (XDH), which belongs to the family of xanthine oxidoreductases and preferentially reduces nicotinamide adenine dinucleotide (NAD(+)), was shown to contribute to the overall production of the 6TX intermediate as well as the final product 6TUA in the presence of NAD(+) in human liver cytosol.	NAD	113-146	xanthine dehydrogenase	Homo sapiens	24-27
24824603-9	2014	Xanthine dehydrogenase (XDH), which belongs to the family of xanthine oxidoreductases and preferentially reduces nicotinamide adenine dinucleotide (NAD(+)), was shown to contribute to the overall production of the 6TX intermediate as well as the final product 6TUA in the presence of NAD(+) in human liver cytosol.	NAD	148-154	xanthine dehydrogenase	Homo sapiens	0-22
24824603-9	2014	Xanthine dehydrogenase (XDH), which belongs to the family of xanthine oxidoreductases and preferentially reduces nicotinamide adenine dinucleotide (NAD(+)), was shown to contribute to the overall production of the 6TX intermediate as well as the final product 6TUA in the presence of NAD(+) in human liver cytosol.	NAD	148-154	xanthine dehydrogenase	Homo sapiens	24-27
24824603-9	2014	Xanthine dehydrogenase (XDH), which belongs to the family of xanthine oxidoreductases and preferentially reduces nicotinamide adenine dinucleotide (NAD(+)), was shown to contribute to the overall production of the 6TX intermediate as well as the final product 6TUA in the presence of NAD(+) in human liver cytosol.	NAD	284-290	xanthine dehydrogenase	Homo sapiens	0-22
24824603-9	2014	Xanthine dehydrogenase (XDH), which belongs to the family of xanthine oxidoreductases and preferentially reduces nicotinamide adenine dinucleotide (NAD(+)), was shown to contribute to the overall production of the 6TX intermediate as well as the final product 6TUA in the presence of NAD(+) in human liver cytosol.	NAD	284-290	xanthine dehydrogenase	Homo sapiens	24-27
19933368-9	2010	Because it has been suggested that TrxR from D. radiodurans may have dual cofactor specificity (can utilize both NADH and NADPH), D. radiodurans TrxR was tested for its ability to utilize NADH as well.	NAD	113-117	DR_1982	Deinococcus radiodurans R1	35-39
25007980-8	2014	Only the ERbeta agonist, DPN, increased fear generalization when testing occurred 24h after injection.	NAD	25-28	estrogen receptor 2	Homo sapiens	9-15
19933368-9	2010	Because it has been suggested that TrxR from D. radiodurans may have dual cofactor specificity (can utilize both NADH and NADPH), D. radiodurans TrxR was tested for its ability to utilize NADH as well.	NAD	113-117	DR_1982	Deinococcus radiodurans R1	145-149
19933368-9	2010	Because it has been suggested that TrxR from D. radiodurans may have dual cofactor specificity (can utilize both NADH and NADPH), D. radiodurans TrxR was tested for its ability to utilize NADH as well.	NAD	188-192	DR_1982	Deinococcus radiodurans R1	35-39
19933368-9	2010	Because it has been suggested that TrxR from D. radiodurans may have dual cofactor specificity (can utilize both NADH and NADPH), D. radiodurans TrxR was tested for its ability to utilize NADH as well.	NAD	188-192	DR_1982	Deinococcus radiodurans R1	145-149
24796879-6	2014	Furthermore, in primary cultured astrocytes, we demonstrated that E2 up-regulated Ndrg2 mRNA and protein expression in a dose- and time-dependent manner and that the ERbeta agonist DPN but not the ERalpha agonist PPT up-regulated Ndrg2 expression.	NAD	181-184	estrogen receptor 2 (beta)	Mus musculus	166-172
19812894-1	2010	Peroxisomal malate dehydrogenase (PMDH) oxidises NADH produced by fatty acid beta-oxidation during seed germination and seedling growth.	NAD	49-53	malate dehydrogenase	Arabidopsis thaliana	12-32
24796879-8	2014	After the OVX mice received continuous subcutaneous injections of 50mug/kg E2, 100mug/kg E2 or the ERbeta agonist DPN for 10 days, the Ndrg2 expression significantly increased compared with that of the OVX mice.	NAD	114-117	estrogen receptor 2 (beta)	Mus musculus	99-105
24920882-3	2014	DATA SOURCES: Correlation of porin redox activity and expression of autism is based on extensive literature, especially studies of antibodies, identification of cytosolic nicotinamide adenine dinucleotide reduced (NADH) dehydrogenase activity in the VDAC, and evidence for extreme sensitivity of the dehydrogenase to a mercurial.	NAD	171-204	voltage dependent anion channel 1	Homo sapiens	29-34
19736255-1	2010	Nicotinamide phosphoribosyltransferase (NAMPT) is a cytokine hormone and rate-limiting enzyme involved in production of NAD and therefore affects a variety of cellular functions requiring NAD.	NAD	120-123	nicotinamide phosphoribosyltransferase pseudogene 1	Gallus gallus	0-38
19736255-1	2010	Nicotinamide phosphoribosyltransferase (NAMPT) is a cytokine hormone and rate-limiting enzyme involved in production of NAD and therefore affects a variety of cellular functions requiring NAD.	NAD	120-123	nicotinamide phosphoribosyltransferase pseudogene 1	Gallus gallus	40-45
19736255-1	2010	Nicotinamide phosphoribosyltransferase (NAMPT) is a cytokine hormone and rate-limiting enzyme involved in production of NAD and therefore affects a variety of cellular functions requiring NAD.	NAD	188-191	nicotinamide phosphoribosyltransferase pseudogene 1	Gallus gallus	0-38
19736255-1	2010	Nicotinamide phosphoribosyltransferase (NAMPT) is a cytokine hormone and rate-limiting enzyme involved in production of NAD and therefore affects a variety of cellular functions requiring NAD.	NAD	188-191	nicotinamide phosphoribosyltransferase pseudogene 1	Gallus gallus	40-45
24784564-7	2014	NAD+ is essential for PARP activity and these data suggest that IDO mediates treatment resistance independent of immunity and at least partially due to a previously unrecognized role for IDO in DNA repair.	NAD	0-4	collagen type XI alpha 2 chain	Homo sapiens	22-26
19736255-2	2010	Spermatogenesis and testicular steroidogenesis are likely to depend on NAD-dependent reactions and may therefore be affected by changes in testicular NAMPT expression.	NAD	71-74	nicotinamide phosphoribosyltransferase pseudogene 1	Gallus gallus	150-155
19764902-0	2009	Silencing of the mitochondrial NADH shuttle component aspartate-glutamate carrier AGC1/Aralar1 in INS-1E cells and rat islets.	NAD	31-35	aggrecan	Rattus norvegicus	82-86
19764902-6	2009	Compared with control INS-1E cells, down-regulation of AGC1 blunted NADH formation (-57%; P&lt;0.05), increased lactate production (+16%; P&lt;0.001) and inhibited glucose oxidation (-22%; P&lt;0.01).	NAD	68-72	aggrecan	Rattus norvegicus	55-59
24668813-3	2014	We find that hVDAC1 possesses one major binding region for ATP, UTP, and GTP that partially overlaps with a previously determined NADH binding site.	NAD	130-134	voltage dependent anion channel 1	Homo sapiens	13-19
19846558-8	2009	Sdt1 overexpression is growth-inhibitory to cells in a manner that depends on its active site and correlates with reduced cellular NAD(+).	NAD	131-137	nucleotidase	Saccharomyces cerevisiae S288C	0-4
24423185-6	2014	Estradiol- or DPN-induced slowing of 5-HT clearance mediated by ERbeta was blocked after inhibition of MAPK/ERK1/2 but not of PI3K/Akt signaling pathways.	NAD	14-17	mitogen activated protein kinase 3	Rattus norvegicus	103-107
24423185-6	2014	Estradiol- or DPN-induced slowing of 5-HT clearance mediated by ERbeta was blocked after inhibition of MAPK/ERK1/2 but not of PI3K/Akt signaling pathways.	NAD	14-17	mitogen activated protein kinase 3	Rattus norvegicus	108-114
19929023-7	2009	With AdN(3), complexes 1, 2, and 5 react similarly to form bis(imido) U(6+) complexes, (C(5)Me(5))(X)U(=NAd)(2).	NAD	104-107	complement factor D	Homo sapiens	5-8
24113812-4	2014	Gox2036 had a strict requirement for NAD+/NADH as the cofactor.	NAD	37-41	acetoin reductase	Gluconobacter oxydans 621H	0-7
24113812-4	2014	Gox2036 had a strict requirement for NAD+/NADH as the cofactor.	NAD	42-46	acetoin reductase	Gluconobacter oxydans 621H	0-7
24216299-6	2014	Then the administration of selective ERalpha agonist PPT partly reversed Aroclor 1254-induced alteration in Bcl-2, caspase-3 and cyclin D1 protein expression while selective ERbeta agonist DPN accelerated it.	NAD	189-192	estrogen receptor 2 (beta)	Mus musculus	174-180
19535819-6	2009	FATP1 silenced 3T3-L1 adipocytes exhibited decreased tricarboxylic acid cycle activity, increased cellular NAD(+)/NADH, increased fatty acid oxidation, and increased lactate production indicative of altered mitochondrial energy metabolism.	NAD	107-113	solute carrier family 27 member 1	Homo sapiens	0-5
19535819-6	2009	FATP1 silenced 3T3-L1 adipocytes exhibited decreased tricarboxylic acid cycle activity, increased cellular NAD(+)/NADH, increased fatty acid oxidation, and increased lactate production indicative of altered mitochondrial energy metabolism.	NAD	114-118	solute carrier family 27 member 1	Homo sapiens	0-5
24144555-6	2014	Results indicated that OMCN treated at 800 C with largest BET surface area and highest amounts of pyrindinic N showed improved electrocatalytic activity for H2O2, nitrobenzene, and NADH in neutral solution.	NAD	181-185	delta/notch like EGF repeat containing	Homo sapiens	58-61
19801601-8	2009	Moreover, in vitro assays demonstrated that histone acetyltransferase p300 can catalyze H3 Lys(23) propionylation, whereas histone deacetylase Sir2 can remove this modification in the presence of NAD(+).	NAD	196-202	E1A binding protein p300	Homo sapiens	70-74
19936064-0	2009	Catastrophic NAD+ depletion in activated T lymphocytes through Nampt inhibition reduces demyelination and disability in EAE.	NAD	13-17	nicotinamide phosphoribosyltransferase	Homo sapiens	63-68
24595043-6	2014	Triose phosphate isomerase, enolase and alcohol dehydrogenase involved in glycosis were up-regulated, while pyruvate dehydrogenase, citrate synthase and isocitrate dehydrogenase with NAD as the coenzyme involved in TCA pathway were down-regulated.	NAD	183-186	citrate synthase	Homo sapiens	132-148
19936064-1	2009	Nicotinamide phosphoribosyltransferase (Nampt) inhibitors such as FK866 are potent inhibitors of NAD(+) synthesis that show promise for the treatment of different forms of cancer.	NAD	97-103	nicotinamide phosphoribosyltransferase	Homo sapiens	0-38
19936064-1	2009	Nicotinamide phosphoribosyltransferase (Nampt) inhibitors such as FK866 are potent inhibitors of NAD(+) synthesis that show promise for the treatment of different forms of cancer.	NAD	97-103	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
19936064-5	2009	We show that activated, but not resting, T lymphocytes undergo massive NAD(+) depletion upon FK866-mediated Nampt inhibition.	NAD	71-77	nicotinamide phosphoribosyltransferase	Homo sapiens	108-113
19855187-6	2009	NAM phosphoribosyltransferase (Nampt) is a rate-limiting enzyme in the NAD(+) salvage pathway.	NAD	71-77	nicotinamide phosphoribosyltransferase	Homo sapiens	0-29
19855187-6	2009	NAM phosphoribosyltransferase (Nampt) is a rate-limiting enzyme in the NAD(+) salvage pathway.	NAD	71-77	nicotinamide phosphoribosyltransferase	Homo sapiens	31-36
24052229-7	2014	Moreover, we showed that BA-related NADP pool build-up is associated with NADK increase which we suspect decreased NAD(+) levels and consequentially lowered SIRT1 amounts in the rat blood cytosol.	NAD	115-121	NAD kinase	Rattus norvegicus	74-78
19855187-7	2009	We have recently demonstrated that Nampt is an important regulator of NAD(+) and autophagy in cardiomyocytes.	NAD	70-76	nicotinamide phosphoribosyltransferase	Homo sapiens	35-40
24366394-1	2014	Sirt6, a member of the mammalian sirtuin family, is a protein that is located in the nucleus and is an NAD+-dependent deacetylase important in the control of metabolic activity and genome stability.	NAD	103-106	sirtuin 6	Homo sapiens	0-5
19458327-9	2009	RDH10 can use both NAD(+) and NADP(+) as cofactors for 11-cis-RDH activity, although NAD(+) cofactor confers more robust activity.	NAD	19-25	retinol dehydrogenase 5	Homo sapiens	55-65
24438340-0	2014	Steroid receptor coactivator 1 is an integrator of glucose and NAD+/NADH homeostasis.	NAD	63-67	nuclear receptor coactivator 1	Homo sapiens	0-30
24438340-0	2014	Steroid receptor coactivator 1 is an integrator of glucose and NAD+/NADH homeostasis.	NAD	68-72	nuclear receptor coactivator 1	Homo sapiens	0-30
19703994-2	2009	We describe findings indicating that GMX1778 is a potent and specific inhibitor of the NAD(+) biosynthesis enzyme nicotinamide phosphoribosyltransferase (NAMPT).	NAD	87-93	nicotinamide phosphoribosyltransferase	Homo sapiens	114-152
19703994-2	2009	We describe findings indicating that GMX1778 is a potent and specific inhibitor of the NAD(+) biosynthesis enzyme nicotinamide phosphoribosyltransferase (NAMPT).	NAD	87-93	nicotinamide phosphoribosyltransferase	Homo sapiens	154-159
27896073-1	2014	BACKGROUND: Citrin, encoded by SLC25A13, is a component of the malate-aspartate shuttle, which is the main NADH-transporting system in the liver.	NAD	107-111	solute carrier family 25 member 13	Homo sapiens	12-18
19703994-4	2009	Selective inhibition by GMX1778 of NAMPT blocks the production of NAD(+) and results in tumor cell death.	NAD	66-72	nicotinamide phosphoribosyltransferase	Homo sapiens	35-40
19654329-2	2009	Growing evidence indicates that PBEF is a nicotinamide phosphoribosyltransferase involved in the mammalian salvage pathway of NAD synthesis.	NAD	126-129	nicotinamide phosphoribosyltransferase	Homo sapiens	32-36
27896073-1	2014	BACKGROUND: Citrin, encoded by SLC25A13, is a component of the malate-aspartate shuttle, which is the main NADH-transporting system in the liver.	NAD	107-111	solute carrier family 25 member 13	Homo sapiens	31-39
25486197-4	2014	In addition, it is worth noting that: (i) NAD incubation induced increased levels of BRCA1 in a concentration-dependent manner; (ii) Nampt knockdown-mediated reduction in NAD levels was effective at inhibiting BRCA1 expression; and (iii) the overexpression of Nampt led to higher NAD levels and a subsequent increase in BRCA1 levels in primary ovarian cancer cells and A2780, HO-8910 and ES2 ovarian cancer cell lines.	NAD	42-45	nicotinamide phosphoribosyltransferase	Homo sapiens	133-138
19720202-11	2009	(CAS)2 was also applied to detection of NAD+, with a D.L.	NAD	40-44	neural precursor cell expressed, developmentally down-regulated 9	Homo sapiens	1-6
25486197-4	2014	In addition, it is worth noting that: (i) NAD incubation induced increased levels of BRCA1 in a concentration-dependent manner; (ii) Nampt knockdown-mediated reduction in NAD levels was effective at inhibiting BRCA1 expression; and (iii) the overexpression of Nampt led to higher NAD levels and a subsequent increase in BRCA1 levels in primary ovarian cancer cells and A2780, HO-8910 and ES2 ovarian cancer cell lines.	NAD	42-45	nicotinamide phosphoribosyltransferase	Homo sapiens	260-265
25486197-4	2014	In addition, it is worth noting that: (i) NAD incubation induced increased levels of BRCA1 in a concentration-dependent manner; (ii) Nampt knockdown-mediated reduction in NAD levels was effective at inhibiting BRCA1 expression; and (iii) the overexpression of Nampt led to higher NAD levels and a subsequent increase in BRCA1 levels in primary ovarian cancer cells and A2780, HO-8910 and ES2 ovarian cancer cell lines.	NAD	171-174	nicotinamide phosphoribosyltransferase	Homo sapiens	133-138
25486197-4	2014	In addition, it is worth noting that: (i) NAD incubation induced increased levels of BRCA1 in a concentration-dependent manner; (ii) Nampt knockdown-mediated reduction in NAD levels was effective at inhibiting BRCA1 expression; and (iii) the overexpression of Nampt led to higher NAD levels and a subsequent increase in BRCA1 levels in primary ovarian cancer cells and A2780, HO-8910 and ES2 ovarian cancer cell lines.	NAD	171-174	nicotinamide phosphoribosyltransferase	Homo sapiens	260-265
19606062-0	2009	Axonal and cell body protection by nicotinamide adenine dinucleotide in tumor necrosis factor-induced optic neuropathy.	NAD	35-68	tumor necrosis factor-like	Rattus norvegicus	72-93
19606062-6	2009	Nicotinamide adenine dinucleotide also prevented TNF-induced axonal loss and delayed retinal ganglion cell loss 2 months after TNF injection.	NAD	0-33	tumor necrosis factor-like	Rattus norvegicus	49-52
19606062-6	2009	Nicotinamide adenine dinucleotide also prevented TNF-induced axonal loss and delayed retinal ganglion cell loss 2 months after TNF injection.	NAD	0-33	tumor necrosis factor-like	Rattus norvegicus	127-130
25486197-4	2014	In addition, it is worth noting that: (i) NAD incubation induced increased levels of BRCA1 in a concentration-dependent manner; (ii) Nampt knockdown-mediated reduction in NAD levels was effective at inhibiting BRCA1 expression; and (iii) the overexpression of Nampt led to higher NAD levels and a subsequent increase in BRCA1 levels in primary ovarian cancer cells and A2780, HO-8910 and ES2 ovarian cancer cell lines.	NAD	171-174	nicotinamide phosphoribosyltransferase	Homo sapiens	133-138
25486197-4	2014	In addition, it is worth noting that: (i) NAD incubation induced increased levels of BRCA1 in a concentration-dependent manner; (ii) Nampt knockdown-mediated reduction in NAD levels was effective at inhibiting BRCA1 expression; and (iii) the overexpression of Nampt led to higher NAD levels and a subsequent increase in BRCA1 levels in primary ovarian cancer cells and A2780, HO-8910 and ES2 ovarian cancer cell lines.	NAD	171-174	nicotinamide phosphoribosyltransferase	Homo sapiens	260-265
23888946-1	2014	Nicotinamide phosphoribosyl transferase (Nampt) is the rate-limiting enzyme for the salvage biosynthesis of nicotinamide adenine dinucleotide (NAD).	NAD	108-141	nicotinamide phosphoribosyltransferase	Homo sapiens	0-39
19606062-7	2009	Microglia identified by immunohistochemistry were increased in the optic nerves after TNF injection; this increase was inhibited by NAD treatment.	NAD	132-135	tumor necrosis factor-like	Rattus norvegicus	86-89
19606062-8	2009	These results suggest that axonal nicotinamide mononucleotide adenylyltransferase 1 and NAD declines are associated with TNF-induced optic nerve axonal degeneration and that axonal protection of NAD may be related to its inhibitory effect on microglial activation.	NAD	88-91	tumor necrosis factor-like	Rattus norvegicus	121-124
23888946-1	2014	Nicotinamide phosphoribosyl transferase (Nampt) is the rate-limiting enzyme for the salvage biosynthesis of nicotinamide adenine dinucleotide (NAD).	NAD	108-141	nicotinamide phosphoribosyltransferase	Homo sapiens	41-46
23888946-1	2014	Nicotinamide phosphoribosyl transferase (Nampt) is the rate-limiting enzyme for the salvage biosynthesis of nicotinamide adenine dinucleotide (NAD).	NAD	143-146	nicotinamide phosphoribosyltransferase	Homo sapiens	0-39
23888946-1	2014	Nicotinamide phosphoribosyl transferase (Nampt) is the rate-limiting enzyme for the salvage biosynthesis of nicotinamide adenine dinucleotide (NAD).	NAD	143-146	nicotinamide phosphoribosyltransferase	Homo sapiens	41-46
19478080-1	2009	In mammals, nicotinamide phosphoribosyltransferase (NAMPT) and nicotinamide mononucleotide adenylyltransferase 1 (NMNAT-1) constitute a nuclear NAD(+) salvage pathway which regulates the functions of NAD(+)-dependent enzymes such as the protein deacetylase SIRT1.	NAD	144-150	nicotinamide phosphoribosyltransferase	Homo sapiens	12-50
24727683-9	2014	On the other hand, the AhR antagonists restored the IS-induced decrease in the NAD(+) content in association with an improvement in the iNampt activity and ameliorated the senescence-related changes.	NAD	79-85	aryl hydrocarbon receptor	Homo sapiens	23-26
19478080-1	2009	In mammals, nicotinamide phosphoribosyltransferase (NAMPT) and nicotinamide mononucleotide adenylyltransferase 1 (NMNAT-1) constitute a nuclear NAD(+) salvage pathway which regulates the functions of NAD(+)-dependent enzymes such as the protein deacetylase SIRT1.	NAD	144-150	nicotinamide phosphoribosyltransferase	Homo sapiens	52-57
19478080-1	2009	In mammals, nicotinamide phosphoribosyltransferase (NAMPT) and nicotinamide mononucleotide adenylyltransferase 1 (NMNAT-1) constitute a nuclear NAD(+) salvage pathway which regulates the functions of NAD(+)-dependent enzymes such as the protein deacetylase SIRT1.	NAD	144-150	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	63-112
19478080-1	2009	In mammals, nicotinamide phosphoribosyltransferase (NAMPT) and nicotinamide mononucleotide adenylyltransferase 1 (NMNAT-1) constitute a nuclear NAD(+) salvage pathway which regulates the functions of NAD(+)-dependent enzymes such as the protein deacetylase SIRT1.	NAD	144-150	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	114-121
19478080-1	2009	In mammals, nicotinamide phosphoribosyltransferase (NAMPT) and nicotinamide mononucleotide adenylyltransferase 1 (NMNAT-1) constitute a nuclear NAD(+) salvage pathway which regulates the functions of NAD(+)-dependent enzymes such as the protein deacetylase SIRT1.	NAD	200-206	nicotinamide phosphoribosyltransferase	Homo sapiens	12-50
19478080-1	2009	In mammals, nicotinamide phosphoribosyltransferase (NAMPT) and nicotinamide mononucleotide adenylyltransferase 1 (NMNAT-1) constitute a nuclear NAD(+) salvage pathway which regulates the functions of NAD(+)-dependent enzymes such as the protein deacetylase SIRT1.	NAD	200-206	nicotinamide phosphoribosyltransferase	Homo sapiens	52-57
19478080-1	2009	In mammals, nicotinamide phosphoribosyltransferase (NAMPT) and nicotinamide mononucleotide adenylyltransferase 1 (NMNAT-1) constitute a nuclear NAD(+) salvage pathway which regulates the functions of NAD(+)-dependent enzymes such as the protein deacetylase SIRT1.	NAD	200-206	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	63-112
19478080-1	2009	In mammals, nicotinamide phosphoribosyltransferase (NAMPT) and nicotinamide mononucleotide adenylyltransferase 1 (NMNAT-1) constitute a nuclear NAD(+) salvage pathway which regulates the functions of NAD(+)-dependent enzymes such as the protein deacetylase SIRT1.	NAD	200-206	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	114-121
19478080-4	2009	In this study we show that stable short hairpin RNA-mediated knockdown of NAMPT or NMNAT-1 in MCF-7 breast cancer cells reduces total cellular NAD(+) levels and alters global patterns of gene expression.	NAD	143-149	nicotinamide phosphoribosyltransferase	Homo sapiens	74-79
24727683-10	2014	Taken together, these results indicate that IS impairs the iNampt-NAD(+)-Sirt1 system via AhR activation, which in turn promotes endothelial senescence.	NAD	66-72	aryl hydrocarbon receptor	Homo sapiens	90-93
19478080-4	2009	In this study we show that stable short hairpin RNA-mediated knockdown of NAMPT or NMNAT-1 in MCF-7 breast cancer cells reduces total cellular NAD(+) levels and alters global patterns of gene expression.	NAD	143-149	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	83-90
19478080-9	2009	This mechanism, in collaboration with NAMPT-dependent regulation of nuclear NAD(+) production, establishes an important pathway for transcription regulation by NAD(+).	NAD	76-82	nicotinamide phosphoribosyltransferase	Homo sapiens	38-43
24163442-1	2014	Sirtuin 6 (SIRT6), a member of the mammalian sirtuin family, is a nuclear deacetylase with substrate-specific NAD(+)-dependent activity.	NAD	110-116	sirtuin 6	Homo sapiens	0-9
19478080-9	2009	This mechanism, in collaboration with NAMPT-dependent regulation of nuclear NAD(+) production, establishes an important pathway for transcription regulation by NAD(+).	NAD	160-166	nicotinamide phosphoribosyltransferase	Homo sapiens	38-43
19500728-6	2009	We conclude that in the testis, caput epididymidis and bulbourethral gland of the immature pig, NADP(+)- and NAD(+)-dependent 11betaHSD enzymes catalyse net inactivation of cortisol, suggesting a physiological role for these enzymes in limiting local actions of glucocorticoids within these male reproductive tissues prior to puberty.	NAD	109-115	hydroxysteroid 11-beta dehydrogenase 2	Sus scrofa	126-135
24163442-1	2014	Sirtuin 6 (SIRT6), a member of the mammalian sirtuin family, is a nuclear deacetylase with substrate-specific NAD(+)-dependent activity.	NAD	110-116	sirtuin 6	Homo sapiens	11-16
24260155-9	2013	In addition, DPN treatment (an ERbeta agonist) induced the ARE-luciferase reporter gene, promoting Nrf2 nuclear translocation.	NAD	13-16	estrogen receptor 2	Homo sapiens	31-37
23831226-1	2013	NADH-Cytochrome b5 reductase (b5R), a flavoprotein consisting of NADH and flavin adenine dinucleotide (FAD) binding domains, catalyzes electron transfer from the two-electron carrier NADH to the one-electron carrier cytochrome b5 (Cb5).	NAD	65-69	cytochrome b5 reductase 3	Homo sapiens	30-33
24155910-1	2013	Among the enzymes involved in NAD homeostasis, nicotinamide mononucleotide adenylyltransferases (NMNAT1-3) are central to intracellular NAD formation.	NAD	136-139	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	97-103
24155910-2	2013	Although NMNAT3 is postulated to be a mitochondrial enzyme contributing to NAD-dependent organelle functioning, information on endogenous proteins is lacking.	NAD	75-78	nicotinamide nucleotide adenylyltransferase 3	Homo sapiens	9-15
19381393-4	2009	This biosensor used 3-alpha-hydroxysteroid dehydrogenase (3alpha-HSD) (EC 1.1.1.50) immobilized on the thick-film screen-printed working electrode to detect the enzymatically generated NADH.	NAD	185-189	aldo-keto reductase family 1 member C3	Homo sapiens	20-56
24155910-7	2013	Data of the present study modify the scenario of the origin of mitochondrial NAD by showing that, in human cells, NMNAT3 is absent in mitochondria, and, akin to plants and yeast, cytosolic NAD maintains the mitochondrial NAD pool.	NAD	77-80	nicotinamide nucleotide adenylyltransferase 3	Homo sapiens	114-120
19381393-4	2009	This biosensor used 3-alpha-hydroxysteroid dehydrogenase (3alpha-HSD) (EC 1.1.1.50) immobilized on the thick-film screen-printed working electrode to detect the enzymatically generated NADH.	NAD	185-189	aldo-keto reductase family 1 member C3	Homo sapiens	58-68
24555099-4	2013	RcFAH12 requires an electron supply from NADH:cytochrome b5 reductase (CBR1) and cytochrome b5 (Cb5) to synthesize ricinoleic acid.	NAD	41-45	oleate hydroxylase FAH12	Ricinus communis	0-7
23601674-5	2013	Importantly, we show that the zinc-deficient SOD1-induced motor defect can be ameliorated by supplementing the endogenous fly respiratory chain machinery with the single-subunit NADH-ubiquinone oxidoreductase from yeast (NADH is nicotinamide adenine dinucleotide, reduced form.).	NAD	178-182	Superoxide dismutase 1	Drosophila melanogaster	45-49
19410549-5	2009	During fasting, NAD in liver mitochondria increases, thereby triggering SIRT5 deacetylation of CPS1 and adaptation to the increase in amino acid catabolism.	NAD	16-19	sirtuin 5	Mus musculus	72-77
23601674-5	2013	Importantly, we show that the zinc-deficient SOD1-induced motor defect can be ameliorated by supplementing the endogenous fly respiratory chain machinery with the single-subunit NADH-ubiquinone oxidoreductase from yeast (NADH is nicotinamide adenine dinucleotide, reduced form.).	NAD	229-262	Superoxide dismutase 1	Drosophila melanogaster	45-49
24204194-0	2013	Dependence of tumor cell lines and patient-derived tumors on the NAD salvage pathway renders them sensitive to NAMPT inhibition with GNE-618.	NAD	65-68	nicotinamide phosphoribosyltransferase	Homo sapiens	111-116
19109034-1	2009	Nicotinamide phosphoribosyltransferase (Nampt) converts nicotinamide to nicotinamide mononucleotide (NMN), a key nicotinamide adenine dinucleotide (NAD) intermediate.	NAD	148-151	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
19109034-2	2009	Previously identified as a cytokine pre-B-cell colony-enhancing factor and controversially claimed as an insulin-mimetic hormone visfatin, Nampt has recently drawn much attention in several fields, including NAD biology, metabolism and inflammation.	NAD	208-211	nicotinamide phosphoribosyltransferase	Homo sapiens	139-144
19109034-3	2009	As a NAD biosynthetic enzyme, Nampt regulates the activity of NAD-consuming enzymes such as sirtuins and influences a variety of metabolic and stress responses.	NAD	5-8	nicotinamide phosphoribosyltransferase	Homo sapiens	30-35
19109034-3	2009	As a NAD biosynthetic enzyme, Nampt regulates the activity of NAD-consuming enzymes such as sirtuins and influences a variety of metabolic and stress responses.	NAD	62-65	nicotinamide phosphoribosyltransferase	Homo sapiens	30-35
24204194-2	2013	A key enzyme in the NAD salvage pathway is nicotinamide phosphoribosyl transferase (NAMPT), and here, we describe GNE-618, an NAMPT inhibitor that depletes NAD and induces cell death in vitro and in vivo.	NAD	20-23	nicotinamide phosphoribosyltransferase	Homo sapiens	43-82
24204194-2	2013	A key enzyme in the NAD salvage pathway is nicotinamide phosphoribosyl transferase (NAMPT), and here, we describe GNE-618, an NAMPT inhibitor that depletes NAD and induces cell death in vitro and in vivo.	NAD	20-23	nicotinamide phosphoribosyltransferase	Homo sapiens	84-89
19158096-2	2009	Previously, the NADH kinase reaction catalyzed by Pos5p, rather than the NAD kinase reaction followed by the NADP(+)-dependent dehydrogenase reaction, had been regarded as a critical source of mitochondrial NADPH, which plays vital roles in various mitochondrial functions.	NAD	16-19	NADH kinase	Saccharomyces cerevisiae S288C	50-55
24204194-2	2013	A key enzyme in the NAD salvage pathway is nicotinamide phosphoribosyl transferase (NAMPT), and here, we describe GNE-618, an NAMPT inhibitor that depletes NAD and induces cell death in vitro and in vivo.	NAD	20-23	nicotinamide phosphoribosyltransferase	Homo sapiens	126-131
24204194-2	2013	A key enzyme in the NAD salvage pathway is nicotinamide phosphoribosyl transferase (NAMPT), and here, we describe GNE-618, an NAMPT inhibitor that depletes NAD and induces cell death in vitro and in vivo.	NAD	156-159	nicotinamide phosphoribosyltransferase	Homo sapiens	43-82
24204194-2	2013	A key enzyme in the NAD salvage pathway is nicotinamide phosphoribosyl transferase (NAMPT), and here, we describe GNE-618, an NAMPT inhibitor that depletes NAD and induces cell death in vitro and in vivo.	NAD	156-159	nicotinamide phosphoribosyltransferase	Homo sapiens	84-89
24204194-2	2013	A key enzyme in the NAD salvage pathway is nicotinamide phosphoribosyl transferase (NAMPT), and here, we describe GNE-618, an NAMPT inhibitor that depletes NAD and induces cell death in vitro and in vivo.	NAD	156-159	nicotinamide phosphoribosyltransferase	Homo sapiens	126-131
19013440-8	2009	AKR1B10 catalyzed 4-MP reduction with a 30-fold increase in activity using NADPH as cofactor compared with NADH.	NAD	107-111	aldo-keto reductase family 1 member B10	Homo sapiens	0-7
24204194-3	2013	While cells proficient for nicotinic acid phosphoribosyl transferase (NAPRT1) can be protected from NAMPT inhibition as they convert nicotinic acid (NA) to NAD independent of the salvage pathway, this protection only occurs if NA is added before NAD depletion.	NAD	156-159	nicotinamide phosphoribosyltransferase	Homo sapiens	100-105
24204194-3	2013	While cells proficient for nicotinic acid phosphoribosyl transferase (NAPRT1) can be protected from NAMPT inhibition as they convert nicotinic acid (NA) to NAD independent of the salvage pathway, this protection only occurs if NA is added before NAD depletion.	NAD	246-249	nicotinamide phosphoribosyltransferase	Homo sapiens	100-105
24204194-7	2013	Thus, we show that dependence of tumor cells on the NAD salvage pathway renders them sensitive to GNE-618 in vitro and in vivo, and our data support further evaluation of the use of NAMPT mRNA and protein levels as predictors of overall sensitivity.	NAD	52-55	nicotinamide phosphoribosyltransferase	Homo sapiens	182-187
24048848-5	2013	Dorsal hippocampal (DH) infusion of ERalpha (PPT) or ERbeta (DPN) agonists enhanced novel object recognition and object placement memory in ovariectomized female mice in an ERK-dependent manner, suggesting that these receptors influence memory by rapidly activating hippocampal cell signaling.	NAD	61-64	estrogen receptor 2 (beta)	Mus musculus	53-59
23747282-2	2013	The first assay is based on the reduction of Delta(1)-pyrroline-5-carboxylate (P5C), generated from ornithine by OAT, using human pyrroline 5-carboxylate reductase 1 (PYCR1), which results in the concomitant oxidation of NADH (nicotinamide adenine dinucleotide, reduced form) to NAD+ (nicotinamide adenine dinucleotide, oxidized form).	NAD	279-283	ornithine aminotransferase	Homo sapiens	113-116
23747282-2	2013	The first assay is based on the reduction of Delta(1)-pyrroline-5-carboxylate (P5C), generated from ornithine by OAT, using human pyrroline 5-carboxylate reductase 1 (PYCR1), which results in the concomitant oxidation of NADH (nicotinamide adenine dinucleotide, reduced form) to NAD+ (nicotinamide adenine dinucleotide, oxidized form).	NAD	285-318	ornithine aminotransferase	Homo sapiens	113-116
18996949-7	2009	A model linking .NO, mitochondria, MnSOD and its acetylation/deacetylation by sirtuins (NAD+-dependent class III histone deacetylases) may be the basis for a potentially new powerful therapeutic intervention in the ageing process.	NAD	88-92	superoxide dismutase 2	Homo sapiens	35-40
23880765-7	2013	By specifically silencing or overexpressing CD38 and CD73, we demonstrated that endogenous CD73 enables, whereas CD38 impairs, the conversion of extracellular NMN to NR as a precursor for intracellular NAD(+) biosynthesis in human cells.	NAD	202-208	5'-nucleotidase ecto	Homo sapiens	91-95
23868449-7	2013	Pos5 is a NADH kinase of Saccharomyces cerevisiae that predominantly phosphorylates NADH to produce NADPH.	NAD	10-14	NADH kinase	Saccharomyces cerevisiae S288C	0-4
19074645-2	2009	Pre-B cell colony-enhancing factor/ nicotinamide phosphoribosyltransferase/visfatin has been characterized as a novel adipokine with a potential role in glucose metabolism and nicotinamide dinucleotide (NAD) generation.	NAD	176-201	nicotinamide phosphoribosyltransferase	Homo sapiens	75-83
19074645-2	2009	Pre-B cell colony-enhancing factor/ nicotinamide phosphoribosyltransferase/visfatin has been characterized as a novel adipokine with a potential role in glucose metabolism and nicotinamide dinucleotide (NAD) generation.	NAD	203-206	nicotinamide phosphoribosyltransferase	Homo sapiens	75-83
19074645-9	2009	Higher visfatin levels were associated with higher hepatic glucose production (r = 0.53, P &lt; 0.05) and also with a higher arterial ketone body ratio (KBR) (r = 0.48, P &lt; 0.05), an indicator of increased hepatic NAD generation.	NAD	217-220	nicotinamide phosphoribosyltransferase	Homo sapiens	7-15
19074645-11	2009	Plasma visfatin in cirrhosis is not associated with insulin resistance but correlates with hepatic glucose production and the arterial KBR, indicating a potential link between the NAD-generating properties of visfatin and metabolism.	NAD	180-183	nicotinamide phosphoribosyltransferase	Homo sapiens	7-15
19074645-11	2009	Plasma visfatin in cirrhosis is not associated with insulin resistance but correlates with hepatic glucose production and the arterial KBR, indicating a potential link between the NAD-generating properties of visfatin and metabolism.	NAD	180-183	nicotinamide phosphoribosyltransferase	Homo sapiens	209-217
24284888-1	2013	The NAD-synthesizing enzyme NMNAT2 is critical for axon survival in primary culture and its depletion may contribute to axon degeneration in a variety of neurodegenerative disorders.	NAD	4-7	nicotinamide nucleotide adenylyltransferase 2	Mus musculus	28-34
19151729-2	2009	The high expression of nicotinamide phosphoribosyltransferase (Nampt), an enzyme involved in the nicotinamide-dependent NAD biosynthetic pathway, in cells of the immune system has led us to examine the potential relationship between NAD metabolism and inflammation.	NAD	120-123	nicotinamide phosphoribosyltransferase	Homo sapiens	23-61
19151729-4	2009	Using a positive screen, we have identified Sirt6, a member of the sirtuin family, as the NAD-dependent enzyme able to regulate TNF production by acting at a post-transcriptional step.	NAD	90-93	sirtuin 6	Homo sapiens	44-49
18996448-1	2009	The alpha-ketoglutarate dehydrogenase complex (KGDHC) which catalyzes the conversion of alpha-ketoglutarate to succinyl-CoA and NADH in mitochondria, is known to generate O(2).- in vitro.	NAD	128-132	oxoglutarate dehydrogenase	Rattus norvegicus	4-37
19071085-1	2009	We examined in HepG2 cells whether glucose-induced changes in AMP-activated protein kinase (AMPK) activity could be mediated by SIRT1, an NAD(+)-dependent histone/protein deacetylase that has been linked to the increase in longevity caused by caloric restriction.	NAD	138-144	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	62-90
19071085-1	2009	We examined in HepG2 cells whether glucose-induced changes in AMP-activated protein kinase (AMPK) activity could be mediated by SIRT1, an NAD(+)-dependent histone/protein deacetylase that has been linked to the increase in longevity caused by caloric restriction.	NAD	138-144	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	92-96
19001417-1	2009	Quantitative basis for Urh1 and purine nucleoside phosphorylase function in NAD+ metabolism.	NAD	76-80	trifunctional uridine nucleosidase/nicotinamide riboside hydrolase/nicotinic acid riboside hydrolase	Saccharomyces cerevisiae S288C	23-27
19130305-1	2009	For the past several years, it has been demonstrated that the NAD-dependent protein deacetylase Sirt1 and nicotinamide phosphoribosyltransferase (Nampt)-mediated systemic NAD biosynthesis together play a critical role in the regulation of metabolism and possibly aging in mammals.	NAD	62-65	nicotinamide phosphoribosyltransferase	Homo sapiens	106-144
19130305-1	2009	For the past several years, it has been demonstrated that the NAD-dependent protein deacetylase Sirt1 and nicotinamide phosphoribosyltransferase (Nampt)-mediated systemic NAD biosynthesis together play a critical role in the regulation of metabolism and possibly aging in mammals.	NAD	62-65	nicotinamide phosphoribosyltransferase	Homo sapiens	146-151
19130305-1	2009	For the past several years, it has been demonstrated that the NAD-dependent protein deacetylase Sirt1 and nicotinamide phosphoribosyltransferase (Nampt)-mediated systemic NAD biosynthesis together play a critical role in the regulation of metabolism and possibly aging in mammals.	NAD	171-174	nicotinamide phosphoribosyltransferase	Homo sapiens	106-144
19130305-1	2009	For the past several years, it has been demonstrated that the NAD-dependent protein deacetylase Sirt1 and nicotinamide phosphoribosyltransferase (Nampt)-mediated systemic NAD biosynthesis together play a critical role in the regulation of metabolism and possibly aging in mammals.	NAD	171-174	nicotinamide phosphoribosyltransferase	Homo sapiens	146-151
19130305-3	2009	Conceptually, in the NAD World, systemic NAD biosynthesis mediated by intra- and extracellular Nampt functions as a driver that keeps up the pace of metabolism in multiple tissues/organs, and the NAD-dependent deacetylase Sirt1 serves as a universal mediator that executes metabolic effects in a tissue-dependent manner in response to changes in systemic NAD biosynthesis.	NAD	21-24	nicotinamide phosphoribosyltransferase	Homo sapiens	95-100
19130305-3	2009	Conceptually, in the NAD World, systemic NAD biosynthesis mediated by intra- and extracellular Nampt functions as a driver that keeps up the pace of metabolism in multiple tissues/organs, and the NAD-dependent deacetylase Sirt1 serves as a universal mediator that executes metabolic effects in a tissue-dependent manner in response to changes in systemic NAD biosynthesis.	NAD	41-44	nicotinamide phosphoribosyltransferase	Homo sapiens	95-100
19130305-3	2009	Conceptually, in the NAD World, systemic NAD biosynthesis mediated by intra- and extracellular Nampt functions as a driver that keeps up the pace of metabolism in multiple tissues/organs, and the NAD-dependent deacetylase Sirt1 serves as a universal mediator that executes metabolic effects in a tissue-dependent manner in response to changes in systemic NAD biosynthesis.	NAD	41-44	nicotinamide phosphoribosyltransferase	Homo sapiens	95-100
19130305-3	2009	Conceptually, in the NAD World, systemic NAD biosynthesis mediated by intra- and extracellular Nampt functions as a driver that keeps up the pace of metabolism in multiple tissues/organs, and the NAD-dependent deacetylase Sirt1 serves as a universal mediator that executes metabolic effects in a tissue-dependent manner in response to changes in systemic NAD biosynthesis.	NAD	41-44	nicotinamide phosphoribosyltransferase	Homo sapiens	95-100
19372760-0	2009	NAD and axon degeneration: from the Wlds gene to neurochemistry.	NAD	0-3	wallerian degeneration	Mus musculus	36-40
19372760-6	2009	The phenotype is attributed to the overexpression of a chimeric protein Wlds which contains a short fragment of the ubiquitin assembly protein UFD2 and the full-length nicotinamide adenine dinucleotide (NAD) synthetic enzyme Nicotinamide mononucleotide adenylyl-transferase-1 (Nmnat-1).	NAD	168-201	wallerian degeneration	Mus musculus	72-76
19390693-8	2009	Within the nucleotides tested, ATP, GTP and NAD show same level of inhibition on SVOP-FLAG labeling.	NAD	44-47	SV2 related protein	Homo sapiens	81-85
19390693-9	2009	Dose dependent studies indicated that SVOP demonstrates the highest affinity for NAD, in contrast to SV2, which binds both NAD and ATP with equal affinity.	NAD	81-84	SV2 related protein	Homo sapiens	38-42
19390693-9	2009	Dose dependent studies indicated that SVOP demonstrates the highest affinity for NAD, in contrast to SV2, which binds both NAD and ATP with equal affinity.	NAD	123-126	SV2 related protein	Homo sapiens	38-42
19128206-4	2008	A new mechanism for visfatin/NAD (nicotinamide adenine dinucleotide)-induced oxidative stress is presented involving redox cycling catalyzed by xanthine dehydrogenase and NADH oxidase.	NAD	29-32	nicotinamide phosphoribosyltransferase	Homo sapiens	20-28
19128206-4	2008	A new mechanism for visfatin/NAD (nicotinamide adenine dinucleotide)-induced oxidative stress is presented involving redox cycling catalyzed by xanthine dehydrogenase and NADH oxidase.	NAD	34-67	nicotinamide phosphoribosyltransferase	Homo sapiens	20-28
18835417-5	2008	Transactivation assays using mouse ERalpha and ERbeta showed that 10(-10)M DES activated both ER subtypes and that the ERalpha agonist (propyl pyrazole triol, PPT) and the ERbeta agonist (diarylpropionitrile, DPN) selectively activated their respective ERs at 10(-9)M. Neonatal female mice were injected subcutaneously with DES, PPT or DPN and the animals were examined at 13 and 15 weeks of age, respectively.	NAD	209-212	estrogen receptor 2 (beta)	Mus musculus	172-178
18835417-5	2008	Transactivation assays using mouse ERalpha and ERbeta showed that 10(-10)M DES activated both ER subtypes and that the ERalpha agonist (propyl pyrazole triol, PPT) and the ERbeta agonist (diarylpropionitrile, DPN) selectively activated their respective ERs at 10(-9)M. Neonatal female mice were injected subcutaneously with DES, PPT or DPN and the animals were examined at 13 and 15 weeks of age, respectively.	NAD	336-339	estrogen receptor 2 (beta)	Mus musculus	172-178
18805792-5	2008	In vitro studies using a range of substrates for different P450 enzymes showed that in hepatic microsomal cytochrome b5 null NADH-mediated metabolism was essentially abolished for most substrates, and the NADPH-dependent metabolism of many substrates was reduced by 50-90%.	NAD	125-129	cytochrome b5 type A (microsomal)	Mus musculus	106-119
18995842-3	2008	We found that the NAD(+)-dependent histone deacetylase SIRT2 deacetylates p300 in vitro and in cells.	NAD	18-24	E1A binding protein p300	Homo sapiens	74-78
18854029-1	2008	BACKGROUND: Human ART4, carrier of the GPI-(glycosyl-phosphatidylinositol) anchored Dombrock blood group antigens, is an apparently inactive member of the mammalian mono-ADP-ribosyltransferase (ART) family named after the enzymatic transfer of a single ADP-ribose moiety from NAD+ to arginine residues of extracellular target proteins.	NAD	276-280	ADP-ribosyltransferase 3 (inactive)	Homo sapiens	18-21
18664402-1	2008	A family of cell surface and growth-related proteins, designated ECTO-NOX proteins, carry out both copper-dependent NADH and hydroquinone oxidation and protein disulfide-thiol interchange.	NAD	116-120	tripartite motif containing 33	Homo sapiens	65-69
18664402-6	2008	Here, we provide results from Cu(II)Cl(2) solutions that demonstrate that ECTO-NOX-/Cu(II)-catalyzed oscillations in NADH oxidation are phased by exposure to low frequency electromagnetic fields.	NAD	117-121	tripartite motif containing 33	Homo sapiens	74-78
23679915-1	2013	Nicotinamide phoshophoribosyltransferase (NAMPT) plays a key role in the replenishment of the NAD pool in cells.	NAD	94-97	nicotinamide phosphoribosyltransferase	Homo sapiens	42-47
23968400-1	2013	BACKGROUND: Nicotinamide phosphoribosyltransferase (NAMPT) is the limiting enzyme in one of pathways of synthesis of Nicotinamide Adenine Dinucleotide, a redox coenzyme.	NAD	117-150	nicotinamide phosphoribosyltransferase	Homo sapiens	12-50
23946398-1	2013	NMNAT2 is an NAD(+)-synthesizing enzyme with an essential axon maintenance role in primary culture neurons.	NAD	13-19	nicotinamide nucleotide adenylyltransferase 2	Mus musculus	0-6
23597856-4	2013	It is unknown, however, whether changes in NAD(+) levels can influence p65 acetylation and cellular inflammatory responses.	NAD	43-49	RELA proto-oncogene, NF-kB subunit	Homo sapiens	71-74
23597856-11	2013	These findings demonstrate that PARP-1-induced changes in NAD(+) levels can modulate NF-kappaB transcriptional activity through effects on p65 acetylation.	NAD	58-64	RELA proto-oncogene, NF-kB subunit	Homo sapiens	139-142
23639789-7	2013	Same as CsA pretreatment, Ngb overexpression significantly reduced OGD-induced mPTP opening markers including mitochondria swelling, mitochondrial NAD(+) release, and cytochrome c (Cyt c) release in primary cultured neurons.	NAD	147-153	neuroglobin	Mus musculus	26-29
23639789-8	2013	Recombinant Ngb incubation significantly reduced OGD-induced NAD(+) release and Cyt c release from isolated mitochondria.	NAD	61-67	neuroglobin	Mus musculus	12-15
23639789-9	2013	In contrast, Ngb knockdown significantly increased OGD-induced neuron death, and increased OGD-induced mitochondrial NAD(+) release and Cyt c release as well, and these outcomes could be rescued by CsA pretreatment.	NAD	117-123	neuroglobin	Mus musculus	13-16
23774812-3	2013	Aldosterone and mineralocorticoid-receptor activation initiate an inflammatory response by increasing the generation of reactive oxygen species by nicotinamide adenine dinucleotide phosphate (NADPH) oxidase and mitochondria.	NAD	147-180	nuclear receptor subfamily 3 group C member 2	Homo sapiens	16-42
23770670-4	2013	We recently identified a pathway by which the AHR target gene TiPARP (TCDD-inducible poly(ADP-ribose) polymerase) contributes to TCDD suppression of transcription of phosphoenolpyruvate carboxykinase (PEPCK), a key regulator of gluconeogenesis, by consuming NAD(+) and decreasing Sirtuin 1 activation of the peroxisome proliferator-activated receptor gamma coactivator 1alpha (PGC1alpha), a transcriptional activator of PEPCK.	NAD	258-264	aryl hydrocarbon receptor	Homo sapiens	46-49
23673559-0	2013	Cloning, chromosomal characterization and FISH mapping of the NAD(+)-dependent histone deacetylase gene sirtuin 5 in the mouse.	NAD	62-68	sirtuin 5	Mus musculus	104-113
23673559-1	2013	Sirtuin 5 (SIRT5) is a nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase, belonging to the silent information regulator 2 (Sir2) family of sirtuin histone deacetylases (sirtuins).	NAD	23-56	sirtuin 5	Mus musculus	0-9
23673559-1	2013	Sirtuin 5 (SIRT5) is a nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase, belonging to the silent information regulator 2 (Sir2) family of sirtuin histone deacetylases (sirtuins).	NAD	23-56	sirtuin 5	Mus musculus	11-16
23673559-1	2013	Sirtuin 5 (SIRT5) is a nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase, belonging to the silent information regulator 2 (Sir2) family of sirtuin histone deacetylases (sirtuins).	NAD	58-61	sirtuin 5	Mus musculus	0-9
23335597-4	2013	Unexpectedly, overexpression of other genes in the salvage pathway for NAD(+) biosynthesis, including QNS1, NPT1 and PNC1 also protected against proteotoxicity.	NAD	71-77	nicotinamidase	Saccharomyces cerevisiae S288C	117-121
23646183-6	2013	The activation of these clock genes in vitro was not observed when we used mutated dCtBP which carries amino acid substitutions in NAD+ domain.	NAD	131-135	Clock	Drosophila melanogaster	24-29
23202346-4	2013	In the mixture solution of D-glucose and D-xylose containing coenzyme NAD+ (the oxidized form of nicotinamide adenine dinucleotide), the Nafion/GOD/XDH-bacteria/MWNTs modified electrode exhibited quasi-reversible oxidation-reduction peak at -0.5 V (vs. saturated calomel electrode, SCE) originating from the catalytic oxidation of D-glucose, and oxidation peak at +0.55 V(vs. SCE) responding to the oxidation of NADH (the reduced form of nicotinamide adenine dinucleotide) by the carbon nanotubes, where NADH is the resultant product of coenzyme NAD+ involved in the catalysis of D-xylose by XDH-displayed bacteria.	NAD	97-130	xanthine dehydrogenase	Homo sapiens	148-151
23202346-4	2013	In the mixture solution of D-glucose and D-xylose containing coenzyme NAD+ (the oxidized form of nicotinamide adenine dinucleotide), the Nafion/GOD/XDH-bacteria/MWNTs modified electrode exhibited quasi-reversible oxidation-reduction peak at -0.5 V (vs. saturated calomel electrode, SCE) originating from the catalytic oxidation of D-glucose, and oxidation peak at +0.55 V(vs. SCE) responding to the oxidation of NADH (the reduced form of nicotinamide adenine dinucleotide) by the carbon nanotubes, where NADH is the resultant product of coenzyme NAD+ involved in the catalysis of D-xylose by XDH-displayed bacteria.	NAD	97-130	xanthine dehydrogenase	Homo sapiens	592-595
23429506-8	2013	RESULTS: PRX2 attenuated reactive oxygen species, DNA damage, nicotinamide adenine dinucleotide depletion, and cell death.	NAD	62-95	peroxiredoxin 2	Mus musculus	9-13
23616928-13	2013	Identification of MNADK immediately suggests a model in which NADK and MNADK are responsible for de novo synthesis of NADP(+) in cytosol and mitochondria, respectively, and therefore provides novel insights into understanding the sources and mechanisms of mitochondrial NADP(+) and NADH production in human cells.	NAD	282-286	NAD kinase 2, mitochondrial	Homo sapiens	18-23
23616928-13	2013	Identification of MNADK immediately suggests a model in which NADK and MNADK are responsible for de novo synthesis of NADP(+) in cytosol and mitochondria, respectively, and therefore provides novel insights into understanding the sources and mechanisms of mitochondrial NADP(+) and NADH production in human cells.	NAD	282-286	NAD kinase 2, mitochondrial	Homo sapiens	71-76
23199080-3	2013	In vitro studies also suggest that the beneficial effects of mGluR5 activation involve nicotinamide adenine dinucleotide phosphate (NADPH) oxidase inhibition in activated microglia.	NAD	87-120	glutamate receptor, ionotropic, kainate 1	Mus musculus	61-67
23116202-1	2013	Saccharomyces cerevisiae has three distinct inner mitochondrial membrane NADH dehydrogenases mediating the transfer of electrons from NADH to CoQ (coenzyme Q): Nde1p, Nde2p and Ndi1p.	NAD	73-77	NADH-ubiquinone reductase (H(+)-translocating) NDI1	Saccharomyces cerevisiae S288C	177-182
18452539-0	2008	Cloning and characterization of a NAD+-dependent glycerol-3-phosphate dehydrogenase gene from Candida glycerinogenes, an industrial glycerol producer.	NAD	34-37	glycerol-3-phosphate dehydrogenase	Saccharomyces cerevisiae S288C	49-83
23116202-2	2013	The active site of Ndi1p faces the matrix side, whereas the enzymatic activities of Nde1p and Nde2p are restricted to the intermembrane space side, where they are responsible for cytosolic NADH oxidation.	NAD	189-193	NADH-ubiquinone reductase (H(+)-translocating) NDI1	Saccharomyces cerevisiae S288C	19-24
23321587-4	2013	Sensitivity analysis of the factors in the enzyme system affecting dye removal examined by an artificial neural network model shows that the relative importance of enzyme ratio between azoreductase and glucose 1-dehydrogenase was 22%, followed by dye concentration (27%), NAD(+) concentration (23%) and glucose concentration (22%), indicating none of the variables could be ignored in the enzyme system.	NAD	272-278	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	202-225
18704666-3	2008	Furanonaphthoquinones (FNQs) induced caspase-dependent apoptosis via the production of NADH-dependent reactive oxygen species (ROS) by VDAC1.	NAD	87-91	voltage dependent anion channel 1	Homo sapiens	135-140
24171767-1	2013	NAD+ biosynthesis through nicotinamide phosphoribosyltransferase (NAMPT) holds potential as a target for the treatment of inflammatory disorders due to NAD(+)"s role in immune cell signaling and metabolism.	NAD	0-4	nicotinamide phosphoribosyltransferase	Homo sapiens	26-64
18485875-4	2008	Here we find that GzmA accesses the mitochondrial matrix to cleave the complex I protein NDUFS3, an iron-sulfur subunit of the NADH:ubiquinone oxidoreductase complex I, after Lys56 to interfere with NADH oxidation and generate superoxide anions.	NAD	127-131	granzyme A	Homo sapiens	18-22
24171767-1	2013	NAD+ biosynthesis through nicotinamide phosphoribosyltransferase (NAMPT) holds potential as a target for the treatment of inflammatory disorders due to NAD(+)"s role in immune cell signaling and metabolism.	NAD	0-4	nicotinamide phosphoribosyltransferase	Homo sapiens	66-71
18485875-4	2008	Here we find that GzmA accesses the mitochondrial matrix to cleave the complex I protein NDUFS3, an iron-sulfur subunit of the NADH:ubiquinone oxidoreductase complex I, after Lys56 to interfere with NADH oxidation and generate superoxide anions.	NAD	199-203	granzyme A	Homo sapiens	18-22
24171767-1	2013	NAD+ biosynthesis through nicotinamide phosphoribosyltransferase (NAMPT) holds potential as a target for the treatment of inflammatory disorders due to NAD(+)"s role in immune cell signaling and metabolism.	NAD	152-158	nicotinamide phosphoribosyltransferase	Homo sapiens	26-64
23055259-4	2013	Using yeast two-hybrid screening assays, we found that beta- but not alpha-hOGG1 directly interacts with the mitochondrial protein NADH:ubiquinone oxidoreductase 1 beta subcomplex 10 (NDUFB10), an integral factor in Complex 1 on the mitochondrial inner membrane.	NAD	131-135	NADH:ubiquinone oxidoreductase subunit B10	Homo sapiens	184-191
18728403-4	2008	Pre-B-cell colony enhancing factor 1 gene (PBEF1) encodes Nicotinamide phosphoribosyltransferase (NAmPRTase), which catalyses the rate limiting step in the salvage pathway of NAD metabolism in mammalian cells.	NAD	175-178	nicotinamide phosphoribosyltransferase	Homo sapiens	0-36
18728403-4	2008	Pre-B-cell colony enhancing factor 1 gene (PBEF1) encodes Nicotinamide phosphoribosyltransferase (NAmPRTase), which catalyses the rate limiting step in the salvage pathway of NAD metabolism in mammalian cells.	NAD	175-178	nicotinamide phosphoribosyltransferase	Homo sapiens	43-48
18728403-4	2008	Pre-B-cell colony enhancing factor 1 gene (PBEF1) encodes Nicotinamide phosphoribosyltransferase (NAmPRTase), which catalyses the rate limiting step in the salvage pathway of NAD metabolism in mammalian cells.	NAD	175-178	nicotinamide phosphoribosyltransferase	Homo sapiens	58-96
23186252-3	2013	HYPOTHESIS: NAD/EDM in the American Quarter Horse (QH) is caused by a mutation in TTPA.	NAD	12-16	alpha tocopherol transfer protein	Equus caballus	82-86
18381895-3	2008	Here we show that the mitochondrial components of the malate-aspartate NADH shuttle (Mdh1 [malate dehydrogenase] and Aat1 [aspartate amino transferase]) and the glycerol-3-phosphate shuttle (Gut2, glycerol-3-phosphate dehydrogenase) are novel longevity factors in the CR pathway in yeast.	NAD	71-75	malate dehydrogenase MDH1	Saccharomyces cerevisiae S288C	85-89
18381895-3	2008	Here we show that the mitochondrial components of the malate-aspartate NADH shuttle (Mdh1 [malate dehydrogenase] and Aat1 [aspartate amino transferase]) and the glycerol-3-phosphate shuttle (Gut2, glycerol-3-phosphate dehydrogenase) are novel longevity factors in the CR pathway in yeast.	NAD	71-75	glycerol-3-phosphate dehydrogenase	Saccharomyces cerevisiae S288C	197-231
22907882-6	2013	Pollen deficient in the nicotinate/nicotinamide mononucleotide adenyltransferase (NMNAT) gene, encoding a key enzyme in NAD biosynthesis, and a lack of NAD+ accumulation in the gametophyte, showed precocious pollen tube germination inside the anther locule and vigorous tube growth under high-humidity conditions.	NAD	120-123	nicotinate/nicotinamide mononucleotide adenyltransferase	Arabidopsis thaliana	24-80
18337721-5	2008	Here we show that the human SIRT6 protein is an NAD+-dependent, histone H3 lysine 9 (H3K9) deacetylase that modulates telomeric chromatin.	NAD	48-52	sirtuin 6	Homo sapiens	28-33
22907882-6	2013	Pollen deficient in the nicotinate/nicotinamide mononucleotide adenyltransferase (NMNAT) gene, encoding a key enzyme in NAD biosynthesis, and a lack of NAD+ accumulation in the gametophyte, showed precocious pollen tube germination inside the anther locule and vigorous tube growth under high-humidity conditions.	NAD	120-123	nicotinate/nicotinamide mononucleotide adenyltransferase	Arabidopsis thaliana	82-87
23086953-0	2012	The NAD+-dependent histone deacetylase SIRT6 promotes cytokine production and migration in pancreatic cancer cells by regulating Ca2+ responses.	NAD	4-8	sirtuin 6	Homo sapiens	39-44
17822775-10	2008	ERbeta agonist DPN induced completely different results.	NAD	15-18	estrogen receptor 2	Homo sapiens	0-6
18344610-9	2008	mRNAs of nucleoside transporter (NT), ENT1, ENT2, CNT, and CNT3 were expressed in neutrophils; and their inhibitors, inosine, uridine, and s-(4-nitrobenzyl)-6-thioinosine, reduced the [Ca(2+)](i) rise induced by beta-NAD(+) and fMLP.	NAD	212-223	solute carrier family 29 member 1 (Augustine blood group)	Homo sapiens	38-42
18344610-9	2008	mRNAs of nucleoside transporter (NT), ENT1, ENT2, CNT, and CNT3 were expressed in neutrophils; and their inhibitors, inosine, uridine, and s-(4-nitrobenzyl)-6-thioinosine, reduced the [Ca(2+)](i) rise induced by beta-NAD(+) and fMLP.	NAD	212-223	solute carrier family 28 member 3	Homo sapiens	59-63
18206804-3	2008	Reactive oxygen species formation by the nicotinamide adenine dinucleotide phosphate oxidases Nox1 and Nox2 in arteries is a consequence of an activation of the enzymes by different stimuli such as growth factors, cytokines, and cardiovascular risk factors (cigarette smoke, high blood pressure, oxidized lipids).	NAD	41-74	NADPH oxidase 1	Homo sapiens	94-98
17921302-8	2007	The purified PrnF protein catalyzes reduction of flavin adenine dinucleotide (FAD) by NADH with a k(cat) of 65 s(-1) (K(m) = 3.2 muM for FAD and 43.1 muM for NADH) and supplies reduced FAD to the PrnD oxygenase component.	NAD	86-90	prion like protein doppel	Homo sapiens	196-200
17853438-3	2007	In the present study we used the MPT inhibitor cyclosporine-A (CsA) to preserve mitochondrial NAD(+) pools during PARP-1 activation and thereby provide an estimate of mitochondrial NAD(+) pool size in different cell types.	NAD	94-100	excision repaiross-complementing rodent repair deficiency, complementation group 8	Mus musculus	63-66
17853438-3	2007	In the present study we used the MPT inhibitor cyclosporine-A (CsA) to preserve mitochondrial NAD(+) pools during PARP-1 activation and thereby provide an estimate of mitochondrial NAD(+) pool size in different cell types.	NAD	181-187	excision repaiross-complementing rodent repair deficiency, complementation group 8	Mus musculus	63-66
17853438-6	2007	Inhibition of the mitochondrial permeability transition with cyclosporine-A (CsA) prevented PARP-1-induced NAD(+) depletion to a varying degree in the four cell types tested.	NAD	107-113	excision repaiross-complementing rodent repair deficiency, complementation group 8	Mus musculus	77-80
17853438-7	2007	CsA preserved 83.5% +/- 5.2% of total cellular NAD(+) in rat cardiac myocytes, 85.7% +/- 8.9% in mouse cardiac myocytes, 55.9% +/- 12.9% in mouse neurons, and 22.4% +/- 7.3% in mouse astrocytes.	NAD	47-53	excision repaiross-complementing rodent repair deficiency, complementation group 8	Mus musculus	0-3
17853438-8	2007	CsA preserved nearly 100% of NAD(+) content in mitochondria isolated from these cells.	NAD	29-35	excision repaiross-complementing rodent repair deficiency, complementation group 8	Mus musculus	0-3
17983577-2	2007	A study in this issue of Cell Metabolism (Revollo et al., 2007b) demonstrates that nicotinamide phosphoribosyltransferase (Nampt), also known as PBEF or visfatin, is a secreted enzyme and a source of systemic NAD.	NAD	209-212	nicotinamide phosphoribosyltransferase	Homo sapiens	83-121
17983577-2	2007	A study in this issue of Cell Metabolism (Revollo et al., 2007b) demonstrates that nicotinamide phosphoribosyltransferase (Nampt), also known as PBEF or visfatin, is a secreted enzyme and a source of systemic NAD.	NAD	209-212	nicotinamide phosphoribosyltransferase	Homo sapiens	123-128
17983577-2	2007	A study in this issue of Cell Metabolism (Revollo et al., 2007b) demonstrates that nicotinamide phosphoribosyltransferase (Nampt), also known as PBEF or visfatin, is a secreted enzyme and a source of systemic NAD.	NAD	209-212	nicotinamide phosphoribosyltransferase	Homo sapiens	145-149
17983577-2	2007	A study in this issue of Cell Metabolism (Revollo et al., 2007b) demonstrates that nicotinamide phosphoribosyltransferase (Nampt), also known as PBEF or visfatin, is a secreted enzyme and a source of systemic NAD.	NAD	209-212	nicotinamide phosphoribosyltransferase	Homo sapiens	153-161
17983577-3	2007	The authors show that Nampt-mediated NAD synthesis is necessary for beta cell function, providing fresh insights into the pathophysiology of metabolic diseases.	NAD	37-40	nicotinamide phosphoribosyltransferase	Homo sapiens	22-27
17983808-2	2007	We recently showed that reactive oxygen species (ROS) produced by nicotinamide adenine dinucleotide phosphate (NADPH) oxidase Nox4 mediate the antiapoptotic effect of growth factors.	NAD	66-99	NADPH oxidase 4	Homo sapiens	126-130
17803971-6	2007	Results of these analyses demonstrated that both the ERalpha-selective agonist, PPT (100 pM), and the ERbeta-selective agonist, DPN (100 pM), were effective in dynamically but differentially regulating intracellular calcium (Ca(2+)) signaling in hippocampal neurons.	NAD	128-131	estrogen receptor 2	Homo sapiens	102-108
17914902-1	2007	The eukaryotic nicotinamide riboside kinase (Nrk) pathway, which is induced in response to nerve damage and promotes replicative life span in yeast, converts nicotinamide riboside to nicotinamide adenine dinucleotide (NAD+) by phosphorylation and adenylylation.	NAD	183-216	Nik related kinase	Homo sapiens	45-48
17914902-1	2007	The eukaryotic nicotinamide riboside kinase (Nrk) pathway, which is induced in response to nerve damage and promotes replicative life span in yeast, converts nicotinamide riboside to nicotinamide adenine dinucleotide (NAD+) by phosphorylation and adenylylation.	NAD	218-222	Nik related kinase	Homo sapiens	45-48
17673460-9	2007	NDB2 and NDB4 fusion proteins were NADH-specific, and NDB2 was stimulated by Ca(2+).	NAD	35-39	NAD(P)H dehydrogenase B2	Arabidopsis thaliana	0-4
17655326-1	2007	Recent computer simulations of the cysteine nucleophilic attack on propanal in human mitochondrial aldehyde dehydrogenase (ALDH2) yielded an unexpected result: the chemically reasonable formation of a dead-end cysteine-cofactor adduct when NAD+ was in the "hydride transfer" position.	NAD	240-244	aldehyde dehydrogenase 2 family member	Homo sapiens	123-128
17501721-6	2007	In membrane preparations, NOX4 activity was selective for NADPH over NADH and did not require the addition of cytosol.	NAD	69-73	NADPH oxidase 4	Homo sapiens	26-30
17440754-2	2007	A steady-state kinetics study of XD showed that it catalyses NADH oxidation, leading to the formation of one O2*- molecule and half a H(2)O(2) molecule per NADH molecule, at rates 3 times those observed for XO (29.2 +/- 1.6 and 9.38 +/- 0.31 min(-1), respectively).	NAD	61-65	xanthine dehydrogenase	Rattus norvegicus	33-35
17440754-2	2007	A steady-state kinetics study of XD showed that it catalyses NADH oxidation, leading to the formation of one O2*- molecule and half a H(2)O(2) molecule per NADH molecule, at rates 3 times those observed for XO (29.2 +/- 1.6 and 9.38 +/- 0.31 min(-1), respectively).	NAD	156-160	xanthine dehydrogenase	Rattus norvegicus	33-35
17440754-3	2007	EPR spectra of NADH-reduced XD and XO were qualitatively similar, but they were quantitatively quite different.	NAD	15-19	xanthine dehydrogenase	Rattus norvegicus	28-30
17402939-1	2007	The effect of pH on the initial-rate kinetic behaviour of BVR-A (biliverdin-IXalpha reductase) exhibits an alkaline optimum with NADPH as cofactor, but a neutral optimum with NADH as cofactor.	NAD	175-179	biliverdin reductase A	Homo sapiens	58-63
17402939-1	2007	The effect of pH on the initial-rate kinetic behaviour of BVR-A (biliverdin-IXalpha reductase) exhibits an alkaline optimum with NADPH as cofactor, but a neutral optimum with NADH as cofactor.	NAD	175-179	biliverdin reductase A	Homo sapiens	65-93
17567466-7	2007	These studies identify a critical role for nicotinamide adenine dinucleotide phosphate (NADPH) oxidase-derived reactive oxygen species in the activation of ERK1/2 and subsequent production of TNFalpha in Kupffer cells after chronic ethanol feeding.	NAD	43-76	mitogen-activated protein kinase 3	Mus musculus	156-162
17565174-1	2007	In the NAD biosynthetic pathway, nicotinamide phosphoribosyltransferase (NMPRTase; EC 2.4.2.12) plays an important role in catalyzing the synthesis of nicotinamide mononucleotide from nicotinamide and 5"-phosphoribosyl-1"-pyrophosphate.	NAD	7-10	nicotinamide phosphoribosyltransferase	Homo sapiens	33-71
17565174-1	2007	In the NAD biosynthetic pathway, nicotinamide phosphoribosyltransferase (NMPRTase; EC 2.4.2.12) plays an important role in catalyzing the synthesis of nicotinamide mononucleotide from nicotinamide and 5"-phosphoribosyl-1"-pyrophosphate.	NAD	7-10	nicotinamide phosphoribosyltransferase	Homo sapiens	73-81
17988016-3	2007	The results of our investigation have also shown that the part of metabolic changes caused by long-term usage of alcohol, can be caused by direct influence of ethanol or its metabolites on those or other enzymatic proteins or receptors, and their functions can quickly be normalized after the abolition of alcohol (NAD+ contents, alpha-ketoglutarate dehydrogenase activity and some others).	NAD	315-319	oxoglutarate dehydrogenase	Rattus norvegicus	330-363
17430113-17	2007	Distinct among the NAD precursors, nicotinic acid specifically activates the g-protein coupled receptor (GPCR) GPR109a to produce the IDO-inducing tolerogenic prostaglandins PGE(2) and PGD(2).	NAD	19-22	adrenoceptor alpha 1A	Homo sapiens	105-109
17362982-1	2007	This study was designed to investigate whether treatment with an estrogen receptor-beta (ER-beta)-selective agonist (2,3-bis(4-hydroxyphenyl)-propionitrile, DPN) can provide cardioprotection in female mice lacking endogenous estrogen.	NAD	157-160	estrogen receptor 2 (beta)	Mus musculus	65-87
17362982-1	2007	This study was designed to investigate whether treatment with an estrogen receptor-beta (ER-beta)-selective agonist (2,3-bis(4-hydroxyphenyl)-propionitrile, DPN) can provide cardioprotection in female mice lacking endogenous estrogen.	NAD	157-160	estrogen receptor 2 (beta)	Mus musculus	89-96
17362982-9	2007	Gene profiling showed that treatment with DPN resulted in upregulation of a number of protective genes such as heat shock protein 70, the antiapoptotic protein, growth arrest and DNA damage 45 beta, and cyclooxygenase 2.	NAD	42-45	prostaglandin-endoperoxide synthase 2	Mus musculus	203-219
17298031-1	2007	Enzyme-based reagentless biosensors were developed using the model system of glucose dehydrogenase (GDH) and its nicotinamide adenine dinucleotide cofactor (NAD+).	NAD	113-146	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	77-98
17298031-1	2007	Enzyme-based reagentless biosensors were developed using the model system of glucose dehydrogenase (GDH) and its nicotinamide adenine dinucleotide cofactor (NAD+).	NAD	113-146	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	100-103
17298031-1	2007	Enzyme-based reagentless biosensors were developed using the model system of glucose dehydrogenase (GDH) and its nicotinamide adenine dinucleotide cofactor (NAD+).	NAD	157-161	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	77-98
17298031-1	2007	Enzyme-based reagentless biosensors were developed using the model system of glucose dehydrogenase (GDH) and its nicotinamide adenine dinucleotide cofactor (NAD+).	NAD	157-161	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	100-103
17298031-4	2007	The bioaffinity interactions between the NAD+ and GDH were secured by cross-linking the system with the glutaric dialdehyde (GDI)-modified CHIT.	NAD	41-45	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	50-53
17203264-4	2007	NADH is converted to NAD+ by applying hexacyanoferrate(III) as oxidant in the presence of DI.	NAD	0-4	dihydrolipoamide dehydrogenase	Homo sapiens	90-92
17203264-4	2007	NADH is converted to NAD+ by applying hexacyanoferrate(III) as oxidant in the presence of DI.	NAD	21-25	dihydrolipoamide dehydrogenase	Homo sapiens	90-92
17253767-9	2007	Conversely, NAD inhibits the Abeta-ABAD interaction.	NAD	12-15	succinate-CoA ligase ADP-forming subunit beta	Homo sapiens	29-34
17092593-4	2007	In a coupled-enzyme system comprising HSDH and formate dehydrogenase (FDH), a two-fold increase in production rate of androsterone was obtained when utilizing [Bmim][lactate] with NADH regeneration.	NAD	180-184	alcohol dehydrogenase 5 (class III), chi polypeptide	Homo sapiens	70-73
17060362-5	2007	Moreover, in a simplified CFS using purified mutant cytochrome b558 and recombinant p67phox, p47phox, and Rac1proteins, we found that the Km for NADPH and for NADH was about three times higher than those of purified WT cytochrome b558, indicating that the Leu505Arg mutation induces a slight decrease of the affinity for NADPH and NADH.	NAD	159-163	neutrophil cytosolic factor 2	Homo sapiens	84-91
17060362-5	2007	Moreover, in a simplified CFS using purified mutant cytochrome b558 and recombinant p67phox, p47phox, and Rac1proteins, we found that the Km for NADPH and for NADH was about three times higher than those of purified WT cytochrome b558, indicating that the Leu505Arg mutation induces a slight decrease of the affinity for NADPH and NADH.	NAD	331-335	neutrophil cytosolic factor 2	Homo sapiens	84-91
17097644-4	2006	Recombinant Ara2p showed NAD+-specific ARA activity with Km=0.78 mM to d-arabinose, which is 200-fold lower than that for the conventional NADP+-specific ARA, Ara1p.	NAD	25-29	D-arabinose 1-dehydrogenase (NAD(P)(+)) ARA2	Saccharomyces cerevisiae S288C	12-17
17097644-5	2006	Gene disruptant of ARA2 lost entire NAD+-specific ARA activity and the conspicuous increase in intracellular eAsA by exogenous d-arabinose feeding, while the double knockout mutant of ARA1 and ARA2 still retained measurable amount of eAsA.	NAD	36-40	D-arabinose 1-dehydrogenase (NAD(P)(+)) ARA2	Saccharomyces cerevisiae S288C	19-23
17029795-6	2006	In contrast, the levels of NAD dependent alpha-aminoadipate-delta-semialdehyde dehydrogenase (AASDH), a cytosolic enzyme important to alphaAA production from alphaAAS, was not influenced by PQQ dietary status.	NAD	27-30	aminoadipate-semialdehyde dehydrogenase	Rattus norvegicus	41-92
17029795-6	2006	In contrast, the levels of NAD dependent alpha-aminoadipate-delta-semialdehyde dehydrogenase (AASDH), a cytosolic enzyme important to alphaAA production from alphaAAS, was not influenced by PQQ dietary status.	NAD	27-30	aminoadipate-semialdehyde dehydrogenase	Rattus norvegicus	94-99
16999835-5	2006	We propose that NAD+ depletion in the nox2 mutant results in reduced acetyl-CoA production, which perturbs FA biosynthesis and hence blocks growth in aerobiosis.	NAD	16-20	cytochrome b-245, beta polypeptide	Mus musculus	38-42
16905546-6	2006	Further experiments showed accumulation of NADH and NRH, cofactors for NQO1 and NQO2, indicating altered intracellular redox status.	NAD	43-47	N-ribosyldihydronicotinamide quinone reductase 2	Mus musculus	80-84
16901503-7	2006	Although the relationship between the insulin-mimetic property and the enzymatic function of visfatin has not been clearly established, our structures raise the intriguing possibility that the glucose metabolism and the NAD biosynthesis are linked by visfatin.	NAD	220-223	nicotinamide phosphoribosyltransferase	Homo sapiens	251-259
22700872-2	2012	Our present study provides evidence that the ERbeta agonist, 2,3-bis-(4-hydroxy-phenyl)-propionitrile (DPN), and the selective estrogen receptor modulator tamoxifen (Tam), inhibit estrogen-induced DNA damage and mammary tumorigenesis in the aromatase transgenic (Arom) mouse model.	NAD	103-106	estrogen receptor 2 (beta)	Mus musculus	45-51
22843771-0	2012	Lipopolysaccharide-induced murine embryonic resorption involves nitric oxide-mediated inhibition of the NAD+-dependent 15-hydroxyprostaglandin dehydrogenase.	NAD	104-108	hydroxyprostaglandin dehydrogenase 15 (NAD)	Mus musculus	119-156
16783373-1	2006	Nicotinamide phosphoribosyltransferase (Nampt) synthesizes nicotinamide mononucleotide (NMN) from nicotinamide in a mammalian NAD+ biosynthetic pathway and is required for SirT1 activity in vivo.	NAD	126-130	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
16604356-3	2006	For [(eta 6-hmb)Ru(en)Cl]PF6, the rate of reaction is independent of NAD+ concentration and shows saturation kinetics with respect to formate concentration.	NAD	69-73	sperm associated antigen 17	Homo sapiens	25-28
22967613-0	2012	Enzyme biosensor for androsterone based on 3alpha-hydroxysteroid dehydrogenase immobilized onto a carbon nanotubes/ionic liquid/NAD+ composite electrode.	NAD	128-132	aldo-keto reductase family 1 member C3	Homo sapiens	43-78
16618099-0	2006	Crystal structures of the short-chain flavin reductase HpaC from Sulfolobus tokodaii strain 7 in its three states: NAD(P)(+)(-)free, NAD(+)(-)bound, and NADP(+)(-)bound.	NAD	133-139	flavin reductase family protein	Sulfurisphaera tokodaii str. 7	38-54
22967613-1	2012	A 3alpha-hydrosteroid biosensor for androsterone determination has been prepared by immobilizing the enzyme 3alpha-hydroxysteroid dehydrogenase (3alpha-HSD) in a composite electrode platform constituted of a mixture of multi-walled carbon nanotubes (MWCNTs), octylpyridinium hexafluorophosphate (OPPF(6)) ionic liquid and NAD(+) cofactor.	NAD	322-328	aldo-keto reductase family 1 member C3	Homo sapiens	108-143
16605250-4	2006	Structures of FDH.adenosine 5"-diphosphate ribose (ADP-ribose) and E67L.NAD(H) binary complexes were determined.	NAD	72-78	alcohol dehydrogenase 5 (class III), chi polypeptide	Homo sapiens	14-17
22967613-1	2012	A 3alpha-hydrosteroid biosensor for androsterone determination has been prepared by immobilizing the enzyme 3alpha-hydroxysteroid dehydrogenase (3alpha-HSD) in a composite electrode platform constituted of a mixture of multi-walled carbon nanotubes (MWCNTs), octylpyridinium hexafluorophosphate (OPPF(6)) ionic liquid and NAD(+) cofactor.	NAD	322-328	aldo-keto reductase family 1 member C3	Homo sapiens	145-155
16605250-13	2006	Steps involved in the binding of the coenzyme to the FDH active site are also discerned from the unique conformation of the coenzyme in one of the subunits of the E67L.NAD(H) binary complex.	NAD	168-174	alcohol dehydrogenase 5 (class III), chi polypeptide	Homo sapiens	53-56
22829588-7	2012	Model-predicted levels of TGF-beta1 protein and mRNA were largely confirmed experimentally but also suggested the presence of other mechanisms of regulation of TGF-beta1 by NAD(+).	NAD	173-179	transforming growth factor, beta 1	Mus musculus	160-169
22829588-8	2012	Thus, in vitro and in silico evidence points to NAD(+) as a novel modulator of TGF-beta1.	NAD	48-54	transforming growth factor, beta 1	Mus musculus	79-88
22700429-7	2012	Knockdown of different VDAC isoforms, especially of the least abundant isoform, VDAC3, also decreases DeltaPsi(m), cellular ATP, and NADH/NAD+, suggesting that VDAC1 and VDAC2 are most inhibited by free tubulin.	NAD	133-137	voltage dependent anion channel 1	Homo sapiens	160-165
16955758-3	2006	The method was based upon measurement of NADH generated from NAD+ during oxidation of bile acid by immobilized 3alpha-HSD with a color reagent consisting of nitrobluetetrazolium (NBT) chloride salt and immobilized diaphorase in 0.065 M sodium phosphate buffer (pH 7.0).	NAD	61-65	dihydrolipoamide dehydrogenase	Homo sapiens	214-224
22700429-7	2012	Knockdown of different VDAC isoforms, especially of the least abundant isoform, VDAC3, also decreases DeltaPsi(m), cellular ATP, and NADH/NAD+, suggesting that VDAC1 and VDAC2 are most inhibited by free tubulin.	NAD	138-142	voltage dependent anion channel 1	Homo sapiens	160-165
22920924-5	2012	We demonstrate that deletion of TDH3 but not TDH2 and TDH1 (encoding glyceraldehyde-3-phosphate dehydrogenase: GAPDH) abolishes NADH oscillations.	NAD	128-132	glyceraldehyde-3-phosphate dehydrogenase (phosphorylating) TDH3	Saccharomyces cerevisiae S288C	32-36
16460752-3	2006	Here we report the apoenzyme structure of GPD1 determined by multiwavelength anomalous diffraction phasing, and other complex structures with small molecules (NAD+ and DHAP) by the molecular replacement method.	NAD	159-163	glycerol-3-phosphate dehydrogenase 1	Homo sapiens	42-46
16356938-1	2006	CtBP family members, CtBP1 and CtBP2, are unique transcriptional regulators that adapt a metabolic enzyme fold, and their activities are regulated by NAD(H)-binding.	NAD	150-156	C-terminal binding protein 1	Homo sapiens	21-26
22767592-3	2012	However, human SIRT5 (sirtuin 5), which has been reported to exhibit little deacetylase activity, was recently identified as an NAD-dependent demalonylase and desuccinylase.	NAD	128-131	sirtuin 5	Homo sapiens	15-20
22767592-3	2012	However, human SIRT5 (sirtuin 5), which has been reported to exhibit little deacetylase activity, was recently identified as an NAD-dependent demalonylase and desuccinylase.	NAD	128-131	sirtuin 5	Homo sapiens	22-31
22767592-5	2012	Previously, we solved the crystal structure of a SIRT5-succinyl-lysine peptide-NAD complex.	NAD	79-82	sirtuin 5	Homo sapiens	49-54
22767592-6	2012	Here, we present two more structures: a binary complex of SIRT5 with an H3K9 succinyl peptide and a binary complex of SIRT5 with a bicyclic intermediate obtained by incubating SIRT5-H3K9 thiosuccinyl peptide co-crystals with NAD.	NAD	225-228	sirtuin 5	Homo sapiens	118-123
16872525-3	2006	Its synthesis is the result of cyclooxygenase (COX) and prostaglandin E synthase (PGES) activities whereas NAD+-dependent 15 hydroxy prostaglandin dehydrogenase (15-PGDH) is the key enzyme implicated in the catabolism of PGE2.	NAD	107-111	hydroxyprostaglandin dehydrogenase 15 (NAD)	Mus musculus	122-160
22767592-6	2012	Here, we present two more structures: a binary complex of SIRT5 with an H3K9 succinyl peptide and a binary complex of SIRT5 with a bicyclic intermediate obtained by incubating SIRT5-H3K9 thiosuccinyl peptide co-crystals with NAD.	NAD	225-228	sirtuin 5	Homo sapiens	118-123
16872525-3	2006	Its synthesis is the result of cyclooxygenase (COX) and prostaglandin E synthase (PGES) activities whereas NAD+-dependent 15 hydroxy prostaglandin dehydrogenase (15-PGDH) is the key enzyme implicated in the catabolism of PGE2.	NAD	107-111	hydroxyprostaglandin dehydrogenase 15 (NAD)	Mus musculus	162-169
22704488-3	2012	Nicotinamide phosphoribosyltransferase (Nampt), which is involved in nicotinamide adenine dinucleotide metabolism, is overexpressed in a variety of tumors.	NAD	69-102	nicotinamide phosphoribosyltransferase	Homo sapiens	0-38
16368957-2	2006	To defend itself against oxidative/nitrosative stress, M. tuberculosis expresses an NADH-dependent peroxidase and peroxynitrite reductase that is encoded by ahpC, ahpD, lpd, and dlaT.	NAD	84-88	dihydrolipoamide S-acetyltransferase (E2 component of pyruvate dehydrogenase complex)	Mus musculus	178-182
16051711-2	2005	ATPase activity was determined by enzymatic coupling of ATP resynthesis to the oxidation of NADH.	NAD	92-96	dynein axonemal heavy chain 8	Homo sapiens	0-6
15935693-1	2005	Arylformamidase (AFMID) is the second enzyme of the kynurenine pathway metabolizing tryptophan to nicotinic acid and nicotinamide adenine dinucleotide cofactors.	NAD	117-150	arylformamidase	Mus musculus	0-15
15935693-1	2005	Arylformamidase (AFMID) is the second enzyme of the kynurenine pathway metabolizing tryptophan to nicotinic acid and nicotinamide adenine dinucleotide cofactors.	NAD	117-150	arylformamidase	Mus musculus	17-22
16118205-1	2005	Nicotinamide mononucleotide adenylyltransferase (NMNAT) is the central enzyme of the NAD biosynthetic pathway.	NAD	85-88	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	0-47
16118205-1	2005	Nicotinamide mononucleotide adenylyltransferase (NMNAT) is the central enzyme of the NAD biosynthetic pathway.	NAD	85-88	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	49-54
16118205-6	2005	Moreover, as opposed to preferred NAD+ synthesis by NMNAT1, the other two isoforms could also form NADH directly from the reduced nicotinamide mononucleotide, supporting a hitherto unknown pathway of NAD generation.	NAD	34-38	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	52-58
16118205-6	2005	Moreover, as opposed to preferred NAD+ synthesis by NMNAT1, the other two isoforms could also form NADH directly from the reduced nicotinamide mononucleotide, supporting a hitherto unknown pathway of NAD generation.	NAD	99-103	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	52-58
16118205-6	2005	Moreover, as opposed to preferred NAD+ synthesis by NMNAT1, the other two isoforms could also form NADH directly from the reduced nicotinamide mononucleotide, supporting a hitherto unknown pathway of NAD generation.	NAD	34-37	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	52-58
16190762-4	2005	To develop an imaging agent for ERbeta, we synthesized a fluoroethyl analogue of DPN (2,3-bis(4-hydroxyphenyl)propanonitrile), a known ERbeta-selective ligand.	NAD	81-84	estrogen receptor 2 (beta)	Mus musculus	32-38
16190762-4	2005	To develop an imaging agent for ERbeta, we synthesized a fluoroethyl analogue of DPN (2,3-bis(4-hydroxyphenyl)propanonitrile), a known ERbeta-selective ligand.	NAD	81-84	estrogen receptor 2 (beta)	Mus musculus	135-141
16166628-9	2005	Instead, the NAD+-dependent deacetylase SIRT1 can potently induce MEF2 deacetylation.	NAD	13-17	myocyte enhancer factor 2A	Homo sapiens	66-70
16140404-1	2005	Mono-ADP-ribosyltransferase (ART) 4 belongs to a family of ectoenzymes that catalyze the transfer of ADP-ribose from NAD+ to a target protein.	NAD	117-121	ADP-ribosyltransferase 3 (inactive)	Homo sapiens	0-27
16140031-7	2005	Since significantly higher NADH/NAD+ ratios were previously observed in cultures of the arcA mutant strain compared to the wild type it seems that the cytochrome o oxidase (the product of cyoABCDE) cannot efficiently support aerobic respiration when the cells are grown under microaerobic conditions.	NAD	27-31	arginine deiminase	Escherichia coli	88-92
16140031-7	2005	Since significantly higher NADH/NAD+ ratios were previously observed in cultures of the arcA mutant strain compared to the wild type it seems that the cytochrome o oxidase (the product of cyoABCDE) cannot efficiently support aerobic respiration when the cells are grown under microaerobic conditions.	NAD	32-36	arginine deiminase	Escherichia coli	88-92
15718414-6	2005	An important role for nicotinamide adenine dinucleotide (NADPH) oxidase in LT-induced microbicidal activity was indicated by the fact that bacterial killing was abrogated by the NADPH oxidase inhibitor diphenyleneiodonium (DPI; 10 microM) and in AMs derived from gp91phox-deficient mice.	NAD	22-55	cytochrome b-245, beta polypeptide	Mus musculus	263-271
15845888-13	2005	The phagocyte-type cytosolic components, p47phox and p67phox, significantly enhanced the NADH-induced superoxide production of the BAEC membranes, whereas the components failed to increase the NADPH-induced superoxide production.	NAD	89-93	neutrophil cytosolic factor 1	Rattus norvegicus	41-48
15752713-0	2005	Porin and cytochrome oxidase containing contact sites involved in the oxidation of cytosolic NADH.	NAD	93-97	voltage dependent anion channel 1	Homo sapiens	0-5
15752713-3	2005	Dextran sulfate (500 kDa), known to interact with porin (the voltage-dependent anion channel), other than to inhibit the release of ATP synthesized inside the mitochondria, greatly decreases the activity of exogenous NADH/cyto-c system of intact mitochondria but has no effect on the reconstituted system made of mitoplasts and external membrane preparations.	NAD	217-221	voltage dependent anion channel 1	Homo sapiens	50-55
15752713-4	2005	The results obtained are consistent with the existence of specific contact sites containing cytochrome oxidase and porin, as components of the inner and the outer membrane respectively, involved in the oxidation of cytosolic NADH.	NAD	225-229	voltage dependent anion channel 1	Homo sapiens	115-120
15773895-0	2005	Role of NAD-dependent deacetylases SIRT1 and SIRT2 in radiation and cisplatin-induced cell death in vertebrate cells.	NAD	8-11	sirtuin 1	Gallus gallus	35-40
15773895-1	2005	Yeast Sir2 is a nicotinamide adenine dinucleotide (NAD)-dependent histone deacetylase that plays a central role in transcriptional silencing, chromosomal stability, DNA damage response and aging.	NAD	16-49	sirtuin 1	Gallus gallus	6-10
15773895-1	2005	Yeast Sir2 is a nicotinamide adenine dinucleotide (NAD)-dependent histone deacetylase that plays a central role in transcriptional silencing, chromosomal stability, DNA damage response and aging.	NAD	51-54	sirtuin 1	Gallus gallus	6-10
15707940-2	2005	The amino acid dehydrogenases were NAD+-dependent phenylalanine (EC 1.4.1.20), alanine (EC 1.4.1.1), and leucine (EC 1.4.1.9) dehydrogenases from various microbial species and NAD(P)+-dependent glutamate dehydrogenase from bovine liver (GDH; EC 1.4.1.3).	NAD	35-38	glucose dehydrogenase	Bos taurus	237-240
15707940-5	2005	The one exception to this was the dual-cofactor-specific GDH from bovine liver, which showed no affinity for N6-linked NAD+ but was biospecifically adsorbed to S6-linked NAD+ derivatives in the presence of its soluble KBEC ligand.	NAD	119-123	glucose dehydrogenase	Bos taurus	57-60
15857752-2	2005	Three-dimensional models of ternary complexes of human 17beta-HSD_8 with NAD cofactor and two chemically distinct substrates, the BKR substrate {CH3-(CH2)(12)-CO-CH(2)-CO-S-[ACP]} and the HSD substrate {estradiol} have been constructed (the atomic coordinates are available on request; e-mail: pletnev@hwi.buffalo.edu).	NAD	73-76	carbohydrate sulfotransferase 3	Homo sapiens	62-65
15557339-7	2005	Using single deletion mutants of Nde1p or Nde2p, we have shown that glycerol 3-phosphate oxidation via Gut2p is inhibited fully when NADH is oxidized via Nde1p, whereas only 50% of glycerol 3-phosphate oxidation is inhibited when Nde2p is functioning.	NAD	133-137	glycerol-3-phosphate dehydrogenase	Saccharomyces cerevisiae S288C	103-108
15269213-3	2004	We found a profound defect in oxidative phosphorylation, a test of integrated mitochondrial function, in clk-1 mitochondria fueled by NADH-linked electron donors, i.e. complex I-dependent substrates.	NAD	134-138	5-demethoxyubiquinone hydroxylase, mitochondrial	Caenorhabditis elegans	105-110
15530458-12	2004	Thus 3-hydroxyanthranilate 3,4-dioxygenase may be an important regulatory mechanism in the control of the flow of tryptophan along the kynurenine pathway to NAD in hypercholesterolemic rabbits.	NAD	157-160	3-hydroxyanthranilate 3,4-dioxygenase	Oryctolagus cuniculus	5-42
22704488-3	2012	Nicotinamide phosphoribosyltransferase (Nampt), which is involved in nicotinamide adenine dinucleotide metabolism, is overexpressed in a variety of tumors.	NAD	69-102	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
22550069-4	2012	NAD kinase (NADK) catalyzes the de novo formation of NADP(+) by phosphorylation of NAD(+).	NAD	83-89	NAD kinase	Rattus norvegicus	0-10
22550069-4	2012	NAD kinase (NADK) catalyzes the de novo formation of NADP(+) by phosphorylation of NAD(+).	NAD	83-89	NAD kinase	Rattus norvegicus	12-16
15627379-1	2004	NAD+-dependent formate dehydrogenase (FDH) is an abundant enzyme that plays an important role in energy supply of methylotrophic microorganisms and in response to stress in plants.	NAD	0-4	alcohol dehydrogenase 5 (class III), chi polypeptide	Homo sapiens	15-36
22687599-5	2012	To study the functions of Frm2, we measured the nitroreductase activity of purified Frm2 on 4-nitroquinoline-N-oxide (4-NQO) using NADH.	NAD	131-135	type II nitroreductase	Saccharomyces cerevisiae S288C	84-88
15627379-1	2004	NAD+-dependent formate dehydrogenase (FDH) is an abundant enzyme that plays an important role in energy supply of methylotrophic microorganisms and in response to stress in plants.	NAD	0-4	alcohol dehydrogenase 5 (class III), chi polypeptide	Homo sapiens	38-41
15247292-2	2004	In this report, we have identified an NAD(+)-binding site within human UGDH by photoaffinity labeling with a specific probe, [(32)P]nicotinamide 2-azidoadenosine dinucleotide (2N(3) NAD(+)), and cassette mutagenesis.	NAD	38-44	UDP-glucose 6-dehydrogenase	Homo sapiens	71-75
15247292-6	2004	Amino acid sequencing and compositional analysis identified the NAD(+)-binding site of UGDH as the region containing the sequence ICCIGAXYVGGPT, corresponding to Ile-7 through Thr-19 of the amino acid sequence of human UGDH.	NAD	64-70	UDP-glucose 6-dehydrogenase	Homo sapiens	87-91
22570471-5	2012	GMX1778 is a specific inhibitor of nicotinamide phosphoribosyltransferase, a rate-limiting enzyme required for the regeneration of NAD(+) from nicotinamide.	NAD	131-137	nicotinamide phosphoribosyltransferase	Homo sapiens	35-73
15247292-6	2004	Amino acid sequencing and compositional analysis identified the NAD(+)-binding site of UGDH as the region containing the sequence ICCIGAXYVGGPT, corresponding to Ile-7 through Thr-19 of the amino acid sequence of human UGDH.	NAD	64-70	UDP-glucose 6-dehydrogenase	Homo sapiens	219-223
15247292-12	2004	These results indicate that Gly-13 plays an important role for efficient binding of NAD(+) to human UGDH.	NAD	84-90	UDP-glucose 6-dehydrogenase	Homo sapiens	100-104
22539348-4	2012	In Saccharomyces cerevisiae, the nicotinamidase Pnc1 converts NAM to nicotinic acid (NA), which is then used as a substrate by the NAD(+) salvage pathway enzyme NA phosphoribosyltransferase (Npt1).	NAD	131-137	nicotinamidase	Saccharomyces cerevisiae S288C	48-52
16857098-1	2004	In the present work we have quantified some enzymatic activities, related to NAD+ metabolism, in lymphocytes of healthy donors and of patients affected by B-cell chronic lymphocytic leukemia (B-CLL): NADase activity for NAD+ degradation and NMN adenylyltransferase (NMNAT) activity for NAD+ biosynthesis.	NAD	77-81	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	241-264
16857098-1	2004	In the present work we have quantified some enzymatic activities, related to NAD+ metabolism, in lymphocytes of healthy donors and of patients affected by B-cell chronic lymphocytic leukemia (B-CLL): NADase activity for NAD+ degradation and NMN adenylyltransferase (NMNAT) activity for NAD+ biosynthesis.	NAD	77-81	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	266-271
16857098-1	2004	In the present work we have quantified some enzymatic activities, related to NAD+ metabolism, in lymphocytes of healthy donors and of patients affected by B-cell chronic lymphocytic leukemia (B-CLL): NADase activity for NAD+ degradation and NMN adenylyltransferase (NMNAT) activity for NAD+ biosynthesis.	NAD	220-224	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	241-264
22539348-9	2012	The INAM-induced increase in NAD(+) was strongly dependent on Pnc1 and Npt1, suggesting that INAM increases flux through the NAD(+) salvage pathway.	NAD	29-35	nicotinamidase	Saccharomyces cerevisiae S288C	62-66
16857098-1	2004	In the present work we have quantified some enzymatic activities, related to NAD+ metabolism, in lymphocytes of healthy donors and of patients affected by B-cell chronic lymphocytic leukemia (B-CLL): NADase activity for NAD+ degradation and NMN adenylyltransferase (NMNAT) activity for NAD+ biosynthesis.	NAD	220-224	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	266-271
16857098-1	2004	In the present work we have quantified some enzymatic activities, related to NAD+ metabolism, in lymphocytes of healthy donors and of patients affected by B-cell chronic lymphocytic leukemia (B-CLL): NADase activity for NAD+ degradation and NMN adenylyltransferase (NMNAT) activity for NAD+ biosynthesis.	NAD	220-224	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	241-264
22539348-9	2012	The INAM-induced increase in NAD(+) was strongly dependent on Pnc1 and Npt1, suggesting that INAM increases flux through the NAD(+) salvage pathway.	NAD	125-131	nicotinamidase	Saccharomyces cerevisiae S288C	62-66
16857098-1	2004	In the present work we have quantified some enzymatic activities, related to NAD+ metabolism, in lymphocytes of healthy donors and of patients affected by B-cell chronic lymphocytic leukemia (B-CLL): NADase activity for NAD+ degradation and NMN adenylyltransferase (NMNAT) activity for NAD+ biosynthesis.	NAD	220-224	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	266-271
22539348-10	2012	Part of this effect was mediated by the NR salvage pathways, which generate NAM as a product and require Pnc1 to produce NAD(+).	NAD	121-127	nicotinamidase	Saccharomyces cerevisiae S288C	105-109
22268572-7	2012	Large-scale transcriptomic analyses indicated that NAD promoted the induction of various pathogen-related genes such as the salicylic acid (SA)-responsive defence marker PR1.	NAD	51-54	pathogenesis-related protein 1	Arabidopsis thaliana	170-173
22207083-7	2012	We further showed that both agonists to estrogen receptor (ER), DPN (ERbeta) and PPT (ERalpha), as well as estrogenic natural compounds including soy isoflavones attenuated D+T-induced PSA production.	NAD	64-67	estrogen receptor 2	Homo sapiens	69-75
15310905-2	2004	In Wallerian degeneration slow (wlds) mice, Wallerian degeneration in response to axonal injury is delayed because of a mutation that results in overexpression of a chimeric protein (Wlds) composed of the ubiquitin assembly protein Ufd2a and the nicotinamide adenine dinucleotide (NAD) biosynthetic enzyme Nmnat1.	NAD	246-279	ubiquitination factor E4B	Mus musculus	232-237
15310905-2	2004	In Wallerian degeneration slow (wlds) mice, Wallerian degeneration in response to axonal injury is delayed because of a mutation that results in overexpression of a chimeric protein (Wlds) composed of the ubiquitin assembly protein Ufd2a and the nicotinamide adenine dinucleotide (NAD) biosynthetic enzyme Nmnat1.	NAD	281-284	ubiquitination factor E4B	Mus musculus	232-237
22339434-6	2012	Formation of adducts of ALDH1A1 and ALDH2 with acrolein increased their K(d) values for NAD(+) by 2- and 3-fold, respectively.	NAD	88-94	aldehyde dehydrogenase 2 family member	Homo sapiens	36-41
15288585-2	2004	ALDH activity, measured by aldehyde-induced NADH formation, was strongly depressed in the tolerant arteries.	NAD	44-48	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	0-4
15206932-7	2004	Kinetic parameters of EhPGDH were similar to those of mammalian PGDH, for example the preference of NADH cofactor, substrate specificities and salt-reversible substrate inhibition.	NAD	100-104	phosphoglycerate dehydrogenase	Homo sapiens	24-28
15206932-9	2004	The E. histolytica lysate contained PGDH activity of 26 nmol NADH utilized per min per mg of lysate protein in the reverse direction, which consisted 0.2-0.4% of a total soluble protein.	NAD	61-65	phosphoglycerate dehydrogenase	Homo sapiens	36-40
22339434-8	2012	These results suggested that both binding sites, those for aldehyde and NAD(+) in ALDH2, are targets for the inactivation by lipid peroxidation products.	NAD	72-78	aldehyde dehydrogenase 2 family member	Homo sapiens	82-87
22348967-2	2012	Visfatin can regulate immune action and is involved in the NAD+ salvage pathway.	NAD	59-63	nicotinamide phosphoribosyltransferase	Homo sapiens	0-8
22315973-2	2012	The mechanisms underlying WldS -mediated axonal protection are unclear, although many studies have attributed WldS neuroprotection to the NAD+-synthesizing Nmnat1 portion of the fusion protein.	NAD	138-142	wallerian degeneration	Mus musculus	110-114
22315973-5	2012	Moreover, NAD+ synthesis is not required since enzymatically-inactive WldS still protects.	NAD	10-14	wallerian degeneration	Mus musculus	70-74
22179235-10	2012	ORF-3 was predicted to have 42% identity to the daidzein reductase of Lactococcus strain 20-92 and belonged to the NADH:flavin oxidoreductase family.	NAD	115-119	hypothetical protein	Escherichia coli	0-5
22145797-9	2012	Instead, the positive charge of the NAD(+) ring, deprotonation of Asp429, and capping of the bulk surface of the flavin by the NAD(+) molecule all contribute to altering E(sq/hq) upon NAD(+) binding to XDH.	NAD	127-133	xanthine dehydrogenase	Homo sapiens	202-205
22145797-9	2012	Instead, the positive charge of the NAD(+) ring, deprotonation of Asp429, and capping of the bulk surface of the flavin by the NAD(+) molecule all contribute to altering E(sq/hq) upon NAD(+) binding to XDH.	NAD	127-133	xanthine dehydrogenase	Homo sapiens	202-205
22123821-1	2012	Biosynthesis of UDP-glucuronic acid by UDP-glucose 6-dehydrogenase (UGDH) occurs through the four-electron oxidation of the UDP-glucose C6 primary alcohol in two NAD(+)-dependent steps.	NAD	162-168	UDP-glucose 6-dehydrogenase	Homo sapiens	39-66
22123821-1	2012	Biosynthesis of UDP-glucuronic acid by UDP-glucose 6-dehydrogenase (UGDH) occurs through the four-electron oxidation of the UDP-glucose C6 primary alcohol in two NAD(+)-dependent steps.	NAD	162-168	UDP-glucose 6-dehydrogenase	Homo sapiens	68-72
22113203-2	2012	Nicotinamide phosphoribosyltransferase (Nampt, also known as visfatin), the rate-limiting enzyme in mammalian NAD (+)  biosynthesis, protects against ischemic stroke through inhibiting neuronal apoptosis and necrosis.	NAD	110-117	nicotinamide phosphoribosyltransferase	Homo sapiens	0-38
22113203-2	2012	Nicotinamide phosphoribosyltransferase (Nampt, also known as visfatin), the rate-limiting enzyme in mammalian NAD (+)  biosynthesis, protects against ischemic stroke through inhibiting neuronal apoptosis and necrosis.	NAD	110-117	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
22113203-2	2012	Nicotinamide phosphoribosyltransferase (Nampt, also known as visfatin), the rate-limiting enzyme in mammalian NAD (+)  biosynthesis, protects against ischemic stroke through inhibiting neuronal apoptosis and necrosis.	NAD	110-117	nicotinamide phosphoribosyltransferase	Homo sapiens	61-69
14680476-7	2004	Furthermore we find that GCY1, encoding a putative glycerol dehydrogenase, GPP2, encoding a NAD-dependent glycerol-3-phosphate phosphatase, and DCS2, a homologue to a decapping enzyme, have decreased mRNA levels in the yap4 -deleted strain.	NAD	92-95	glycerol 2-dehydrogenase (NADP(+)) GCY1	Saccharomyces cerevisiae S288C	25-29
21933152-0	2012	The high-resolution crystal structure of periplasmic Haemophilus influenzae NAD nucleotidase reveals a novel enzymatic function of human CD73 related to NAD metabolism.	NAD	76-79	5'-nucleotidase ecto	Homo sapiens	137-141
14694147-5	2004	XOR requires molybdopterin, iron-sulphur centres, and FAD as cofactors and has two interconvertible forms, xanthine oxidase and xanthine dehydrogenase, which transfer electrons from xanthine to oxygen and NAD(+), respectively, yielding superoxide, hydrogen peroxide and NADH.	NAD	205-211	xanthine dehydrogenase	Homo sapiens	0-3
14694147-5	2004	XOR requires molybdopterin, iron-sulphur centres, and FAD as cofactors and has two interconvertible forms, xanthine oxidase and xanthine dehydrogenase, which transfer electrons from xanthine to oxygen and NAD(+), respectively, yielding superoxide, hydrogen peroxide and NADH.	NAD	205-211	xanthine dehydrogenase	Homo sapiens	128-150
14694147-5	2004	XOR requires molybdopterin, iron-sulphur centres, and FAD as cofactors and has two interconvertible forms, xanthine oxidase and xanthine dehydrogenase, which transfer electrons from xanthine to oxygen and NAD(+), respectively, yielding superoxide, hydrogen peroxide and NADH.	NAD	270-274	xanthine dehydrogenase	Homo sapiens	0-3
21933152-6	2012	Sequence and structural analysis of H. influenzae NadN led us to discover that human CD73 is capable of processing both NAD and NMN, therefore disclosing a possible novel function of human CD73 in systemic NAD metabolism.	NAD	120-123	5'-nucleotidase ecto	Homo sapiens	85-89
14694147-5	2004	XOR requires molybdopterin, iron-sulphur centres, and FAD as cofactors and has two interconvertible forms, xanthine oxidase and xanthine dehydrogenase, which transfer electrons from xanthine to oxygen and NAD(+), respectively, yielding superoxide, hydrogen peroxide and NADH.	NAD	270-274	xanthine dehydrogenase	Homo sapiens	128-150
14699012-3	2004	Physiological concentrations of cytosolic NADH inhibited ryanodine receptor type 2 (RyR2)-mediated Ca2+-induced Ca2+ release (CICR) from SR membranes (IC50=120 micromol/L) and significantly lowered single channel open probability.	NAD	42-46	ryanodine receptor 2	Rattus norvegicus	84-88
21933152-6	2012	Sequence and structural analysis of H. influenzae NadN led us to discover that human CD73 is capable of processing both NAD and NMN, therefore disclosing a possible novel function of human CD73 in systemic NAD metabolism.	NAD	120-123	5'-nucleotidase ecto	Homo sapiens	189-193
21933152-6	2012	Sequence and structural analysis of H. influenzae NadN led us to discover that human CD73 is capable of processing both NAD and NMN, therefore disclosing a possible novel function of human CD73 in systemic NAD metabolism.	NAD	206-209	5'-nucleotidase ecto	Homo sapiens	85-89
21933152-6	2012	Sequence and structural analysis of H. influenzae NadN led us to discover that human CD73 is capable of processing both NAD and NMN, therefore disclosing a possible novel function of human CD73 in systemic NAD metabolism.	NAD	206-209	5'-nucleotidase ecto	Homo sapiens	189-193
22044451-1	2012	Pre-B-cell colony-enhancing factor (PBEF) is known as a rate-limiting enzyme that converts nicotinamide (NAM) to NMN in the salvage pathway of mammalian NAD+ biosynthesis.	NAD	153-157	nicotinamide phosphoribosyltransferase	Homo sapiens	0-34
14699012-9	2004	These data indicate that NADH oxidation is tightly linked to, and essential for, negative regulation of the RyR2 complex and is a likely component of an important physiological negative-feedback mechanism coupling SR Ca2+ fluxes and mitochondrial energy production.	NAD	25-29	ryanodine receptor 2	Rattus norvegicus	108-112
22044451-1	2012	Pre-B-cell colony-enhancing factor (PBEF) is known as a rate-limiting enzyme that converts nicotinamide (NAM) to NMN in the salvage pathway of mammalian NAD+ biosynthesis.	NAD	153-157	nicotinamide phosphoribosyltransferase	Homo sapiens	36-40
22044451-4	2012	Our results showed that the treatments of neurons with NAM and NAD+, the substrate and downstream product of PBEF, respectively, significantly reduced neuronal death after OGD and glutamate excitotoxicity, while treatment of neurons treated with FK866, a PBEF inhibitor, increased neuronal death after OGD.	NAD	63-67	nicotinamide phosphoribosyltransferase	Homo sapiens	109-113
15630200-4	2004	Furthermore, NADH-dependent ferricyanide reduction associated with VDAC1 is not sensitive to the anion channel inhibitors DIDS and dextran sulfate.	NAD	13-17	voltage dependent anion channel 1	Homo sapiens	67-72
22044451-4	2012	Our results showed that the treatments of neurons with NAM and NAD+, the substrate and downstream product of PBEF, respectively, significantly reduced neuronal death after OGD and glutamate excitotoxicity, while treatment of neurons treated with FK866, a PBEF inhibitor, increased neuronal death after OGD.	NAD	63-67	nicotinamide phosphoribosyltransferase	Homo sapiens	255-259
22044451-9	2012	We conclude that PBEF has a neuroprotective effect in ischemia through its enzymatic activity for NAD+ production that can ameliorate mitochondrial dysfunction.	NAD	98-102	nicotinamide phosphoribosyltransferase	Homo sapiens	17-21
22768255-5	2012	Our studies demonstrate a novel role for the NAD(+)-biosynthetic enzyme Nicotinamide phosphoribosyltransferase (Nampt) in maintaining de novo lipogenesis in prostate cancer (PCa) cells.	NAD	45-51	nicotinamide phosphoribosyltransferase	Homo sapiens	72-110
21706687-5	2004	In the second part, students are asked to design a soluble redox chain between NADH and cytochrome c using catalytic amounts of redox-active dyes.	NAD	79-83	LOC104968582	Bos taurus	88-100
15588129-2	2004	In the presence of NADH or NADPH, diaphorase can convert selected NO donors, glycerol trinitrate (GTN) and formaldoxime (FAL) to nitrites and nitrates with NO as an intermediate.	NAD	19-23	dihydrolipoamide dehydrogenase	Homo sapiens	34-44
15588129-8	2004	Reaction of FAL with diaphorase was lowered with SOD by 38 % indicating the partial participation of superoxide anion probably generated by the reaction of diaphorase with NADH or NADPH.	NAD	172-176	dihydrolipoamide dehydrogenase	Homo sapiens	21-31
15588129-8	2004	Reaction of FAL with diaphorase was lowered with SOD by 38 % indicating the partial participation of superoxide anion probably generated by the reaction of diaphorase with NADH or NADPH.	NAD	172-176	dihydrolipoamide dehydrogenase	Homo sapiens	156-166
14500716-4	2003	Modification of the pyrophosphate binding region, involving residues Thr-155, Ala-160, and Leu-263, indicates that this region is involved in determining coenzyme specificity and that selected alterations of these positions produce FNR enzymes that are able to bind NAD+.	NAD	266-270	ferredoxin reductase	Homo sapiens	232-235
12940934-6	2003	Hemichannels constituted of Cx43, the main connexin expressed by astrocytes, are permeable to small physiologically significant molecules, such as ATP, NAD+ and glutamate, and may mediate paracrine as well as autocrine signalling.	NAD	152-156	gap junction protein alpha 1	Homo sapiens	28-32
12872159-5	2003	In the presence of NADH, Pak1 superphosphorylates CtBP and inhibits CtBP dehydrogenase activity, suggesting that preferential phosphorylation of active CtBP may alter secondary structures and influence both enzymatic and corepressor functions.	NAD	19-23	p21 (RAC1) activated kinase 1	Homo sapiens	25-29
12872159-5	2003	In the presence of NADH, Pak1 superphosphorylates CtBP and inhibits CtBP dehydrogenase activity, suggesting that preferential phosphorylation of active CtBP may alter secondary structures and influence both enzymatic and corepressor functions.	NAD	19-23	C-terminal binding protein 1	Homo sapiens	50-54
12872159-5	2003	In the presence of NADH, Pak1 superphosphorylates CtBP and inhibits CtBP dehydrogenase activity, suggesting that preferential phosphorylation of active CtBP may alter secondary structures and influence both enzymatic and corepressor functions.	NAD	19-23	C-terminal binding protein 1	Homo sapiens	68-72
12872159-5	2003	In the presence of NADH, Pak1 superphosphorylates CtBP and inhibits CtBP dehydrogenase activity, suggesting that preferential phosphorylation of active CtBP may alter secondary structures and influence both enzymatic and corepressor functions.	NAD	19-23	C-terminal binding protein 1	Homo sapiens	68-72
12810547-4	2003	AKR1C2 is expressed in prostate, and in vitro it will catalyze the nicotinamide adenine dinucleotide (NAD(+))-dependent oxidation of 3alpha-androstanediol (3alpha-diol) to 5alpha-dihydrotestosterone (5alpha-DHT).	NAD	67-100	aldo-keto reductase family 1 member C2	Homo sapiens	0-6
12810547-4	2003	AKR1C2 is expressed in prostate, and in vitro it will catalyze the nicotinamide adenine dinucleotide (NAD(+))-dependent oxidation of 3alpha-androstanediol (3alpha-diol) to 5alpha-dihydrotestosterone (5alpha-DHT).	NAD	102-109	aldo-keto reductase family 1 member C2	Homo sapiens	0-6
12810547-5	2003	This reaction is potently inhibited by reduced NAD phosphate (NADPH), indicating that the NAD(+): NADPH ratio in cells will determine whether AKR1C2 makes 5alpha-DHT.	NAD	90-96	aldo-keto reductase family 1 member C2	Homo sapiens	142-148
12756024-1	2003	A case of type I methaemoglobinaemia observed in a Polish subject with compound heterozygosity for two mutations in the reduced nicotinamide adenine dinucleotide (NADH) cytochrome b5 reductase (b5R) gene is described.	NAD	128-161	cytochrome b5 reductase 3	Homo sapiens	180-192
12756024-1	2003	A case of type I methaemoglobinaemia observed in a Polish subject with compound heterozygosity for two mutations in the reduced nicotinamide adenine dinucleotide (NADH) cytochrome b5 reductase (b5R) gene is described.	NAD	128-161	cytochrome b5 reductase 3	Homo sapiens	194-197
12756024-1	2003	A case of type I methaemoglobinaemia observed in a Polish subject with compound heterozygosity for two mutations in the reduced nicotinamide adenine dinucleotide (NADH) cytochrome b5 reductase (b5R) gene is described.	NAD	163-167	cytochrome b5 reductase 3	Homo sapiens	180-192
12756024-1	2003	A case of type I methaemoglobinaemia observed in a Polish subject with compound heterozygosity for two mutations in the reduced nicotinamide adenine dinucleotide (NADH) cytochrome b5 reductase (b5R) gene is described.	NAD	163-167	cytochrome b5 reductase 3	Homo sapiens	194-197
12727306-1	2003	We have previously speculated that elevated levels of nicotinamide N-methyltransferase (NNMT), the primary catabolic enzyme of nicotinamide, may result in reduced Complex I activity in idiopathic Parkinson"s disease (IPD) in two ways: (1) reduction in the levels of nicotinamide available for nicotinamide adenine dinucleotide synthesis; and (2) increased methylation of compounds such as tetrahydroisoquinolines and beta-carbolines, which are potent Complex I inhibitors.	NAD	293-326	nicotinamide N-methyltransferase	Homo sapiens	54-86
12727306-1	2003	We have previously speculated that elevated levels of nicotinamide N-methyltransferase (NNMT), the primary catabolic enzyme of nicotinamide, may result in reduced Complex I activity in idiopathic Parkinson"s disease (IPD) in two ways: (1) reduction in the levels of nicotinamide available for nicotinamide adenine dinucleotide synthesis; and (2) increased methylation of compounds such as tetrahydroisoquinolines and beta-carbolines, which are potent Complex I inhibitors.	NAD	293-326	nicotinamide N-methyltransferase	Homo sapiens	88-92
12710131-4	2003	Immunoreactivity for versican was negative in benign melanocytic nevi, positive in NAD (ranging from weakly to intensely positive), and intensely positive in malignant melanoma.	NAD	83-86	versican	Homo sapiens	21-29
12710131-6	2003	Our results suggest that versican expression may be of value for distinguishing NAD from benign melanocytic nevi and for distinguishing severe NAD from mild and moderate NAD.	NAD	80-83	versican	Homo sapiens	25-33
12710131-6	2003	Our results suggest that versican expression may be of value for distinguishing NAD from benign melanocytic nevi and for distinguishing severe NAD from mild and moderate NAD.	NAD	143-146	versican	Homo sapiens	25-33
12892045-7	2003	While NAD(+)-dependent glutamate dehydrogenase (GDH-NAD+) activity also rose progressively during the recovering time, the cognate NADH-dependent glutamate dehydrogenase (GDH-NADH) activity decreased.	NAD	6-12	glutamate dehydrogenase	Solanum lycopersicum	48-51
12702242-1	2003	Under anaerobic conditions, Saccharomyces cerevisiae uses NADH-dependent glycerol-3-phosphate dehydrogenase (Gpd1p and Gpd2p) to re-oxidize excess NADH, yielding substantial amounts of glycerol.	NAD	58-62	glycerol-3-phosphate dehydrogenase	Saccharomyces cerevisiae S288C	73-107
12702242-1	2003	Under anaerobic conditions, Saccharomyces cerevisiae uses NADH-dependent glycerol-3-phosphate dehydrogenase (Gpd1p and Gpd2p) to re-oxidize excess NADH, yielding substantial amounts of glycerol.	NAD	147-151	glycerol-3-phosphate dehydrogenase	Saccharomyces cerevisiae S288C	73-107
12604204-3	2003	The structure of the FDH.NAD(H) binary complex reported here, in conjunction with the other complexes of FDH, provide the structural basis of the kinetic observations.	NAD	25-31	alcohol dehydrogenase 5 (class III), chi polypeptide	Homo sapiens	21-24
12604204-3	2003	The structure of the FDH.NAD(H) binary complex reported here, in conjunction with the other complexes of FDH, provide the structural basis of the kinetic observations.	NAD	25-31	alcohol dehydrogenase 5 (class III), chi polypeptide	Homo sapiens	105-108
12604204-8	2003	In the FDH.NAD(H) binary complex reported here, Glu67 is added to the coordination environment of the active site zinc and the distance between the water molecule and zinc is increased.	NAD	11-17	alcohol dehydrogenase 5 (class III), chi polypeptide	Homo sapiens	7-10
12604214-1	2003	Human NAD(+)-dependent microsomal short-chain dehydrogenase/reductase RoDH-4 oxidizes all-trans-retinol, 13-cis-retinol and 3alpha-hydroxysteroids to corresponding retinaldehydes and 3-ketones.	NAD	6-12	retinol dehydrogenase 16	Homo sapiens	70-76
12555668-3	2002	Recently, a bacterial protein encoded by nadV, a gene from the prokaryote Haemophilus ducreyi displaying significant homology with PBEF, has been identified as a nicotinamide phosphoribosyltranferase (NAmPRTase), an enzyme involved in nicotinamide adenine dinucleotide (NAD) biosynthesis.	NAD	235-268	nadV	[Haemophilus] ducreyi	41-45
12555668-3	2002	Recently, a bacterial protein encoded by nadV, a gene from the prokaryote Haemophilus ducreyi displaying significant homology with PBEF, has been identified as a nicotinamide phosphoribosyltranferase (NAmPRTase), an enzyme involved in nicotinamide adenine dinucleotide (NAD) biosynthesis.	NAD	270-273	nadV	[Haemophilus] ducreyi	41-45
12117413-6	2002	NMN-adenylyltransferase was then used to convert nicotinic acid-adenine dinucleotide into NAD in the presence of high concentrations of NMN.	NAD	90-93	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	0-23
22768255-5	2012	Our studies demonstrate a novel role for the NAD(+)-biosynthetic enzyme Nicotinamide phosphoribosyltransferase (Nampt) in maintaining de novo lipogenesis in prostate cancer (PCa) cells.	NAD	45-51	nicotinamide phosphoribosyltransferase	Homo sapiens	112-117
12117413-7	2002	The resultant NAD was amplified by a cycling assay involving alcohol dehydrogenase and diaphorase.	NAD	14-17	dihydrolipoamide dehydrogenase	Homo sapiens	87-97
22384032-4	2012	In addition, impaired complex I activity, which is well documented in PD, reduces the availability of the NAD(+) co-factor required by multiple ALDH isoforms to catalyze the removal of biogenic aldehydes.	NAD	106-112	aldehyde dehydrogenase family 3, subfamily A1	Mus musculus	144-148
12419229-5	2002	In addition, both a cofactor-dependent conformational change, with NAD(+) and NADH being equivalently effective, and the active site residues are linked to the binding of the PXDLS consensus recognition motif on repressors, such as E1A and RIP140.	NAD	67-73	nuclear receptor interacting protein 1	Homo sapiens	240-246
12419229-5	2002	In addition, both a cofactor-dependent conformational change, with NAD(+) and NADH being equivalently effective, and the active site residues are linked to the binding of the PXDLS consensus recognition motif on repressors, such as E1A and RIP140.	NAD	78-82	nuclear receptor interacting protein 1	Homo sapiens	240-246
22295107-5	2012	The treatment with estradiol (E2), anti-estrogenic agents 4-hydroxytamoxifen and ICI 182780, ERbeta specific ligand DPN and GPR30 agonist G1 led to a rapid activation of p-ERK1/2, suggesting the involvement of ERalpha36, ERbeta and GPR30 in the non-genomic signaling pathway in these cells.	NAD	116-119	estrogen receptor 2	Homo sapiens	93-99
12200115-2	2002	The present study describes biotransformation of RDX via route 3 by a diaphorase (EC 1.8.1.4) from Clostridium kluyveri using NADH as electron donor.	NAD	126-130	dihydrolipoamide dehydrogenase	Homo sapiens	70-80
22295107-5	2012	The treatment with estradiol (E2), anti-estrogenic agents 4-hydroxytamoxifen and ICI 182780, ERbeta specific ligand DPN and GPR30 agonist G1 led to a rapid activation of p-ERK1/2, suggesting the involvement of ERalpha36, ERbeta and GPR30 in the non-genomic signaling pathway in these cells.	NAD	116-119	estrogen receptor 2	Homo sapiens	221-227
22033928-12	2011	Our data suggest that Cx43 has a dual function exporting NAD(+) and importing cADPR into the cell to activate intracellular calcium mobilization.	NAD	57-63	gap junction protein, alpha 3	Mus musculus	22-26
12032156-1	2002	In the yeast Saccharomyces cerevisiae, the two most important systems for conveying excess cytosolic NADH to the mitochondrial respiratory chain are external NADH dehydrogenase (Nde1p/Nde2p) and the glycerol-3-phosphate dehydrogenase shuttle.	NAD	101-105	glycerol-3-phosphate dehydrogenase	Saccharomyces cerevisiae S288C	199-233
12032156-6	2002	Second, the activation of NADH dehydrogenase inhibited the Gut2p in such a manner that, at a saturating concentration of NADH, glycerol 3-phosphate is not used as respiratory substrate.	NAD	26-30	glycerol-3-phosphate dehydrogenase	Saccharomyces cerevisiae S288C	59-64
21890492-3	2011	The NDI1 mediated electron transfer from NADH to Co-Q, bypassed the defective complex I and restored oxidative phosphorylation in the host cells.	NAD	41-45	NADH-ubiquinone reductase (H(+)-translocating) NDI1	Saccharomyces cerevisiae S288C	4-8
12432938-1	2002	The primary catabolic pathway of prostaglandins and related eicosanoids is initiated by the oxidation of 15(S)-hydroxyl group catalyzed by NAD+-dependent 15-hydroxyprostaglandin dehydrogenase (15-PGDH) followed by the reduction of delta13 double bond catalyzed by NADPH/NADH dependent delta13-15-ketoprostaglandin reductase (13-PGR).	NAD	270-274	progesterone receptor	Homo sapiens	328-331
21890893-7	2011	Nicotinamide phosphoribosyltransferase (NAMPT) that synthesizes NAD(+) required for SIRT1 activation exerts similar effects on CIITA activity.	NAD	64-70	nicotinamide phosphoribosyltransferase	Homo sapiens	0-38
21890893-7	2011	Nicotinamide phosphoribosyltransferase (NAMPT) that synthesizes NAD(+) required for SIRT1 activation exerts similar effects on CIITA activity.	NAD	64-70	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
12011039-3	2002	We demonstrate in HeLa cells but not in normal diploid fibroblasts that modest increases in the expression level of uncoupling protein 2 (UCP-2) leads to a rapid and dramatic fall in mitochondrial membrane potential and to a reduction of mitochondrial NADH and intracellular ATP.	NAD	252-256	uncoupling protein 2	Homo sapiens	116-136
21930696-4	2011	We analyzed human DLD mutations linked to strikingly different clinical phenotypes, including E340K, D444V, R447G, and R460G in the dimer interface domain that are responsible for severe multisystem disorders of infancy and G194C in the NAD(+)-binding domain that is typically associated with milder presentations.	NAD	237-243	dihydrolipoamide dehydrogenase	Homo sapiens	18-21
12011039-3	2002	We demonstrate in HeLa cells but not in normal diploid fibroblasts that modest increases in the expression level of uncoupling protein 2 (UCP-2) leads to a rapid and dramatic fall in mitochondrial membrane potential and to a reduction of mitochondrial NADH and intracellular ATP.	NAD	252-256	uncoupling protein 2	Homo sapiens	138-143
12079352-10	2002	Finally, structural comparison with the members of the broad FNR structural family also provides an explanation for the high specificity exhibited by FNR for NADP+/H versus NAD+/H.	NAD	173-177	ferredoxin reductase	Homo sapiens	61-64
12079352-10	2002	Finally, structural comparison with the members of the broad FNR structural family also provides an explanation for the high specificity exhibited by FNR for NADP+/H versus NAD+/H.	NAD	173-177	ferredoxin reductase	Homo sapiens	150-153
11959140-1	2002	The final step in the biosynthesis of nicotinamide-adenine dinucleotide, a major coenzyme in cellular redox reactions and involved in intracellular signaling, is catalyzed by the enzyme nicotinamide mononucleotide adenylyltransferase (NMNAT).	NAD	38-71	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	235-240
11966438-5	2002	NMNAT is the rate-limiting step in the synthesis of NAD and NAD analogues.	NAD	52-55	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	0-5
11966438-5	2002	NMNAT is the rate-limiting step in the synthesis of NAD and NAD analogues.	NAD	60-63	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	0-5
11966442-3	2002	BR 5"-monophosphate is then converted to the active metabolite benzamide adenine dinucleotide (BAD) by NMN adenylyltransferase, the rate-limiting enzyme in the biosynthesis of NAD.	NAD	176-179	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	103-126
11744691-5	2002	Lipoamide dehydrogenase, a component of the alpha-ketoglutarate dehydrogenase complex and two other mitochondrial complexes, catalyzes the transfer of reducing equivalents from the bound dihydrolipoate of the neighboring dihydrolipoamide acyltransferase subunit to NAD(+).	NAD	265-271	dihydrolipoamide dehydrogenase	Sus scrofa	0-23
11744691-10	2002	Lipoamide dehydrogenase also catalyzes NADH oxidation by oxygen, yielding hydrogen peroxide as the major product and superoxide radical as a minor product.	NAD	39-43	dihydrolipoamide dehydrogenase	Sus scrofa	0-23
11772410-5	2002	The resultant NAD(+) can then be coupled to a cycling assay involving alcohol dehydrogenase and diaphorase.	NAD	14-20	dihydrolipoamide dehydrogenase	Homo sapiens	96-106
11687219-15	2001	Also the way of NAD(+)-reduction is unknown, since a gene equivalent to ferredoxin-NADP(+) reductase is not present in the genome.	NAD	16-22	ferredoxin reductase	Homo sapiens	72-100
11313358-12	2001	A structural comparison of ADP-hep 6-epimerase with UDP-galactose 4-epimerase, which utilizes an NAD(+) cofactor, has identified the regions of ADP-hep 6-epimerase, which defines its specificity for NADP(+).	NAD	97-103	UDP-galactose-4-epimerase	Homo sapiens	52-77
11425497-7	2001	Ghost AFR reductase activity can also be differentiated from NADH-dependent ferricyanide reductase(s) by its sensitivity to the detergent Triton X-100 and insensitivity to enzymatic digestion with cathepsin D.	NAD	61-65	cathepsin D	Homo sapiens	197-208
11418649-7	2001	Further analyses revealed that natural knockout mice for Art2.a (C57BL/6) or Art2.b (NZW) were resistant to NAD-mediated apoptosis.	NAD	108-111	ADP-ribosyltransferase 2a	Mus musculus	57-63
11274199-2	2001	Recently, hexameric connexin 43 (Cx43) hemichannels have been shown to release cytosolic NAD(+) from isolated murine fibroblasts (Bruzzone, S., Guida, L., Zocchi, E., Franco, L. and De Flora, A.	NAD	89-95	gap junction protein, alpha 3	Mus musculus	33-37
11370674-1	2001	Saccharomyces cerevisiae mitochondria contain an NADH:Q6 oxidoreductase (internal NADH dehydrogenase) encoded by NDI1 gene in chromosome XIII.	NAD	49-53	NADH-ubiquinone reductase (H(+)-translocating) NDI1	Saccharomyces cerevisiae S288C	113-117
11424356-2	2001	We investigated 23 patients who had both DPN and sufficient ADPN innervation to the EDB on the intramuscular distribution of DPN and ADPN innervation to the medial and lateral side of the EDB.	NAD	61-64	vesicle associated membrane protein 8	Homo sapiens	84-87
11424356-2	2001	We investigated 23 patients who had both DPN and sufficient ADPN innervation to the EDB on the intramuscular distribution of DPN and ADPN innervation to the medial and lateral side of the EDB.	NAD	61-64	vesicle associated membrane protein 8	Homo sapiens	188-191
11424356-6	2001	DPN enters to the EDB from the medial side, and ADPN from the lateral side of the EDB.	NAD	0-3	vesicle associated membrane protein 8	Homo sapiens	18-21
11424356-9	2001	This study clarified that a biased larger DPN innervation and smaller ADPN innervation to the medial side of the EDB, and vice versa to the lateral side of the EDB in the majority cases.	NAD	42-45	vesicle associated membrane protein 8	Homo sapiens	113-116
11295830-1	2001	Hereditary methemoglobinemia due to reduced nicotin amide adenine dinucleotide (NADH)-cytochrome b5 reductase (b5r) deficiency is classified into an erythrocyte type (I) and a generalized type (II).	NAD	44-78	cytochrome b5 reductase 3	Homo sapiens	111-114
11295830-1	2001	Hereditary methemoglobinemia due to reduced nicotin amide adenine dinucleotide (NADH)-cytochrome b5 reductase (b5r) deficiency is classified into an erythrocyte type (I) and a generalized type (II).	NAD	80-84	cytochrome b5 reductase 3	Homo sapiens	111-114
11224565-1	2001	Biliverdin reductase (BVR) is a soluble cytoplasmic enzyme that catalyzes the conversion of biliverdin to bilirubin using NADH or NADPH as electron donor.	NAD	122-126	biliverdin reductase A	Homo sapiens	0-20
11224565-1	2001	Biliverdin reductase (BVR) is a soluble cytoplasmic enzyme that catalyzes the conversion of biliverdin to bilirubin using NADH or NADPH as electron donor.	NAD	122-126	biliverdin reductase A	Homo sapiens	22-25
11159544-0	2001	Seven new mutations in the nicotinamide adenine dinucleotide reduced-cytochrome b(5) reductase gene leading to methemoglobinemia type I. Cytochrome b(5) reductase (b5R) deficiency manifests itself in 2 distinct ways.	NAD	27-60	cytochrome b5 reductase 3	Homo sapiens	164-167
11169102-2	2001	We demonstrate here that the catalytic domain of SpvB as well bacterial extracts containing full-length SpvB modifies a 43 kDa protein from macrophage-like J774-A.1 and epithelial MDCK cells as shown by label transfer from [32P]-nicotinamide adenine dinucleotide (NAD) to the 43 kDa protein.	NAD	229-262	virulence protein	Salmonella enterica	49-53
11169102-2	2001	We demonstrate here that the catalytic domain of SpvB as well bacterial extracts containing full-length SpvB modifies a 43 kDa protein from macrophage-like J774-A.1 and epithelial MDCK cells as shown by label transfer from [32P]-nicotinamide adenine dinucleotide (NAD) to the 43 kDa protein.	NAD	229-262	virulence protein	Salmonella enterica	104-108
11169102-2	2001	We demonstrate here that the catalytic domain of SpvB as well bacterial extracts containing full-length SpvB modifies a 43 kDa protein from macrophage-like J774-A.1 and epithelial MDCK cells as shown by label transfer from [32P]-nicotinamide adenine dinucleotide (NAD) to the 43 kDa protein.	NAD	264-267	virulence protein	Salmonella enterica	49-53
11169102-2	2001	We demonstrate here that the catalytic domain of SpvB as well bacterial extracts containing full-length SpvB modifies a 43 kDa protein from macrophage-like J774-A.1 and epithelial MDCK cells as shown by label transfer from [32P]-nicotinamide adenine dinucleotide (NAD) to the 43 kDa protein.	NAD	264-267	virulence protein	Salmonella enterica	104-108
11169102-5	2001	The isolated catalytic domain of SpvB mediated transfer of 32P from [32P]-NAD to actins from various sources in vitro, whereas isolated eukaryotic control proteins or bacterial proteins were not modified.	NAD	74-77	virulence protein	Salmonella enterica	33-37
11306026-5	2001	We recently published a 2.6 A structure of a binary complex between ALDH2 and NAD(+) in which the predominant conformation of the cofactor differed between different subunits in the structure.	NAD	78-84	aldehyde dehydrogenase 2 family member	Homo sapiens	68-73
11162776-1	2001	The ubiquitous NAD+ kinase (NADK) is the only known enzyme to catalyze formation of NADP+ from NAD+.	NAD	15-19	NAD kinase	Rattus norvegicus	28-32
11341914-3	2001	HSD efficiently reduces aspartate semialdehyde to homoserine (Hse) using either NADH or NADPH with kcat/Km in the order of 10(6-7) M(-1) x s(-1) at pH 7.5.	NAD	80-84	homoserine dehydrogenase	Saccharomyces cerevisiae S288C	0-3
22076378-0	2011	Sirt5 is a NAD-dependent protein lysine demalonylase and desuccinylase.	NAD	11-14	sirtuin 5	Homo sapiens	0-5
11095954-4	2000	As a competitive PARP inhibitor (K(i) = 60 nM), GPI 6150 protected the P388D1 cells against hydrogen peroxide cytotoxicity, by preventing PARP activation and the depletion of NAD(+), the substrate for PARP.	NAD	175-181	glucose-6-phosphate isomerase 1	Mus musculus	48-51
21664449-5	2011	Purified rMGEno exhibited alpha-enolase catalytic activity that it could reflect the conversion of NADH to NAD(+).	NAD	99-103	enolase 1, (alpha)	Gallus gallus	26-39
11042259-3	2000	The rescued mutants display a partially re-established transcriptional control of the osmostress-induced expression of GPD1, a target gene of the HOG pathway encoding NAD(+)-dependent glycerol 3-phosphate dehydrogenase, and a partially recovered hyperosmolarity-induced production of glycerol.	NAD	167-173	glycerol-3-phosphate dehydrogenase	Saccharomyces cerevisiae S288C	184-218
21664449-5	2011	Purified rMGEno exhibited alpha-enolase catalytic activity that it could reflect the conversion of NADH to NAD(+).	NAD	107-113	enolase 1, (alpha)	Gallus gallus	26-39
10842169-2	2000	The GPD1 gene encodes NAD(+)-dependent glycerol-3-phosphate dehydrogenase, a key enzyme in the production of the compatible solute glycerol.	NAD	22-28	glycerol-3-phosphate dehydrogenase	Saccharomyces cerevisiae S288C	39-73
21600982-5	2011	The ERbeta-specific agonist DPN increased [(3)H]-thymidine incorporation in all four thyroid cancer cell lines, whereas the ERalpha-specific agonist PPT increased growth only in NPA and WRO.	NAD	28-31	estrogen receptor 2	Homo sapiens	4-10
10744737-1	2000	Chloroplast ferredoxin-NADP(+) reductase has a 32,000-fold preference for NADPH over NADH, consistent with its main physiological role of NADP(+) photoreduction for de novo carbohydrate biosynthesis.	NAD	85-89	ferredoxin reductase	Homo sapiens	12-40
21733762-0	2011	Glucose sensing by electrogenerated chemiluminescence of glucose-dehydrogenase produced NADH on electrodeposited redox hydrogel.	NAD	88-92	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	57-78
10702312-1	2000	The penultimate step in carnitine biosynthesis is mediated by gamma-trimethylaminobutyraldehyde dehydrogenase (EC 1.2.1.47), a cytosolic NAD(+)-dependent aldehyde dehydrogenase that converts gamma-trimethylaminobutyraldehyde into gamma-butyrobetaine.	NAD	137-143	aldehyde dehydrogenase 9 family, member A1	Rattus norvegicus	62-109
21545843-1	2011	Nicotinamide phosphoribosyltransferase (Nampt/visfatin/PBEF) has been identified as a rate-limiting NAD(+) biosynthetic enzyme and an adipokine found in the circulation.	NAD	100-106	nicotinamide phosphoribosyltransferase pseudogene 1	Gallus gallus	0-38
10684881-3	2000	In the presence of glutamate, L-glutamic dehydrogenase (GDH) reduces NAD(+) to NADH, a product that fluoresces when excited with UV light.	NAD	69-75	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	30-54
10684881-3	2000	In the presence of glutamate, L-glutamic dehydrogenase (GDH) reduces NAD(+) to NADH, a product that fluoresces when excited with UV light.	NAD	69-75	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	56-59
10684881-3	2000	In the presence of glutamate, L-glutamic dehydrogenase (GDH) reduces NAD(+) to NADH, a product that fluoresces when excited with UV light.	NAD	79-83	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	30-54
10684881-3	2000	In the presence of glutamate, L-glutamic dehydrogenase (GDH) reduces NAD(+) to NADH, a product that fluoresces when excited with UV light.	NAD	79-83	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	56-59
10684881-4	2000	Theoretically, provided that GDH and NAD(+) are present in the bathing saline, the release of glutamate from stimulated astrocytes can be optically detected by monitoring the accumulation of NADH.	NAD	191-195	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	29-32
10606766-1	2000	We report the characterization of two enzymes that catalyze NAD(+)-dependent 9-cis-retinol dehydrogenase activity in rat liver cystol.	NAD	60-66	retinol dehydrogenase 5	Rattus norvegicus	77-104
10604966-1	2000	Xanthine oxidoreductase (XOR) is a mammalian enzyme that possesses a series of redox centers, which use either NAD(+) or molecular oxygen for oxidation of the purines xanthine and hypoxanthine to uric acid.	NAD	111-117	xanthine dehydrogenase	Homo sapiens	0-23
10604966-1	2000	Xanthine oxidoreductase (XOR) is a mammalian enzyme that possesses a series of redox centers, which use either NAD(+) or molecular oxygen for oxidation of the purines xanthine and hypoxanthine to uric acid.	NAD	111-117	xanthine dehydrogenase	Homo sapiens	25-28
10497258-1	1999	We report that the NAD-dependent Escherichia coli DNA ligase can support the growth of Saccharomyces cerevisiae strains deleted singly for CDC9 or doubly for CDC9 plus LIG4.	NAD	19-22	DNA ligase (ATP) DNL4	Saccharomyces cerevisiae S288C	168-172
10359773-6	1999	It was determined that inactivation of alpha-ketoglutarate dehydrogenase is responsible, in large part, for observed reperfusion-induced declines in NADH-linked respiration.	NAD	149-153	oxoglutarate dehydrogenase	Rattus norvegicus	39-72
10192400-4	1999	Raldh2 is an NAD-dependent aldehyde dehydrogenase with high substrate specificity for retinaldehyde.	NAD	13-16	aldehyde dehydrogenase family 1, subfamily A2	Mus musculus	0-6
10075667-6	1999	The flavin and iron-sulfur centers of inactivated XO were reduced by dithionite and reoxidized readily with oxygen, and inactivated XDH retained electron transfer activities from NADH to electron acceptors, consistent with the conclusion that the flavin and iron-sulfur centers of the inactivated enzyme both remained intact.	NAD	179-183	xanthine dehydrogenase	Homo sapiens	132-135
10698572-2	1999	Additional incorporation of glucose dehydrogenase in the enzymatic sequence results in regeneration of NADH provided that glucose is present in the carrier stream and incorporation of a dialysis membrane provides operational stability to the biosensor.	NAD	103-107	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	28-49
9884310-9	1999	The stoichiometry of 1:1 between the consumption of ND and the formation of NADH for the formation of HNQ implies that rat lens aldose reductase catalyzes a 2e- oxidation of ND to yield the corresponding ketol, which is autoxidized to NQ.	NAD	76-80	aldo-keto reductase family 1 member B1	Rattus norvegicus	128-144
10232052-3	1999	11 beta-HSD2 is a high affinity NAD-dependent dehydrogenase that protects the mineralocorticoid receptor from glucocorticoid excess; mutations in the HSD11B2 gene explain an inherited form of hypertension, the syndrome of apparent mineralocorticoid excess in which cortisol acts as a potent mineralocorticoid.	NAD	32-35	nuclear receptor subfamily 3 group C member 2	Homo sapiens	78-104
9834970-0	1998	NADH: ubiquinone oxidoreductase inhibitors block induction of ornithine decarboxylase activity in MCF-7 human breast cancer cells.	NAD	0-4	ornithine decarboxylase 1	Homo sapiens	62-85
9834970-6	1998	It is therefore proposed that NADH: ubiquinone oxidoreductase inhibitors block multiple and possibly reactive oxygen species-modulated pathways which regulate ornithine decarboxylase activity.	NAD	30-34	ornithine decarboxylase 1	Homo sapiens	159-182
9774405-0	1998	A novel, non-redox-regulated NAD-dependent malate dehydrogenase from chloroplasts of Arabidopsis thaliana L. We report a novel plastidic NAD-dependent malate dehydrogenase (EC 1.	NAD	29-32	malate dehydrogenase	Arabidopsis thaliana	43-63
9607316-1	1998	Xanthine oxidoreductase (XOR) catalyses the reduction of the therapeutic organic nitrate, nitroglycerin (glyceryl trinitrate, GTN), as well as inorganic nitrate and nitrite, to nitric oxide (NO) under hypoxic conditions in the presence of NADH.	NAD	239-243	xanthine dehydrogenase	Homo sapiens	0-23
9607316-1	1998	Xanthine oxidoreductase (XOR) catalyses the reduction of the therapeutic organic nitrate, nitroglycerin (glyceryl trinitrate, GTN), as well as inorganic nitrate and nitrite, to nitric oxide (NO) under hypoxic conditions in the presence of NADH.	NAD	239-243	xanthine dehydrogenase	Homo sapiens	25-28
9588172-1	1998	To identify the cytochrome b5 residues responsible for the electrostatic interaction with NADH-cytochrome b5 reductase (b5R), we prepared and characterized the cytochrome b5 mutants in which Glu41, Glu42, Glu63, Asp70, and Glu73 were replaced by Ala, utilizing site-directed mutagenesis and the expression system for cytochrome b5 in Escherichia coli.	NAD	90-94	cytochrome b5 reductase 3	Homo sapiens	120-123
9367520-2	1997	To investigate the specificity and target proteins of the arginine-specific mono-ADP-ribosyltransferase (mADP-RT) in rabbit skeletal muscle T-tubules (TT) biotin- or digoxigenin-coupled NAD-derivatives were synthesized.	NAD	186-189	ecto-ADP-ribosyltransferase 3	Oryctolagus cuniculus	76-103
9344673-0	1997	Molecular cloning and characterization of the human mitochondrial NADH:oxidoreductase 10-kDa gene (NDUFV3).	NAD	66-70	NADH:ubiquinone oxidoreductase subunit V3	Homo sapiens	99-105
9378235-22	1997	Through the lipoamide dehydrogenase-dependent reduction of lipoic acid, the cell can draw on its NADH pool for antioxidant activity additionally to its NADPH pool, which is usually consumed during oxidative stress.	NAD	97-101	dihydrolipoamide dehydrogenase	Homo sapiens	12-35
21545843-1	2011	Nicotinamide phosphoribosyltransferase (Nampt/visfatin/PBEF) has been identified as a rate-limiting NAD(+) biosynthetic enzyme and an adipokine found in the circulation.	NAD	100-106	nicotinamide phosphoribosyltransferase pseudogene 1	Gallus gallus	40-45
21545843-1	2011	Nicotinamide phosphoribosyltransferase (Nampt/visfatin/PBEF) has been identified as a rate-limiting NAD(+) biosynthetic enzyme and an adipokine found in the circulation.	NAD	100-106	nicotinamide phosphoribosyltransferase pseudogene 1	Gallus gallus	46-54
21602353-5	2011	UDP-glucose dehydrogenase (UGD) is responsible for the NAD-dependent 2-fold oxidation of UDP-glucose (UDP-Glc) to UDP-glucuronic acid (UDP-GlcA), which is a key step in cepacian biosynthesis.	NAD	55-58	UDP-glucose 6-dehydrogenase	Homo sapiens	0-25
9244391-0	1997	Mutations in the IDH2 gene encoding the catalytic subunit of the yeast NAD+-dependent isocitrate dehydrogenase can be suppressed by mutations in the CIT1 gene encoding citrate synthase and other genes of oxidative metabolism.	NAD	71-74	citrate (Si)-synthase CIT1	Saccharomyces cerevisiae S288C	149-153
21602353-5	2011	UDP-glucose dehydrogenase (UGD) is responsible for the NAD-dependent 2-fold oxidation of UDP-glucose (UDP-Glc) to UDP-glucuronic acid (UDP-GlcA), which is a key step in cepacian biosynthesis.	NAD	55-58	UDP-glucose 6-dehydrogenase	Homo sapiens	27-30
20824484-1	2011	The GPD2 gene, encoding NAD(+)-dependent glycerol-3-phosphate dehydrogenase in an industrial ethanol-producing strain of Saccharomyces cerevisiae, was deleted.	NAD	24-30	glycerol-3-phosphate dehydrogenase	Saccharomyces cerevisiae S288C	41-75
9388747-0	1997	Elevated circulating plasma NADH oxidising activity of xanthine oxidoreductase in plasma.	NAD	28-32	xanthine dehydrogenase	Homo sapiens	55-78
21477609-6	2011	Our data further confirm that therapeutic activation of ERbeta by DPN, an ERbeta agonist, blocks letrozole-resistant tumor growth in a xenograft model.	NAD	66-69	estrogen receptor 2 (beta)	Mus musculus	56-62
9240456-4	1997	In addition the IgG also inhibited NADH-dependent cytochrome c reduction in the same preparation.	NAD	35-39	cytochrome c	Zea mays	50-62
21477609-6	2011	Our data further confirm that therapeutic activation of ERbeta by DPN, an ERbeta agonist, blocks letrozole-resistant tumor growth in a xenograft model.	NAD	66-69	estrogen receptor 2 (beta)	Mus musculus	74-80
21477609-7	2011	Interestingly, DPN exerted tumor growth inhibition only in the presence of the AI letrozole, suggesting that combination therapy including ERbeta activators and AI may be used in the clinical setting treating AI resistant breast cancer.	NAD	15-18	estrogen receptor 2 (beta)	Mus musculus	139-145
21380727-5	2011	In the presence of NAD(+), the complex of keratin 1 and lectin was dissociated, what was recorded during elution of its separate components out of affinity columns and by decrease of their apparent molecular masses during gel-filtration.	NAD	19-25	keratin 1	Homo sapiens	42-51
23604305-3	1997	XDH acts on these same substrates but utilizes NAD as a cofactor to produce NADH instead of  O2 (-) and uric acid.	NAD	47-50	xanthine dehydrogenase	Homo sapiens	0-3
23604305-3	1997	XDH acts on these same substrates but utilizes NAD as a cofactor to produce NADH instead of  O2 (-) and uric acid.	NAD	76-80	xanthine dehydrogenase	Homo sapiens	0-3
21471938-6	2011	Pretreatment with MPG (0.5, 5 and 50 mug/mL) restored the ACh-induced relaxations (R(max): 92.29% +- 2.93, 91.02% +- 4.54 and 88.31 +- 2.36, respectively) in the presence of beta-NADH.	NAD	174-183	N-methylpurine-DNA glycosylase	Rattus norvegicus	18-21
21471938-9	2011	MPG also markedly inhibited the beta-NADH-induced generation of the superoxide radicals.	NAD	32-41	N-methylpurine-DNA glycosylase	Rattus norvegicus	0-3
9226256-1	1997	The structural gene (FDH1) coding for NAD(+)-dependent formate dehydrogenase (FDH) was cloned from a genomic library of Candida boidinii, and the FDH1 gene was disrupted in the C. boidinii genome (fdh1 delta) by one-step gene disruption.	NAD	38-44	formate dehydrogenase (NAD+)	Saccharomyces cerevisiae S288C	21-25
9226256-1	1997	The structural gene (FDH1) coding for NAD(+)-dependent formate dehydrogenase (FDH) was cloned from a genomic library of Candida boidinii, and the FDH1 gene was disrupted in the C. boidinii genome (fdh1 delta) by one-step gene disruption.	NAD	38-44	formate dehydrogenase (NAD+)	Saccharomyces cerevisiae S288C	146-150
21734824-6	2011	The soluble recombinant BmADH, produced at low-growth temperature, was instrumental in catalyzing the ethanol-dependent reduction of NAD(+), thereby indicating ethanol as one of the substrates of BmADH.	NAD	133-139	putative alcohol dehydrogenase	Bombyx mori	24-29
9226256-1	1997	The structural gene (FDH1) coding for NAD(+)-dependent formate dehydrogenase (FDH) was cloned from a genomic library of Candida boidinii, and the FDH1 gene was disrupted in the C. boidinii genome (fdh1 delta) by one-step gene disruption.	NAD	38-44	formate dehydrogenase (NAD+)	Saccharomyces cerevisiae S288C	197-201
21734824-6	2011	The soluble recombinant BmADH, produced at low-growth temperature, was instrumental in catalyzing the ethanol-dependent reduction of NAD(+), thereby indicating ethanol as one of the substrates of BmADH.	NAD	133-139	putative alcohol dehydrogenase	Bombyx mori	196-201
20388721-5	2011	In addition, an outline of the variety of immunological processes depending on the activity of nicotinamide phosphoribosyltransferase (Nampt), the key enzyme of the salvage pathway of NAD+ synthesis, is presented.	NAD	184-188	nicotinamide phosphoribosyltransferase	Homo sapiens	95-133
9207200-1	1997	The mouse NAD+-dependent 15-hydroxyprostaglandin dehydrogenase (15-PGDH) gene and its 5"-flanking region was cloned from a 129 mouse ES bacteriophage P1 genomic library.	NAD	10-14	hydroxyprostaglandin dehydrogenase 15 (NAD)	Mus musculus	64-71
20388721-5	2011	In addition, an outline of the variety of immunological processes depending on the activity of nicotinamide phosphoribosyltransferase (Nampt), the key enzyme of the salvage pathway of NAD+ synthesis, is presented.	NAD	184-188	nicotinamide phosphoribosyltransferase	Homo sapiens	135-140
21224467-6	2011	HES1-induced PARP1 activation leads to self-ADP ribosylation of PARP1, consumption of nicotinamide adenine dinucleotide(+), diminished adenosine triphosphate levels, and translocation of apoptosis-inducing factor from mitochondria to the nucleus, resulting in apoptosis in B-ALL but not T-cell ALL.	NAD	86-119	hes family bHLH transcription factor 1	Homo sapiens	0-4
21246601-2	2011	Nicotinamide phosphoribosyltransferase (Nampt) is the rate-limiting enzyme in mammalian nicotinamide adenine dinucleotide (NAD)(+) biosynthesis and contributes to cell fate decisions.	NAD	88-121	nicotinamide phosphoribosyltransferase	Homo sapiens	0-38
21246601-2	2011	Nicotinamide phosphoribosyltransferase (Nampt) is the rate-limiting enzyme in mammalian nicotinamide adenine dinucleotide (NAD)(+) biosynthesis and contributes to cell fate decisions.	NAD	88-121	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
21246601-2	2011	Nicotinamide phosphoribosyltransferase (Nampt) is the rate-limiting enzyme in mammalian nicotinamide adenine dinucleotide (NAD)(+) biosynthesis and contributes to cell fate decisions.	NAD	123-130	nicotinamide phosphoribosyltransferase	Homo sapiens	0-38
21246601-2	2011	Nicotinamide phosphoribosyltransferase (Nampt) is the rate-limiting enzyme in mammalian nicotinamide adenine dinucleotide (NAD)(+) biosynthesis and contributes to cell fate decisions.	NAD	123-130	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
20940012-6	2011	Increased nicotinamide adenine dinucleotide phosphate (NADHP) oxidase activity and apoptosis induction, regulated by mitochondrial signal pathway through an increased pro-apoptotic Bax/BcL(2) ratio and caspase 3 activity, were demonstrated.	NAD	10-43	caspase 3	Rattus norvegicus	202-211
21586363-4	2011	The CD38/CD157 family of extracellular NADases degrades NAD(+) and generates Ca(2+)-active metabolites, including cyclic ADP ribose and ADP ribose.	NAD	56-62	bone marrow stromal cell antigen 1	Mus musculus	9-14
21048160-6	2010	A search for the histone deacetylase (HDAC) that counterbalances CLOCK activity revealed that SIRT1, a nicotinamide adenin dinucleotide (NAD(+))-dependent HDAC, functions in a circadian manner.	NAD	137-144	clock circadian regulator	Homo sapiens	65-70
9283625-5	1997	After 8 h of preincubation with insulin (5 micrograms/ml), the activity of the enzyme ATP-citrate lyase in cultured Sertoli cells was increased from 0.19 to 0.34 nmol NAD+ formed microgram protein-1 min-1.	NAD	167-171	ATP citrate lyase	Rattus norvegicus	86-103
9092820-2	1997	In this work, we show that the two flavin-based enzymes ferredoxin-NADP+ reductase and xanthine oxidase catalyze the reductive activation of 1 by NADPH and NADH, respectively.	NAD	156-160	ferredoxin reductase	Homo sapiens	56-82
20696207-1	2010	OBJECTIVE: The nicotinamide phosphoribosyltransferase (Nampt) inhibitor APO866 depletes intracellular nicotinamide adenine dinucleotide (NAD(+)) and shows promising anticancer activity in preclinical studies.	NAD	102-135	nicotinamide phosphoribosyltransferase	Homo sapiens	15-53
20696207-1	2010	OBJECTIVE: The nicotinamide phosphoribosyltransferase (Nampt) inhibitor APO866 depletes intracellular nicotinamide adenine dinucleotide (NAD(+)) and shows promising anticancer activity in preclinical studies.	NAD	102-135	nicotinamide phosphoribosyltransferase	Homo sapiens	55-60
20696207-1	2010	OBJECTIVE: The nicotinamide phosphoribosyltransferase (Nampt) inhibitor APO866 depletes intracellular nicotinamide adenine dinucleotide (NAD(+)) and shows promising anticancer activity in preclinical studies.	NAD	137-143	nicotinamide phosphoribosyltransferase	Homo sapiens	15-53
20696207-1	2010	OBJECTIVE: The nicotinamide phosphoribosyltransferase (Nampt) inhibitor APO866 depletes intracellular nicotinamide adenine dinucleotide (NAD(+)) and shows promising anticancer activity in preclinical studies.	NAD	137-143	nicotinamide phosphoribosyltransferase	Homo sapiens	55-60
20692795-6	2010	RESULTS: LOX-1 protein expression was markedly lower after exposure to oxLDL in HUVECs pretreated with ellagic acid or diphenyleneiodonium, a well-known inhibitor of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, than in HUVECs exposed to oxLDL alone, suggesting that ellagic acid deactivates NADPH oxidase.	NAD	166-199	oxidized low density lipoprotein receptor 1	Homo sapiens	9-14
20876337-5	2010	The slow-growing mmdh1mmdh2 mutant has elevated leaf respiration rate in the dark and light, without loss of photosynthetic capacity, suggesting that mMDH normally uses NADH to reduce oxaloacetate to malate, which is then exported to the cytosol, rather than to drive mitochondrial respiration.	NAD	169-173	Lactate/malate dehydrogenase family protein	Arabidopsis thaliana	17-27
20798610-4	2010	In response to stress, FoxO1 dissociated from an NAD(+)-dependent histone deacetylase SIRT2 and FoxO1 thus became acetylated and in turn bound to Atg7, an E1-like protein, to influence the autophagic process leading to cell death.	NAD	49-55	autophagy related 7	Homo sapiens	146-150
20531298-6	2010	Recently, it became clear that the energy sensor, AMP-activated kinase (AMPK) translates the effects of energy stress into altered Sirt1 activity by regulating the intracellular level of its co-substrate nicotinamide adenine dinucleotide (NAD)(+).	NAD	239-242	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	50-70
20531298-6	2010	Recently, it became clear that the energy sensor, AMP-activated kinase (AMPK) translates the effects of energy stress into altered Sirt1 activity by regulating the intracellular level of its co-substrate nicotinamide adenine dinucleotide (NAD)(+).	NAD	239-242	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	72-76
19879981-9	2010	Recent studies on the NAD(+) biosynthetic enzymes in the salvage pathway, nicotinamide phosphoribosyltransferase (NAMPT) and nicotinamide mononucleotide adenylyltransferase 1 (NMNAT-1), have revealed important functions for these enzymes in SIRT1-dependent transcription regulation.	NAD	22-28	nicotinamide phosphoribosyltransferase	Homo sapiens	74-112
19879981-9	2010	Recent studies on the NAD(+) biosynthetic enzymes in the salvage pathway, nicotinamide phosphoribosyltransferase (NAMPT) and nicotinamide mononucleotide adenylyltransferase 1 (NMNAT-1), have revealed important functions for these enzymes in SIRT1-dependent transcription regulation.	NAD	22-28	nicotinamide phosphoribosyltransferase	Homo sapiens	114-119
19879981-9	2010	Recent studies on the NAD(+) biosynthetic enzymes in the salvage pathway, nicotinamide phosphoribosyltransferase (NAMPT) and nicotinamide mononucleotide adenylyltransferase 1 (NMNAT-1), have revealed important functions for these enzymes in SIRT1-dependent transcription regulation.	NAD	22-28	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	125-174
19879981-9	2010	Recent studies on the NAD(+) biosynthetic enzymes in the salvage pathway, nicotinamide phosphoribosyltransferase (NAMPT) and nicotinamide mononucleotide adenylyltransferase 1 (NMNAT-1), have revealed important functions for these enzymes in SIRT1-dependent transcription regulation.	NAD	22-28	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	176-183
20608974-8	2010	Finally, we show that PPARgamma ligands increase NAD(+) production in primary human macrophages and that this regulation is dampened in the presence of visfatin small interfering RNA or by the visfatin-specific inhibitor FK866.	NAD	49-55	nicotinamide phosphoribosyltransferase	Homo sapiens	193-201
20608974-9	2010	Taken together, our results suggest that PPARgamma regulates the expression of visfatin in macrophages, leading to increased levels of NAD(+).	NAD	135-141	nicotinamide phosphoribosyltransferase	Homo sapiens	79-87
20647743-1	2010	Nampt/PBEF/visfatin is the rate-limiting enzyme that catalyzes the first step in NAD biosynthesis from nicotinamide and regulates growth, apoptosis and angiogenesis of mammalian cells.	NAD	81-84	nicotinamide phosphoribosyltransferase	Homo sapiens	0-5
20543840-5	2010	In response to stress, FoxO1 was acetylated by dissociation from sirtuin-2 (SIRT2), a NAD(+)-dependent histone deacetylase, and the acetylated FoxO1 bound to Atg7, an E1-like protein, to influence the autophagic process leading to cell death.	NAD	86-92	autophagy related 7	Homo sapiens	158-162
20609415-4	2010	By combining chemical proteomics with biochemical and cellular pharmacology we have determined that CB30865 cytotoxicity is due to subnanomolar inhibition of nicotinamide phosphoribosyltransferase (Nampt), an enzyme present in the NAD biosynthetic pathway.	NAD	231-234	nicotinamide phosphoribosyltransferase	Homo sapiens	158-196
20609415-4	2010	By combining chemical proteomics with biochemical and cellular pharmacology we have determined that CB30865 cytotoxicity is due to subnanomolar inhibition of nicotinamide phosphoribosyltransferase (Nampt), an enzyme present in the NAD biosynthetic pathway.	NAD	231-234	nicotinamide phosphoribosyltransferase	Homo sapiens	198-203
20609415-5	2010	Cancer cells develop dependence on Nampt due to increased energy requirements and the elevated activity of NAD consuming enzymes such as sirtuins and mono and poly(ADP-ribose) polymerases (PARPs).	NAD	107-110	nicotinamide phosphoribosyltransferase	Homo sapiens	35-40
20457531-1	2010	Nicotinamide mononucleotide adenylyltransferase (NMNAT) catalyzes the formation of nicotinamide adenine dinucleotide (NAD).	NAD	118-121	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	0-47
20457531-1	2010	Nicotinamide mononucleotide adenylyltransferase (NMNAT) catalyzes the formation of nicotinamide adenine dinucleotide (NAD).	NAD	118-121	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	49-54
20370672-2	2010	Although first discovery of this molecule as PBEF suggested primarily a cytokine function, its rediscovery as the key enzyme in nicotinamide adenine dinucleotide (NAD) generation has considerably widened its biological perspective.	NAD	128-161	nicotinamide phosphoribosyltransferase	Homo sapiens	45-49
20370672-2	2010	Although first discovery of this molecule as PBEF suggested primarily a cytokine function, its rediscovery as the key enzyme in nicotinamide adenine dinucleotide (NAD) generation has considerably widened its biological perspective.	NAD	163-166	nicotinamide phosphoribosyltransferase	Homo sapiens	45-49
20181750-10	2010	These results indicated that AtNUDX6 is a modulator of NADH rather than ADP-Rib metabolism and that, through induction of TRX-h5 expression, AtNUDX6 significantly impacts the plant immune response as a positive regulator of NPR1-dependent SA signaling pathways.	NAD	55-59	thioredoxin H-type 5	Arabidopsis thaliana	122-128
20068028-7	2010	A peculiar P450, P450nor, receives electrons directly from NADH for the reduction of nitric oxide.	NAD	59-63	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	11-15
19824993-1	2010	BACKGROUND: We previously reported that an NAD-dependent in situ retinoic acid supply system, which comprises some isoforms of alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH) and provides retinoic acid from retinol via a 2-step oxidation process, exists in the rat esophagus.	NAD	43-46	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	159-181
19824993-1	2010	BACKGROUND: We previously reported that an NAD-dependent in situ retinoic acid supply system, which comprises some isoforms of alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH) and provides retinoic acid from retinol via a 2-step oxidation process, exists in the rat esophagus.	NAD	43-46	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	183-187
19485930-2	2010	Visfatin, which plays a role in nicotinamide adenine dinucleotide (NAD) biosynthesis, has been implicated in inflammatory states.	NAD	32-65	nicotinamide phosphoribosyltransferase	Homo sapiens	0-8
19485930-2	2010	Visfatin, which plays a role in nicotinamide adenine dinucleotide (NAD) biosynthesis, has been implicated in inflammatory states.	NAD	67-70	nicotinamide phosphoribosyltransferase	Homo sapiens	0-8
19934346-7	2010	However, expression of either mutant blocked the effects of insulin on glucose-stimulated nicotinamide adenine dinucleotide and nicotinamide adenine dinucleotide phosphate reduction, suggesting defects in posttranslational regulation of GCK.	NAD	90-123	glucokinase	Mus musculus	237-240
21335947-6	2010	The E2-induced Ngb increase requires estrogen receptor (ER) beta, but not ERalpha, as evaluated by the mimetic effect of ERbeta-specific agonist DPN and by the blockage of E2 effect in ERbeta-silenced SK-N-BE cells.	NAD	145-148	estrogen receptor 2	Homo sapiens	121-127
19966463-7	2009	Adh3 might thus play a crucial role in the control of the NADH/NAD(+) balance in mitochondria.	NAD	58-62	alcohol dehydrogenase ADH3	Saccharomyces cerevisiae S288C	0-4
19966463-7	2009	Adh3 might thus play a crucial role in the control of the NADH/NAD(+) balance in mitochondria.	NAD	63-69	alcohol dehydrogenase ADH3	Saccharomyces cerevisiae S288C	0-4
19855088-6	2009	The effect of E2 was mimicked by the ERbeta agonist 2,3-bis(4-hydroxyphenyl)-propionitrile (DPN).	NAD	92-95	estrogen receptor 2 (beta)	Mus musculus	37-43
19855088-7	2009	Activation of ERbeta by DPN enhanced glucose-induced Ca(2+) signals and insulin release.	NAD	24-27	estrogen receptor 2 (beta)	Mus musculus	14-20
19720090-5	2009	NAD(+) levels and SIRT1 activity were also decreased with Tat treatment.	NAD	0-6	tyrosine aminotransferase	Homo sapiens	58-61
19289152-5	2009	In this review, I will follow the process of conceptual development from the heterochromatin island hypothesis to a novel, comprehensive concept of a systemic regulatory network for mammalian aging, named "NAD World," summarizing recent studies on the mammalian NAD-dependent deacetylase Sirt1 and nicotinamide phosphoribosyltransferase (Nampt)-mediated systemic NAD biosynthesis.	NAD	206-209	nicotinamide phosphoribosyltransferase	Homo sapiens	298-336
19596275-3	2009	The present study generated a profile of synaptic proteins altered by administration of estradiol benzoate, the ERalpha selective agonist PPT (1,3,5-tris (4-hydroxyphenyl)-4-propyl-1H-pyrazole) and the ERbeta selective agonist DPN (2,3-bis (4-hydroxyphenyl) propionitrile) alone and in combination in comparison to vehicle in the CA1 region of the dorsal hippocampus.	NAD	227-230	tachykinin, precursor 1	Rattus norvegicus	138-141
19596275-4	2009	In the stratum radiatum, estradiol, DPN, and PPT increased PSD-95 and AMPA-type glutamate receptor subunit GluR1.	NAD	36-39	discs large MAGUK scaffold protein 4	Rattus norvegicus	59-65
19641205-1	2009	The mitochondrial aspartate-glutamate carrier isoform 1 (AGC1), specific to neurons and muscle, supplies aspartate to the cytosol and, as a component of the malate-aspartate shuttle, enables mitochondrial oxidation of cytosolic NADH, thought to be important in providing energy for neurons in the central nervous system.	NAD	228-232	solute carrier family 25 member 12	Homo sapiens	57-61
19581491-4	2009	METHODS AND RESULTS: We treated ovariectomized C57BL/6J mice with the ER-beta selective agonist 2,2-bis(4-hydroxyphenyl)-proprionitrile (DPN), 17beta-estradiol (E2), or vehicle using Alzet minipumps for 2 weeks.	NAD	137-140	estrogen receptor 2 (beta)	Mus musculus	70-77
19581491-7	2009	To test the specificity of DPN, we treated ER-beta-knockout mice with DPN.	NAD	70-73	estrogen receptor 2 (beta)	Mus musculus	43-50
19581491-8	2009	However, no cardioprotective effect of DPN was found in ER-beta-knockout mice, indicating that the DPN-induced cardioprotection occurs through the activation of ER-beta.	NAD	99-102	estrogen receptor 2 (beta)	Mus musculus	161-168
19416720-2	2009	An enzyme activity was observed in nuclear protein fractions that utilized either NADP(+) or NAD(+), but not NADPH and NADH, as pyridine nucleotide cofactor with K(m) values of 12+/-2 and 390+/-2microM, compared to the K(m) for microsomal 11betaHSD1 of 43+/-8 and 264+/-24microM, respectively.	NAD	93-99	RNA, U1 small nuclear 1	Homo sapiens	228-249
19416720-2	2009	An enzyme activity was observed in nuclear protein fractions that utilized either NADP(+) or NAD(+), but not NADPH and NADH, as pyridine nucleotide cofactor with K(m) values of 12+/-2 and 390+/-2microM, compared to the K(m) for microsomal 11betaHSD1 of 43+/-8 and 264+/-24microM, respectively.	NAD	119-123	RNA, U1 small nuclear 1	Homo sapiens	228-249
19461540-1	2009	UNLABELLED: Nampt/pre-B-cell colony-enhancing factor/visfatin (visfatin) release from adipocytes has recently been suggested to be nutrient responsive and linked to systemic nicotinamide adenine dinucleotide biosynthesis and regulation of pancreatic beta-cell function.	NAD	174-207	nicotinamide phosphoribosyltransferase	Homo sapiens	53-61
19461540-1	2009	UNLABELLED: Nampt/pre-B-cell colony-enhancing factor/visfatin (visfatin) release from adipocytes has recently been suggested to be nutrient responsive and linked to systemic nicotinamide adenine dinucleotide biosynthesis and regulation of pancreatic beta-cell function.	NAD	174-207	nicotinamide phosphoribosyltransferase	Homo sapiens	63-71
19426698-2	2009	The first step of the nicotinamide-dependent NAD-rescue pathway is operated by nicotinamide phosphoribosyl transferase (NaPRT) forming nicotinamide mononucleotide (NMN).	NAD	45-48	nicotinamide phosphoribosyltransferase	Homo sapiens	79-118
19426698-2	2009	The first step of the nicotinamide-dependent NAD-rescue pathway is operated by nicotinamide phosphoribosyl transferase (NaPRT) forming nicotinamide mononucleotide (NMN).	NAD	45-48	nicotinamide phosphoribosyltransferase	Homo sapiens	120-125
19426698-8	2009	Evidence that the inhibitor of NAD resynthesis FK866 selectively inhibits NaPRT having no effect on NMNAT activity is also provided.	NAD	31-34	nicotinamide phosphoribosyltransferase	Homo sapiens	74-79
19428988-11	2009	Both PPT, a specific ERalpha agonist, and DPN, a specific ERbeta agonist, inhibited GnRH gene expression in GN11 cells, but only DPN inhibited GnRH gene expression in GT1-7 cells, consistent with their undetectable levels of ERalpha expression.	NAD	42-45	estrogen receptor 2 (beta)	Mus musculus	58-64
19264808-5	2009	ER alpha and ER beta agonists PPT and DPN inhibited and 4-OHT increased miR-21 expression.	NAD	38-41	estrogen receptor 2	Homo sapiens	13-20
19403820-4	2009	The Wld(s) protein consists of the N-terminal portion of the ubiquitination factor Ube4b fused to the nicotinamide adenine dinucleotide (NAD(+)) biosynthetic enzyme nicotinamide mononucleotide adenylyl transferase 1 (Nmnat1).	NAD	102-135	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	165-215
19403820-4	2009	The Wld(s) protein consists of the N-terminal portion of the ubiquitination factor Ube4b fused to the nicotinamide adenine dinucleotide (NAD(+)) biosynthetic enzyme nicotinamide mononucleotide adenylyl transferase 1 (Nmnat1).	NAD	137-144	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	165-215
19196867-1	2009	APO866 inhibits nicotinamide phosphoribosyltransferase (NMPRTase), a key enzyme involved in nicotinamide adenine dinucleotide (NAD) biosynthesis from the natural precursor nicotinamide.	NAD	92-125	nicotinamide phosphoribosyltransferase	Homo sapiens	16-54
19196867-1	2009	APO866 inhibits nicotinamide phosphoribosyltransferase (NMPRTase), a key enzyme involved in nicotinamide adenine dinucleotide (NAD) biosynthesis from the natural precursor nicotinamide.	NAD	92-125	nicotinamide phosphoribosyltransferase	Homo sapiens	56-64
19196867-1	2009	APO866 inhibits nicotinamide phosphoribosyltransferase (NMPRTase), a key enzyme involved in nicotinamide adenine dinucleotide (NAD) biosynthesis from the natural precursor nicotinamide.	NAD	127-130	nicotinamide phosphoribosyltransferase	Homo sapiens	16-54
19196867-1	2009	APO866 inhibits nicotinamide phosphoribosyltransferase (NMPRTase), a key enzyme involved in nicotinamide adenine dinucleotide (NAD) biosynthesis from the natural precursor nicotinamide.	NAD	127-130	nicotinamide phosphoribosyltransferase	Homo sapiens	56-64
19183134-3	2009	Ethanol metabolism also causes an increase in the free reduced nicotinamide adenine dinucleotide (NADH) in cells, which might reasonably be expected to decrease the retinol oxidation rate by product inhibition of ADH isoforms.	NAD	63-96	alcohol dehydrogenase 7 (class IV), mu or sigma polypeptide	Homo sapiens	99-102
19302375-3	2009	Nicotinamide phosphoribosyltransferase (Nampt), also known as PBEF and visfatin, is rate-limiting for NAD+ salvage from nicotinamide and confers resistance to oxidative stress via SIRT1.	NAD	102-106	nicotinamide phosphoribosyltransferase	Homo sapiens	0-38
19302375-3	2009	Nicotinamide phosphoribosyltransferase (Nampt), also known as PBEF and visfatin, is rate-limiting for NAD+ salvage from nicotinamide and confers resistance to oxidative stress via SIRT1.	NAD	102-106	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
19302375-3	2009	Nicotinamide phosphoribosyltransferase (Nampt), also known as PBEF and visfatin, is rate-limiting for NAD+ salvage from nicotinamide and confers resistance to oxidative stress via SIRT1.	NAD	102-106	nicotinamide phosphoribosyltransferase	Homo sapiens	62-66
19302375-3	2009	Nicotinamide phosphoribosyltransferase (Nampt), also known as PBEF and visfatin, is rate-limiting for NAD+ salvage from nicotinamide and confers resistance to oxidative stress via SIRT1.	NAD	102-106	nicotinamide phosphoribosyltransferase	Homo sapiens	71-79
19122206-4	2009	Both of the Fprs have a lower K(m) value for NADPH than for NADH in the diaphorase assays.	NAD	60-64	dihydrolipoamide dehydrogenase	Homo sapiens	72-82
19122206-5	2009	With NADH as electron donor, FprB also has a high specific constant (k(cat)/K(m)) in the diaphorase assay.	NAD	5-9	dihydrolipoamide dehydrogenase	Homo sapiens	89-99
19460292-7	2009	One of the identified proteins is dihydrolipoamide dehydrogenase (DLDH), a component of the alpha-ketoglutarate dehydrogenase (KGDH) complex, which uses NAD(+) as a substrate.	NAD	153-159	dihydrolipoamide dehydrogenase	Homo sapiens	34-64
19460292-7	2009	One of the identified proteins is dihydrolipoamide dehydrogenase (DLDH), a component of the alpha-ketoglutarate dehydrogenase (KGDH) complex, which uses NAD(+) as a substrate.	NAD	153-159	dihydrolipoamide dehydrogenase	Homo sapiens	66-70
19109034-0	2009	Nampt: linking NAD biology, metabolism and cancer.	NAD	15-18	nicotinamide phosphoribosyltransferase	Homo sapiens	0-5
19109034-1	2009	Nicotinamide phosphoribosyltransferase (Nampt) converts nicotinamide to nicotinamide mononucleotide (NMN), a key nicotinamide adenine dinucleotide (NAD) intermediate.	NAD	113-146	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
19351597-0	2009	CtBP1/BARS Gly172--&gt;Glu mutant structure: impairing NAD(H)-binding and dimerization.	NAD	55-61	C-terminal binding protein 1	Homo sapiens	0-5
19351597-0	2009	CtBP1/BARS Gly172--&gt;Glu mutant structure: impairing NAD(H)-binding and dimerization.	NAD	55-61	C-terminal binding protein 1	Homo sapiens	6-10
19276158-6	2009	Because lactate dehydrogenase-A (LDH-A), also a HIF-1alpha target, promotes fermentative glycolysis (conversion of pyruvate to lactate), a step essential for regenerating NAD+, we asked whether FH-deficient cells would be exquisitely sensitive to LDH-A blockade.	NAD	171-175	lactate dehydrogenase A	Mus musculus	8-31
19276158-6	2009	Because lactate dehydrogenase-A (LDH-A), also a HIF-1alpha target, promotes fermentative glycolysis (conversion of pyruvate to lactate), a step essential for regenerating NAD+, we asked whether FH-deficient cells would be exquisitely sensitive to LDH-A blockade.	NAD	171-175	lactate dehydrogenase A	Mus musculus	33-38
19276158-6	2009	Because lactate dehydrogenase-A (LDH-A), also a HIF-1alpha target, promotes fermentative glycolysis (conversion of pyruvate to lactate), a step essential for regenerating NAD+, we asked whether FH-deficient cells would be exquisitely sensitive to LDH-A blockade.	NAD	171-175	lactate dehydrogenase A	Mus musculus	247-252
19237596-2	2009	This unusual chimeric protein fuses a 70-amino acid N-terminal sequence from the Ube4b multiubiquitination factor with the nicotinamide adenine dinucleotide-synthesizing enzyme nicotinamide mononucleotide adenylyl transferase 1.	NAD	123-156	ubiquitination factor E4B	Mus musculus	81-86
19173061-6	2009	In the presence of the auxiliary enzyme DI, the PQI was reduced back to PAP and the resulting oxidized form of DI was finally regenerated in its reduced native state by its natural substrate, NADH.	NAD	192-196	dihydrolipoamide dehydrogenase	Homo sapiens	40-42
19173061-6	2009	In the presence of the auxiliary enzyme DI, the PQI was reduced back to PAP and the resulting oxidized form of DI was finally regenerated in its reduced native state by its natural substrate, NADH.	NAD	192-196	dihydrolipoamide dehydrogenase	Homo sapiens	111-113
19113843-1	2009	The logic network composed of three enzymes (alcohol dehydrogenase, glucose dehydrogenase, and glucose oxidase) operating in concert as four concatenated logic gates (AND/OR), was designed to process four different chemical input signals (NADH, acetaldehyde, glucose, and oxygen).	NAD	239-243	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	68-89
19372760-6	2009	The phenotype is attributed to the overexpression of a chimeric protein Wlds which contains a short fragment of the ubiquitin assembly protein UFD2 and the full-length nicotinamide adenine dinucleotide (NAD) synthetic enzyme Nicotinamide mononucleotide adenylyl-transferase-1 (Nmnat-1).	NAD	203-206	wallerian degeneration	Mus musculus	72-76
19149599-0	2009	Nicotinamide phosphoribosyltransferase (Nampt): a link between NAD biology, metabolism, and diseases.	NAD	63-66	nicotinamide phosphoribosyltransferase	Homo sapiens	0-38
19149599-0	2009	Nicotinamide phosphoribosyltransferase (Nampt): a link between NAD biology, metabolism, and diseases.	NAD	63-66	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
19149599-2	2009	Among them, nicotinamide phosphoribosyltransferase (Nampt) has drawn much attention in several different fields, including NAD biology, metabolism, and immunomodulatory response.	NAD	123-126	nicotinamide phosphoribosyltransferase	Homo sapiens	12-50
19149599-2	2009	Among them, nicotinamide phosphoribosyltransferase (Nampt) has drawn much attention in several different fields, including NAD biology, metabolism, and immunomodulatory response.	NAD	123-126	nicotinamide phosphoribosyltransferase	Homo sapiens	52-57
19149599-5	2009	Intracellular Nampt (iNampt) is an essential enzyme in the NAD biosynthetic pathway starting from nicotinamide.	NAD	59-62	nicotinamide phosphoribosyltransferase	Homo sapiens	14-19
19149599-6	2009	On the other hand, an extracellular form of this protein has been reported to act as a cytokine named PBEF, an insulin-mimetic hormone named visfatin, or an extracellular NAD biosynthetic enzyme named eNampt.	NAD	171-174	nicotinamide phosphoribosyltransferase	Homo sapiens	102-106
19149599-7	2009	This review article summarizes the research history and reported functions of this unique protein and discusses the pathophysiological significance of Nampt as an NAD biosynthetic enzyme vs. a potential inflammatory cytokine in diverse biological contexts.	NAD	163-166	nicotinamide phosphoribosyltransferase	Homo sapiens	151-156
19149606-7	2009	Because SIRT activity depends on cellular NAD+ availability, enzymes involved in NAD+ biosynthesis, including nicotinamide phosphoribosyltransferase (Nampt), may also be valuable pharmaceutical targets for managing CVD.	NAD	81-85	nicotinamide phosphoribosyltransferase	Homo sapiens	110-148
19390637-5	2009	We found that Saccharomyces cerevisiae cells null for all GAPDH paralogues (Tdh1, Tdh2, and Tdh3) survived the counter-selection of a GAPDH-encoding plasmid when the NAD(+) metabolizing deacetylase Sir2 was overexpressed.	NAD	166-172	glyceraldehyde-3-phosphate dehydrogenase (phosphorylating) TDH3	Saccharomyces cerevisiae S288C	92-96
18957417-7	2008	Finally, alterations in the NAD salvage pathway enzyme nicotinamide phosphoribosyltransferase led to changes in NAD levels, SirT activity, and cartilage-specific gene expression in human chondrocytes.	NAD	28-31	nicotinamide phosphoribosyltransferase	Homo sapiens	55-93
18957417-7	2008	Finally, alterations in the NAD salvage pathway enzyme nicotinamide phosphoribosyltransferase led to changes in NAD levels, SirT activity, and cartilage-specific gene expression in human chondrocytes.	NAD	112-115	nicotinamide phosphoribosyltransferase	Homo sapiens	55-93
19020091-2	2008	Cotransforming rho degrees cells with the NADH dehydrogenase of Saccharomyces cerevisiae, Ndi1 and Aox recovered the NADH DH/CoQ reductase and the CoQ oxidase activities.	NAD	42-46	NADH-ubiquinone reductase (H(+)-translocating) NDI1	Saccharomyces cerevisiae S288C	90-94
19020091-4	2008	Coexpression of AOX and NDI1 further improves the recycling of NAD(+).	NAD	63-69	NADH-ubiquinone reductase (H(+)-translocating) NDI1	Saccharomyces cerevisiae S288C	24-28
19011746-5	2008	Recent findings suggest that ADH3-mediated GSNO reduction and subsequent product formation responds to redox states in terms of NADH availability and glutathione levels.	NAD	128-132	alcohol dehydrogenase 5 (class III), chi polypeptide	Homo sapiens	29-33
9050836-0	1997	Unexpected genetic and structural relationships of a long-forgotten flavoenzyme to NAD(P)H:quinone reductase (DT-diaphorase) A mammalian cytosolic FAD-dependent enzyme that catalyzes the reduction of quinones by N-ribosyl- and N-alkyldihydronicotinamides, but not by NADH, NADPH, or NMNH (reduced nicotinamide mononucleotide), was isolated from bovine kidney more than 30 years ago [S. Liao, J. T. Dulaney and H. G. Williams-Ashman (1962) J. Biol.	NAD	267-271	crystallin zeta	Homo sapiens	83-108
9050836-9	1997	Recombinant human QR2: (i) reacts with N-ribosyl- and N-alkyldihydronicotinamides, but not with NADH, NADPH, or NMNH; (ii) is very weakly inhibited by dicumarol or Cibacron blue; (iii) is very potently inhibited by benzo[a]pyrene.	NAD	96-100	N-ribosyldihydronicotinamide:quinone reductase 2	Homo sapiens	18-21
9048877-0	1997	A human cDNA encoding the homologue of NADH: ubiquinone oxidoreductase subunit B13.	NAD	39-43	NADH:ubiquinone oxidoreductase subunit A5	Homo sapiens	79-82
9054620-6	1997	The DNA repair-associated enzyme, poly(ADPribose) polymerase (PARP), was similarly elevated and was associated with significant decreases in the substrate for ADPribose polymer synthesis, nicotinamide adenine dinucleotide (NAD).	NAD	188-221	poly (ADP-ribose) polymerase 1	Rattus norvegicus	34-60
9054620-6	1997	The DNA repair-associated enzyme, poly(ADPribose) polymerase (PARP), was similarly elevated and was associated with significant decreases in the substrate for ADPribose polymer synthesis, nicotinamide adenine dinucleotide (NAD).	NAD	223-226	poly (ADP-ribose) polymerase 1	Rattus norvegicus	34-60
8981046-3	1997	The mitochondrial NADH-dependent dihydrolipoamide dehydrogenase exhibits a marked preference for R(+)-lipoate, whereas NADPH-dependent glutathione reductase shows slightly greater activity toward the S(-)-lipoate stereoisomer.	NAD	18-22	glutathione-disulfide reductase	Rattus norvegicus	135-156
9000459-6	1997	11beta-HSD-2 is a much higher affinity, NAD-dependent, exclusive 11beta-dehydrogenase (glucocorticoid inactivating enzyme), which, when colocalized with otherwise nonselective mineralocorticoid receptors (MR), ensures selective access for aldosterone in vivo.	NAD	40-43	hydroxysteroid 11-beta dehydrogenase 2	Homo sapiens	0-12
9021153-0	1997	Cloning of the human NADH: ubiquinone oxidoreductase subunit B13: localization to chromosome 7q32 and identification of a pseudogene on 11p15.	NAD	21-25	NADH:ubiquinone oxidoreductase subunit A5	Homo sapiens	61-64
8806761-1	1996	Evidence suggests that one or more cysteine residues may be important for the activity of human placental NAD(+)-dependent 15-hydroxyprostaglandin dehydrogenase (15-PGDH).	NAD	106-112	15-hydroxyprostaglandin dehydrogenase	Homo sapiens	162-169
8774727-10	1996	In addition for [G353D]xanthine dehydrogenase, there was an increase in apparent Km values both for NAD+ and NADH.	NAD	100-104	rosy	Drosophila melanogaster	23-45
8774727-10	1996	In addition for [G353D]xanthine dehydrogenase, there was an increase in apparent Km values both for NAD+ and NADH.	NAD	109-113	rosy	Drosophila melanogaster	23-45
8663387-3	1996	beta3 was crystallized as a ternary complex with the coenzyme NAD+ and the competitive inhibitor 4-iodopyrazole.	NAD	62-66	eukaryotic translation elongation factor 1 beta 2 pseudogene 2	Homo sapiens	0-5
8692916-1	1996	The catalytic, or third domain of Pseudomonas exotoxin A (PEIII) catalyzes the transfer of ADP ribose from nicotinamide adenine dinucleotide (NAD) to elongation factor-2 in eukaryotic cells, inhibiting protein synthesis.	NAD	107-140	eukaryotic translation elongation factor 2	Homo sapiens	150-169
8692916-1	1996	The catalytic, or third domain of Pseudomonas exotoxin A (PEIII) catalyzes the transfer of ADP ribose from nicotinamide adenine dinucleotide (NAD) to elongation factor-2 in eukaryotic cells, inhibiting protein synthesis.	NAD	142-145	eukaryotic translation elongation factor 2	Homo sapiens	150-169
18768589-8	2008	Visfatin stimuli also enhanced intracellular NAD levels, and treatment with FK866, which is a specific inhibitor of nicotinamide phosphoribosyltransferase (Nampt), significantly inhibited visfatin-induced NAD synthesis and glucose uptake.	NAD	45-48	nicotinamide phosphoribosyltransferase	Homo sapiens	0-8
18768589-8	2008	Visfatin stimuli also enhanced intracellular NAD levels, and treatment with FK866, which is a specific inhibitor of nicotinamide phosphoribosyltransferase (Nampt), significantly inhibited visfatin-induced NAD synthesis and glucose uptake.	NAD	205-208	nicotinamide phosphoribosyltransferase	Homo sapiens	0-8
18768589-8	2008	Visfatin stimuli also enhanced intracellular NAD levels, and treatment with FK866, which is a specific inhibitor of nicotinamide phosphoribosyltransferase (Nampt), significantly inhibited visfatin-induced NAD synthesis and glucose uptake.	NAD	205-208	nicotinamide phosphoribosyltransferase	Homo sapiens	116-154
18768589-8	2008	Visfatin stimuli also enhanced intracellular NAD levels, and treatment with FK866, which is a specific inhibitor of nicotinamide phosphoribosyltransferase (Nampt), significantly inhibited visfatin-induced NAD synthesis and glucose uptake.	NAD	205-208	nicotinamide phosphoribosyltransferase	Homo sapiens	188-196
18815383-7	2008	AtNUDX19 showed pyrophosphohydrolase activity toward both NADH (335.3+/-5.4 microm) and NADPH (36.9+/-3.5 microm).	NAD	58-62	nudix hydrolase homolog 19	Arabidopsis thaliana	0-8
18678867-3	2008	PNC1 is thought to exert its effect on yeast life span by modulating cellular nicotinamide and NAD levels, resulting in increased activity of Sir2 family class III histone deacetylases.	NAD	95-98	nicotinamidase	Saccharomyces cerevisiae S288C	0-4
18627174-2	2008	The activity of PDHK2 is regulated by a variety of metabolites such as pyruvate, NAD (+), NADH, CoA, and acetyl-CoA.	NAD	81-88	pyruvate dehydrogenase kinase 2	Homo sapiens	16-21
18627174-2	2008	The activity of PDHK2 is regulated by a variety of metabolites such as pyruvate, NAD (+), NADH, CoA, and acetyl-CoA.	NAD	90-94	pyruvate dehydrogenase kinase 2	Homo sapiens	16-21
18412547-7	2008	Hence, considering the high cytosolic NAD(+)/NADH ratio, formaldehyde probably triggers ADH3-mediated GSNO reduction by enzyme-bound cofactor recycling and might result in a decrease in cellular S-NO (S-nitrosothiol) content in vivo.	NAD	38-44	alcohol dehydrogenase 5 (class III), chi polypeptide	Homo sapiens	88-92
18412547-7	2008	Hence, considering the high cytosolic NAD(+)/NADH ratio, formaldehyde probably triggers ADH3-mediated GSNO reduction by enzyme-bound cofactor recycling and might result in a decrease in cellular S-NO (S-nitrosothiol) content in vivo.	NAD	45-49	alcohol dehydrogenase 5 (class III), chi polypeptide	Homo sapiens	88-92
18445470-7	2008	Subsequent action of glucose dehydrogenase (EC 1.1.1.47) and diaphorase (EC 1.6.99.2) in the presence of glucose and 2-(4-iodophenyl)-3-(4-nitrophenyl)-5-(2,4-disulfophenyl)-2H-tetrazolium (WST-1) acts to cycle the formed NAD between its oxidized and reduced forms, resulting in the production of WST-1 formazan, which is monitored at 450 nm.	NAD	222-225	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	21-42
18445470-7	2008	Subsequent action of glucose dehydrogenase (EC 1.1.1.47) and diaphorase (EC 1.6.99.2) in the presence of glucose and 2-(4-iodophenyl)-3-(4-nitrophenyl)-5-(2,4-disulfophenyl)-2H-tetrazolium (WST-1) acts to cycle the formed NAD between its oxidized and reduced forms, resulting in the production of WST-1 formazan, which is monitored at 450 nm.	NAD	222-225	dihydrolipoamide dehydrogenase	Homo sapiens	61-71
18569334-12	2008	The NAD+ dependent retinol oxidation catalyzed by xanthine dehydrogenase is strictly dependent on cellular retinol binding proteins and is inhibited by oxypurinol.	NAD	4-8	xanthine dehydrogenase	Homo sapiens	50-72
18298409-1	2008	Cytosolic NAD-dependent glyceraldehyde 3-P dehydrogenase (GAPDH; GapC; EC 1.2.1.12) catalyzes the oxidation of triose phosphates during glycolysis in all organisms, but additional functions of the protein has been put forward.	NAD	10-13	glyceraldehyde-3-phosphate dehydrogenase C subunit 1	Arabidopsis thaliana	65-69
18412408-1	2008	Binding free energies between coenzyme (FAD and NADH) and the apoenzyme of NADH-cytochrome b5 reductase (b5R) were estimated by applying the continuum Poisson-Boltzmann (PB) model to structures sampled from molecular dynamics simulations in explicit water molecules.	NAD	48-52	cytochrome b5 reductase 3	Homo sapiens	105-108
18332217-3	2008	We identify on protein expression arrays novel cyclin E-Cdk2 substrates, including SIRT2, a member of the Sirtuin family of NAD(+)-dependent deacetylases that targets alpha-tubulin.	NAD	124-130	cyclin dependent kinase 2	Homo sapiens	56-60
17936613-4	2008	The ERalpha agonist, PPT, is shown as estradiol to modulate hippocampal NMDA receptors and AMPA receptors in cortex and striatum of ovariectomized rats whereas the ERbeta agonist DPN is inactive.	NAD	179-182	tachykinin, precursor 1	Rattus norvegicus	21-24
8663150-1	1996	Human CD38 is a 45-kDa transmembrane protein that acts as a bifunctional ectoenzyme, catalyzing the synthesis of cyclic ADP-ribose (cADPR) from NAD+ and the hydrolysis of cADPR to ADP-ribose.	NAD	144-148	CD38 molecule	Homo sapiens	6-10
8694840-5	1996	Chase experiments with high NAD concentration resulted in the formation of poly(ADP-ribosyl)ated p53 protein shifted to 64 kD.	NAD	28-31	transformation related protein 53, pseudogene	Mus musculus	97-100
21619301-5	1996	In the presence of excess nicotinamide adenine dinucleotide (NAD(+)), GDH converts glutamate to alpha-ketoglutarate while simultaneously reducing NAD(+) to NADH.	NAD	26-59	glutamate dehydrogenase 1	Homo sapiens	70-73
21619301-5	1996	In the presence of excess nicotinamide adenine dinucleotide (NAD(+)), GDH converts glutamate to alpha-ketoglutarate while simultaneously reducing NAD(+) to NADH.	NAD	61-67	glutamate dehydrogenase 1	Homo sapiens	70-73
8706705-1	1996	The lymphocyte cell surface antigen, CD38, which has an amino acid sequence similar to Aplysia ADP-ribosyl cyclase, catalyzes not only the hydrolysis of NAD+ and 1-(5-phospho-beta-D-ribosyl) adenosine 5"-phosphate cyclic anhydride (cyclic ADP-ribose) but also the formation of cyclic ADP-ribose from NAD+.	NAD	153-157	CD38 molecule	Homo sapiens	37-41
8706705-1	1996	The lymphocyte cell surface antigen, CD38, which has an amino acid sequence similar to Aplysia ADP-ribosyl cyclase, catalyzes not only the hydrolysis of NAD+ and 1-(5-phospho-beta-D-ribosyl) adenosine 5"-phosphate cyclic anhydride (cyclic ADP-ribose) but also the formation of cyclic ADP-ribose from NAD+.	NAD	300-304	CD38 molecule	Homo sapiens	37-41
8706705-5	1996	Zinc ions inhibited the NAD+ glycohydrolase reaction catalyzed by MBP-CD38 in an uncompetitive manner, whereas they enhanced the ADP-ribosyl cyclase reaction without affecting the Km value for NAD+.	NAD	24-28	CD38 molecule	Homo sapiens	70-74
8656275-0	1996	[3H]dihydrorotenone binding to NADH: ubiquinone reductase (complex I) of the electron transport chain: an autoradiographic study.	NAD	31-35	NADH:ubiquinone oxidoreductase subunit A5	Homo sapiens	37-57
8652544-6	1996	The abortive complexes are transformed into active E.NAD+ by denaturation of the purified enzyme at 4 degrees C in 6 M guanidine hydrochloride buffered at pH 7.0 in the presence of 0.126 mM NAD+ for 3 h, followed by dilution of guanidine hydrochloride to 0.18 M and of NAD+ to 0.076 mM for 2 h. The renatured enzyme is fully active and contains negligible amounts of NADH and uridine nucleotides.	NAD	367-371	Aldehyde dehydrogenase	Escherichia coli	53-56
8652544-6	1996	The abortive complexes are transformed into active E.NAD+ by denaturation of the purified enzyme at 4 degrees C in 6 M guanidine hydrochloride buffered at pH 7.0 in the presence of 0.126 mM NAD+ for 3 h, followed by dilution of guanidine hydrochloride to 0.18 M and of NAD+ to 0.076 mM for 2 h. The renatured enzyme is fully active and contains negligible amounts of NADH and uridine nucleotides.	NAD	367-371	Aldehyde dehydrogenase	Escherichia coli	190-193
8652544-6	1996	The abortive complexes are transformed into active E.NAD+ by denaturation of the purified enzyme at 4 degrees C in 6 M guanidine hydrochloride buffered at pH 7.0 in the presence of 0.126 mM NAD+ for 3 h, followed by dilution of guanidine hydrochloride to 0.18 M and of NAD+ to 0.076 mM for 2 h. The renatured enzyme is fully active and contains negligible amounts of NADH and uridine nucleotides.	NAD	367-371	Aldehyde dehydrogenase	Escherichia coli	190-193
8652544-10	1996	The ultraviolet/visible absorption spectrum of E.NAD+ from denaturation-renaturation experiments reveals the presence of a broad absorption band extending from 300 nm to beyond 360 nm that cannot be attributed to NADH and appears to be a charge-transfer band.	NAD	213-217	Aldehyde dehydrogenase	Escherichia coli	49-52
17967884-10	2008	Although monomeric CtBP1 is proficient in the recruiting of both core and auxiliary components, NAD(H)-dependent dimerization is required for transcriptional repression.	NAD	96-102	C-terminal binding protein 1	Homo sapiens	19-24
17936786-5	2007	The stable short hairpin (sh)RNA-mediated knockdown of Oxa1l in HEK293 cells resulted in markedly decreased steady-state levels and ATP hydrolytic activity of the F(1)F(o)-ATP synthase and moderately reduced levels and activity of NADH:ubiquinone oxidoreductase (complex I).	NAD	231-235	OXA1L mitochondrial inner membrane protein	Homo sapiens	55-60
17886038-5	2007	They inhibited NADH production by acting specifically on aconitase for O(2)*(-) and alpha-ketoglutarate dehydrogenase for H(2)O(2) and HO*.	NAD	15-19	oxoglutarate dehydrogenase	Rattus norvegicus	84-117
17889652-3	2007	Rodents fasted for 48 hr show increased levels of the NAD(+) biosynthetic enzyme Nampt and a concomitant increase in mitochondrial NAD(+).	NAD	54-60	nicotinamide phosphoribosyltransferase	Homo sapiens	81-86
17889652-4	2007	Increased Nampt provides protection against cell death and requires an intact mitochondrial NAD(+) salvage pathway as well as the mitochondrial NAD(+)-dependent deacetylases SIRT3 and SIRT4.	NAD	92-98	nicotinamide phosphoribosyltransferase	Homo sapiens	10-15
17640960-6	2007	However, the activation of estrogen receptor (ER)-beta with a specific agonist, DPN [2,3-bis(4-hydroxyphenol)-propionitrile], prevented the development of prostatic hyperplasia and inflammation in testosterone-treated LuRKO mice.	NAD	80-83	estrogen receptor 2 (beta)	Mus musculus	27-54
8622631-9	1996	Anti-cytochrome b5 IgG decreased NADPH- and NADH-dependent HER formation, and this was associated with inhibition of superoxide formation with both reductants.	NAD	44-48	cytochrome b5 type A	Homo sapiens	5-18
17706937-0	2007	Expression of Ndi1p, an alternative NADH:ubiquinone oxidoreductase, increases mitochondrial membrane potential in a C. elegans model of mitochondrial disease.	NAD	36-40	NADH-ubiquinone reductase (H(+)-translocating) NDI1	Saccharomyces cerevisiae S288C	14-19
17634376-7	2007	Both were prevented, however, by forced expression of the NDI1 nicotinamide adenine dinucleotide (NADH)-quinone-oxidoreductase of Saccharomyces cerevisiae, which can restore NADH oxidation in complex I-deficient mammalian cells and stimulation of energy production via anaerobic glycolysis.	NAD	63-96	NADH-ubiquinone reductase (H(+)-translocating) NDI1	Saccharomyces cerevisiae S288C	58-62
8609401-0	1996	Regulation of CTL by ecto-nictinamide adenine dinucleotide (NAD) involves ADP-ribosylation of a p56lck-associated protein.	NAD	60-63	LCK proto-oncogene, Src family tyrosine kinase	Homo sapiens	96-102
8609401-5	1996	This enzyme is a glycosyl-phosphatidylinositol-anchored protein releasable from the surface of cytotoxic T cells by glycosyl-phosphatidylinositol-specific phospholipase C. Release of arginine-specific mono-ADP-ribosyltransferase results in failure of extracellular NAD to downmodulate p56lck kinase activity.	NAD	265-268	LCK proto-oncogene, Src family tyrosine kinase	Homo sapiens	285-291
8609401-6	1996	Concomitant to suppression of the kinase by NAD, CD8 mediated transmembrane signaling and p56lck kinase activation are inhibited.	NAD	44-47	LCK proto-oncogene, Src family tyrosine kinase	Homo sapiens	90-96
17634376-7	2007	Both were prevented, however, by forced expression of the NDI1 nicotinamide adenine dinucleotide (NADH)-quinone-oxidoreductase of Saccharomyces cerevisiae, which can restore NADH oxidation in complex I-deficient mammalian cells and stimulation of energy production via anaerobic glycolysis.	NAD	98-102	NADH-ubiquinone reductase (H(+)-translocating) NDI1	Saccharomyces cerevisiae S288C	58-62
17634376-7	2007	Both were prevented, however, by forced expression of the NDI1 nicotinamide adenine dinucleotide (NADH)-quinone-oxidoreductase of Saccharomyces cerevisiae, which can restore NADH oxidation in complex I-deficient mammalian cells and stimulation of energy production via anaerobic glycolysis.	NAD	174-178	NADH-ubiquinone reductase (H(+)-translocating) NDI1	Saccharomyces cerevisiae S288C	58-62
8608153-7	1996	Disruption of the MTD1 gene in this strain resulted in undetectable CHO-THF, indicating that the NAD-dependent CH2-THF dehydrogenase was responsible for CHO-THF production in the ade3 deletion strain.	NAD	97-100	methylenetetrahydrofolate dehydrogenase (NAD(+))	Saccharomyces cerevisiae S288C	18-22
17442666-5	2007	The K(m) values of PA2022 and PA3559 for UDP-glucose are approximately 0.1 and 0.4 mM, whereas the K(m) values for NAD(+) are 0.5 and 2.0 mM, respectively.	NAD	115-121	UDP-glucose 6-dehydrogenase	Pseudomonas aeruginosa PAO1	19-25
8608153-7	1996	Disruption of the MTD1 gene in this strain resulted in undetectable CHO-THF, indicating that the NAD-dependent CH2-THF dehydrogenase was responsible for CHO-THF production in the ade3 deletion strain.	NAD	97-100	trifunctional formate-tetrahydrofolate ligase/methenyltetrahydrofolate cyclohydrolase/methylenetetrahydrofolate dehydrogenase ADE3	Saccharomyces cerevisiae S288C	179-183
17307730-2	2007	We identified a relationship between aging of human vascular smooth muscle cells (SMCs) and nicotinamide phosphoribosyltransferase (Nampt/PBEF/Visfatin), the rate-limiting enzyme for NAD+ salvage from nicotinamide.	NAD	183-187	nicotinamide phosphoribosyltransferase	Homo sapiens	92-130
8852827-4	1996	11 beta-HSD-2 is NAD(+)-dependent, has a Km in the nanomolar range, exhibits only oxidase activity, and colocalizes with the MR in the kidney, so is likely to serve as the gatekeeper for the MR. We have further characterized 11 beta-HSD activity in JEG-3 cells, a cell line derived from a human choriocarcinoma which was reported to have only the high affinity, NAD(+)-dependent 11 beta-HSD-2.	NAD	17-23	hydroxysteroid 11-beta dehydrogenase 2	Homo sapiens	0-13
8852827-4	1996	11 beta-HSD-2 is NAD(+)-dependent, has a Km in the nanomolar range, exhibits only oxidase activity, and colocalizes with the MR in the kidney, so is likely to serve as the gatekeeper for the MR. We have further characterized 11 beta-HSD activity in JEG-3 cells, a cell line derived from a human choriocarcinoma which was reported to have only the high affinity, NAD(+)-dependent 11 beta-HSD-2.	NAD	362-368	hydroxysteroid 11-beta dehydrogenase 2	Homo sapiens	0-13
17307730-2	2007	We identified a relationship between aging of human vascular smooth muscle cells (SMCs) and nicotinamide phosphoribosyltransferase (Nampt/PBEF/Visfatin), the rate-limiting enzyme for NAD+ salvage from nicotinamide.	NAD	183-187	nicotinamide phosphoribosyltransferase	Homo sapiens	132-137
8963661-0	1996	NADH in the pyramidal cell layer of hippocampal regions CA1 and CA3 upon selective inhibition and uncoupling of oxidative phosphorylation.	NAD	0-4	carbonic anhydrase 1	Rattus norvegicus	56-59
8963661-6	1996	The CA1/CA3 ratio of NADH fluorescence mildly decreased to 0.92 +/- 0.04 (mean +/- S.D.)	NAD	21-25	carbonic anhydrase 1	Rattus norvegicus	4-7
17307730-2	2007	We identified a relationship between aging of human vascular smooth muscle cells (SMCs) and nicotinamide phosphoribosyltransferase (Nampt/PBEF/Visfatin), the rate-limiting enzyme for NAD+ salvage from nicotinamide.	NAD	183-187	nicotinamide phosphoribosyltransferase	Homo sapiens	138-142
17307730-2	2007	We identified a relationship between aging of human vascular smooth muscle cells (SMCs) and nicotinamide phosphoribosyltransferase (Nampt/PBEF/Visfatin), the rate-limiting enzyme for NAD+ salvage from nicotinamide.	NAD	183-187	nicotinamide phosphoribosyltransferase	Homo sapiens	143-151
12893455-5	1996	AcH metabolism by liver mitochondrial aldehyde dehydrogenase (ALDH) was studied by following AcH disappearance rate and the formation of NADH at 340 nm in the incubation medium.	NAD	137-141	aldehyde dehydrogenase 2 family member	Rattus norvegicus	24-60
17307730-6	2007	Nampt-mediated SMC lifespan extension was associated with increased activity of the NAD+-dependent longevity enzyme SIRT1 and was abrogated in Nampt-overexpressing cells transduced with a dominant-negative form of SIRT1 (H363Y).	NAD	84-88	nicotinamide phosphoribosyltransferase	Homo sapiens	0-5
17315258-1	2007	Mammalian mitochondrial dihydrolipoamide dehydrogenase (DLDH, EC 1.8.1.4) catalyzes NAD(+)-dependent oxidation of dihydrolipoamide in vivo and can also act as a diaphorase catalyzing in vitro nicotinamide adenine dinucleotide (reduced form) (NADH)-dependent reduction of electron-accepting molecules such as ubiquinone and nitroblue tetrazolium (NBT).	NAD	84-90	dihydrolipoamide dehydrogenase	Homo sapiens	56-60
17315258-1	2007	Mammalian mitochondrial dihydrolipoamide dehydrogenase (DLDH, EC 1.8.1.4) catalyzes NAD(+)-dependent oxidation of dihydrolipoamide in vivo and can also act as a diaphorase catalyzing in vitro nicotinamide adenine dinucleotide (reduced form) (NADH)-dependent reduction of electron-accepting molecules such as ubiquinone and nitroblue tetrazolium (NBT).	NAD	192-225	dihydrolipoamide dehydrogenase	Homo sapiens	56-60
17315258-1	2007	Mammalian mitochondrial dihydrolipoamide dehydrogenase (DLDH, EC 1.8.1.4) catalyzes NAD(+)-dependent oxidation of dihydrolipoamide in vivo and can also act as a diaphorase catalyzing in vitro nicotinamide adenine dinucleotide (reduced form) (NADH)-dependent reduction of electron-accepting molecules such as ubiquinone and nitroblue tetrazolium (NBT).	NAD	242-246	dihydrolipoamide dehydrogenase	Homo sapiens	56-60
17268245-0	2007	The regulation of nicotinamide adenine dinucleotide biosynthesis by Nampt/PBEF/visfatin in mammals.	NAD	18-51	nicotinamide phosphoribosyltransferase	Homo sapiens	68-73
17268245-0	2007	The regulation of nicotinamide adenine dinucleotide biosynthesis by Nampt/PBEF/visfatin in mammals.	NAD	18-51	nicotinamide phosphoribosyltransferase	Homo sapiens	74-78
17268245-0	2007	The regulation of nicotinamide adenine dinucleotide biosynthesis by Nampt/PBEF/visfatin in mammals.	NAD	18-51	nicotinamide phosphoribosyltransferase	Homo sapiens	79-87
17268245-4	2007	This review summarizes the latest knowledge on the NAD biosynthetic pathways and focuses on one of the key NAD biosynthetic enzymes, namely, nicotinamide phosphoribosyltransferase.	NAD	51-54	nicotinamide phosphoribosyltransferase	Homo sapiens	141-179
17268245-4	2007	This review summarizes the latest knowledge on the NAD biosynthetic pathways and focuses on one of the key NAD biosynthetic enzymes, namely, nicotinamide phosphoribosyltransferase.	NAD	107-110	nicotinamide phosphoribosyltransferase	Homo sapiens	141-179
17268245-6	2007	Nicotinamide phosphoribosyltransferase (Nampt) is the rate-limiting enzyme that converts nicotinamide to nicotinamide mononucleotide in the NAD biosynthetic pathway from nicotinamide in mammals.	NAD	140-143	nicotinamide phosphoribosyltransferase	Homo sapiens	0-38
17268245-6	2007	Nicotinamide phosphoribosyltransferase (Nampt) is the rate-limiting enzyme that converts nicotinamide to nicotinamide mononucleotide in the NAD biosynthetic pathway from nicotinamide in mammals.	NAD	140-143	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
17268245-8	2007	SUMMARY: We propose that the presumed multiple effects of Nampt/PBEF/visfatin may be entirely explained by its role as an intra and extracellular NAD biosynthetic enzyme.	NAD	146-149	nicotinamide phosphoribosyltransferase	Homo sapiens	58-63
17268245-8	2007	SUMMARY: We propose that the presumed multiple effects of Nampt/PBEF/visfatin may be entirely explained by its role as an intra and extracellular NAD biosynthetic enzyme.	NAD	146-149	nicotinamide phosphoribosyltransferase	Homo sapiens	64-68
17268245-8	2007	SUMMARY: We propose that the presumed multiple effects of Nampt/PBEF/visfatin may be entirely explained by its role as an intra and extracellular NAD biosynthetic enzyme.	NAD	146-149	nicotinamide phosphoribosyltransferase	Homo sapiens	69-77
17268245-9	2007	We also propose a new model of Namp/PBEF/visfatin-mediated systemic NAD biosynthesis and its possible physiological significance.	NAD	68-71	nicotinamide phosphoribosyltransferase	Homo sapiens	36-40
17268245-9	2007	We also propose a new model of Namp/PBEF/visfatin-mediated systemic NAD biosynthesis and its possible physiological significance.	NAD	68-71	nicotinamide phosphoribosyltransferase	Homo sapiens	41-49
17335512-0	2007	Nicotinamidase participates in the salvage pathway of NAD biosynthesis in Arabidopsis.	NAD	54-57	nicotinamidase	Saccharomyces cerevisiae S288C	0-14
17335512-7	2007	Plants homozygous for a null AtNIC1 allele, nic1-1, have lower levels of NAD and NADP under normal growth conditions, indicating that AtNIC1 participates in a yeast-type NAD salvage pathway.	NAD	73-76	nicotinamidase 1	Arabidopsis thaliana	29-35
17335512-7	2007	Plants homozygous for a null AtNIC1 allele, nic1-1, have lower levels of NAD and NADP under normal growth conditions, indicating that AtNIC1 participates in a yeast-type NAD salvage pathway.	NAD	73-76	nicotinamidase 1	Arabidopsis thaliana	44-48
17335512-7	2007	Plants homozygous for a null AtNIC1 allele, nic1-1, have lower levels of NAD and NADP under normal growth conditions, indicating that AtNIC1 participates in a yeast-type NAD salvage pathway.	NAD	73-76	nicotinamidase 1	Arabidopsis thaliana	134-140
17335512-7	2007	Plants homozygous for a null AtNIC1 allele, nic1-1, have lower levels of NAD and NADP under normal growth conditions, indicating that AtNIC1 participates in a yeast-type NAD salvage pathway.	NAD	81-84	nicotinamidase 1	Arabidopsis thaliana	29-35
17335512-7	2007	Plants homozygous for a null AtNIC1 allele, nic1-1, have lower levels of NAD and NADP under normal growth conditions, indicating that AtNIC1 participates in a yeast-type NAD salvage pathway.	NAD	81-84	nicotinamidase 1	Arabidopsis thaliana	44-48
17335512-7	2007	Plants homozygous for a null AtNIC1 allele, nic1-1, have lower levels of NAD and NADP under normal growth conditions, indicating that AtNIC1 participates in a yeast-type NAD salvage pathway.	NAD	81-84	nicotinamidase 1	Arabidopsis thaliana	134-140
17355872-0	2007	Structural basis of inhibition of the human NAD+-dependent deacetylase SIRT5 by suramin.	NAD	44-47	sirtuin 5	Homo sapiens	71-76
17270012-3	2007	AtNMNAT catalyzed the synthesis of nicotinate adenine dinucleotide (NaAD) from nicotinate mononucleotide (NaMN) in the Preiss-Handler-dependent pathway, and of nicotinamide adenine dinucleotide (NAD) from nicotiamide mononucleotide (NMN) in the Preiss-Handler-independent pathway.	NAD	160-193	nicotinate/nicotinamide mononucleotide adenyltransferase	Arabidopsis thaliana	0-7
8787900-7	1996	The gene encodes a 36.7-kDa protein with homology to a family of bacterial NAD+-dependent, D-specific 2-hydroxyacid dehydrogenases which includes both D-lactate dehydrogenase and the enterococcal vancomycin resistance protein VanH and is therefore designated ddh.	NAD	75-79	vancomycin resistance protein VanH	Staphylococcus aureus	226-230
8613810-3	1996	Two isoforms exist: 11 beta-HSD1, a bidirectional NADPH-dependent enzyme, and 11 beta-HSD2, an NAD(+)-dependent exclusive 11 beta-dehydrogenase (corticosterone-inactivating enzyme).	NAD	95-101	hydroxysteroid 11-beta dehydrogenase 2	Homo sapiens	50-90
8770980-2	1996	Both NADP, and NAD-dependent isoforms of 11 beta-HSD have been described.	NAD	5-8	hydroxysteroid 11-beta dehydrogenase 2	Homo sapiens	41-48
8770980-3	1996	An NAD-dependent isoform of 11 beta-HSD (11 beta-HSD2) was recently cloned from human kidney.	NAD	3-6	hydroxysteroid 11-beta dehydrogenase 2	Homo sapiens	28-35
8770980-3	1996	An NAD-dependent isoform of 11 beta-HSD (11 beta-HSD2) was recently cloned from human kidney.	NAD	3-6	hydroxysteroid 11-beta dehydrogenase 2	Homo sapiens	41-53
8770980-11	1996	These results support the view that the NAD-dependent isoform of 11 beta-HSD (11 beta-HSD2) provides mineralocorticoid specificity by inactivating glucocorticoids in an autocrine fashion.	NAD	40-43	hydroxysteroid 11-beta dehydrogenase 2	Homo sapiens	65-72
8770980-11	1996	These results support the view that the NAD-dependent isoform of 11 beta-HSD (11 beta-HSD2) provides mineralocorticoid specificity by inactivating glucocorticoids in an autocrine fashion.	NAD	40-43	hydroxysteroid 11-beta dehydrogenase 2	Homo sapiens	78-90
12226176-5	1996	Surprisingly, the regenerative potentiality in dividing protoplasts was specifically correlated with a higher NADH-peroxidase activity, which resulted in a net H2O2 accumulation in the cells.	NAD	110-114	peroxidase N1	Nicotiana tabacum	115-125
8898563-13	1996	Several bacterial toxin and eukaryotic mono-ADP-ribosyltransferases, and perhaps other NAD-utilizing enzymes such as the RT6 alloantigens share regions of amino acid sequence similarity, which form, in part, the catalytic site.	NAD	87-90	ADP-ribosyltransferase 2, pseudogene	Homo sapiens	121-124
8554320-0	1995	Role of cytochrome b5 in NADH-dependent microsomal reduction of ferric complexes, lipid peroxidation, and hydrogen peroxide generation.	NAD	25-29	cytochrome b5 type A	Homo sapiens	8-21
8554320-1	1995	The NADH-dependent microsomal electron transfer system consists of NADH-cytochrome b5 reductase and cytochrome b5, which donates reducing equivalents to fatty acyl desaturase, cytochrome P450, and other reactions.	NAD	4-8	cytochrome b5 type A	Homo sapiens	72-85
8554320-1	1995	The NADH-dependent microsomal electron transfer system consists of NADH-cytochrome b5 reductase and cytochrome b5, which donates reducing equivalents to fatty acyl desaturase, cytochrome P450, and other reactions.	NAD	4-8	cytochrome b5 type A	Homo sapiens	100-113
17270012-3	2007	AtNMNAT catalyzed the synthesis of nicotinate adenine dinucleotide (NaAD) from nicotinate mononucleotide (NaMN) in the Preiss-Handler-dependent pathway, and of nicotinamide adenine dinucleotide (NAD) from nicotiamide mononucleotide (NMN) in the Preiss-Handler-independent pathway.	NAD	195-198	nicotinate/nicotinamide mononucleotide adenyltransferase	Arabidopsis thaliana	0-7
17270012-6	2007	Disruption of the AtNMNAT gene (atnmnat mutant) was characterized by a decrease in NAD content in pollen.	NAD	83-86	nicotinate/nicotinamide mononucleotide adenyltransferase	Arabidopsis thaliana	18-25
17270012-6	2007	Disruption of the AtNMNAT gene (atnmnat mutant) was characterized by a decrease in NAD content in pollen.	NAD	83-86	nicotinate/nicotinamide mononucleotide adenyltransferase	Arabidopsis thaliana	32-39
17194138-2	2007	The approach was illustrated in the case of the bioelectrocatalytic oxidation of NADH by a diaphorase oxidoreductase in the presence of a ferrocene mediator.	NAD	81-85	dihydrolipoamide dehydrogenase	Homo sapiens	91-101
17937376-3	2007	The affinity complexes of glucose dehydrogenase (GDH) with the NADP(+) cofactor or alcohol dehydrogenase (AlcDH) with the NAD(+) cofactor were crosslinked with glutaric dialdehyde and the biomolecule-functionalized SWCNT materials were deposited on glassy carbon electrodes.	NAD	122-128	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	26-47
17937376-3	2007	The affinity complexes of glucose dehydrogenase (GDH) with the NADP(+) cofactor or alcohol dehydrogenase (AlcDH) with the NAD(+) cofactor were crosslinked with glutaric dialdehyde and the biomolecule-functionalized SWCNT materials were deposited on glassy carbon electrodes.	NAD	122-128	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	49-52
17126728-9	2006	At a high salt concentration, the nicotinamide adenine dinucleotide reduced (NADH)-GDH activity was stimulated concomitantly with the increasing NH(4)(+) contents and proteolysis activity in the leaves and roots.	NAD	34-67	glutamate dehydrogenase	Solanum lycopersicum	83-86
16817779-5	2006	Kinetic analysis revealed that inhibition of DT and ETA by HNP1 was competitive with respect to eEF2 and uncompetitive against NAD+ substrates.	NAD	127-131	endothelin receptor type A	Homo sapiens	52-55
16760478-3	2006	We constructed a diploid strain heterozygous for disruption of POS5, encoding mitochondrial NADH kinase, UTR1, cytosolic NAD kinase, and YEF1, a UTR1-homologous gene we characterized as encoding a low specific activity cytosolic NAD kinase.	NAD	92-95	NADH kinase	Saccharomyces cerevisiae S288C	63-67
16760478-8	2006	Purified Yef1 has similar nucleoside triphosphate specificity but substantially lower specific activity and less discrimination in favor of NAD versus NADH phosphorylation than Utr1.	NAD	140-143	NADH/NAD(+) kinase	Saccharomyces cerevisiae S288C	9-13
16760478-8	2006	Purified Yef1 has similar nucleoside triphosphate specificity but substantially lower specific activity and less discrimination in favor of NAD versus NADH phosphorylation than Utr1.	NAD	151-155	NADH/NAD(+) kinase	Saccharomyces cerevisiae S288C	9-13
16762039-6	2006	Here, we show that HIC1 interacts with both CtBP1 and CtBP2 and that this interaction is stimulated by agents increasing NADH levels.	NAD	121-125	C-terminal binding protein 1	Homo sapiens	44-49
16783373-0	2006	Structure of Nampt/PBEF/visfatin, a mammalian NAD+ biosynthetic enzyme.	NAD	46-50	nicotinamide phosphoribosyltransferase	Homo sapiens	13-18
16783373-0	2006	Structure of Nampt/PBEF/visfatin, a mammalian NAD+ biosynthetic enzyme.	NAD	46-50	nicotinamide phosphoribosyltransferase	Homo sapiens	19-23
16783373-0	2006	Structure of Nampt/PBEF/visfatin, a mammalian NAD+ biosynthetic enzyme.	NAD	46-50	nicotinamide phosphoribosyltransferase	Homo sapiens	24-32
8543910-6	1995	The unidirectional 11 beta-HSD2 dehydrogenase activity was identified by its distinct cofactor preference (NAD), and by its unique ability to metabolize dexamethasone (Dex).	NAD	107-110	11-beta-hydroxysteroid dehydrogenase type 2	Ovis aries	19-31
16652391-6	2006	Strains overexpressing ADH6 had increased HMF conversion activity in cell-free crude extracts with both NADPH and NADH as co-factors.	NAD	114-118	NADP-dependent alcohol dehydrogenase	Saccharomyces cerevisiae S288C	23-27
8553368-2	1995	We report here on the ability of ATA to inhibit the activity of several NAD(H)/NADP(H)-requiring enzymes (purified or cellular homogenates), including lactic dehydrogenase, alcohol dehydrogenase, cytochrome c reductase, ethoxycoumarin o-dealkylase, isocitric dehydrogenase, glutathione reductase and glucose-6-phosphate dehydrogenase.	NAD	72-78	glutathione-disulfide reductase	Rattus norvegicus	274-295
16955758-3	2006	The method was based upon measurement of NADH generated from NAD+ during oxidation of bile acid by immobilized 3alpha-HSD with a color reagent consisting of nitrobluetetrazolium (NBT) chloride salt and immobilized diaphorase in 0.065 M sodium phosphate buffer (pH 7.0).	NAD	41-45	aldo-keto reductase family 1 member C3	Homo sapiens	111-121
7573423-9	1995	In contrast, the primary regulatory factors causing greater PDHa during recovery were lower ATP/ADP and NADH/NAD and increased concentrations of pyruvate and H+.	NAD	104-108	pyruvate dehydrogenase E1 subunit alpha 1	Homo sapiens	60-64
16955758-3	2006	The method was based upon measurement of NADH generated from NAD+ during oxidation of bile acid by immobilized 3alpha-HSD with a color reagent consisting of nitrobluetetrazolium (NBT) chloride salt and immobilized diaphorase in 0.065 M sodium phosphate buffer (pH 7.0).	NAD	41-45	dihydrolipoamide dehydrogenase	Homo sapiens	214-224
7573423-9	1995	In contrast, the primary regulatory factors causing greater PDHa during recovery were lower ATP/ADP and NADH/NAD and increased concentrations of pyruvate and H+.	NAD	104-107	pyruvate dehydrogenase E1 subunit alpha 1	Homo sapiens	60-64
16955758-3	2006	The method was based upon measurement of NADH generated from NAD+ during oxidation of bile acid by immobilized 3alpha-HSD with a color reagent consisting of nitrobluetetrazolium (NBT) chloride salt and immobilized diaphorase in 0.065 M sodium phosphate buffer (pH 7.0).	NAD	61-65	aldo-keto reductase family 1 member C3	Homo sapiens	111-121
7616297-2	1995	Poly(ADP-ribose) is synthesized from NAD+ by a nuclear enzyme, poly(ADP-ribose)polymerase, which is activated by DNA strand breaks.	NAD	37-41	poly (ADP-ribose) polymerase 1	Rattus norvegicus	63-89
16435395-8	2006	The selective 5-HT1A antagonist WAY-100635 (3 mg/kg) prevented the increased NADH fluorescence after 8-OH-DPAT, but had no own effect.	NAD	77-81	5-hydroxytryptamine receptor 1A	Rattus norvegicus	14-20
7476212-0	1995	Cloning and characterization of GPD2, a second gene encoding sn-glycerol 3-phosphate dehydrogenase (NAD+) in Saccharomyces cerevisiae, and its comparison with GPD1.	NAD	100-104	glycerol-3-phosphate dehydrogenase (NAD(+)) GPD2	Saccharomyces cerevisiae S288C	32-36
16371511-2	2006	The C-terminal region, derived from NAD(+) synthesizing enzyme Nmnat1, is reported to confer neuroprotection in vitro.	NAD	36-42	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	63-69
7766625-5	1995	A pKa of 9.6 was found for the binary complex of Cd2(111mCd)Cd2LADH with NAD+.	NAD	73-77	CD2 molecule	Equus caballus	49-52
7766625-7	1995	No pH dependency was detected for the binary complex of Cd2(111mCd)Cd2LADH with NADH within the pH range measured (pH 8.3-11.5).	NAD	80-84	CD2 molecule	Equus caballus	56-59
7721841-5	1995	The additional site(s) of modification, utilized at higher NAD concentrations, were located in the 63-kDa N-terminal segment of integrin alpha 7.	NAD	59-62	integrin alpha 7	Mus musculus	128-144
7721706-10	1995	Adjacent to cooA are two genes, nadB and nadC, with predicted products similar to proteins in other bacteria that catalyze reactions in the de novo synthesis of NAD.	NAD	161-164	CS1 fimbrial subunit A precursor	Escherichia coli	12-16
7836368-6	1995	Overexpression of p32 in Cos cells produced a membrane-bound stereospecific 11-cis retinol dehydrogenase, active in the presence of NAD+ as cofactor but not in the presence of NADP.	NAD	132-136	retinol dehydrogenase 5	Bos taurus	18-21
8527489-1	1995	Cyclic ADP-ribose is generated from NAD+ in glucose-stimulated beta-cells by CD38.	NAD	36-40	CD38 molecule	Homo sapiens	77-81
7926004-4	1994	Such changes could reflect a substantial loss in the energy conserving function of NADH:ubiquinone reductase and thus explain the pathological effect of the ND4/11,778 mutation.	NAD	83-87	mitochondrially encoded NADH dehydrogenase 4	Homo sapiens	157-160
8051714-1	1994	It has been proposed that the activation of poly(ADP-ribose) polymerase (Papirmeister et al., 1985), which results from the presence of strand breaks in bis-(beta-chloroethyl)sulfide (BCES) damaged DNA, causes depletion in the level of nicotinamide adenine dinucleotide (NAD) leading to cell death.	NAD	236-269	poly (ADP-ribose) polymerase 1	Rattus norvegicus	44-71
8051714-1	1994	It has been proposed that the activation of poly(ADP-ribose) polymerase (Papirmeister et al., 1985), which results from the presence of strand breaks in bis-(beta-chloroethyl)sulfide (BCES) damaged DNA, causes depletion in the level of nicotinamide adenine dinucleotide (NAD) leading to cell death.	NAD	271-274	poly (ADP-ribose) polymerase 1	Rattus norvegicus	44-71
8347142-8	1993	This drop was prevented by co-incubation with 3AB, indicating that PADPRP activation was the cause of the NAD depletion.	NAD	106-109	poly [ADP-ribose] polymerase 1	Cricetulus griseus	67-73
8358221-3	1993	One of the fractions, which bound to a cellulose phosphate column, was able to reduce the soluble cytochrome b5, using NADH as an electron donor.	NAD	119-123	cytochrome b5 type A	Homo sapiens	98-111
8261576-3	1993	Mechanism studies showed that endogenous PARP activity (incorporation of tritiated nicotinamide adenine dinucleotide, [3H]-NAD) was 2.6 times higher in O-342/DDP than in O-342 cells and that the presence of 2.5 mM NA during the incubation with the isotope resulted in 73.3% inhibition of the enzyme activity in O-342/DDP cells but in only about 30% inhibition in the sensitive line.	NAD	83-116	poly (ADP-ribose) polymerase 1	Rattus norvegicus	41-45
8261576-3	1993	Mechanism studies showed that endogenous PARP activity (incorporation of tritiated nicotinamide adenine dinucleotide, [3H]-NAD) was 2.6 times higher in O-342/DDP than in O-342 cells and that the presence of 2.5 mM NA during the incubation with the isotope resulted in 73.3% inhibition of the enzyme activity in O-342/DDP cells but in only about 30% inhibition in the sensitive line.	NAD	123-126	poly (ADP-ribose) polymerase 1	Rattus norvegicus	41-45
8454571-5	1993	Such an extract labeled with [32P]NAD+ was analyzed by immunoprecipitation with anti-RNA polymerase I (pol I) antibody; a protein with M(r) 130 kDa was detected.	NAD	34-38	polymerase (DNA directed), iota	Mus musculus	103-108
8454571-8	1993	These results suggest that the activation by NAD+ is due to enhancement of the formation of initiation complex by mono ADP-ribosylation of the second-largest subunit (130 kDa) of pol I.	NAD	45-49	polymerase (DNA directed), iota	Mus musculus	179-184
1327782-9	1992	The NADH:acceptor reductase was capable of reducing either one- or two-electron acceptors, such as horse heart cytochrome c or 2,6-dichloroindophenol, at an optimal pH of 8.5.	NAD	4-8	cytochrome c, somatic	Equus caballus	111-123
1418308-6	1992	In group C, the rate constant of NADH fluorescence decreased significantly (P &lt; 0.05) from the control value of 8.31 +/- 0.21 x 10(-3) (sec-1) to 4.97 +/- 0.15 x 10(-3) and 5.58 +/- 0.16 x 10(-3) (mean +/- SEM) at 12 and 24 h after cold preservation, respectively.	NAD	33-37	secretory blood group 1	Rattus norvegicus	139-144
1411581-3	1992	MMP-8 is activated by hypochlorous acid produced by myeloperoxidase from hydrogen peroxide and chloride ion and by the hydroxyl radical produced in Haber Weiss reaction fed by superoxide produced by, eg, NADPH (reduced nicotinamide adenine dinucleotide) oxidase and xanthine oxidase.	NAD	219-252	matrix metallopeptidase 8	Homo sapiens	0-5
1508959-1	1992	The presence of endogenous inhibitors of NAD(+)-dependent 15-hydroxyprostaglandin dehydrogenase (PGDH) has been indicated by increasing total activity after the initial purification step of PGDH in human placenta.	NAD	41-47	15-hydroxyprostaglandin dehydrogenase	Homo sapiens	97-101
1508959-1	1992	The presence of endogenous inhibitors of NAD(+)-dependent 15-hydroxyprostaglandin dehydrogenase (PGDH) has been indicated by increasing total activity after the initial purification step of PGDH in human placenta.	NAD	41-47	15-hydroxyprostaglandin dehydrogenase	Homo sapiens	190-194
16668941-0	1992	Expression in Escherichia coli of Cytochrome c Reductase Activity from a Maize NADH:Nitrate Reductase Complementary DNA.	NAD	79-83	nitrate reductase [NADH] 1	Zea mays	84-101
16668941-2	1992	Zmnr1S was shown to be an NADH:nitrate reductase clone by nucleotide sequencing and comparison of its deduced amino acid sequence to Zmnr1.	NAD	26-30	nitrate reductase [NADH] 1	Zea mays	31-48
16668941-4	1992	The cell lysate contained NADH:cytochrome c reductase activity, which is a characteristic partial activity of NADH:nitrate reductase dependent on the cytochrome b and flavin adenine dinucleotide domains.	NAD	26-30	nitrate reductase [NADH] 1	Zea mays	115-132
16668941-4	1992	The cell lysate contained NADH:cytochrome c reductase activity, which is a characteristic partial activity of NADH:nitrate reductase dependent on the cytochrome b and flavin adenine dinucleotide domains.	NAD	110-114	nitrate reductase [NADH] 1	Zea mays	115-132
1350433-4	1992	GDH catalyzes the formation of NADH, and GPT drives the GDH reaction by removing a reaction product and regenerating glutamate.	NAD	31-35	glutamate dehydrogenase 1	Homo sapiens	56-59
1740142-6	1992	Km values for NAD were calculated to be 30 microM with beta/gamma-actin, 35 microM with alpha-actin and 20 microM with gamma-actin.	NAD	14-17	actin, beta	Gallus gallus	55-71
1740142-6	1992	Km values for NAD were calculated to be 30 microM with beta/gamma-actin, 35 microM with alpha-actin and 20 microM with gamma-actin.	NAD	14-17	actin, beta	Gallus gallus	66-71
1909571-8	1991	On the basis of the amino acid sequence, the NQO2 gene was found to be located 1.7 kilobase pairs upstream of the gene for NADH-binding subunit (NQO1).	NAD	123-127	N-ribosyldihydronicotinamide:quinone reductase 2	Homo sapiens	45-49
1874176-4	1991	The relative rates of activity with various substrates (CoQ0 approximately equal to durohydroquinone greater than menadione greater than duroquinone greater than CoQ6 = CoQ10 greater than ferricyanide) were similar to those described previously for quinone reductase from liver Dicumarol, chlorpromazine, and T3 were much more potent inhibitors of the enzyme when NADPH was the coenzyme than when NADH was the coenzyme.	NAD	397-401	coenzyme Q6, monooxygenase	Homo sapiens	162-166
1652057-1	1991	We found that cells of Saccharomyces cerevisiae have an elevated level of the NAD-dependent glutamate dehydrogenase (NAD-GDH; encoded by the GDH2 gene) when grown with a nonfermentable carbon source or with limiting amounts of glucose, even in the presence of the repressing nitrogen source glutamine.	NAD	78-81	glutamate dehydrogenase (NAD(+))	Saccharomyces cerevisiae S288C	141-145
1652057-3	1991	This UAS was found to be separable from a neighboring element which is necessary for the nitrogen source regulation of the gene, and strains deficient for the GLN3 gene product, required for expression of NAD-GDH during growth with the activating nitrogen source glutamate, were unaffected for the expression of NAD-GDH during growth with activating carbon sources.	NAD	205-208	nitrogen-responsive transcriptional regulator GLN3	Saccharomyces cerevisiae S288C	159-163
1776672-1	1991	Alcohol dehydrogenase (ADH) and glucose-6-phosphate dehydrogenase (G6PDH) activities of cetyltrimethylammonium bromide permeabilized baker"s yeast whole cells were employed to prepare reduced nicotinamide nucleotides NADH and NADPH from their corresponding oxidised forms.	NAD	217-221	glucose-6-phosphate dehydrogenase	Saccharomyces cerevisiae S288C	32-65
1776672-1	1991	Alcohol dehydrogenase (ADH) and glucose-6-phosphate dehydrogenase (G6PDH) activities of cetyltrimethylammonium bromide permeabilized baker"s yeast whole cells were employed to prepare reduced nicotinamide nucleotides NADH and NADPH from their corresponding oxidised forms.	NAD	217-221	glucose-6-phosphate dehydrogenase	Saccharomyces cerevisiae S288C	67-72
1840553-4	1991	Crude cell extracts from E. coli grown under several different conditions show weak but measurable ALDH enzyme activity that prefers NADP+ over NAD+ as coenzyme; however, aldH gene expression appears to be very low, since no specific transcripts derived from the novel gene can be detected on Northern blots of RNA isolated from these cells.	NAD	144-148	Aldehyde dehydrogenase	Escherichia coli	99-103
2124504-2	1990	Studies have suggested that in Lactobacillus casei dihydrofolate reductase Arg-43, the homologous residue at this position, plays an important role in the binding of NADPH and in the differentiation of Km values for NADPH and NADH.	NAD	226-230	dihydrofolate reductase	Homo sapiens	51-74
2369123-2	1990	The reduction of exogenous cytochrome b5 by microsomes was low at 1.2 microM cytochrome b5 (3.9 or 2.7 nmol/min/mg protein, respectively, with NADH or NADPH).	NAD	143-147	cytochrome b5 type A	Homo sapiens	27-40
2369123-2	1990	The reduction of exogenous cytochrome b5 by microsomes was low at 1.2 microM cytochrome b5 (3.9 or 2.7 nmol/min/mg protein, respectively, with NADH or NADPH).	NAD	143-147	cytochrome b5 type A	Homo sapiens	77-90
2369123-6	1990	MgCl2 also stimulated cytochrome b5 reduction with a EC50 value of 1.0 mM in the NADH system or 0.6 mM in the NADPH system.	NAD	81-85	cytochrome b5 type A	Homo sapiens	22-35
2369123-8	1990	The Km value for cytochrome b5 was decreased and the Vmax was increased by calcium with either the NADH- or the NADPH-dependent system.	NAD	99-103	cytochrome b5 type A	Homo sapiens	17-30
2126460-2	1990	Residue Asn313 is involved together with the carboxyamide moiety of the nicotinamide ring in a complex network of hydrogen bonding interactions which fix the position of the pyridinium ring of NAD to which hydride transfer occurs at the C-4 position in the catalytic reaction.	NAD	193-196	complement C4A (Rodgers blood group)	Homo sapiens	237-240
2350175-3	1990	The specific activity of the lung PGDH in pregnant rabbits (25- to 28-day gestations) was 36.7 nmol NADH formed/min/mg protein compared to 0.3 nmol NADH formed/min/mg protein in nonpregnant rabbits.	NAD	100-104	15-hydroxyprostaglandin dehydrogenase	Homo sapiens	34-38
2350175-3	1990	The specific activity of the lung PGDH in pregnant rabbits (25- to 28-day gestations) was 36.7 nmol NADH formed/min/mg protein compared to 0.3 nmol NADH formed/min/mg protein in nonpregnant rabbits.	NAD	148-152	15-hydroxyprostaglandin dehydrogenase	Homo sapiens	34-38
2350175-7	1990	An immunochemically reactive protein also was observed in the ovary of 25- to 28-day pregnant rabbits and the specific activity of the ovary PGDH was 19.3 nmol NADH formed/min/mg protein.	NAD	160-164	15-hydroxyprostaglandin dehydrogenase	Homo sapiens	141-145
2116938-6	1990	3-Aminobenzamide (3-ABA), an ADPRT inhibitor, prevented the depletion of intracellular NAD+ by MMS or MNNG treatment and potentiated cytotoxicity.	NAD	87-91	poly [ADP-ribose] polymerase 1	Cricetulus griseus	29-34
31427442-6	2019	Cells were primed with LPS with or without subsequent NLRP3 activation with ATP or cholesterol crystals to analyze the effects of NAD+ levels on TLR4-mediated NF-kappaB activation and NLRP3 activity, respectively.	NAD	130-134	toll like receptor 4	Homo sapiens	145-149
31427442-10	2019	Hence, we suggest a novel mechanism in which NAD+ affects TLR4 signal transduction.	NAD	45-49	toll like receptor 4	Homo sapiens	58-62
34856334-5	2022	Silent information regulator 2 or SIR2 or more commonly known as sirtuins are NAD+ dependent histone deacetylase.	NAD	78-81	sirtuin 2	Homo sapiens	0-30
34856334-5	2022	Silent information regulator 2 or SIR2 or more commonly known as sirtuins are NAD+ dependent histone deacetylase.	NAD	78-81	sirtuin 2	Homo sapiens	34-38
34987507-12	2021	Collectively, our data suggest that NAD+ depletion provides a non-transcriptional priming signal for NLRP3 activation via mitochondrial perinuclear clustering, and aging-associated NAD+ decline can trigger NLRP3 inflammasome activation in ATP-rich environments.	NAD	36-40	NLR family, pyrin domain containing 3	Mus musculus	101-106
34987507-12	2021	Collectively, our data suggest that NAD+ depletion provides a non-transcriptional priming signal for NLRP3 activation via mitochondrial perinuclear clustering, and aging-associated NAD+ decline can trigger NLRP3 inflammasome activation in ATP-rich environments.	NAD	181-185	NLR family, pyrin domain containing 3	Mus musculus	206-211
34959937-9	2021	Also, TGPN and PNY stimulated NAD-dependent deacetylase sirtuin-1(SIRT1), peroxisome proliferator-activated receptor gamma coactivator-1 alpha (PGC-1alpha), nuclear respiratory factor 1,2, mitochondrial transcription factor A, along with mitochondrial DNA content via SIRT1/PGC-1alpha signaling.	NAD	30-33	sirtuin 1	Mus musculus	66-71
34959937-9	2021	Also, TGPN and PNY stimulated NAD-dependent deacetylase sirtuin-1(SIRT1), peroxisome proliferator-activated receptor gamma coactivator-1 alpha (PGC-1alpha), nuclear respiratory factor 1,2, mitochondrial transcription factor A, along with mitochondrial DNA content via SIRT1/PGC-1alpha signaling.	NAD	30-33	sirtuin 1	Mus musculus	268-273
34525347-5	2021	The third edit was a knockout of the ecto-enzyme CD38, which hydrolyzes NAD+.	NAD	72-76	CD38 molecule	Homo sapiens	49-53
34402126-6	2021	Of the 361 compounds detected in the liver, 41 compounds, including amino acids related to the Cit-arginine (Arg) cycle, argininosuccinic acid, Arg, ornithine, and Cit, as well as gamma aminobutyric acid, glycine, histidine, and nicotinamide adenine dinucleotide were abundant in l-Cit-treated livers.	NAD	229-262	citron rho-interacting serine/threonine kinase	Homo sapiens	282-285
34695733-6	2021	It could be demonstrated that the stalled intermediate formed by the reaction of Sirt2-bound thiomyristoylated peptide and NAD+ has IC50 values below 200 pM.	NAD	123-127	sirtuin 2	Homo sapiens	81-86
34591326-1	2021	BACKGROUND: Sirtuin 3 (SIRT3), a mitochondrial NAD+ -dependent deacetylase, has received much attention for its effect on metabolism and aging.	NAD	47-50	sirtuin 3	Mus musculus	12-21
34591326-1	2021	BACKGROUND: Sirtuin 3 (SIRT3), a mitochondrial NAD+ -dependent deacetylase, has received much attention for its effect on metabolism and aging.	NAD	47-50	sirtuin 3	Mus musculus	23-28
34591326-11	2021	RESULTS: In parallel with the imbalanced NAD+ /NADH ratio, the SIRT3 expression was significantly decreased in the alveolar bones of the aged mice, accompanied by a global elevation of protein acetylation levels.	NAD	41-45	sirtuin 3	Mus musculus	63-68
34591326-11	2021	RESULTS: In parallel with the imbalanced NAD+ /NADH ratio, the SIRT3 expression was significantly decreased in the alveolar bones of the aged mice, accompanied by a global elevation of protein acetylation levels.	NAD	47-51	sirtuin 3	Mus musculus	63-68
34748530-2	2021	Here, we report that the genetic and pharmacological inhibition of nicotinamide phosphoribosyltransferase (Nampt), the rate-limiting enzyme in the salvage pathway of NAD+ biosynthesis, reduced oxidative stress, inflammation, and keratinocyte DNA damage, hyperproliferation, and cell death in zebrafish models of chronic skin inflammation, while all these effects were reversed by NAD+ supplementation.	NAD	166-170	nicotinamide phosphoribosyltransferase 1	Danio rerio	67-105
34748530-2	2021	Here, we report that the genetic and pharmacological inhibition of nicotinamide phosphoribosyltransferase (Nampt), the rate-limiting enzyme in the salvage pathway of NAD+ biosynthesis, reduced oxidative stress, inflammation, and keratinocyte DNA damage, hyperproliferation, and cell death in zebrafish models of chronic skin inflammation, while all these effects were reversed by NAD+ supplementation.	NAD	166-170	nicotinamide phosphoribosyltransferase 1	Danio rerio	107-112
34748530-2	2021	Here, we report that the genetic and pharmacological inhibition of nicotinamide phosphoribosyltransferase (Nampt), the rate-limiting enzyme in the salvage pathway of NAD+ biosynthesis, reduced oxidative stress, inflammation, and keratinocyte DNA damage, hyperproliferation, and cell death in zebrafish models of chronic skin inflammation, while all these effects were reversed by NAD+ supplementation.	NAD	380-384	nicotinamide phosphoribosyltransferase 1	Danio rerio	67-105
34748530-2	2021	Here, we report that the genetic and pharmacological inhibition of nicotinamide phosphoribosyltransferase (Nampt), the rate-limiting enzyme in the salvage pathway of NAD+ biosynthesis, reduced oxidative stress, inflammation, and keratinocyte DNA damage, hyperproliferation, and cell death in zebrafish models of chronic skin inflammation, while all these effects were reversed by NAD+ supplementation.	NAD	380-384	nicotinamide phosphoribosyltransferase 1	Danio rerio	107-112
34355499-2	2021	SIRT1 is a NAD+-dependent class III histone deacetylase, widely expresses in BLA.	NAD	11-14	sirtuin 1	Mus musculus	0-5
34725423-1	2021	Lactate dehydrogenase (LDH) catalyses the conversion of pyruvate to lactate and NADH to NAD+; it has two isoforms, LDHA and LDHB.	NAD	80-84	lactate dehydrogenase B	Homo sapiens	124-128
34725423-1	2021	Lactate dehydrogenase (LDH) catalyses the conversion of pyruvate to lactate and NADH to NAD+; it has two isoforms, LDHA and LDHB.	NAD	88-92	lactate dehydrogenase B	Homo sapiens	124-128
17068635-13	2006	Treatment of platelets with ONOO- (50-300 microM) resulted in decreased activities of NADH : ubiquinone oxidoreductase, succinate dehydrogenase and cytochrome oxidase.	NAD	86-90	hydroxysteroid 17-beta dehydrogenase 6	Homo sapiens	104-118
34725423-4	2021	Here, we developed a high-throughput mass spectrometry screening system using an LDHB enzyme assay by detecting NADH and NAD+.	NAD	112-116	lactate dehydrogenase B	Homo sapiens	81-85
34725423-4	2021	Here, we developed a high-throughput mass spectrometry screening system using an LDHB enzyme assay by detecting NADH and NAD+.	NAD	121-125	lactate dehydrogenase B	Homo sapiens	81-85
16484774-0	2006	Assignment of the NAD-dependent deacetylase sirtuin 5 gene (SIRT5) to human chromosome band 6p23 by in situ hybridization.	NAD	18-21	sirtuin 5	Homo sapiens	44-53
34718606-1	2022	SIRT3 is an NAD+-dependent protein deacetylase localized in mitochondria.	NAD	12-15	sirtuin 3	Rattus norvegicus	0-5
16484774-0	2006	Assignment of the NAD-dependent deacetylase sirtuin 5 gene (SIRT5) to human chromosome band 6p23 by in situ hybridization.	NAD	18-21	sirtuin 5	Homo sapiens	60-65
34771251-4	2021	After conversion into diesters of different lengths, the CALB-catalyzed polymerization of these monomers with 1,4-butanediol resulted in short oligomers with a DPn up to 5.	NAD	160-163	calbindin 1	Homo sapiens	57-61
16484774-1	2006	Sirtuin 5 (SIRT5) is a nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase and belongs to the Silent information regulator 2 (Sir2) family of sirtuin histone deacetylases (HDACs), which play a central role in epigenetic gene silencing, DNA repair and recombination, cell-cycle, microtubule organization, and in the regulation of aging.	NAD	23-56	sirtuin 5	Homo sapiens	0-9
16484774-1	2006	Sirtuin 5 (SIRT5) is a nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase and belongs to the Silent information regulator 2 (Sir2) family of sirtuin histone deacetylases (HDACs), which play a central role in epigenetic gene silencing, DNA repair and recombination, cell-cycle, microtubule organization, and in the regulation of aging.	NAD	23-56	sirtuin 5	Homo sapiens	11-16
34835990-2	2021	Among these enzymes, CD38 can be seen under two perspectives: as the enzyme synthesizing Ca2+-mobilizing second messenger, starting from NAD+, and as the major NAD+-consumer, to be inhibited to increase NAD+ levels.	NAD	137-141	CD38 molecule	Homo sapiens	21-25
34835990-2	2021	Among these enzymes, CD38 can be seen under two perspectives: as the enzyme synthesizing Ca2+-mobilizing second messenger, starting from NAD+, and as the major NAD+-consumer, to be inhibited to increase NAD+ levels.	NAD	160-164	CD38 molecule	Homo sapiens	21-25
16484774-1	2006	Sirtuin 5 (SIRT5) is a nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase and belongs to the Silent information regulator 2 (Sir2) family of sirtuin histone deacetylases (HDACs), which play a central role in epigenetic gene silencing, DNA repair and recombination, cell-cycle, microtubule organization, and in the regulation of aging.	NAD	58-61	sirtuin 5	Homo sapiens	0-9
34835990-2	2021	Among these enzymes, CD38 can be seen under two perspectives: as the enzyme synthesizing Ca2+-mobilizing second messenger, starting from NAD+, and as the major NAD+-consumer, to be inhibited to increase NAD+ levels.	NAD	203-207	CD38 molecule	Homo sapiens	21-25
16484774-1	2006	Sirtuin 5 (SIRT5) is a nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase and belongs to the Silent information regulator 2 (Sir2) family of sirtuin histone deacetylases (HDACs), which play a central role in epigenetic gene silencing, DNA repair and recombination, cell-cycle, microtubule organization, and in the regulation of aging.	NAD	58-61	sirtuin 5	Homo sapiens	11-16
16321804-4	2005	Aconitase in the Krebs cycle is more vulnerable than alpha-KGDH to ROS but as long as alpha-KGDH is functional NADH generation in the Krebs cycle is maintained.	NAD	111-115	oxoglutarate dehydrogenase	Homo sapiens	86-96
34675216-2	2021	Sirtuin 3 (SIRT3), an important mitochondrial NAD+dependent decarboxylase and a major regulator of cellular energy metabolism and antioxidant defense, is integral to maintaining normal mitochondrial function.	NAD	46-50	sirtuin 3	Bos taurus	0-9
34675216-2	2021	Sirtuin 3 (SIRT3), an important mitochondrial NAD+dependent decarboxylase and a major regulator of cellular energy metabolism and antioxidant defense, is integral to maintaining normal mitochondrial function.	NAD	46-50	sirtuin 3	Bos taurus	11-16
16321804-5	2005	NADH supply to the respiratory chain is limited only when alpha-KGDH is also inhibited by ROS.	NAD	0-4	oxoglutarate dehydrogenase	Homo sapiens	58-68
16321804-6	2005	In addition being a key target, alpha-KGDH is able to generate ROS during its catalytic function, which is regulated by the NADH/NAD+ ratio.	NAD	124-128	oxoglutarate dehydrogenase	Homo sapiens	32-42
16321804-6	2005	In addition being a key target, alpha-KGDH is able to generate ROS during its catalytic function, which is regulated by the NADH/NAD+ ratio.	NAD	129-133	oxoglutarate dehydrogenase	Homo sapiens	32-42
34618304-0	2022	Purification of Angiotensin-Converting Enzyme (ACE) from Sheep Kidney and Inhibition Effect of Reduced Nicotinamide Adenine Dinucleotide (NADH) on Purified ACE Activity.	NAD	103-136	angiotensin-converting enzyme	Ovis aries	16-45
34618304-0	2022	Purification of Angiotensin-Converting Enzyme (ACE) from Sheep Kidney and Inhibition Effect of Reduced Nicotinamide Adenine Dinucleotide (NADH) on Purified ACE Activity.	NAD	103-136	angiotensin-converting enzyme	Ovis aries	47-50
34618304-0	2022	Purification of Angiotensin-Converting Enzyme (ACE) from Sheep Kidney and Inhibition Effect of Reduced Nicotinamide Adenine Dinucleotide (NADH) on Purified ACE Activity.	NAD	103-136	angiotensin-converting enzyme	Ovis aries	156-159
16007178-6	2005	The ERbeta-selective agonist 2,3-bis(4-hydroxy-phenyl)-propionitrile (DPN) inhibited cell growth and induced apoptosis.	NAD	70-73	estrogen receptor 2 (beta)	Mus musculus	4-10
34618304-0	2022	Purification of Angiotensin-Converting Enzyme (ACE) from Sheep Kidney and Inhibition Effect of Reduced Nicotinamide Adenine Dinucleotide (NADH) on Purified ACE Activity.	NAD	138-142	angiotensin-converting enzyme	Ovis aries	16-45
34618304-0	2022	Purification of Angiotensin-Converting Enzyme (ACE) from Sheep Kidney and Inhibition Effect of Reduced Nicotinamide Adenine Dinucleotide (NADH) on Purified ACE Activity.	NAD	138-142	angiotensin-converting enzyme	Ovis aries	47-50
34618304-0	2022	Purification of Angiotensin-Converting Enzyme (ACE) from Sheep Kidney and Inhibition Effect of Reduced Nicotinamide Adenine Dinucleotide (NADH) on Purified ACE Activity.	NAD	138-142	angiotensin-converting enzyme	Ovis aries	156-159
16382292-3	2005	The constitutive xanthine dehydrogenase form of this enzyme generally uses NAD(+) as an electron acceptor, whereas the post-translational xanthine oxidase form uses molecular oxygen and yields four units of reactive oxygen species per unit of transformed substrate.	NAD	75-81	xanthine dehydrogenase	Homo sapiens	17-39
34464722-9	2021	Blockade of JAK2 or STAT3 phosphorylation significantly reduced the ability of DPN to down-regulate P2X7R expression and the ability of ERB-041 and DPN to inhibit IL-1beta release from RAW264.7 cells.	NAD	79-82	Janus kinase 2	Mus musculus	12-16
16087479-2	2005	In this study, it was shown that purified rat liver XO and xanthine dehydrogenase (XD) catalyse the NADH oxidation, generating O*- and inducing the peroxidation of liposomes, in a NADH and enzyme concentration-dependent manner.	NAD	100-104	xanthine dehydrogenase	Rattus norvegicus	59-81
34529976-5	2021	Loss of DRP1 (shDRP1) resulted in extensive ultrastructural and functional remodeling of mitochondria, characterized by pleomorphic enlargement, increased electron density of the matrix, and defective NADH and succinate oxidation.	NAD	201-205	dynamin 1 like	Homo sapiens	8-12
34509469-7	2021	Decreasing tissue NAD+ concentrations have been ascribed to an imbalance between biosynthesis and consumption of the dinucleotide, resulting from, for instance, reduced levels of the rate limiting enzyme NAMPT along with an increased activation state of the NAD+-consuming enzymes PARPs and CD38.	NAD	18-22	CD38 molecule	Homo sapiens	291-295
34509469-7	2021	Decreasing tissue NAD+ concentrations have been ascribed to an imbalance between biosynthesis and consumption of the dinucleotide, resulting from, for instance, reduced levels of the rate limiting enzyme NAMPT along with an increased activation state of the NAD+-consuming enzymes PARPs and CD38.	NAD	258-262	CD38 molecule	Homo sapiens	291-295
34603081-13	2021	Moreover, the expression of NAD+-consuming enzymes sirtuin 3 (SIRT3) and CD38 decreased significantly in CKD rats.	NAD	28-32	sirtuin 3	Rattus norvegicus	51-60
34603081-13	2021	Moreover, the expression of NAD+-consuming enzymes sirtuin 3 (SIRT3) and CD38 decreased significantly in CKD rats.	NAD	28-32	sirtuin 3	Rattus norvegicus	62-67
16087479-2	2005	In this study, it was shown that purified rat liver XO and xanthine dehydrogenase (XD) catalyse the NADH oxidation, generating O*- and inducing the peroxidation of liposomes, in a NADH and enzyme concentration-dependent manner.	NAD	180-184	xanthine dehydrogenase	Rattus norvegicus	59-81
15983043-4	2005	ALDH2*2 has an increased Km for its coenzyme, NAD+, and a decreased kcat, which lead to low activity in vivo.	NAD	46-50	aldehyde dehydrogenase 2 family member	Homo sapiens	0-5
34567409-16	2021	Mechanically, these beneficial effects were attributed to the inhibition of NLRP3 inflammasome activation and myocardial inflammatory response by regulating the NAD+-Sirtuin3-MnSOD signaling pathway.	NAD	161-165	NLR family, pyrin domain containing 3	Mus musculus	76-81
34567409-16	2021	Mechanically, these beneficial effects were attributed to the inhibition of NLRP3 inflammasome activation and myocardial inflammatory response by regulating the NAD+-Sirtuin3-MnSOD signaling pathway.	NAD	161-165	sirtuin 3	Mus musculus	166-174
16109413-2	2005	Mammalian mitochondria are thought to synthesize fatty acids, but evidence for the key ACP component was lacking since the only reported ACP was the SDAP subunit of the membrane-bound NADH:ubiquinone oxidoreductase, We report that most of the SDAP is found in the soluble (matrix) fraction of bovine heart mitochondria and is therefore available to carry the intermediates of type II fatty acid synthesis.	NAD	184-188	NADH:ubiquinone oxidoreductase subunit AB1	Homo sapiens	137-140
34571997-11	2021	Since the SIRT3 activity is NAD+ dependent, these results might parallel changes in glucose metabolism under pathologic reduction in mitochondrial NAD+ pools.	NAD	28-32	sirtuin 3	Mus musculus	10-15
34571997-11	2021	Since the SIRT3 activity is NAD+ dependent, these results might parallel changes in glucose metabolism under pathologic reduction in mitochondrial NAD+ pools.	NAD	147-151	sirtuin 3	Mus musculus	10-15
34314389-6	2021	Lsd1 knockout reduces NAD+-dependent SIRT1 and SIRT7 deacetylase activity, leading to hyperacetylation and hypofunctioning of GABPbeta and PGC-1alpha, the major transcriptional factor/cofactor for nuclear-encoded mitochondrial genes.	NAD	22-25	sirtuin 1	Mus musculus	37-42
15946682-3	2005	To catalyze the oxidation of dihydrolipoamide, hE3 uses two molecules: non-covalently bound FAD and a transiently bound substrate, NAD+.	NAD	131-135	dihydrolipoamide dehydrogenase	Homo sapiens	47-50
34302821-2	2021	These strategies include supplementing with NAD+ precursors, small molecule activation of NAD+ biosynthetic enzymes, and treatment with small molecule inhibitors of NAD+ consuming enzymes such as CD38, SARM1 or members of the PARP family.	NAD	165-169	CD38 molecule	Homo sapiens	196-200
15946682-4	2005	To address the catalytic mechanism of hE3 and the structural basis for E3 deficiency, the crystal structures of hE3 in the presence of NAD+ or NADH have been determined at resolutions of 2.5A and 2.1A, respectively.	NAD	135-139	dihydrolipoamide dehydrogenase	Homo sapiens	112-115
15946682-4	2005	To address the catalytic mechanism of hE3 and the structural basis for E3 deficiency, the crystal structures of hE3 in the presence of NAD+ or NADH have been determined at resolutions of 2.5A and 2.1A, respectively.	NAD	143-147	dihydrolipoamide dehydrogenase	Homo sapiens	112-115
15946682-6	2005	The structure of oxidized hE3 with NAD+ bound demonstrates that the nicotinamide moiety is not proximal to the FAD.	NAD	35-39	dihydrolipoamide dehydrogenase	Homo sapiens	26-29
34190541-1	2021	(R)-3-Hydroxybutyrate dehydrogenase (HBDH) catalyzes the NADH-dependent reduction of 3-oxocarboxylates to (R)-3-hydroxycarboxylates.	NAD	57-61	3-hydroxybutyrate dehydrogenase 1	Homo sapiens	37-41
15946682-8	2005	This is the first time that this mechanistically requisite conformation of NAD+ or NADH has been observed in E3 from any species.	NAD	75-79	dihydrolipoamide dehydrogenase	Homo sapiens	109-111
34087956-5	2021	Mechanistic studies of replicative cellular senescence in the presence or absence of NLRX1 in vitro reveal that NLRX1-deficient fibroblasts fail to maintain optimal NAD+ /NADH ratio, which instigates the decline of SIRT1 and the activation of mTOR, p16INK4A , and p53, leading to the increase in senescence-associated beta-galactosidase (SA-beta-gal)-positive cells.	NAD	165-169	sirtuin 1	Mus musculus	215-220
34087956-5	2021	Mechanistic studies of replicative cellular senescence in the presence or absence of NLRX1 in vitro reveal that NLRX1-deficient fibroblasts fail to maintain optimal NAD+ /NADH ratio, which instigates the decline of SIRT1 and the activation of mTOR, p16INK4A , and p53, leading to the increase in senescence-associated beta-galactosidase (SA-beta-gal)-positive cells.	NAD	165-169	mechanistic target of rapamycin kinase	Mus musculus	243-247
34087956-5	2021	Mechanistic studies of replicative cellular senescence in the presence or absence of NLRX1 in vitro reveal that NLRX1-deficient fibroblasts fail to maintain optimal NAD+ /NADH ratio, which instigates the decline of SIRT1 and the activation of mTOR, p16INK4A , and p53, leading to the increase in senescence-associated beta-galactosidase (SA-beta-gal)-positive cells.	NAD	165-169	transformation related protein 53, pseudogene	Mus musculus	264-267
15946682-8	2005	This is the first time that this mechanistically requisite conformation of NAD+ or NADH has been observed in E3 from any species.	NAD	83-87	dihydrolipoamide dehydrogenase	Homo sapiens	109-111
15946682-10	2005	The current hE3 structures show directly that the disease-causing mutations occur at three locations in the human enzyme: the dimer interface, the active site, and the FAD and NAD(+)-binding sites.	NAD	176-182	dihydrolipoamide dehydrogenase	Homo sapiens	12-15
15947248-6	2005	Intracellular nicotinamide adenine dinucleotide (NAD+) content was increased in PBEF-overexpressing SMCs and decreased in PBEF-knockdown SMCs.	NAD	14-47	nicotinamide phosphoribosyltransferase	Homo sapiens	80-84
34087956-5	2021	Mechanistic studies of replicative cellular senescence in the presence or absence of NLRX1 in vitro reveal that NLRX1-deficient fibroblasts fail to maintain optimal NAD+ /NADH ratio, which instigates the decline of SIRT1 and the activation of mTOR, p16INK4A , and p53, leading to the increase in senescence-associated beta-galactosidase (SA-beta-gal)-positive cells.	NAD	171-175	sirtuin 1	Mus musculus	215-220
15947248-6	2005	Intracellular nicotinamide adenine dinucleotide (NAD+) content was increased in PBEF-overexpressing SMCs and decreased in PBEF-knockdown SMCs.	NAD	14-47	nicotinamide phosphoribosyltransferase	Homo sapiens	122-126
15947248-6	2005	Intracellular nicotinamide adenine dinucleotide (NAD+) content was increased in PBEF-overexpressing SMCs and decreased in PBEF-knockdown SMCs.	NAD	49-53	nicotinamide phosphoribosyltransferase	Homo sapiens	80-84
34175838-8	2021	Further analysis revealed that acacetin effect on Sirt6 was mediated by Sirt1 activation and increase of NAD+/NADH ratio.	NAD	105-109	sirtuin 6	Rattus norvegicus	50-55
34175838-8	2021	Further analysis revealed that acacetin effect on Sirt6 was mediated by Sirt1 activation and increase of NAD+/NADH ratio.	NAD	110-114	sirtuin 6	Rattus norvegicus	50-55
15947248-6	2005	Intracellular nicotinamide adenine dinucleotide (NAD+) content was increased in PBEF-overexpressing SMCs and decreased in PBEF-knockdown SMCs.	NAD	49-53	nicotinamide phosphoribosyltransferase	Homo sapiens	122-126
15947248-7	2005	Furthermore, NAD+-dependent protein deacetylase activity was found to be essential for SMC maturation and was increased by PBEF.	NAD	13-16	nicotinamide phosphoribosyltransferase	Homo sapiens	123-127
15947248-10	2005	These findings identify PBEF as a regulator of NAD+-dependent reactions in SMCs, reactions that promote, among other potential processes, the acquisition of a mature SMC phenotype.	NAD	47-51	nicotinamide phosphoribosyltransferase	Homo sapiens	24-28
34172715-3	2021	The coenzyme nicotinamide adenine dinucleotide (NAD+) is essential for both mitochondrial bioenergetics and nuclear DNA repair through NAD+-consuming poly (ADP-ribose) polymerases (PARPs).	NAD	13-46	Poly-(ADP-ribose) polymerase	Drosophila melanogaster	181-186
15960593-5	2005	The NAD+ is recycled to NADH by the enzyme glucose dehydrogenase, which obtains the necessary electrons from oxidation of glucose.	NAD	4-8	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	43-64
34172715-3	2021	The coenzyme nicotinamide adenine dinucleotide (NAD+) is essential for both mitochondrial bioenergetics and nuclear DNA repair through NAD+-consuming poly (ADP-ribose) polymerases (PARPs).	NAD	48-52	Poly-(ADP-ribose) polymerase	Drosophila melanogaster	181-186
34172715-9	2021	We suggest that enhancing the availability of NAD+ by either vitamin B supplements or the inhibition of NAD+-dependent enzymes such as PARPs are potential therapies for Alzheimer"s disease.	NAD	46-50	Poly-(ADP-ribose) polymerase	Drosophila melanogaster	135-140
34172715-9	2021	We suggest that enhancing the availability of NAD+ by either vitamin B supplements or the inhibition of NAD+-dependent enzymes such as PARPs are potential therapies for Alzheimer"s disease.	NAD	104-108	Poly-(ADP-ribose) polymerase	Drosophila melanogaster	135-140
15960593-5	2005	The NAD+ is recycled to NADH by the enzyme glucose dehydrogenase, which obtains the necessary electrons from oxidation of glucose.	NAD	24-28	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	43-64
15866519-3	2005	Afmid-catalyzed hydrolysis of N-formyl-kynurenine is a key step in tryptophan metabolism and biosynthesis of kynurenine-derived products including kynurenic acid, quinolinic acid, nicotinamide, NAD, and NADP.	NAD	194-197	arylformamidase	Mus musculus	0-5
34155309-1	2021	SIRT2, an NAD+-dependent histone deacetylase, has been shown to play a pivotal role in various physiological processes, however, its role in cancer is currently controversial.	NAD	10-13	sirtuin 2	Mus musculus	0-5
34142751-4	2021	Human non-stenotic valves (n = 10) actively converted NAD+ and NMN via both CD73 and NAD+ -glycohydrolase (CD38) according to our analysis with RP-HPLC and immunofluorescence.	NAD	54-58	CD38 molecule	Homo sapiens	107-111
34142751-5	2021	In stenotic valves (n = 50), due to reduced CD73 activity, NAD+ was degraded predominantly by CD38 and additionally by ALP and eNPP1.	NAD	59-63	CD38 molecule	Homo sapiens	94-98
34142751-7	2021	CD38 was also primarily engaged in human vascular NAD+ metabolism.	NAD	50-54	CD38 molecule	Homo sapiens	0-4
34142751-8	2021	Studies using specific ecto-enzyme inhibitors and CD73-/- mice confirmed that CD73 is not the only enzyme involved in NAD+ and NMN hydrolysis and that CD38 had a significant contribution to these pathways.	NAD	118-122	5' nucleotidase, ecto	Mus musculus	78-82
33271594-1	2021	Caloric restriction (CR) has been shown repeatedly to prolong the lifespan in laboratory animals, with its benefits dependent on molecular targets forming part of the nutrient signaling network, including the NAD-dependent deacetylase silent mating type information regulation 2 homologue 1 (SIRT1).	NAD	209-212	sirtuin 1	Mus musculus	292-297
34629356-2	2021	Nicotinamide adenine dinucleotide kinase (NAD kinase) catalyzes the phosphorylation of NAD+ to NADP+ in the presence of ATP (ATP-NAD kinase).	NAD	87-91	NAD kinase	Homo sapiens	0-40
34629356-2	2021	Nicotinamide adenine dinucleotide kinase (NAD kinase) catalyzes the phosphorylation of NAD+ to NADP+ in the presence of ATP (ATP-NAD kinase).	NAD	87-91	NAD kinase	Homo sapiens	42-52
34629356-3	2021	Novel NAD kinase that explicitly phosphorylates NAD+ to NADP+ using poly(P), besides ATP (ATP/poly(P)-NAD kinase), was found in bacteria, in particular, Gram-positive bacteria, and the gene encoding ATP/poly(P)-NAD kinase was also newly identified in Mycobacterium tuberculosis H37Rv.	NAD	48-52	NAD kinase	Homo sapiens	6-16
34629356-3	2021	Novel NAD kinase that explicitly phosphorylates NAD+ to NADP+ using poly(P), besides ATP (ATP/poly(P)-NAD kinase), was found in bacteria, in particular, Gram-positive bacteria, and the gene encoding ATP/poly(P)-NAD kinase was also newly identified in Mycobacterium tuberculosis H37Rv.	NAD	48-52	NAD kinase	Homo sapiens	102-112
35358824-2	2022	The enzymatic activity of SIRT2 is dependent on nicotinamide adenine dinucleotide (NAD+) and SIRT2 regulates post-translational modifications that are responsible for deacetylation of lysine residues in histone and non-histone substrates.	NAD	48-81	sirtuin 2	Homo sapiens	26-31
35358824-2	2022	The enzymatic activity of SIRT2 is dependent on nicotinamide adenine dinucleotide (NAD+) and SIRT2 regulates post-translational modifications that are responsible for deacetylation of lysine residues in histone and non-histone substrates.	NAD	83-87	sirtuin 2	Homo sapiens	26-31
35599350-7	2022	ERbeta knock down in the colons of mice with DSS-induced colitis resulted in significant reduction of the protection of arctigenin and DPN against the mucosal barrier.	NAD	135-138	estrogen receptor 1 (alpha)	Mus musculus	0-6
35609862-12	2022	Because NADH oxidation is required for cellular glycolytic activity, we propose that the mitochondrial outer membrane protein mitoNEET may promote glycolysis by transferring electrons from FMNH2 to oxygen or ubiquinone-10 in mitochondria.	NAD	8-12	CDGSH iron sulfur domain 1	Homo sapiens	126-134
35538652-8	2022	Furthermore, NAD+-mediated mitonuclear protein imbalance and UPRmt are probably regulated by deacetylase Sirtuin1 (SIRT1).	NAD	13-17	sirtuin 1	Mus musculus	105-113
35538652-8	2022	Furthermore, NAD+-mediated mitonuclear protein imbalance and UPRmt are probably regulated by deacetylase Sirtuin1 (SIRT1).	NAD	13-17	sirtuin 1	Mus musculus	115-120
35420434-3	2022	Our previous study revealed that CD38 overexpression decreased cellular nicotinamide adenine dinucleotide (NAD+) levels and caused cells to undergo EMT.	NAD	72-105	CD38 molecule	Homo sapiens	33-37
35420434-3	2022	Our previous study revealed that CD38 overexpression decreased cellular nicotinamide adenine dinucleotide (NAD+) levels and caused cells to undergo EMT.	NAD	107-111	CD38 molecule	Homo sapiens	33-37
35602958-3	2022	Here, we surprisingly found that although Cd38 deficiency partially reverses NAD+ degradation and T cell dysfunction in vitro, the terminal exhausted differentiation of adoptively transferred CD8+ T cells in tumor is not impacted by either deficiency or overexpression of CD38.	NAD	77-81	CD38 molecule	Homo sapiens	42-46
35602958-5	2022	Therefore, our results suggest that decreased NAD+ are correlated with T cell dysfunction, but deficiency of CD38 is not enough for rescuing NAD+ in tumor infiltrated CD8+ T cells and fails to increase the efficacy of antitumor T cell therapy.	NAD	141-145	CD38 molecule	Homo sapiens	109-113
35410407-9	2022	Furthermore, downstream of NAD+, the dynamics of the intracellular ATP concentration paralleled those of NAD+, and ATP-dependent caspase-9 activation via apoptosome formation was thus impaired under strong H2O2 stimulation.	NAD	27-31	caspase 9	Homo sapiens	129-138
35266458-4	2022	In the presence of NADH, NNP displayed high selectivity for NTR, a strong fluorescence enhancement (108 fold), and a low detection limit (3.6 ng mL-1).	NAD	19-23	L1 cell adhesion molecule	Mus musculus	145-149
35408935-5	2022	Results demonstrated that TKTL1 knockdown results in a decrease in TKT, glucose-6-phosphate dehydrogenase (G6PD) and glyceraldehyde-3-phosphate dehydrogenase (GAPDH) activities and impairs the hypoxia-induced overexpression of G6PD and GAPDH, all having significant impacts on the redox capacity of NADPH- and NADH-related cells.	NAD	310-314	transketolase like 1	Homo sapiens	26-31
35408818-6	2022	Accordingly, FK866, a NAMPT inhibitor, and quercetin, a Sirt1 agonist, have favorable effects on the maintenance of NAD+ homeostasis and renal function in db/db mice.	NAD	116-120	sirtuin 1	Mus musculus	56-61
35294260-6	2022	In vitro, P2X7R+ CD8 T cells were susceptible to ART1-mediated ADP-ribosylation and NICD, which was exacerbated upon blockade of the NAD+-degrading ADP-ribosyl cyclase CD38.	NAD	133-137	CD38 molecule	Homo sapiens	168-172
35372451-3	2022	Sirtuin 3 (SIRT3) which located in the mitochondria is the NAD-dependent deacetylase protein.	NAD	59-62	sirtuin 3	Mus musculus	0-9
35372451-3	2022	Sirtuin 3 (SIRT3) which located in the mitochondria is the NAD-dependent deacetylase protein.	NAD	59-62	sirtuin 3	Mus musculus	11-16
35138178-5	2022	The enzyme CD38, one of the main NAD-consuming enzymes, is a key component of NAD homeostasis.	NAD	33-36	CD38 molecule	Homo sapiens	11-15
35138178-5	2022	The enzyme CD38, one of the main NAD-consuming enzymes, is a key component of NAD homeostasis.	NAD	78-81	CD38 molecule	Homo sapiens	11-15
35138178-6	2022	The majority of CD38 is localized in the plasma membrane with its catalytic domain facing the extracellular environment, likely for the purpose of controlling systemic levels of NAD.	NAD	178-181	CD38 molecule	Homo sapiens	16-20
35138178-8	2022	Here we review potential roles of CD38 in health and disease and postulate ways in which CD38 dysregulation causes changes in NAD homeostasis and contributes to the pathophysiology of multiple conditions.	NAD	126-129	CD38 molecule	Homo sapiens	34-38
35138178-8	2022	Here we review potential roles of CD38 in health and disease and postulate ways in which CD38 dysregulation causes changes in NAD homeostasis and contributes to the pathophysiology of multiple conditions.	NAD	126-129	CD38 molecule	Homo sapiens	89-93
35138178-12	2022	Thus, understanding dysregulation of NAD homeostasis by CD38 may open new avenues for the treatment of human diseases.	NAD	37-40	CD38 molecule	Homo sapiens	56-60
35195252-5	2022	Specifically, FoxOs regulate mitochondrial biogenesis by dampening NRF1-Tfam and c-Myc-Tfam cascades directly, and inhibiting NAD-Sirt1-Pgc1alpha cascade indirectly by inducing Hmox1 or repressing Fxn and Urod.	NAD	126-129	heme oxygenase 1	Homo sapiens	177-182
34699038-6	2022	A combination of NNMT and its related genetic (Nmnat1, Nampt, Cyp2e1, Nrk1, Cd38) and proteic analyses and also the NAD + levels demonstrated the dynamical and depot-specific remodeling of NAD metabolism in different adipose tissues in response to cold exposure.	NAD	189-192	cytochrome P450, family 2, subfamily e, polypeptide 1	Mus musculus	62-68
34981667-12	2022	Mechanistically, mitochondrial fission increased the acetylation level of sterol regulatory element-binding protein 1 (SREBP1) and peroxisome proliferator-activated receptor coactivator 1 alpha (PGC-1alpha) by suppressing nicotinamide adenine dinucleotide (NAD+)/Sirtuin 1 (SIRT1) signaling.	NAD	222-255	sterol regulatory element binding transcription factor 1	Homo sapiens	74-117
34981667-12	2022	Mechanistically, mitochondrial fission increased the acetylation level of sterol regulatory element-binding protein 1 (SREBP1) and peroxisome proliferator-activated receptor coactivator 1 alpha (PGC-1alpha) by suppressing nicotinamide adenine dinucleotide (NAD+)/Sirtuin 1 (SIRT1) signaling.	NAD	222-255	sterol regulatory element binding transcription factor 1	Homo sapiens	119-125
15882838-7	2005	Differences in enzyme activities and inhibitor profiles between the WST-1-reducing NADH oxidoreductase enzyme in the presence of NADH or mPMS and the ECTO-NOX family are reconciled in terms of the different purification methods and assay systems used to study these proteins.	NAD	83-87	tripartite motif containing 33	Homo sapiens	150-154
35036692-5	2022	A comparison to the highly homologous porcine (sus scrofa) MDH1 ternary structures leads to the conclusion that only small conformational differences are needed to accommodate binding by NAD+ or other NAD+ mimetics.	NAD	187-191	malate dehydrogenase 1	Sus scrofa	59-63
35036692-5	2022	A comparison to the highly homologous porcine (sus scrofa) MDH1 ternary structures leads to the conclusion that only small conformational differences are needed to accommodate binding by NAD+ or other NAD+ mimetics.	NAD	201-205	malate dehydrogenase 1	Sus scrofa	59-63
15865448-3	2005	RDH12 exhibits approximately 2000-fold lower K(m) values for NADP(+) and NADPH than for NAD(+) and NADH and recognizes both retinoids and lipid peroxidation products (C(9) aldehydes) as substrates.	NAD	88-94	retinol dehydrogenase 12	Homo sapiens	0-5
16667152-3	1989	NADH:nitrate reductase activity and enzyme protein, as measured with an enzyme-linked immunosorbent assay, increased in parallel during the 8 h nitrate treatment in air, but in O(2) the levels of enzyme activity and protein were depressed.	NAD	0-4	nitrate reductase [NADH] 1	Zea mays	5-22
16667152-4	1989	NADH:nitrate reductase mRNA levels were the same in the air-and O(2)-treated leaves.	NAD	0-4	nitrate reductase [NADH] 1	Zea mays	5-22
15865448-3	2005	RDH12 exhibits approximately 2000-fold lower K(m) values for NADP(+) and NADPH than for NAD(+) and NADH and recognizes both retinoids and lipid peroxidation products (C(9) aldehydes) as substrates.	NAD	99-103	retinol dehydrogenase 12	Homo sapiens	0-5
2611200-5	1989	These trends in binding can be rationalized by considering the behavior of the analogues in the first two chemical steps of the mechanism: NAD+-mediated oxidation at C-5 and enolization at C-6 (the first part of the E1cB elimination of inorganic phosphate).	NAD	139-143	complement C5	Homo sapiens	166-169
15710617-7	2005	P450 BM3 W1046A/W106H FAD and reductase domains are efficient NADH-dependent ferricyanide reductases with selectivity coefficients (k(cat)/K(m)(NADPH)/k(cat)/K(m)(NADH)) of 1.5, 67, and 8571 for the W1046A, W1046H, and wild-type reductase domains, respectively.	NAD	62-66	presenilin 1	Homo sapiens	22-25
2507334-3	1989	The selection strategy for obtaining cells deficient in activity of poly(ADP-ribose) polymerase was based on the ability of this enzyme to deplete cellular NAD in response to high levels of DNA damage.	NAD	156-159	poly [ADP-ribose] polymerase 1	Cricetulus griseus	68-95
16666879-0	1989	cDNA Clones for Corn Leaf NADH:Nitrate Reductase and Chloroplast NAD(P):Glyceraldehyde-3-Phosphate Dehydrogenase : Characterization of the Clones and Analysis of the Expression of the Genes in Leaves as Influenced by Nitrate in the Light and Dark.	NAD	26-30	nitrate reductase [NADH] 1	Zea mays	31-48
16666879-3	1989	The deduced amino acid sequence of Zmnrl was nearly identical to peptide sequences of corn leaf NADH:nitrate reductase.	NAD	96-100	nitrate reductase [NADH] 1	Zea mays	101-118
2722875-2	1989	When the reactions catalyzed by alanine racemase (EC 5.1.1.1) and L-alanine dehydrogenase (EC 1.4.1.1), which is pro-R specific for the C-4 hydrogen transfer of NADH, are coupled in 2H2O, [4R-2H]NADH is exclusively produced.	NAD	161-165	complement C4A (Rodgers blood group)	Homo sapiens	136-139
2722875-4	1989	We have established a simple procedure for the in situ analysis of stereospecificity of C-4 hydrogen transfer of NADH by an NAD-dependent dehydrogenase by combination with either of the above two couples of enzymes in the same reaction mixture.	NAD	113-117	complement C4A (Rodgers blood group)	Homo sapiens	88-91
2722875-5	1989	When the C-4 hydrogen of NAD+ is fully retained after sufficient incubation, the stereospecificity of hydrogen transfer by a dehydrogenase is the same as that of alanine dehydrogenase or leucine dehydrogenase.	NAD	25-29	complement C4A (Rodgers blood group)	Homo sapiens	9-12
2722875-6	1989	However, when the C-4 hydrogen of NAD+ is exchanged with deuterium, the enzyme to be examined shows the different stereospecificity from alanine dehydrogenase or leucine dehydrogenase.	NAD	34-38	complement C4A (Rodgers blood group)	Homo sapiens	18-21
2727306-1	1989	The activity of NAD+-dependent PGDH was measured in the cytosolic fractions (100,000 x g) of uterine tissues obtained from transsexual, pregnant and non-pregnant women.	NAD	16-20	15-hydroxyprostaglandin dehydrogenase	Homo sapiens	31-35
15699053-6	2005	Thus, phosphorylation of xanthosine by cytosolic 5"-nucleotidase circumvents the activity of IMP dehydrogenase, a rate-limiting enzyme, catalyzing the NAD(+)-dependent conversion of IMP to XMP at the branch point of de novo nucleotide synthesis, thus leading to the generation of guanine nucleotides.	NAD	151-157	5'-nucleotidase ecto	Homo sapiens	49-64
15551062-8	2005	The rate of ethanol, 2-ethoxyethanol (2-EE), ethylene glycol, 2-phenoxyethanol (2-PE) and 2-BE conversion to alkoxyacetic acid by ADH/ALDH in these fractions was continuously monitored by UV spectrophotometry via the conversion of NAD+ to NADH at 340 nm.	NAD	231-235	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	134-138
15551062-8	2005	The rate of ethanol, 2-ethoxyethanol (2-EE), ethylene glycol, 2-phenoxyethanol (2-PE) and 2-BE conversion to alkoxyacetic acid by ADH/ALDH in these fractions was continuously monitored by UV spectrophotometry via the conversion of NAD+ to NADH at 340 nm.	NAD	239-243	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	134-138
15456401-4	2005	The present study with bovine liver catalase and [14C]NADPH and [14C]NADH revealed that unbound NADPH or NADH are substrates for an internal reductase and transhydrogenase reaction respectively; the unbound NADPH or NADH cause tightly bound NADP+ to become NADPH without becoming tightly bound themselves.	NAD	105-109	catalase	Bos taurus	36-44
15456401-4	2005	The present study with bovine liver catalase and [14C]NADPH and [14C]NADH revealed that unbound NADPH or NADH are substrates for an internal reductase and transhydrogenase reaction respectively; the unbound NADPH or NADH cause tightly bound NADP+ to become NADPH without becoming tightly bound themselves.	NAD	105-109	catalase	Bos taurus	36-44
15677321-2	2005	We report selective binding of IP3R to GAPDH, whose activity leads to the local generation of NADH to regulate intracellular calcium signaling.	NAD	94-98	inositol 1,4,5-trisphosphate receptor type 3	Homo sapiens	31-35
15677321-4	2005	Addition of native GAPDH and NAD+ to WT IP3R stimulates calcium release, whereas no stimulation occurs with C992S/995S IP3R that cannot bind GAPDH.	NAD	29-33	inositol 1,4,5-trisphosphate receptor type 3	Homo sapiens	40-44
23045123-1	2005	NADH cytochrome b(5) reductase (b(5)R; EC 1.6.2.2; Diaphorase I; NADH: ferricytochrome b(5) oxidoreductase) is an FAD-containing protein, which, along with the hemoprotein cytochrome b(5) (cyt b(5)), mediates electron transfer from NADH to fatty acid desaturases, P450 oxidases, methemoglobin, and ascorbyl free radical.	NAD	0-4	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	264-268
2751392-2	1989	Testicular cytosolic LDH-X activity was determined by oxidation of reduced nicotinamide adenine dinucleotide (NADH).	NAD	75-108	lactate dehydrogenase C	Rattus norvegicus	21-26
2751392-2	1989	Testicular cytosolic LDH-X activity was determined by oxidation of reduced nicotinamide adenine dinucleotide (NADH).	NAD	110-114	lactate dehydrogenase C	Rattus norvegicus	21-26
15381699-5	2004	We found that Nampt was the rate-limiting component in this mammalian NAD biosynthesis pathway.	NAD	70-73	nicotinamide phosphoribosyltransferase	Homo sapiens	14-19
15650244-5	2004	Connexin 43 (Cx43) hemichannels mediate an equilibrative transport of NAD+ from the cytosol to the active site of CD38 (either ectocellular or intravesicular).	NAD	70-74	gap junction protein alpha 1	Homo sapiens	0-11
3143698-1	1988	Nicotinamide adenine dinucleotide is utilized as the substrate of a chromatin-bound enzyme, poly(ADP-ribose) polymerase.	NAD	0-33	poly (ADP-ribose) polymerase 1	Rattus norvegicus	92-119
2459594-1	1988	Isolated and purified microsomal NADH-cytochrome b5 reductase (EC 1.6.2.2) was incubated with bleomycin (BLM) and FeCl3 in the presence of NADH.	NAD	33-37	cytochrome b5 type A	Homo sapiens	38-51
15650244-5	2004	Connexin 43 (Cx43) hemichannels mediate an equilibrative transport of NAD+ from the cytosol to the active site of CD38 (either ectocellular or intravesicular).	NAD	70-74	gap junction protein alpha 1	Homo sapiens	13-17
15604828-2	2004	The pnta and pntb genes encoding for the alpha- and beta-subunits were cloned and co-expressed with NADP+-dependent alcohol dehydrogenase (ADH) from Lactobacillus kefir and NAD+-dependent formate dehydrogenase (FDH) from Candida boidinii.	NAD	173-177	alcohol dehydrogenase 5 (class III), chi polypeptide	Homo sapiens	211-214
2459594-2	1988	Only when purified cytochrome b5 was added could an increased NADH consumption be observed indicating redox cycling of the BLM-Fe(III) complex.	NAD	62-66	cytochrome b5 type A	Homo sapiens	19-32
2459594-10	1988	The results reveal that the BLM-Fe(III) complex undergoes redox cycling by the microsomal NADH-dependent cytochrome b5 reductase-cytochrome b5 system.	NAD	90-94	cytochrome b5 type A	Homo sapiens	105-118
2459594-10	1988	The results reveal that the BLM-Fe(III) complex undergoes redox cycling by the microsomal NADH-dependent cytochrome b5 reductase-cytochrome b5 system.	NAD	90-94	cytochrome b5 type A	Homo sapiens	129-142
17191791-2	2004	We reproducibly observed that pol beta is an efficient covalent target for ADP-ribose polymers under standard conditions of enzymatically catalyzed ADP-ribosylation of betaNAD+ as a substrate.	NAD	168-176	DNA polymerase beta	Homo sapiens	30-38
15210723-2	2004	We here report that respiratory-deficient cells become strictly dependent on the Gpd2p isoform of the NAD(+)-linked glycerol-3-phosphate dehydrogenase (Gpd).	NAD	102-108	glycerol-3-phosphate dehydrogenase	Saccharomyces cerevisiae S288C	81-84
3136680-2	1988	The assay uses a coupled enzyme system in which liberated CO2 is reacted with phosphoenolpyruvate and phosphoenolpyruvate carboxylase to form oxaloacetate, which in turn is reduced by malate dehydrogenase to L-malate concomitantly with the oxidation of NADH to NAD.	NAD	253-257	phosphoenolpyruvate carboxykinase 1	Homo sapiens	102-133
3136680-2	1988	The assay uses a coupled enzyme system in which liberated CO2 is reacted with phosphoenolpyruvate and phosphoenolpyruvate carboxylase to form oxaloacetate, which in turn is reduced by malate dehydrogenase to L-malate concomitantly with the oxidation of NADH to NAD.	NAD	253-256	phosphoenolpyruvate carboxykinase 1	Homo sapiens	102-133
3348868-1	1988	New inhibitor or inhibitors of nicotinamide-adenine dinucleotide-dependent 15-hydroxyprostaglandin dehydrogenase (PGDH) activity were found in breast milk but not in powdered milk.	NAD	31-64	15-hydroxyprostaglandin dehydrogenase	Homo sapiens	114-118
15308223-3	2004	The resulting modified electrode was efficient for the ferricyanide-mediated NADH oxidation catalyzed by a diaphorase.	NAD	77-81	dihydrolipoamide dehydrogenase	Homo sapiens	107-117
33873776-13	2004	Sir2 is an NAD dependant histone deacetylase 37 VIII.	NAD	11-14	cytochrome c oxidase subunit 8A	Homo sapiens	48-52
3122752-1	1988	The thioredoxin peptide Trp-Cys-Gly-Pro-Cys-Lys, which contains the redox active dithiol, was found to be reduced by lipoamide in a coupled reaction with lipoamide dehydrogenase and NADH.	NAD	182-186	thioredoxin	Homo sapiens	4-15
15196936-0	2004	Dihydrolipoamide dehydrogenase from porcine heart catalyzes NADH-dependent scavenging of nitric oxide.	NAD	60-64	dihydrolipoamide dehydrogenase	Homo sapiens	0-30
3342923-2	1988	Neocuproine binding to ceruloplasmin markedly increases the chlorpromazine-ceruloplasmin-catalyzed oxidation of NADH.	NAD	112-116	ceruloplasmin	Homo sapiens	23-36
3342923-2	1988	Neocuproine binding to ceruloplasmin markedly increases the chlorpromazine-ceruloplasmin-catalyzed oxidation of NADH.	NAD	112-116	ceruloplasmin	Homo sapiens	75-88
15196936-1	2004	Dihydrolipoamide dehydrogenase (DLDH; EC 1.8.1.4) from porcine heart is capable of using nitric oxide (NO) as an electron acceptor, with NADH as the electron donor, forming nitrate in the reaction.	NAD	137-141	dihydrolipoamide dehydrogenase	Homo sapiens	0-30
3662534-7	1987	These data indicate that omega 6-hydroxy fatty acids, in addition to prostaglandins, are also substrates of the lung NAD+-dependent PGDH and that the enzyme does not require the cyclopentane ring of prostaglandins.	NAD	117-121	15-hydroxyprostaglandin dehydrogenase	Homo sapiens	132-136
15196936-1	2004	Dihydrolipoamide dehydrogenase (DLDH; EC 1.8.1.4) from porcine heart is capable of using nitric oxide (NO) as an electron acceptor, with NADH as the electron donor, forming nitrate in the reaction.	NAD	137-141	dihydrolipoamide dehydrogenase	Homo sapiens	32-36
15174865-2	2004	The beta N-O turns and beta N-O helices that involve a nine-membered-ring intramolecular hydrogen bond between NH(i)(+2) and CO(i), which have been found previously in peptides of beta(2,2)-aminoxy acids (NH(2)OCH(2)CMe(2)COOH), are also present in those beta(3)-aminoxy peptides.	NAD	125-130	potassium calcium-activated channel subfamily M regulatory beta subunit 2	Homo sapiens	180-188
3120517-1	1987	A number of prostaglandins and mono-hydroxylated fatty acids were investigated as substrates for NAD-dependent 15-prostaglandin dehydrogenase (15-PGDH) obtained from human HL-60 cells.	NAD	97-100	15-hydroxyprostaglandin dehydrogenase	Homo sapiens	143-150
15078171-1	2004	The enzyme nicotinamide mononucleotide adenylyltransferase (NMNAT), a member of the nucleotidyltransferase alpha/beta phosphodiesterase superfamily, catalyzes the reaction NMN + ATP = NAD + PPi, representing the final step in the biosynthesis of NAD, a molecule playing a fundamental role as a cofactor in cellular redox reactions.	NAD	184-187	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	60-65
3479888-3	1987	The strict requirement for NAD coupled with other characteristics of the reaction indicate that the enzyme is the NAD-dependent 15-prostaglandin dehydrogenase (15-PGDH).	NAD	27-30	15-hydroxyprostaglandin dehydrogenase	Homo sapiens	160-167
3479888-3	1987	The strict requirement for NAD coupled with other characteristics of the reaction indicate that the enzyme is the NAD-dependent 15-prostaglandin dehydrogenase (15-PGDH).	NAD	114-117	15-hydroxyprostaglandin dehydrogenase	Homo sapiens	160-167
3111756-6	1987	We propose the following hypothesis for the LDH-IgG complex formation: LDH can recognize the gamma-Fab region of IgG at the NAD+ binding site of the molecule, but the affinity of the LDH molecule for immunoglobulin is much weaker than that for NADH or 5"-AMP.	NAD	124-128	FA complementation group B	Homo sapiens	99-102
14516279-1	2004	NMNAT (nicotinamide 5"-mononucleotide adenylyltransferase; EC 2.7.7.1) catalyses the transfer of the adenylyl group from ATP to NMN to form NAD.	NAD	140-143	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	0-5
14516279-1	2004	NMNAT (nicotinamide 5"-mononucleotide adenylyltransferase; EC 2.7.7.1) catalyses the transfer of the adenylyl group from ATP to NMN to form NAD.	NAD	140-143	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	7-57
14977171-3	2004	Aerobically, it has been shown that the external NADH dehydrogenase, Nde1p and Nde2p, as well as the glycerol-3-phosphate dehydrogenase shuttle, comprising the cytoplasmic glycerol-3-phosphate dehydrogenase, Gpdlp, and the mitochondrial glycerol-3-phosphate dehydrogenase, Gut2p, are the most important mechanisms for mitochondrial oxidation of cytosolic NADH.	NAD	49-53	glycerol-3-phosphate dehydrogenase	Saccharomyces cerevisiae S288C	172-206
3107571-7	1987	These data suggest that, in both differentiated and undifferentiated HL-60 cells, an NAD-dependent enzyme, apparently 15-prostaglandin dehydrogenase (15-PGDH), is expressed and catalyzes the conversion of HHT to KHT.	NAD	85-88	15-hydroxyprostaglandin dehydrogenase	Homo sapiens	118-148
3107571-7	1987	These data suggest that, in both differentiated and undifferentiated HL-60 cells, an NAD-dependent enzyme, apparently 15-prostaglandin dehydrogenase (15-PGDH), is expressed and catalyzes the conversion of HHT to KHT.	NAD	85-88	15-hydroxyprostaglandin dehydrogenase	Homo sapiens	150-157
3630023-1	1987	Partially purified preparation of sorbitol dehydrogenase, isolated from hepatocytes of bovine liver tissue, was active at a wide range of pH exhibiting the maximal activity at pH 9.0 in presence of NAD but not of NADP.	NAD	198-201	sorbitol dehydrogenase	Bos taurus	34-56
3622897-3	1987	The ceruloplasmin oxidase activity is markedly enhanced when promazine is added in the presence of NADH; possibly through a change in enzyme conformation.	NAD	99-103	ceruloplasmin	Homo sapiens	4-17
3099790-0	1986	Modulation of rat polymorphonuclear leukocyte 5-lipoxygenase activity by 5-HPETE and NADH-dependent flavin inhibition.	NAD	85-89	arachidonate 5-lipoxygenase	Rattus norvegicus	46-60
16665101-1	1986	Bromphenol blue, which was reduced with dithionite, was found to support nitrate reduction catalyzed by squash NADH:nitrate reductase at a rate about 5 times greater than NADH with freshly prepared enzyme and 10 times or more with enzyme having been frozen and thawed.	NAD	111-115	nitrate reductase [NADH] 1	Zea mays	116-133
16665101-1	1986	Bromphenol blue, which was reduced with dithionite, was found to support nitrate reduction catalyzed by squash NADH:nitrate reductase at a rate about 5 times greater than NADH with freshly prepared enzyme and 10 times or more with enzyme having been frozen and thawed.	NAD	171-175	nitrate reductase [NADH] 1	Zea mays	116-133
16665101-5	1986	When squash NADH:nitrate reductase activity was inactivated with p-hydroxymercuribenzoate or denatured by heating at 40 degrees C, the bromphenol blue nitrate reductase activity was not lost.	NAD	12-16	nitrate reductase [NADH] 1	Zea mays	17-34
16665101-5	1986	When squash NADH:nitrate reductase activity was inactivated with p-hydroxymercuribenzoate or denatured by heating at 40 degrees C, the bromphenol blue nitrate reductase activity was not lost.	NAD	12-16	nitrate reductase [NADH] 1	Zea mays	151-168
16665054-3	1986	We demonstrate in this work that scutella of very young maize seedlings contain NADH NR almost exclusively and that this activity is gradually replaced, as the seedling ages, with NAD(P)H NR.	NAD	80-84	nitrate reductase [NADH] 1	Zea mays	85-87
16665054-4	1986	Leaves in the seedlings contain exclusively the NADH NR activity.	NAD	48-52	nitrate reductase [NADH] 1	Zea mays	53-55
16665054-9	1986	The same pattern of NADH NR and NAD(P)H NR activities was found in unorganized as well as in organized callus, in recognizable root-like and even in green shoot-like material, both activities being present in all these tissues.	NAD	20-24	nitrate reductase [NADH] 1	Zea mays	25-27
16665054-10	1986	An examination of the NR complement in different organs of a number of siblings originating from a cross involving transposon Mu-containing parents and having different levels of leaf NADH NR activity shows that the leaf NADH NR activity content and the scutellum NAD(P)H NR activity content are relatively independent of each other, indicating that the genetic programs specifying the NR content of these organs are not tightly coupled, if at all.	NAD	184-188	nitrate reductase [NADH] 1	Zea mays	189-191
16665054-10	1986	An examination of the NR complement in different organs of a number of siblings originating from a cross involving transposon Mu-containing parents and having different levels of leaf NADH NR activity shows that the leaf NADH NR activity content and the scutellum NAD(P)H NR activity content are relatively independent of each other, indicating that the genetic programs specifying the NR content of these organs are not tightly coupled, if at all.	NAD	184-188	nitrate reductase [NADH] 1	Zea mays	189-191
16665054-10	1986	An examination of the NR complement in different organs of a number of siblings originating from a cross involving transposon Mu-containing parents and having different levels of leaf NADH NR activity shows that the leaf NADH NR activity content and the scutellum NAD(P)H NR activity content are relatively independent of each other, indicating that the genetic programs specifying the NR content of these organs are not tightly coupled, if at all.	NAD	184-188	nitrate reductase [NADH] 1	Zea mays	189-191
16665054-10	1986	An examination of the NR complement in different organs of a number of siblings originating from a cross involving transposon Mu-containing parents and having different levels of leaf NADH NR activity shows that the leaf NADH NR activity content and the scutellum NAD(P)H NR activity content are relatively independent of each other, indicating that the genetic programs specifying the NR content of these organs are not tightly coupled, if at all.	NAD	184-188	nitrate reductase [NADH] 1	Zea mays	189-191
16665054-10	1986	An examination of the NR complement in different organs of a number of siblings originating from a cross involving transposon Mu-containing parents and having different levels of leaf NADH NR activity shows that the leaf NADH NR activity content and the scutellum NAD(P)H NR activity content are relatively independent of each other, indicating that the genetic programs specifying the NR content of these organs are not tightly coupled, if at all.	NAD	221-225	nitrate reductase [NADH] 1	Zea mays	22-24
3778875-15	1986	The product 3-fluorooxalacetate is thus released from phosphoenolpyruvate carboxykinase as the keto form and is reduced more rapidly by reduced nicotinamide adenine dinucleotide with malate dehydrogenase than by the occurrence of tautomerization.	NAD	144-177	malic enzyme 1	Gallus gallus	183-203
3955788-0	1986	Unique properties of NADPH- and NADH-dependent metabolism of p-nitroanisole catalyzed by cytochrome P-450 isozyme 2 in pulmonary and hepatic microsomal preparations from rabbits.	NAD	32-36	cytochrome P450 2B4	Oryctolagus cuniculus	89-115
3004411-4	1985	In addition, 8-N3-Ado was found to participate in the first step in the catalytic mechanism for AdoHcyase, resulting in conversion of enzyme-bound NAD+ to NADH, although it was not a substrate for the full enzyme-catalysed reaction.	NAD	147-151	adenosylhomocysteinase	Homo sapiens	96-105
3004411-4	1985	In addition, 8-N3-Ado was found to participate in the first step in the catalytic mechanism for AdoHcyase, resulting in conversion of enzyme-bound NAD+ to NADH, although it was not a substrate for the full enzyme-catalysed reaction.	NAD	155-159	adenosylhomocysteinase	Homo sapiens	96-105
3935115-6	1985	The P-450 hemoproteins involved primarily in both the NADH- and NADPH-supported deethylation of NP are the P1-450 type, i.e. they are markedly induced by MC and inhibited by alpha-napthoflavone.	NAD	54-58	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	107-113
2867182-3	1985	Ph CL 28A inhibited human placental PGDH non-competitively with regard both to substrate PGF2 alpha (Ki = 18.7 +/- 0.9 nM) and the NAD+ cofactor (Ki = 57.6 +/- 2.9 nM); inhibition was greatly reduced at pH greater than or equal to 8.0.	NAD	131-135	15-hydroxyprostaglandin dehydrogenase	Homo sapiens	36-40
4074667-2	1985	In the dark, N3-NAD can replace NAD as a cosubstrate for the mitochondrial D-(-)-beta-hydroxybutyrate dehydrogenase (BDH).	NAD	16-19	3-hydroxybutyrate dehydrogenase 1	Homo sapiens	75-115
4074667-2	1985	In the dark, N3-NAD can replace NAD as a cosubstrate for the mitochondrial D-(-)-beta-hydroxybutyrate dehydrogenase (BDH).	NAD	16-19	3-hydroxybutyrate dehydrogenase 1	Homo sapiens	117-120
4074667-3	1985	With purified, phospholipid-reconstituted BDH and NAD as the variable substrate, the apparent Km and Vmax values were respectively 0.25 mM and 62.5 mumol min-1 (mg of protein)-1.	NAD	50-53	3-hydroxybutyrate dehydrogenase 1	Homo sapiens	42-45
4074667-7	1985	The photoinhibition of BDH in the presence of N3-NAD was prevented nearly completely by addition of NADH, NAD plus beta-hydroxybutyrate, or NAD plus 2-methylmalonate and partially by addition of NAD.	NAD	100-104	3-hydroxybutyrate dehydrogenase 1	Homo sapiens	23-26
4074667-7	1985	The photoinhibition of BDH in the presence of N3-NAD was prevented nearly completely by addition of NADH, NAD plus beta-hydroxybutyrate, or NAD plus 2-methylmalonate and partially by addition of NAD.	NAD	49-52	3-hydroxybutyrate dehydrogenase 1	Homo sapiens	23-26
4074667-7	1985	The photoinhibition of BDH in the presence of N3-NAD was prevented nearly completely by addition of NADH, NAD plus beta-hydroxybutyrate, or NAD plus 2-methylmalonate and partially by addition of NAD.	NAD	100-103	3-hydroxybutyrate dehydrogenase 1	Homo sapiens	23-26
4074667-7	1985	The photoinhibition of BDH in the presence of N3-NAD was prevented nearly completely by addition of NADH, NAD plus beta-hydroxybutyrate, or NAD plus 2-methylmalonate and partially by addition of NAD.	NAD	100-103	3-hydroxybutyrate dehydrogenase 1	Homo sapiens	23-26
4074667-8	1985	Moreover, the presence of NADH prevented, and prior partial modification of BDH at the NAD(H)-protectable site by N-ethylmaleimide decreased, the incorporation of radioactivity into BDH from photoirradiated [3H]N3-NAD.	NAD	26-30	3-hydroxybutyrate dehydrogenase 1	Homo sapiens	76-79
4074667-8	1985	Moreover, the presence of NADH prevented, and prior partial modification of BDH at the NAD(H)-protectable site by N-ethylmaleimide decreased, the incorporation of radioactivity into BDH from photoirradiated [3H]N3-NAD.	NAD	26-30	3-hydroxybutyrate dehydrogenase 1	Homo sapiens	182-185
4074667-8	1985	Moreover, the presence of NADH prevented, and prior partial modification of BDH at the NAD(H)-protectable site by N-ethylmaleimide decreased, the incorporation of radioactivity into BDH from photoirradiated [3H]N3-NAD.	NAD	87-93	3-hydroxybutyrate dehydrogenase 1	Homo sapiens	76-79
4074667-8	1985	Moreover, the presence of NADH prevented, and prior partial modification of BDH at the NAD(H)-protectable site by N-ethylmaleimide decreased, the incorporation of radioactivity into BDH from photoirradiated [3H]N3-NAD.	NAD	87-93	3-hydroxybutyrate dehydrogenase 1	Homo sapiens	182-185
3987871-1	1985	In gerbil adrenal cortex the activity of intramitochondrial NADP-linked isocitric dehydrogenase (IDH) is up to 10-fold greater than the NAD-linked IDH.	NAD	60-63	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	97-100
16663992-1	1985	The proton translocation coupled to the electron flux from succinate, exogenous NADH, and NAD(+)-linked substrates (malate and isocitrate) to cytochrome c and to oxygen was studied in purified potato (Solanum tuberosum) mitochondria using oxygen and ferricyanide pulse techniques.	NAD	90-96	cytochrome c	Solanum tuberosum	142-154
6377948-4	1984	Preincubation with propiolaldehyde in the absence of NAD produces inactivation with K1 values of 1.6 microM for E1 and 1.8 microM for E2.	NAD	53-56	small nucleolar RNA, H/ACA box 73A	Homo sapiens	112-120
6323357-3	1984	The activity of glucose-6-phosphate dehydrogenase is greatly in excess of that of the kinase and was unaffected by the constituents of the kinase incubation medium (ATP, Mg2+ and NAD+) either alone or in combination.	NAD	179-183	glucose-6-phosphate 1-dehydrogenase	Cavia porcellus	16-49
6140197-1	1983	Mullerian inhibiting substance (MIS), a glycoprotein from the fetal testis causing regression of the embryonic Mullerian duct, can be inhibited in vitro in the presence of Mn2+ by a wide range of nucleotides including GTP, NAD, ATP, AMP, and several nonhydrolyzable synthetic ATP analogs.	NAD	223-226	anti-Mullerian hormone	Rattus norvegicus	32-35
6887859-6	1983	The C-2 reaction was greatly enhanced by NADPH or NADH and exhibited the greatest velocity in the microsomal formation in the presence of NADH.	NAD	50-54	complement C2	Rattus norvegicus	4-7
6887859-6	1983	The C-2 reaction was greatly enhanced by NADPH or NADH and exhibited the greatest velocity in the microsomal formation in the presence of NADH.	NAD	138-142	complement C2	Rattus norvegicus	4-7
6887859-7	1983	The C-2 reaction exhibited saturation with respect to substrate and NADH with apparent KM of 1.82 microM and 0.34 mM respectively and Vmax of 81.3-76.3 pmol/mg protein/60 min.	NAD	68-72	complement C2	Rattus norvegicus	4-7
6887859-9	1983	These data indicate that male rat brain estrogen hydroxylase is specific for the C-2 position, is NADH dependent and thus different from the corresponding liver enzyme.	NAD	98-102	complement C2	Rattus norvegicus	81-84
6830592-6	1983	The Michaelis constants of bacterial luciferase for FMNH2 and decanal were 3 X 10(-6) M and 8 X 10(-7) M, respectively, and those of oxidoreductase for FMN and NADH were 6.1 X 10(-6) M and 1.6 X 10(-5) M, respectively.	NAD	160-164	formin 1	Homo sapiens	52-55
6634835-7	1983	Deuterium transfer from chiral [1-2H] ethanols and [2-2H] glycerol in hepatocytes indicated that cytosolic malate dehydrogenase and lactate dehydrogenase were not completely equilibrated, whereas there was no difference in the utilization of NADH formed at alcohol dehydrogenase and at glycerol-3-phosphate dehydrogenase.	NAD	242-246	malate dehydrogenase 1	Homo sapiens	97-127
7161259-6	1982	The synergistic effect with the addition of the NADH-linked electron transport system was more remarkable at the lower reduction levels of cytochrome b5 in the steady state.	NAD	48-52	cytochrome b5 type A	Homo sapiens	139-152
14977171-3	2004	Aerobically, it has been shown that the external NADH dehydrogenase, Nde1p and Nde2p, as well as the glycerol-3-phosphate dehydrogenase shuttle, comprising the cytoplasmic glycerol-3-phosphate dehydrogenase, Gpdlp, and the mitochondrial glycerol-3-phosphate dehydrogenase, Gut2p, are the most important mechanisms for mitochondrial oxidation of cytosolic NADH.	NAD	49-53	glycerol-3-phosphate dehydrogenase	Saccharomyces cerevisiae S288C	172-206
14977171-3	2004	Aerobically, it has been shown that the external NADH dehydrogenase, Nde1p and Nde2p, as well as the glycerol-3-phosphate dehydrogenase shuttle, comprising the cytoplasmic glycerol-3-phosphate dehydrogenase, Gpdlp, and the mitochondrial glycerol-3-phosphate dehydrogenase, Gut2p, are the most important mechanisms for mitochondrial oxidation of cytosolic NADH.	NAD	49-53	glycerol-3-phosphate dehydrogenase	Saccharomyces cerevisiae S288C	273-278
14522996-9	2003	NAD+ analogues including beta-2"-deoxy-2"-fluororibo-NAD+ and a His-to-Ala mutant were used to probe the mechanism of nicotinamide-ribosyl cleavage and acetyl group transfer.	NAD	0-4	potassium calcium-activated channel subfamily M regulatory beta subunit 2	Homo sapiens	25-31
7092806-2	1982	The pKa of the phenolic hydroxy group of the Tyr(3NO2)-237 residue in pig heart [Tyr(3NO2)237]lactate dehydrogenase is 7.2 in the apoenzyme, 7.4 in the enzyme-NADH complex and 7.8 in the enzyme-NADH-oxamate complex.	NAD	159-163	protein kinase cAMP-activated catalytic subunit alpha	Sus scrofa	4-7
7092806-8	1982	Temperature-jump relaxation experiments of the enzyme saturated with NADH but fractionally saturated with oxamate are interpreted to show that the pKa of the nitrotyrosine residue responds to a protein rearrangement after oxamate binds to the binary enzyme-NADH complex.	NAD	69-73	protein kinase cAMP-activated catalytic subunit alpha	Sus scrofa	147-150
7092806-8	1982	Temperature-jump relaxation experiments of the enzyme saturated with NADH but fractionally saturated with oxamate are interpreted to show that the pKa of the nitrotyrosine residue responds to a protein rearrangement after oxamate binds to the binary enzyme-NADH complex.	NAD	257-261	protein kinase cAMP-activated catalytic subunit alpha	Sus scrofa	147-150
6284133-0	1982	Evidence that poly(ADP-ribose) polymerase is involved in the loss of NAD from cultured rat liver cells.	NAD	69-72	poly (ADP-ribose) polymerase 1	Rattus norvegicus	14-41
7128914-0	1982	Nicotinamide adenine dinucleotide and nicotinamide adenine dinucleotide phosphate-dependent reduction of mammalian hepatic microsomal cytochrome b5: some properties of the enzyme system catalyzing the endogenous reduction of pyridine nucleotides.	NAD	0-33	cytochrome b5 type A	Homo sapiens	134-147
7128914-6	1982	The rates of reduction of cytochrome b5 and auto-oxidation of reduced cytochrome b5 were, however, much slower in NAD+ supplemented reaction media than in those supplemented with NADH.	NAD	114-118	cytochrome b5 type A	Homo sapiens	26-39
14609736-0	2003	Adenosine binding sites at S-adenosylhomocysteine hydrolase are controlled by the NAD+/NADH ratio of the enzyme.	NAD	82-86	adenosylhomocysteinase	Bos taurus	27-59
7128914-6	1982	The rates of reduction of cytochrome b5 and auto-oxidation of reduced cytochrome b5 were, however, much slower in NAD+ supplemented reaction media than in those supplemented with NADH.	NAD	114-118	cytochrome b5 type A	Homo sapiens	70-83
7128914-6	1982	The rates of reduction of cytochrome b5 and auto-oxidation of reduced cytochrome b5 were, however, much slower in NAD+ supplemented reaction media than in those supplemented with NADH.	NAD	179-183	cytochrome b5 type A	Homo sapiens	26-39
7128914-6	1982	The rates of reduction of cytochrome b5 and auto-oxidation of reduced cytochrome b5 were, however, much slower in NAD+ supplemented reaction media than in those supplemented with NADH.	NAD	179-183	cytochrome b5 type A	Homo sapiens	70-83
14609736-0	2003	Adenosine binding sites at S-adenosylhomocysteine hydrolase are controlled by the NAD+/NADH ratio of the enzyme.	NAD	87-91	adenosylhomocysteinase	Bos taurus	27-59
14612543-5	2003	We identified the first low molecular weight compound, designated FK866, which induces apoptosis by highly specific, noncompetitive inhibition of nicotinamide phosphoribosyltransferase (NAPRT), a key enzyme in the regulation of NAD+ biosynthesis from the natural precursor nicotinamide.	NAD	228-232	nicotinamide phosphoribosyltransferase	Homo sapiens	146-184
14612543-5	2003	We identified the first low molecular weight compound, designated FK866, which induces apoptosis by highly specific, noncompetitive inhibition of nicotinamide phosphoribosyltransferase (NAPRT), a key enzyme in the regulation of NAD+ biosynthesis from the natural precursor nicotinamide.	NAD	228-232	nicotinamide phosphoribosyltransferase	Homo sapiens	186-191
7034777-9	1981	The analogue 3-pyridine-carboxaldehyde adenine dinucleotide, a potent activator of the aldehyde dehydrogenase, was a poor substrate compared with NAD+.	NAD	146-150	Aldehyde dehydrogenase	Escherichia coli	87-109
12975482-6	2003	Incubation with NAD+ prevented cytomix-induced derangements in the expression and localization of the tight junction proteins occludin and zonula occludens-1 in Caco-2 cells.	NAD	16-20	occludin	Homo sapiens	126-134
6265441-2	1981	During oxidation of exogenous NADH there is a fast and complete reduction of cytochrome b5 while endogenous or added exogenous cytochrome c become 10-15% and 100% reduced, respectively.	NAD	30-34	cytochrome b5 type A	Homo sapiens	77-90
6265441-3	1981	The reoxidation of cytochrome b5, after exhaustion of NADH, precedes that of cytochrome c.	NAD	54-58	cytochrome b5 type A	Homo sapiens	19-32
19330139-0	2003	Spectroscopic Analyses of Oscillations in ECTO-NOX-Catalyzed Oxidation of NADH.	NAD	74-78	tripartite motif containing 33	Homo sapiens	42-46
6265441-4	1981	NADH oxidation is blocked by mersalyl, an inhibitor of NADH-cytochrome b5 reductase.	NAD	0-4	cytochrome b5 type A	Homo sapiens	60-73
6265441-8	1981	It is concluded that aerobic oxidation of exogenous NADH involves the following pathway: NADH leads to NADH-cytochrome b5 reductase leads to cytochrome b5 leads to intermembrane cytochrome c leads to cytochrome oxidase leads to oxygen.	NAD	52-56	cytochrome b5 type A	Homo sapiens	108-121
6265441-8	1981	It is concluded that aerobic oxidation of exogenous NADH involves the following pathway: NADH leads to NADH-cytochrome b5 reductase leads to cytochrome b5 leads to intermembrane cytochrome c leads to cytochrome oxidase leads to oxygen.	NAD	52-56	cytochrome b5 type A	Homo sapiens	141-154
6265441-8	1981	It is concluded that aerobic oxidation of exogenous NADH involves the following pathway: NADH leads to NADH-cytochrome b5 reductase leads to cytochrome b5 leads to intermembrane cytochrome c leads to cytochrome oxidase leads to oxygen.	NAD	89-93	cytochrome b5 type A	Homo sapiens	108-121
6265441-8	1981	It is concluded that aerobic oxidation of exogenous NADH involves the following pathway: NADH leads to NADH-cytochrome b5 reductase leads to cytochrome b5 leads to intermembrane cytochrome c leads to cytochrome oxidase leads to oxygen.	NAD	89-93	cytochrome b5 type A	Homo sapiens	141-154
19330139-1	2003	Spectroscopic strategies that substantiate periodic oscillations in low rates of NADH oxidation exhibited by ECTO-NOX proteins at the animal and plant cell surface are described.	NAD	81-85	tripartite motif containing 33	Homo sapiens	109-113
6972374-9	1981	An electron flow from NADH via cytochrome b5 can be utilized as the second electron for the O-deethylase reaction of 7-ethoxycoumarin catalyzed by reconstituted systems containing P-450(2) and P-448(2) when both NADH-cytochrome b5 reductase and cytochrome b5 are included in the system, although the cytochrome has no stimulatory effect at all on the deethylase activity of these two cytochrome P-450"s.	NAD	22-26	cytochrome b5 type A	Homo sapiens	31-44
12727869-5	2003	POS5 encodes a protein that is homologous to NAD(+) and NADH kinases, and we show here that recombinant Pos5p has NADH kinase activity.	NAD	45-51	NADH kinase	Saccharomyces cerevisiae S288C	0-4
6972374-9	1981	An electron flow from NADH via cytochrome b5 can be utilized as the second electron for the O-deethylase reaction of 7-ethoxycoumarin catalyzed by reconstituted systems containing P-450(2) and P-448(2) when both NADH-cytochrome b5 reductase and cytochrome b5 are included in the system, although the cytochrome has no stimulatory effect at all on the deethylase activity of these two cytochrome P-450"s.	NAD	22-26	cytochrome b5 type A	Homo sapiens	217-230
6972374-9	1981	An electron flow from NADH via cytochrome b5 can be utilized as the second electron for the O-deethylase reaction of 7-ethoxycoumarin catalyzed by reconstituted systems containing P-450(2) and P-448(2) when both NADH-cytochrome b5 reductase and cytochrome b5 are included in the system, although the cytochrome has no stimulatory effect at all on the deethylase activity of these two cytochrome P-450"s.	NAD	22-26	cytochrome b5 type A	Homo sapiens	217-230
12727869-5	2003	POS5 encodes a protein that is homologous to NAD(+) and NADH kinases, and we show here that recombinant Pos5p has NADH kinase activity.	NAD	45-51	NADH kinase	Saccharomyces cerevisiae S288C	104-109
7286604-0	1981	NAD-linked mitochondrial aldehyde dehydrogenase in the rat testis.	NAD	0-3	aldehyde dehydrogenase 2 family member	Rattus norvegicus	11-47
12892045-7	2003	While NAD(+)-dependent glutamate dehydrogenase (GDH-NAD+) activity also rose progressively during the recovering time, the cognate NADH-dependent glutamate dehydrogenase (GDH-NADH) activity decreased.	NAD	6-12	glutamate dehydrogenase	Solanum lycopersicum	171-174
12892045-7	2003	While NAD(+)-dependent glutamate dehydrogenase (GDH-NAD+) activity also rose progressively during the recovering time, the cognate NADH-dependent glutamate dehydrogenase (GDH-NADH) activity decreased.	NAD	131-135	glutamate dehydrogenase	Solanum lycopersicum	171-174
12892045-7	2003	While NAD(+)-dependent glutamate dehydrogenase (GDH-NAD+) activity also rose progressively during the recovering time, the cognate NADH-dependent glutamate dehydrogenase (GDH-NADH) activity decreased.	NAD	175-179	glutamate dehydrogenase	Solanum lycopersicum	171-174
12892045-8	2003	This result allows us to propose that the ammonia produced by the stress-induced protein catabolism is detoxified and re-assimilated by the GDH-NADH isoenzyme.	NAD	144-148	glutamate dehydrogenase	Solanum lycopersicum	140-143
12646198-1	2003	Retinol dehydrogenase-4 (RoDH-4) converts retinol and 13-cis-retinol to corresponding aldehydes in human liver and skin in the presence of NAD(+).	NAD	139-145	retinol dehydrogenase 16	Homo sapiens	0-23
7449761-0	1980	Direct enzyme titration curve of NADH: cytochrome b5 reductase by combined isoelectric focusing/electrophoresis.	NAD	33-37	cytochrome b5 type A	Homo sapiens	39-52
7449761-2	1980	Methemoglobin reduction in human red cells involves successively an electron transport from NADH to a soluble form of cytochrome b5 (step 1) and from cytochrome b5 to methemoglobin (step 2).	NAD	92-96	cytochrome b5 type A	Homo sapiens	118-131
7449761-3	1980	Step 1 is catalysed by an enzyme, soluble NADH:cytochrome b5 reductase (EC 1.6.2.2).	NAD	42-46	cytochrome b5 type A	Homo sapiens	47-60
7008786-1	1980	A number of reactive dichlorotriazine dyes specifically and irreversibly inactivate pig heart lactate dehydrogenase, yeast glucose 6-phosphate dehydrogenase and yeast hexokinase at sites competitive with NAD+, NADP+, and ATP respectively.	NAD	204-208	glucose-6-phosphate dehydrogenase	Saccharomyces cerevisiae S288C	123-156
7388066-6	1980	The results obtained suggest that upon interaction with NAD the brain GDH reveals a relatively higher affinity for L-glutamate and L-ketoglutarate as compared to the liver enzyme.	NAD	56-59	glutamate dehydrogenase 1	Homo sapiens	70-73
7424738-7	1980	The fourth human brain enzyme ("SSA reductase") differs from the other forms in its ability to use NADH as well as or better than NADPH as cofactor, and in its molecular weight, which is nearly twice that of the other forms.	NAD	99-103	aldo-keto reductase family 7 member A2	Homo sapiens	17-46
227369-9	1979	This is the only route for oxidation of NADH and succinate in the cytochrome c-deficient mutant in all growth conditions.	NAD	40-44	MEXAM1_RS12150	Methylobacterium extorquens AM1	66-78
227369-10	1979	During carbon-limited growth the cytochrome c becomes bound to the membrane in such a way that it can mediate between cytochromes b and a/a(3), hence becoming involved in proton translocation and ATP synthesis during NADH and succinate oxidation.	NAD	217-221	MEXAM1_RS12150	Methylobacterium extorquens AM1	33-45
721806-3	1978	After [3H]ADP-ribosylation by [3H]nad+ and diphtheria toxin, EF-2 was digested with trypsin and a homogeneous [3H]ADP-ribosyl peptide was isolated by chromatography on DEAE-Sephadex and dihydroxyboryl-substituted cellulose.	NAD	34-38	elongation factor 2	Saccharomyces cerevisiae S288C	61-65
196649-2	1977	The Michaelis constants for EF-2 and NAD are 0.15 and 1.4 muM, respectively.	NAD	37-40	eukaryotic translation elongation factor 2	Homo sapiens	28-32
196649-4	1977	Based on these and earlier results, we propose an ordered sequential mechanism for the reaction; the sequence of binding of substrates is NAD, followed by EF-2.	NAD	138-141	eukaryotic translation elongation factor 2	Homo sapiens	155-159
19038-1	1977	Hepatic NADH-cytochrome b5 reductase was reduced by 1 mol of dithionite or NADH per mol of enzyme-bound FAD, without forming a stable semiquinone or intermediate during the titrations.	NAD	8-12	cytochrome b5 type A	Homo sapiens	13-26
19038-6	1977	Potentiometric titration of NADH-cytochrome b5 reductase at pH 7.0 with dithionite gave a midpoint potential of -258 mV; titration with NADH gave -160 mV.	NAD	28-32	cytochrome b5 type A	Homo sapiens	33-46
19038-6	1977	Potentiometric titration of NADH-cytochrome b5 reductase at pH 7.0 with dithionite gave a midpoint potential of -258 mV; titration with NADH gave -160 mV.	NAD	136-140	cytochrome b5 type A	Homo sapiens	33-46
15177-2	1977	Reduced nicotinamide adenine dinucleotide (NADH) or reduced nicotinamide adenine dinucleotide phosphate (NADPH) (0.87 mM) served as electron donors, and effectively prompted the delta6-desaturase activities with yields of about 1.1 to 1.3 nmol per mg of protein in 10 min.	NAD	8-41	fatty acid desaturase 2	Rattus norvegicus	178-195
15177-2	1977	Reduced nicotinamide adenine dinucleotide (NADH) or reduced nicotinamide adenine dinucleotide phosphate (NADPH) (0.87 mM) served as electron donors, and effectively prompted the delta6-desaturase activities with yields of about 1.1 to 1.3 nmol per mg of protein in 10 min.	NAD	43-47	fatty acid desaturase 2	Rattus norvegicus	178-195
12751-8	1976	A partial purification of the NAD-linked "malic" enzyme from Glossina was effected by DEAE-cellulose chromatography, which separated the enzyme from malate dehydrogenase and NADP-linked "malic" enzyme, but not from oxaloacetate decarboxylase.	NAD	30-33	Malate dehydrogenase 1	Drosophila melanogaster	149-169
12646198-1	2003	Retinol dehydrogenase-4 (RoDH-4) converts retinol and 13-cis-retinol to corresponding aldehydes in human liver and skin in the presence of NAD(+).	NAD	139-145	retinol dehydrogenase 16	Homo sapiens	25-31
15206771-9	2003	Tryptophan-NAD pathway was initiated by cleavage of indole ring of tryptophan by TDO in the liver and IDO in many organs.	NAD	11-14	indoleamine 2,3-dioxygenase 1	Rattus norvegicus	102-105
177074-5	1976	This antimycin-A-resistant, NADH-consuming respiration is absent, when no cytochrome c is added to the reaction medium.	NAD	28-32	cytochrome c	Solanum tuberosum	74-86
14695919-4	2003	The reduction of ubiquinone by lipoamide dehydrogenase and glutathione reductase is potently stimulated by zinc and the highest rate of reduction is achieved at acidic pH and the rates are equal with either NADPH or NADH as co-factors.	NAD	216-220	dihydrolipoamide dehydrogenase	Homo sapiens	31-54
167022-3	1975	When a small amount of NADH-cytochrome b5 reductase is bound liposomes simultaneously with cytochrome b5, the two proteins catalyze the reduction of cytochrome c by NADH.	NAD	23-27	cytochrome b5 type A	Homo sapiens	28-41
167022-3	1975	When a small amount of NADH-cytochrome b5 reductase is bound liposomes simultaneously with cytochrome b5, the two proteins catalyze the reduction of cytochrome c by NADH.	NAD	23-27	cytochrome b5 type A	Homo sapiens	91-104
239543-0	1975	Role of cytochrome b5 in the NADH synergism of NADPH-dependent reactions of the cytochrome P-450 monooxygenase system of hepatic microsomes.	NAD	29-33	cytochrome b5 type A	Homo sapiens	8-21
239543-0	1975	Role of cytochrome b5 in the NADH synergism of NADPH-dependent reactions of the cytochrome P-450 monooxygenase system of hepatic microsomes.	NAD	29-33	cytochrome P450 family 20 subfamily A member 1	Homo sapiens	80-110
1138993-3	1975	Enzymic oxidation of UDP-glucose-6-3-H with calf liver UDP-glucose dehydrogenase was found to proceed with direct transfer of the hydrogen from C-6 of UDP-glucose onto NAD.	NAD	168-171	UDP-glucose 6-dehydrogenase	Bos taurus	55-80
4374132-0	1974	Reduced nicotinamide adenine dinucleotide-cytochrome b5 reductase and cytochrome b5 as electron carriers in NADH-supported cytochrome P-450 -dependent enzyme activities in liver microsomes.	NAD	108-112	cytochrome b5 type A	Homo sapiens	42-55
4374132-0	1974	Reduced nicotinamide adenine dinucleotide-cytochrome b5 reductase and cytochrome b5 as electron carriers in NADH-supported cytochrome P-450 -dependent enzyme activities in liver microsomes.	NAD	108-112	cytochrome b5 type A	Homo sapiens	70-83
4156646-1	1974	Quantitative evaluation of the cytochrome b5 content in the NADPH and NADH oxidation chains].	NAD	70-74	cytochrome b5 type A	Homo sapiens	31-44
4366168-2	1974	The involvement of cytochrome b5 in the NADH-dependent hydroxylation of 3,4-benzpyrene by a reconstituted cytochrome P-448-containing system.	NAD	40-44	cytochrome b5 type A	Homo sapiens	19-32
4151403-0	1974	Immunochemical evidence for the participation of cytochrome b5 in the NADH synergism of the NADPH-dependent mono-oxidase system of hepatic microsomes.	NAD	70-74	cytochrome b5 type A	Homo sapiens	49-62
19396987-8	1974	(4) It is postulated that with pyruvate as substrate, recycling of carbon via pyruvate carboxylase, phosphoenolpyruvate carboxylase and pyruvate kinase (ATP: pyruvate phosphotransferase, EC 2.7.1.40) is an important, energy-requiring, mechanism for the transfer of the proportion of NADH not directly associated with gluconeogenesis.	NAD	283-287	phosphoenolpyruvate carboxykinase 1	Homo sapiens	100-131
16658530-3	1973	Activity of the root and scutella nitrate reductase was obtained with either NADH or NADPH, but that of the root enzyme with NADPH was only demonstrated in the absence of phosphate.Before leaf expansion, the nitrate reductase in the maize seedling was mainly in the scutellum.	NAD	77-81	nitrate reductase [NADH] 1	Zea mays	34-51
4297937-6	1968	The results are interpreted as indicating that the cyclization proceeds by an aldol condensation in which C-5 is oxidized by NAD(+) in a tightly-bound ternary complex, and that the apparent loss of (3)H when untreated enzyme is used is due to an isotope effect.	NAD	125-131	complement C5	Rattus norvegicus	106-109
16656864-1	1968	With respect to cofactor requirements, NADH, and FMNH(2) were equally effective as electron donors for nitrate reductase obtained from leaves of maize, marrow, and spinach, when the cofactors were supplied in optimal concentrations.	NAD	39-43	nitrate reductase [NADH] 1	Zea mays	103-120
16656864-5	1968	Unity of NADH to FMNH(2) activities were obtained during: A) purification procedures (4 step, 30-fold); B) induction of nitrate reductase in corn seedlings with nitrate; and C) inactivation of nitrate reductase in intact or excised corn seedlings.	NAD	9-13	nitrate reductase [NADH] 1	Zea mays	120-137
16656864-5	1968	Unity of NADH to FMNH(2) activities were obtained during: A) purification procedures (4 step, 30-fold); B) induction of nitrate reductase in corn seedlings with nitrate; and C) inactivation of nitrate reductase in intact or excised corn seedlings.	NAD	9-13	nitrate reductase [NADH] 1	Zea mays	193-210
16656864-6	1968	The NADH- and FMNH(2)-dependent activities were not additive.A half-life for nitrate reductase of approximately 4 hours was estimated from the inactivation studies with excised corn seedlings.	NAD	4-8	nitrate reductase [NADH] 1	Zea mays	77-94
16656864-8	1968	This was verified by reactivation with exogenous cysteine.Based on these current findings, and previous work, it is concluded that nitrate reductase is a single moiety with the ability to utilize either NADH or FMNH(2) as cofactor.	NAD	203-207	nitrate reductase [NADH] 1	Zea mays	131-148
16656864-9	1968	However the high concentration of FMNH(2) required for optimal activity suggests that in vivo NADH is the electron donor and that nitrate reductase in higher plants should be designated NADH:nitrate reductase (E.C.	NAD	94-98	nitrate reductase [NADH] 1	Zea mays	191-208
16656864-9	1968	However the high concentration of FMNH(2) required for optimal activity suggests that in vivo NADH is the electron donor and that nitrate reductase in higher plants should be designated NADH:nitrate reductase (E.C.	NAD	186-190	nitrate reductase [NADH] 1	Zea mays	130-147
16656864-9	1968	However the high concentration of FMNH(2) required for optimal activity suggests that in vivo NADH is the electron donor and that nitrate reductase in higher plants should be designated NADH:nitrate reductase (E.C.	NAD	186-190	nitrate reductase [NADH] 1	Zea mays	191-208
4291561-9	1967	In the thorax, cytochrome c oxidase and the dehydrogenases for glycerophosphate, isocitrate (NAD-dependent), succinate and malate appeared initially in small particles (less than 1mu in diameter).	NAD	93-96	Cytochrome c oxidase subunit 4	Drosophila melanogaster	15-35
33689947-5	2021	Our results showed that exposure to PFOS inhibited silent information regulator 1 (SIRT1) activity, and molecular simulation showed PFOS could fit into the pocket overlapped with the nicotinamide adenine dinucleotide (NAD+) binding cavity in SIRT1.	NAD	183-216	sirtuin 1	Mus musculus	51-81
33689947-5	2021	Our results showed that exposure to PFOS inhibited silent information regulator 1 (SIRT1) activity, and molecular simulation showed PFOS could fit into the pocket overlapped with the nicotinamide adenine dinucleotide (NAD+) binding cavity in SIRT1.	NAD	183-216	sirtuin 1	Mus musculus	83-88
33689947-5	2021	Our results showed that exposure to PFOS inhibited silent information regulator 1 (SIRT1) activity, and molecular simulation showed PFOS could fit into the pocket overlapped with the nicotinamide adenine dinucleotide (NAD+) binding cavity in SIRT1.	NAD	183-216	sirtuin 1	Mus musculus	242-247
33689947-5	2021	Our results showed that exposure to PFOS inhibited silent information regulator 1 (SIRT1) activity, and molecular simulation showed PFOS could fit into the pocket overlapped with the nicotinamide adenine dinucleotide (NAD+) binding cavity in SIRT1.	NAD	218-222	sirtuin 1	Mus musculus	51-81
33689947-5	2021	Our results showed that exposure to PFOS inhibited silent information regulator 1 (SIRT1) activity, and molecular simulation showed PFOS could fit into the pocket overlapped with the nicotinamide adenine dinucleotide (NAD+) binding cavity in SIRT1.	NAD	218-222	sirtuin 1	Mus musculus	83-88
33689947-5	2021	Our results showed that exposure to PFOS inhibited silent information regulator 1 (SIRT1) activity, and molecular simulation showed PFOS could fit into the pocket overlapped with the nicotinamide adenine dinucleotide (NAD+) binding cavity in SIRT1.	NAD	218-222	sirtuin 1	Mus musculus	242-247
33958376-0	2021	Salvaging the endothelium in acute respiratory distress syndrome: a druggable intersection between TLR4 and NAD+ signalling.	NAD	108-112	toll like receptor 4	Homo sapiens	99-103
14695919-4	2003	The reduction of ubiquinone by lipoamide dehydrogenase and glutathione reductase is potently stimulated by zinc and the highest rate of reduction is achieved at acidic pH and the rates are equal with either NADPH or NADH as co-factors.	NAD	216-220	glutathione-disulfide reductase	Homo sapiens	59-80
12602510-4	2002	From the viewpoint of the metabolic functions of citrin as aspartate glutamate carrier in urea synthesis and NADH shuttle, symptoms of CTLN2 and neonatal intrahepatic cholestasis caused by citrin deficiency are analyzed.	NAD	109-113	solute carrier family 25 member 13	Homo sapiens	49-55
33444676-1	2021	Sirtuin 6 (SIRT6), a member of the Sirtuin family, acts as nicotinamide adenine dinucleotide (NAD)-dependent protein deacetylase, mono-adenosine diphosphate (ADP)-ribosyltransferase, and fatty acid deacylase, and plays critical roles in inflammation, aging, glycolysis, and DNA repair.	NAD	59-92	sirtuin 6	Rattus norvegicus	0-9
33444676-1	2021	Sirtuin 6 (SIRT6), a member of the Sirtuin family, acts as nicotinamide adenine dinucleotide (NAD)-dependent protein deacetylase, mono-adenosine diphosphate (ADP)-ribosyltransferase, and fatty acid deacylase, and plays critical roles in inflammation, aging, glycolysis, and DNA repair.	NAD	59-92	sirtuin 6	Rattus norvegicus	11-16
33444676-1	2021	Sirtuin 6 (SIRT6), a member of the Sirtuin family, acts as nicotinamide adenine dinucleotide (NAD)-dependent protein deacetylase, mono-adenosine diphosphate (ADP)-ribosyltransferase, and fatty acid deacylase, and plays critical roles in inflammation, aging, glycolysis, and DNA repair.	NAD	94-97	sirtuin 6	Rattus norvegicus	0-9
33444676-1	2021	Sirtuin 6 (SIRT6), a member of the Sirtuin family, acts as nicotinamide adenine dinucleotide (NAD)-dependent protein deacetylase, mono-adenosine diphosphate (ADP)-ribosyltransferase, and fatty acid deacylase, and plays critical roles in inflammation, aging, glycolysis, and DNA repair.	NAD	94-97	sirtuin 6	Rattus norvegicus	11-16
12602510-4	2002	From the viewpoint of the metabolic functions of citrin as aspartate glutamate carrier in urea synthesis and NADH shuttle, symptoms of CTLN2 and neonatal intrahepatic cholestasis caused by citrin deficiency are analyzed.	NAD	109-113	solute carrier family 25 member 13	Homo sapiens	189-195
12424587-2	2002	Citrin, an aspartate glutamate carrier in mitochondria, is an essential component of the malate-aspartate NADH shuttle.	NAD	106-110	solute carrier family 25 member 13	Homo sapiens	0-6
12271621-1	2002	The selenium(IV) diimide AdN=Se=NAd (Ad = 1-adamantyl) adopts a monomeric structure with a Z,E configuration in the solid state whereas the seleninylamine OSe(mu-NBut)2SeO crystallizes as the cis-dimer.	NAD	32-35	complement factor D	Homo sapiens	25-28
12200299-8	2002	Metabolic control analysis values calculated by the model indicate that the NAD(+)-dependent glycerol 3-phosphate dehydrogenase-catalyzed reaction has a flux control coefficient (C(J)v1) of approximately 0.85 and exercises the majority of the control of flux through the pathway.	NAD	76-82	glycerol-3-phosphate dehydrogenase	Saccharomyces cerevisiae S288C	93-127
12065597-3	2002	Efficient assembly of biotin synthase as a model Fe/S protein required anaerobic conditions, dithiothreitol, cysteine, ATP, and NADH.	NAD	128-132	biotin synthase	Saccharomyces cerevisiae S288C	22-37
12135624-5	2002	The EtOH loss was significantly higher (than the loss observed during metabolism of EtOH alone) only in EtOH-Hex and EtOH-Hep systems, which may be explained by the fact that reoxidation of NADH to NAD+ is quicker in these systems than dissociation of the alcohol dehydrogenase (ADH)-NADH complex.	NAD	190-194	hematopoietically expressed homeobox	Rattus norvegicus	109-112
12135624-5	2002	The EtOH loss was significantly higher (than the loss observed during metabolism of EtOH alone) only in EtOH-Hex and EtOH-Hep systems, which may be explained by the fact that reoxidation of NADH to NAD+ is quicker in these systems than dissociation of the alcohol dehydrogenase (ADH)-NADH complex.	NAD	198-202	hematopoietically expressed homeobox	Rattus norvegicus	109-112
12135624-5	2002	The EtOH loss was significantly higher (than the loss observed during metabolism of EtOH alone) only in EtOH-Hex and EtOH-Hep systems, which may be explained by the fact that reoxidation of NADH to NAD+ is quicker in these systems than dissociation of the alcohol dehydrogenase (ADH)-NADH complex.	NAD	284-288	hematopoietically expressed homeobox	Rattus norvegicus	109-112
12054821-2	2002	Compared to the structures of bovine GDH that were complexed with coenzyme and substrate, the NAD binding domain is rotated away from the glutamate-binding domain.	NAD	94-97	glutamate dehydrogenase 1, mitochondrial	Bos taurus	37-40
12269395-5	2002	Cyanamide, a potent inhibitor of aldehyde dehydrogenase (ALDH), markedly decreased the formation of NLA from racemic NDP in the enzyme reaction system of rat liver mitochondria with NAD+.	NAD	182-186	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	33-55
12269395-5	2002	Cyanamide, a potent inhibitor of aldehyde dehydrogenase (ALDH), markedly decreased the formation of NLA from racemic NDP in the enzyme reaction system of rat liver mitochondria with NAD+.	NAD	182-186	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	57-61
11788603-3	2002	Human NMNAT displays unique dual substrate specificity toward both NMN and NaMN, thus flexible in participating in both de novo and salvage pathways of NAD synthesis.	NAD	152-155	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	6-11
11788603-6	2002	We have solved the crystal structures of human NMNAT in complex with NAD, deamido-NAD, and a non-hydrolyzable TAD analogue beta-CH(2)-TAD.	NAD	69-72	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	47-52
11939620-11	2002	CONCLUSION: We conclude that insulin increases cGMP production in VSMC with iNOS by raising the cell NADH/NAD+ redox state, which may increase the availability of iNOS-derived NO.	NAD	101-105	nitric oxide synthase 2	Canis lupus familiaris	76-80
11816029-3	2002	A yeast strain in which the NAMase gene, hereafter named PNC1, was deleted shows a decreased intracellular NAD(+) concentration, consistent with the loss of NAMase activity in the null mutant.	NAD	107-113	nicotinamidase	Saccharomyces cerevisiae S288C	28-34
11816029-3	2002	A yeast strain in which the NAMase gene, hereafter named PNC1, was deleted shows a decreased intracellular NAD(+) concentration, consistent with the loss of NAMase activity in the null mutant.	NAD	107-113	nicotinamidase	Saccharomyces cerevisiae S288C	57-61
11816029-6	2002	These results suggest that NAMase helps yeast cells to adapt to various stress conditions and nutrient depletion, most likely via the activation of NAD-dependent biological processes.	NAD	148-151	nicotinamidase	Saccharomyces cerevisiae S288C	27-33
11679583-7	2002	The changes in NAD(T), NADH, NAD(+), NADP(T), and NADP(+) were progressive and observed primarily in the cerebellum of 4-month-old Atm(-/-) mice.	NAD	23-27	ataxia telangiectasia mutated	Mus musculus	131-134
11708925-9	2001	Furthermore, the addition of a second nitrile group beta to the nitrile in DPN or the addition of a methyl substitutent at an ortho position on the beta-aromatic ring increases the affinity and selectivity of these compounds for ERbeta.	NAD	75-78	estrogen receptor 2	Homo sapiens	229-235
11705403-8	2001	The K(m,NAD) for Tpt1 is substrate dependent: K(m,NAD) is 10 microM with ligated tRNA, 200 microM with pApA(p)pA, and 600 microM with pApApA(p).	NAD	8-11	tRNA 2'-phosphotransferase	Saccharomyces cerevisiae S288C	17-21
11705403-8	2001	The K(m,NAD) for Tpt1 is substrate dependent: K(m,NAD) is 10 microM with ligated tRNA, 200 microM with pApA(p)pA, and 600 microM with pApApA(p).	NAD	50-53	tRNA 2'-phosphotransferase	Saccharomyces cerevisiae S288C	17-21
11551228-0	2001	13C NMR analysis of electrostatic interactions between NAD+ and active site residues of UDP-galactose 4-epimerase: implications for the activation induced by uridine nucleotides.	NAD	55-59	UDP-galactose-4-epimerase	Homo sapiens	88-113
11551228-1	2001	UDP-galactose 4-epimerase contains the coenzyme NAD+ bound tightly at the active site.	NAD	48-52	UDP-galactose-4-epimerase	Homo sapiens	0-25
11528236-11	2001	Aldose reductase utilizes both NADPH and with lower affinity NADH as coenzymes.	NAD	61-65	aldo-keto reductase family 1 member B1	Oryctolagus cuniculus	0-16
33930374-0	2021	CD38 and MGluR1 as possible signaling molecules involved in epileptogenesis: a potential role for NAD+ homeostasis.	NAD	98-102	CD38 molecule	Homo sapiens	0-4
33930374-6	2021	An increase in expression of CD38/NADase activity was observed during the kindling procedure in hippocampus that represent it as one of the most important NAD degrading enzymes during epileptogenesis.	NAD	34-37	CD38 molecule	Homo sapiens	29-33
33528041-8	2021	Nmnat3 gene expression is suppressed by HIF1alpha, a transcription factor that is stabilized by mitochondrial translation dysfunction, suggesting that HIF1alpha-Nmnat3-mediated NAD+ production is important for lysosomal function.	NAD	177-181	hypoxia inducible factor 1, alpha subunit	Mus musculus	40-49
33528041-8	2021	Nmnat3 gene expression is suppressed by HIF1alpha, a transcription factor that is stabilized by mitochondrial translation dysfunction, suggesting that HIF1alpha-Nmnat3-mediated NAD+ production is important for lysosomal function.	NAD	177-181	hypoxia inducible factor 1, alpha subunit	Mus musculus	151-160
33418473-6	2021	ATP hydrolysis was thus catalyzed by ADH1A...NAD+ enzymatic complexes absorbed at the IF extremities protruding out of the capillary matrix.	NAD	45-49	alcohol dehydrogenase 1A (class I), alpha polypeptide	Homo sapiens	37-42
33734555-5	2021	We further show that boosting intracellular NAD+ levels with nicotinamide riboside (NR) prevents senescence and SASP by promoting mitophagy in a PINK1-dependent manner.	NAD	44-48	PTEN induced putative kinase 1	Mus musculus	145-150
33795658-4	2021	The NAD+-dependent Sirtuin1 (Sirt1) deacetylates FoxOs and beta-catenin in osteoblast progenitors and, thereby, increases bone mass.	NAD	4-8	sirtuin 1	Mus musculus	19-27
33795658-4	2021	The NAD+-dependent Sirtuin1 (Sirt1) deacetylates FoxOs and beta-catenin in osteoblast progenitors and, thereby, increases bone mass.	NAD	4-8	sirtuin 1	Mus musculus	29-34
11319814-1	2001	Pseudomonas aeruginosa exotoxin A (ETA) is a member of the family of bacterial ADP-ribosylating toxins that use NAD(+) as the ADP-ribose donor.	NAD	112-118	endothelin receptor type A	Homo sapiens	23-33
33795658-6	2021	We found decreased levels of NAD+ in osteoblast progenitor cultures from old mice, associated with increased acetylation of FoxO1 and markers of cell senescence.	NAD	29-33	forkhead box O1	Mus musculus	124-129
33795658-7	2021	The NAD+ precursor nicotinamide riboside (NR) abrogated FoxO1 and beta-catenin acetylation and several marker of cellular senescence, and increased the osteoblastogenic capacity of cells from old mice.	NAD	4-8	forkhead box O1	Mus musculus	56-61
33645541-3	2021	SmoS is a dehydrogenase that catalyzes the oxidation of the commonly occurring sugar alcohols sorbitol and galactitol to fructose and tagatose, respectively, using NAD+ as a cofactor.	NAD	164-168	L-iditol 2-dehydrogenase	Sinorhizobium meliloti 1021	0-4
33796837-4	2021	To address these questions, we develop a comprehensive mathematical model that represents the circadian pathway in the mouse liver, together with the insulin/IGF-1 pathway, mTORC1, AMPK, NAD+, and the NAD+ -consuming factor SIRT1.	NAD	201-205	sirtuin 1	Mus musculus	224-229
33335015-1	2021	Resveratrol affords protection against reactive oxygen species (ROS)-related diseases via activation of SIRT1, an NAD+-dependent deacetylase.	NAD	114-117	sirtuin 1	Mus musculus	104-109
33597293-3	2021	Here, we show that IFN signaling, present in a subset of PDAC tumors, substantially lowers NAD(H) levels through up-regulating the expression of NAD-consuming enzymes PARP9, PARP10, and PARP14.	NAD	91-94	poly(ADP-ribose) polymerase family member 9	Homo sapiens	167-172
33385367-4	2021	Since positively charged groove including substrate- and NAD+-binding sites is proposed as potential binding site for alpha-synuclein and RNA, GAPDH was glycated on residues in grooves and randomly distributed over the whole surface.	NAD	57-61	synuclein alpha	Homo sapiens	118-133
33353981-2	2021	NAD+ is also an essential cofactor for non-redox NAD+-dependent enzymes, including sirtuins, CD38 and poly(ADP-ribose) polymerases.	NAD	0-4	CD38 molecule	Homo sapiens	93-97
33353981-2	2021	NAD+ is also an essential cofactor for non-redox NAD+-dependent enzymes, including sirtuins, CD38 and poly(ADP-ribose) polymerases.	NAD	49-53	CD38 molecule	Homo sapiens	93-97
33461448-4	2021	The synthesis and degradation of NAD+ and transport of its key intermediates among cell compartments play an important role to maintain optimal NAD levels, for regulation of NAD+ -utilizing enzymes, such as sirtuins (Sirt), poly-ADP-ribose polymerases, and CD38/157 enzymes, either intracellularly as well as extracellularly.	NAD	33-37	CD38 molecule	Homo sapiens	257-261
33461448-4	2021	The synthesis and degradation of NAD+ and transport of its key intermediates among cell compartments play an important role to maintain optimal NAD levels, for regulation of NAD+ -utilizing enzymes, such as sirtuins (Sirt), poly-ADP-ribose polymerases, and CD38/157 enzymes, either intracellularly as well as extracellularly.	NAD	33-36	CD38 molecule	Homo sapiens	257-261
33461448-4	2021	The synthesis and degradation of NAD+ and transport of its key intermediates among cell compartments play an important role to maintain optimal NAD levels, for regulation of NAD+ -utilizing enzymes, such as sirtuins (Sirt), poly-ADP-ribose polymerases, and CD38/157 enzymes, either intracellularly as well as extracellularly.	NAD	174-178	CD38 molecule	Homo sapiens	257-261
33462707-8	2021	Although a number of different mechanisms may be at play in each case, a common theme is that resveratrol and NAD both enhance the activity of SIRT1.	NAD	110-113	sirtuin 1	Mus musculus	143-148
33462707-9	2021	Moreover, many of the physiologic improvements observed with resveratrol and NAD precursors are consistent with modulation of known SIRT1 targets.	NAD	77-80	sirtuin 1	Mus musculus	132-137
33441761-6	2021	Further studies on cytochrome b5 (CYB5), an alternative NADH-dependent electron donor indicated particularly strong support of CYP2C8-dependent amodiaquine N-deethylation by CYB5 and this was confirmed by genetic CYB5 single- and POR/CYB5 double-knockout.	NAD	56-60	cytochrome b5 type A	Homo sapiens	19-32
33441761-6	2021	Further studies on cytochrome b5 (CYB5), an alternative NADH-dependent electron donor indicated particularly strong support of CYP2C8-dependent amodiaquine N-deethylation by CYB5 and this was confirmed by genetic CYB5 single- and POR/CYB5 double-knockout.	NAD	56-60	cytochrome b5 type A	Homo sapiens	34-38
33441761-6	2021	Further studies on cytochrome b5 (CYB5), an alternative NADH-dependent electron donor indicated particularly strong support of CYP2C8-dependent amodiaquine N-deethylation by CYB5 and this was confirmed by genetic CYB5 single- and POR/CYB5 double-knockout.	NAD	56-60	cytochrome b5 type A	Homo sapiens	174-178
33441761-6	2021	Further studies on cytochrome b5 (CYB5), an alternative NADH-dependent electron donor indicated particularly strong support of CYP2C8-dependent amodiaquine N-deethylation by CYB5 and this was confirmed by genetic CYB5 single- and POR/CYB5 double-knockout.	NAD	56-60	cytochrome b5 type A	Homo sapiens	174-178
33441761-6	2021	Further studies on cytochrome b5 (CYB5), an alternative NADH-dependent electron donor indicated particularly strong support of CYP2C8-dependent amodiaquine N-deethylation by CYB5 and this was confirmed by genetic CYB5 single- and POR/CYB5 double-knockout.	NAD	56-60	cytochrome b5 type A	Homo sapiens	174-178
33441761-8	2021	In summary our results show that POR/NADPH- and CYB5/NADH-electron transport systems influence human drug metabolizing CYPs differentially and differently than mouse Cyps.	NAD	53-57	cytochrome b5 type A	Homo sapiens	48-52
33171124-6	2021	Importantly, high NAMPT-expressing tumors are more sensitive to anti-PD-L1 treatment and NAD+ augmentation enhances the efficacy of anti-PD-L1 antibody in immunotherapy-resistant tumors.	NAD	89-93	CD274 molecule	Homo sapiens	137-142
33290962-9	2021	Treatment with NAD + also inhibited the expressions of NLRP3 and modulated the differentiation of Th1 and Th17 cells, reduced the expressions of the pro-inflammatory factors IL-1beta, IL-2, IL-18, IFN-gamma and IL-17, and increased the expression of anti-inflammatory IL-10.	NAD	15-20	NLR family, pyrin domain containing 3	Mus musculus	55-60
33290962-9	2021	Treatment with NAD + also inhibited the expressions of NLRP3 and modulated the differentiation of Th1 and Th17 cells, reduced the expressions of the pro-inflammatory factors IL-1beta, IL-2, IL-18, IFN-gamma and IL-17, and increased the expression of anti-inflammatory IL-10.	NAD	15-20	interleukin 1 alpha	Mus musculus	174-182
33290962-9	2021	Treatment with NAD + also inhibited the expressions of NLRP3 and modulated the differentiation of Th1 and Th17 cells, reduced the expressions of the pro-inflammatory factors IL-1beta, IL-2, IL-18, IFN-gamma and IL-17, and increased the expression of anti-inflammatory IL-10.	NAD	15-20	interleukin 2	Mus musculus	184-188
33290962-12	2021	Our results indicate that NAD + suppresses the NLRP3 inflammasome at least in part through the activation of autophagy to relieve the symptoms of EAE.	NAD	26-31	NLR family, pyrin domain containing 3	Mus musculus	47-52
33053398-2	2021	In diabetic cornea, the NAD+-consuming enzyme SIRT1 was down-regulated and contributed to the delayed wound healing.	NAD	24-28	sirtuin 1	Mus musculus	46-51
33053398-12	2021	Furthermore, in DM mice, NAD+ and its precursors nicotinamide mononucleotide and nicotinamide riboside also facilitated corneal epithelial and nerve regeneration, accompanied with the recovered expression of SIRT1 and phosphorylated EGFR, AKT, and ERK1/2 in epithelium and corneal sensitivity.	NAD	25-29	sirtuin 1	Mus musculus	208-213
33053398-12	2021	Furthermore, in DM mice, NAD+ and its precursors nicotinamide mononucleotide and nicotinamide riboside also facilitated corneal epithelial and nerve regeneration, accompanied with the recovered expression of SIRT1 and phosphorylated EGFR, AKT, and ERK1/2 in epithelium and corneal sensitivity.	NAD	25-29	epidermal growth factor receptor	Mus musculus	233-237
33264406-2	2020	While it has been shown that eukaryotic DNA ligases utilize ATP as the adenylation donor, it was recently reported that human DNA ligase IV can also utilize NAD+ and, to a lesser extent ADP-ribose, as the source of the adenylate group and that NAD+, unlike ATP, enhances ligation by supporting multiple catalytic cycles.	NAD	157-161	DNA ligase 4	Homo sapiens	126-139
33264406-2	2020	While it has been shown that eukaryotic DNA ligases utilize ATP as the adenylation donor, it was recently reported that human DNA ligase IV can also utilize NAD+ and, to a lesser extent ADP-ribose, as the source of the adenylate group and that NAD+, unlike ATP, enhances ligation by supporting multiple catalytic cycles.	NAD	244-248	DNA ligase 4	Homo sapiens	126-139
33264406-3	2020	Since this unexpected finding has significant implications for our understanding of the mechanisms and regulation of DNA double strand break repair, we attempted to confirm that NAD+ and ADP-ribose can be used as co-factors by human DNA ligase IV.	NAD	178-182	DNA ligase 4	Homo sapiens	233-246
33264406-5	2020	Moreover, we find that ligation by de-adenylated DNA ligase IV is dependent upon ATP not NAD+ or ADP-ribose.	NAD	89-93	DNA ligase 4	Homo sapiens	49-62
33010255-5	2020	The present study was undertaken to elucidate whether the NAD-dependent protein deacetylase sirtuin isoform SIRT1 is an upstream mediator of hypoxic PC-induced protection, and to assess the efficacy of the SIRT1-activating polyphenol Resveratrol as a pharmacologic preconditioning therapy.	NAD	58-61	sirtuin 1	Mus musculus	108-113
33011272-1	2020	NAD kinase (NADK) is required for the de novo synthesis of NADP+ from NAD+.	NAD	70-74	NAD kinase	Homo sapiens	0-10
33011272-1	2020	NAD kinase (NADK) is required for the de novo synthesis of NADP+ from NAD+.	NAD	70-74	NAD kinase	Homo sapiens	12-16
33011272-6	2020	This was mirrored by a rapid reduction in NAD+ levels, suggesting that NADK had been activated.	NAD	42-46	NAD kinase	Homo sapiens	71-75
33324653-1	2020	Proteins from the poly(ADP-ribose) polymerase (PARP) family, such as PARP1 and PARP2, use NAD+ as a substrate to catalyze the synthesis of polymeric chains consisting of ADP-ribose units covalently attached to an acceptor molecule.	NAD	90-94	poly(ADP-ribose) polymerase 2	Arabidopsis thaliana	69-74
33228716-1	2020	Sirtuin 1 (SIRT1), is a nicotinamide adenine dinucleotide (NAD+)-dependent protein deacetylase and a candidate gene for depression.	NAD	24-57	sirtuin 1	Mus musculus	0-9
33228716-1	2020	Sirtuin 1 (SIRT1), is a nicotinamide adenine dinucleotide (NAD+)-dependent protein deacetylase and a candidate gene for depression.	NAD	24-57	sirtuin 1	Mus musculus	11-16
33228716-1	2020	Sirtuin 1 (SIRT1), is a nicotinamide adenine dinucleotide (NAD+)-dependent protein deacetylase and a candidate gene for depression.	NAD	59-63	sirtuin 1	Mus musculus	0-9
33228716-1	2020	Sirtuin 1 (SIRT1), is a nicotinamide adenine dinucleotide (NAD+)-dependent protein deacetylase and a candidate gene for depression.	NAD	59-63	sirtuin 1	Mus musculus	11-16
33183342-3	2020	Nicotinamide adenine dinucleotide phosphate oxidase (NADPH oxidase, NOX) has been indicated in Abeta pathology; however, whether and how it affects tau pathology are not yet clear.	NAD	0-33	amyloid beta (A4) precursor protein	Mus musculus	95-100
33182523-4	2020	Intracellularly, visfatin/iNAMPT plays a regulatory role in NAD+ biosynthesis and thereby affects many NAD-dependent proteins such as sirtuins, PARPs, MARTs and CD38/157.	NAD	60-64	CD38 molecule	Homo sapiens	161-165
33182523-4	2020	Intracellularly, visfatin/iNAMPT plays a regulatory role in NAD+ biosynthesis and thereby affects many NAD-dependent proteins such as sirtuins, PARPs, MARTs and CD38/157.	NAD	60-63	CD38 molecule	Homo sapiens	161-165
32606138-0	2020	Poly(ADP-ribose) glycohydrolase inhibition sequesters NAD+ to potentiate the metabolic lethality of alkylating chemotherapy in IDH mutant tumor cells.	NAD	54-58	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	127-130
11319814-1	2001	Pseudomonas aeruginosa exotoxin A (ETA) is a member of the family of bacterial ADP-ribosylating toxins that use NAD(+) as the ADP-ribose donor.	NAD	112-118	endothelin receptor type A	Homo sapiens	35-38
33199923-0	2020	CD38-expressing macrophages drive age-related NAD+ decline.	NAD	46-50	CD38 molecule	Homo sapiens	0-4
11319814-3	2001	A fluorometric assay involving the use of etheno-beta-nicotinamide adenine dinucleotide (epsilon-NAD(+)), an analog of NAD(+), has been found to provide a rapid, reliable, and sensitive procedure for assessing the kinetic parameters of this class of enzymes including ETA and its C-terminal fragment, PE24.	NAD	97-103	endothelin receptor type A	Homo sapiens	268-271
33199924-0	2020	Senescent cells promote tissue NAD+ decline during ageing via the activation of CD38+ macrophages.	NAD	31-35	CD38 molecule	Homo sapiens	80-84
33199924-4	2020	These M1-like macrophages express high levels of the NAD-consuming enzyme CD38 and have enhanced CD38-dependent NADase activity, thereby reducing tissue NAD levels.	NAD	53-56	CD38 molecule	Homo sapiens	74-78
11328592-6	2001	The purified Pmb5 showed the typical absorption spectrum of cytochrome b(5) with an asymmetric peak at 556 nm and a shoulder at 560 nm upon reduction with NADH and NADH-cytochrome b(5) reductase.	NAD	155-159	cytochrome b5 type A	Gallus gallus	60-75
33199924-4	2020	These M1-like macrophages express high levels of the NAD-consuming enzyme CD38 and have enhanced CD38-dependent NADase activity, thereby reducing tissue NAD levels.	NAD	112-115	CD38 molecule	Homo sapiens	97-101
33199925-0	2020	CD38 ecto-enzyme in immune cells is induced during aging and regulates NAD+ and NMN levels.	NAD	71-75	CD38 molecule	Homo sapiens	0-4
11275476-6	2001	4-ABP(NHOH) dose-dependently induced 8-hydroxy-2"-deoxyguanosine (8-OHdG) formation in the presence of Cu(ll) and NADH.	NAD	114-118	amine oxidase copper containing 1	Homo sapiens	2-5
33036972-2	2020	Here, we show that nicotinamide adenine dinucleotide (NAD+), administered during a critical window of prenatal development, in a mouse model with dysfunctional endothelial gamma-aminobutyric acid type A (GABAA) receptors (Gabrb3 endothelial cell knockout mice), results in a synergistic repair of impaired angiogenesis and normalization of brain development, thus preventing the acquisition of abnormal behavioral symptoms.	NAD	19-52	gamma-aminobutyric acid (GABA) A receptor, subunit beta 3	Mus musculus	222-228
33036972-2	2020	Here, we show that nicotinamide adenine dinucleotide (NAD+), administered during a critical window of prenatal development, in a mouse model with dysfunctional endothelial gamma-aminobutyric acid type A (GABAA) receptors (Gabrb3 endothelial cell knockout mice), results in a synergistic repair of impaired angiogenesis and normalization of brain development, thus preventing the acquisition of abnormal behavioral symptoms.	NAD	54-58	gamma-aminobutyric acid (GABA) A receptor, subunit beta 3	Mus musculus	222-228
11248244-0	2001	Characterization of recombinant human nicotinamide mononucleotide adenylyl transferase (NMNAT), a nuclear enzyme essential for NAD synthesis.	NAD	127-130	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	38-86
11248244-0	2001	Characterization of recombinant human nicotinamide mononucleotide adenylyl transferase (NMNAT), a nuclear enzyme essential for NAD synthesis.	NAD	127-130	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	88-93
33020580-4	2020	Combining structural analyses of cryo-electron microscopy data with molecular dynamic simulations, here we show that the cofactor NADH is a key player in the GDH regulation process.	NAD	130-134	glutamate dehydrogenase 1	Homo sapiens	158-161
11248244-1	2001	Nicotinamide mononucleotide adenylyl transferase (NMNAT) is an essential enzyme in all organisms, because it catalyzes a key step of NAD synthesis.	NAD	133-136	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	0-48
33020580-5	2020	Our structural analysis indicates that, binding to the regulatory sites in proximity of the antenna region, NADH acts as a positive allosteric modulator by enhancing both the affinity of the inhibitor GTP binding and inhibition of GDH catalytic activity.	NAD	108-112	glutamate dehydrogenase 1	Homo sapiens	231-234
11248244-1	2001	Nicotinamide mononucleotide adenylyl transferase (NMNAT) is an essential enzyme in all organisms, because it catalyzes a key step of NAD synthesis.	NAD	133-136	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	50-55
33020580-6	2020	We further show that the binding of GTP to the NADH-bound GDH activates a triangular allosteric network, interlinking the inhibitor with regulatory and catalytic sites.	NAD	47-51	glutamate dehydrogenase 1	Homo sapiens	58-61
11231268-8	2001	Ellman"s reagent, 5,5"-dithiobis (2-nitrobenzoic acid) (DTNB), which binds close to the NAD(+) binding site, thus abolishing coenzyme binding in the wild-type enzyme, also reacts with D165S but has no effect on C320S.	NAD	88-94	dystrobrevin beta	Homo sapiens	56-60
11231268-11	2001	DTNB-modified 5 : 1 hybrids, with only one subunit capable of binding coenzyme, showed classical Michaelis-Menten kinetics when the NAD(+) concentration was varied, whereas removal of the thionitrobenzoate moieties that blocked the other five coenzyme binding sites in the hexamer reinstated nonlinear behaviour, suggesting that "nonlinear" behaviour of the native enzyme and the hybrid with six coenzyme binding sites depends on binding to multiple sites.	NAD	132-138	dystrobrevin beta	Homo sapiens	0-4
11230512-3	2001	ATPase activity was determined by enzymatic coupling of ATP resynthesis to the oxidation of NADH.	NAD	92-96	dynein axonemal heavy chain 8	Homo sapiens	0-6
11032835-5	2001	The membrane fraction of kidney-derived human embryonic kidney (HEK) 293 cells, expressing NOX4, exhibits NADH- and NADPH-dependent superoxide-producing activities, both of which are inhibited by diphenylene iodonium, an agent known to block oxygen sensing, and decreased in cells expressing antisense NOX4 mRNA.	NAD	106-110	NADPH oxidase 4	Homo sapiens	91-95
11400110-3	2001	It also catalyzed the photoreduction of NADP+ or NAD+ in the presence of ascorbate as an electron donor and ferredoxin-NADP+ reductase as the coupling enzyme.	NAD	49-53	ferredoxin reductase	Homo sapiens	108-134
18628906-2	2001	It encodes, all on the same strand, seven subunits of NADH: ubiquinone oxidoreductase (ND1-6, ND4L), apocytochrome b (COB), three subunits of cytochrome oxidase (COX1, 2, 3), three subunits of ATP synthetase (ATP6, 8 and 9), small and large ribosomal RNAs and an incomplete set of tRNAs.	NAD	54-58	nd1	Yarrowia lipolytica	87-92
33041769-6	2020	Following the excessive activity of poly(ADP-ribose) polymerase-1 depletes NAD+/ATP in the cells.	NAD	75-79	poly (ADP-ribose) polymerase 1	Rattus norvegicus	36-65
32828286-7	2020	The preference of NADP+ over NAD+ was significantly subjected by a pair of Ser37 and Arg38, whose manners were similar to other Gfo/Idh/MocA members.	NAD	29-33	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	132-135
32717131-6	2020	Thus, the membrane organization of endolysosomal CD38, a signal-mediated transport system for NADP+ and luminal NAD+ biosynthetic enzymes integrate signals from a chemokine and cAMP to specify the spatiotemporal mobilization of Ca2+ to drive cell migration.	NAD	112-116	CD38 molecule	Homo sapiens	49-53
32445867-4	2020	Here, we explore the FMN binding site in mitoNEET by using FMN analogs and find that lumiflavin, like FMN, at nanomolar concentrations can mediate the redox transition of the mitoNEET [2Fe-2S] clusters in the presence of flavin reductase and NADH (100 muM) under aerobic conditions.	NAD	242-246	CDGSH iron sulfur domain 1	Homo sapiens	175-183
18628906-2	2001	It encodes, all on the same strand, seven subunits of NADH: ubiquinone oxidoreductase (ND1-6, ND4L), apocytochrome b (COB), three subunits of cytochrome oxidase (COX1, 2, 3), three subunits of ATP synthetase (ATP6, 8 and 9), small and large ribosomal RNAs and an incomplete set of tRNAs.	NAD	54-58	nd4L	Yarrowia lipolytica	94-98
32700357-1	2020	Sirtuin 2 (SIRT2) is an NAD+ dependent deacetylase that is the most abundant sirtuin protein in the brain.	NAD	24-27	sirtuin 2	Mus musculus	0-9
11099492-0	2001	Connexin 43 hemi channels mediate Ca2+-regulated transmembrane NAD+ fluxes in intact cells.	NAD	63-67	gap junction protein alpha 1	Homo sapiens	0-11
32700357-1	2020	Sirtuin 2 (SIRT2) is an NAD+ dependent deacetylase that is the most abundant sirtuin protein in the brain.	NAD	24-27	sirtuin 2	Mus musculus	11-16
31679456-6	2020	Vascular smooth muscle cells silenced for the mitochondrial complex I subunit Ndufc2 gene (NADH:ubiquinone oxidoreductase subunit C2) and cerebral endothelial cells isolated from SHRSP were also used to assess autophagy/mitophagy and mitochondrial function in response to high salt levels.	NAD	91-95	NADH:ubiquinone oxidoreductase subunit C2	Homo sapiens	78-84
32493816-1	2020	Sirtuin 2 (Sirt2), an NAD+-dependent protein deacetylase, deacetylates tubulin, AKT, and other proteins.	NAD	22-25	sirtuin 2	Homo sapiens	0-9
32493816-1	2020	Sirtuin 2 (Sirt2), an NAD+-dependent protein deacetylase, deacetylates tubulin, AKT, and other proteins.	NAD	22-25	sirtuin 2	Homo sapiens	11-16
32711564-5	2020	We also demonstrated that ectopic expression of SIRT2, a cytoplasmic NAD+ - dependent deacetylase, suppresses the defects of HDAC6 knockdown neurons.	NAD	69-72	sirtuin 2	Homo sapiens	48-53
32699629-11	2020	Integrated analysis of the altered metabolites and gene expression revealed the high expression level of MDH1 in the grain-fed group might contribute to the mitochondrial NADH oxidation and spermidine metabolism for adapting the deletion mtDNA copy number.	NAD	171-175	malate dehydrogenase 1	Bos taurus	105-109
32220640-5	2020	Co-factor (NADH) was anchored in ZIF-8 by ion exchange between PEI (positive charge) and co-factor (negative charge), and regenerated through GDH embedded in the ZIF-8, thus keeping high activity of FateDH.	NAD	11-15	glutamate dehydrogenase 1	Homo sapiens	142-145
32432680-5	2020	The NAD+-dependent protein SIRT1 deacetylates RECQL4 in vitro and in cells thereby controlling the interaction between OGG1 and RECQL4 after DNA repair and maintaining RECQL4 in a low acetylated state.	NAD	4-8	RecQ like helicase 4	Homo sapiens	46-52
32432680-5	2020	The NAD+-dependent protein SIRT1 deacetylates RECQL4 in vitro and in cells thereby controlling the interaction between OGG1 and RECQL4 after DNA repair and maintaining RECQL4 in a low acetylated state.	NAD	4-8	8-oxoguanine DNA glycosylase	Homo sapiens	119-123
32432680-5	2020	The NAD+-dependent protein SIRT1 deacetylates RECQL4 in vitro and in cells thereby controlling the interaction between OGG1 and RECQL4 after DNA repair and maintaining RECQL4 in a low acetylated state.	NAD	4-8	RecQ like helicase 4	Homo sapiens	128-134
32432680-5	2020	The NAD+-dependent protein SIRT1 deacetylates RECQL4 in vitro and in cells thereby controlling the interaction between OGG1 and RECQL4 after DNA repair and maintaining RECQL4 in a low acetylated state.	NAD	4-8	RecQ like helicase 4	Homo sapiens	128-134
32461692-5	2020	Using LbNOX, we demonstrate that NADH reductive stress mediates the effects of GCKR variation on many metabolic traits, including circulating triglyceride levels, glucose tolerance and FGF21 levels.	NAD	33-37	glucokinase regulator	Homo sapiens	79-83
32569316-3	2020	In this study, we isolated a chilling hypersensitive Arabidopsis thaliana mutant named qs-2 and identified the causal mutation in the gene encoding quinolinate synthase (QS) critical for NAD biosynthesis.	NAD	187-190	quinolinate synthase	Arabidopsis thaliana	148-168
32569316-3	2020	In this study, we isolated a chilling hypersensitive Arabidopsis thaliana mutant named qs-2 and identified the causal mutation in the gene encoding quinolinate synthase (QS) critical for NAD biosynthesis.	NAD	187-190	quinolinate synthase	Arabidopsis thaliana	170-172
32544883-6	2020	Collectively, this study revealed potential roles of miR-9 and miR-29a as contributors to DPN development through the SHH signaling pathway by binding to ISL1.	NAD	90-93	ISL LIM homeobox 1	Rattus norvegicus	154-158
32502419-2	2020	(2020) now show that nicotinamide adenine dinucleotide (NAD+) can restore robust circadian gene expression and behavior in aged mice through SIRT1-dependent deacetylation of the core clock protein PER2.	NAD	21-54	sirtuin 1	Mus musculus	141-146
32502419-2	2020	(2020) now show that nicotinamide adenine dinucleotide (NAD+) can restore robust circadian gene expression and behavior in aged mice through SIRT1-dependent deacetylation of the core clock protein PER2.	NAD	56-60	sirtuin 1	Mus musculus	141-146
32278117-8	2020	The change trend of SIRT1 is quite the same as that of NAD+/NADH ratio.	NAD	55-59	sirtuin 1	Mus musculus	20-25
32278117-8	2020	The change trend of SIRT1 is quite the same as that of NAD+/NADH ratio.	NAD	60-64	sirtuin 1	Mus musculus	20-25
32045672-8	2020	Also, the pathways of NAD+ synthesis were inhibited, resulting in the reduced activity of sirtuin 3 (SIRT3).	NAD	22-25	sirtuin 3	Mus musculus	90-99
32045672-8	2020	Also, the pathways of NAD+ synthesis were inhibited, resulting in the reduced activity of sirtuin 3 (SIRT3).	NAD	22-25	sirtuin 3	Mus musculus	101-106
32063085-2	2020	Sirtuin2 (Sirt2), an NAD+-dependent deacetylase, appears to play detrimental roles in liver injury.	NAD	21-24	sirtuin 2	Mus musculus	0-8
32063085-2	2020	Sirtuin2 (Sirt2), an NAD+-dependent deacetylase, appears to play detrimental roles in liver injury.	NAD	21-24	sirtuin 2	Mus musculus	10-15
32415082-5	2020	LDHB knockdown caused downregulation of mitochondrial functions in auditory cell line, University of Bristol/organ of Corti 1 (UB/OC1) with decreased NAD+ and increased hypoxia inducing factor-1alpha.	NAD	150-154	lactate dehydrogenase B	Mus musculus	0-4
32415082-7	2020	On the contrary, the induction of LDHB expression caused enhanced mitochondrial functions, including changes in mitochondrial respiratory subunits, mitochondrial membrane potentials, ATP, and the NAD+/NADH ratio.	NAD	196-200	lactate dehydrogenase B	Mus musculus	34-38
32415082-7	2020	On the contrary, the induction of LDHB expression caused enhanced mitochondrial functions, including changes in mitochondrial respiratory subunits, mitochondrial membrane potentials, ATP, and the NAD+/NADH ratio.	NAD	201-205	lactate dehydrogenase B	Mus musculus	34-38
32169417-0	2020	Modulation of aryl hydrocarbon receptor (AHR) and the NAD+-consuming enzyme CD38: Searches of therapeutic options for nonalcoholic fatty liver disease (NAFLD).	NAD	54-58	CD38 molecule	Homo sapiens	76-80
32169417-2	2020	Recently, evidence has been obtained that AHR is involved in NAD+ and energy homeostasis in cooperation with NAD+-consuming enzymes including CD38, TiPARP and sirtuins.	NAD	109-113	CD38 molecule	Homo sapiens	142-146
32072193-13	2020	Furthermore, immunoprecipitation and mass spectrometry analysis indicated that AKAP1 interacted with the NADH-ubiquinone oxidoreductase 75 kDa subunit (NDUFS1).	NAD	105-120	A kinase (PRKA) anchor protein 1	Mus musculus	79-84
31912134-9	2020	Cytoplasmic NAD(P)-dependent 10-formyl-tetrahydrofolate dehydrogenase (Aldh1/1) and mitochondrial NAD(P)-dependent 10-formyl-tetrahydrofolate dehydrogenase (Aldh1/2) , genes responsible for the catabolism of 10-formylTHF, were very weakly expressed in PP, low in livers of F and N, and reached the significantly higher adult levels in J.	NAD	12-18	aldehyde dehydrogenase 2 family member	Rattus norvegicus	71-155
32301489-9	2020	Western blot showed that NAD+ treatment up-regulated the expression of p-STAT6 and SIRT1.	NAD	25-29	sirtuin 1	Mus musculus	83-88
31900976-16	2020	HINT2 overexpression restored mitochondrial NAD levels; this was dependent on nicotinamide mononucleotide(NMN).	NAD	44-47	histidine triad nucleotide binding protein 2	Mus musculus	0-5
31900976-18	2020	CONCLUSION: HINT2 overexpression protects cardiac function in adult mice after myocardial infarction by maintaining mitochondrial NAD homeostasis.	NAD	130-133	histidine triad nucleotide binding protein 2	Mus musculus	12-17
11099492-6	2001	Bidirectional NAD+ transport in isolated Cx43-expressing mur ine 3T3 fibroblasts was affected by known modulators of connexin-mediated intercellular coupling and was completely inhibited by treatment of the cells with a Cx43-antisense oligonucleotide.	NAD	14-18	gap junction protein alpha 1	Homo sapiens	41-45
11099492-6	2001	Bidirectional NAD+ transport in isolated Cx43-expressing mur ine 3T3 fibroblasts was affected by known modulators of connexin-mediated intercellular coupling and was completely inhibited by treatment of the cells with a Cx43-antisense oligonucleotide.	NAD	14-18	gap junction protein alpha 1	Homo sapiens	220-224
11099492-7	2001	NAD+ transport in proteoliposomes reconstituted with 3T3 membrane proteins was inhibited in the presence of a monoclonal anti-Cx43 antibody.	NAD	0-4	gap junction protein alpha 1	Homo sapiens	126-130
32480246-3	2020	One such enzyme, CD38, utilizes NAD to produce several metabolites, including cyclic ADP ribose (cADPR), which is involved in calcium signaling in airway smooth muscle (ASM).	NAD	32-35	CD38 molecule	Homo sapiens	17-21
11099492-8	2001	Finally, Cx43 immunopurified to homogeneity was reconstituted in unilamellar proteoliposomes, which displayed full NAD+-transporting activity.	NAD	115-119	gap junction protein alpha 1	Homo sapiens	9-13
32480246-3	2020	One such enzyme, CD38, utilizes NAD to produce several metabolites, including cyclic ADP ribose (cADPR), which is involved in calcium signaling in airway smooth muscle (ASM).	NAD	32-35	H19 imprinted maternally expressed transcript	Homo sapiens	169-172
32235505-2	2020	DHS catalyses the transfer of a 4-aminobutyl moiety of polyamine spermidine to a specific lysine of eukaryotic translation factor 5A (eIF5A) precursor in a nicotinamide adenine dinucleotide (NAD)-dependent manner.	NAD	156-189	eukaryotic translation initiation factor 5A	Homo sapiens	100-132
32235505-2	2020	DHS catalyses the transfer of a 4-aminobutyl moiety of polyamine spermidine to a specific lysine of eukaryotic translation factor 5A (eIF5A) precursor in a nicotinamide adenine dinucleotide (NAD)-dependent manner.	NAD	156-189	eukaryotic translation initiation factor 5A	Homo sapiens	134-139
11099492-9	2001	This finding is the first evidence that connexin hemichannels can mediate transmembrane fluxes of a nucleotide in whole cells: The pleiotropy of NAD+-dependent cellular events, including redox reactions, signaling, and DNA repair, implicates Cx43 hemichannels in intercellular NAD+ trafficking, which suggests new paracrine functions of NAD.	NAD	145-149	gap junction protein alpha 1	Homo sapiens	242-246
11099492-9	2001	This finding is the first evidence that connexin hemichannels can mediate transmembrane fluxes of a nucleotide in whole cells: The pleiotropy of NAD+-dependent cellular events, including redox reactions, signaling, and DNA repair, implicates Cx43 hemichannels in intercellular NAD+ trafficking, which suggests new paracrine functions of NAD.	NAD	145-148	gap junction protein alpha 1	Homo sapiens	242-246
11124972-4	2000	The rotenone-induced increase in reduced nicotinamide adenine dinucleotide (phosphate) [NAD(P)H] fluorescence reflecting the amount of NADH available for the respiratory chain was also diminished by H(2)O(2), and the effect exerted at small concentrations (&lt;/=50 microm) of the oxidant was completely prevented by 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU), an inhibitor of glutathione reductase.	NAD	135-139	glutathione-disulfide reductase	Homo sapiens	378-399
32235505-2	2020	DHS catalyses the transfer of a 4-aminobutyl moiety of polyamine spermidine to a specific lysine of eukaryotic translation factor 5A (eIF5A) precursor in a nicotinamide adenine dinucleotide (NAD)-dependent manner.	NAD	191-194	eukaryotic translation initiation factor 5A	Homo sapiens	100-132
32235505-2	2020	DHS catalyses the transfer of a 4-aminobutyl moiety of polyamine spermidine to a specific lysine of eukaryotic translation factor 5A (eIF5A) precursor in a nicotinamide adenine dinucleotide (NAD)-dependent manner.	NAD	191-194	eukaryotic translation initiation factor 5A	Homo sapiens	134-139
11113971-2	2000	NAD(+)-dependent glycerol-3-phosphate dehydrogenase in S. cerevisiae is present in two isoforms, coded for by two different genes, GPD1 and GPD2.	NAD	0-6	glycerol-3-phosphate dehydrogenase	Saccharomyces cerevisiae S288C	17-51
10978156-3	2000	This NAD(+)-dependent enzyme belongs to the family of zinc-dependent alcohol dehydrogenases with 40 kDa subunits and is also called ADH3 or chi-ADH.	NAD	5-11	alcohol dehydrogenase 5 (class III), chi polypeptide	Homo sapiens	132-136
32231086-8	2020	Using FurNAD-RNAs, we discovered that the eukaryotic glycohydrolase CD38 processes NAD-capped RNA in vitro into ADP-ribose-modified-RNA and nicotinamide and therefore might act as a decapping enzyme in vivo.	NAD	9-12	CD38 molecule	Homo sapiens	68-72
31859031-1	2020	Sirtuin 1 (Sirt1) is a NAD+-dependent deacetylase capable of countering age-related neurodegeneration, but the basis of Sirt1 neuroprotection remains elusive.	NAD	23-26	sirtuin 1	Mus musculus	0-9
31859031-1	2020	Sirtuin 1 (Sirt1) is a NAD+-dependent deacetylase capable of countering age-related neurodegeneration, but the basis of Sirt1 neuroprotection remains elusive.	NAD	23-26	sirtuin 1	Mus musculus	11-16
31859031-4	2020	Transcription-factor binding-site analysis of downregulated genes yielded Sirt1 target sites, and we observed reduced Sirt1 activity in the SCA7 mouse cerebellum with NAD+ depletion.	NAD	167-171	sirtuin 1	Mus musculus	118-123
10840044-2	2000	l-3-Hydroxyacyl-CoA dehydrogenase reversibly catalyzes the conversion of l-3-hydroxyacyl-CoA to 3-ketoacyl-CoA concomitant with the reduction of NAD(+) to NADH as part of the beta-oxidation spiral.	NAD	145-151	enoyl-CoA hydratase and 3-hydroxyacyl CoA dehydrogenase	Homo sapiens	0-33
32075690-11	2020	Boosting NAD+ levels through the NRK2 pathway using the precursor nicotinamide riboside elevated NAD+/NADH but had no effect to mitigate ER stress and dysfunctional mitochondrial respiratory capacity or acetyl-CoA metabolism.	NAD	9-12	nicotinamide riboside kinase 2	Mus musculus	33-37
32075690-11	2020	Boosting NAD+ levels through the NRK2 pathway using the precursor nicotinamide riboside elevated NAD+/NADH but had no effect to mitigate ER stress and dysfunctional mitochondrial respiratory capacity or acetyl-CoA metabolism.	NAD	97-100	nicotinamide riboside kinase 2	Mus musculus	33-37
32075690-11	2020	Boosting NAD+ levels through the NRK2 pathway using the precursor nicotinamide riboside elevated NAD+/NADH but had no effect to mitigate ER stress and dysfunctional mitochondrial respiratory capacity or acetyl-CoA metabolism.	NAD	102-106	nicotinamide riboside kinase 2	Mus musculus	33-37
10840044-2	2000	l-3-Hydroxyacyl-CoA dehydrogenase reversibly catalyzes the conversion of l-3-hydroxyacyl-CoA to 3-ketoacyl-CoA concomitant with the reduction of NAD(+) to NADH as part of the beta-oxidation spiral.	NAD	155-159	enoyl-CoA hydratase and 3-hydroxyacyl CoA dehydrogenase	Homo sapiens	0-33
10837478-5	2000	PGR/LTB(4)DH catalyzed the NADH-dependent reduction of 15-oxo-LXA(4) to yield 13,14-dihydro-15-oxo-LXA(4).	NAD	27-31	progesterone receptor	Homo sapiens	0-3
10856427-6	2000	The lack of protection was due, in part, to low catalytic activity of hALDH3 towards aldophosphamide, since, with NAD as cofactor, the catalytic efficiency of homogeneous, recombinant hALDH3 for aldophosphamide oxidation was shown to be about seven times lower than that of recombinant hALDH1.	NAD	114-117	aldehyde dehydrogenase 3 family member A1	Homo sapiens	70-76
31825806-1	2020	Cytochrome b5 reductase is an enzyme with the ability to generate superoxide anion at the expenses of NADH.	NAD	102-106	cytochrome b5 type A	Homo sapiens	0-13
31825806-6	2020	Upon complex formation with cytochrome b5 reductase, juglone is able to act as an electron acceptor leading to NADH consumption stimulation and increase of superoxide anion production by the reductase.	NAD	111-115	cytochrome b5 type A	Homo sapiens	28-41
10781607-0	2000	The iscS gene in Escherichia coli is required for the biosynthesis of 4-thiouridine, thiamin, and NAD.	NAD	98-101	NFS1 cysteine desulfurase	Homo sapiens	4-8
31773269-3	2020	This interaction leads to the formation of one-electron reduced cobalamin, cob(II)alamin, and proceeds via water substitution on aquacobalamin by NADH and further decomposition of NADH-Co(III) complex to cob(II)alamin and NADH +.	NAD	146-150	metabolism of cobalamin associated B	Homo sapiens	75-78
32005247-0	2020	Targeting the NAD+ salvage pathway suppresses APC mutation-driven colorectal cancer growth and Wnt/beta-catenin signaling via increasing Axin level.	NAD	14-17	catenin beta 1	Homo sapiens	99-111
10781607-14	2000	Thus, IscS plays a significant and specific role at the top of a potentially broad sulfur transfer cascade that is required for the biosynthesis of thiamin, NAD, Fe-S clusters, and thionucleosides.	NAD	157-160	NFS1 cysteine desulfurase	Homo sapiens	6-10
10807796-1	2000	Recessive congenital methemoglobinemia due to nicotinamide adenine dinucleotide (NADH)-cytochrome b5 reductase (b5R) deficiency is classified into 2 clinical types: type 1 (erythrocyte type) and type 2 (generalized type).	NAD	46-79	cytochrome b5 reductase 3	Homo sapiens	98-110
32013131-1	2020	The NAD-hydrolyzing ecto-enzyme CD38 is overexpressed by multiple myeloma and other hematological malignancies.	NAD	4-7	CD38 molecule	Homo sapiens	32-36
31820972-8	2020	A crystal structure of the most potent compound, compound 7, bound to InhA revealed the inhibitor to occupy a hydrophobic pocket implicated in binding the aliphatic portions of InhA substrates but distant from the NADH cofactor, i.e., in a site distinct from those occupied by the great majority of known InhA inhibitors.	NAD	214-218	NADH-dependent enoyl-[ACP] reductase	Mycobacterium tuberculosis H37Rv	70-74
10807796-1	2000	Recessive congenital methemoglobinemia due to nicotinamide adenine dinucleotide (NADH)-cytochrome b5 reductase (b5R) deficiency is classified into 2 clinical types: type 1 (erythrocyte type) and type 2 (generalized type).	NAD	46-79	cytochrome b5 reductase 3	Homo sapiens	112-115
10807796-1	2000	Recessive congenital methemoglobinemia due to nicotinamide adenine dinucleotide (NADH)-cytochrome b5 reductase (b5R) deficiency is classified into 2 clinical types: type 1 (erythrocyte type) and type 2 (generalized type).	NAD	81-85	cytochrome b5 reductase 3	Homo sapiens	112-115
10779683-1	2000	The well known NADP-specific isocitrate dehydrogenase (IDH) obtained from pig heart was found to oxidize NADH with accompanying consumption of oxygen (NADH:O(2)=1:1) in presence of polyvanadate.	NAD	105-109	isocitrate dehydrogenase [NADP] cytoplasmic	Sus scrofa	55-58
10779683-1	2000	The well known NADP-specific isocitrate dehydrogenase (IDH) obtained from pig heart was found to oxidize NADH with accompanying consumption of oxygen (NADH:O(2)=1:1) in presence of polyvanadate.	NAD	151-155	isocitrate dehydrogenase [NADP] cytoplasmic	Sus scrofa	55-58
10779683-2	2000	This activity of the soluble IDH-protein has the following features common with the previously described membrane-enzymes: heat-sensitive, active only with NADH but not NADPH, increased rates in acidic pH, dependence on concentrations of the enzyme, NADH, decavanadate and metavanadate (the two constituents of polyvanadate), and sensitivity to SOD and EDTA.	NAD	156-160	isocitrate dehydrogenase [NADP] cytoplasmic	Sus scrofa	29-32
31625260-5	2020	Furthermore, old NLRP3 KO mice showed an inhibition of the PI3K/AKT/mTOR pathway and autophagy improvement, compared with old wild mice and preserved Nampt-mediated NAD+ levels with increased SIRT1 protein expression.	NAD	165-168	NLR family, pyrin domain containing 3	Mus musculus	17-22
10779683-2	2000	This activity of the soluble IDH-protein has the following features common with the previously described membrane-enzymes: heat-sensitive, active only with NADH but not NADPH, increased rates in acidic pH, dependence on concentrations of the enzyme, NADH, decavanadate and metavanadate (the two constituents of polyvanadate), and sensitivity to SOD and EDTA.	NAD	250-254	isocitrate dehydrogenase [NADP] cytoplasmic	Sus scrofa	29-32
10779683-3	2000	Utilizing NADH as the electron source the IDH protein was able to reduce decavanadate but not metavanadate.	NAD	10-14	isocitrate dehydrogenase [NADP] cytoplasmic	Sus scrofa	42-45
10639079-4	2000	Furthermore, the PEG-chlorophyllin conjugate catalyzed the photoreduction of NADP(+) or NAD(+) in the presence of ascorbate as an electron donor and ferredoxin-NADP(+) reductase as the coupling enzyme.	NAD	88-94	ferredoxin reductase	Homo sapiens	149-177
31301008-5	2020	Interaction force and the corresponding amino acid residues between IDH and NAD+ or NADP+ were parsed by docking.	NAD	76-80	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	68-71
10559442-1	1999	The peroxisomal isoform of ascorbate peroxidase (APX) is a novel membrane isoform that functions in the regeneration of NAD(+) and protection against toxic reactive oxygen species.	NAD	120-126	L-ascorbate peroxidase 2, cytosolic	Nicotiana tabacum	49-52
31954883-3	2020	We investigated the role of Sirtuin 2 (SIRT2), a NAD-dependent protein deacetylase, in intestinal epithelial cell (IEC) proliferation and differentiation and the mechanism by which SIRT2 contributes to maintenance of intestinal cell homeostasis METHODS: IECs were collected from SIRT2-deficient mice and patients with IBD.	NAD	49-52	sirtuin 2	Mus musculus	28-37
31954883-3	2020	We investigated the role of Sirtuin 2 (SIRT2), a NAD-dependent protein deacetylase, in intestinal epithelial cell (IEC) proliferation and differentiation and the mechanism by which SIRT2 contributes to maintenance of intestinal cell homeostasis METHODS: IECs were collected from SIRT2-deficient mice and patients with IBD.	NAD	49-52	sirtuin 2	Mus musculus	39-44
10425679-10	1999	GTP and NADH inhibit GDH by keeping the catalytic cleft in a closed conformation.	NAD	8-12	glucose dehydrogenase	Bos taurus	21-24
31672920-3	2019	Accordingly, for more than 20 years it has remained unresolved how CD38 can use cytosolic substrates such as NAD and NADP to produce messengers that target intracellular Ca2+-stores.	NAD	109-112	CD38 molecule	Homo sapiens	67-71
10403632-9	1999	The above findings raise the possibility that a cytochrome P450-like protein, that can receive electrons from NADH, possibly through cytochrome b5 reductase, is present in the hepatic microsomes of rats and mice, and is capable of catalysing the bioactivation of aromatic amines through N-hydroxylation.	NAD	110-114	cytochrome P450, family 4, subfamily v, polypeptide 3	Rattus norvegicus	48-76
31598701-5	2019	Pyruvate represses histone gene expression by inducing the expression of NAD+ biosynthesis enzyme, nicotinamide phosphoribosyltransferase (NAMPT) via myocyte enhancer factor 2C (MEF2C), which then increases NAD+ levels and activates the histone deacetylase activity of SIRT1.	NAD	73-76	myocyte enhancer factor 2C	Homo sapiens	150-176
31598701-5	2019	Pyruvate represses histone gene expression by inducing the expression of NAD+ biosynthesis enzyme, nicotinamide phosphoribosyltransferase (NAMPT) via myocyte enhancer factor 2C (MEF2C), which then increases NAD+ levels and activates the histone deacetylase activity of SIRT1.	NAD	73-76	myocyte enhancer factor 2C	Homo sapiens	178-183
31754701-2	2019	The nicotinamide-adenine dinucleotide (NAD+)-dependent deacetylase enzyme, Sirtuin 1 (SIRT1), can prevent activation of these pathways and promote axonal regeneration.	NAD	4-37	sirtuin 1	Mus musculus	75-84
10328830-2	1999	Functional inactivation of the mitochondrial sHsps with murine Hsp25 antibody indicated that these sHsps protect NADH:ubiquinone oxidoreductase and NADH dehydrogenase activity (i.e., complex I) in submitochondrial vesicles during heat and oxidative stress.	NAD	113-117	heat shock protein family B (small) member 1	Rattus norvegicus	63-68
31754701-2	2019	The nicotinamide-adenine dinucleotide (NAD+)-dependent deacetylase enzyme, Sirtuin 1 (SIRT1), can prevent activation of these pathways and promote axonal regeneration.	NAD	4-37	sirtuin 1	Mus musculus	86-91
31754701-2	2019	The nicotinamide-adenine dinucleotide (NAD+)-dependent deacetylase enzyme, Sirtuin 1 (SIRT1), can prevent activation of these pathways and promote axonal regeneration.	NAD	39-43	sirtuin 1	Mus musculus	75-84
31754701-2	2019	The nicotinamide-adenine dinucleotide (NAD+)-dependent deacetylase enzyme, Sirtuin 1 (SIRT1), can prevent activation of these pathways and promote axonal regeneration.	NAD	39-43	sirtuin 1	Mus musculus	86-91
31754701-12	2019	In dorsal root ganglion protein extracts from nSIRT1OE mice, the NAD+-consuming enzyme PARP1 was deactivated and the major deacetylated protein was identified to be an E3 protein ligase, NEDD4-1, a protein required for axonal growth, regeneration and proteostasis in neurodegenerative diseases.	NAD	65-69	neural precursor cell expressed, developmentally down-regulated 4	Mus musculus	187-194
31608530-10	2019	Treatment with DPN resulted in the up-regulation of CREB and BDNF expressions, while PPT up-regulated expression of CREB without affecting BDNF levels.	NAD	15-18	cAMP responsive element binding protein 1	Rattus norvegicus	52-56
10383997-1	1999	: In the yeasts Saccharomyces cerevisiae and Debaryomyces hansenii, glycerol-3-phosphate dehydrogenase (NAD+-GPD) is believed to be the enzyme controlling the synthesis of glycerol in osmotically challenged cells.	NAD	104-108	glycerol-3-phosphate dehydrogenase	Saccharomyces cerevisiae S288C	68-102
10329026-10	1999	It encodes a protein that, using NAD+ as a preferred cofactor, utilizes free and CRBP-bound all-trans-retinol and steroids as substrates.	NAD	33-37	retinol binding protein 1	Homo sapiens	81-85
31693862-5	2019	Here, sirtuin 1 (SIRT1), an NAD-dependent deacetylase, was demonstrated to activate mouse PFs independent of its deacetylase activity.	NAD	28-31	sirtuin 1	Mus musculus	6-15
31693862-5	2019	Here, sirtuin 1 (SIRT1), an NAD-dependent deacetylase, was demonstrated to activate mouse PFs independent of its deacetylase activity.	NAD	28-31	sirtuin 1	Mus musculus	17-22
10215845-0	1999	In the Nicotiana sylvestris CMSII mutant, a recombination-mediated change 5" to the first exon of the mitochondrial nad1 gene is associated with lack of the NADH:ubiquinone oxidoreductase (complex I) NAD1 subunit.	NAD	157-161	NADH dehydrogenase subunit 1	Nicotiana sylvestris	116-120
31703292-8	2019	Finally, Dicer gene deletion reduced the copy number of mitochondrially encoded 1,4-Dihydronicotinamide adenine dinucleotide (NADH): ubiquinone oxidoreductase core subunit 6 (MT-ND6), a mitochondrial-encoded gene, in C-MSC.	NAD	80-124	dicer 1, ribonuclease III	Homo sapiens	9-14
31703292-8	2019	Finally, Dicer gene deletion reduced the copy number of mitochondrially encoded 1,4-Dihydronicotinamide adenine dinucleotide (NADH): ubiquinone oxidoreductase core subunit 6 (MT-ND6), a mitochondrial-encoded gene, in C-MSC.	NAD	126-130	dicer 1, ribonuclease III	Homo sapiens	9-14
9895226-7	1999	The data obtained suggests that: (1) expression of ADH and XOR or AOX in breast tissue provides the enzymes that generate ROS; (2) metabolism of alcohol produces acetaldehyde and NADH that can both be substrates for XOR or AOX and thereby result in ROS formation; and (3) ROS generated by XOR or AOX can induce the carcinogenic mutations and DNA damage found in breast cancer.	NAD	179-183	xanthine dehydrogenase	Homo sapiens	59-62
31657440-0	2019	Pyridoxamine-phosphate oxidases and pyridoxamine-phosphate oxidase-related proteins catalyze the oxidation of 6-NAD(P)H to NAD(P).	NAD	110-119	pyridoxamine 5'-phosphate oxidase	Rattus norvegicus	36-66
31657440-0	2019	Pyridoxamine-phosphate oxidases and pyridoxamine-phosphate oxidase-related proteins catalyze the oxidation of 6-NAD(P)H to NAD(P).	NAD	112-115	pyridoxamine 5'-phosphate oxidase	Rattus norvegicus	36-66
9895226-7	1999	The data obtained suggests that: (1) expression of ADH and XOR or AOX in breast tissue provides the enzymes that generate ROS; (2) metabolism of alcohol produces acetaldehyde and NADH that can both be substrates for XOR or AOX and thereby result in ROS formation; and (3) ROS generated by XOR or AOX can induce the carcinogenic mutations and DNA damage found in breast cancer.	NAD	179-183	xanthine dehydrogenase	Homo sapiens	216-219
31657440-2	2019	They are known to be oxidized to NAD(P)+ by mammalian renalase, an FAD-linked enzyme mainly present in heart and kidney, and by related bacterial enzymes.	NAD	33-40	renalase, FAD dependent amine oxidase	Homo sapiens	54-62
9895226-7	1999	The data obtained suggests that: (1) expression of ADH and XOR or AOX in breast tissue provides the enzymes that generate ROS; (2) metabolism of alcohol produces acetaldehyde and NADH that can both be substrates for XOR or AOX and thereby result in ROS formation; and (3) ROS generated by XOR or AOX can induce the carcinogenic mutations and DNA damage found in breast cancer.	NAD	179-183	xanthine dehydrogenase	Homo sapiens	216-219
31624074-8	2019	The results showed that either a HFD or dSir2 knockdown remarkably increased cardiac TG level and d FAS expression, reduced heart fractional shortening and diastolic diameter, increased arrhythmia index, and decreased heart NAD+ level, dSIR2 protein, dSir2 and PGC-1alpha expression levels.	NAD	224-227	Sirtuin 1	Drosophila melanogaster	40-45
9915792-1	1999	The last step of tRNA splicing in yeast is catalyzed by Tpt1 protein, which transfers the 2"-phosphate from ligated tRNA to NAD to produce ADP-ribose 1"-2"-cyclic phosphate (Appr&gt;p).	NAD	124-127	tRNA 2'-phosphotransferase	Saccharomyces cerevisiae S288C	56-60
31624074-9	2019	Contrarily, either exercise or dSir2 overexpression remarkably reduced heart TG level, dFAS expression and arrhythmia index, and notably increased heart fractional shortening, diastolic diameter, NAD+ level, dSIR2 level, and heart dSir2 and PGC-1alpha expression.	NAD	196-199	Sirtuin 1	Drosophila melanogaster	31-36
31624074-10	2019	Therefore, we declared that exercise training could improve lipotoxic cardiomyopathy induced by a HFD or cardiac dSir2 knockdown in old Drosophila The NAD+/dSIR2/PGC-1alpha pathway activation was an important molecular mechanism of exercise resistance against lipotoxic cardiomyopathy.	NAD	151-154	Sirtuin 1	Drosophila melanogaster	113-118
31624074-10	2019	Therefore, we declared that exercise training could improve lipotoxic cardiomyopathy induced by a HFD or cardiac dSir2 knockdown in old Drosophila The NAD+/dSIR2/PGC-1alpha pathway activation was an important molecular mechanism of exercise resistance against lipotoxic cardiomyopathy.	NAD	151-154	Sirtuin 1	Drosophila melanogaster	156-161
10403507-6	1999	These findings suggest that raised NAD concentrations in HPRT- erythrocytes are due to enhanced synthesis as a result of increased enzyme activities.	NAD	35-38	hypoxanthine phosphoribosyltransferase 1	Homo sapiens	57-61
31636473-1	2019	BACKGROUND: Sirtuin 1 (SIRT1) is a nicotinamide adenine dinucleotide (NAD+)-dependent protein deacetylase that is involved in various diseases, including cancers, metabolic diseases, and inflammation-associated diseases.	NAD	35-68	sirtuin 1	Mus musculus	12-21
31636473-1	2019	BACKGROUND: Sirtuin 1 (SIRT1) is a nicotinamide adenine dinucleotide (NAD+)-dependent protein deacetylase that is involved in various diseases, including cancers, metabolic diseases, and inflammation-associated diseases.	NAD	35-68	sirtuin 1	Mus musculus	23-28
31636473-1	2019	BACKGROUND: Sirtuin 1 (SIRT1) is a nicotinamide adenine dinucleotide (NAD+)-dependent protein deacetylase that is involved in various diseases, including cancers, metabolic diseases, and inflammation-associated diseases.	NAD	70-74	sirtuin 1	Mus musculus	12-21
31636473-1	2019	BACKGROUND: Sirtuin 1 (SIRT1) is a nicotinamide adenine dinucleotide (NAD+)-dependent protein deacetylase that is involved in various diseases, including cancers, metabolic diseases, and inflammation-associated diseases.	NAD	70-74	sirtuin 1	Mus musculus	23-28
9870556-2	1998	3HAO participates in de novo biosynthesis of NAD in mammalian kidney and liver, and it is present in low concentrations in brain where its function is controversial.	NAD	45-48	3-hydroxyanthranilate 3,4-dioxygenase	Homo sapiens	0-4
31681271-5	2019	In contrast, high dose endotoxin drove a shift of NAD synthesis pathway from early NAMPT-dependent NAD salvage to late indoleamine 2,3-dioxygenase-1 (IDO1)-dependent NAD de novo biosynthesis, leading to persistent immune suppression.	NAD	50-53	indoleamine 2,3-dioxygenase 1	Homo sapiens	119-148
31681271-5	2019	In contrast, high dose endotoxin drove a shift of NAD synthesis pathway from early NAMPT-dependent NAD salvage to late indoleamine 2,3-dioxygenase-1 (IDO1)-dependent NAD de novo biosynthesis, leading to persistent immune suppression.	NAD	50-53	indoleamine 2,3-dioxygenase 1	Homo sapiens	150-154
31681271-6	2019	This is resulted from the IDO1-dependent expansion of nuclear NAD pool and nuclear NAD-dependent prolongation of sirtuin1 (SIRT1)-directed epigenetics of immune tolerance.	NAD	62-65	indoleamine 2,3-dioxygenase 1	Homo sapiens	26-30
31681271-7	2019	Inhibition of IDO1 activity predominantly decreased nuclear NAD level, which promoted sequential dissociations of immunosuppressive SIRT1 and RelB from the promoter of pro-inflammatory TNF-alpha gene and broke endotoxin tolerance.	NAD	60-63	indoleamine 2,3-dioxygenase 1	Homo sapiens	14-18
31681271-8	2019	Thus, NAMPT-NAD-SIRT1 axis adapts pro-inflammation, but IDO1-NAD-SIRT1-RelB axis sustains endotoxin tolerance during acute inflammatory response.	NAD	61-64	indoleamine 2,3-dioxygenase 1	Homo sapiens	56-60
9860297-0	1998	The nuclear-encoded human NADH:ubiquinone oxidoreductase NDUFA8 subunit: cDNA cloning, chromosomal localization, tissue distribution, and mutation detection in complex-I-deficient patients.	NAD	26-30	NADH:ubiquinone oxidoreductase subunit A8	Homo sapiens	57-63
9860297-1	1998	We report the cloning of the cDNA sequence of the nuclear-encoded NDUFA8 subunit of NADH: ubiquinone oxidoreductase, the first mitochondrial respiratory chain complex.	NAD	84-88	NADH:ubiquinone oxidoreductase subunit A8	Homo sapiens	66-72
9873629-1	1998	Electroenzymatic reduction of NAD+ to NADH for subsequent use in enzymatic synthesis has been carried out at carbon electrodes bearing lipoamide dehydrogenase (LiDH) immobilized under a Nafion film.	NAD	38-42	dihydrolipoamide dehydrogenase	Homo sapiens	135-158
31590397-12	2019	(4) Conclusion: Under high glucose conditions, decreases in the reducing power may be linked to DNA oxidative damage and apoptosis via activation of the NMNAT-NAD-PARP-SIRT axis.	NAD	159-162	poly (ADP-ribose) polymerase 1	Rattus norvegicus	163-167
31590397-13	2019	Rb1 provides an advantage during high glucose-induced cell damage by targeting the NAD-PARP-SIRT signaling pathway and modulating the redox state in RCECs.	NAD	83-86	poly (ADP-ribose) polymerase 1	Rattus norvegicus	87-91
31353811-6	2019	We elucidated that the reduction of cellular NAD+ during the aging process was an important contributor for ARHL; it facilitated oxidative stress and pro-inflammatory responses in the cochlear tissue through regulating sirtuins that alter various signaling pathways, such as NF-kappaB, p53, and IDH2.	NAD	45-49	transformation related protein 53, pseudogene	Mus musculus	286-289
31347918-3	2019	NAD is directly involved in various metabolic processes and may indirectly regulate metabolic gene expression through Sirt1, an NAD-dependent protein deacetylase.	NAD	0-3	sirtuin 1	Mus musculus	118-123
9873629-1	1998	Electroenzymatic reduction of NAD+ to NADH for subsequent use in enzymatic synthesis has been carried out at carbon electrodes bearing lipoamide dehydrogenase (LiDH) immobilized under a Nafion film.	NAD	38-42	dihydrolipoamide dehydrogenase	Homo sapiens	160-164
31347918-3	2019	NAD is directly involved in various metabolic processes and may indirectly regulate metabolic gene expression through Sirt1, an NAD-dependent protein deacetylase.	NAD	128-131	sirtuin 1	Mus musculus	118-123
31347918-8	2019	On the other hand, the NAD level was increased in Tg-Nampt mice at baseline but not during PO, possibly due to increased consumption of NAD by Sirt1.	NAD	23-26	sirtuin 1	Mus musculus	143-148
9689052-7	1998	Added NADH did not serve as the substrate, suggesting that the expressed Ndi1 enzyme was located on the matrix side of the inner mitochondrial membranes.	NAD	6-10	NADH-ubiquinone reductase (H(+)-translocating) NDI1	Saccharomyces cerevisiae S288C	73-77
31347918-8	2019	On the other hand, the NAD level was increased in Tg-Nampt mice at baseline but not during PO, possibly due to increased consumption of NAD by Sirt1.	NAD	136-139	sirtuin 1	Mus musculus	143-148
30993413-6	2019	Mac1 appears to work with the Hst1-Sum1-Rfm1 complex to repress the expression of de novo NAD+ biosynthesis genes.	NAD	90-94	Rfm1p	Saccharomyces cerevisiae S288C	40-44
9689052-11	1998	These results indicated that the S. cerevisiae Ndi1 was expressed functionally in CCL16-B2 cells and catalyzed electron transfer from NADH in the matrix to ubiquinone-10 in the inner mitochondrial membranes.	NAD	134-138	NADH-ubiquinone reductase (H(+)-translocating) NDI1	Saccharomyces cerevisiae S288C	47-51
31433161-7	2019	The lysine acylation of RalB is regulated by SIRT2, a member of the sirtuin family of nicotinamide adenine dinucleotide (NAD)-dependent protein lysine deacylases.	NAD	86-119	RAS like proto-oncogene B	Homo sapiens	24-28
9695367-3	1998	RESULTS: The cytochemical reaction for diaphorase/NADH revealed disorders of the mitochondrial activity and subtle and drastic malformations in the spermatozoa midpieces.	NAD	50-54	dihydrolipoamide dehydrogenase	Homo sapiens	39-49
31433161-7	2019	The lysine acylation of RalB is regulated by SIRT2, a member of the sirtuin family of nicotinamide adenine dinucleotide (NAD)-dependent protein lysine deacylases.	NAD	86-119	sirtuin 2	Homo sapiens	45-50
31433161-7	2019	The lysine acylation of RalB is regulated by SIRT2, a member of the sirtuin family of nicotinamide adenine dinucleotide (NAD)-dependent protein lysine deacylases.	NAD	121-124	RAS like proto-oncogene B	Homo sapiens	24-28
31433161-7	2019	The lysine acylation of RalB is regulated by SIRT2, a member of the sirtuin family of nicotinamide adenine dinucleotide (NAD)-dependent protein lysine deacylases.	NAD	121-124	sirtuin 2	Homo sapiens	45-50
31422819-11	2019	Correcting the highly oxidized cytosolic NAD-redox state by pyruvate supplementation restored serine biosynthesis in GOT2-deficient cells.	NAD	41-44	glutamic-oxaloacetic transaminase 2	Homo sapiens	117-121
31611752-0	2019	Up-regulation of miR-381 inhibits NAD+ salvage pathway and promotes apoptosis in breast cancer cells.	NAD	34-37	microRNA 381	Homo sapiens	17-24
9599007-2	1998	When the effects of different gabapentin concentrations on GDH activities were studied in the direction of reductive amination of 2-oxoglutarate with NADPH as a coenzyme, a marked activation was observed for both isoproteins, whereas both isoproteins showed activation to a lesser extent with NADH as a coenzyme.	NAD	293-297	glutamate dehydrogenase 1, mitochondrial	Bos taurus	59-62
31611752-9	2019	Our results revealed that the 3"-UTR of NAMPT was a direct target of miR-381 and its up-regulation decreased NAMPT gene and protein expression, leading to a notable reduction in intracellular NAD and subsequently cell survival and induction of apoptosis.	NAD	192-195	microRNA 381	Homo sapiens	69-76
31447857-2	2019	The dinucleotide NAD+ has also been proposed to be a P2Y11 receptor ligand but its role is less clear.	NAD	17-21	purinergic receptor P2Y11	Homo sapiens	53-58
31447857-9	2019	In conclusion, our data indicate that an AMPK-NAMPT-NAD+ signaling axis promotes P2Y11 receptor expression during M2 polarization of human macrophages in response to IL-10.	NAD	52-56	purinergic receptor P2Y11	Homo sapiens	81-86
9405293-10	1998	NADH alone stimulated the activities of PDK1 and PDK2 by 20 and 30% respectively.	NAD	0-4	pyruvate dehydrogenase kinase 2	Homo sapiens	49-53
31102152-1	2019	Sirt1, also known as the longevity gene, is an NAD+-dependent class III histone deacetylase that has been extensively studied in multiple areas of research including cellular metabolism, longevity, cancer, autoimmunity, and immunity.	NAD	47-51	sirtuin 1	Mus musculus	0-5
9336832-12	1997	This suggests that all of the ADP-ribosylating enzymes that are structurally homologous to DT and ETA will bind a highly similar conformation of NAD.	NAD	145-148	endothelin receptor type A	Homo sapiens	98-101
31168681-5	2019	We show that the mitochondrial NAD pool is elevated in the mod1 mutant.	NAD	31-34	NAD(P)-binding Rossmann-fold superfamily protein	Arabidopsis thaliana	59-63
31168681-6	2019	The som592 mutation fully suppressed mitochondrial NADH hyper-accumulation, ROS production, and PCD in the mod1 mutant, indicating a causal relationship between mitochondrial NAD accumulation and ROS/PCD phenotypes.	NAD	51-55	NAD(P)-binding Rossmann-fold superfamily protein	Arabidopsis thaliana	107-111
31168681-6	2019	The som592 mutation fully suppressed mitochondrial NADH hyper-accumulation, ROS production, and PCD in the mod1 mutant, indicating a causal relationship between mitochondrial NAD accumulation and ROS/PCD phenotypes.	NAD	51-54	NAD(P)-binding Rossmann-fold superfamily protein	Arabidopsis thaliana	107-111
9286695-1	1997	In this paper we present the entire genomic sequence as well as the cDNA sequence of two new human genes encoding the gamma subunit of the NAD(+)-dependent isocitrate dehydrogenase (H-IDH gamma) and the translocon-associated protein delta subunit (TRAP delta).	NAD	139-145	isocitrate dehydrogenase (NAD(+)) 3 non-catalytic subunit gamma	Homo sapiens	184-193
9234667-8	1997	Acetaldehyde accumulated through the competitive regeneration of NADH via GPDH.	NAD	65-69	glycerol-3-phosphate dehydrogenase	Saccharomyces cerevisiae S288C	74-78
30472140-0	2019	NAD binding by human CD38 analyzed by Trp189 fluorescence.	NAD	0-3	CD38 molecule	Homo sapiens	21-25
30472140-1	2019	The NAD-glycohydrolase/ADP-ribosyl cyclase CD38 catalyzes the metabolism of nicotinamide adenine dinucleotide (NAD) to the Ca2+ mobilizing second messengers ADP-ribose (ADPR), 2"-deoxy-ADPR, and cyclic ADP-ribose (cADPR).	NAD	76-109	CD38 molecule	Homo sapiens	43-47
30472140-1	2019	The NAD-glycohydrolase/ADP-ribosyl cyclase CD38 catalyzes the metabolism of nicotinamide adenine dinucleotide (NAD) to the Ca2+ mobilizing second messengers ADP-ribose (ADPR), 2"-deoxy-ADPR, and cyclic ADP-ribose (cADPR).	NAD	4-7	CD38 molecule	Homo sapiens	43-47
30472140-2	2019	In the present study, we investigated binding and metabolism of NAD by a soluble fragment of human CD38, sCD38, and its catalytically inactive mutant by monitoring changes in endogenous tryptophan (Trp) fluorescence.	NAD	64-67	CD38 molecule	Homo sapiens	99-103
31053044-8	2019	Our data show that the NAD metabolites interfere with early events associated with differentiation of THP-1 cells along the monocytic path and that they affect LPS-induced biological responses of the cell line.	NAD	23-26	interferon regulatory factor 6	Homo sapiens	160-163
9207238-0	1997	Identification of alternative first exons of NADH-cytochrome b5 reductase gene expressed ubiquitously in human cells.	NAD	45-49	cytochrome b5 reductase 3	Homo sapiens	61-73
31275331-3	2019	NADK is a key enzyme for NADP (including NADP+ and NADPH) biosynthesis by phosphorylating NAD (including NAD+ and NADH) and therefore, maintains the balance between NAD pool and NADP pool through an allosteric regulation mode.	NAD	105-109	NAD kinase	Homo sapiens	0-4
31275331-3	2019	NADK is a key enzyme for NADP (including NADP+ and NADPH) biosynthesis by phosphorylating NAD (including NAD+ and NADH) and therefore, maintains the balance between NAD pool and NADP pool through an allosteric regulation mode.	NAD	114-118	NAD kinase	Homo sapiens	0-4
31275331-3	2019	NADK is a key enzyme for NADP (including NADP+ and NADPH) biosynthesis by phosphorylating NAD (including NAD+ and NADH) and therefore, maintains the balance between NAD pool and NADP pool through an allosteric regulation mode.	NAD	25-28	NAD kinase	Homo sapiens	0-4
31275331-4	2019	In addition, the two respective derivatives from NAD+ (substrate of NADK) and NADP+ (product of NADK), cyclic ADP-ribose (cADPR) and nicotinic acid adenine dinucleotide phosphate (NAADP), have been considered to be the important messengers for intracellular Ca2+ homeostasis which could finally influence the combination between CaM and NADK, forming a feedback regulation mechanism.	NAD	49-53	NAD kinase	Homo sapiens	68-72
9182988-7	1997	The potential involvement of reactive oxygen species arising from NADH oxidation by xanthine oxidoreductase in ischaemia-reperfusion injury and other disease states, as well as in normal signal transduction, is discusssed.	NAD	66-70	xanthine dehydrogenase	Homo sapiens	84-107
31275331-4	2019	In addition, the two respective derivatives from NAD+ (substrate of NADK) and NADP+ (product of NADK), cyclic ADP-ribose (cADPR) and nicotinic acid adenine dinucleotide phosphate (NAADP), have been considered to be the important messengers for intracellular Ca2+ homeostasis which could finally influence the combination between CaM and NADK, forming a feedback regulation mechanism.	NAD	49-53	NAD kinase	Homo sapiens	96-100
31275331-4	2019	In addition, the two respective derivatives from NAD+ (substrate of NADK) and NADP+ (product of NADK), cyclic ADP-ribose (cADPR) and nicotinic acid adenine dinucleotide phosphate (NAADP), have been considered to be the important messengers for intracellular Ca2+ homeostasis which could finally influence the combination between CaM and NADK, forming a feedback regulation mechanism.	NAD	49-53	NAD kinase	Homo sapiens	96-100
9505366-3	1997	Aldose reductase inhibitors partially restored Na+, K(+)-ATP-ase activity in sciatic nerve of diabetic rats and redox state of nicotinamide adenine dinucleotides.	NAD	127-161	aldo-keto reductase family 1 member B1	Rattus norvegicus	0-16
30930169-4	2019	Administration of the NAD(+) precursor nicotinamide mononucleotide maintains telomere length, dampens the DNA damage response and p53, improves mitochondrial function, and, functionally, rescues liver fibrosis in a partially Sirt1-dependent manner.	NAD	22-28	transformation related protein 53, pseudogene	Mus musculus	130-133
30930169-4	2019	Administration of the NAD(+) precursor nicotinamide mononucleotide maintains telomere length, dampens the DNA damage response and p53, improves mitochondrial function, and, functionally, rescues liver fibrosis in a partially Sirt1-dependent manner.	NAD	22-28	sirtuin 1	Mus musculus	225-230
9083059-14	1997	Thus, our data suggest that domain I of CaM plays a key role in the differential activation of NAD kinase exhibited by SCaM-1 and SCaM-4.	NAD	95-98	calmodulin	Glycine max	130-136
30771486-3	2019	We have investigated the role of the NAD+-dependent Class III deacetylase SIRT1 in the adaptive response to MG in mouse oocytes and ovary.	NAD	37-41	sirtuin 1	Mus musculus	74-79
9008232-3	1997	Four genes not previously described in psoriasis--connexin 26, a gap junction protein; squamous cell carcinoma antigen-1 (SCCA1), a serine protease inhibitor; and mitochondrial NAD subunits 5 and 6--were identified as having very high expression levels in psoriatic skin.	NAD	177-180	serpin family B member 3	Homo sapiens	87-120
31127273-1	2019	Sirtuin 1 (Sirt1) is an NAD-dependent class III deacetylase that functions as a cellular energy sensor.	NAD	24-27	sirtuin 1	Mus musculus	0-9
31127273-1	2019	Sirtuin 1 (Sirt1) is an NAD-dependent class III deacetylase that functions as a cellular energy sensor.	NAD	24-27	sirtuin 1	Mus musculus	11-16
31214171-1	2019	CD38 (Cluster of Differentiation 38) is a multifunctional ecto-enzyme that metabolizes NAD+ and mediates nicotinamide dinucleotide (NAD+) and extracellular nucleotide homeostasis as well as intracellular calcium.	NAD	87-91	CD38 molecule	Homo sapiens	0-4
31214171-1	2019	CD38 (Cluster of Differentiation 38) is a multifunctional ecto-enzyme that metabolizes NAD+ and mediates nicotinamide dinucleotide (NAD+) and extracellular nucleotide homeostasis as well as intracellular calcium.	NAD	87-91	CD38 molecule	Homo sapiens	6-35
31214171-1	2019	CD38 (Cluster of Differentiation 38) is a multifunctional ecto-enzyme that metabolizes NAD+ and mediates nicotinamide dinucleotide (NAD+) and extracellular nucleotide homeostasis as well as intracellular calcium.	NAD	105-130	CD38 molecule	Homo sapiens	0-4
31214171-1	2019	CD38 (Cluster of Differentiation 38) is a multifunctional ecto-enzyme that metabolizes NAD+ and mediates nicotinamide dinucleotide (NAD+) and extracellular nucleotide homeostasis as well as intracellular calcium.	NAD	105-130	CD38 molecule	Homo sapiens	6-35
31214171-1	2019	CD38 (Cluster of Differentiation 38) is a multifunctional ecto-enzyme that metabolizes NAD+ and mediates nicotinamide dinucleotide (NAD+) and extracellular nucleotide homeostasis as well as intracellular calcium.	NAD	132-136	CD38 molecule	Homo sapiens	0-4
31214171-1	2019	CD38 (Cluster of Differentiation 38) is a multifunctional ecto-enzyme that metabolizes NAD+ and mediates nicotinamide dinucleotide (NAD+) and extracellular nucleotide homeostasis as well as intracellular calcium.	NAD	132-136	CD38 molecule	Homo sapiens	6-35
31214171-4	2019	Of greatest significance is the role of CD38 as an ecto-enzyme capable of modulating extracellular NAD+ precursor availability: 1 to bacteria unable to perform de novo synthesis of NAD+; and 2 in aged parenchyma impacted by the accumulation of immune cells during the process of "inflammaging".	NAD	99-103	CD38 molecule	Homo sapiens	40-44
31214171-4	2019	Of greatest significance is the role of CD38 as an ecto-enzyme capable of modulating extracellular NAD+ precursor availability: 1 to bacteria unable to perform de novo synthesis of NAD+; and 2 in aged parenchyma impacted by the accumulation of immune cells during the process of "inflammaging".	NAD	181-185	CD38 molecule	Homo sapiens	40-44
31214171-5	2019	We also discuss the paradoxical role of CD38 as a modulator of intracellular NAD+, particularly in tumor immunity.	NAD	77-81	CD38 molecule	Homo sapiens	40-44
30763605-8	2019	Besides, NAD(H) activated the efflux of mitochondrial AN via ANT.	NAD	9-15	solute carrier family 25 member 6	Homo sapiens	61-64
30718260-10	2019	Consistent with known effects of mitochondrial fragmentation on metabolism, fluorescence lifetime imaging microscopy of endogenous NADH showed that PAI1 promotes glycolysis in cell-based assays, orthotopic tumor xenografts, and lung metastases.	NAD	131-135	serpin family E member 1	Homo sapiens	148-152
31179321-11	2019	When proteins with fold change &gt;1.2 or &lt;0.84 and P value &lt; 0.05 between groups were considered differentially expressed, the expression of 10 proteins, including CD38, involved in the nicotinamide adenine dinucleotide (NAD) metabolism and signaling pathway showed significant changes in IBD.	NAD	193-226	CD38 molecule	Homo sapiens	171-175
31179321-11	2019	When proteins with fold change &gt;1.2 or &lt;0.84 and P value &lt; 0.05 between groups were considered differentially expressed, the expression of 10 proteins, including CD38, involved in the nicotinamide adenine dinucleotide (NAD) metabolism and signaling pathway showed significant changes in IBD.	NAD	228-231	CD38 molecule	Homo sapiens	171-175
30648291-1	2019	Apart from its vital function as a redox cofactor, nicotinamide adenine dinucleotide (NAD+ ) has emerged as a crucial substrate for NAD+ -consuming enzymes, including poly(ADP-ribosyl)transferase 1 (PARP1) and CD38/CD157.	NAD	51-84	CD38 molecule	Homo sapiens	210-214
30648291-1	2019	Apart from its vital function as a redox cofactor, nicotinamide adenine dinucleotide (NAD+ ) has emerged as a crucial substrate for NAD+ -consuming enzymes, including poly(ADP-ribosyl)transferase 1 (PARP1) and CD38/CD157.	NAD	86-90	CD38 molecule	Homo sapiens	210-214
30648291-1	2019	Apart from its vital function as a redox cofactor, nicotinamide adenine dinucleotide (NAD+ ) has emerged as a crucial substrate for NAD+ -consuming enzymes, including poly(ADP-ribosyl)transferase 1 (PARP1) and CD38/CD157.	NAD	132-136	CD38 molecule	Homo sapiens	210-214
30846598-3	2019	Akt phosphorylates NAD kinase (NADK), the sole cytosolic enzyme that catalyzes the synthesis of NADP+ from NAD+ (the oxidized form of NADH), on three serine residues (Ser44, Ser46, and Ser48) within an amino-terminal domain.	NAD	107-111	NAD kinase	Homo sapiens	19-29
30846598-3	2019	Akt phosphorylates NAD kinase (NADK), the sole cytosolic enzyme that catalyzes the synthesis of NADP+ from NAD+ (the oxidized form of NADH), on three serine residues (Ser44, Ser46, and Ser48) within an amino-terminal domain.	NAD	107-111	NAD kinase	Homo sapiens	31-35
30846598-3	2019	Akt phosphorylates NAD kinase (NADK), the sole cytosolic enzyme that catalyzes the synthesis of NADP+ from NAD+ (the oxidized form of NADH), on three serine residues (Ser44, Ser46, and Ser48) within an amino-terminal domain.	NAD	134-138	NAD kinase	Homo sapiens	19-29
30846598-3	2019	Akt phosphorylates NAD kinase (NADK), the sole cytosolic enzyme that catalyzes the synthesis of NADP+ from NAD+ (the oxidized form of NADH), on three serine residues (Ser44, Ser46, and Ser48) within an amino-terminal domain.	NAD	134-138	NAD kinase	Homo sapiens	31-35
30692130-0	2019	The E3 ligase Highwire promotes synaptic transmission by targeting the NAD-synthesizing enzyme dNmnat.	NAD	71-74	Nicotinamide mononucleotide adenylyltransferase	Drosophila melanogaster	95-101
30692130-3	2019	Highwire targets the NAD+ biosynthetic and axoprotective enzyme dNmnat to regulate axonal injury responses.	NAD	21-25	Nicotinamide mononucleotide adenylyltransferase	Drosophila melanogaster	64-70
30692130-6	2019	Catalytically active dNmnat is required to drive defects in evoked release, and depletion of a second NAD+ synthesizing enzyme is sufficient to suppress these defects in highwire mutants, suggesting that excess NAD+ biosynthesis is the mechanism inhibiting neurotransmission.	NAD	211-215	Nicotinamide mononucleotide adenylyltransferase	Drosophila melanogaster	21-27
30496552-0	2019	Human DNA ligase IV is able to use NAD+ as an alternative adenylation donor for DNA ends ligation.	NAD	35-39	DNA ligase 4	Homo sapiens	6-19
30496552-2	2019	Here, we report that human DNA ligase IV, a key enzyme in DNA double-strand break (DSB) repair, is able to use NAD+ as a substrate for double-stranded DNA ligation.	NAD	111-115	DNA ligase 4	Homo sapiens	27-40
30457689-6	2019	The NADH fluorescence intensity measured by two-photon excitation fluorescence (TPEF) microscopy was consistently increased in CRC cell lines, azoxymethane/dextran sodium sulfate (AOM/DSS)-induced CRC tissues and tumor tissues from CRC patients.	NAD	4-8	transmembrane protein with EGF like and two follistatin like domains 2	Homo sapiens	80-84
30457689-8	2019	Collectively, our results suggest that NAMPT-mediated upregulation of the NAD(H) pool protects cancer cells against detrimental oxidative stress and that detecting NADH fluorescence by TPEF microscopy could be a potential method for monitoring CRC progression.	NAD	164-168	transmembrane protein with EGF like and two follistatin like domains 2	Homo sapiens	185-189
30761140-5	2019	Such increased alpha-tubulin acetylation was significantly suppressed either by resveratrol or NAD+ (coenzyme required for deacetylase activity of SIRT2), or by genetic knockdown of MEC-17 (gene encoding alpha-tubulin acetyltransferase 1).	NAD	95-99	sirtuin 2	Mus musculus	147-152
30761140-6	2019	Concurrently, the paclitaxel-mediated enhancement of NLRP3 inflammasome activation was significantly suppressed by resveratrol, NAD+, or MEC-17 knockdown, indicating the involvement of paclitaxel-induced alpha-tubulin acetylation in the augmentation of NLRP3 inflammasome activation.	NAD	128-132	NLR family, pyrin domain containing 3	Mus musculus	53-58
29567265-6	2019	Animals were randomly treated with 17beta-estradiol (E2), DPN (ERbeta selective agonist), or their respective vehicles, PBS and DMSO.	NAD	58-61	estrogen receptor 2	Rattus norvegicus	63-69
30537007-3	2019	According to this model, increased catalytic activity of CD38 may reduce CD4 T cells" cytoplasmic nicotin-amide adenine dinucleotide (NAD), leading to a chronic Warburg effect.	NAD	98-132	CD38 molecule	Homo sapiens	57-61
30537007-3	2019	According to this model, increased catalytic activity of CD38 may reduce CD4 T cells" cytoplasmic nicotin-amide adenine dinucleotide (NAD), leading to a chronic Warburg effect.	NAD	134-137	CD38 molecule	Homo sapiens	57-61
30201537-3	2019	We found that ERalpha and/or ERbeta activation using their agonists (0.5 mg/kg E2, PPT or DPN) ameliorate memory impairment in the Morris water maze and Y-maze tests, increase hippocampal neurogenesis and prevent hippocampal apoptotic responses.	NAD	90-93	estrogen receptor 1 (alpha)	Mus musculus	14-21
30246917-0	2019	Steric hindrance controls pyridine nucleotide specificity of a flavin-dependent NADH:quinone oxidoreductase.	NAD	80-84	crystallin zeta	Homo sapiens	85-107
30246917-1	2019	The crystal structure of the NADH:quinone oxidoreductase PA1024 has been solved in complex with NAD+ to 2.2 A resolution.	NAD	29-33	crystallin zeta	Homo sapiens	34-56
30246917-1	2019	The crystal structure of the NADH:quinone oxidoreductase PA1024 has been solved in complex with NAD+ to 2.2 A resolution.	NAD	96-100	crystallin zeta	Homo sapiens	34-56
30246917-5	2019	P78, P82, and P84 provide internal rigidity to the loop, whereas Q80 serves as an active site latch that secures the NAD+ within the binding pocket.	NAD	117-121	microspherule protein 1	Homo sapiens	0-3
30246917-8	2019	Steric constraints between the adenosine ribose of NAD+ , P78, and Q80, control the strict specificity of the enzyme for NADH.	NAD	121-125	microspherule protein 1	Homo sapiens	58-61
30619489-5	2018	In this paper, we investigated the effects of changes in the cellular content of NAD+ on CLS by altering the expression of mitochondrial NAD+ carriers, namely Ndt1 and Ndt2.	NAD	81-85	NAD+ transporter	Saccharomyces cerevisiae S288C	159-163
30619489-5	2018	In this paper, we investigated the effects of changes in the cellular content of NAD+ on CLS by altering the expression of mitochondrial NAD+ carriers, namely Ndt1 and Ndt2.	NAD	137-141	NAD+ transporter	Saccharomyces cerevisiae S288C	159-163
30619489-7	2018	In particular, lack of both carriers decreases NAD+ content and extends CLS, whereas NDT1 overexpression increases NAD+ content and reduces CLS.	NAD	115-119	NAD+ transporter	Saccharomyces cerevisiae S288C	85-89
30552101-4	2018	RNA profiling revealed that TRM from liver and small intestine express P2RX7, a damage/danger-associated molecular pattern (DAMP) receptor that is triggered by extracellular nucleotides (ATP, NAD+).	NAD	192-196	tremor	Mus musculus	28-31
30552101-6	2018	Tissue damage induced during routine isolation of liver lymphocytes led to P2RX7 activation and resulted in selective cell death of TRM P2RX7 activation in vivo by exogenous NAD+ led to a specific depletion of TRM while retaining TCIRC The effect was absent in P2RX7-deficient mice and after P2RX7 blockade.	NAD	174-178	tremor	Mus musculus	132-135
30552101-6	2018	Tissue damage induced during routine isolation of liver lymphocytes led to P2RX7 activation and resulted in selective cell death of TRM P2RX7 activation in vivo by exogenous NAD+ led to a specific depletion of TRM while retaining TCIRC The effect was absent in P2RX7-deficient mice and after P2RX7 blockade.	NAD	174-178	tremor	Mus musculus	210-213
30552101-7	2018	TCR triggering down-regulated P2RX7 expression and made TRM resistant to NAD-induced cell death.	NAD	73-76	tremor	Mus musculus	56-59
30358055-3	2018	Demonstrated herein is the incorporation of a natural flavin cofactor (FMN) into the specific microenvironment of a water-soluble polymer which allows the efficient reduction of the FMN by NADH in aqueous solution.	NAD	189-193	formin 1	Homo sapiens	71-74
30358055-3	2018	Demonstrated herein is the incorporation of a natural flavin cofactor (FMN) into the specific microenvironment of a water-soluble polymer which allows the efficient reduction of the FMN by NADH in aqueous solution.	NAD	189-193	formin 1	Homo sapiens	182-185
30533032-1	2018	The NAD+-dependent deacetylase SIRT2 is unique amongst sirtuins as it is effective in the cytosol, as well as the mitochondria.	NAD	4-7	sirtuin 2	Mus musculus	31-36
30053027-0	2018	Rescue of biosynthesis of nicotinamide adenine dinucleotide protects the heart in cardiomyopathy caused by lamin A/C gene mutation.	NAD	26-59	lamin A/C	Homo sapiens	107-116
30053027-5	2018	We showed here that NAD+ salvage pathway was altered in the heart of mouse and human carrying LMNA mutation, leading to an alteration of one of NAD+ co-substrate enzymes, PARP-1.	NAD	20-24	lamin A/C	Homo sapiens	94-98
30053027-5	2018	We showed here that NAD+ salvage pathway was altered in the heart of mouse and human carrying LMNA mutation, leading to an alteration of one of NAD+ co-substrate enzymes, PARP-1.	NAD	144-148	lamin A/C	Homo sapiens	94-98
30222979-1	2018	NADH cytochrome b5 reductase mediates electron transfer from NADH to cytochrome b5 utilizing flavin adenine dinucleotide as a redox cofactor.	NAD	0-4	cytochrome b5 type A	Homo sapiens	5-18
30222979-1	2018	NADH cytochrome b5 reductase mediates electron transfer from NADH to cytochrome b5 utilizing flavin adenine dinucleotide as a redox cofactor.	NAD	0-4	cytochrome b5 type A	Homo sapiens	69-82
30416740-12	2018	Taken together, NAD+ reduction in the CA1 region contributes to development of age-associated cognitive dysfunction, aspects of which may be prevented or treated by enhancing NAD+ availability through supplementation of NAD+ intermediates, such as NMN.	NAD	16-20	carbonic anhydrase 1	Mus musculus	38-41
30416740-12	2018	Taken together, NAD+ reduction in the CA1 region contributes to development of age-associated cognitive dysfunction, aspects of which may be prevented or treated by enhancing NAD+ availability through supplementation of NAD+ intermediates, such as NMN.	NAD	175-179	carbonic anhydrase 1	Mus musculus	38-41
30416740-12	2018	Taken together, NAD+ reduction in the CA1 region contributes to development of age-associated cognitive dysfunction, aspects of which may be prevented or treated by enhancing NAD+ availability through supplementation of NAD+ intermediates, such as NMN.	NAD	175-179	carbonic anhydrase 1	Mus musculus	38-41
30291911-11	2018	In addition, a decrease in SIRT1 activity due to a reduction in the NAD+/NADH ratio by PARP-1 hyperactivation was associated with AIC through increased nuclear factor (NF)-kappaB p65 and p53 acetylation in both WT and NQO1-/- mice.	NAD	68-72	sirtuin 1	Mus musculus	27-32
30291911-11	2018	In addition, a decrease in SIRT1 activity due to a reduction in the NAD+/NADH ratio by PARP-1 hyperactivation was associated with AIC through increased nuclear factor (NF)-kappaB p65 and p53 acetylation in both WT and NQO1-/- mice.	NAD	73-77	sirtuin 1	Mus musculus	27-32
30291911-12	2018	While an elevation in NAD+/NADH ratio via NQO1 enzymatic action using dunnione recovered SIRT1 activity and subsequently deacetylated NF-kappaB p65 and p53, however not in NQO1-/- mice, thereby attenuating AIC.	NAD	22-26	sirtuin 1	Mus musculus	89-94
30291911-12	2018	While an elevation in NAD+/NADH ratio via NQO1 enzymatic action using dunnione recovered SIRT1 activity and subsequently deacetylated NF-kappaB p65 and p53, however not in NQO1-/- mice, thereby attenuating AIC.	NAD	22-26	transformation related protein 53, pseudogene	Mus musculus	152-155
30291911-12	2018	While an elevation in NAD+/NADH ratio via NQO1 enzymatic action using dunnione recovered SIRT1 activity and subsequently deacetylated NF-kappaB p65 and p53, however not in NQO1-/- mice, thereby attenuating AIC.	NAD	27-31	sirtuin 1	Mus musculus	89-94
30179604-1	2018	BACKGROUND: Nicotinamide adenine dinucleotide (NAD)-dependent deacetylase SIRT1 is an important regulator of hypothalamic neuronal function.	NAD	12-45	sirtuin 1	Mus musculus	74-79
30179604-1	2018	BACKGROUND: Nicotinamide adenine dinucleotide (NAD)-dependent deacetylase SIRT1 is an important regulator of hypothalamic neuronal function.	NAD	47-50	sirtuin 1	Mus musculus	74-79
30179604-6	2018	Extracellular NAD was imported into N1 hypothalamic neuronal cells in a connexin 43-dependent and CD73-independent manner.	NAD	14-17	5' nucleotidase, ecto	Mus musculus	98-102
30179604-8	2018	Exogenous NAD suppressed NPY and AgRP transcriptional activity, which was mediated by SIRT1 and FOXO1.	NAD	10-13	sirtuin 1	Mus musculus	86-91
30179604-8	2018	Exogenous NAD suppressed NPY and AgRP transcriptional activity, which was mediated by SIRT1 and FOXO1.	NAD	10-13	forkhead box O1	Mus musculus	96-101
30356033-7	2018	RESULTS The data demonstrated that CtBP1 directly bound to the promoters of MPC1 and MPC2 and transcriptionally repressed them, leading to increased levels of free NADH in the cytosol and nucleus, thus positively feeding back CtBP1"s functions.	NAD	164-168	C-terminal binding protein 1	Mus musculus	35-40
30356033-9	2018	CONCLUSIONS Our data indicate that MPC1 and MPC2 are principal mediators that link CtBP1-mediated transcription regulation to NADH production.	NAD	126-130	C-terminal binding protein 1	Mus musculus	83-88
30356033-10	2018	The discovery of CtBP1 as an NADH regulator in addition to being an NADH sensor shows that CtBP1 is at the center of tumor metabolism and transcription control.	NAD	29-33	C-terminal binding protein 1	Mus musculus	17-22
30356033-10	2018	The discovery of CtBP1 as an NADH regulator in addition to being an NADH sensor shows that CtBP1 is at the center of tumor metabolism and transcription control.	NAD	29-33	C-terminal binding protein 1	Mus musculus	91-96
30356033-10	2018	The discovery of CtBP1 as an NADH regulator in addition to being an NADH sensor shows that CtBP1 is at the center of tumor metabolism and transcription control.	NAD	68-72	C-terminal binding protein 1	Mus musculus	17-22
30356033-10	2018	The discovery of CtBP1 as an NADH regulator in addition to being an NADH sensor shows that CtBP1 is at the center of tumor metabolism and transcription control.	NAD	68-72	C-terminal binding protein 1	Mus musculus	91-96
29763382-5	2018	Finally, stable KDM2B-knockdown cell lines exhibit displacement of NAD+-dependent deacetylase sirtuin-1 (SIRT1) from chromatin, with concomitant increases in H3K79 methylation and H4K16 acetylation.	NAD	67-70	lysine demethylase 2B	Homo sapiens	16-21
30106119-3	2018	Sirtuin 3 (Sirt3) is a member of the sirtuin family of NAD+-dependent enzymes with homology to Saccharomyces cerevisiae gene silent information regulator 2.	NAD	55-59	sirtuin 3	Mus musculus	11-16
30258629-0	2018	CD38 is methylated in prostate cancer and regulates extracellular NAD.	NAD	66-69	CD38 molecule	Homo sapiens	0-4
30258629-2	2018	We recently reported that human prostate cancer can be initiated following oncogene expression in progenitor-like luminal cells marked by low expression of the NAD+-consuming enzyme CD38.	NAD	160-164	CD38 molecule	Homo sapiens	182-186
30258629-3	2018	CD38 expression is reduced in prostate cancer compared to benign prostate, suggesting that tumor cells may reduce CD38 expression in order to enhance pools of NAD+.	NAD	159-163	CD38 molecule	Homo sapiens	0-4
30258629-6	2018	CD38 was inducibly over-expressed in benign and malignant human prostate cell lines in order to determine the effects on cell proliferation and levels of NAD+ and NADH.	NAD	154-158	CD38 molecule	Homo sapiens	0-4
30258629-6	2018	CD38 was inducibly over-expressed in benign and malignant human prostate cell lines in order to determine the effects on cell proliferation and levels of NAD+ and NADH.	NAD	163-167	CD38 molecule	Homo sapiens	0-4
30258629-15	2018	Our study provides support for CD38 as a regulator of extracellular, but not intracellular, NAD+ in epithelial cells.	NAD	92-96	CD38 molecule	Homo sapiens	31-35
30258629-16	2018	These findings suggest that repression of CD38 by methylation may serve to increase the availability of extracellular NAD+ in prostate cancer tissues.	NAD	118-122	CD38 molecule	Homo sapiens	42-46
29797808-8	2018	Based on the evidence accumulated thus far, we propose a clinical intervention for the restoration of aged HSC function by improving mitochondrial function through NAD+ precursor supplementation.	NAD	164-168	fucosyltransferase 1 (H blood group)	Homo sapiens	107-110
29753648-7	2018	Using 1H-nuclear magnetic resonance metabolomic analysis, we found that the content of NAD and NMN were increased in the VTA of cocaine-conditioned mice; moreover, the expression of SIRT1 was also upregulated.	NAD	87-90	sirtuin 1	Mus musculus	182-187
29753648-9	2018	Our results suggest that NAMPT-mediated NAD biosynthesis may modify cocaine behavioral effects through SIRT1.	NAD	40-43	sirtuin 1	Mus musculus	103-108
29753648-10	2018	Moreover, our findings reveal that the interplay between NAD biosynthesis and SIRT1 regulation may comprise a novel regulatory pathway that responds to chronic cocaine stimuli.	NAD	57-60	sirtuin 1	Mus musculus	78-83
30127395-5	2018	QPRT+/- mice exhibited higher quinolinate, lower NAD+, and higher AKI susceptibility.	NAD	49-53	quinolinate phosphoribosyltransferase	Mus musculus	0-4
29859505-1	2018	The human enzyme 17beta-hydroxysteroid dehydrogenase 14 (17beta-HSD14) oxidizes the hydroxyl group at position 17 of estradiol and 5-androstenediol using NAD+ as cofactor.	NAD	154-158	hydroxysteroid 17-beta dehydrogenase 14	Homo sapiens	17-55
29859505-1	2018	The human enzyme 17beta-hydroxysteroid dehydrogenase 14 (17beta-HSD14) oxidizes the hydroxyl group at position 17 of estradiol and 5-androstenediol using NAD+ as cofactor.	NAD	154-158	hydroxysteroid 17-beta dehydrogenase 14	Homo sapiens	57-69
29957526-1	2018	Human sirtuin 2 (SIRT2) is a nicotinamide adenine dinucleotide (NAD+)-dependent deacylase, and is implicated in human diseases including cancer.	NAD	29-62	sirtuin 2	Homo sapiens	6-15
29957526-1	2018	Human sirtuin 2 (SIRT2) is a nicotinamide adenine dinucleotide (NAD+)-dependent deacylase, and is implicated in human diseases including cancer.	NAD	29-62	sirtuin 2	Homo sapiens	17-22
29957526-1	2018	Human sirtuin 2 (SIRT2) is a nicotinamide adenine dinucleotide (NAD+)-dependent deacylase, and is implicated in human diseases including cancer.	NAD	64-67	sirtuin 2	Homo sapiens	6-15
29957526-1	2018	Human sirtuin 2 (SIRT2) is a nicotinamide adenine dinucleotide (NAD+)-dependent deacylase, and is implicated in human diseases including cancer.	NAD	64-67	sirtuin 2	Homo sapiens	17-22
29760313-1	2018	Sirtuin-1 (SIRT1) is a nicotinamide adenine dinucleotide (NAD+)-dependent histone deacetylase with a large number of protein substrates.	NAD	23-56	sirtuin 1	Canis lupus familiaris	0-9
29760313-1	2018	Sirtuin-1 (SIRT1) is a nicotinamide adenine dinucleotide (NAD+)-dependent histone deacetylase with a large number of protein substrates.	NAD	23-56	sirtuin 1	Canis lupus familiaris	11-16
29760313-1	2018	Sirtuin-1 (SIRT1) is a nicotinamide adenine dinucleotide (NAD+)-dependent histone deacetylase with a large number of protein substrates.	NAD	58-62	sirtuin 1	Canis lupus familiaris	0-9
29760313-1	2018	Sirtuin-1 (SIRT1) is a nicotinamide adenine dinucleotide (NAD+)-dependent histone deacetylase with a large number of protein substrates.	NAD	58-62	sirtuin 1	Canis lupus familiaris	11-16
30026729-6	2018	Elevated NAD+ levels induced by KL1333 triggered the activation of SIRT1 and AMPK, and subsequently activated PGC-1alpha in these cells.	NAD	9-13	PPARG coactivator 1 alpha	Sus scrofa	110-120
30069485-3	2018	NAD+-sensing nuclear sirtuin1 (SIRT1) epigenetically guards immune and metabolic homeostasis during sepsis.	NAD	0-4	sirtuin 1	Mus musculus	21-29
30069485-3	2018	NAD+-sensing nuclear sirtuin1 (SIRT1) epigenetically guards immune and metabolic homeostasis during sepsis.	NAD	0-4	sirtuin 1	Mus musculus	31-36
30069485-8	2018	These findings support the unifying concept that nuclear NAD+ sensor SIRT1 broadly coordinates innate and adaptive immune reprogramming during sepsis and is a druggable immunometabolic enhancement target.	NAD	57-61	sirtuin 1	Mus musculus	69-74
29444200-1	2018	Aims: Sirtuin 3 (Sirt3) is a mitochondrial, nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase that reduces oxidative stress by activation of superoxide dismutase 2 (SOD2).	NAD	44-77	sirtuin 3	Mus musculus	6-15
29444200-1	2018	Aims: Sirtuin 3 (Sirt3) is a mitochondrial, nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase that reduces oxidative stress by activation of superoxide dismutase 2 (SOD2).	NAD	44-77	sirtuin 3	Mus musculus	17-22
29444200-1	2018	Aims: Sirtuin 3 (Sirt3) is a mitochondrial, nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase that reduces oxidative stress by activation of superoxide dismutase 2 (SOD2).	NAD	79-82	sirtuin 3	Mus musculus	6-15
29444200-1	2018	Aims: Sirtuin 3 (Sirt3) is a mitochondrial, nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase that reduces oxidative stress by activation of superoxide dismutase 2 (SOD2).	NAD	79-82	sirtuin 3	Mus musculus	17-22
29444200-13	2018	Therefore, enhancing SIRT3 activity by pan-sirtuin activating NAD+-boosters may provide a novel therapeutic target to prevent or treat thrombotic arterial occlusion in myocardial infarction or stroke.	NAD	62-66	sirtuin 3	Mus musculus	21-26
29676938-0	2018	The Development of a Biotinylated NAD+-Applied Human Poly(ADP-Ribose) Polymerase 3 (PARP3) Enzymatic Assay.	NAD	34-38	poly(ADP-ribose) polymerase family member 3	Homo sapiens	53-82
29676938-0	2018	The Development of a Biotinylated NAD+-Applied Human Poly(ADP-Ribose) Polymerase 3 (PARP3) Enzymatic Assay.	NAD	34-38	poly(ADP-ribose) polymerase family member 3	Homo sapiens	84-89
29676938-4	2018	Herein, we describe a modified PARP3 screening assay using biotinylated NAD+ as the specialized substrate.	NAD	72-76	poly(ADP-ribose) polymerase family member 3	Homo sapiens	31-36
29676938-5	2018	This method relies on the activity of PARP3 to transfer the biotinylated NAD+ onto a histone protein to form ADP-ribosylated histone.	NAD	73-77	poly(ADP-ribose) polymerase family member 3	Homo sapiens	38-43
29905535-4	2018	NAD+ levels declined with age and correlated directly with decreased nicotinamide phosphoribosyltransferase (NAMPT) expression, increased expression of senescence markers (p16INK4a, p21Waf/Cip1, ApoJ, CTGF and beta-galactosidase) and significant reductions in SIRT1 expression and activity.	NAD	0-4	clusterin	Mus musculus	195-199
29905535-4	2018	NAD+ levels declined with age and correlated directly with decreased nicotinamide phosphoribosyltransferase (NAMPT) expression, increased expression of senescence markers (p16INK4a, p21Waf/Cip1, ApoJ, CTGF and beta-galactosidase) and significant reductions in SIRT1 expression and activity.	NAD	0-4	galactosidase, beta 1	Mus musculus	210-228
29905535-4	2018	NAD+ levels declined with age and correlated directly with decreased nicotinamide phosphoribosyltransferase (NAMPT) expression, increased expression of senescence markers (p16INK4a, p21Waf/Cip1, ApoJ, CTGF and beta-galactosidase) and significant reductions in SIRT1 expression and activity.	NAD	0-4	sirtuin 1	Mus musculus	260-265
29685963-0	2018	New chemical tools for probing activity and inhibition of the NAD+-dependent lysine deacylase sirtuin 2.	NAD	62-66	sirtuin 2	Homo sapiens	94-103
29685974-1	2018	SIRT2 is a member of the human sirtuin family of proteins and possesses NAD+-dependent lysine deacetylase/deacylase activity.	NAD	72-76	sirtuin 2	Homo sapiens	0-5
29721585-3	2018	Furthermore, the up-regulated LONP increased mitochondrial ROS generation to promote cell survival, cell proliferation, epithelial-mesenchymal transition, and cell migration, which was attributed to the up-regulation of NADH:ubiquinone oxidoreductase core subunit S8 via interaction with chaperone Lon under hypoxic or oxidative stress in tumorigenesis.	NAD	220-224	lon peptidase 1, mitochondrial	Homo sapiens	30-34
29721585-3	2018	Furthermore, the up-regulated LONP increased mitochondrial ROS generation to promote cell survival, cell proliferation, epithelial-mesenchymal transition, and cell migration, which was attributed to the up-regulation of NADH:ubiquinone oxidoreductase core subunit S8 via interaction with chaperone Lon under hypoxic or oxidative stress in tumorigenesis.	NAD	220-224	lon peptidase 1, mitochondrial	Homo sapiens	298-301
29679549-7	2018	Our results indicated that CHM-1 increased the expression of SIRT2 protein, an NAD-dependent tubulin deacetylase.	NAD	79-82	sirtuin 2	Homo sapiens	61-66
29571013-6	2018	In addition, a partial GDH structure was docked to the Sirt4-NAD+ complex model.	NAD	61-65	glutamate dehydrogenase 1	Homo sapiens	23-26
29571013-7	2018	In the ternary complex model of Sirt4-NAD+-GDH, the acetylated lysine 171 of GDH is located close to NAD+.	NAD	38-42	glutamate dehydrogenase 1	Homo sapiens	43-46
29508376-2	2018	Depending on several parameters like extracellular NAD+ , P2X7 can be ADP-ribosylated rapidly by adjacent ARTC2.2 resulting in susceptibilities to apoptosis to a varying extent.	NAD	51-55	ADP-ribosyltransferase 2b	Mus musculus	106-111
29524843-0	2018	Regulation of the mechanism of Type-II NADH: Quinone oxidoreductase from S. aureus.	NAD	39-43	AT695_RS05530	Staphylococcus aureus	45-67
29524843-1	2018	Type-II NADH:quinone oxidoreductases (NDH-2s) are membrane proteins involved in respiratory chains and the only enzymes with NADH:quinone oxidoreductase activity expressed in Staphylococcus aureus (S. aureus), one of the most common causes of clinical infections.	NAD	8-12	AT695_RS05530	Staphylococcus aureus	13-35
29852001-10	2018	This was the case for mutants in the NAD+-independent deacetylase complex subunits Clr1, Clr2 and Clr3, the casein kinase CK2 subunit Ckb1, the ubiquitin ligase component Pof3, and the CENP-B homologue Cbp1, as well as for double mutants lacking Swi6 and Brl2, Pof3, or Cbp1.	NAD	37-41	centromere protein B	Homo sapiens	185-191
29892266-4	2018	Sirtuin 1 (SIRT1) is a protein deacetylase depended on nicotinamide adenine dinucleotide.	NAD	55-88	sirtuin 1	Mus musculus	0-9
29892266-4	2018	Sirtuin 1 (SIRT1) is a protein deacetylase depended on nicotinamide adenine dinucleotide.	NAD	55-88	sirtuin 1	Mus musculus	11-16
29977153-8	2018	However, re-expression of CD38 in the knockdown clones reversed the effect on Sirt1/NF-kappaB/TLR2 signaling, which is NAD-dependent.	NAD	119-122	sirtuin 1	Mus musculus	78-83
29751795-10	2018	Moreover, GOT1-null cells accumulated NADH and displayed a decreased ratio of NADH/NAD+ with nutrient depletion.	NAD	38-42	glutamic-oxaloacetic transaminase 1	Homo sapiens	10-14
29751795-10	2018	Moreover, GOT1-null cells accumulated NADH and displayed a decreased ratio of NADH/NAD+ with nutrient depletion.	NAD	78-82	glutamic-oxaloacetic transaminase 1	Homo sapiens	10-14
29751795-10	2018	Moreover, GOT1-null cells accumulated NADH and displayed a decreased ratio of NADH/NAD+ with nutrient depletion.	NAD	83-87	glutamic-oxaloacetic transaminase 1	Homo sapiens	10-14
29604959-10	2018	Extracellular NAD+ stimulated Ca2+ signaling in each ATP-responsive MSC by involving P2Y11.	NAD	14-18	purinergic receptor P2Y11	Homo sapiens	85-90
29752474-5	2018	Mechanistically, the interaction between CHES1 and ERalpha enhanced the recruitment of nicotinamide adenine dinucleotide (NAD+) deacetylase Sirtuin 1 (SIRT1), and it further induced SIRT1-mediated ERalpha deacetylation and repression on the promoter-binding enrichment of ERalpha.	NAD	87-120	forkhead box N3	Homo sapiens	41-46
29447131-3	2018	Using unbiased proteomic and metabolic high-throughput profiling on a unique in-house-generated isogenic model of ERCC1 deficiency, we found marked metabolic rewiring of ERCC1-deficient populations, including decreased levels of the metabolite NAD+ and reduced expression of the rate-limiting NAD+ biosynthetic enzyme nicotinamide phosphoribosyltransferase (NAMPT).	NAD	244-248	ERCC excision repair 1, endonuclease non-catalytic subunit	Homo sapiens	114-119
29447131-3	2018	Using unbiased proteomic and metabolic high-throughput profiling on a unique in-house-generated isogenic model of ERCC1 deficiency, we found marked metabolic rewiring of ERCC1-deficient populations, including decreased levels of the metabolite NAD+ and reduced expression of the rate-limiting NAD+ biosynthetic enzyme nicotinamide phosphoribosyltransferase (NAMPT).	NAD	293-297	ERCC excision repair 1, endonuclease non-catalytic subunit	Homo sapiens	114-119
29193800-8	2018	Palmitate pre-treatment reduced expression of the Bmal1 downstream target, nicotinamide phosphoribosyltransferase, the rate-limiting enzyme in the synthesis of NAD+ .	NAD	160-164	aryl hydrocarbon receptor nuclear translocator-like	Mus musculus	50-55
29368147-8	2018	Adduct formation (i.e. 10-(deoxyguanosin-N2-yl)-7,8,9-trihydroxy-7,8,9,10-tetrahydro-BaP [dG-N2-BPDE]) correlated with observed CYP1A activity and metabolite formation (i.e. BaP-7,8-dihydrodiol) when NADPH or NADH was used as enzymatic cofactors.	NAD	209-213	prohibitin 2	Mus musculus	85-88
29156373-2	2018	Breakdown of acetaldehyde by aldehyde dehydrogenase 2 (ALDH2) in the mitochondria consumes NAD+ and generates reactive oxygen/nitrogen species, which represents a fundamental mechanism in the pathogenesis of alcoholic liver disease (ALD).	NAD	91-95	aldehyde dehydrogenase 2, mitochondrial	Mus musculus	29-53
29156373-2	2018	Breakdown of acetaldehyde by aldehyde dehydrogenase 2 (ALDH2) in the mitochondria consumes NAD+ and generates reactive oxygen/nitrogen species, which represents a fundamental mechanism in the pathogenesis of alcoholic liver disease (ALD).	NAD	91-95	aldehyde dehydrogenase 2, mitochondrial	Mus musculus	55-60
29482842-2	2018	The protein CD38 (cluster of differentiation 38) is a multifunctional enzyme that degrades NAD and modulates cellular NAD homeostasis.	NAD	91-94	CD38 molecule	Homo sapiens	12-16
29482842-2	2018	The protein CD38 (cluster of differentiation 38) is a multifunctional enzyme that degrades NAD and modulates cellular NAD homeostasis.	NAD	91-94	CD38 molecule	Homo sapiens	18-47
29482842-2	2018	The protein CD38 (cluster of differentiation 38) is a multifunctional enzyme that degrades NAD and modulates cellular NAD homeostasis.	NAD	118-121	CD38 molecule	Homo sapiens	12-16
29482842-2	2018	The protein CD38 (cluster of differentiation 38) is a multifunctional enzyme that degrades NAD and modulates cellular NAD homeostasis.	NAD	118-121	CD38 molecule	Homo sapiens	18-47
29562167-4	2018	By virtue of a change in cellular redox homeostasis, IDH1-mutated cells synthesize excess glutamine-derived proline through enhanced activity of pyrroline 5-carboxylate reductase 1 (PYCR1), coupled to NADH oxidation.	NAD	201-205	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	53-57
29721150-6	2018	Sirt3 modulates age-associated mitochondrial biology and function via lysine deacetylation of target proteins, and we show that its regulation depends on its nitration status and is benefited by the improved NAD+/NADH ratio in aged p66Shc(-/-) brain mitochondria.	NAD	208-212	sirtuin 3	Mus musculus	0-5
29721150-6	2018	Sirt3 modulates age-associated mitochondrial biology and function via lysine deacetylation of target proteins, and we show that its regulation depends on its nitration status and is benefited by the improved NAD+/NADH ratio in aged p66Shc(-/-) brain mitochondria.	NAD	213-217	sirtuin 3	Mus musculus	0-5
29536043-4	2018	We present a quantitative approach to detecting both functional and structural metabolic biomarkers noninvasively, relying on endogenous TPEF from two coenzymes, NADH (reduced form of nicotinamide adenine dinucleotide) and FAD (flavin adenine dinucleotide).	NAD	162-166	transmembrane protein with EGF like and two follistatin like domains 2	Homo sapiens	137-141
29536043-4	2018	We present a quantitative approach to detecting both functional and structural metabolic biomarkers noninvasively, relying on endogenous TPEF from two coenzymes, NADH (reduced form of nicotinamide adenine dinucleotide) and FAD (flavin adenine dinucleotide).	NAD	184-217	transmembrane protein with EGF like and two follistatin like domains 2	Homo sapiens	137-141
29317496-9	2018	We showed that decreased nicotinamide mononucleotide adenylyltransferase (Nma1/Nma2) levels probably caused the NAD+ defects, and NMA1-oe was sufficient to restore NAD+ NatB-mediated N-terminal acetylation of Nma1 and Nma2 appears essential for maintaining NAD+ levels.	NAD	164-168	nicotinamide-nucleotide adenylyltransferase NMA1	Saccharomyces cerevisiae S288C	130-134
29317496-9	2018	We showed that decreased nicotinamide mononucleotide adenylyltransferase (Nma1/Nma2) levels probably caused the NAD+ defects, and NMA1-oe was sufficient to restore NAD+ NatB-mediated N-terminal acetylation of Nma1 and Nma2 appears essential for maintaining NAD+ levels.	NAD	164-168	nicotinamide-nucleotide adenylyltransferase NMA1	Saccharomyces cerevisiae S288C	130-134
29194006-5	2018	Kinetic characterization of the fusion GST-hLDHA protein toward GSH and NADH, suggested retention of functional activities of GST and hLDHA in fused protein as indicated by the kinetic parameters km and kcat/km.	NAD	72-76	glutathione S-transferase kappa 1	Homo sapiens	39-42
29194006-5	2018	Kinetic characterization of the fusion GST-hLDHA protein toward GSH and NADH, suggested retention of functional activities of GST and hLDHA in fused protein as indicated by the kinetic parameters km and kcat/km.	NAD	72-76	glutathione S-transferase kappa 1	Homo sapiens	126-129
29401458-7	2018	Sem1 maintains high cellular NADH levels, controls mitochondria integrity during stress and developmental transition.	NAD	29-33	SEM1 26S proteasome subunit	Homo sapiens	0-4
8977386-1	1997	Streptozotocin, which induces diabetes mellitus in experimental animals, has been reported to be taken up by beta-cells by means of the glucose transporter 2 (GLUT2) and then reduce the cellular level of NAD+, leading to necrosis of the beta-cells.	NAD	204-208	solute carrier family 2 member 2	Rattus norvegicus	136-157
29470101-5	2018	The recombinant human GDH enzyme showed expected properties such as adenosine diphosphate activation and nicotinamide adenine dinucleotide/nicotinamide adenine dinucleotide phosphate dual recognition.	NAD	105-138	glutamate dehydrogenase 1	Homo sapiens	22-25
28847709-4	2018	Recently, some flavonoids were shown to inhibit poly (ADP-ribose) polymerases (PARPs) and cyclic ADP-ribose (cADP) synthases (CD38 and CD157), elevate intracellular nicotinamide adenine dinucleotide+ (NAD+) levels and activate NAD+ dependent sirtuin -mediated signaling pathways.	NAD	165-199	CD38 molecule	Homo sapiens	126-130
28847709-4	2018	Recently, some flavonoids were shown to inhibit poly (ADP-ribose) polymerases (PARPs) and cyclic ADP-ribose (cADP) synthases (CD38 and CD157), elevate intracellular nicotinamide adenine dinucleotide+ (NAD+) levels and activate NAD+ dependent sirtuin -mediated signaling pathways.	NAD	201-205	CD38 molecule	Homo sapiens	126-130
28847709-4	2018	Recently, some flavonoids were shown to inhibit poly (ADP-ribose) polymerases (PARPs) and cyclic ADP-ribose (cADP) synthases (CD38 and CD157), elevate intracellular nicotinamide adenine dinucleotide+ (NAD+) levels and activate NAD+ dependent sirtuin -mediated signaling pathways.	NAD	227-231	CD38 molecule	Homo sapiens	126-130
8977386-1	1997	Streptozotocin, which induces diabetes mellitus in experimental animals, has been reported to be taken up by beta-cells by means of the glucose transporter 2 (GLUT2) and then reduce the cellular level of NAD+, leading to necrosis of the beta-cells.	NAD	204-208	solute carrier family 2 member 2	Rattus norvegicus	159-164
29405961-2	2018	Sirtuin-1 (Sirt1) is a ubiquitously-expressed NAD-dependent protein deacetylase which plays a key role in numerous cellular processes, including cellular differentiation and metabolism.	NAD	46-49	sirtuin 1	Mus musculus	0-9
9058195-1	1997	The substrate-binding sites of NADP-dependent isocitrate dehydrogenase and NAD-dependent 3-isopropylmalate dehydrogenase from Thermus thermophilus were analyzed by site-directed mutagenesis.	NAD	31-34	3-isopropylmalate dehydrogenase	Thermus thermophilus HB8	89-120
29405961-2	2018	Sirtuin-1 (Sirt1) is a ubiquitously-expressed NAD-dependent protein deacetylase which plays a key role in numerous cellular processes, including cellular differentiation and metabolism.	NAD	46-49	sirtuin 1	Mus musculus	11-16
29129787-0	2018	CD38-NAD+Axis Regulates Immunotherapeutic Anti-Tumor T Cell Response.	NAD	5-9	CD38 molecule	Homo sapiens	0-4
29129787-5	2018	Importantly, T cells with reduced surface expression of the NADase CD38 exhibited intrinsically higher NAD+, enhanced oxidative phosphorylation, higher glutaminolysis, and altered mitochondrial dynamics that vastly improved tumor control.	NAD	103-107	CD38 molecule	Homo sapiens	67-71
29129787-7	2018	Thus, strategies targeting the CD38-NAD+ axis could increase the efficacy of anti-tumor adoptive T cell therapy.	NAD	36-40	CD38 molecule	Homo sapiens	31-35
29298345-7	2018	In untreated human cells, regions with high intensity immunostaining for NQO1 co-localize with acetyl alpha-tubulin and the NAD+-dependent deacetylase Sirt2 on the centrosome(s), the mitotic spindle and midbody during cell division.	NAD	124-128	sirtuin 2	Homo sapiens	151-156
29298345-8	2018	These data provide evidence that during the centriole duplication cycle NQO1 may provide NAD+ for Sirt2-mediated deacetylation of microtubules.	NAD	89-93	sirtuin 2	Homo sapiens	98-103
30097868-2	2018	ARH1 hydrolyzes mono(ADP-ribosyl)ated arginine, which results from actions of cholera toxin and other nicotinamide adenine dinucleotide (NAD+):arginine ADP-ribosyl-transferases, while ARH3 hydrolyzes poly(ADP-ribose) and O-acetyl-ADP-ribose, resulting from the action of poly(ADP-ribose) polymerases and sirtuins, respectively.	NAD	102-135	ADP-ribosylserine hydrolase	Homo sapiens	184-188
30097868-2	2018	ARH1 hydrolyzes mono(ADP-ribosyl)ated arginine, which results from actions of cholera toxin and other nicotinamide adenine dinucleotide (NAD+):arginine ADP-ribosyl-transferases, while ARH3 hydrolyzes poly(ADP-ribose) and O-acetyl-ADP-ribose, resulting from the action of poly(ADP-ribose) polymerases and sirtuins, respectively.	NAD	137-141	ADP-ribosylserine hydrolase	Homo sapiens	184-188
29185343-8	2017	Our results suggest that PQQ-inducible mitochondrial biogenesis can be attributed to activation of the SIRT1/PGC-1alpha signaling pathway by enhancing cellular NAD+ formation.	NAD	160-164	sirtuin 1	Mus musculus	103-108
29034432-3	2017	Herein, we report that an uncharacterized open reading frame YKL071W from S. cerevisiae encodes a novel "classical" short-chain dehydrogenase/reductase (SDR) protein with NADH-dependent enzymatic activities for reduction of furfural (FF), glycolaldehyde (GA), formaldehyde (FA), and benzaldehyde (BZA).	NAD	171-175	short-chain dehydrogenase/reductase	Saccharomyces cerevisiae S288C	116-151
29034432-3	2017	Herein, we report that an uncharacterized open reading frame YKL071W from S. cerevisiae encodes a novel "classical" short-chain dehydrogenase/reductase (SDR) protein with NADH-dependent enzymatic activities for reduction of furfural (FF), glycolaldehyde (GA), formaldehyde (FA), and benzaldehyde (BZA).	NAD	171-175	short-chain dehydrogenase/reductase	Saccharomyces cerevisiae S288C	153-156
29054115-2	2017	ADP-ribosylation is carried out by ADP-ribosyltransferase proteins, such as poly (ADP-ribose) polymerases (PARPs) that transfer either monomer or polymers of ADP-ribose onto the molecular targets by using nicotinamide adenine dinucleotide (NAD+ ) as a cofactor.	NAD	205-238	poly(ADP-ribose) polymerase family member 3	Homo sapiens	107-112
29054115-2	2017	ADP-ribosylation is carried out by ADP-ribosyltransferase proteins, such as poly (ADP-ribose) polymerases (PARPs) that transfer either monomer or polymers of ADP-ribose onto the molecular targets by using nicotinamide adenine dinucleotide (NAD+ ) as a cofactor.	NAD	240-244	poly(ADP-ribose) polymerase family member 3	Homo sapiens	107-112
28898552-6	2017	Interestingly, NPP5 is able to cleave nicotinamide adenine dinucleotide (NAD), suggesting a potential role of this enzyme in NAD-based neurotransmission.	NAD	38-71	ectonucleotide pyrophosphatase/phosphodiesterase family member 5	Homo sapiens	15-19
28898552-6	2017	Interestingly, NPP5 is able to cleave nicotinamide adenine dinucleotide (NAD), suggesting a potential role of this enzyme in NAD-based neurotransmission.	NAD	73-76	ectonucleotide pyrophosphatase/phosphodiesterase family member 5	Homo sapiens	15-19
28898552-6	2017	Interestingly, NPP5 is able to cleave nicotinamide adenine dinucleotide (NAD), suggesting a potential role of this enzyme in NAD-based neurotransmission.	NAD	125-128	ectonucleotide pyrophosphatase/phosphodiesterase family member 5	Homo sapiens	15-19
28970491-6	2017	We conclude that replication stress via Rev1-deficiency contributes to metabolic stress caused by compromized mitochondrial function via the PARP-NAD+-SIRT1-PGC1alpha axis.	NAD	146-150	sirtuin 1	Mus musculus	151-156
28397297-5	2017	The activity of PFK in boar spermatozoa enzymatic extracts was 1.70 +- 0.19 U/1010 spermatozoa, the activity of NAD- and NADP-dependent IDH was 0.111 +- 0.005 U/1010 and 2.22 +- 0.14 U/1010 spermatozoa, respectively, and the activity of MDH was 4.24 +- 0.38 U/1010 spermatozoa.	NAD	112-115	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	136-139
28778545-2	2017	Among them, we have recently identified SIRT2, a class III NAD+-dependent HDAC, as being oppositely regulated by stress and antidepressants.	NAD	59-63	sirtuin 2	Mus musculus	40-45
27590140-1	2017	Sirtuin 1 (SIRT1) is a nicotinamide adenine dinucleotide (NAD+)-dependent lysine deacetylase that regulates longevity and enhances mitochondrial metabolism.	NAD	23-56	sirtuin 1	Mus musculus	0-9
27590140-1	2017	Sirtuin 1 (SIRT1) is a nicotinamide adenine dinucleotide (NAD+)-dependent lysine deacetylase that regulates longevity and enhances mitochondrial metabolism.	NAD	23-56	sirtuin 1	Mus musculus	11-16
27590140-1	2017	Sirtuin 1 (SIRT1) is a nicotinamide adenine dinucleotide (NAD+)-dependent lysine deacetylase that regulates longevity and enhances mitochondrial metabolism.	NAD	58-62	sirtuin 1	Mus musculus	0-9
27590140-1	2017	Sirtuin 1 (SIRT1) is a nicotinamide adenine dinucleotide (NAD+)-dependent lysine deacetylase that regulates longevity and enhances mitochondrial metabolism.	NAD	58-62	sirtuin 1	Mus musculus	11-16
28813682-6	2017	SIRT3 activity being nicotinamide adenine dinucleotide (NAD)+ level-dependent, we show that NAD+ is orchestrated by both feeding rhythms and the circadian clock through the NAD+ salvage pathway but also via the nicotinamide riboside pathway.	NAD	21-54	sirtuin 3	Mus musculus	0-5
28813682-6	2017	SIRT3 activity being nicotinamide adenine dinucleotide (NAD)+ level-dependent, we show that NAD+ is orchestrated by both feeding rhythms and the circadian clock through the NAD+ salvage pathway but also via the nicotinamide riboside pathway.	NAD	56-61	sirtuin 3	Mus musculus	0-5
28813682-6	2017	SIRT3 activity being nicotinamide adenine dinucleotide (NAD)+ level-dependent, we show that NAD+ is orchestrated by both feeding rhythms and the circadian clock through the NAD+ salvage pathway but also via the nicotinamide riboside pathway.	NAD	92-96	sirtuin 3	Mus musculus	0-5
28813682-6	2017	SIRT3 activity being nicotinamide adenine dinucleotide (NAD)+ level-dependent, we show that NAD+ is orchestrated by both feeding rhythms and the circadian clock through the NAD+ salvage pathway but also via the nicotinamide riboside pathway.	NAD	173-177	sirtuin 3	Mus musculus	0-5
28786950-12	2017	In summary, PSPC protected against HFD-induced hepatic inflammation by boosting NAD+ level to inhibit NLRP3 inflammasome activation.	NAD	80-84	NLR family, pyrin domain containing 3	Mus musculus	102-107
28671819-0	2017	Efficient Reduction of Vertebrate Cytoglobins by the Cytochrome b5/Cytochrome b5 Reductase/NADH System.	NAD	91-95	cytochrome b5 type A	Homo sapiens	53-66
28671819-0	2017	Efficient Reduction of Vertebrate Cytoglobins by the Cytochrome b5/Cytochrome b5 Reductase/NADH System.	NAD	91-95	cytochrome b5 type A	Homo sapiens	67-80
28625978-1	2017	IDH1-mutant gliomas are dependent upon the canonical coenzyme NAD+ for survival.	NAD	62-66	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	0-4
28625978-3	2017	We therefore hypothesized that a strategy combining NAD+ biosynthesis inhibitors with the alkylating chemotherapeutic agent temozolomide could potentiate NAD+ depletion-mediated cytotoxicity in mutant IDH1 cancer cells.	NAD	52-56	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	201-205
28625978-3	2017	We therefore hypothesized that a strategy combining NAD+ biosynthesis inhibitors with the alkylating chemotherapeutic agent temozolomide could potentiate NAD+ depletion-mediated cytotoxicity in mutant IDH1 cancer cells.	NAD	154-158	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	201-205
28625978-6	2017	In IDH1-mutant-expressing cells, this consumption reduced further the abnormally lowered basal steady-state levels of NAD+, introducing a window of hypervulnerability to NAD+ biosynthesis inhibitors.	NAD	118-122	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	3-7
28625978-6	2017	In IDH1-mutant-expressing cells, this consumption reduced further the abnormally lowered basal steady-state levels of NAD+, introducing a window of hypervulnerability to NAD+ biosynthesis inhibitors.	NAD	170-174	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	3-7
28625978-9	2017	Thus, we find IDH1-mutant cancers have distinct metabolic stress responses to chemotherapy-induced DNA damage and that combination regimens targeting nonredundant NAD+ pathways yield potent anticancer efficacy in vivo Such targeting of convergent metabolic pathways in genetically selected cancers could minimize treatment toxicity and improve durability of response to therapy.	NAD	163-167	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	14-18
28246130-0	2017	Nicotinamide Mononucleotide, an NAD+ Precursor, Rescues Age-Associated Susceptibility to AKI in a Sirtuin 1-Dependent Manner.	NAD	32-36	sirtuin 1	Mus musculus	98-107
28432149-18	2017	The underlying mechanism involves a profound increase in the hydrolysis of ATP/NAD and AMP, resulting primarily from the upregulation of pyrophosphatases and CD73.	NAD	79-82	5' nucleotidase, ecto	Mus musculus	158-162
28263970-6	2017	Here we demonstrate, using a variety of cancer cell lines as well as activated primary T cells, that cytosolic malate dehydrogenase 1 (MDH1) is an alternative to LDH as a supplier of NAD.	NAD	183-186	malate dehydrogenase 1	Homo sapiens	101-131
9040540-6	1997	Compared with control values, liver PARP activity was enhanced in rats fed the 12% MCFD diet but was lower in MCFND-fed rats following a further reduction in liver NAD concentration.	NAD	164-167	poly (ADP-ribose) polymerase 1	Rattus norvegicus	36-40
28263970-6	2017	Here we demonstrate, using a variety of cancer cell lines as well as activated primary T cells, that cytosolic malate dehydrogenase 1 (MDH1) is an alternative to LDH as a supplier of NAD.	NAD	183-186	malate dehydrogenase 1	Homo sapiens	135-139
28263970-9	2017	Together, our findings suggest that proliferating cells rely on both MDH1 and LDH to replenish cytosolic NAD, and that therapies designed at targeting glycolysis must consider both dehydrogenases.	NAD	105-108	malate dehydrogenase 1	Homo sapiens	69-73
9040540-7	1997	These changes in PARP activity associated with lower NAD concentrations may slow DNA repair and enhance DNA damage.	NAD	53-56	poly (ADP-ribose) polymerase 1	Rattus norvegicus	17-21
28808418-3	2017	Sirtuins are a group of conserved nicotinamide adenine dinucleotide (NAD+) dependent histone and/or protein deacetylases belonging to the silent information regulator 2 (Sir2) family.	NAD	34-67	sirtuin 2	Homo sapiens	138-168
8759717-2	1996	The human leukocyte surface Ag CD38 was recently identified as a nicotinamide adenine dinucleotide (NAD)(+)-glycohydrolase ecto-enzyme, degrading NAD into nicotinamide and ADP-ribose.	NAD	65-98	CD38 molecule	Homo sapiens	31-35
28808418-3	2017	Sirtuins are a group of conserved nicotinamide adenine dinucleotide (NAD+) dependent histone and/or protein deacetylases belonging to the silent information regulator 2 (Sir2) family.	NAD	34-67	sirtuin 2	Homo sapiens	170-174
28808418-3	2017	Sirtuins are a group of conserved nicotinamide adenine dinucleotide (NAD+) dependent histone and/or protein deacetylases belonging to the silent information regulator 2 (Sir2) family.	NAD	69-72	sirtuin 2	Homo sapiens	138-168
28808418-3	2017	Sirtuins are a group of conserved nicotinamide adenine dinucleotide (NAD+) dependent histone and/or protein deacetylases belonging to the silent information regulator 2 (Sir2) family.	NAD	69-72	sirtuin 2	Homo sapiens	170-174
28461337-6	2017	In the presence of FMN, NADH, and flavin reductase, which reduces FMN to FMNH2 using NADH as the electron donor, mitoNEET mediates oxidation of NADH with a concomitant reduction of oxygen.	NAD	24-28	CDGSH iron sulfur domain 1	Homo sapiens	113-121
8759717-2	1996	The human leukocyte surface Ag CD38 was recently identified as a nicotinamide adenine dinucleotide (NAD)(+)-glycohydrolase ecto-enzyme, degrading NAD into nicotinamide and ADP-ribose.	NAD	100-103	CD38 molecule	Homo sapiens	31-35
8759717-2	1996	The human leukocyte surface Ag CD38 was recently identified as a nicotinamide adenine dinucleotide (NAD)(+)-glycohydrolase ecto-enzyme, degrading NAD into nicotinamide and ADP-ribose.	NAD	146-149	CD38 molecule	Homo sapiens	31-35
8759717-4	1996	Two other nucleotide-hydrolyzing activities were induced on the T cell surface concomitantly with CD38: the human PC-1 molecule, a nucleotide phosphodiesterase/pyrophosphatase that produces AMP from NAD or ADP-ribose, and a nucleotidase that produces adenosine from AMP, but which may be distinct from the CD73 5"-nucleotidase.	NAD	199-202	CD38 molecule	Homo sapiens	98-102
28659951-9	2017	We provide evidence that the NAD(H) binding domain of AN is relevant in this context as proteins carrying mutations in this domain localize to a much higher degree to SGs and strongly reduce AN dimerization and its interaction with one interactor but not the others.	NAD	29-35	NAD(P)-binding Rossmann-fold superfamily protein	Arabidopsis thaliana	54-56
28659951-9	2017	We provide evidence that the NAD(H) binding domain of AN is relevant in this context as proteins carrying mutations in this domain localize to a much higher degree to SGs and strongly reduce AN dimerization and its interaction with one interactor but not the others.	NAD	29-35	NAD(P)-binding Rossmann-fold superfamily protein	Arabidopsis thaliana	191-193
8694855-1	1996	NADH-dependent 7-ethoxycoumarin O-deethylation activities could be reconstituted in systems containing cytochrome b5 (b5), NADH-b5 reductase, and bacterial recombinant P450 2E1 in 100 mM potassium phosphate buffer (pH 7.4) containing a synthetic phospholipid mixture and cholate.	NAD	0-4	cytochrome b5 type A	Homo sapiens	103-116
28537485-9	2017	The NAD+/PARP1/SIRT1 axis may link NAD+ levels and DNA damage with the apparent epigenomic DNA methylation clocks that have been described.	NAD	4-8	sirtuin 1	Mus musculus	15-20
28537485-9	2017	The NAD+/PARP1/SIRT1 axis may link NAD+ levels and DNA damage with the apparent epigenomic DNA methylation clocks that have been described.	NAD	35-39	sirtuin 1	Mus musculus	15-20
21619301-5	1996	In the presence of excess nicotinamide adenine dinucleotide (NAD(+)), GDH converts glutamate to alpha-ketoglutarate while simultaneously reducing NAD(+) to NADH.	NAD	146-152	glutamate dehydrogenase 1	Homo sapiens	70-73
21619301-5	1996	In the presence of excess nicotinamide adenine dinucleotide (NAD(+)), GDH converts glutamate to alpha-ketoglutarate while simultaneously reducing NAD(+) to NADH.	NAD	156-160	glutamate dehydrogenase 1	Homo sapiens	70-73
8660685-0	1996	Interaction of ferric complexes with NADH-cytochrome b5 reductase and cytochrome b5: lipid peroxidation, H2O2 generation, and ferric reduction.	NAD	37-41	cytochrome b5 type A	Homo sapiens	42-55
8660685-0	1996	Interaction of ferric complexes with NADH-cytochrome b5 reductase and cytochrome b5: lipid peroxidation, H2O2 generation, and ferric reduction.	NAD	37-41	cytochrome b5 type A	Homo sapiens	70-83
28558019-9	2017	We found that high levels of DEK significantly reprogrammed cellular metabolism and altered the abundances of amino acids, TCA cycle intermediates and the glycolytic end products lactate, alanine and NAD+.	NAD	200-204	DEK proto-oncogene	Homo sapiens	29-32
8660685-2	1996	NADH-dependent microsomal electron transfer involves the enzymes NADH-cytochrome b5 reductase and cytochrome b5.	NAD	0-4	cytochrome b5 type A	Homo sapiens	70-83
8660685-2	1996	NADH-dependent microsomal electron transfer involves the enzymes NADH-cytochrome b5 reductase and cytochrome b5.	NAD	0-4	cytochrome b5 type A	Homo sapiens	98-111
8858566-1	1996	Poly(ADP-ribose) polymerase (PARP) is a nuclear enzyme which catalyzes the transfer of ADP-ribose units from NAD+ to a variety of nuclear proteins under the stimulation of DNA strand break.	NAD	109-113	poly [ADP-ribose] polymerase 1	Cricetulus griseus	0-27
27460777-2	2017	Currently, only the mitochondrial sirtuins (SIRT3-5) and SIRT1 have been shown to direct mitochondrial function; however, Aims: NAD-dependent protein deacetylase sirtuin-2 (SIRT2), the primary cytoplasmic sirtuin, is not yet reported to associate with mitochondria.	NAD	128-131	sirtuin 3	Mus musculus	44-51
27460777-2	2017	Currently, only the mitochondrial sirtuins (SIRT3-5) and SIRT1 have been shown to direct mitochondrial function; however, Aims: NAD-dependent protein deacetylase sirtuin-2 (SIRT2), the primary cytoplasmic sirtuin, is not yet reported to associate with mitochondria.	NAD	128-131	sirtuin 1	Mus musculus	57-62
27460777-2	2017	Currently, only the mitochondrial sirtuins (SIRT3-5) and SIRT1 have been shown to direct mitochondrial function; however, Aims: NAD-dependent protein deacetylase sirtuin-2 (SIRT2), the primary cytoplasmic sirtuin, is not yet reported to associate with mitochondria.	NAD	128-131	sirtuin 2	Mus musculus	162-171
28978015-7	2017	Moreover, the ALDH1A1 mutants that retained their GSH/DHLA-dependent NAD+ reduction activity but lost their aldehyde-dehydrogenase activity were able to decrease the NAD+/NADH ratio and to rescue the impaired growth of ALDH1A1/3A1 double knockout tumor cells.	NAD	69-73	aldehyde dehydrogenase 1 family member A1	Homo sapiens	14-21
28978015-7	2017	Moreover, the ALDH1A1 mutants that retained their GSH/DHLA-dependent NAD+ reduction activity but lost their aldehyde-dehydrogenase activity were able to decrease the NAD+/NADH ratio and to rescue the impaired growth of ALDH1A1/3A1 double knockout tumor cells.	NAD	69-73	aldehyde dehydrogenase 1 family member A1	Homo sapiens	219-226
8858566-1	1996	Poly(ADP-ribose) polymerase (PARP) is a nuclear enzyme which catalyzes the transfer of ADP-ribose units from NAD+ to a variety of nuclear proteins under the stimulation of DNA strand break.	NAD	109-113	poly [ADP-ribose] polymerase 1	Cricetulus griseus	29-33
28978015-7	2017	Moreover, the ALDH1A1 mutants that retained their GSH/DHLA-dependent NAD+ reduction activity but lost their aldehyde-dehydrogenase activity were able to decrease the NAD+/NADH ratio and to rescue the impaired growth of ALDH1A1/3A1 double knockout tumor cells.	NAD	166-170	aldehyde dehydrogenase 1 family member A1	Homo sapiens	14-21
28978015-7	2017	Moreover, the ALDH1A1 mutants that retained their GSH/DHLA-dependent NAD+ reduction activity but lost their aldehyde-dehydrogenase activity were able to decrease the NAD+/NADH ratio and to rescue the impaired growth of ALDH1A1/3A1 double knockout tumor cells.	NAD	166-170	aldehyde dehydrogenase 1 family member A1	Homo sapiens	219-226
8635236-7	1996	The PARS inhibitors 3-aminobenzamide (1 mmol/L), nicotinamide (1 mmol/L), and PD 128763 (100 mumol/L) inhibited the reduction in cellular NAD+ and ATP and the suppression of mitochondrial respiration in response to LPS and IFN-gamma stimulation.	NAD	138-142	interferon gamma	Rattus norvegicus	223-232
28978015-7	2017	Moreover, the ALDH1A1 mutants that retained their GSH/DHLA-dependent NAD+ reduction activity but lost their aldehyde-dehydrogenase activity were able to decrease the NAD+/NADH ratio and to rescue the impaired growth of ALDH1A1/3A1 double knockout tumor cells.	NAD	171-175	aldehyde dehydrogenase 1 family member A1	Homo sapiens	14-21
28978015-7	2017	Moreover, the ALDH1A1 mutants that retained their GSH/DHLA-dependent NAD+ reduction activity but lost their aldehyde-dehydrogenase activity were able to decrease the NAD+/NADH ratio and to rescue the impaired growth of ALDH1A1/3A1 double knockout tumor cells.	NAD	171-175	aldehyde dehydrogenase 1 family member A1	Homo sapiens	219-226
8615810-1	1996	Deoxyhypusine synthase is an NAD(+)-dependent enzyme that catalyses the formation of a deoxyhypusine residue on the eukaryotic initiation factor 5A (eIF-5A) precursor by transferring an aminobutyl moiety from spermidine to the epsilon-amino group of a unique lysine residue.	NAD	29-35	eukaryotic translation initiation factor 5A	Homo sapiens	116-147
28288933-4	2017	Our results suggest a beneficial effect of prune extract on hyperhomocysteinemia with reduction of homocysteine level by its conversion on to SAH by S-adenosylhomocysteine hydrolase, which is activated by NAD+, a by-product of NAD(P)H: quinone oxydo reductase-1.	NAD	205-209	S-adenosylhomocysteine hydrolase	Mus musculus	149-181
8615810-1	1996	Deoxyhypusine synthase is an NAD(+)-dependent enzyme that catalyses the formation of a deoxyhypusine residue on the eukaryotic initiation factor 5A (eIF-5A) precursor by transferring an aminobutyl moiety from spermidine to the epsilon-amino group of a unique lysine residue.	NAD	29-35	eukaryotic translation initiation factor 5A	Homo sapiens	149-155
8630392-2	1996	It has been recently shown that CD38 displays three enzymatic activities: hydrolysis of NAD+ to ADP-ribose, synthesis of cyclic ADP-ribose from NAD+, and hydrolysis of cyclic ADP-ribose to ADP-ribose.	NAD	88-92	CD38 molecule	Homo sapiens	32-36
28074060-9	2017	Novel common pathways including increased induction of an NAD+-dependent protein deacetylase sirtuin-1 that may reduce NF-kappaB signalling, and increased STAT3 activation may reduce LPS activation.	NAD	58-62	sirtuin 1	Mus musculus	93-102
28449683-14	2017	On the one hand, the inhibition of NAMPT reduced the production of NAD+ through inhibiting the NAD+ salvage pathway, resulting in the decrease of Sirt1 activity, and then attenuated the deacetylation of SREBP1 in which the inhibition of SREBP1 activity promoted the expressions of FASN and ACC.	NAD	67-71	sirtuin 1	Mus musculus	146-151
28449683-14	2017	On the one hand, the inhibition of NAMPT reduced the production of NAD+ through inhibiting the NAD+ salvage pathway, resulting in the decrease of Sirt1 activity, and then attenuated the deacetylation of SREBP1 in which the inhibition of SREBP1 activity promoted the expressions of FASN and ACC.	NAD	67-71	sterol regulatory element binding transcription factor 1	Mus musculus	203-209
28449683-14	2017	On the one hand, the inhibition of NAMPT reduced the production of NAD+ through inhibiting the NAD+ salvage pathway, resulting in the decrease of Sirt1 activity, and then attenuated the deacetylation of SREBP1 in which the inhibition of SREBP1 activity promoted the expressions of FASN and ACC.	NAD	67-71	sterol regulatory element binding transcription factor 1	Mus musculus	237-243
28449683-14	2017	On the one hand, the inhibition of NAMPT reduced the production of NAD+ through inhibiting the NAD+ salvage pathway, resulting in the decrease of Sirt1 activity, and then attenuated the deacetylation of SREBP1 in which the inhibition of SREBP1 activity promoted the expressions of FASN and ACC.	NAD	95-99	sirtuin 1	Mus musculus	146-151
8630392-2	1996	It has been recently shown that CD38 displays three enzymatic activities: hydrolysis of NAD+ to ADP-ribose, synthesis of cyclic ADP-ribose from NAD+, and hydrolysis of cyclic ADP-ribose to ADP-ribose.	NAD	144-148	CD38 molecule	Homo sapiens	32-36
8632430-4	1996	Our results, based on striking similarities in molecular volume and electrostatic isopotential between MPA and cofactor NAD+, lead to the suggestion that MPA is capable of binding to the nicotinamide site of IMPD and mimicking the NAD+ inverse regulation of the enzyme.	NAD	120-124	inosine monophosphate dehydrogenase 1	Homo sapiens	208-212
8632430-4	1996	Our results, based on striking similarities in molecular volume and electrostatic isopotential between MPA and cofactor NAD+, lead to the suggestion that MPA is capable of binding to the nicotinamide site of IMPD and mimicking the NAD+ inverse regulation of the enzyme.	NAD	231-235	inosine monophosphate dehydrogenase 1	Homo sapiens	208-212
28533928-1	2017	BACKGROUND/AIMS: Nicotinic acid (NA), a lipid-lowering drug, serves as a source of NAD+, the cofactor for Sirt1.	NAD	83-87	sirtuin 1	Mus musculus	106-111
8611186-8	1996	Affinity chromatography and affinity labelling studies suggest that 11 beta-HSD2 has a compulsory ordered mechanism, with NAD+ binding first, followed by a conformational change allowing glucocorticoid binding with high affinity.	NAD	122-126	hydroxysteroid 11-beta dehydrogenase 2	Homo sapiens	68-80
28404626-7	2017	Expression analysis by quantitative reverse transcription polymerase chain reaction of extracellular purine degrading enzymes and P1 and P2 receptors on T cells isolated from the injured heart revealed profound upregulation of the enzymatic machinery for hydrolysis of extracellular adenosine triphosphate and nicotinamide adenine dinucleotide, both pathways converging in the formation of AMP and adenosine via CD73.	NAD	310-343	zinc finger protein 185	Mus musculus	130-139
8561495-1	1996	NADH-dependent testosterone 6 beta-hydroxylation and nifedipine oxidation activities could be reconstituted in systems containing cytochrome b5 (b5), NADH-b5 reductase, and bacterial recombinant cytochrome P450 (P450) 3A4 with a synthetic phospholipid mixture, cholate, MgCl2, and reduced glutathione.	NAD	0-4	cytochrome b5 type A	Homo sapiens	130-143
28270525-2	2017	The NAD+-dependent deacetylase SIRT1 serves as a guardian against metabolic disorders in multiple tissues.	NAD	4-8	sirtuin 1	Mus musculus	31-36
7496532-2	1995	The role of the IMP2 gene product in the regulation of carbon catabolite repressible enzymes maltase, invertase, alcohol dehydrogenase, NAD-dependent glutamate dehydrogenase (NAD-GDH) and L-lactate:ferricytochrome-c oxidoreductase (L-LCR) was also analysed.	NAD	136-139	endopeptidase catalytic subunit	Saccharomyces cerevisiae S288C	16-20
28413470-7	2017	Enrichment analyses showed that NADH:Ubiquinone Oxidoreductase Core Subunit V2 (NDUFV2) was involved in several neurological diseases, including oxidative phosphorylation, Alzheimer"s disease, Parkinson"s disease and Huntington"s disease.	NAD	32-36	NADH:ubiquinone oxidoreductase core subunit V2	Rattus norvegicus	80-86
7565631-0	1995	Nicotinamide adenine dinucleotide (phosphate): quinone oxidoreductase (DT-diaphorase) as a target for bioreductive antitumor quinones: quinone cytotoxicity and selectivity in human lung and breast cancer cell lines.	NAD	0-33	crystallin zeta	Homo sapiens	47-69
28219011-1	2017	Aldehyde dehydrogenase 2 (ALDH2), one of 19 ALDH superfamily members, catalyzes the NAD+-dependent oxidation of aldehydes to their respective carboxylic acids.	NAD	84-88	aldehyde dehydrogenase 1 family member A1	Homo sapiens	26-30
28373875-2	2017	One set of ectoenzymes-CD39, CD38, CD203a, and CD73-leads to the generation of adenosine (ADO) by metabolizing ATP and NAD+.	NAD	119-123	ectonucleoside triphosphate diphosphohydrolase 1	Homo sapiens	23-27
28373875-2	2017	One set of ectoenzymes-CD39, CD38, CD203a, and CD73-leads to the generation of adenosine (ADO) by metabolizing ATP and NAD+.	NAD	119-123	CD38 molecule	Homo sapiens	29-33
7612640-9	1995	The kinetics support the mechanism of the overall reaction where NADH is oxidized by the protein-Ru(NH3)3+(6) complex in which positively charged electron acceptor is bound at the specific site close to FMN, thus stabilizing the flavosemiquinone intermediate.	NAD	65-69	formin 1	Homo sapiens	203-206
30090498-2	2017	SIRT1, a NAD+-dependent histone deacetylase, can play a neuroprotective role in brain injury.	NAD	9-12	sirtuin 1	Mus musculus	0-5
7556871-3	1995	Radiometric conversion assay using adrenal cortical tissues revealed extremely high levels of 11 beta-HSD activity which was characteristic of 11 beta-HSD2 in that it was NAD-dependent and displayed a Km for cortisol of 41 +/- 4 nM.	NAD	171-174	11-beta-hydroxysteroid dehydrogenase type 2	Ovis aries	143-155
7755589-5	1995	It is 55, 43 and 44% identical with yeast NAD(+)-specific IDH2, yeast NAD(+)-specific IDH1 and monkey NAD(+)-specific IDH gamma-subunit (IDH gamma) respectively.	NAD	42-48	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	58-61
7755589-5	1995	It is 55, 43 and 44% identical with yeast NAD(+)-specific IDH2, yeast NAD(+)-specific IDH1 and monkey NAD(+)-specific IDH gamma-subunit (IDH gamma) respectively.	NAD	70-76	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	86-89
7755589-5	1995	It is 55, 43 and 44% identical with yeast NAD(+)-specific IDH2, yeast NAD(+)-specific IDH1 and monkey NAD(+)-specific IDH gamma-subunit (IDH gamma) respectively.	NAD	70-76	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	86-89
7733677-0	1995	Transient kinetics of intracomplex electron transfer in the human cytochrome b5 reductase-cytochrome b5 system: NAD+ modulates protein-protein binding and electron transfer.	NAD	112-116	cytochrome b5 type A	Homo sapiens	66-79
7733677-0	1995	Transient kinetics of intracomplex electron transfer in the human cytochrome b5 reductase-cytochrome b5 system: NAD+ modulates protein-protein binding and electron transfer.	NAD	112-116	cytochrome b5 type A	Homo sapiens	90-103
12228428-4	1995	Asparagine (1 mM) or glutamine (1 mM), potential products of that hydrolysis, inhibited the induction of NADH-dependent root NR in the dry system by about 70%.	NAD	105-109	nitrate reductase [NADH] 1	Zea mays	125-127
7696141-7	1995	These studies demonstrate that exon 6 of the rat CYP17 is essential for CYP17 activity, and may be structurally related to the NAD-linked prokaryote alpha/beta F supersecondary element.	NAD	127-130	cytochrome P450, family 17, subfamily a, polypeptide 1	Rattus norvegicus	49-54
7883010-1	1995	Directed mutagenesis has been used to identify a set of amino acids in the Pichia stipitis xylitol dehydrogenase, encoded by the xylitol dehydrogenase gene XYL2, which is involved in specific NAD binding.	NAD	192-195	D-xylulose reductase XYL2	Saccharomyces cerevisiae S288C	156-160
7851527-3	1995	CD38 purified from human erythrocyte membranes has been recently shown to undergo stable oligomerization induced by either NAD+ or beta-mercaptoethanol.	NAD	123-127	CD38 molecule	Homo sapiens	0-4
7603972-5	1995	The NAD(P)H:quinone oxidoreductase was able to use NADH or NADPH as the electron donor.	NAD	51-55	crystallin zeta	Homo sapiens	12-34
7656579-1	1995	The enzyme 11 beta-hydroxysteroid dehydrogenase type 2 (11 beta HSD2) is an NAD-dependent, high-affinity isoform that potently inactivates glucocorticoids.	NAD	76-79	hydroxysteroid 11-beta dehydrogenase 2	Homo sapiens	4-68
7775378-4	1995	CD38 antigen has an amino acid sequence homologous to Aplysia ADP-ribosyl cyclase which generates cyclic adenosine diphosphoribose (cADPR) and nicotinamide (NA) from beta-NAD+.	NAD	166-175	CD38 molecule	Homo sapiens	0-4
7775378-7	1995	On the other hand, CD38 NADase utilized the NAD analogs to form ADP-ribose and NA.	NAD	24-27	CD38 molecule	Homo sapiens	19-23
7859916-2	1994	A ubiquitous low affinity NADP+ dependent enzyme (11 beta HSD1) and a tissue specific, high affinity NAD+ dependent form (11 beta HSD2) of 11 beta HSD exist.	NAD	101-105	hydroxysteroid 11-beta dehydrogenase 2	Homo sapiens	122-134
7812715-5	1994	This catalytically competent fragment of nitrate reductase consists of two domains, the amino-terminal lobe, which binds FAD, and the carboxy-terminal lobe, which presumably binds NADH, connected by a linker region.	NAD	180-184	nitrate reductase [NADH] 1	Zea mays	41-58
7815897-8	1994	Co-incubation with 2-CdA and the poly-ADP-ribose synthetase inhibitor 3-MOB, which is known to render cells resistant to 2-CdA toxicity by preventing cellular nicotinamide adenine dinucleotide (NAD)- and adenosine triphosphase-depletion, also reversed the effect of 2-CdA on lipid accumulation.	NAD	159-192	cytidine deaminase	Mus musculus	21-24
7815897-8	1994	Co-incubation with 2-CdA and the poly-ADP-ribose synthetase inhibitor 3-MOB, which is known to render cells resistant to 2-CdA toxicity by preventing cellular nicotinamide adenine dinucleotide (NAD)- and adenosine triphosphase-depletion, also reversed the effect of 2-CdA on lipid accumulation.	NAD	194-197	cytidine deaminase	Mus musculus	21-24
7985780-3	1994	Deoxyhypusine synthase, an NAD(+)-dependent enzyme, catalyzes the first step of hypusine formation on the eIF-5A precursor.	NAD	27-33	eukaryotic translation initiation factor 5A	Homo sapiens	106-112
8155713-4	1994	The Michaelis constants for ALDH-1 and -2, determined from initial velocities (for ALDH-1) and single reaction progress curves (for ALDH-2), are 180 +/- 10 microM and 0.20 +/- 0.02 microM, respectively (pH 7.5 and 9.5, saturating NAD+ in both cases).	NAD	230-234	aldehyde dehydrogenase 1 family member A1	Homo sapiens	28-41
8155713-4	1994	The Michaelis constants for ALDH-1 and -2, determined from initial velocities (for ALDH-1) and single reaction progress curves (for ALDH-2), are 180 +/- 10 microM and 0.20 +/- 0.02 microM, respectively (pH 7.5 and 9.5, saturating NAD+ in both cases).	NAD	230-234	aldehyde dehydrogenase 1 family member A1	Homo sapiens	28-34
8106462-13	1994	The balance of LDH, plasma membrane lactate transport, and mitochondrial glycerol phosphate dehydrogenase activities therefore appear to be important in beta- and INS-1 cell glucose recognition to ensure that mitochondrial oxidation is the principle fate of pyruvate and NADH produced by glycolysis.	NAD	271-275	insulin 1	Rattus norvegicus	163-168
8297331-9	1994	NADH/lipoamide-stimulated vitamin K epoxide reduction is uncoupled by traces of Triton X-100, suggesting that microsomal lipoamide reductase and vitamin K epoxide reductase are associated.	NAD	0-4	vitamin K epoxide reductase complex subunit 1	Homo sapiens	145-172
8177224-1	1993	Rat kidney microsomal fraction is able to catalyze the enzymatic desaturation of eicosatrienoic acid (20:3n-6) to arachidonic acid (20:4n-6) by the delta 5 desaturase pathway, in the presence of reduced nicotinamide adenine dinucleotide (NADH), adenosinetriphosphate (ATP) and coenzyme A (CoA).	NAD	203-236	fatty acid desaturase 1	Rattus norvegicus	148-166
8177224-1	1993	Rat kidney microsomal fraction is able to catalyze the enzymatic desaturation of eicosatrienoic acid (20:3n-6) to arachidonic acid (20:4n-6) by the delta 5 desaturase pathway, in the presence of reduced nicotinamide adenine dinucleotide (NADH), adenosinetriphosphate (ATP) and coenzyme A (CoA).	NAD	238-242	fatty acid desaturase 1	Rattus norvegicus	148-166
8226835-0	1993	Interaction of non-myristoylated NADH-cytochrome b5 reductase with cytochrome b5-dimyristoylphosphatidylcholine vesicles.	NAD	33-37	cytochrome b5 type A	Homo sapiens	38-51
8226835-0	1993	Interaction of non-myristoylated NADH-cytochrome b5 reductase with cytochrome b5-dimyristoylphosphatidylcholine vesicles.	NAD	33-37	cytochrome b5 type A	Homo sapiens	67-80
7901008-2	1993	These growth defects could be suppressed by an over-expression on a multi-copy plasmid of the structural gene GDH2 coding for the NAD-dependent glutamate dehydrogenase.	NAD	130-133	glutamate dehydrogenase (NAD(+))	Saccharomyces cerevisiae S288C	110-114
27817132-5	2017	In 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis in rats, weight loss, higher DAI scores, increased visceromotor responses, and inflammatory responses were reversed by application of DPN or ERB-041.	NAD	196-199	estrogen receptor 2	Rattus norvegicus	203-206
28215489-5	2017	We observed that neonatal exposure to PPT, DPN and ICI induced the early onset of abnormal estrous cyclicity after sexual maturation, suggesting that the compounds capable of inducing delayed effects are not limited to ERalpha agonists.	NAD	43-46	estrogen receptor 1	Rattus norvegicus	219-226
8391315-6	1993	NADH-induced loss of the enzyme activity in diluted solutions is accompanied with the synchronous appearance of a fluorescence characteristic for free FMN.	NAD	0-4	formin 1	Homo sapiens	151-154
7683100-3	1993	The nuclear enzyme poly(ADP-ribose) polymerase (pADPRP), a chromatin-bound catalytic protein, utilizing NAD+ as a substrate, was tested by a radiometric procedure.	NAD	104-108	poly (ADP-ribose) polymerase 1	Rattus norvegicus	19-46
28707004-3	2017	We show that Mtb down-regulates sirtuin 1 (SIRT1), a nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase, in monocytes/macrophages, TB animal models, and TB patients with active disease.	NAD	53-86	sirtuin 1	Mus musculus	43-48
28707004-3	2017	We show that Mtb down-regulates sirtuin 1 (SIRT1), a nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase, in monocytes/macrophages, TB animal models, and TB patients with active disease.	NAD	88-91	sirtuin 1	Mus musculus	43-48
28073696-1	2017	SIRT2 is a NAD-dependent deacetylase and inhibition of SIRT2 has a broad anticancer activity.	NAD	11-14	sirtuin 2	Homo sapiens	0-5
28122227-5	2017	Reduced p53 activity in HFD-fed Mdm2C305F/C305F mice resulted in higher levels of p53 downregulated targets GLUT4 and SIRT1, leading to increased biosynthesis of NAD+, and increased energy expenditure.	NAD	162-166	transformation related protein 53, pseudogene	Mus musculus	8-11
28122227-5	2017	Reduced p53 activity in HFD-fed Mdm2C305F/C305F mice resulted in higher levels of p53 downregulated targets GLUT4 and SIRT1, leading to increased biosynthesis of NAD+, and increased energy expenditure.	NAD	162-166	transformation related protein 53, pseudogene	Mus musculus	82-85
28122227-5	2017	Reduced p53 activity in HFD-fed Mdm2C305F/C305F mice resulted in higher levels of p53 downregulated targets GLUT4 and SIRT1, leading to increased biosynthesis of NAD+, and increased energy expenditure.	NAD	162-166	sirtuin 1	Mus musculus	118-123
29393101-1	2017	The sirtuin SIRT1 is a highly conserved nicotinamide adenine dinucleotide (NAD)-dependent protein deacetylase known to have protective effects against a wide range of neurological disorders.	NAD	40-73	sirtuin 1	Mus musculus	12-17
29393101-1	2017	The sirtuin SIRT1 is a highly conserved nicotinamide adenine dinucleotide (NAD)-dependent protein deacetylase known to have protective effects against a wide range of neurological disorders.	NAD	75-78	sirtuin 1	Mus musculus	12-17
7683100-3	1993	The nuclear enzyme poly(ADP-ribose) polymerase (pADPRP), a chromatin-bound catalytic protein, utilizing NAD+ as a substrate, was tested by a radiometric procedure.	NAD	104-108	poly (ADP-ribose) polymerase 1	Rattus norvegicus	48-54
8486360-10	1993	For 3 of these, the corresponding cDNAs were isolated: clone CD60A1 codes for the cation-dependent mannose 6-phosphate receptor, clone CC6 is a human homologue of the bovine 39-kDa nuclear-encoded NADH:ubiquinone oxidoreductase subunit, and CD18 belongs to the family of tumor necrosis factor receptor proteins.	NAD	197-201	NADH:ubiquinone oxidoreductase subunit A9	Homo sapiens	135-138
8444804-4	1993	This result suggests that orf2 may also be involved in NAD biosynthesis and that nadB and orf2 are in the same operon.	NAD	55-58	hypothetical protein	Bacillus subtilis	26-30
27689878-3	2017	Here we report that Fbxo7 deficiency is associated with reduced cellular NAD+ levels, which results in increased mitochondrial NADH redox index and impaired activity of complex I in the electron transport chain.	NAD	73-77	F-box protein 7	Homo sapiens	20-25
27689878-3	2017	Here we report that Fbxo7 deficiency is associated with reduced cellular NAD+ levels, which results in increased mitochondrial NADH redox index and impaired activity of complex I in the electron transport chain.	NAD	127-131	F-box protein 7	Homo sapiens	20-25
26731773-6	2017	Nine different species from Nicotinamide adenine dinucleotide (NADH) dehydrogenase 5 (ND5) protein sequences were tested as an example to demonstrate our method.	NAD	28-61	mitochondrially encoded NADH dehydrogenase 5	Homo sapiens	86-89
8468781-5	1993	This indicates that ARp well reflects the cytosolic redox state, i.e. cytosolic [NAD+]/[NADH], and also [ATP]/[ADP][Pi] theoretically.	NAD	81-85	mesencephalic astrocyte derived neurotrophic factor	Homo sapiens	20-23
8468781-5	1993	This indicates that ARp well reflects the cytosolic redox state, i.e. cytosolic [NAD+]/[NADH], and also [ATP]/[ADP][Pi] theoretically.	NAD	88-92	mesencephalic astrocyte derived neurotrophic factor	Homo sapiens	20-23
28479736-7	2017	METHOD: The inhibitory activity for 15-PGDH inhibitors was evaluated using fluorescence spectrophotometer by measuring the formation of NADH at 468 nm following excitation at 340 nm.	NAD	136-140	15-hydroxyprostaglandin dehydrogenase	Homo sapiens	36-43
1444452-4	1992	Flux through the 3-hydroxyisobutyrate dehydrogenase was more sensitive to regulation by the mitochondrial NADH/NAD+ ratio than flux through the branched-chain alpha-ketoacid dehydrogenase.	NAD	106-110	3-hydroxyisobutyrate dehydrogenase	Rattus norvegicus	17-51
27769837-5	2016	The previously observed preference of renalase from Pseudomonas for NAD-derived substrates over those derived from NADP is accounted for by the structure of the enzyme in complex with NADPH.	NAD	68-71	renalase, FAD dependent amine oxidase	Homo sapiens	38-46
1444452-4	1992	Flux through the 3-hydroxyisobutyrate dehydrogenase was more sensitive to regulation by the mitochondrial NADH/NAD+ ratio than flux through the branched-chain alpha-ketoacid dehydrogenase.	NAD	111-115	3-hydroxyisobutyrate dehydrogenase	Rattus norvegicus	17-51
1489089-3	1992	NAD+- and (ADP-ribose)-derivatized agarose beads were recognized as polymer acceptors by the nuclear enzyme poly(ADP-ribose) polymerase.	NAD	0-4	poly (ADP-ribose) polymerase 1	Rattus norvegicus	108-135
27683265-6	2016	Immunohistochemistry of NAD+-dependent deacetylase SIRTUIN 1 (SIRT1) in neonatal ovary revealed that increasing SIRT1 expression in oocyte nuclei was inversely related to decreasing free/bound NADH during the primordial to primary follicle transition.	NAD	24-28	sirtuin 1	Mus musculus	51-60
27683265-6	2016	Immunohistochemistry of NAD+-dependent deacetylase SIRTUIN 1 (SIRT1) in neonatal ovary revealed that increasing SIRT1 expression in oocyte nuclei was inversely related to decreasing free/bound NADH during the primordial to primary follicle transition.	NAD	24-28	sirtuin 1	Mus musculus	62-67
27683265-6	2016	Immunohistochemistry of NAD+-dependent deacetylase SIRTUIN 1 (SIRT1) in neonatal ovary revealed that increasing SIRT1 expression in oocyte nuclei was inversely related to decreasing free/bound NADH during the primordial to primary follicle transition.	NAD	24-28	sirtuin 1	Mus musculus	112-117
27683265-6	2016	Immunohistochemistry of NAD+-dependent deacetylase SIRTUIN 1 (SIRT1) in neonatal ovary revealed that increasing SIRT1 expression in oocyte nuclei was inversely related to decreasing free/bound NADH during the primordial to primary follicle transition.	NAD	193-197	sirtuin 1	Mus musculus	51-60
27683265-6	2016	Immunohistochemistry of NAD+-dependent deacetylase SIRTUIN 1 (SIRT1) in neonatal ovary revealed that increasing SIRT1 expression in oocyte nuclei was inversely related to decreasing free/bound NADH during the primordial to primary follicle transition.	NAD	193-197	sirtuin 1	Mus musculus	62-67
27683265-6	2016	Immunohistochemistry of NAD+-dependent deacetylase SIRTUIN 1 (SIRT1) in neonatal ovary revealed that increasing SIRT1 expression in oocyte nuclei was inversely related to decreasing free/bound NADH during the primordial to primary follicle transition.	NAD	193-197	sirtuin 1	Mus musculus	112-117
1544629-6	1992	Ethanol exposure of hepatocytes in culture for 2 hr, however, decreased the Km for NAD+ of poly (ADP-ribose) polymerase.	NAD	83-87	poly (ADP-ribose) polymerase 1	Rattus norvegicus	91-119
28043598-5	2016	Nicotinamide adenine dinucleotide is coded by the ndh gene, and its overexpresion may lead cross-resistance between INH and ETH drugs.	NAD	0-33	GLIS family zinc finger 3	Homo sapiens	50-53
27761584-4	2016	Within the niche, NAD+ is able to activate a discontinuous adenosinergic pathway that relies upon CD38, CD203a, and CD73 or TRACP, according to the environmental pH.	NAD	18-22	CD38 molecule	Homo sapiens	98-102
1544629-7	1992	Both nicotinamide and 5-aminobenzamide, which are inhibitors of poly (ADP-ribose) polymerase, prevented the decrease in NAD+ produced by 2-hr exposure of hepatocytes in culture to 100 mmol/L ethanol.	NAD	120-124	poly (ADP-ribose) polymerase 1	Rattus norvegicus	64-92
27587602-11	2016	Besides, significantly increased protein levels of transforming growth factor beta1 (TGF-beta1), gene expression of TGF-beta1, connective tissue growth factor (CTGF), p22 phox and gp91 phox subunits of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, as well as increased media thickness and aortic media area/lumen area (AM/LA) in the untreated hypertensive rats were significantly reduced (p &lt; 0.05) to control levels by all treatments.	NAD	202-235	cellular communication network factor 2	Rattus norvegicus	127-158
1737776-2	1992	S-Adenosylhomocysteine hydrolase (SAHase) was resolved into apoenzyme and NAD+ by acidic ammonium sulfate treatment.	NAD	74-78	adenosylhomocysteinase	Homo sapiens	0-32
27687729-5	2016	The synergistic increase in nuclear p53 and FOXO3 by exercise can facilitate their known interaction in transactivating Sirtuin 1 (SIRT1), a NAD+-dependent histone deacetylase that mediates adaptation to various stresses.	NAD	141-145	transformation related protein 53, pseudogene	Mus musculus	36-39
27687729-5	2016	The synergistic increase in nuclear p53 and FOXO3 by exercise can facilitate their known interaction in transactivating Sirtuin 1 (SIRT1), a NAD+-dependent histone deacetylase that mediates adaptation to various stresses.	NAD	141-145	sirtuin 1	Mus musculus	120-129
27687729-5	2016	The synergistic increase in nuclear p53 and FOXO3 by exercise can facilitate their known interaction in transactivating Sirtuin 1 (SIRT1), a NAD+-dependent histone deacetylase that mediates adaptation to various stresses.	NAD	141-145	sirtuin 1	Mus musculus	131-136
1737776-2	1992	S-Adenosylhomocysteine hydrolase (SAHase) was resolved into apoenzyme and NAD+ by acidic ammonium sulfate treatment.	NAD	74-78	adenosylhomocysteinase	Homo sapiens	34-40
1737776-4	1992	Reduced SAHase (ENADH) that was prepared by reconstitution of the apoenzyme with NADH was catalytically inactive.	NAD	17-21	adenosylhomocysteinase	Homo sapiens	8-14
1737776-15	1992	Since SAHase reduced by adenosine was not highly fluorescent, enzyme-bound intermediates quenched the fluorescence of enzyme-bound NADH.	NAD	131-135	adenosylhomocysteinase	Homo sapiens	6-12
1682801-0	1991	Role of the complex upstream region of the GDH2 gene in nitrogen regulation of the NAD-linked glutamate dehydrogenase in Saccharomyces cerevisiae.	NAD	83-86	glutamate dehydrogenase (NAD(+))	Saccharomyces cerevisiae S288C	43-47
27452907-5	2016	The NAD+-dependent histone deacetylase sirtuin (SIRT)1 amplified the pro-apoptotic effect by deacetylating FOXO3a, which induced EGR1 binding to the Bim promoter and activated Bim expression.	NAD	4-8	early growth response 1	Homo sapiens	129-133
27452907-5	2016	The NAD+-dependent histone deacetylase sirtuin (SIRT)1 amplified the pro-apoptotic effect by deacetylating FOXO3a, which induced EGR1 binding to the Bim promoter and activated Bim expression.	NAD	4-8	BCL2 like 11	Homo sapiens	149-152
27452907-5	2016	The NAD+-dependent histone deacetylase sirtuin (SIRT)1 amplified the pro-apoptotic effect by deacetylating FOXO3a, which induced EGR1 binding to the Bim promoter and activated Bim expression.	NAD	4-8	BCL2 like 11	Homo sapiens	176-179
27759041-4	2016	By interacting with nicotinamide phosphoribosyltransferase (NAMPT), a protein involved in NAD biosynthesis, PCNA coordinates glycolysis and survival, especially in HL-60R cells.	NAD	90-93	proliferating cell nuclear antigen	Homo sapiens	108-112
1682801-1	1991	We analyzed the upstream region of the GDH2 gene, which encodes the NAD-linked glutamate dehydrogenase in Saccharomyces cerevisiae, for elements important for the regulation of the gene by the nitrogen source.	NAD	68-71	glutamate dehydrogenase (NAD(+))	Saccharomyces cerevisiae S288C	39-43
27562971-8	2016	Decreasing NADH pharmacologically with MTOB or genetically blocking CtBP1 with siRNA upregulated the cyclin-dependent genes (p15 and p21) and proapoptotic regulators (NOXA and PERP), attenuated proliferation, corrected the glycolytic reprogramming phenotype of PH-Fibs, and augmented transcription of the anti-inflammatory gene HMOX1.	NAD	11-15	heme oxygenase 1	Homo sapiens	328-333
1897935-7	1991	Pretreatment of microsomes with an antibody to cytochrome b5 reductase inhibited microsomal NADH-dependent reduction of DES Q to DES by 55%.	NAD	92-96	cytochrome b5 type A	Homo sapiens	47-60
27703264-4	2016	Nv-derived SDR orthologues generally had higher epimerisation rates, which were also influenced by NAD+ availability.	NAD	99-103	short-chain dehydrogenase/reductase	Nasonia vitripennis	11-14
1898726-0	1991	Structural role of serine 127 in the NADH-binding site of human NADH-cytochrome b5 reductase.	NAD	37-41	cytochrome b5 type A	Homo sapiens	69-82
27566573-3	2016	Here, we establish a mechanistic link from L-type amino acid transporter 1 (LAT1) mediated transport of tryptophan and the subsequent de-novo NAD+ synthesis to SIRT1-FOXO1 regulated apoptotic signaling in A549 cells in response to NQO1 activation.	NAD	142-146	solute carrier family 7 member 5	Homo sapiens	43-74
27566573-3	2016	Here, we establish a mechanistic link from L-type amino acid transporter 1 (LAT1) mediated transport of tryptophan and the subsequent de-novo NAD+ synthesis to SIRT1-FOXO1 regulated apoptotic signaling in A549 cells in response to NQO1 activation.	NAD	142-146	solute carrier family 7 member 5	Homo sapiens	76-80
27566573-5	2016	Decreased uptake of tryptophan due to the downregulation of LAT1 coordinates with PARP-1 hyperactivation to induce rapid depletion of NAD+ pool.	NAD	134-138	solute carrier family 7 member 5	Homo sapiens	60-64
27566573-6	2016	Particularly, the LAT1-NAD+-SIRT1 signaling is activated in tumor tissues of patients with non-small cell lung cancer.	NAD	23-27	solute carrier family 7 member 5	Homo sapiens	18-22
1898726-9	1991	Ser-127----Pro mutant and Ser-127----Ala mutant showed very low Kcat/Km (NADH) values (5 x 10(7) and 3.5 x 10(7) s-1 M-1, respectively) with cytochrome b5 as an electron acceptor, than that of the wild-type enzyme (Kcat/Km (NADH) = 179 x 10(7) s-1 M-1), while the Kcat/Km (cytochrome b5) value for each enzyme was similar.	NAD	73-77	cytochrome b5 type A	Homo sapiens	141-154
1898726-9	1991	Ser-127----Pro mutant and Ser-127----Ala mutant showed very low Kcat/Km (NADH) values (5 x 10(7) and 3.5 x 10(7) s-1 M-1, respectively) with cytochrome b5 as an electron acceptor, than that of the wild-type enzyme (Kcat/Km (NADH) = 179 x 10(7) s-1 M-1), while the Kcat/Km (cytochrome b5) value for each enzyme was similar.	NAD	73-77	cytochrome b5 type A	Homo sapiens	273-286
27404282-0	2016	NADH:Cytochrome b5 Reductase and Cytochrome b5 Can Act as Sole Electron Donors to Human Cytochrome P450 1A1-Mediated Oxidation and DNA Adduct Formation by Benzo[a]pyrene.	NAD	0-4	cytochrome b5 type A	Homo sapiens	5-18
1964451-4	1990	An antibody against cytochrome b5 markedly reduced the CMP-NeuAc hydroxylase activity when added to incubation mixture containing either NADH or NADPH as an electron donor.	NAD	137-141	cytochrome b5 type A	Homo sapiens	20-33
27404282-0	2016	NADH:Cytochrome b5 Reductase and Cytochrome b5 Can Act as Sole Electron Donors to Human Cytochrome P450 1A1-Mediated Oxidation and DNA Adduct Formation by Benzo[a]pyrene.	NAD	0-4	cytochrome b5 type A	Homo sapiens	33-46
27404282-0	2016	NADH:Cytochrome b5 Reductase and Cytochrome b5 Can Act as Sole Electron Donors to Human Cytochrome P450 1A1-Mediated Oxidation and DNA Adduct Formation by Benzo[a]pyrene.	NAD	0-4	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	88-107
27404282-3	2016	We also studied the efficiencies of the coenzymes of these reductases, NADPH as a coenzyme of POR, and NADH as a coenzyme of CBR, to mediate BaP oxidation.	NAD	103-107	prohibitin 2	Homo sapiens	141-144
2124504-3	1990	A Lys-54 to Gln-54 mutant (K54Q) of hDHFR has been constructed by oligodeoxynucleotide-directed mutagenesis in order to study the role of Lys-54 in differentiating Km and Kcat values for NADPH and NADH as well as in other functions of hDHFR.	NAD	197-201	dihydrofolate reductase	Homo sapiens	36-41
2116938-1	1990	Alkylating agents cause a marked depletion of cellular NAD+ levels by activating nuclear ADP-ribosyl transferase (ADPRT), which utilizes NAD+ as a substrate in the synthesis of poly(ADP-ribose).	NAD	55-59	poly [ADP-ribose] polymerase 1	Cricetulus griseus	89-112
2116938-1	1990	Alkylating agents cause a marked depletion of cellular NAD+ levels by activating nuclear ADP-ribosyl transferase (ADPRT), which utilizes NAD+ as a substrate in the synthesis of poly(ADP-ribose).	NAD	55-59	poly [ADP-ribose] polymerase 1	Cricetulus griseus	114-119
2116938-1	1990	Alkylating agents cause a marked depletion of cellular NAD+ levels by activating nuclear ADP-ribosyl transferase (ADPRT), which utilizes NAD+ as a substrate in the synthesis of poly(ADP-ribose).	NAD	137-141	poly [ADP-ribose] polymerase 1	Cricetulus griseus	89-112
27334978-7	2016	Mutations in the IDH1/2 genes are central to gliomagenesis in a high proportion of grade II and III gliomas, and ongoing trials are examining vaccines against IDH1, small molecular inhibitors of IDH1 and IDH2, and metabolic components including NAD+ depletion to target IDH-mutated gliomas.	NAD	245-249	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	17-23
27334978-7	2016	Mutations in the IDH1/2 genes are central to gliomagenesis in a high proportion of grade II and III gliomas, and ongoing trials are examining vaccines against IDH1, small molecular inhibitors of IDH1 and IDH2, and metabolic components including NAD+ depletion to target IDH-mutated gliomas.	NAD	245-249	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	17-21
27334978-7	2016	Mutations in the IDH1/2 genes are central to gliomagenesis in a high proportion of grade II and III gliomas, and ongoing trials are examining vaccines against IDH1, small molecular inhibitors of IDH1 and IDH2, and metabolic components including NAD+ depletion to target IDH-mutated gliomas.	NAD	245-249	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	17-20
2116938-1	1990	Alkylating agents cause a marked depletion of cellular NAD+ levels by activating nuclear ADP-ribosyl transferase (ADPRT), which utilizes NAD+ as a substrate in the synthesis of poly(ADP-ribose).	NAD	137-141	poly [ADP-ribose] polymerase 1	Cricetulus griseus	114-119
2156280-3	1990	Stimulation of poly(ADP-ribose) polymerase activity of nuclei was a function of radiation dose and correlated with the decrease in the NAD content of nervous tissue.	NAD	135-138	poly (ADP-ribose) polymerase 1	Rattus norvegicus	15-42
27307252-2	2016	UDP-glucose dehydrogenase (UGDH) catalyzes the NAD(+)-dependent oxidation of UDP-glucose to UDP-glucuronate, an essential precursor for androgen inactivation by the prostate glucuronidation enzymes UGT2B15 and UGT2B17.	NAD	47-53	UDP glucuronosyltransferase family 2 member B15	Homo sapiens	198-205
27307252-2	2016	UDP-glucose dehydrogenase (UGDH) catalyzes the NAD(+)-dependent oxidation of UDP-glucose to UDP-glucuronate, an essential precursor for androgen inactivation by the prostate glucuronidation enzymes UGT2B15 and UGT2B17.	NAD	47-53	UDP glucuronosyltransferase family 2 member B17	Homo sapiens	210-217
27311481-1	2016	Deacetylation of alpha-tubulin at lysine 40 is catalyzed by two enzymes, the NAD-dependent deacetylase SIRT2 and the NAD-independent deacetylase HDAC6, in apparently redundant reactions.	NAD	77-80	sirtuin 2	Homo sapiens	103-108
27311481-1	2016	Deacetylation of alpha-tubulin at lysine 40 is catalyzed by two enzymes, the NAD-dependent deacetylase SIRT2 and the NAD-independent deacetylase HDAC6, in apparently redundant reactions.	NAD	117-120	sirtuin 2	Homo sapiens	103-108
27107935-4	2016	Upregulation of Cyclin D2 and incorporation of [methyl-(3)H]thymidine induced by DPN were also blocked by PKF118-310, a compound that disrupts beta-catenin-TCF (T-cell-specific transcription factor) complex, suggesting the involvement of beta-catenin in the estradiol effects in PC-3 cells.	NAD	81-84	catenin beta 1	Homo sapiens	143-155
27107935-4	2016	Upregulation of Cyclin D2 and incorporation of [methyl-(3)H]thymidine induced by DPN were also blocked by PKF118-310, a compound that disrupts beta-catenin-TCF (T-cell-specific transcription factor) complex, suggesting the involvement of beta-catenin in the estradiol effects in PC-3 cells.	NAD	81-84	catenin beta 1	Homo sapiens	238-250
27107935-7	2016	Treatment of PC-3 cells with 17beta-estradiol or DPN markedly increased non-phosphorylated beta-catenin expression.	NAD	49-52	catenin beta 1	Homo sapiens	91-103
27404390-5	2016	During ethanol metabolism, a low NAD(+)/NADH ratio repressed NAD-dependent deacetylase sirtuin 1 (SIRT1) activity, concomitantly resulting in increased acetylated PPARgamma with high transcriptional activity.	NAD	33-36	sirtuin 1	Mus musculus	87-96
27404390-5	2016	During ethanol metabolism, a low NAD(+)/NADH ratio repressed NAD-dependent deacetylase sirtuin 1 (SIRT1) activity, concomitantly resulting in increased acetylated PPARgamma with high transcriptional activity.	NAD	33-36	sirtuin 1	Mus musculus	98-103
27226634-3	2016	The extrinsic arm contains binding sites for NADH, the primary electron acceptor FMN, and seven iron-sulfur clusters that form a pathway for electrons linking FMN to the terminal electron acceptor, ubiquinone, which is bound in a tunnel in the region of the junction between the arms.	NAD	45-49	formin 1	Homo sapiens	159-162
27264869-5	2016	Depletion of endogenous MDM2 in p53-deficient cells impairs serine/glycine metabolism, the NAD(+)/NADH ratio, and glutathione (GSH) recycling, impacting their redox state and tumorigenic potential.	NAD	91-97	transformed mouse 3T3 cell double minute 2	Mus musculus	24-28
27264869-5	2016	Depletion of endogenous MDM2 in p53-deficient cells impairs serine/glycine metabolism, the NAD(+)/NADH ratio, and glutathione (GSH) recycling, impacting their redox state and tumorigenic potential.	NAD	91-97	transformation related protein 53, pseudogene	Mus musculus	32-35
27264869-5	2016	Depletion of endogenous MDM2 in p53-deficient cells impairs serine/glycine metabolism, the NAD(+)/NADH ratio, and glutathione (GSH) recycling, impacting their redox state and tumorigenic potential.	NAD	98-102	transformed mouse 3T3 cell double minute 2	Mus musculus	24-28
27264869-5	2016	Depletion of endogenous MDM2 in p53-deficient cells impairs serine/glycine metabolism, the NAD(+)/NADH ratio, and glutathione (GSH) recycling, impacting their redox state and tumorigenic potential.	NAD	98-102	transformation related protein 53, pseudogene	Mus musculus	32-35
27085036-3	2016	Autophagy is regulated by silent information regulator-1 (SIRT1), a NAD+-dependent histone deacetylase.	NAD	68-71	sirtuin 1	Mus musculus	26-56
27085036-3	2016	Autophagy is regulated by silent information regulator-1 (SIRT1), a NAD+-dependent histone deacetylase.	NAD	68-71	sirtuin 1	Mus musculus	58-63
26923291-4	2016	In this study, we elucidated that Sphk1/S1P upregulates sirtuin 1 (SIRT1), a NAD+ dependent deacetylases protease which exerts multiple cellular functions, to regulate the proliferation and migration of endothelial cells.	NAD	77-80	sphingosine kinase 1	Homo sapiens	34-39
27003727-4	2016	For IDI-2 from the pathogenic bacterium Streptococcus pneumoniae, the flavin can be treated kinetically as a dissociable cosubstrate in incubations with IPP and excess NADH.	NAD	168-172	isopentenyl-diphosphate delta isomerase 2	Homo sapiens	4-9
27003727-10	2016	Dithionite reduction of FMN in the IDI-2 FMN and IPP mixture was biphasic with k(red)(IDI-2 FMN IPP (fast)) = 326 s(-1) and k(red)(IDI-2 FMN IPP (slow)) = 6.9 s(-1) The pseudo-first-order rate constant for the slow component was similar to those for NADH reduction of the flavin in the IDI-2 FMN and IPP mixture and may reflect a rate-limiting conformational change in the enzyme.	NAD	250-254	isopentenyl-diphosphate delta isomerase 2	Homo sapiens	35-40
26982234-3	2016	Kinetic studies revealed that a representative SIRT2 inhibitor acted competitively against both NAD(+) and the peptide substrate, an inhibitory modality that was supported by our computational study.	NAD	96-102	sirtuin 2	Homo sapiens	47-52
33810495-1	2021	L-aspartate (Asp) serves as a central building block, in addition to being a constituent of proteins, for many metabolic processes in most organisms, such as biosynthesis of other amino acids, nucleotides, nicotinamide adenine dinucleotide (NAD), the tricarboxylic acid (TCA) cycle and glycolysis pathway intermediates, and hormones, which are vital for growth and defense.	NAD	206-239	assembly factor for spindle microtubules	Homo sapiens	13-16
33810495-1	2021	L-aspartate (Asp) serves as a central building block, in addition to being a constituent of proteins, for many metabolic processes in most organisms, such as biosynthesis of other amino acids, nucleotides, nicotinamide adenine dinucleotide (NAD), the tricarboxylic acid (TCA) cycle and glycolysis pathway intermediates, and hormones, which are vital for growth and defense.	NAD	241-244	assembly factor for spindle microtubules	Homo sapiens	13-16
33802063-8	2021	These results suggest that NAD+-mediated SIRT1 activation facilitates mitochondrial fission through activation of Drp1 by suppressing its phosphorylation and accelerating its dephosphorylation.	NAD	27-31	dynamin 1 like	Homo sapiens	114-118
31427442-0	2019	Low Cellular NAD+ Compromises Lipopolysaccharide-Induced Inflammatory Responses via Inhibiting TLR4 Signal Transduction in Human Monocytes.	NAD	13-17	toll like receptor 4	Homo sapiens	95-99
31427442-3	2019	In this study, we explored how NAD+ affects TLR4 and NOD-like receptor with a PYD-domain 3 (NLRP3) inflammasome activation, two key innate immune responses.	NAD	31-35	toll like receptor 4	Homo sapiens	44-48
25361036-5	2014	Interestingly, injection of PJ34, a PARP-1 inhibitor, in aged mice increased SIRT-1 activity by preserving intracellular NAD+ content, which resulted in higher skeletal muscle mitochondrial biogenesis and performance.	NAD	121-125	sirtuin 1	Mus musculus	77-83
26933806-2	2016	C-terminal binding protein 1 (CtBP1) is a co-repressor of tumor suppressor genes that is activated by low NAD+/NADH ratio.	NAD	106-110	C-terminal binding protein 1	Mus musculus	0-28
26933806-2	2016	C-terminal binding protein 1 (CtBP1) is a co-repressor of tumor suppressor genes that is activated by low NAD+/NADH ratio.	NAD	106-110	C-terminal binding protein 1	Mus musculus	30-35
26933806-2	2016	C-terminal binding protein 1 (CtBP1) is a co-repressor of tumor suppressor genes that is activated by low NAD+/NADH ratio.	NAD	111-115	C-terminal binding protein 1	Mus musculus	0-28
18814027-2	2009	PAR modification of VEGF was found to be related with the changes in NAD(+) associated with a shift in LDH isoenzymes.	NAD	69-75	lactate dehydrogenase B	Homo sapiens	103-106
26933806-2	2016	C-terminal binding protein 1 (CtBP1) is a co-repressor of tumor suppressor genes that is activated by low NAD+/NADH ratio.	NAD	111-115	C-terminal binding protein 1	Mus musculus	30-35
26891996-5	2016	In astrocytes, 2.5-20 nM 17beta-estradiol (E2) or 10 nM DPN (ERbeta agonist) not 10 nM PPT (ERalpha agonist), significantly increased GFAP expression.	NAD	56-59	glial fibrillary acidic protein	Mus musculus	134-138
26620563-4	2016	Furthermore, CerS1, -2, and -6 are hyperacetylated in the mitochondria of SIRT3-null mice, and SIRT3 directly deacetylates the ceramide synthases in a NAD(+)-dependent manner that increases enzyme activity.	NAD	151-157	sirtuin 3	Mus musculus	74-79
26620563-4	2016	Furthermore, CerS1, -2, and -6 are hyperacetylated in the mitochondria of SIRT3-null mice, and SIRT3 directly deacetylates the ceramide synthases in a NAD(+)-dependent manner that increases enzyme activity.	NAD	151-157	sirtuin 3	Mus musculus	95-100
34962581-8	2021	The levels of pyruvate, nicotinamide adenine dinucleotide, and reactive oxygen species decreased significantly upon ldh knockout, and the activity of isocitrate dehydrogenase and malate dehydrogenase decreased.	NAD	24-57	L-lactate dehydrogenase	Staphylococcus xylosus	116-119
26794150-0	2016	Functional characterization of NAD dependent de-acetylases SIRT1 and SIRT2 in B-Cell Chronic Lymphocytic Leukemia (CLL).	NAD	31-34	sirtuin 2	Homo sapiens	69-74
34987507-0	2021	Intracellular NAD+ Depletion Confers a Priming Signal for NLRP3 Inflammasome Activation.	NAD	14-18	NLR family, pyrin domain containing 3	Mus musculus	58-63
34871367-5	2021	These NAD+-consuming enzymes include PARPs, sirtuins, CD38, and SARM1.	NAD	6-10	CD38 molecule	Homo sapiens	54-58
26414199-1	2016	The nicotinamide adenine dinucleotide-dependent protein deacetylase silent information regulator 2 (Sir2) regulates cellular lifespan in several organisms.	NAD	4-37	sirtuin 2	Homo sapiens	68-98
34950703-10	2021	SERCA inhibition, which also reduces ER/SR Ca2+ levels had similar effects to both NAD+ and cADPR on O-GlcNAc and ER stress responses to glucose deprivation.	NAD	83-87	O-linked N-acetylglucosamine (GlcNAc) transferase	Homo sapiens	101-109
27110038-0	2016	NADPH- and NADH-dependent metabolism of and DNA adduct formation by benzo[a]pyrene catalyzed with rat hepatic microsomes and cytochrome P450 1A1.	NAD	11-15	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	125-144
34950703-11	2021	The observation that NAD+, cADPR, and caffeine all attenuated the increase in O-GlcNAc and ER stress in response to glucose deprivation, suggests a potential common mechanism, linked to ER/SR Ca2+ levels, underlying their activation.	NAD	21-25	O-linked N-acetylglucosamine (GlcNAc) transferase	Homo sapiens	78-86
34637964-8	2021	Interestingly, CD38 inhibition without significant elevation of intracellular NAD+ also decreased IL-1beta release driven by MSU crystals in THP-1 macrophages.	NAD	78-82	interleukin 1 alpha	Mus musculus	98-106
27362524-2	2016	Mitochondrial Sirtuin 3 (SIRT3), which belongs to an evolutionary conserved family of NAD+-dependent deacetylases, is a key regulator of the mitochondrial respiratory chain, ATP production, and fatty acid beta-oxidation, and it exerts an antioxidant activity.	NAD	86-89	sirtuin 3	Mus musculus	14-23
27362524-2	2016	Mitochondrial Sirtuin 3 (SIRT3), which belongs to an evolutionary conserved family of NAD+-dependent deacetylases, is a key regulator of the mitochondrial respiratory chain, ATP production, and fatty acid beta-oxidation, and it exerts an antioxidant activity.	NAD	86-89	sirtuin 3	Mus musculus	25-30
34531546-12	2021	The mechanisms underlying ROF neuroprotective effects appear to be associated with NAD+/SIRT1-dependent activation of lysosomal function.	NAD	83-87	sirtuin 1	Mus musculus	88-93
27073590-5	2016	SIRT1 is an NAD(+)-dependent histone/protein deacetylase that plays roles in diverse cellular processes, including stress resistance and cell survival.	NAD	12-18	sirtuin 1	Mus musculus	0-5
34903884-0	2021	NADH inhibition of SIRT1 links energy state to transcription during time-restricted feeding.	NAD	0-4	sirtuin 1	Mus musculus	19-24
26627442-6	2016	Cytochrome b light chain (CYBA), encoded by a polymorphic gene, which is a critical component of the nicotinamide adenine dinucleotide (NADH)/NADPH oxidase system and plays an important role in electron transport and superoxide anion production, is located on chromosome band 16q24 and has six exons spanning almost 7.76 kb of genomic DNA.	NAD	101-134	cytochrome b-245 alpha chain	Homo sapiens	0-24
26627442-6	2016	Cytochrome b light chain (CYBA), encoded by a polymorphic gene, which is a critical component of the nicotinamide adenine dinucleotide (NADH)/NADPH oxidase system and plays an important role in electron transport and superoxide anion production, is located on chromosome band 16q24 and has six exons spanning almost 7.76 kb of genomic DNA.	NAD	101-134	cytochrome b-245 alpha chain	Homo sapiens	26-30
26627442-6	2016	Cytochrome b light chain (CYBA), encoded by a polymorphic gene, which is a critical component of the nicotinamide adenine dinucleotide (NADH)/NADPH oxidase system and plays an important role in electron transport and superoxide anion production, is located on chromosome band 16q24 and has six exons spanning almost 7.76 kb of genomic DNA.	NAD	136-140	cytochrome b-245 alpha chain	Homo sapiens	0-24
34903884-1	2021	In mammals, circadian rhythms are entrained to the light cycle and drive daily oscillations in levels of NAD+, a cosubstrate of the class III histone deacetylase sirtuin 1 (SIRT1) that associates with clock transcription factors.	NAD	105-109	sirtuin 1	Mus musculus	162-171
26627442-6	2016	Cytochrome b light chain (CYBA), encoded by a polymorphic gene, which is a critical component of the nicotinamide adenine dinucleotide (NADH)/NADPH oxidase system and plays an important role in electron transport and superoxide anion production, is located on chromosome band 16q24 and has six exons spanning almost 7.76 kb of genomic DNA.	NAD	136-140	cytochrome b-245 alpha chain	Homo sapiens	26-30
26470683-5	2015	Furthermore, the coexpression of S. cerevisiae ZWF1 and ACS1 genes in the DWM strain increased intracellular concentrations of NADPH and NADH and improved maximum xylitol productivity by 17%, relative to that for the DWM strain.	NAD	137-141	glucose-6-phosphate dehydrogenase	Saccharomyces cerevisiae S288C	47-51
34903884-1	2021	In mammals, circadian rhythms are entrained to the light cycle and drive daily oscillations in levels of NAD+, a cosubstrate of the class III histone deacetylase sirtuin 1 (SIRT1) that associates with clock transcription factors.	NAD	105-109	sirtuin 1	Mus musculus	173-178
34903884-6	2021	Enzymatic analyses reveal that NADH inhibits SIRT1 in vitro, corresponding with reduced deacetylation of SIRT1 substrates during TRF-CR in vivo.	NAD	31-35	sirtuin 1	Mus musculus	45-50
34903884-6	2021	Enzymatic analyses reveal that NADH inhibits SIRT1 in vitro, corresponding with reduced deacetylation of SIRT1 substrates during TRF-CR in vivo.	NAD	31-35	sirtuin 1	Mus musculus	105-110
34903884-8	2021	Our findings reveal that the hepatic NADH cycle links nutrient state to whole-body energetics through the rhythmic regulation of SIRT1.	NAD	37-41	sirtuin 1	Mus musculus	129-134
26209889-7	2015	RESULTS: HIF-2alpha activated the NAMPT-NAD(+)-SIRT axis in chondrocytes by upregulating NAMPT, which stimulated NAD(+) synthesis and thereby activated SIRT family members.	NAD	40-46	endothelial PAS domain protein 1	Mus musculus	9-19
34789130-8	2021	It is noted that the genotoxic behavior of STZ in animals is accomplished through a reduction of nicotinamide adenine dinucleotide (NAD+) in pancreatic beta-cells via the GLUT2 (Glucose transporter 2), which can cause cellular damage by DNA (Deoxyribonucleic acid) strand breaks that lead to cell death.	NAD	97-130	solute carrier family 2 member 2	Rattus norvegicus	171-176
26209889-7	2015	RESULTS: HIF-2alpha activated the NAMPT-NAD(+)-SIRT axis in chondrocytes by upregulating NAMPT, which stimulated NAD(+) synthesis and thereby activated SIRT family members.	NAD	113-119	endothelial PAS domain protein 1	Mus musculus	9-19
26209889-11	2015	CONCLUSION: The reciprocal regulation of HIF-2alpha and the NAMPT-NAD(+)-SIRT axis in articular chondrocytes is involved in OA cartilage destruction caused by HIF-2alpha or NAMPT.	NAD	66-72	endothelial PAS domain protein 1	Mus musculus	159-169
34789130-8	2021	It is noted that the genotoxic behavior of STZ in animals is accomplished through a reduction of nicotinamide adenine dinucleotide (NAD+) in pancreatic beta-cells via the GLUT2 (Glucose transporter 2), which can cause cellular damage by DNA (Deoxyribonucleic acid) strand breaks that lead to cell death.	NAD	97-130	solute carrier family 2 member 2	Rattus norvegicus	178-199
26616331-1	2015	Nicotinamide mononucleotide adenylyltransferase (NMNAT) is a conserved enzyme in the NAD synthetic pathway.	NAD	85-88	Nicotinamide mononucleotide adenylyltransferase	Drosophila melanogaster	0-47
34789130-8	2021	It is noted that the genotoxic behavior of STZ in animals is accomplished through a reduction of nicotinamide adenine dinucleotide (NAD+) in pancreatic beta-cells via the GLUT2 (Glucose transporter 2), which can cause cellular damage by DNA (Deoxyribonucleic acid) strand breaks that lead to cell death.	NAD	132-136	solute carrier family 2 member 2	Rattus norvegicus	171-176
26616331-1	2015	Nicotinamide mononucleotide adenylyltransferase (NMNAT) is a conserved enzyme in the NAD synthetic pathway.	NAD	85-88	Nicotinamide mononucleotide adenylyltransferase	Drosophila melanogaster	49-54
34789130-8	2021	It is noted that the genotoxic behavior of STZ in animals is accomplished through a reduction of nicotinamide adenine dinucleotide (NAD+) in pancreatic beta-cells via the GLUT2 (Glucose transporter 2), which can cause cellular damage by DNA (Deoxyribonucleic acid) strand breaks that lead to cell death.	NAD	132-136	solute carrier family 2 member 2	Rattus norvegicus	178-199
26618989-9	2015	HPLC measurements and protein localization analysis highlight Nmnat1-Rbp7a as the only known cytoplasmic and presumably endoplasmic reticulum (ER) specific NAD+ catalyzing enzyme.	NAD	156-160	nicotinamide nucleotide adenylyltransferase 1	Danio rerio	62-68
26618989-10	2015	These studies, taken together with previously documented NAD+ dependent interaction of RBPs with ER-associated enzymes of retinal catalysis, implicate functions of this newly described NMNAT1-Rbp7 fusion protein in retinol oxidation.	NAD	57-61	nicotinamide nucleotide adenylyltransferase 1	Danio rerio	185-191
34789130-9	2021	NA is a biochemical precursor of NAD+, and it is a poly-ADP-ribose-polymerase-1 (PARP-1) inhibitor.	NAD	33-37	poly (ADP-ribose) polymerase 1	Rattus norvegicus	51-79
34789130-9	2021	NA is a biochemical precursor of NAD+, and it is a poly-ADP-ribose-polymerase-1 (PARP-1) inhibitor.	NAD	33-37	poly (ADP-ribose) polymerase 1	Rattus norvegicus	81-87
34758848-3	2021	Sirtuin 3 (SIRT3), a mitochondrial NAD+-dependent deacetylase, modulates the activities of several substrates involving in autophagy and energy metabolism.	NAD	35-38	sirtuin 3	Mus musculus	0-9
34758848-3	2021	Sirtuin 3 (SIRT3), a mitochondrial NAD+-dependent deacetylase, modulates the activities of several substrates involving in autophagy and energy metabolism.	NAD	35-38	sirtuin 3	Mus musculus	11-16
34769515-5	2021	Dunnione increases the cellular NAD+ levels in lung tissues of tumor-bearing mice to restore the declining sirtuin 1 (SIRT1) activity, thus deacetylating nuclear factor-kappa B (NF-kappaB) and preventing the overexpression of tissue factor in bronchial epithelial and vascular endothelial cells.	NAD	32-36	sirtuin 1	Mus musculus	107-116
26579709-6	2015	We show, for the first time, that IDO mediates human tumor cell resistance to the candidate anticancer drugs FK866 (an NAD+ inhibitor), methoxyamine (MX, a base excision repair [BER] inhibitor) and approved anticancer drugs pemetrexed (a folate anti-metabolite) and gemcitabine (a nucleoside analogue), and combined treatment with pemetrexed and MX, in the absence of immune cells.	NAD	119-123	indoleamine 2,3-dioxygenase 1	Homo sapiens	34-37
34769515-5	2021	Dunnione increases the cellular NAD+ levels in lung tissues of tumor-bearing mice to restore the declining sirtuin 1 (SIRT1) activity, thus deacetylating nuclear factor-kappa B (NF-kappaB) and preventing the overexpression of tissue factor in bronchial epithelial and vascular endothelial cells.	NAD	32-36	sirtuin 1	Mus musculus	118-123
34506725-2	2021	Here, we elucidate a transcellular signaling mechanism by which oligodendrocytes support axonal energy metabolism via transcellular delivery of NAD-dependent deacetylase SIRT2.	NAD	144-147	sirtuin 2	Mus musculus	170-175
26463129-0	2015	Negishi cross-coupling enabled synthesis of novel NAD(+)-dependent DNA ligase inhibitors and SAR development.	NAD	50-56	ubiquitin conjugating enzyme E2 K	Homo sapiens	71-77
26522369-5	2015	Pharmacological inhibition of Nampt by FK866 or depletion of monocytes/macrophages by clodronate liposomes disrupted the homeostatic mechanism of myocardial NAD(+) levels and NAD(+)-dependent Sirt1 activity, leading to susceptibility to cardiomyocyte apoptosis and cardiac decompensation in pressure-overloaded mice.	NAD	175-181	sirtuin 1	Mus musculus	192-197
34559251-6	2021	As examples, the present commentary tries to integrate responses of AHR and NAD+-consuming enzymes (PARP7/TiPARP, CD38 and sirtuins) into infectious and stress-induced inflammatory responses, the latter exemplified by nonalcoholic fatty liver disease (NAFLD).	NAD	76-80	CD38 molecule	Homo sapiens	114-118
25761756-8	2015	While the expression and activity of the NAD(+) dependent deacetylase sirtuin 1, a ChREBP-negative target, were down-regulated in the liver of alcohol-fed mice, they were restored to control levels upon ChREBP silencing.	NAD	41-47	sirtuin 1	Mus musculus	70-79
34182004-3	2021	METHODS: In this paper, microvascular endothelial function was assessed in FH patients and healthy controls using flow mediated skin fluorescence (FMSF), based on measurements of nicotinamide adenine dinucleotide fluorescence intensity during brachial artery occlusion (ischemic response, IR) and immediately after occlusion (hyperemic response, HR).	NAD	179-212	low density lipoprotein receptor	Homo sapiens	75-77
34777396-6	2021	Furthermore, we identified CD38 as an inflammatory mediator of exhausted monocytes, associated with a drastic depletion of cellular NAD+; elevation of ROS; and compromise of mitochondria respiration, representative of septic monocytes.	NAD	132-136	CD38 molecule	Homo sapiens	27-31
25546019-5	2015	Both Connexin and Pannexin hemichannels may mediate release of paracrine molecules that in turn propagate cell death messages by releasing intracellular mediators, such as ATP, NAD(+), or glutamate or by abnormally prolonged opening to allow cell edema.	NAD	177-183	LOC100128922	Homo sapiens	5-13
26089537-3	2015	BPZE1-DC induces CD4(+) and CD8(+) T lymphocytes to express 2 sets of ectoenzymes generating ADO: 1 set is part of the conventional CD39/CD73 pathway, which uses ATP as substrate, whereas the other is part of the CD38/CD203a/CD73 pathway and metabolizes NAD(+).	NAD	254-260	5' nucleotidase, ecto	Mus musculus	137-141
26407304-4	2015	Here, we provide the first full-length molecular models of SIRT2 in the absence and presence of NAD+.	NAD	96-100	sirtuin 2	Homo sapiens	59-64
26189030-2	2015	Using NAD(+) as a substrate, they poly(ADP-ribosyl)ate TRF1 (regulating lengths of telomeres), NuMA (facilitating mitosis) and axin (in wnt/beta-catenin signalling).	NAD	6-12	catenin beta 1	Homo sapiens	140-152
26237213-7	2015	Characterization of P173G hAIF indicates that the stacking of P173 against the isoalloxazine ring is relevant to determine the flavin environment and to modulate the enzyme affinity for NADH.	NAD	186-190	NADH:ubiquinone oxidoreductase subunit B11	Homo sapiens	20-24
25934569-1	2015	Inhibitors of PARP-1(Poly(ADP-ribose) polymerase-1) act by competing with NAD(+), the enzyme physiological substrate, which play a protective role in many pathological conditions characterized by PARP-1 overactivation.	NAD	74-80	poly (ADP-ribose) polymerase 1	Rattus norvegicus	14-50
25934569-1	2015	Inhibitors of PARP-1(Poly(ADP-ribose) polymerase-1) act by competing with NAD(+), the enzyme physiological substrate, which play a protective role in many pathological conditions characterized by PARP-1 overactivation.	NAD	74-80	poly (ADP-ribose) polymerase 1	Rattus norvegicus	14-20
26200012-6	2015	Further, ERRalpha was required for the regulation of NF-kappaB signaling by controlling p65 acetylation via maintenance of NAD(+) levels and sirtuin 1 activation.	NAD	123-129	v-rel reticuloendotheliosis viral oncogene homolog A (avian)	Mus musculus	88-91
26060246-10	2015	Knockdown of NAD-dependent deacetylase sirtuin 1 (SIRT1) and SIRT2 inhibited the progrowth action of Nampt-NAD axis, whereas knockdown of SIRT1, SIRT2, and SIRT6 compromised the prodifferentiation effect of Nampt-NAD axis.	NAD	13-16	sirtuin 1	Mus musculus	50-55
26060246-10	2015	Knockdown of NAD-dependent deacetylase sirtuin 1 (SIRT1) and SIRT2 inhibited the progrowth action of Nampt-NAD axis, whereas knockdown of SIRT1, SIRT2, and SIRT6 compromised the prodifferentiation effect of Nampt-NAD axis.	NAD	13-16	sirtuin 2	Mus musculus	145-150
26060246-10	2015	Knockdown of NAD-dependent deacetylase sirtuin 1 (SIRT1) and SIRT2 inhibited the progrowth action of Nampt-NAD axis, whereas knockdown of SIRT1, SIRT2, and SIRT6 compromised the prodifferentiation effect of Nampt-NAD axis.	NAD	107-110	sirtuin 1	Mus musculus	50-55
26060246-10	2015	Knockdown of NAD-dependent deacetylase sirtuin 1 (SIRT1) and SIRT2 inhibited the progrowth action of Nampt-NAD axis, whereas knockdown of SIRT1, SIRT2, and SIRT6 compromised the prodifferentiation effect of Nampt-NAD axis.	NAD	107-110	sirtuin 2	Mus musculus	61-66
26060246-10	2015	Knockdown of NAD-dependent deacetylase sirtuin 1 (SIRT1) and SIRT2 inhibited the progrowth action of Nampt-NAD axis, whereas knockdown of SIRT1, SIRT2, and SIRT6 compromised the prodifferentiation effect of Nampt-NAD axis.	NAD	107-110	sirtuin 2	Mus musculus	145-150
26060246-10	2015	Knockdown of NAD-dependent deacetylase sirtuin 1 (SIRT1) and SIRT2 inhibited the progrowth action of Nampt-NAD axis, whereas knockdown of SIRT1, SIRT2, and SIRT6 compromised the prodifferentiation effect of Nampt-NAD axis.	NAD	107-110	sirtuin 1	Mus musculus	50-55
26060246-10	2015	Knockdown of NAD-dependent deacetylase sirtuin 1 (SIRT1) and SIRT2 inhibited the progrowth action of Nampt-NAD axis, whereas knockdown of SIRT1, SIRT2, and SIRT6 compromised the prodifferentiation effect of Nampt-NAD axis.	NAD	107-110	sirtuin 2	Mus musculus	61-66
26060246-10	2015	Knockdown of NAD-dependent deacetylase sirtuin 1 (SIRT1) and SIRT2 inhibited the progrowth action of Nampt-NAD axis, whereas knockdown of SIRT1, SIRT2, and SIRT6 compromised the prodifferentiation effect of Nampt-NAD axis.	NAD	107-110	sirtuin 2	Mus musculus	145-150
26074075-2	2015	The NAD(+)-dependent deacetylase SirT1 orchestrates metabolism, cellular survival, and growth.	NAD	4-10	sirtuin 1	Mus musculus	33-38
26098879-3	2015	Sirtuin1 (SIRT1) belongs to the family of NAD-dependent de-acyetylases and is modulated by cellular redox.	NAD	42-45	sirtuin 1	Mus musculus	10-15
34509469-2	2021	NAD+ is also important in cellular signalling as it is consumed by PARPs, SARM1, sirtuins and CD38.	NAD	0-4	CD38 molecule	Homo sapiens	94-98
34694148-3	2021	Augmentation of NAD+ by oral administration of a precursor, nicotinamide riboside (NR), reduces senescence of affected cells, attenuates DNA damage and neuroinflammation in the transgenic APP/PS1 murine model of AD.	NAD	16-20	presenilin 1	Mus musculus	192-195
26078397-7	2015	GST inhibitors also induced intracellular oxidative stress (measured by dihydrorhodamine 123 and dichlorofluorescein fluorescence), caused alterations in overall intracellular redox status (as evidenced by NAD(+)/NADH ratios), and increased protein carbonyl formation.	NAD	206-212	hematopoietic prostaglandin D synthase	Mus musculus	0-3
26078397-7	2015	GST inhibitors also induced intracellular oxidative stress (measured by dihydrorhodamine 123 and dichlorofluorescein fluorescence), caused alterations in overall intracellular redox status (as evidenced by NAD(+)/NADH ratios), and increased protein carbonyl formation.	NAD	213-217	hematopoietic prostaglandin D synthase	Mus musculus	0-3
25450233-3	2015	Here we present the first human ALDH1A1 structure, as the apo-enzyme and in complex with its cofactor NADH to a resolution of 1.75 and 2.1A, respectfully.	NAD	102-106	aldehyde dehydrogenase 1 family member A1	Homo sapiens	32-39
26023773-3	2015	Mitotic repression of Pol I transcription correlates with transient nucleolar enrichment of the NAD(+)-dependent deacetylase SIRT1, which deacetylates another subunit of SL1, TAFI68.	NAD	96-102	TATA-box binding protein associated factor, RNA polymerase I subunit C	Homo sapiens	170-173
25897714-8	2015	Cocrystallization of SIRT2 with myristoylated peptide and NAD(+) yielded a co-complex structure with reaction product 2"-O-myristoyl-ADP-ribose, revealing a latent hydrophobic cavity to accommodate the long chain acyl group, and suggesting a general mechanism for long chain deacylation.	NAD	58-64	sirtuin 2	Homo sapiens	21-26
25921090-0	2015	SIRT1-Mediated eNAMPT Secretion from Adipose Tissue Regulates Hypothalamic NAD+ and Function in Mice.	NAD	75-79	sirtuin 1	Mus musculus	0-5
25475438-2	2015	SIRT1 is a NAD-dependent protein deacetylase possessing antiaging activities in a wide range of organisms.	NAD	11-14	sirtuin 1	Mus musculus	0-5
26018518-1	2015	BACKGROUND: Isocitrate dehydrogenase (IDH) catalyzes the oxidative decarboxylation of isocitrate to yield alpha-ketoglutarate (alpha-KG) with production of reduced nicotinamide adenine dinucleotide (NADH).	NAD	164-197	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	12-36
26018518-1	2015	BACKGROUND: Isocitrate dehydrogenase (IDH) catalyzes the oxidative decarboxylation of isocitrate to yield alpha-ketoglutarate (alpha-KG) with production of reduced nicotinamide adenine dinucleotide (NADH).	NAD	164-197	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	38-41
26018518-1	2015	BACKGROUND: Isocitrate dehydrogenase (IDH) catalyzes the oxidative decarboxylation of isocitrate to yield alpha-ketoglutarate (alpha-KG) with production of reduced nicotinamide adenine dinucleotide (NADH).	NAD	199-203	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	12-36
26018518-1	2015	BACKGROUND: Isocitrate dehydrogenase (IDH) catalyzes the oxidative decarboxylation of isocitrate to yield alpha-ketoglutarate (alpha-KG) with production of reduced nicotinamide adenine dinucleotide (NADH).	NAD	199-203	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	38-41
26018518-2	2015	Dysfunctional IDH leads to reduced production of alpha-KG and NADH and increased production of 2-hydroxyglutarate, an oncometabolite.	NAD	62-66	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	14-17
25933096-10	2015	Importantly, NAD+ rescued impaired fatty acid oxidation in hepatocytes deficient for either OXPHOS or SIRT3.	NAD	13-17	sirtuin 3	Mus musculus	102-107
25722455-4	2015	Elevated matrix NADH, in turn, diminished the cytosolic NAD(+)/NADH ratio and triggered a subsequent downregulation of the NAD(+)-dependent deacetylase sirtuin 1 (SIRT1).	NAD	16-20	sirtuin 1	Mus musculus	163-168
25722455-4	2015	Elevated matrix NADH, in turn, diminished the cytosolic NAD(+)/NADH ratio and triggered a subsequent downregulation of the NAD(+)-dependent deacetylase sirtuin 1 (SIRT1).	NAD	123-129	sirtuin 1	Mus musculus	163-168
25341378-2	2015	This study tested the hypothesis that metabolic inhibition caused by cyanide-induced chemical anoxia plus glucose deprivation promotes both release of mitochondrial NAD(H) in response to opening of the permeability transition pore (PTP) and NAD(P)(H) degradation through activation of poly (ADP-ribose) polymerase (PARP).	NAD	165-171	poly (ADP-ribose) polymerase 1	Rattus norvegicus	285-313
25813492-0	2015	NAD+ treatment can prevent rotenone-induced increases in DNA damage, Bax levels and nuclear translocation of apoptosis-inducing factor in differentiated PC12 cells.	NAD	0-4	BCL2 associated X, apoptosis regulator	Rattus norvegicus	69-72
25813492-5	2015	We found that NAD(+) treatment can markedly attenuate the rotenone-induced increases in the levels of Bax and nuclear translocation of AIF in the cells.	NAD	14-20	BCL2 associated X, apoptosis regulator	Rattus norvegicus	102-105
34089817-0	2021	Modulation of NAD+ biosynthesis activates SIRT1 and resist cisplatin-induced ototoxicity.	NAD	14-18	sirtuin 1	Mus musculus	42-47
34745743-5	2021	In this study, we use TPEF imaging to acquire high-resolution fluorescence images from two coenzymes, NAD(P)H (reduced form of nicotinamide adenine dinucleotide) and FAD (flavin adenine dinucleotide), within human fibroblasts and keratinocytes in response to B3 (a nicotinamide precursor) supplementation and/or UV irradiation, without addition of exogenous labels.	NAD	127-160	transmembrane protein with EGF like and two follistatin like domains 2	Homo sapiens	22-26
34777762-3	2021	In this study, we find that rare-earth elements (REEs) can enhance the activity of NAD+-dependent glutamate dehydrogenase (GDH) toward highly sensitive electrochemical biosensing of glutamate in vivo.	NAD	83-86	glutamate dehydrogenase 1	Homo sapiens	123-126
34777762-6	2021	With the potential effect of REE cations on NAD+ electrochemistry being ruled out, homogeneous kinetic assays by steady-state and stopped-flow spectroscopy reveal a two-fold enhancement in the intrinsic reaction rate of GDH by introducing Yb3+, mainly through accelerating the rate-determining NADH releasing step during the catalytic cycle.	NAD	44-48	glutamate dehydrogenase 1	Homo sapiens	220-223
34777762-6	2021	With the potential effect of REE cations on NAD+ electrochemistry being ruled out, homogeneous kinetic assays by steady-state and stopped-flow spectroscopy reveal a two-fold enhancement in the intrinsic reaction rate of GDH by introducing Yb3+, mainly through accelerating the rate-determining NADH releasing step during the catalytic cycle.	NAD	294-298	glutamate dehydrogenase 1	Homo sapiens	220-223
34777762-7	2021	In-depth structural investigations using small angle X-ray scattering and infrared spectroscopy indicate that Yb3+ induces the backbone compaction of GDH and subtle beta-sheet transitions in the active site, which may reduce the energetic barrier to NADH dissociation from the binding pocket as further suggested by molecular dynamics simulation.	NAD	250-254	glutamate dehydrogenase 1	Homo sapiens	150-153
34183378-11	2021	These findings indicate that the NAD+/SIRT2 pathway plays an important role in CYP3A regulation during NAFLD.	NAD	33-37	sirtuin 2	Mus musculus	38-43
34504490-5	2021	Our results show that extracellular NAD+ reduces the enzymatic activity of CD73 HEK cells co-transfected with CD73/ARTC2.2.	NAD	36-40	5' nucleotidase, ecto	Mus musculus	75-79
34504490-5	2021	Our results show that extracellular NAD+ reduces the enzymatic activity of CD73 HEK cells co-transfected with CD73/ARTC2.2.	NAD	36-40	5' nucleotidase, ecto	Mus musculus	110-114
34504490-6	2021	Importantly, NAD+ significantly reduced CD73 activity on WT CD8 T cells compared to ARTC2ko CD8 T cells or WT CD8 T cells treated with an ARTC2.2-blocking nanobody.	NAD	13-17	5' nucleotidase, ecto	Mus musculus	40-44
34483906-4	2021	Sirtuin 1 (SIRT1), an NAD+-dependent deacetylase, plays a vital role in hepatic steatosis and inflammation.	NAD	22-25	sirtuin 1	Mus musculus	0-9
25772354-1	2015	The NAD+-dependent protein deacetylase SIRT1 regulates energy metabolism, responses to stress, and aging by deacetylating many different proteins, including histones and transcription factors.	NAD	4-8	sirtuin 1	Mus musculus	39-44
25549554-4	2015	Molecular docking showed that the tetrahydropyridoindole scaffold was positioned in the NAD + pocket and the acetylated substrate channel of the sirtuin 2 protein by van der Waals/hydrophobic, H bonding and stacking interactions.	NAD	88-93	sirtuin 2	Homo sapiens	145-154
25600643-0	2015	The NAD(+)-dependent SIRT1 deacetylase translates a metabolic switch into regulatory epigenetics in skeletal muscle stem cells.	NAD	4-10	sirtuin 1	Mus musculus	21-26
25497549-9	2015	In addition, the levels of norepinephrine in serum as well as nicotinamide adenine dinucleotide (NAD(+)) and ATP in myocardium were determined, which implied that cardiac protection of renalase against I/R may be related, at least in part, to its metabolism of catecholamine and regulation of energy.	NAD	62-95	renalase, FAD-dependent amine oxidase	Mus musculus	185-193
25497549-9	2015	In addition, the levels of norepinephrine in serum as well as nicotinamide adenine dinucleotide (NAD(+)) and ATP in myocardium were determined, which implied that cardiac protection of renalase against I/R may be related, at least in part, to its metabolism of catecholamine and regulation of energy.	NAD	97-103	renalase, FAD-dependent amine oxidase	Mus musculus	185-193
24990614-5	2015	Through the enzymatic conversion of NAD into ADPR (ADP-ribose) and cADPR (cyclic ADP-ribose), CD38 increases cytoplasmic Ca(2+) concentrations, positively influencing proliferation and signaling mediated via chemokine receptors or integrins.	NAD	36-39	CD38 molecule	Homo sapiens	94-98
25590809-2	2015	Reducing NAD(+) pools by inhibiting NAMPT primed pancreatic ductal adenocarcinoma (PDA) cells for poly(ADP ribose) polymerase (PARP1)-dependent cell death induced by the targeted cancer therapeutic, beta-lapachone (beta-lap, ARQ761), independent of poly(ADP ribose) (PAR) accumulation.	NAD	9-15	LAP	Homo sapiens	204-207
34483906-4	2021	Sirtuin 1 (SIRT1), an NAD+-dependent deacetylase, plays a vital role in hepatic steatosis and inflammation.	NAD	22-25	sirtuin 1	Mus musculus	11-16
34303733-6	2021	Furthermore, pretreatment with specific ERalpha agonist PPT (1 muM) significantly attenuated the above PFOS-induced effects while specific ERbeta agonist DPN (1 muM) accelerated them.	NAD	154-157	estrogen receptor 1 (alpha)	Mus musculus	139-145
34393764-1	2021	Silence information regulator 3 (SIRT3) is an NAD+ dependent deacetylase enzyme that enhances the function of key mitochondrial proteins.	NAD	46-49	sirtuin 3	Mus musculus	0-31
34393764-1	2021	Silence information regulator 3 (SIRT3) is an NAD+ dependent deacetylase enzyme that enhances the function of key mitochondrial proteins.	NAD	46-49	sirtuin 3	Mus musculus	33-38
34190541-1	2021	(R)-3-Hydroxybutyrate dehydrogenase (HBDH) catalyzes the NADH-dependent reduction of 3-oxocarboxylates to (R)-3-hydroxycarboxylates.	NAD	57-61	3-hydroxybutyrate dehydrogenase 1	Homo sapiens	0-35
34278224-5	2021	Results: GP referral accuracy was found to be 63% for strabismus cases, 50% for reduced vision/amblyopia cases, 45% for NAD cases, 100% of nystagmus cases and 92% of "other" cases.	NAD	120-123	ring finger protein 130	Homo sapiens	9-11
34484659-1	2021	Sirtuin 1 (SIRT1), the NAD-dependent histone deacetylase, has been extensively investigated due to its cognitive protective effect.	NAD	23-26	sirtuin 1	Mus musculus	0-9
34484659-1	2021	Sirtuin 1 (SIRT1), the NAD-dependent histone deacetylase, has been extensively investigated due to its cognitive protective effect.	NAD	23-26	sirtuin 1	Mus musculus	11-16
35381294-7	2022	Mechanistically, the inhibiting effect was attributed to the direct and indirect regulatory effect of DDIT3 on SIRT1 (sirtuin1, silent mating type information regulation protein type 1, a member of NAD+ dependent class III histone deacetylases).	NAD	198-201	DNA-damage inducible transcript 3	Mus musculus	102-107
35381294-7	2022	Mechanistically, the inhibiting effect was attributed to the direct and indirect regulatory effect of DDIT3 on SIRT1 (sirtuin1, silent mating type information regulation protein type 1, a member of NAD+ dependent class III histone deacetylases).	NAD	198-201	sirtuin 1	Mus musculus	111-116
35381294-7	2022	Mechanistically, the inhibiting effect was attributed to the direct and indirect regulatory effect of DDIT3 on SIRT1 (sirtuin1, silent mating type information regulation protein type 1, a member of NAD+ dependent class III histone deacetylases).	NAD	198-201	sirtuin 1	Mus musculus	118-126
35504092-7	2022	Subsequently, the increased NAD+ upregulated the expression of Sirt1, SOD2 and attenuated DNA damage.	NAD	28-32	sirtuin 1	Mus musculus	63-68
35490894-11	2022	CONCLUSION: In view of the findings, crocin ameliorates depression in mice, which may be associated with regulating NAMPT-NAD+-SIRT1 pathway.	NAD	122-126	sirtuin 1	Mus musculus	127-132
35196577-8	2022	Additionally, Sirt3 transcript and protein expressions were found up-regulated in both of the HF old male offspring skeletal muscle (1.42-fold) (P<.05) and palmitic acid (PA) treated L6 myotubes (1.32-fold) (P<.05), accompanied with increase in nicotinamide adenine dinucleotide (NAD+) in HF old male offspring skeletal muscle (P<.05).	NAD	245-278	sirtuin 3	Rattus norvegicus	14-19
25287541-4	2015	The effects observed long after perinatal asphyxia can be explained by over-expression of sentinel proteins, such as poly(ADP-ribose) polymerase-1 (PARP-1), competing for oxidised nicotinamide adenine dinucleotide (NAD(+)) during re-oxygenation.	NAD	180-213	poly (ADP-ribose) polymerase 1	Rattus norvegicus	117-146
25287541-4	2015	The effects observed long after perinatal asphyxia can be explained by over-expression of sentinel proteins, such as poly(ADP-ribose) polymerase-1 (PARP-1), competing for oxidised nicotinamide adenine dinucleotide (NAD(+)) during re-oxygenation.	NAD	180-213	poly (ADP-ribose) polymerase 1	Rattus norvegicus	148-154
25287541-4	2015	The effects observed long after perinatal asphyxia can be explained by over-expression of sentinel proteins, such as poly(ADP-ribose) polymerase-1 (PARP-1), competing for oxidised nicotinamide adenine dinucleotide (NAD(+)) during re-oxygenation.	NAD	215-221	poly (ADP-ribose) polymerase 1	Rattus norvegicus	117-146
25287541-4	2015	The effects observed long after perinatal asphyxia can be explained by over-expression of sentinel proteins, such as poly(ADP-ribose) polymerase-1 (PARP-1), competing for oxidised nicotinamide adenine dinucleotide (NAD(+)) during re-oxygenation.	NAD	215-221	poly (ADP-ribose) polymerase 1	Rattus norvegicus	148-154
25529796-8	2015	Thus, the NAD(+)-dependent inhibition of SOD2 activity and ROS by SIRT1 provides a gatekeeper function to reduce PARK2-mediated mitophagy and aberrant cell survival.	NAD	10-16	parkin RBR E3 ubiquitin protein ligase	Homo sapiens	113-118
25048519-6	2015	Our working hypothesis, to be discussed and partially tested herein, is that CD38, and likely BST1/CD157--both NAD(+) -consuming enzymes, are active in the myeloma niche and lead a discontinuous chain of ectoenzymes whose final products are exploited by the neoplastic plasma cell as part of its local survival strategy.	NAD	111-117	CD38 molecule	Homo sapiens	77-81
26558285-5	2015	Finally, low sirtuin-1 and sirtuin-3 gene expressions due to higher NADH/NAD in Cmah-null mice decreased Foxo-1 and MnSOD gene expression, suggesting that oxidative stress may result in mitochondrial dysfunction in Cmah-null mouse.	NAD	68-71	sirtuin 1	Mus musculus	13-22
26558285-5	2015	Finally, low sirtuin-1 and sirtuin-3 gene expressions due to higher NADH/NAD in Cmah-null mice decreased Foxo-1 and MnSOD gene expression, suggesting that oxidative stress may result in mitochondrial dysfunction in Cmah-null mouse.	NAD	68-71	sirtuin 3	Mus musculus	27-36
26558285-5	2015	Finally, low sirtuin-1 and sirtuin-3 gene expressions due to higher NADH/NAD in Cmah-null mice decreased Foxo-1 and MnSOD gene expression, suggesting that oxidative stress may result in mitochondrial dysfunction in Cmah-null mouse.	NAD	68-71	forkhead box O1	Mus musculus	105-111
25666794-5	2015	A number of studies have further indicated that multiple NAD(+)-dependent enzymes such as sirtuins, polymerase(ADP-ribose) polymerases (PARPs) and CD38 mediate cell death and multiple biological processes.	NAD	57-63	CD38 molecule	Homo sapiens	147-151
25535715-9	2014	The values of Km and Vmax with NADH of the bacterium was found to be 0.818 mug mL-1 and 0.085 mug mL-1.min-1.mg-1 protein, respectively.	NAD	31-35	L1 cell adhesion molecule	Mus musculus	79-83
25535715-9	2014	The values of Km and Vmax with NADH of the bacterium was found to be 0.818 mug mL-1 and 0.085 mug mL-1.min-1.mg-1 protein, respectively.	NAD	31-35	L1 cell adhesion molecule	Mus musculus	98-102
25453901-0	2014	Inhibition of de novo NAD(+) synthesis by oncogenic URI causes liver tumorigenesis through DNA damage.	NAD	22-28	URI1 prefoldin like chaperone	Homo sapiens	52-55
25453901-3	2014	URI inhibits aryl hydrocarbon (AhR)- and estrogen receptor (ER)-mediated transcription of enzymes implicated in L-tryptophan/kynurenine/nicotinamide adenine dinucleotide (NAD(+)) metabolism, thereby causing DNA damage at early stages of tumorigenesis.	NAD	136-169	URI1 prefoldin like chaperone	Homo sapiens	0-3
25453901-3	2014	URI inhibits aryl hydrocarbon (AhR)- and estrogen receptor (ER)-mediated transcription of enzymes implicated in L-tryptophan/kynurenine/nicotinamide adenine dinucleotide (NAD(+)) metabolism, thereby causing DNA damage at early stages of tumorigenesis.	NAD	171-177	URI1 prefoldin like chaperone	Homo sapiens	0-3
25257342-6	2014	The nicotinamidase PNC-1, a key NAD+ salvage pathway component, was largely required for DR to increase lifespan but not two healthspan indicators: movement and stress resistance.	NAD	32-36	Isochorismatase domain-containing protein	Caenorhabditis elegans	19-24
35196577-8	2022	Additionally, Sirt3 transcript and protein expressions were found up-regulated in both of the HF old male offspring skeletal muscle (1.42-fold) (P<.05) and palmitic acid (PA) treated L6 myotubes (1.32-fold) (P<.05), accompanied with increase in nicotinamide adenine dinucleotide (NAD+) in HF old male offspring skeletal muscle (P<.05).	NAD	280-284	sirtuin 3	Rattus norvegicus	14-19
35585057-7	2022	Interestingly, while inhibition of FSP1 caused RPE cell death, which was aggravated by SIO exposure, overexpression of FSP1 effectively protected RPE cells from SIO-induced injury, accompanied by a significant down-regulation of CoQ10/NADH and lipid peroxidation.	NAD	235-239	atlastin GTPase 1	Mus musculus	119-123
35176139-6	2022	Furthermore, the interaction of LDHA and eEF2 was dependent on NADH, a coenzyme of LDHA.	NAD	63-67	eukaryotic translation elongation factor 2	Homo sapiens	41-45
35176139-7	2022	NADH-competitive inhibitors of LDHA could release eEF2 from the LDHA pool, up-regulate translation and enhance MK maturation in vitro.	NAD	0-4	eukaryotic translation elongation factor 2	Homo sapiens	50-54
35563503-6	2022	Simultaneous measurements of oxygen consumption, membrane potential, NADH, and the ubiquinone redox state were correlated to ProDH activity and F1FO-ATPase directionality.	NAD	69-73	proline dehydrogenase	Mus musculus	125-130
35438990-5	2022	EPR spectroscopy and density functional theory calculations revealed that this compound features a high-spin Co(I) center that is antiferromagnetically coupled to a PDI radical anion.	NAD	109-114	peptidyl arginine deiminase 1	Homo sapiens	165-168
35302710-4	2022	Specifically, abrogation of SCO2 increased NAD+ regenerating reactions and decreased glucose oxidation through citric acid cycle while enhancing pyruvate carboxylation.	NAD	43-47	synthesis of cytochrome C oxidase 2	Homo sapiens	28-32
35429545-2	2022	CD38 is a major mammalian nicotinamide adenine dinucleotide (NAD)+ glycohydrolase expressed on T cells, and appears to be an important modulator of T cell response in tumor models.	NAD	26-59	CD38 molecule	Homo sapiens	0-4
24912433-7	2014	Native top-down ISD of the hADH dimer shows that each subunit (E and S chains) binds not only to two zinc atoms, but also the NAD/NADH ligand, with a higher NAD/NADH binding preference for the S chain relative to the E chain.	NAD	126-129	alcohol dehydrogenase 1A (class I), alpha polypeptide	Homo sapiens	27-31
24912433-7	2014	Native top-down ISD of the hADH dimer shows that each subunit (E and S chains) binds not only to two zinc atoms, but also the NAD/NADH ligand, with a higher NAD/NADH binding preference for the S chain relative to the E chain.	NAD	130-134	alcohol dehydrogenase 1A (class I), alpha polypeptide	Homo sapiens	27-31
24912433-7	2014	Native top-down ISD of the hADH dimer shows that each subunit (E and S chains) binds not only to two zinc atoms, but also the NAD/NADH ligand, with a higher NAD/NADH binding preference for the S chain relative to the E chain.	NAD	130-133	alcohol dehydrogenase 1A (class I), alpha polypeptide	Homo sapiens	27-31
24912433-7	2014	Native top-down ISD of the hADH dimer shows that each subunit (E and S chains) binds not only to two zinc atoms, but also the NAD/NADH ligand, with a higher NAD/NADH binding preference for the S chain relative to the E chain.	NAD	161-165	alcohol dehydrogenase 1A (class I), alpha polypeptide	Homo sapiens	27-31
35429545-2	2022	CD38 is a major mammalian nicotinamide adenine dinucleotide (NAD)+ glycohydrolase expressed on T cells, and appears to be an important modulator of T cell response in tumor models.	NAD	61-64	CD38 molecule	Homo sapiens	0-4
35452563-1	2022	Emerging evidence suggests an important role for SIRT1, a nicotinamide adenine dinucleotide (NAD)-dependent deacetylase in cancer development, progression and therapeutic resistance; making it a viable therapeutic target.	NAD	58-91	sirtuin 1	Mus musculus	49-54
24496572-6	2014	Calorie restriction increases the intracellular levels of the essential pyridine nucleotide, nicotinamide adenine dinucleotide (NAD(+)), a co-substrate for the sirtuin 1 (Sirt1, silent mating-type information regulator 2 homolog 1) activity and a cofactor for oxidative phosphorylation and ATP synthesis.	NAD	93-126	sirtuin 1	Mus musculus	160-169
24496572-6	2014	Calorie restriction increases the intracellular levels of the essential pyridine nucleotide, nicotinamide adenine dinucleotide (NAD(+)), a co-substrate for the sirtuin 1 (Sirt1, silent mating-type information regulator 2 homolog 1) activity and a cofactor for oxidative phosphorylation and ATP synthesis.	NAD	93-126	sirtuin 1	Mus musculus	171-176
24496572-6	2014	Calorie restriction increases the intracellular levels of the essential pyridine nucleotide, nicotinamide adenine dinucleotide (NAD(+)), a co-substrate for the sirtuin 1 (Sirt1, silent mating-type information regulator 2 homolog 1) activity and a cofactor for oxidative phosphorylation and ATP synthesis.	NAD	128-134	sirtuin 1	Mus musculus	160-169
24496572-6	2014	Calorie restriction increases the intracellular levels of the essential pyridine nucleotide, nicotinamide adenine dinucleotide (NAD(+)), a co-substrate for the sirtuin 1 (Sirt1, silent mating-type information regulator 2 homolog 1) activity and a cofactor for oxidative phosphorylation and ATP synthesis.	NAD	128-134	sirtuin 1	Mus musculus	171-176
35452563-1	2022	Emerging evidence suggests an important role for SIRT1, a nicotinamide adenine dinucleotide (NAD)-dependent deacetylase in cancer development, progression and therapeutic resistance; making it a viable therapeutic target.	NAD	93-96	sirtuin 1	Mus musculus	49-54
24496572-7	2014	Promotion of intracellular NAD(+) anabolism is speculated to induce neuroprotective effects against amyloid-beta-peptide (Abeta) toxicity in some models for Alzheimer"s disease (AD).	NAD	27-33	amyloid beta (A4) precursor protein	Mus musculus	122-127
35418200-3	2022	We report high-resolution three-dimensional ALDH1A3 structures for the apo-enzyme, the NAD+ complex and a binary complex with ATP.	NAD	87-91	aldehyde dehydrogenase 1 family member A3	Homo sapiens	44-51
24496572-8	2014	The NAD(+)-dependent histone deacetylase, Sirt1, has been implicated in the ageing process.	NAD	4-8	sirtuin 1	Mus musculus	42-47
25451262-5	2014	Finally, beta-lap activated Sirt1 by increasing the intracellular NAD(+)/NADH ratio, which was accompanied by increased mtDNA content.	NAD	66-72	LAP	Homo sapiens	14-17
25451262-5	2014	Finally, beta-lap activated Sirt1 by increasing the intracellular NAD(+)/NADH ratio, which was accompanied by increased mtDNA content.	NAD	73-77	LAP	Homo sapiens	14-17
25248746-1	2014	S-Adenosylhomocysteine hydrolase (SAHH) is an NAD(+)-dependent tetrameric enzyme that catalyzes the breakdown of S-adenosylhomocysteine to adenosine and homocysteine and is important in cell growth and the regulation of gene expression.	NAD	46-52	adenosylhomocysteinase	Homo sapiens	0-32
25248746-1	2014	S-Adenosylhomocysteine hydrolase (SAHH) is an NAD(+)-dependent tetrameric enzyme that catalyzes the breakdown of S-adenosylhomocysteine to adenosine and homocysteine and is important in cell growth and the regulation of gene expression.	NAD	46-52	adenosylhomocysteinase	Homo sapiens	34-38
25248746-5	2014	X-ray crystal structures of 408-acetylated SAHH and dually acetylated SAHH have been determined and reveal perturbations in the C-terminal hydrogen bonding patterns, a region of the protein important for NAD(+) binding.	NAD	204-210	adenosylhomocysteinase	Homo sapiens	43-47
25248746-5	2014	X-ray crystal structures of 408-acetylated SAHH and dually acetylated SAHH have been determined and reveal perturbations in the C-terminal hydrogen bonding patterns, a region of the protein important for NAD(+) binding.	NAD	204-210	adenosylhomocysteinase	Homo sapiens	70-74
25440059-0	2014	A high-fat diet and NAD(+) activate Sirt1 to rescue premature aging in cockayne syndrome.	NAD	20-26	sirtuin 1	Mus musculus	36-41
25064694-4	2014	Here, we have found that a 24h-long exposure to slightly decreased ambient fractional concentration of oxygen (20% oxygen), which is an equivalent to oxygen tension at 350m above sea level, significantly increased levels of SUR2A in the heart despite that this drop of oxygen did not affect levels of O2, CO2 and hematocrit in the blood or myocardial levels of ATP, lactate and NAD/NADH/NAD(+).	NAD	387-393	ATP-binding cassette, sub-family C (CFTR/MRP), member 9	Mus musculus	224-229
24814981-5	2014	In response to NAD depletion caused by inhibition of NAD synthesis from nicotinamide, alpha-tubulin was hyperacetylated.	NAD	15-18	tubulin alpha 1b	Homo sapiens	86-99
24814981-5	2014	In response to NAD depletion caused by inhibition of NAD synthesis from nicotinamide, alpha-tubulin was hyperacetylated.	NAD	53-56	tubulin alpha 1b	Homo sapiens	86-99
24814981-7	2014	Likewise, decreasing the rate of endogenous NAD consumption using an inhibitor of poly-ADP-ribosylation also stabilized the acetylation of alpha-tubulin.	NAD	44-47	tubulin alpha 1b	Homo sapiens	139-152
24814981-8	2014	Conversely, the level of acetylated alpha-tubulin decreased when NAD synthesis was enhanced by overexpression of an NAD biosynthetic enzyme.	NAD	65-68	tubulin alpha 1b	Homo sapiens	36-49
24814981-8	2014	Conversely, the level of acetylated alpha-tubulin decreased when NAD synthesis was enhanced by overexpression of an NAD biosynthetic enzyme.	NAD	116-119	tubulin alpha 1b	Homo sapiens	36-49
24814981-10	2014	Furthermore, we provide evidence confirming that the NAD-dependent regulation of tubulin acetylation is mediated by SIRT2.	NAD	53-56	sirtuin 2	Homo sapiens	116-121
25340584-5	2014	We could show for NAD-dependent lactate dehydrogenase B (LDHB) and NAD-dependent malate dehydrogenase 1 (MDH1) that translational readthrough results in C-terminally extended protein variants containing a peroxisomal targeting signal 1 (PTS1).	NAD	18-21	lactate dehydrogenase B	Homo sapiens	32-55
25340584-5	2014	We could show for NAD-dependent lactate dehydrogenase B (LDHB) and NAD-dependent malate dehydrogenase 1 (MDH1) that translational readthrough results in C-terminally extended protein variants containing a peroxisomal targeting signal 1 (PTS1).	NAD	18-21	lactate dehydrogenase B	Homo sapiens	57-61
25108014-1	2014	Cardiac overexpression of locally acting muscle-restricted (m)IGF-1 and the consequent downstream activation of NAD(+)-dependent protein deacetylase sirtuin 1 (SIRT1) trigger potent cardiac antioxidative and antihypertrophic effects.	NAD	112-118	sirtuin 1	Mus musculus	149-158
25108014-1	2014	Cardiac overexpression of locally acting muscle-restricted (m)IGF-1 and the consequent downstream activation of NAD(+)-dependent protein deacetylase sirtuin 1 (SIRT1) trigger potent cardiac antioxidative and antihypertrophic effects.	NAD	112-118	sirtuin 1	Mus musculus	160-165
25092517-7	2014	Specific ER antagonists MPP and PHTPP potentiated the NP-induced loss of mitochondrial membrane potential and increase in lactate dehydrogenase (LDH) release whereas, ER agonists PPT and DPN inhibited these effects.	NAD	187-190	estrogen receptor 1 (alpha)	Mus musculus	9-11
25092517-7	2014	Specific ER antagonists MPP and PHTPP potentiated the NP-induced loss of mitochondrial membrane potential and increase in lactate dehydrogenase (LDH) release whereas, ER agonists PPT and DPN inhibited these effects.	NAD	187-190	estrogen receptor 1 (alpha)	Mus musculus	167-169
25268725-0	2014	Design, synthesis and SAR studies of NAD analogues as potent inhibitors towards CD38 NADase.	NAD	37-40	CD38 molecule	Homo sapiens	80-84
25268725-1	2014	Nicotinamide adenine dinucleotide (NAD), one of the most important coenzymes in the cells, is a substrate of the signaling enzyme CD38, by which NAD is converted to a second messenger, cyclic ADP-ribose, which releases calcium from intracellular calcium stores.	NAD	0-33	CD38 molecule	Homo sapiens	130-134
25268725-1	2014	Nicotinamide adenine dinucleotide (NAD), one of the most important coenzymes in the cells, is a substrate of the signaling enzyme CD38, by which NAD is converted to a second messenger, cyclic ADP-ribose, which releases calcium from intracellular calcium stores.	NAD	35-38	CD38 molecule	Homo sapiens	130-134
25268725-1	2014	Nicotinamide adenine dinucleotide (NAD), one of the most important coenzymes in the cells, is a substrate of the signaling enzyme CD38, by which NAD is converted to a second messenger, cyclic ADP-ribose, which releases calcium from intracellular calcium stores.	NAD	145-148	CD38 molecule	Homo sapiens	130-134
25401025-3	2014	Co-localized TPEF and THG imaging on tryptophan and NADH in cells indicates that the change of scattering property is largely originating from the morphological change of metabolic proteins induced by acetic acids.	NAD	52-56	transmembrane protein with EGF like and two follistatin like domains 2	Homo sapiens	13-17
25401025-4	2014	Further TPEF imaging on NADH and FAD in cells confirms that this change is irreversible when acetic acid concentration is higher than 1.2%.	NAD	24-28	transmembrane protein with EGF like and two follistatin like domains 2	Homo sapiens	8-12
24786309-2	2014	NAD(+) also plays an important role in the regulation of NAD(+)-consuming enzymes, including sirtuins, poly-ADP-ribose polymerases (PARPs), and CD38/157 ectoenzymes.	NAD	0-6	CD38 molecule	Homo sapiens	144-148
24786309-2	2014	NAD(+) also plays an important role in the regulation of NAD(+)-consuming enzymes, including sirtuins, poly-ADP-ribose polymerases (PARPs), and CD38/157 ectoenzymes.	NAD	57-63	CD38 molecule	Homo sapiens	144-148
24842055-1	2014	Poly(ADP-ribose) polymerase-1 (PARP-1) activation is a hallmark of oxidative stress-induced cellular injury that can lead to energetic failure and necrotic cell death via depleting the cellular nicotinamide adenine dinucleotide (NAD(+)) and ATP pools.	NAD	194-227	poly (ADP-ribose) polymerase 1	Rattus norvegicus	0-29
24842055-1	2014	Poly(ADP-ribose) polymerase-1 (PARP-1) activation is a hallmark of oxidative stress-induced cellular injury that can lead to energetic failure and necrotic cell death via depleting the cellular nicotinamide adenine dinucleotide (NAD(+)) and ATP pools.	NAD	194-227	poly (ADP-ribose) polymerase 1	Rattus norvegicus	31-37
24842055-1	2014	Poly(ADP-ribose) polymerase-1 (PARP-1) activation is a hallmark of oxidative stress-induced cellular injury that can lead to energetic failure and necrotic cell death via depleting the cellular nicotinamide adenine dinucleotide (NAD(+)) and ATP pools.	NAD	229-235	poly (ADP-ribose) polymerase 1	Rattus norvegicus	0-29
24842055-1	2014	Poly(ADP-ribose) polymerase-1 (PARP-1) activation is a hallmark of oxidative stress-induced cellular injury that can lead to energetic failure and necrotic cell death via depleting the cellular nicotinamide adenine dinucleotide (NAD(+)) and ATP pools.	NAD	229-235	poly (ADP-ribose) polymerase 1	Rattus norvegicus	31-37
25054226-6	2014	A key factor for the production of 2-butanol was the availability of NADH, which was achieved by growing cells lacking the GPD1 and GPD2 isogenes under anaerobic conditions.	NAD	69-73	glycerol-3-phosphate dehydrogenase (NAD(+)) GPD2	Saccharomyces cerevisiae S288C	132-136
25009184-4	2014	Further mechanistic studies show that p53 directly activates expression of the NAD(+)-dependent histone deacetylase sirtuin 6 (SIRT6), whose interaction with FoxO1 leads to FoxO1 deacetylation and export to the cytoplasm.	NAD	79-85	transformation related protein 53, pseudogene	Mus musculus	38-41
25009184-4	2014	Further mechanistic studies show that p53 directly activates expression of the NAD(+)-dependent histone deacetylase sirtuin 6 (SIRT6), whose interaction with FoxO1 leads to FoxO1 deacetylation and export to the cytoplasm.	NAD	79-85	forkhead box O1	Mus musculus	158-163
25009184-4	2014	Further mechanistic studies show that p53 directly activates expression of the NAD(+)-dependent histone deacetylase sirtuin 6 (SIRT6), whose interaction with FoxO1 leads to FoxO1 deacetylation and export to the cytoplasm.	NAD	79-85	forkhead box O1	Mus musculus	173-178
25013930-2	2014	Here, we report a role for the NAD+-dependent histone deacetylase SIRT1 in the control of anti-bacterial defense.	NAD	31-35	sirtuin 1	Mus musculus	66-71
24952428-1	2014	The silent mating type information regulation 2 homolog 1 gene (Sirt1) encodes an NAD-dependent deacetylase that modifies the activity of well-known transcriptional regulators affected in kidney diseases.	NAD	82-85	sirtuin 1	Mus musculus	64-69
24721563-1	2014	Bovine CD38/NAD(+) glycohydrolase catalyzes the hydrolysis of NAD(+) to nicotinamide and ADP-ribose and the formation of cyclic ADP-ribose via a stepwise reaction mechanism.	NAD	12-18	CD38 molecule	Bos taurus	7-11
24510807-1	2014	Sirtuin 6 (SIRT6) is a NAD-dependent deacetylase involved in lifespan regulation.	NAD	23-26	sirtuin 6	Rattus norvegicus	0-9
24510807-1	2014	Sirtuin 6 (SIRT6) is a NAD-dependent deacetylase involved in lifespan regulation.	NAD	23-26	sirtuin 6	Rattus norvegicus	11-16
24922076-7	2014	Moreover, we show that the induction of cellular NAD(+) levels using beta-lapachone (beta-Lap), whose intracellular target is NQO1, prevents the toxic effects of cisplatin through the regulation of PARP-1 and SIRT1 activity.	NAD	49-55	LAP	Homo sapiens	90-93
35418200-7	2022	At physiological concentrations, ATP inhibits the dehydrogenase activity of ALDH1A3 and other isoforms, with a Ki value of 0.48 mM for ALDH1A3, showing a mixed inhibition type against NAD+.	NAD	184-188	aldehyde dehydrogenase 1 family member A3	Homo sapiens	76-83
35453391-0	2022	Sirtuin 3 Dependent and Independent Effects of NAD+ to Suppress Vascular Inflammation and Improve Endothelial Function in Mice.	NAD	47-51	sirtuin 3	Mus musculus	0-9
35453391-2	2022	Sirtuin 3 (SIRT3) is a nicotinamide adenine dinucleotide (NAD+)-dependent mitochondrial deacetylase, which plays a key role in maintaining normal mitochondrial function.	NAD	23-56	sirtuin 3	Mus musculus	0-9
35453391-2	2022	Sirtuin 3 (SIRT3) is a nicotinamide adenine dinucleotide (NAD+)-dependent mitochondrial deacetylase, which plays a key role in maintaining normal mitochondrial function.	NAD	23-56	sirtuin 3	Mus musculus	11-16
35453391-2	2022	Sirtuin 3 (SIRT3) is a nicotinamide adenine dinucleotide (NAD+)-dependent mitochondrial deacetylase, which plays a key role in maintaining normal mitochondrial function.	NAD	58-62	sirtuin 3	Mus musculus	0-9
35453391-2	2022	Sirtuin 3 (SIRT3) is a nicotinamide adenine dinucleotide (NAD+)-dependent mitochondrial deacetylase, which plays a key role in maintaining normal mitochondrial function.	NAD	58-62	sirtuin 3	Mus musculus	11-16
35453391-6	2022	In human umbilical vein endothelial cells, SIRT3 silencing potentiated the induction of inflammatory factors by IL-1beta, including VCAM-1, ICAM-1, and MCP1, and the impairment of mitochondrial respiration, both of which were alleviated by NAD+ treatment.	NAD	240-244	interleukin 1 alpha	Homo sapiens	112-120
35453391-8	2022	Our results support the SIRT3-dependent and -independent of NAD+ to improve endothelial function in atherosclerosis.	NAD	60-64	sirtuin 3	Mus musculus	24-29
35139656-2	2022	Nicotinamide adenine dinucleotide (NAD+) acts as a signaling molecule, and its levels were used to govern several biological pathways, for example, promoting angiogenesis by SIRT1 (sirtuin 1)-mediated inhibition of Notch signaling to rejuvenate capillary density of old-aged mice.	NAD	0-33	sirtuin 1	Mus musculus	174-179
35139656-2	2022	Nicotinamide adenine dinucleotide (NAD+) acts as a signaling molecule, and its levels were used to govern several biological pathways, for example, promoting angiogenesis by SIRT1 (sirtuin 1)-mediated inhibition of Notch signaling to rejuvenate capillary density of old-aged mice.	NAD	0-33	sirtuin 1	Mus musculus	181-190
35139656-2	2022	Nicotinamide adenine dinucleotide (NAD+) acts as a signaling molecule, and its levels were used to govern several biological pathways, for example, promoting angiogenesis by SIRT1 (sirtuin 1)-mediated inhibition of Notch signaling to rejuvenate capillary density of old-aged mice.	NAD	35-39	sirtuin 1	Mus musculus	174-179
35139656-2	2022	Nicotinamide adenine dinucleotide (NAD+) acts as a signaling molecule, and its levels were used to govern several biological pathways, for example, promoting angiogenesis by SIRT1 (sirtuin 1)-mediated inhibition of Notch signaling to rejuvenate capillary density of old-aged mice.	NAD	35-39	sirtuin 1	Mus musculus	181-190
35406095-6	2022	SIRT3 is a key metabolism-regulating NAD+-dependent protein deacetylase.	NAD	37-40	sirtuin 3	Mus musculus	0-5
25046046-6	2014	The described method was used to measure endogenous NAD(+) levels in mouse blood following oral administration of the nicotinamide phosphoribosyltransferase inhibitor GNE-617.	NAD	52-58	glucosamine (UDP-N-acetyl)-2-epimerase/N-acetylmannosamine kinase	Mus musculus	167-170
24748324-9	2014	Expression analysis in T cell subsets of the lung revealed ATP (Cd39, Cd73) and NAD (Cd38, Cd157, Cd296, Pc-1) degrading enzymes.	NAD	80-83	CD38 molecule	Homo sapiens	85-89
24748324-9	2014	Expression analysis in T cell subsets of the lung revealed ATP (Cd39, Cd73) and NAD (Cd38, Cd157, Cd296, Pc-1) degrading enzymes.	NAD	80-83	polycystin 1, transient receptor potential channel interacting	Homo sapiens	105-109
24660829-3	2014	One NAD-metabolizing enzyme in mammals is CD38, a type II transmembrane protein that converts NAD primarily to adenosine diphosphate ribose (ADPR) and a small amount of cyclic adenosine diphosphate ribose (cADPR).	NAD	4-7	CD38 molecule	Homo sapiens	42-46
24660829-3	2014	One NAD-metabolizing enzyme in mammals is CD38, a type II transmembrane protein that converts NAD primarily to adenosine diphosphate ribose (ADPR) and a small amount of cyclic adenosine diphosphate ribose (cADPR).	NAD	94-97	CD38 molecule	Homo sapiens	42-46
24660829-5	2014	With the efficient NAD-hydrolysis activity, the intracellular CD38 may lead to depletion of cellular NAD, thus producing harmful effects.	NAD	19-22	CD38 molecule	Homo sapiens	62-66
24660829-5	2014	With the efficient NAD-hydrolysis activity, the intracellular CD38 may lead to depletion of cellular NAD, thus producing harmful effects.	NAD	101-104	CD38 molecule	Homo sapiens	62-66
24660829-10	2014	The finding that very little intracellular CD38 exists in these cell lines suggests that the major enzymatic function of CD38 is to hydrolyze extracellular rather than intracellular NAD.	NAD	182-185	CD38 molecule	Homo sapiens	121-125
24936455-1	2014	The NAD-dependent deacetylase SIRT1 is involved in chromatin silencing and genome stability.	NAD	4-7	sirtuin 1	Mus musculus	30-35
35318613-5	2022	In this report, we identify a crucial role for the NAD+-dependent histone deacetylase Sirtuin 1 (Sirt1) downstream of PKA and CREB in dmPGE2-dependent radioprotection of hematopoietic cells.	NAD	51-55	sirtuin 1	Mus musculus	86-95
24480449-2	2014	Sirtuin 1 (Sirt1) is a NAD-dependent deacetylase which is involved in myogenesis.	NAD	23-26	sirtuin 1	Mus musculus	0-9
24480449-2	2014	Sirtuin 1 (Sirt1) is a NAD-dependent deacetylase which is involved in myogenesis.	NAD	23-26	sirtuin 1	Mus musculus	11-16
24337988-2	2014	NAD(+) has emerged as a major signalling molecule that serves as the sole substrate for several enzymatic reactions including the DNA repair enzyme, poly(ADP-ribose) polymerase (PARP), NAD-dependent protein deacetylases or CD38, and transcriptional factors by a new class of histone deacetylases known as sirtuins.	NAD	0-6	poly (ADP-ribose) polymerase 1	Rattus norvegicus	149-176
24337988-2	2014	NAD(+) has emerged as a major signalling molecule that serves as the sole substrate for several enzymatic reactions including the DNA repair enzyme, poly(ADP-ribose) polymerase (PARP), NAD-dependent protein deacetylases or CD38, and transcriptional factors by a new class of histone deacetylases known as sirtuins.	NAD	0-6	poly (ADP-ribose) polymerase 1	Rattus norvegicus	178-182
35318613-5	2022	In this report, we identify a crucial role for the NAD+-dependent histone deacetylase Sirtuin 1 (Sirt1) downstream of PKA and CREB in dmPGE2-dependent radioprotection of hematopoietic cells.	NAD	51-55	sirtuin 1	Mus musculus	97-102
35354042-0	2022	PTIP governs NAD+ metabolism by regulating CD38 expression to drive macrophage inflammation.	NAD	13-17	PAX interacting protein 1	Homo sapiens	0-4
35354042-3	2022	Here, we find that PTIP governs NAD+ metabolism in macrophages by regulating CD38 expression and is required for macrophage inflammation.	NAD	32-36	PAX interacting protein 1	Homo sapiens	19-23
35354042-4	2022	Through integrating histone modifications with NAD+ metabolic gene expression profiling, we identify PTIP as a key factor in regulating CD38 expression, the primary NAD+-consuming enzyme in macrophages.	NAD	47-51	PAX interacting protein 1	Homo sapiens	101-105
35354042-4	2022	Through integrating histone modifications with NAD+ metabolic gene expression profiling, we identify PTIP as a key factor in regulating CD38 expression, the primary NAD+-consuming enzyme in macrophages.	NAD	165-169	PAX interacting protein 1	Homo sapiens	101-105
24723845-5	2014	In the experimental scenario, the effects observed long after perinatal asphyxia have been explained by overexpression of sentinel proteins, such as poly(ADP-ribose) polymerase-1 (PARP-1), competing for NAD(+) during re-oxygenation, leading to the idea that sentinel protein inhibition constitutes a suitable therapeutic strategy.	NAD	203-209	poly (ADP-ribose) polymerase 1	Rattus norvegicus	149-178
24723845-5	2014	In the experimental scenario, the effects observed long after perinatal asphyxia have been explained by overexpression of sentinel proteins, such as poly(ADP-ribose) polymerase-1 (PARP-1), competing for NAD(+) during re-oxygenation, leading to the idea that sentinel protein inhibition constitutes a suitable therapeutic strategy.	NAD	203-209	poly (ADP-ribose) polymerase 1	Rattus norvegicus	180-186
35354042-8	2022	Overall, our findings reveal a critical role for PTIP in fine-tuning the inflammatory responses of macrophages via regulating NAD+ metabolism.	NAD	126-130	PAX interacting protein 1	Homo sapiens	49-53
35392281-3	2022	MI was detected indirectly by the reaction product of myoinositol dehydrogenase (IDH) and cofactor beta-nicotinamide adenine dinucleotide (NAD+).	NAD	139-143	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	81-84
24595244-7	2014	For SCC25, NADH alpha1 is reduced with BGT226 and cisplatin treatment.	NAD	11-15	adrenoceptor alpha 1D	Homo sapiens	16-22
24595244-8	2014	For SCC61, NADH alpha1 is reduced with cetuximab, BGT226, and cisplatin treatment.	NAD	11-15	adrenoceptor alpha 1D	Homo sapiens	16-22
24595244-9	2014	Trends in NADH alpha1 are statistically similar to changes in standard measurements of glycolytic rates after treatment.	NAD	10-14	adrenoceptor alpha 1D	Homo sapiens	15-21
24463048-1	2014	The cofactor-binding site of the NAD(+)-dependent Arabidopsis thaliana aldehyde dehydrogenase ALDH3H1 was analyzed to understand structural features determining cofactor-specificity.	NAD	33-39	aldehyde dehydrogenase 3H1	Arabidopsis thaliana	94-101
35007154-10	2022	The adh mutations were partially suppressed by a deletion of rex, encoding an NAD+/NADH-sensing transcription factor that represses genes functioning in fermentation.	NAD	78-81	alcohol dehydrogenase 1A (class I), alpha polypeptide	Homo sapiens	4-7
25016869-3	2014	The expression of NAD -dependent deacetylase Sirtuin type 3 (SIRT3), which regulates mitochondrial energy production and oxidative stress, and heat shock protein 60 (HSP60), a major biomarker of mitochondrial stress, and the tyrosine hydroxylasic projection from locus coeruleus were analyzed after a 5-day sleep deprivation.	NAD	18-21	sirtuin 3	Mus musculus	45-59
25016869-3	2014	The expression of NAD -dependent deacetylase Sirtuin type 3 (SIRT3), which regulates mitochondrial energy production and oxidative stress, and heat shock protein 60 (HSP60), a major biomarker of mitochondrial stress, and the tyrosine hydroxylasic projection from locus coeruleus were analyzed after a 5-day sleep deprivation.	NAD	18-21	sirtuin 3	Mus musculus	61-66
35264567-4	2022	When we supplement beta-nicotinamide mononucleotide (beta-NMN), an NAD+ precursor, nuclear entry of SIRT2 in OPCs, OPC differentiation, and remyelination were rescued in aged animals.	NAD	67-71	sirtuin 2	Mus musculus	100-105
24295520-0	2014	Overexpression of CD38 decreases cellular NAD levels and alters the expression of proteins involved in energy metabolism and antioxidant defense.	NAD	42-45	CD38 molecule	Homo sapiens	18-22
24295520-2	2014	In the present study, a 35% decrease of cellular NAD level is achieved by stable expression of the N-terminal truncated CD38, a NAD hydrolase.	NAD	49-52	CD38 molecule	Homo sapiens	120-124
35264567-5	2022	We show that the effects on myelination are mediated via the NAD+-SIRT2-H3K18Ac-ID4 axis, and SIRT2 is required for rejuvenating OPCs.	NAD	61-65	sirtuin 2	Mus musculus	66-71
24295520-6	2014	However, down-regulation of mRNA expressions of genes associated with glycolysis, antioxidant, and DNA repair is less significant than the corresponding change in protein expression, suggesting the low NAD level impairs the protein translational machinery in CD38(+) cells.	NAD	202-205	CD38 molecule	Homo sapiens	259-263
24295520-8	2014	Taken together, these results demonstrate that CD38(+) cells are a useful model to study effects of the cellular NAD levels on cellular processes and establish a new linker between cellular NAD levels and oxidative stress.	NAD	113-116	CD38 molecule	Homo sapiens	47-51
35235362-5	2022	By using a series of adipose tissue and brain region-specific loss- and gain-of-function approaches, we implicate impaired nicotinamide adenine dinucleotide (NAD+)/SIRT1 pathway in the nucleus accumbens.	NAD	123-156	sirtuin 1	Mus musculus	164-169
24295520-8	2014	Taken together, these results demonstrate that CD38(+) cells are a useful model to study effects of the cellular NAD levels on cellular processes and establish a new linker between cellular NAD levels and oxidative stress.	NAD	190-193	CD38 molecule	Homo sapiens	47-51
35241643-0	2022	miR-146a impedes the anti-aging effect of AMPK via NAMPT suppression and NAD+/SIRT inactivation.	NAD	73-77	microRNA 146a	Homo sapiens	0-8
35241643-6	2022	Additionally, miR-146a overexpression weakened the metformin-mediated upregulation of NAMPT expression, NAD+ synthesis, SIRT activity, and senescence protection, whereas treatment with the miR-146a inhibitor reversed this effect.	NAD	104-108	microRNA 146a	Homo sapiens	14-22
24186862-4	2014	Furthermore, we observed that flux via AR impaired NAD(+) homeostasis and reduced activity of NAD(+)-dependent deacetylase Sirt-1 leading to acetylation and prolonged expression of Egr-1 in hyperglycemic conditions.	NAD	51-57	aldo-keto reductase family 1, member B3 (aldose reductase)	Mus musculus	39-41
24186862-4	2014	Furthermore, we observed that flux via AR impaired NAD(+) homeostasis and reduced activity of NAD(+)-dependent deacetylase Sirt-1 leading to acetylation and prolonged expression of Egr-1 in hyperglycemic conditions.	NAD	51-57	early growth response 1	Mus musculus	181-186
35241643-10	2022	These findings identified a novel cascade that negatively regulates the NAD+/SIRT pathway by suppressing miR-146a-mediated NAMPT downregulation.	NAD	72-76	microRNA 146a	Homo sapiens	105-113
35241643-12	2022	This mutual inhibitory relationship between miR-146a and AMPK enriches our understanding of the molecular connections between AMPK and SIRT and provides new insight into miRNA-mediated NAD+/SIRT regulation and an intervention point for the prevention of aging and age-related diseases.	NAD	185-189	microRNA 146a	Homo sapiens	44-52
35245456-1	2022	IDO1 oxidizes tryptophan (TRP) to generate kynurenine (KYN), the substrate for 1-carbon and NAD metabolism, and is implicated in pro-cancer pathophysiology and infection biology.	NAD	92-95	indoleamine 2,3-dioxygenase 1	Homo sapiens	0-4
24186862-4	2014	Furthermore, we observed that flux via AR impaired NAD(+) homeostasis and reduced activity of NAD(+)-dependent deacetylase Sirt-1 leading to acetylation and prolonged expression of Egr-1 in hyperglycemic conditions.	NAD	94-100	aldo-keto reductase family 1, member B3 (aldose reductase)	Mus musculus	39-41
24186862-4	2014	Furthermore, we observed that flux via AR impaired NAD(+) homeostasis and reduced activity of NAD(+)-dependent deacetylase Sirt-1 leading to acetylation and prolonged expression of Egr-1 in hyperglycemic conditions.	NAD	94-100	sirtuin 1	Mus musculus	123-129
24186862-4	2014	Furthermore, we observed that flux via AR impaired NAD(+) homeostasis and reduced activity of NAD(+)-dependent deacetylase Sirt-1 leading to acetylation and prolonged expression of Egr-1 in hyperglycemic conditions.	NAD	94-100	early growth response 1	Mus musculus	181-186
35120922-1	2022	The secreted form of the enzyme nicotinamide phosphoribosyltransferase (eNAMPT), which catalyzes a key reaction in intracellular NAD biosynthesis, acts as a damage-associated molecular pattern (DAMP) triggering Toll-like receptor-4 (TLR4)-mediated inflammatory responses.	NAD	129-132	toll like receptor 4	Homo sapiens	211-231
24410488-9	2014	propose a model linking decreased NAD+ to loss of nuclear SIRT1 activity to stabilization of the hypoxia-associated transcription factor hypoxia-inducible factor 1-alpha (HIF-1a).	NAD	34-38	sirtuin 1	Mus musculus	58-63
24410488-9	2014	propose a model linking decreased NAD+ to loss of nuclear SIRT1 activity to stabilization of the hypoxia-associated transcription factor hypoxia-inducible factor 1-alpha (HIF-1a).	NAD	34-38	hypoxia inducible factor 1, alpha subunit	Mus musculus	137-169
24410488-9	2014	propose a model linking decreased NAD+ to loss of nuclear SIRT1 activity to stabilization of the hypoxia-associated transcription factor hypoxia-inducible factor 1-alpha (HIF-1a).	NAD	34-38	hypoxia inducible factor 1, alpha subunit	Mus musculus	171-177
35120922-1	2022	The secreted form of the enzyme nicotinamide phosphoribosyltransferase (eNAMPT), which catalyzes a key reaction in intracellular NAD biosynthesis, acts as a damage-associated molecular pattern (DAMP) triggering Toll-like receptor-4 (TLR4)-mediated inflammatory responses.	NAD	129-132	toll like receptor 4	Homo sapiens	233-237
35301252-7	2022	Ferulic acid also enhances the activation of AMP-activated kinase (AMPK) by increasing expression and activity of its activating kinase LKB1-whereas AMPK in turn amplifies Sirt1 activity by promoting induction of nicotinamide phosphoribosyltranferase, rate-limiting for generation of Sirt1"s obligate substrate NAD+.	NAD	311-315	serine/threonine kinase 11	Homo sapiens	136-140
35441145-1	2022	Sirtuin2 (Sirt2) with its NAD+-dependent deacetylase and defatty-acylase activities plays a central role in the regulation of specific cellular functions.	NAD	26-29	sirtuin 2	Homo sapiens	0-8
35441145-1	2022	Sirtuin2 (Sirt2) with its NAD+-dependent deacetylase and defatty-acylase activities plays a central role in the regulation of specific cellular functions.	NAD	26-29	sirtuin 2	Homo sapiens	10-15
35386537-6	2022	In addition, there are more factors proposed to involve in lymphopenia in COVID-19 infection such as the role of CD38, which functions as NADase and intensifies NAD depletion, which in turn affects NAD+-dependent Sirtuin proteins, as the regulators of cell death and viability.	NAD	161-164	CD38 molecule	Homo sapiens	113-117
35386537-6	2022	In addition, there are more factors proposed to involve in lymphopenia in COVID-19 infection such as the role of CD38, which functions as NADase and intensifies NAD depletion, which in turn affects NAD+-dependent Sirtuin proteins, as the regulators of cell death and viability.	NAD	198-201	CD38 molecule	Homo sapiens	113-117
35137036-7	2022	Expression of S. cerevisiae GPD2, which encodes NAD+-dependent glycerol-3-phosphate dehydrogenase, and GPP1 supported increased glycerol production by oxygen-limited chemostat cultures of O. parapolymorpha.	NAD	48-51	glycerol-3-phosphate dehydrogenase (NAD(+)) GPD2	Saccharomyces cerevisiae S288C	28-32
35203360-1	2022	Nicotinamide adenine dinucleotide (NAD) is a versatile chemical compound serving as a coenzyme in metabolic pathways and as a substrate to support the enzymatic functions of sirtuins (SIRTs), poly (ADP-ribose) polymerase-1 (PARP-1), and cyclic ADP ribose hydrolase (CD38).	NAD	0-33	CD38 molecule	Homo sapiens	266-270
35203360-1	2022	Nicotinamide adenine dinucleotide (NAD) is a versatile chemical compound serving as a coenzyme in metabolic pathways and as a substrate to support the enzymatic functions of sirtuins (SIRTs), poly (ADP-ribose) polymerase-1 (PARP-1), and cyclic ADP ribose hydrolase (CD38).	NAD	35-38	CD38 molecule	Homo sapiens	266-270
35001440-2	2022	At the molecular level, the circadian molecular clock and cellular metabolic state may be interconnected through interactions with the nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase, Sirtuin 1 (SIRT1).	NAD	135-168	sirtuin 1	Mus musculus	199-208
35001440-2	2022	At the molecular level, the circadian molecular clock and cellular metabolic state may be interconnected through interactions with the nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase, Sirtuin 1 (SIRT1).	NAD	135-168	sirtuin 1	Mus musculus	210-215
35001440-2	2022	At the molecular level, the circadian molecular clock and cellular metabolic state may be interconnected through interactions with the nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase, Sirtuin 1 (SIRT1).	NAD	170-174	sirtuin 1	Mus musculus	199-208
35001440-2	2022	At the molecular level, the circadian molecular clock and cellular metabolic state may be interconnected through interactions with the nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase, Sirtuin 1 (SIRT1).	NAD	170-174	sirtuin 1	Mus musculus	210-215
35001440-3	2022	In the nucleus accumbens (NAc), a region important for reward, both SIRT1 and the circadian transcription factor neuronal PAS domain protein 2 (NPAS2) are highly enriched, and both are regulated by the metabolic cofactor NAD+.	NAD	221-225	sirtuin 1	Mus musculus	68-73
35115380-0	2022	BMAL1 drives muscle repair through control of hypoxic NAD+ regeneration in satellite cells.	NAD	54-58	aryl hydrocarbon receptor nuclear translocator-like	Mus musculus	0-5
35115380-7	2022	Finally, hypoxic cell proliferation and myofiber formation in Bmal1-deficient myoblasts are restored by increasing cytosolic NAD+ Together, we identify the MuSC clock as a pivotal regulator of oxygen-dependent myoblast cell fate and muscle repair through the control of the NAD+-driven response to injury.	NAD	125-129	aryl hydrocarbon receptor nuclear translocator-like	Mus musculus	62-67
35115380-7	2022	Finally, hypoxic cell proliferation and myofiber formation in Bmal1-deficient myoblasts are restored by increasing cytosolic NAD+ Together, we identify the MuSC clock as a pivotal regulator of oxygen-dependent myoblast cell fate and muscle repair through the control of the NAD+-driven response to injury.	NAD	274-278	aryl hydrocarbon receptor nuclear translocator-like	Mus musculus	62-67
35013907-23	2022	TREM2 overexpression ameliorates LPS-induced oxidative stress and neuroinflammation through enhancing SIRT3 function via NAD+.	NAD	121-125	sirtuin 3	Mus musculus	102-107
35090502-13	2022	CONCLUSIONS: All these data suggest that NQO1 has a protective effect against oxidative stress and apoptosis in DN, which may be mediated by the regulation of Sirt1 through increasing intracellular NAD+/NADH levels.	NAD	198-202	sirtuin 1	Mus musculus	159-164
24383546-3	2014	Compounds that activate the NAD+-dependent SIRT1 deacetylase prevent neuronal loss in an autoimmune-mediated MS model, but the mechanism of this effect is unknown, and it is unclear whether SIRT1 activating compounds exert similar effects in demyelinating disease induced by other etiologies.	NAD	28-32	sirtuin 1	Mus musculus	43-48
24343700-1	2014	Silent information regulator type-1 (SIRT1) is the best-studied member of the Sirtuin (Sir2) family of nicotinamide dinucleotide (NAD)-dependent class III histone deacetylases (HDACs), but has not yet been explored in cutaneous T-cell lymphoma (CTCL).	NAD	103-128	sirtuin 2	Homo sapiens	87-91
24343700-1	2014	Silent information regulator type-1 (SIRT1) is the best-studied member of the Sirtuin (Sir2) family of nicotinamide dinucleotide (NAD)-dependent class III histone deacetylases (HDACs), but has not yet been explored in cutaneous T-cell lymphoma (CTCL).	NAD	130-133	sirtuin 2	Homo sapiens	87-91
24284820-5	2014	Estrogen receptor (ER) alpha- and ERbeta-selective agonists, propylpyrazole triol (PPT), and 2,3-bis(4-hydroxyphenyl) propionitrile (DPN), respectively, augmented GH mRNA expression and secretion, whereas E2 and PPT, but not DPN increased prolactin (PRL) mRNA levels.	NAD	225-228	estrogen receptor 1 (alpha)	Mus musculus	0-28
23982874-6	2014	A homology model of Homo sapiens ALDH1A1 was built using the crystal structure of NAD-bound sheep liver class I aldehyde dehydrogenase [PDB ID: 1BXS] as a template.	NAD	82-85	aldehyde dehydrogenase 1 family member A1	Homo sapiens	33-40
24360282-5	2013	Deleting SIRT1 accelerates this process, whereas raising NAD(+) levels in old mice restores mitochondrial function to that of a young mouse in a SIRT1-dependent manner.	NAD	57-63	sirtuin 1	Mus musculus	145-150
23834033-2	2013	As SIRT1 deacetylase activity is dependent on NAD(+) levels and the development of compounds that directly activate SIRT1 has been controversial, indirectly activating SIRT1 through enhancing NAD(+) bioavailability has received increasing attention.	NAD	46-52	sirtuin 1	Mus musculus	3-8
23834033-5	2013	Here, we further show that miR-34a reduces NAD(+) levels and SIRT1 activity by targeting NAMPT, the rate-limiting enzyme for NAD(+) biosynthesis.	NAD	125-131	sirtuin 1	Mus musculus	61-66
23990359-7	2013	PPARalpha also cooperates with Sirt1 activated by EPO through modulating the NAD+ level to regulate metabolic activity.	NAD	77-81	sirtuin 1	Mus musculus	31-36
23990359-7	2013	PPARalpha also cooperates with Sirt1 activated by EPO through modulating the NAD+ level to regulate metabolic activity.	NAD	77-81	erythropoietin	Mus musculus	50-53
23831226-1	2013	NADH-Cytochrome b5 reductase (b5R), a flavoprotein consisting of NADH and flavin adenine dinucleotide (FAD) binding domains, catalyzes electron transfer from the two-electron carrier NADH to the one-electron carrier cytochrome b5 (Cb5).	NAD	0-4	cytochrome b5 type A	Homo sapiens	5-18
23831226-1	2013	NADH-Cytochrome b5 reductase (b5R), a flavoprotein consisting of NADH and flavin adenine dinucleotide (FAD) binding domains, catalyzes electron transfer from the two-electron carrier NADH to the one-electron carrier cytochrome b5 (Cb5).	NAD	0-4	cytochrome b5 type A	Homo sapiens	216-229
23831226-1	2013	NADH-Cytochrome b5 reductase (b5R), a flavoprotein consisting of NADH and flavin adenine dinucleotide (FAD) binding domains, catalyzes electron transfer from the two-electron carrier NADH to the one-electron carrier cytochrome b5 (Cb5).	NAD	0-4	cytochrome b5 type A	Homo sapiens	231-234
23860243-7	2013	Analysis of recombinant peroxisomal NADH-dependent HPR1 activity from Arabidopsis in the presence of H2O2, NO, GSH and peroxynitrite showed that the ONOO(-) molecule caused the highest inhibition of activity (51% at 5mM SIN-1), with 5mM H2O2 having no inhibitory effect.	NAD	36-40	dicer-like 1	Arabidopsis thaliana	220-225
24051248-3	2013	Circadian control of the activity of the NAD(+)-dependent deacetylase sirtuin 3 (SIRT3) generated rhythms in the acetylation and activity of oxidative enzymes and respiration in isolated mitochondria, and NAD(+) supplementation restored protein deacetylation and enhanced oxygen consumption in circadian mutant mice.	NAD	41-47	sirtuin 3	Mus musculus	81-86
25309947-9	2013	Nuclear translocation of NAD-dependent histone deacetylase SIRT1 and global chromatin silencing lead to hESC cardiac fate determination, while silencing of pluripotence-associated hsa-miR-302 family and drastic up-regulation of neuroectodermal Hox miRNA hsa-miR-10 family lead to hESC neural fate determination.	NAD	25-28	microRNA 302a	Homo sapiens	180-191
24003916-4	2013	NLRP3 inflammasome inducers reduce the NAD(+) level to inactivate the alpha-tubulin deacetylase Sirtuin 2, resulting in accumulation of acetylated alpha-tubulin.	NAD	39-45	NLR family, pyrin domain containing 3	Mus musculus	0-5
24003916-4	2013	NLRP3 inflammasome inducers reduce the NAD(+) level to inactivate the alpha-tubulin deacetylase Sirtuin 2, resulting in accumulation of acetylated alpha-tubulin.	NAD	39-45	sirtuin 2	Mus musculus	96-105
24009628-1	2013	BACKGROUND: Silent mating type information regulation 2 homolog 1 (SIRT1), an NAD+-dependent deacetylase, might act as a tumor promoter by inhibiting p53, but may also as a tumor suppressor by inhibiting several oncogenes such as beta-catenin and survivin.	NAD	78-81	catenin beta 1	Homo sapiens	230-242
23723308-1	2013	BACKGROUND AND PURPOSE: Sirtuin 1 (SIRT1) is a member of NAD+-dependent protein deacetylases implicated in a wide range of cellular functions and has beneficial properties in pathologies including ischemia/reperfusion processes and neurodegeneration.	NAD	57-60	sirtuin 1	Mus musculus	24-33
23723308-1	2013	BACKGROUND AND PURPOSE: Sirtuin 1 (SIRT1) is a member of NAD+-dependent protein deacetylases implicated in a wide range of cellular functions and has beneficial properties in pathologies including ischemia/reperfusion processes and neurodegeneration.	NAD	57-60	sirtuin 1	Mus musculus	35-40
35090502-13	2022	CONCLUSIONS: All these data suggest that NQO1 has a protective effect against oxidative stress and apoptosis in DN, which may be mediated by the regulation of Sirt1 through increasing intracellular NAD+/NADH levels.	NAD	203-207	sirtuin 1	Mus musculus	159-164
35107007-4	2022	Herein, we propose a strategy of constructing a thylakoid membrane-inspired capsule (TMC) with fortified and tunable NAD+/NADH shuttling to boost the enzyme-photocoupled catalytic process.	NAD	117-121	STT3 oligosaccharyltransferase complex catalytic subunit A	Homo sapiens	85-88
23604553-1	2013	AIMS/HYPOTHESIS: The NAD(+)-dependent protein deacetylase sirtuin (SIRT)1 is thought to be a key regulator of skeletal muscle metabolism.	NAD	21-27	sirtuin 1	Mus musculus	67-73
23575529-2	2013	Adenosine diphosphate ribosyl transferase 2.2 (ART2.2) utilizes extracellular NAD(+) to transfer ADP-ribose to arginine residues of extracellular domains of surface proteins.	NAD	78-84	ADP-ribosyltransferase 2b	Mus musculus	0-45
23575529-2	2013	Adenosine diphosphate ribosyl transferase 2.2 (ART2.2) utilizes extracellular NAD(+) to transfer ADP-ribose to arginine residues of extracellular domains of surface proteins.	NAD	78-84	ADP-ribosyltransferase 2b	Mus musculus	47-53
23575529-3	2013	Here, we show that in the presence of extracellular NAD(+) , ART2.2 caused ADP-ribosylation of CD8-beta on murine CD8(+) T cells in vitro and in vivo.	NAD	52-58	ADP-ribosyltransferase 2b	Mus musculus	61-67
35107007-4	2022	Herein, we propose a strategy of constructing a thylakoid membrane-inspired capsule (TMC) with fortified and tunable NAD+/NADH shuttling to boost the enzyme-photocoupled catalytic process.	NAD	122-126	STT3 oligosaccharyltransferase complex catalytic subunit A	Homo sapiens	85-88
35107007-5	2022	The apparent shuttling number (ASN) of NAD+/NADH for TMC could reach 17.1, ~8 times as high as that of non-integrated EPCS.	NAD	39-43	STT3 oligosaccharyltransferase complex catalytic subunit A	Homo sapiens	53-56
35107007-5	2022	The apparent shuttling number (ASN) of NAD+/NADH for TMC could reach 17.1, ~8 times as high as that of non-integrated EPCS.	NAD	44-48	STT3 oligosaccharyltransferase complex catalytic subunit A	Homo sapiens	53-56
2508731-1	1989	We have isolated a partial 2.0 kb cDNA (pRATC) encoding the entire 489 amino acids of the NAD binding domain located at the C terminus of the rat poly(ADP-ribose) polymerase.	NAD	90-93	poly (ADP-ribose) polymerase 1	Rattus norvegicus	146-173
23228600-5	2013	We also review the recently published finding that cyt-b(5) allosterically augments the activity of 3beta-hydroxysteroid dehydrogenase/Delta(5)-Delta(4) isomerase (3betaHSD), a non cytochrome P450 enzyme, by increasing the enzymes affinity for its cofactor, NAD(+).	NAD	258-264	cytochrome b5 type A	Homo sapiens	51-59
3245385-4	1988	The discussed biphasic kinetics was more regular and distinct in the NADH-dependent reaction as compared with NADPH-dependent hydroxylation of B(a)P. It is suggested that the NADH-specific pathway of electron transport to cytochrome P-450 is necessary for the occurrence of this effect both in NADH- and NADPH supported reaction.	NAD	69-73	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	222-238
23506846-8	2013	Down-regulation of AQP9 significantly increased apoptosis, ROS accumulation, and the NAD(+)/NADH ratio in the RGC-5 cells.	NAD	85-91	aquaporin 9	Mus musculus	19-23
23506846-8	2013	Down-regulation of AQP9 significantly increased apoptosis, ROS accumulation, and the NAD(+)/NADH ratio in the RGC-5 cells.	NAD	92-96	aquaporin 9	Mus musculus	19-23
3245385-4	1988	The discussed biphasic kinetics was more regular and distinct in the NADH-dependent reaction as compared with NADPH-dependent hydroxylation of B(a)P. It is suggested that the NADH-specific pathway of electron transport to cytochrome P-450 is necessary for the occurrence of this effect both in NADH- and NADPH supported reaction.	NAD	175-179	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	222-238
3245385-4	1988	The discussed biphasic kinetics was more regular and distinct in the NADH-dependent reaction as compared with NADPH-dependent hydroxylation of B(a)P. It is suggested that the NADH-specific pathway of electron transport to cytochrome P-450 is necessary for the occurrence of this effect both in NADH- and NADPH supported reaction.	NAD	175-179	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	222-238
3067255-3	1988	Preculture of cells in medium enriched with nicotinic acid, a precursor of NAD, influenced the intracellular NAD concentration only to a small extend in all strains, but enhanced the radiation resistance against UV-C significantly in one rad6 mutant strain.	NAD	75-78	E2 ubiquitin-conjugating protein RAD6	Saccharomyces cerevisiae S288C	238-242
23404532-3	2013	Here we examine the role of an NAD(+) -dependent histone deacetylase, SIRT1, in modulating the neurogenic potential of neural precursors in the neurogenic niches of the adult mouse brain.	NAD	31-37	sirtuin 1	Mus musculus	70-75
2963642-1	1987	The inhibitory action of nicotinic acid, nicotinamide, N-nicotinoyl-gamma-aminobutyric acid, NAD, NADH, NADP, and NADPH on the rabbit skeletal muscle glycogen phosphorylase b has been studied.	NAD	93-96	LOW QUALITY PROTEIN: glycogen phosphorylase, brain form	Oryctolagus cuniculus	150-174
2963642-1	1987	The inhibitory action of nicotinic acid, nicotinamide, N-nicotinoyl-gamma-aminobutyric acid, NAD, NADH, NADP, and NADPH on the rabbit skeletal muscle glycogen phosphorylase b has been studied.	NAD	98-102	LOW QUALITY PROTEIN: glycogen phosphorylase, brain form	Oryctolagus cuniculus	150-174
2963642-3	1987	NADH-binding site of glycogen phosphorylase b subunit was characterized by the sedimentation velocity method.	NAD	0-4	LOW QUALITY PROTEIN: glycogen phosphorylase, brain form	Oryctolagus cuniculus	21-45
2963642-5	1987	AMP-induced association of glycogen phosphorylase b is hindered by NADH.	NAD	67-71	LOW QUALITY PROTEIN: glycogen phosphorylase, brain form	Oryctolagus cuniculus	27-51
3662534-1	1987	The oxidation of the 15-hydroxy group of prostaglandins of the A, E, and F series by the NAD+-dependent prostaglandin dehydrogenase (PGDH) has been well documented.	NAD	89-92	15-hydroxyprostaglandin dehydrogenase	Homo sapiens	104-131
3662534-1	1987	The oxidation of the 15-hydroxy group of prostaglandins of the A, E, and F series by the NAD+-dependent prostaglandin dehydrogenase (PGDH) has been well documented.	NAD	89-92	15-hydroxyprostaglandin dehydrogenase	Homo sapiens	133-137
3427221-4	1987	The dye inhibits in a non-competitive way the fragment A-catalysed transfer of ADP-ribose from NAD to elongation factor 2 (EF2).	NAD	95-98	eukaryotic translation elongation factor 2	Homo sapiens	102-121
3427221-4	1987	The dye inhibits in a non-competitive way the fragment A-catalysed transfer of ADP-ribose from NAD to elongation factor 2 (EF2).	NAD	95-98	eukaryotic translation elongation factor 2	Homo sapiens	123-126
3039339-8	1987	In membranes from day 12 myometrium, the amount of [32P]NAD incorporated by IAP into the Mr = 41,000 peptides (alpha i, subunit of Gi was markedly increased compared to membranes from day 0 tissue.	NAD	56-59	magnesium transporter 1	Rattus norvegicus	76-79
3569267-8	1987	With up to 300-fold NADH----NAD+ conversions for the system using yeast alcohol dehydrogenase and up to 1500-fold NADPH----NADP+ regenerations for the system using glucose-6-phosphate dehydrogenase.	NAD	20-24	glucose-6-phosphate dehydrogenase	Saccharomyces cerevisiae S288C	164-197
3567170-9	1987	At high [E2] and for [E2] greater than [E1] greater than [NADH], E1-NADH X E2 and E1 X NADH-E2 are virtually the only coenzyme-contained species.	NAD	58-62	small nucleolar RNA, H/ACA box 73A	Homo sapiens	65-94
3814652-3	1987	These changes are probably due to the activation of phospholipase A2 and lipid peroxidation, since their inhibitors eliminate with the same efficiency the activation of the external pathway of NADH oxidation both in normal and damaged myocardium.	NAD	193-197	phospholipase A2	Oryctolagus cuniculus	52-68
3785292-5	1986	In contrast, PDHa kinase activity is stimulated by elevated NADH/NAD+ and acetyl CoA/CoA ratios, although it appears that the NADH/NAD+ ratios required for half-maximal stimulation are more than an order of magnitude greater than those reported for mammalian pyruvate dehydrogenase complexes.	NAD	60-64	pyruvate dehydrogenase E1 subunit alpha 1	Homo sapiens	13-17
3785292-5	1986	In contrast, PDHa kinase activity is stimulated by elevated NADH/NAD+ and acetyl CoA/CoA ratios, although it appears that the NADH/NAD+ ratios required for half-maximal stimulation are more than an order of magnitude greater than those reported for mammalian pyruvate dehydrogenase complexes.	NAD	65-69	pyruvate dehydrogenase E1 subunit alpha 1	Homo sapiens	13-17
3785292-5	1986	In contrast, PDHa kinase activity is stimulated by elevated NADH/NAD+ and acetyl CoA/CoA ratios, although it appears that the NADH/NAD+ ratios required for half-maximal stimulation are more than an order of magnitude greater than those reported for mammalian pyruvate dehydrogenase complexes.	NAD	126-130	pyruvate dehydrogenase E1 subunit alpha 1	Homo sapiens	13-17
3785292-5	1986	In contrast, PDHa kinase activity is stimulated by elevated NADH/NAD+ and acetyl CoA/CoA ratios, although it appears that the NADH/NAD+ ratios required for half-maximal stimulation are more than an order of magnitude greater than those reported for mammalian pyruvate dehydrogenase complexes.	NAD	131-135	pyruvate dehydrogenase E1 subunit alpha 1	Homo sapiens	13-17
3091080-6	1986	When purified ferrochelatase was incubated with the low molecular weight form of NADH dehydrogenase prepared from Complex I, heme synthesis from ferric ion occurred by the addition of NADH.	NAD	81-85	FECH	Bos taurus	14-28
3091080-8	1986	These results indicate that ferrous ion is produced by NADH oxidation in Complex I and is then utilized for heme synthesis by ferrochelatase.	NAD	55-59	FECH	Bos taurus	126-140
3769053-6	1986	While the oxygen-containing coumaran and benzofuran both increased the NADH: quinone reductase activity in hepatic cytosol, the nitrogen-containing indole and indole-3-carbinol did not.	NAD	71-75	crystallin, zeta	Mus musculus	77-94
3781468-6	1986	Both NADH and NADPH were able to be electron donors for delta 5-desaturase, but cytochrome P-450 did not take part in the enzyme reaction because CO gas did not inhibit its activity.	NAD	5-9	fatty acid desaturase 1	Rattus norvegicus	56-74
16664639-1	1986	NADH:nitrate reductase was extracted from corn leaves (Zea mays L. W64A x W182E) and purified on blue Sepharose.	NAD	0-4	nitrate reductase [NADH] 1	Zea mays	5-22
16664640-9	1986	Western blots of polyacrylamide gels of native and denatured crude extracts showed that NADH:NR polypeptide was absent prior to treatment with N nutrients, but appeared after nitrate was given in dark or light.	NAD	88-92	nitrate reductase [NADH] 1	Zea mays	93-95
4059037-6	1985	Oxygen saturated CSF superfusion of the ischemic brain cortex restored the cortical NAD/NADH redox state to the preanoxic level (oxidation of NADH).	NAD	84-87	colony stimulating factor 2	Homo sapiens	17-20
23467744-3	2013	Because LDHC is abundant in spermatozoa that utilize aerobic glycolysis for energy requirements, its main function was presumed to be the interconversion of pyruvate to lactate with the concomitant oxidation/reduction of NADH to NAD(+).	NAD	221-225	lactate dehydrogenase C	Homo sapiens	8-12
23467744-3	2013	Because LDHC is abundant in spermatozoa that utilize aerobic glycolysis for energy requirements, its main function was presumed to be the interconversion of pyruvate to lactate with the concomitant oxidation/reduction of NADH to NAD(+).	NAD	229-235	lactate dehydrogenase C	Homo sapiens	8-12
23333241-6	2013	Up-regulation of Iduna reduced the loss of mitochondrial potential and ATP and NAD+ production, but did not affect the mitochondrial dysfunction-induced cytochrome c release, increase of Bax/Bcl-2 ratio, and Caspase-9/Caspase-3 activity.	NAD	79-83	ring finger protein 146	Mus musculus	17-22
24280190-12	2013	Such trigger was mediated by HIF-1alpha, whose stabilization was regulated after recovery of the balance between alpha-ketoglutarate and succinate due to a recuperation of NADH consumption that followed complex I rescue.	NAD	172-176	hypoxia inducible factor 1, alpha subunit	Mus musculus	29-39
23439428-1	2013	Human sirtuin1 (SIRT1), the closest homolog of the yeast sir2 protein, functions as an NAD+-dependent histone and non-histone protein deacetylase in several cellular processes, like energy metabolism, stress responses, aging, etc.	NAD	87-91	sirtuin 1	Mus musculus	16-21
23373462-2	2013	Human nicotinamide phosphoribosyltransferase (NAMPT) replenishes the NAD pool and controls the activities of sirtuins, mono- and poly-(ADP-ribose) polymerases, and NAD nucleosidase.	NAD	69-72	CD38 molecule	Homo sapiens	164-180
24020002-1	2013	The cellular NAD(+)/NADH level controls Sir2 (silent information regulator 2) deacetylase activity in regulating aging in lower species.	NAD	13-19	sirtuin 2	Homo sapiens	40-44
24020002-1	2013	The cellular NAD(+)/NADH level controls Sir2 (silent information regulator 2) deacetylase activity in regulating aging in lower species.	NAD	13-19	sirtuin 2	Homo sapiens	46-76
24020002-1	2013	The cellular NAD(+)/NADH level controls Sir2 (silent information regulator 2) deacetylase activity in regulating aging in lower species.	NAD	20-24	sirtuin 2	Homo sapiens	40-44
24020002-1	2013	The cellular NAD(+)/NADH level controls Sir2 (silent information regulator 2) deacetylase activity in regulating aging in lower species.	NAD	20-24	sirtuin 2	Homo sapiens	46-76
23302720-4	2013	Here, younger mice were found to express higher levels of the NAD(+)-dependent histone deacetylase SIRT1 in the kidney.	NAD	62-68	sirtuin 1	Mus musculus	99-104
23414428-1	2013	Recent studies with genetic deletion of P2Y1 receptor (P2Y1-/-) have clinched its role in enteric purinergic inhibitory neurotransmission and suggested that beta-NAD may be the purinergic inhibitory neurotransmitter in the colon.	NAD	157-165	purinergic receptor P2Y, G-protein coupled 1	Mus musculus	40-53
23297412-2	2013	Here, we show that oral administration of resveratrol, which leads to activation of an NAD(+)-dependent protein deacetylase SIRT1, suppresses cardiac hypertrophy and fibrosis and restores cardiac diastolic function in dystrophin-deficient mdx mice.	NAD	87-93	sirtuin 1	Mus musculus	124-129
23123429-5	2013	CD38 is an enzyme that catalyzes the hydrolysis of nicotinamide adenine dinucleotide (NAD) to ADP-ribose.	NAD	51-84	CD38 molecule	Homo sapiens	0-4
23123429-5	2013	CD38 is an enzyme that catalyzes the hydrolysis of nicotinamide adenine dinucleotide (NAD) to ADP-ribose.	NAD	86-89	CD38 molecule	Homo sapiens	0-4
23123429-6	2013	Here we show that NAD can covalently label CD38 E226D and E226Q mutants but not wild-type CD38.	NAD	18-21	CD38 molecule	Homo sapiens	43-47
23358244-5	2013	Acetylation of K8 was rapidly responsive to changes in glucose levels and was up-regulated in response to nicotinamide adenine dinucleotide (NAD) depletion and in diabetic mouse and human livers.	NAD	106-139	keratin 8	Mus musculus	15-17
23358244-5	2013	Acetylation of K8 was rapidly responsive to changes in glucose levels and was up-regulated in response to nicotinamide adenine dinucleotide (NAD) depletion and in diabetic mouse and human livers.	NAD	141-144	keratin 8	Mus musculus	15-17
23358244-6	2013	The NAD-dependent deacetylase sirtuin 2 (SIRT2) associated with and deacetylated K8.	NAD	4-7	sirtuin 2	Homo sapiens	30-39
23358244-6	2013	The NAD-dependent deacetylase sirtuin 2 (SIRT2) associated with and deacetylated K8.	NAD	4-7	sirtuin 2	Homo sapiens	41-46
22982257-4	2013	Cytotoxicity and transfection efficiency of the obtained SLN:pDNA complexes were evaluated on three different immortalized cell lines: COS-I (African green monkey kidney cell line), HepG2 (human hepatocellular liver carcinoma cell line) and Na1300 (murine neuroblastoma cell line).	NAD	135-140	sarcolipin	Homo sapiens	57-60
23509928-5	2013	beta-NAD(+) inhibited the expression of MMP-1 and MMP-3 triggered by IL-1alpha at gene and protein levels.	NAD	0-11	matrix metallopeptidase 1	Homo sapiens	40-45
23509928-5	2013	beta-NAD(+) inhibited the expression of MMP-1 and MMP-3 triggered by IL-1alpha at gene and protein levels.	NAD	0-11	interleukin 1 alpha	Homo sapiens	69-78
4059037-6	1985	Oxygen saturated CSF superfusion of the ischemic brain cortex restored the cortical NAD/NADH redox state to the preanoxic level (oxidation of NADH).	NAD	88-92	colony stimulating factor 2	Homo sapiens	17-20
4059037-6	1985	Oxygen saturated CSF superfusion of the ischemic brain cortex restored the cortical NAD/NADH redox state to the preanoxic level (oxidation of NADH).	NAD	142-146	colony stimulating factor 2	Homo sapiens	17-20
4059037-7	1985	10(-1) M cyanide, applied after superfusion of the brain cortex with oxygen saturated CSF resulted in comparable NAD reduction to that produced by "non flow anoxia".	NAD	113-116	colony stimulating factor 2	Homo sapiens	86-89
4033124-2	1985	In any incubations under the presence of NADH and NADPH, metabolites hydroxylated at the C-2, C-4, C-6 beta, C-7 alpha and C-7 beta positions were produced.	NAD	41-45	complement C2	Homo sapiens	89-92
4033124-2	1985	In any incubations under the presence of NADH and NADPH, metabolites hydroxylated at the C-2, C-4, C-6 beta, C-7 alpha and C-7 beta positions were produced.	NAD	41-45	complement C4A (Rodgers blood group)	Homo sapiens	94-97
2985614-2	1985	Using polysomal immunoselected rat liver glutathione S-transferase mRNAs, we have constructed cDNA clones using DNA polymerase I, RNase H, and Escherichia coli ligase (NAD+)-mediated second strand cDNA synthesis as described by Gubler and Hoffman (Gubler, U., and Hoffman, B. S. (1983) Gene 25, 263-269).	NAD	168-172	hematopoietic prostaglandin D synthase	Rattus norvegicus	41-66
22876953-4	2013	Specifically, the sirtuin-catalyzed AcK side chain deacetylation is not merely an amide hydrolysis reaction, instead is coupled to the nicotinamide cleavage from beta-nicotinamide adenine dinucleotide (beta-NAD+ or NAD+) with the generation of three enzymatic products, i.e. the deacetylated protein species, nicotinamide, and 2"-O-acetyl-ADP-ribose (2"-O-AADPR).	NAD	162-200	tyrosine kinase non receptor 2	Homo sapiens	36-39
22876953-4	2013	Specifically, the sirtuin-catalyzed AcK side chain deacetylation is not merely an amide hydrolysis reaction, instead is coupled to the nicotinamide cleavage from beta-nicotinamide adenine dinucleotide (beta-NAD+ or NAD+) with the generation of three enzymatic products, i.e. the deacetylated protein species, nicotinamide, and 2"-O-acetyl-ADP-ribose (2"-O-AADPR).	NAD	202-211	tyrosine kinase non receptor 2	Homo sapiens	36-39
22876953-4	2013	Specifically, the sirtuin-catalyzed AcK side chain deacetylation is not merely an amide hydrolysis reaction, instead is coupled to the nicotinamide cleavage from beta-nicotinamide adenine dinucleotide (beta-NAD+ or NAD+) with the generation of three enzymatic products, i.e. the deacetylated protein species, nicotinamide, and 2"-O-acetyl-ADP-ribose (2"-O-AADPR).	NAD	207-211	tyrosine kinase non receptor 2	Homo sapiens	36-39
3000695-0	1985	Change in NAD+/NADH content of S-adenosyl-L-homocysteine hydrolase upon NAD+ reversible inactivation by cAMP and 2"-deoxyadenosine.	NAD	10-14	adenosylhomocysteinase	Homo sapiens	31-66
23527151-5	2013	Hence, we performed 5 ns molecular dynamics (MD) simulation on SIRT2 Apo-form and complexes with substrate/NAD(+) and inhibitor of wild type (WT), Q167A, and H187A.	NAD	107-113	sirtuin 2	Homo sapiens	63-68
23527151-10	2013	Our study unveiled the structural changes of SIRT2 in presence of NAD(+) and inhibitor which should be helpful to improve the inhibitory potency of SIRT2.	NAD	66-72	sirtuin 2	Homo sapiens	45-50
3000695-0	1985	Change in NAD+/NADH content of S-adenosyl-L-homocysteine hydrolase upon NAD+ reversible inactivation by cAMP and 2"-deoxyadenosine.	NAD	15-19	adenosylhomocysteinase	Homo sapiens	31-66
23527151-10	2013	Our study unveiled the structural changes of SIRT2 in presence of NAD(+) and inhibitor which should be helpful to improve the inhibitory potency of SIRT2.	NAD	66-72	sirtuin 2	Homo sapiens	148-153
3000695-0	1985	Change in NAD+/NADH content of S-adenosyl-L-homocysteine hydrolase upon NAD+ reversible inactivation by cAMP and 2"-deoxyadenosine.	NAD	72-76	adenosylhomocysteinase	Homo sapiens	31-66
22967499-7	2012	Addition of leucine to HFD correlated with increased expression of SIRT1 and NAMPT (nicotinamide phosphoribosyltransferase) as well as higher intracellular NAD(+) levels, which decreased acetylation of peroxisome proliferator-activated receptor-gamma coactivator 1alpha (PGC1alpha) and forkhead box O1 (FoxO1).	NAD	156-162	forkhead box O1	Mus musculus	286-301
6152012-7	1984	Glutamine limitation of gln1 structural mutants has the opposite effect, causing elevated levels of NAD-dependent glutamate dehydrogenase even in the presence of ammonia.	NAD	100-103	glutamate--ammonia ligase	Saccharomyces cerevisiae S288C	24-28
22967499-7	2012	Addition of leucine to HFD correlated with increased expression of SIRT1 and NAMPT (nicotinamide phosphoribosyltransferase) as well as higher intracellular NAD(+) levels, which decreased acetylation of peroxisome proliferator-activated receptor-gamma coactivator 1alpha (PGC1alpha) and forkhead box O1 (FoxO1).	NAD	156-162	forkhead box O1	Mus musculus	303-308
23137106-2	2012	Telmisartan has been reported to function as a partial agonist of the peroxisome proliferator-activated receptor (PPAR) gamma, which is also targeted by the nicotinamide adenine dinucleotide (NAD)-dependent deacetylase (SIRT1).	NAD	157-190	sirtuin 1	Mus musculus	220-225
23137106-2	2012	Telmisartan has been reported to function as a partial agonist of the peroxisome proliferator-activated receptor (PPAR) gamma, which is also targeted by the nicotinamide adenine dinucleotide (NAD)-dependent deacetylase (SIRT1).	NAD	192-195	sirtuin 1	Mus musculus	220-225
6329192-1	1984	The sarcoplasmic reticulum and glycogen pellet derived from rabbit skeletal muscle and the sarcolemma and sarcoplasmic reticulum from pig skeletal muscle contains NAD:dependent mono ADP-ribosyltransferase activity toward the guanidine analog, P- nitrobenzylidine aminoguanidine.	NAD	163-166	ADP-ribosyltransferase 3 (inactive)	Sus scrofa	177-204
6327552-5	1984	An inhibitor of ADPRT , m-aminobenzamide, largely prevented the depletion of cellular NAD+ and reduced the rate at which ADPRT activity disappeared during post-irradiation incubation.	NAD	86-90	poly [ADP-ribose] polymerase 1	Cricetulus griseus	16-21
6326802-3	1984	The NAD+-bound reduced enzyme was oxidized by cytochrome b5 via the semiquinone intermediate.	NAD	4-8	cytochrome b5 type A	Homo sapiens	46-59
6326802-9	1984	A mechanism for electron transfer from NADH to cytochrome b5 is discussed on the basis of the one-electron redox potentials of the enzyme and is compared with the electron-transfer mechanism of NADPH-cytochrome P-450 reductase.	NAD	39-43	cytochrome b5 type A	Homo sapiens	47-60
6699018-6	1984	Ninety per cent of the cytochrome b5 in the derivative was reduced with a first order rate constant of 51 s-1 upon the addition of NADH; the transfer of electrons from NADH to the reductase FAD prosthetic group, which is known to be the rate-limiting step in the reductase reaction mechanism, proceeded with an apparent rate constant of 57 s-1 under these conditions.	NAD	131-135	cytochrome b5 type A	Homo sapiens	23-36
6699018-6	1984	Ninety per cent of the cytochrome b5 in the derivative was reduced with a first order rate constant of 51 s-1 upon the addition of NADH; the transfer of electrons from NADH to the reductase FAD prosthetic group, which is known to be the rate-limiting step in the reductase reaction mechanism, proceeded with an apparent rate constant of 57 s-1 under these conditions.	NAD	168-172	cytochrome b5 type A	Homo sapiens	23-36
6323400-9	1984	The physiological relevance of the location and the Ca2+, calmodulin-dependence of the NAD kinase will be discussed.	NAD	87-90	calmodulin1	Zea mays	58-68
6706937-2	1984	Both isomers of phenylserine are substrates for native phenylalanine hydroxylase at pH 6.8 and 25 degrees C, when activity is measured with the use of the dihydropteridine reductase assay coupled with NADH in the presence of the synthetic cofactor, 6-methyl-5,6,7,8-tetrahydropterin.	NAD	201-205	phenylalanine hydroxylase	Rattus norvegicus	55-80
6140197-1	1983	Mullerian inhibiting substance (MIS), a glycoprotein from the fetal testis causing regression of the embryonic Mullerian duct, can be inhibited in vitro in the presence of Mn2+ by a wide range of nucleotides including GTP, NAD, ATP, AMP, and several nonhydrolyzable synthetic ATP analogs.	NAD	223-226	anti-Mullerian hormone	Rattus norvegicus	0-30
6824689-4	1983	Different reducing agents (dithiothreitol, NADPH, NADH, GSH) are effective both in preventing and in reversing ornithine decarboxylase inactivation.	NAD	50-54	ornithine decarboxylase 1	Rattus norvegicus	111-134
6152729-12	1983	Other NAD utilizing enzymes, including representative dehydrogenases and poly ADP ribose polymerase, were, by comparison to mammalian IMPD, resistant to inhibition by TAD.	NAD	6-9	inosine monophosphate dehydrogenase 1	Homo sapiens	134-138
16662626-0	1982	Role of peroxidase in lignification of tobacco cells : I. Oxidation of nicotinamide adenine dinucleotide and formation of hydrogen peroxide by cell wall peroxidases.	NAD	71-104	peroxidase N1	Nicotiana tabacum	8-18
16662626-6	1982	In the presence of both cofactors or Mn(2+) alone, catalase oxidized NADH.	NAD	69-73	catalase isozyme 1	Nicotiana tabacum	51-59
16662626-7	1982	However, if the cofactors were absent or if only dichlorophenol was present, catalase inhibited NADH oxidation.	NAD	96-100	catalase isozyme 1	Nicotiana tabacum	77-85
16662626-9	1982	Superoxide dismutase inhibited NADH oxidation quite significantly indicating the involvement of the superoxide radical in the peroxidase reaction.	NAD	31-35	peroxidase N1	Nicotiana tabacum	126-136
16662626-10	1982	These results are interpreted to mean that the reactions whereby tobacco cell wall peroxidases catalyze NADH-dependent H(2)O(2) formation are similar to those proposed for horseradish peroxidase (Halliwell 1978 Planta 140: 81-88).	NAD	104-108	peroxidase N1	Nicotiana tabacum	83-93
16662627-2	1982	Coniferyl alcohol is the primary substrate for peroxidase-mediated lignification, a process which depends on the generation of H(2)O(2) by NADH oxidation.	NAD	139-143	peroxidase N1	Nicotiana tabacum	47-57
16662627-5	1982	In addition, coniferyl alcohol prevented the conversion of active peroxidase into the inactive intermediate compound III-which is usually formed in the presence of NADH-at equally low concentrations.	NAD	164-168	peroxidase N1	Nicotiana tabacum	66-76
7115785-5	1982	To explain the protection exerted by NAD+ in the presence of oxidized substrate, a transient activated form of the oxidized coenzyme with a 1,4-dihydronicotinamide structure and a positive charge on the C-4 atom is postulated.	NAD	37-41	complement C4A (Rodgers blood group)	Homo sapiens	203-206
7079734-5	1982	In addition, the unusual capacity of S-adenosylhomocysteine hydrolase to form stable complexes with adenosine and its cofactor, nicotinamide adenine dinucleotide, suggest that evolution of its gene may have involved recombination of a portion of the adenosine deaminase gene with an adenine nucleotide domain-coding sequence of another preexisting gene.	NAD	128-161	adenosylhomocysteinase	Homo sapiens	37-69
6216130-5	1982	These effects are both NAD+ and n-octylamine dependent and appear to be due to an activation of the microsomal enzyme causing endogenous reduction of NAD(P)+ and also, in part, to inhibition of the autooxidation of reduced cytochrome b5.	NAD	23-27	cytochrome b5 type A	Homo sapiens	223-236
7030314-9	1981	The enzyme also catalyses the NADH-dependent reduction of horse heart cytochrome c, 2,6-dichlorophenol-indophenol and K3Fe(CN)6.	NAD	30-34	cytochrome c, somatic	Equus caballus	70-82
7213758-11	1981	The use of Leuconostoc mesenteroides glucose-6-phosphate dehydrogenase (D-glucose-6-phosphate: NADP+ 1-oxidoreductase, EC 1.1.1.49), with NAD as cofactor, is recommended for measuring hexokinases in crude tissue preparations to avoid the variable further reduction of nucleotide caused by the action of 6-phosphogluconate dehydrogenase when NADP is used with yeast glucose-6-phosphate dehydrogenase.	NAD	95-98	glucose-6-phosphate dehydrogenase	Saccharomyces cerevisiae S288C	37-70
7213758-11	1981	The use of Leuconostoc mesenteroides glucose-6-phosphate dehydrogenase (D-glucose-6-phosphate: NADP+ 1-oxidoreductase, EC 1.1.1.49), with NAD as cofactor, is recommended for measuring hexokinases in crude tissue preparations to avoid the variable further reduction of nucleotide caused by the action of 6-phosphogluconate dehydrogenase when NADP is used with yeast glucose-6-phosphate dehydrogenase.	NAD	95-98	glucose-6-phosphate dehydrogenase	Saccharomyces cerevisiae S288C	365-398
6972374-10	1981	It has been shown that the second electron for P-448(1) can also be supplied from NADH via cytochrome b5 in a reconstituted acetanilide p-hydroxylase system containing P-448(1), cytochrome b5, and the two reductases.	NAD	82-86	cytochrome b5 type A	Homo sapiens	91-104
6972374-10	1981	It has been shown that the second electron for P-448(1) can also be supplied from NADH via cytochrome b5 in a reconstituted acetanilide p-hydroxylase system containing P-448(1), cytochrome b5, and the two reductases.	NAD	82-86	cytochrome b5 type A	Homo sapiens	178-191
6111437-0	1981	NADH-dependent inducible aryl hydrocarbon hydroxylase activity in rat brain mitochondria.	NAD	0-4	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	25-53
7400118-5	1980	These results apparently suggest that the NADPH-flavin reductase system is able to reduce methemoglobin in erythrocytes at a moderate speed with about 1 microM flavin, and the reduction was estimated to vary from less than 1% to about 20% of that by the NADH-cytochrome b5 reductase system with 1 microM cytochrome b5, depending on the uptake of flavin by human erythrocytes.	NAD	254-258	biliverdin reductase B	Homo sapiens	42-64
22402365-10	2012	Nutrition restriction induced an increase in the level of the miR-140-3p target, NAD+-dependent SIRT1.	NAD	81-85	microRNA 140	Homo sapiens	62-69
230554-1	1979	The higher inhibition of liver microsomal carboxylesterase (CEase) by EPN, as compared to that of acetylcholinesterase (AchE) may be, at least in part, explained by the present findings that NAD potentiated the anti-CEase, but not anti-AchE, action of EPN.	NAD	191-194	acetylcholinesterase	Rattus norvegicus	98-118
22476700-3	2012	In addition, NAD(+) is used as a substrate independent of its redox-carrier function by enzymes like poly(ADP)ribose polymerases, sirtuins and glycohydrolases like CD38.	NAD	13-19	CD38 molecule	Homo sapiens	164-168
22874065-3	2012	Dual oxidase 1 (DUOX1) and DUOX2, originally identified in the thyroid, are nicotinamide adenine dinucleotide phosphate (NADPH) oxidases that are necessary to produce the H2O2 required for thyroid hormone biosynthesis.	NAD	76-109	dual oxidase 2	Rattus norvegicus	27-32
230554-1	1979	The higher inhibition of liver microsomal carboxylesterase (CEase) by EPN, as compared to that of acetylcholinesterase (AchE) may be, at least in part, explained by the present findings that NAD potentiated the anti-CEase, but not anti-AchE, action of EPN.	NAD	191-194	acetylcholinesterase	Rattus norvegicus	236-240
33163-4	1979	2) The hydrolyses of maltodextrin (DPn = 74.4) and soluble starch catalyzed by soybean beta-amylase were investigated in the pH range from 3.0 to 9.1 at 25 degrees C, and the Michaelis constant, Km, and the maximum velocity, V, for each substrate were determined at each pH.	NAD	35-38	beta-amylase	Glycine max	87-99
22829588-0	2012	Identification of a novel pathway of transforming growth factor-beta1 regulation by extracellular NAD+ in mouse macrophages: in vitro and in silico studies.	NAD	98-102	hemoglobin, beta adult major chain	Mus musculus	63-69
22311271-3	2012	The effects observed long after perinatal asphyxia (PA) have been explained by over-expression of sentinel proteins, such as poly(ADP-ribose) polymerase-1 (PARP-1), competing for NAD(+) during re-oxygenation, leading to the idea that sentinel protein inhibition constitutes a therapeutic strategy.	NAD	179-185	poly (ADP-ribose) polymerase 1	Rattus norvegicus	125-154
22311271-3	2012	The effects observed long after perinatal asphyxia (PA) have been explained by over-expression of sentinel proteins, such as poly(ADP-ribose) polymerase-1 (PARP-1), competing for NAD(+) during re-oxygenation, leading to the idea that sentinel protein inhibition constitutes a therapeutic strategy.	NAD	179-185	poly (ADP-ribose) polymerase 1	Rattus norvegicus	156-162
213050-2	1978	In the presence of 1.6 mM-NAD+, isoenzyme LDH-X does not bind to AMP-Sepharose, whereas the other lactate dehydrogenase isoenzymes do.	NAD	26-30	lactate dehydrogenase C	Homo sapiens	42-47
207332-3	1978	The oscillations in the peroxidase (donor: hydrogen-peroxide oxidoreductase, EC 1.11.1.7)-catalyzed reaction between NADH and O2 are undamped when the reaction is carried out in a system open to both substrates and when 2,4-dichlorophenol and methylene blue are present in the solution.	NAD	117-121	Susceptibility to lysis by alloreactive natural killer cells	Homo sapiens	77-81
22547068-7	2012	The use of specific siRNA showed that the changes of Ca(2+) homeostasis induced by NAD(+) precursors are mediated by CD38 and the consequent ADPR-mediated TRPM2 gating.	NAD	83-89	CD38 molecule	Homo sapiens	117-121
22682224-2	2012	In line with this premise, decreased activity of PARP-1 or CD38-both NAD(+) consumers-increases NAD(+) bioavailability, resulting in SIRT1 activation and protection against metabolic disease.	NAD	96-102	CD38 molecule	Homo sapiens	59-63
22487558-1	2012	Arabidopsis mitochondria contain two NAD(+)-malic enzymes, NAD-ME1 and NAD-ME2.	NAD	37-43	NAD-dependent malic enzyme 1	Arabidopsis thaliana	59-66
344312-5	1978	A kinetic isotope effect kH/k3H of 1.7 was observed at C-5, and afforded support for a mechanism involving oxidation of C-5 with NAD.	NAD	129-132	complement C5	Homo sapiens	55-58
22487558-3	2012	Here, the interaction of NAD-ME1 and -2 with fumarate was investigated by kinetic approaches, urea denaturation assays and intrinsic fluorescence quenching, in the absence and presence of NAD(+).	NAD	188-194	NAD-dependent malic enzyme 1	Arabidopsis thaliana	25-39
22487558-5	2012	In contrast, NAD-ME1 fumarate activation was higher at suboptimal NAD(+) concentrations.	NAD	66-72	NAD-dependent malic enzyme 1	Arabidopsis thaliana	13-20
22487558-9	2012	Together, the results indicate that the differential fumarate regulation of Arabidopsis NAD-MEs, which is further modulated by NAD(+) availability, is related to the gaining of an allosteric site for fumarate in NAD-ME1 and an active site-associated inhibition by this C(4)-organic acid in NAD-ME2.	NAD	127-133	NAD-dependent malic enzyme 1	Arabidopsis thaliana	212-219
344312-5	1978	A kinetic isotope effect kH/k3H of 1.7 was observed at C-5, and afforded support for a mechanism involving oxidation of C-5 with NAD.	NAD	129-132	complement C5	Homo sapiens	120-123
190237-4	1977	The toxin A-hPL conjugate retains one-third of the NAD+:EF-2 ADP-ribosyltransferase activity of toxin A, and 26% of the hPL-binding activity to lactogenic receptors.	NAD	51-55	galectin 1	Homo sapiens	12-15
22542455-1	2012	The NAD-dependent histone deacetylase Sirt1 antagonizes p53 transcriptional activity to regulate cell-cycle progression and apoptosis.	NAD	4-7	sirtuin 1	Mus musculus	38-43
22542455-1	2012	The NAD-dependent histone deacetylase Sirt1 antagonizes p53 transcriptional activity to regulate cell-cycle progression and apoptosis.	NAD	4-7	transformation related protein 53, pseudogene	Mus musculus	56-59
794420-5	1976	Incorporation of the reduced pyridine nucleotide NADH into an incubation mixture containing NADPH increased epidermal AHH activity by one-third.	NAD	49-53	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	118-121
22312127-6	2012	Acetylation and stability of wild-type, but not mutant, Foxp3 is enhanced when cells are treated with Ex-527, an inhibitor of the NAD(+)-dependent deacetylase SIRT1.	NAD	130-136	sirtuin 1	Mus musculus	159-164
171253-0	1975	Reduced nicotinamide adenine dinucleotide-activated phosphoenolpyruvate carboxylase in Pseudomonas MA: potential regulation between carbon assimilation and energy production.	NAD	8-41	phosphoenolpyruvate carboxykinase 1	Homo sapiens	52-83
22411915-1	2012	Sir2 is an evolutionarily conserved NAD+ dependent protein.	NAD	36-40	Sirtuin 1	Drosophila melanogaster	0-4
171253-2	1975	The purified phosphoenolpyruvate carboxylase is activated specifically by reduced nicotinamide adenine dinucleotide (KA = 0.2 mM).	NAD	82-115	phosphoenolpyruvate carboxykinase 1	Homo sapiens	13-44
1177492-2	1975	The poly(1-Me-5-VIm)-catalyzed hydrolysis of S12- exhibited saturation in excess catalyst nad in excess substrate.	NAD	90-93	vimentin	Homo sapiens	16-19
22155552-3	2012	Although it was a dual co-factor GDH, activity was greater with NAD(+)/H than with NADP(+)/H.	NAD	64-70	glutamate dehydrogenase 1	Homo sapiens	33-36
239092-4	1975	Glucose 6-phosphate dehydrogenase and 6-phosphogluconate dehydrogenase were specific for NADP+ and were inhibited in a non-competitive manner by NADPH and NADH.	NAD	155-159	glucose-6-phosphate dehydrogenase	Saccharomyces cerevisiae S288C	0-33
22271746-9	2012	These findings demonstrate a restructuring of fermentative metabolism in the adh1 mutant in a way that sustains the recycling (oxidation) of NADH and the survival of the mutant (similar to wild-type cell survival) during dark anoxic growth.	NAD	141-145	uncharacterized protein	Chlamydomonas reinhardtii	77-81
22226197-0	2012	Engineered NADH-dependent GRE2 from Saccharomyces cerevisiae by directed enzyme evolution enhances HMF reduction using additional cofactor NADPH.	NAD	11-15	methylglyoxal reductase (NADPH-dependent) GRE2	Saccharomyces cerevisiae S288C	26-30
235300-10	1975	The maize nitrate reductase, when partially inactivated by NADH and cyanide, was not altered as a substrate for the inactivating enzyme.	NAD	59-63	nitrate reductase [NADH] 1	Zea mays	10-27
22226197-3	2012	YOL151W (GRE2) is a commonly recognized up-regulated gene expressed under stress conditions that encodes reductase activities toward furfural and HMF using cofactor NADH.	NAD	165-169	methylglyoxal reductase (NADPH-dependent) GRE2	Saccharomyces cerevisiae S288C	9-13
235300-11	1975	The maize root inactivating enzyme was also shown to inactivate the nitrate reductase (NADH) in the pea leaf.	NAD	87-91	nitrate reductase [NADH] 1	Zea mays	68-85
22006156-1	2012	The protein encoded by the sirt1 gene is an enzyme, SirT1, that couples the hydrolysis of NAD(+) to the deacetylation of acetyl-lysine residues in substrate proteins.	NAD	90-96	sirtuin 1	Mus musculus	27-32
22006156-1	2012	The protein encoded by the sirt1 gene is an enzyme, SirT1, that couples the hydrolysis of NAD(+) to the deacetylation of acetyl-lysine residues in substrate proteins.	NAD	90-96	sirtuin 1	Mus musculus	52-57
239545-0	1975	Role of cytochrome b5 in NADPH-and NADH-dependent hydroxylation by the reconstituted cytochrome P-450- or P-448-containing system.	NAD	35-39	cytochrome b5 type A	Homo sapiens	8-21
4377102-1	1974	The binding of NAD(+) and NADH to bovine liver UDP-glucose dehydrogenase was studied by using gel-filtration and fluorescence-titration methods.	NAD	15-21	UDP-glucose 6-dehydrogenase	Bos taurus	47-72
21934695-1	2012	The deficiency in the mitochondrial aspartate/glutamate transporter Aralar/AGC1 results in a loss of the malate-aspartate NADH shuttle in the brain neurons, hypomyelination, and additional defects in the brain metabolism.	NAD	122-126	aggrecan	Mus musculus	75-79
22257560-9	2012	The mRNA expression of all EPs and FP are downregulated by estradiol and the ERalpha specific agonist PPT, whereas the ERbeta specific agonist DPN downregulates only EP2 and EP4.	NAD	143-146	estrogen receptor 2	Rattus norvegicus	119-125
22257560-9	2012	The mRNA expression of all EPs and FP are downregulated by estradiol and the ERalpha specific agonist PPT, whereas the ERbeta specific agonist DPN downregulates only EP2 and EP4.	NAD	143-146	prostaglandin E receptor 2	Rattus norvegicus	166-169
4377102-1	1974	The binding of NAD(+) and NADH to bovine liver UDP-glucose dehydrogenase was studied by using gel-filtration and fluorescence-titration methods.	NAD	26-30	UDP-glucose 6-dehydrogenase	Bos taurus	47-72
4397931-6	1970	A number of NADH- and NADPH-oxidizing enzymes are concentrated in the upper part of the gradient and exhibit a certain degree of separation from G6Pase.	NAD	12-16	glucose-6-phosphatase catalytic subunit 1	Rattus norvegicus	145-151
4391279-0	1969	Nonenzymatic reduction and oxidation of myoglobin and hemoglobin by nicotinamide adenine dinucleotides and flavins.	NAD	68-102	myoglobin	Homo sapiens	40-49
22084251-7	2012	Inhibition of deacetylases, including the NAD+-dependent sirtuins, promotes Rictor acetylation and IGF-1-mediated Akt phosphorylation.	NAD	42-46	RPTOR independent companion of MTOR complex 2	Homo sapiens	76-82
21883939-5	2012	A critical source of endothelial ROS is a family of non-phagocytic nicotinamide adenine dinucleotide phosphate (NADPH) oxidases, including the prototypic Nox2-based NADPH oxidases, Nox1, Nox4 and Nox5.	NAD	67-100	NADPH oxidase 5	Homo sapiens	196-200
34059674-4	2021	The acetyltransferase MYST1 stimulated by Acetyl-CoA, and the deacetylase SIRT2 stimulated by NAD +, are identified as direct regulators of PAX7 acetylation and asymmetric division in muscle stem cells.	NAD	94-99	sirtuin 2	Mus musculus	74-79
22694102-3	2012	Unfortunately, SIRT2 complex structure is not available yet, hence molecular docking was carried out to dock the substrate (NAD(+) and acetylated lysine) and inhibitor (sirtinol) in the NAD(+) binding site.	NAD	124-130	sirtuin 2	Homo sapiens	15-20
22694102-3	2012	Unfortunately, SIRT2 complex structure is not available yet, hence molecular docking was carried out to dock the substrate (NAD(+) and acetylated lysine) and inhibitor (sirtinol) in the NAD(+) binding site.	NAD	186-192	sirtuin 2	Homo sapiens	15-20
33749726-3	2021	Overexpression of NMNAT/Nma1, an enzyme in the NAD+ biosynthetic salvage pathway, acts as an efficient suppressor of proteotoxicities in yeast, fly, and mouse models.	NAD	47-51	nicotinamide-nucleotide adenylyltransferase NMA1	Saccharomyces cerevisiae S288C	24-28
22070562-6	2012	Pre-treatment with DPN, an ERbeta agonist, significantly increased ERbeta association with mitochondria.	NAD	19-22	estrogen receptor 2	Rattus norvegicus	27-33
22070562-6	2012	Pre-treatment with DPN, an ERbeta agonist, significantly increased ERbeta association with mitochondria.	NAD	19-22	estrogen receptor 2	Rattus norvegicus	67-73
33749726-8	2021	The NAD+ salvage proteins act by preventing misfolding and, together with the Hsp90 chaperone, promoting the refolding of extended polyQ domains and alpha-synuclein (alpha-Syn).	NAD	4-8	Hsp90 family chaperone HSP82	Saccharomyces cerevisiae S288C	78-83
34009633-8	2021	CONCLUSION: These results indicate that long-term UVA eye irradiation stimulates p53, inhibits the clock gene, and reduces Sirt1 production in the NAD+ constructional system, resulting in reduced memory and learning ability.	NAD	147-151	sirtuin 1	Mus musculus	123-128
22242017-1	2012	Poly(ADP-ribose) polymerase 1 (PARP1), a nuclear protein, utilizes NAD to synthesize poly(AD-Pribose) (pADPr), resulting in both automodification and the modification of acceptor proteins.	NAD	67-70	Poly-(ADP-ribose) polymerase	Drosophila melanogaster	0-29
22242017-1	2012	Poly(ADP-ribose) polymerase 1 (PARP1), a nuclear protein, utilizes NAD to synthesize poly(AD-Pribose) (pADPr), resulting in both automodification and the modification of acceptor proteins.	NAD	67-70	Poly-(ADP-ribose) polymerase	Drosophila melanogaster	31-36
33924243-2	2021	SIRT1, an NAD-dependent deacetylase, was shown to be one of the critical regulators of eNOS.	NAD	10-13	sirtuin 1	Mus musculus	0-5
33924243-2	2021	SIRT1, an NAD-dependent deacetylase, was shown to be one of the critical regulators of eNOS.	NAD	10-13	nitric oxide synthase 3, endothelial cell	Mus musculus	87-91
33936090-6	2021	We therefore discuss these novel findings, examining the possible contribution of NAD+ depletion, along with ADO production, in the immunosuppressive activities of CD38 in the context of human tumors.	NAD	82-86	CD38 molecule	Homo sapiens	164-168
33854178-7	2021	Supplementing preadipocytes with the NAD+ booster nicotinamide mononucleotide (NMN) during differentiation increased expression levels of leptin, SIRT1, and PGC-1alpha and its transcriptional targets, and reduced levels of pro-fibrotic collagens (Col6A1 and Col6A3) in a SIRT1-dependent manner.	NAD	37-41	leptin	Homo sapiens	138-144
33854178-7	2021	Supplementing preadipocytes with the NAD+ booster nicotinamide mononucleotide (NMN) during differentiation increased expression levels of leptin, SIRT1, and PGC-1alpha and its transcriptional targets, and reduced levels of pro-fibrotic collagens (Col6A1 and Col6A3) in a SIRT1-dependent manner.	NAD	37-41	collagen type VI alpha 1 chain	Homo sapiens	247-253
33854178-7	2021	Supplementing preadipocytes with the NAD+ booster nicotinamide mononucleotide (NMN) during differentiation increased expression levels of leptin, SIRT1, and PGC-1alpha and its transcriptional targets, and reduced levels of pro-fibrotic collagens (Col6A1 and Col6A3) in a SIRT1-dependent manner.	NAD	37-41	collagen type VI alpha 3 chain	Homo sapiens	258-264
33846538-0	2021	Nicotinamide riboside, an NAD+ precursor, attenuates inflammation and oxidative stress by activating sirtuin 1 in alcohol-stimulated macrophages.	NAD	26-30	sirtuin 1	Mus musculus	101-110
33846538-12	2021	In conclusion, NR exerts anti-inflammatory and antioxidant properties by abrogating the inhibitory effects of ethanol on the SIRT1 pathway by increasing Sirt1 expression and its activator, NAD+.	NAD	189-193	sirtuin 1	Mus musculus	125-130
33846538-13	2021	Also, SIRT1 activation and normalization of ethanol-induced changes in NAD+/NADH ratios by NR are likely crucial to counteract the changes in energy phenotypes of macrophages exposed to ethanol.	NAD	76-80	sirtuin 1	Mus musculus	6-11
33732455-7	2021	According to the results of protein-protein interaction and Gene Ontology analyses, 14 proteins involved in the negative regulation of macromolecules and mRNA metabolic processes, and protein targeting to the membrane exhibited the largest degree of differential expression in the fibroblasts of patients with PD with a GBA variant, whereas 20 proteins involved in the regulation of biological quality, NAD metabolic process and cytoskeletal organization exhibited the largest degree of differential expression in the fibroblasts of patients with PD with a PARK2 variant.	NAD	403-406	glucosylceramidase beta	Homo sapiens	320-323
33758176-1	2021	Sirtuin 1 (SIRT1) is a nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase belonging to class III histone deacetylases.	NAD	23-56	sirtuin 1	Mus musculus	0-9
33758176-1	2021	Sirtuin 1 (SIRT1) is a nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase belonging to class III histone deacetylases.	NAD	23-56	sirtuin 1	Mus musculus	11-16
33758176-1	2021	Sirtuin 1 (SIRT1) is a nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase belonging to class III histone deacetylases.	NAD	58-62	sirtuin 1	Mus musculus	0-9
33758176-1	2021	Sirtuin 1 (SIRT1) is a nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase belonging to class III histone deacetylases.	NAD	58-62	sirtuin 1	Mus musculus	11-16
33355213-9	2021	The formation velocity of atRA in the presence of NAD+ correlated significantly with the expression of ALDH1A1 and AOX protein.	NAD	50-54	aldehyde dehydrogenase 1 family member A1	Homo sapiens	103-110
33754067-0	2021	NAD+-boosting therapy alleviates nonalcoholic fatty liver disease via stimulating a novel exerkine Fndc5/irisin.	NAD	0-4	fibronectin type III domain containing 5	Mus musculus	99-104
33627431-3	2021	Our analyses of human cancerous tissue revealed that the NAD-dependent deacetylase SIRT2 is up-regulated in early-stage carcinomas of various organs.	NAD	57-60	sirtuin 2	Homo sapiens	83-88
33613454-2	2020	Quinolinate phosphoribosyltransferase (QPRT) is the rate-limiting enzyme in the kynurenine pathway participating in NAD+ generation.	NAD	116-120	quinolinate phosphoribosyltransferase	Mus musculus	0-37
33613454-2	2020	Quinolinate phosphoribosyltransferase (QPRT) is the rate-limiting enzyme in the kynurenine pathway participating in NAD+ generation.	NAD	116-120	quinolinate phosphoribosyltransferase	Mus musculus	39-43
33531400-3	2021	Since the NAD+-dependent protein deacetylase Sirtuin 3 (SIRT3) is an important regulator of mitochondrial metabolism and cellular redox homeostasis, we hypothesized that SIRT3 modulation mediates M. tuberculosis-induced metabolic reprogramming.	NAD	10-13	sirtuin 3	Mus musculus	56-61
33531400-3	2021	Since the NAD+-dependent protein deacetylase Sirtuin 3 (SIRT3) is an important regulator of mitochondrial metabolism and cellular redox homeostasis, we hypothesized that SIRT3 modulation mediates M. tuberculosis-induced metabolic reprogramming.	NAD	10-13	sirtuin 3	Mus musculus	170-175
33360352-2	2021	NQO1 catalyzes the oxidation of NADH to NAD+ and may supplement levels of NAD+ near microtubules to aid SIRT2 deacetylase activity.	NAD	74-78	sirtuin 2	Homo sapiens	104-109
22195961-1	2011	The NAD(+)-dependent deacetylase SIRT1 is an evolutionarily conserved metabolic sensor of the Sirtuin family that mediates homeostatic responses to certain physiological stresses such as nutrient restriction.	NAD	4-10	sirtuin 1	Mus musculus	33-38
22195961-2	2011	Previous reports have implicated fluctuations in intracellular NAD(+) concentrations as the principal regulator of SIRT1 activity.	NAD	63-69	sirtuin 1	Mus musculus	115-120
22195961-3	2011	However, here we have identified a cAMP-induced phosphorylation of a highly conserved serine (S434) located in the SIRT1 catalytic domain that rapidly enhanced intrinsic deacetylase activity independently of changes in NAD(+) levels.	NAD	219-225	sirtuin 1	Mus musculus	115-120
33171124-0	2021	NAD+ Metabolism Maintains Inducible PD-L1 Expression to Drive Tumor Immune Evasion.	NAD	0-4	CD274 molecule	Homo sapiens	36-41
33171124-4	2021	Mechanistically, NAD+ metabolism maintains activity and expression of methylcytosine dioxygenase Tet1 via alpha-ketoglutarate (alpha-KG).	NAD	17-21	tet methylcytosine dioxygenase 1	Homo sapiens	70-101
21950728-1	2011	SIRT1 belongs to the silent information regulator 2 (Sir2) protein family of enzymes and functions as a NAD(+) -dependent class III histone deacetylase.	NAD	104-110	sirtuin 2	Homo sapiens	21-51
32712045-0	2021	Sleeve gastrectomy ameliorated high-fat diet (HFD)-induced non-alcoholic fatty liver disease and upregulated the nicotinamide adenine dinucleotide +/ Sirtuin-1 pathway in mice.	NAD	113-146	sirtuin 1	Mus musculus	150-159
21950728-1	2011	SIRT1 belongs to the silent information regulator 2 (Sir2) protein family of enzymes and functions as a NAD(+) -dependent class III histone deacetylase.	NAD	104-110	sirtuin 2	Homo sapiens	53-57
22013015-6	2011	SirT1 activity was evaluated using an in vitro deacetylation assay and correlated with the NAD(+)-to-NADH ratio.	NAD	91-97	sirtuin 1	Mus musculus	0-5
33290962-0	2021	Nicotinamide adenine dinucleotide treatment alleviates the symptoms of experimental autoimmune encephalomyelitis by activating autophagy and inhibiting the NLRP3 inflammasome.	NAD	0-33	NLR family, pyrin domain containing 3	Mus musculus	156-161
22013015-6	2011	SirT1 activity was evaluated using an in vitro deacetylation assay and correlated with the NAD(+)-to-NADH ratio.	NAD	101-105	sirtuin 1	Mus musculus	0-5
33290962-8	2021	In addition, NAD + increased the expressions of the autophagy-related proteins LC3-II/I and Beclin 1, and reduced the expression of p62.	NAD	13-18	beclin 1, autophagy related	Mus musculus	92-100
21488086-6	2011	We propose that CD38, a main cellular NAD(+) level regulator, can significantly contribute to NAD(+) catabolism.	NAD	38-44	CD38 molecule	Homo sapiens	16-20
33425964-0	2020	Ozone Exposure Induces Metabolic Disorders and NAD+ Depletion Through PARP1 Activation in Spinal Cord Neurons.	NAD	47-51	poly (ADP-ribose) polymerase 1	Rattus norvegicus	70-75
21488086-6	2011	We propose that CD38, a main cellular NAD(+) level regulator, can significantly contribute to NAD(+) catabolism.	NAD	94-100	CD38 molecule	Homo sapiens	16-20
21488086-8	2011	These therapeutic approaches are based on utilizing endogenous intermediates of NAD(+) metabolism that feed into the NAD(+) salvage pathway and also inhibit CD38 activity.	NAD	80-86	CD38 molecule	Homo sapiens	157-161
33425964-13	2020	Moreover, using PARP1 inhibitor can protect SCNs from cytotoxic effects of ozone by preventing NAD+ depletion during ozone exposure.	NAD	95-99	poly (ADP-ribose) polymerase 1	Rattus norvegicus	16-21
21807113-4	2011	Sirt1, a NAD-dependent class III histone deacetylase, has a paradoxical role in tumorigenesis by deacetylating several transcription factors, including p53, E2F1 and forkhead proteins.	NAD	9-12	E2F transcription factor 1	Homo sapiens	157-161
33425964-14	2020	Conclusion: Ozone exposure seems to induce metabolic disorders and NAD+ depletion through excessive PARP1 activation in SCNs.	NAD	67-71	poly (ADP-ribose) polymerase 1	Rattus norvegicus	100-105
33273685-8	2020	We focused on quinolinic acid (QUIN), a metabolic intermediate in the de novo nicotinamide adenine dinucleotide (NAD+) synthesis pathway, which accumulated in the tdh2 deletion cells and was a candidate metabolite to suppress DNA replication fork instability.	NAD	78-111	glyceraldehyde-3-phosphate dehydrogenase (phosphorylating) TDH2	Saccharomyces cerevisiae S288C	163-167
33254438-10	2020	The possible mechanism underlying the antidiabetic effects was revealed by molecular docking analyses examining the binding of beta-sitosterol and stigmasterol with sirtuin 4, an NAD-dependent deacylase enzyme that downregulates leucine-induced and glutamate dehydrogenase-induced insulin secretion.	NAD	179-182	sirtuin 4	Mus musculus	165-174
21188613-3	2011	Under fermentative conditions yeast reoxidizes excess NADH through glycerol production which involves NADH-dependent glycerol-3-phosphate dehydrogenases (Gpd1p and Gpd2p).	NAD	54-58	glycerol-3-phosphate dehydrogenase (NAD(+)) GPD2	Saccharomyces cerevisiae S288C	164-169
21188613-3	2011	Under fermentative conditions yeast reoxidizes excess NADH through glycerol production which involves NADH-dependent glycerol-3-phosphate dehydrogenases (Gpd1p and Gpd2p).	NAD	102-106	glycerol-3-phosphate dehydrogenase (NAD(+)) GPD2	Saccharomyces cerevisiae S288C	164-169
21188613-5	2011	We investigated the possibility of converting this excess NADH to NAD(+) by transforming a double mutant (gpd1 gpd2 ) with alternative oxidoreductase genes that might restore the redox balance and produce either sorbitol or propane-1,2-diol.	NAD	58-62	glycerol-3-phosphate dehydrogenase (NAD(+)) GPD2	Saccharomyces cerevisiae S288C	111-115
21188613-5	2011	We investigated the possibility of converting this excess NADH to NAD(+) by transforming a double mutant (gpd1 gpd2 ) with alternative oxidoreductase genes that might restore the redox balance and produce either sorbitol or propane-1,2-diol.	NAD	66-72	glycerol-3-phosphate dehydrogenase (NAD(+)) GPD2	Saccharomyces cerevisiae S288C	111-115
21652783-2	2011	We previously showed that resveratrol (3,5,4"-trihydroxy-trans-stilbene), an antioxidant and activator of the NAD(+)-dependent protein deacetylase SIRT1, delays the progression of heart failure and prolongs the lifespan of delta-sarcoglycan-deficient hamsters.	NAD	110-116	sirtuin 1	Mus musculus	147-152
33254438-11	2020	The binding affinities between sirtuin 4 and beta-sitosterol, stigmasterol, and NAD were found to be -8.6 kcal/mol, -7.2 kcal/mol and -9.5 kcal/mol, respectively, indicating the probable competition between NAD and the isolated components for sirtuin 4.	NAD	80-83	sirtuin 4	Mus musculus	31-40
33254438-11	2020	The binding affinities between sirtuin 4 and beta-sitosterol, stigmasterol, and NAD were found to be -8.6 kcal/mol, -7.2 kcal/mol and -9.5 kcal/mol, respectively, indicating the probable competition between NAD and the isolated components for sirtuin 4.	NAD	80-83	sirtuin 4	Mus musculus	243-252
33254438-11	2020	The binding affinities between sirtuin 4 and beta-sitosterol, stigmasterol, and NAD were found to be -8.6 kcal/mol, -7.2 kcal/mol and -9.5 kcal/mol, respectively, indicating the probable competition between NAD and the isolated components for sirtuin 4.	NAD	207-210	sirtuin 4	Mus musculus	31-40
32818702-6	2020	In addition, we observed that Wnt3a exacerbated hypoxia-induced mitochondrial dysfunction and cytosolic release of cytochrome C. Furthermore, we found that Sirt3, a mitochondrial NAD+-dependent deacetylase that modulates mitochondrial metabolism and homeostasis, was negatively regulated by Wnt3a.	NAD	179-182	sirtuin 3	Rattus norvegicus	156-161
33020065-4	2020	In the current work, our metabolomic analysis discovered a novel NAD+ adduct with acetylisoniazid (AcINH), a primary INH metabolite mediated by N-acetyltransferase (NAT), and we named it AcINH-NAD.	NAD	65-69	solute carrier family 38, member 3	Mus musculus	144-163
21690092-1	2011	The heme enzyme indoleamine 2,3-dioxygenase (IDO) was found to oxidize NADH under aerobic conditions in the absence of other enzymes or reactants.	NAD	71-75	indoleamine 2,3-dioxygenase 1	Homo sapiens	45-48
21690092-4	2011	Anaerobic reaction of IDO with NADH proceeded only in the presence of a mediator (e.g. methylene blue) and resulted in formation of the ferrous form of the enzyme.	NAD	31-35	indoleamine 2,3-dioxygenase 1	Homo sapiens	22-25
33020065-4	2020	In the current work, our metabolomic analysis discovered a novel NAD+ adduct with acetylisoniazid (AcINH), a primary INH metabolite mediated by N-acetyltransferase (NAT), and we named it AcINH-NAD.	NAD	65-69	solute carrier family 38, member 3	Mus musculus	165-168
21690092-5	2011	We propose that trace amounts of peroxide previously proposed to occur in NADH solutions as well as solid NADH activate IDO and lead to aerobic formation of superoxide and the reactive dioxygen adduct of the enzyme.	NAD	74-78	indoleamine 2,3-dioxygenase 1	Homo sapiens	120-123
33131100-3	2020	Sirtuin 3 (SIRT3), an NAD-dependent deacetylase, is a major cellular sensor of energy metabolism.	NAD	22-25	sirtuin 3	Mus musculus	0-9
21690092-5	2011	We propose that trace amounts of peroxide previously proposed to occur in NADH solutions as well as solid NADH activate IDO and lead to aerobic formation of superoxide and the reactive dioxygen adduct of the enzyme.	NAD	106-110	indoleamine 2,3-dioxygenase 1	Homo sapiens	120-123
21849978-6	2011	This pathway, which involves the biosynthesis and degradation of haem, enables Fh1-deficient cells to use the accumulated TCA cycle metabolites and permits partial mitochondrial NADH production.	NAD	178-182	filamin B	Homo sapiens	79-82
33131100-3	2020	Sirtuin 3 (SIRT3), an NAD-dependent deacetylase, is a major cellular sensor of energy metabolism.	NAD	22-25	sirtuin 3	Mus musculus	11-16
21699903-3	2011	Here we report the renalase crystal structure at 2.5 A resolution together with new data on its interaction with nicotinamide dinucleotides.	NAD	113-139	renalase, FAD dependent amine oxidase	Homo sapiens	19-27
21699903-7	2011	Renalase has an extremely low diaphorase activity, displaying lower k(cat) but higher k(cat)/K(m) for NADH compared to NADPH.	NAD	102-106	renalase, FAD dependent amine oxidase	Homo sapiens	0-8
32758058-8	2020	Low-dose (10 nM) NAD+ precursors (nicotinic acid, nicotinamide mononucleotide, and nicotinamide riboside) synergized with leucine to increase Sirt1 activity in adipocytes, hepatocytes, and muscle cells (30-100%, P < .01) and lifespan in Caenorhabditis elegans (25%, P = .025) and to significantly regress atherosclerotic lesion size and macrophage infiltration in a mouse model of atherosclerosis.	NAD	17-21	sirtuin 1	Mus musculus	142-147
21244356-5	2011	Because sirtuin-2 activity depends on cellular NAD+ availability, mitochondrial regulation of NAD+ levels may contribute to an increase in sirtuin-mediated tubulin deacetylation.	NAD	47-51	sirtuin 2	Homo sapiens	8-17
21244356-5	2011	Because sirtuin-2 activity depends on cellular NAD+ availability, mitochondrial regulation of NAD+ levels may contribute to an increase in sirtuin-mediated tubulin deacetylation.	NAD	94-98	sirtuin 2	Homo sapiens	8-17
20964598-4	2011	Further, we show that NAD(+)(e) activates the purinergic receptor P2Y(11) and a cyclic adenosin monophosphate (cAMP)/cyclic ADP-ribose/[Ca(2+)](i) signaling cascade, involving the opening, unique to MSC, of L-type Ca(2+) channels.	NAD	22-28	purinergic receptor P2Y11	Homo sapiens	46-73
21477609-8	2011	An increase in ERbeta levels, with diminished ERalpha/ERbeta ratio, was observed in the tumors from mice treated with DPN/letrozole combination compared to single agents and control.	NAD	118-121	estrogen receptor 1 (alpha)	Mus musculus	46-53
33061819-0	2020	The NAD-dependent deacetylase SIRT2 regulates T cell differentiation involved in tumor immune response.	NAD	4-7	sirtuin 2	Homo sapiens	30-35
33061819-1	2020	Sirtuin 2 (SIRT2), an NAD+-dependent deacetylase, regulates multiple biologic and pathologic processes including mitosis, genomic integrity, cell homeostasis and tumorigenesis.	NAD	22-25	sirtuin 2	Homo sapiens	0-9
21715639-7	2011	The underlying mechanisms for this shift in differentiation direction involve the astrogenesis promoting Sirt1 via an increased NAD/NADH ratio in ogg1(-/-) cells.	NAD	128-131	sirtuin 1	Mus musculus	105-110
33061819-1	2020	Sirtuin 2 (SIRT2), an NAD+-dependent deacetylase, regulates multiple biologic and pathologic processes including mitosis, genomic integrity, cell homeostasis and tumorigenesis.	NAD	22-25	sirtuin 2	Homo sapiens	11-16
21715639-7	2011	The underlying mechanisms for this shift in differentiation direction involve the astrogenesis promoting Sirt1 via an increased NAD/NADH ratio in ogg1(-/-) cells.	NAD	132-136	sirtuin 1	Mus musculus	105-110
31944172-11	2020	This study shows that sustained high autophagic flux by RUBCN deficiency in PTECs leads to metabolic syndrome concomitantly with an accelerated mobilization of phospholipids from cellular membranes to lysosomes.Abbreviations: ABC: ATP binding cassette; ACADM: acyl-CoA dehydrogenase medium chain; ACTB: actin, beta; ATG: autophagy related; AUC: area under the curve; Baf: bafilomycin A1; BAT: brown adipose tissue; BODIPY: boron-dipyrromethene; BSA: bovine serum albumin; BW: body weight; CAT: chloramphenicol acetyltransferase; CM: complete medium; CPT1A: carnitine palmitoyltransferase 1a, liver; CQ: chloroquine; CTRL: control; EGFP: enhanced green fluorescent protein; CTSD: cathepsin D; EAT: epididymal adipose tissue; EGFR: epidermal growth factor receptor; EIF4EBP1: eukaryotic translation initiation factor 4E binding protein 1; FA: fatty acid; FBS: fetal bovine serum; GTT: glucose tolerance test; HE: hematoxylin and eosin; HFD: high-fat diet; I/R: ischemia-reperfusion; ITT: insulin tolerance test; KAP: kidney androgen regulated protein; KO: knockout; LAMP1: lysosomal associated membrane protein 1; LD: lipid droplet; LRP2: low density lipoprotein receptor related protein 2; MAP1LC3B: microtubule associated protein 1 light chain 3 beta; MAT: mesenteric adipose tissue; MS: mass spectrometry; MTOR: mechanistic target of rapamycin kinase; MTORC1: MTOR complex 1; NDRG1: N-myc downstream regulated 1; NDUFB5: NADH:ubiquinone oxidoreductase subunit B5; NEFA: non-esterified fatty acid; OA: oleic acid; OCT: optimal cutting temperature; ORO: Oil Red O; PAS: Periodic-acid Schiff; PFA: paraformaldehyde; PIK3C3: phosphatidylinositol 3-kinase catalytic subunit type 3; PPARA: peroxisome proliferator activated receptor alpha; PPARGC1A: PPARG coactivator 1 alpha; PTEC: proximal tubular epithelial cell; RAB7A: RAB7A, member RAS oncogene family; RPS6: ribosomal protein S6; RPS6KB1: ribosomal protein S6 kinase B1; RT: reverse transcription; RUBCN: rubicon autophagy regulator; SAT: subcutaneous adipose tissue; SFC: supercritical fluid chromatography; SQSTM1: sequestosome 1; SREBF1: sterol regulatory element binding transcription factor 1; SV-40: simian virus-40; TFEB: transcription factor EB; TG: triglyceride; TS: tissue specific; TUNEL: terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling; UN: urea nitrogen; UQCRB: ubiquinol-cytochrome c reductase binding protein; UVRAG: UV radiation resistance associated; VPS: vacuolar protein sorting; WAT: white adipose tissue.	NAD	1422-1426	RUN domain and cysteine-rich domain containing, Beclin 1-interacting protein	Mus musculus	56-61
21416227-9	2011	Inhibition of PARP significantly increased the levels of ATP and NAD+, phosphorylation of Akt, and Bcl-2/Bax ratio, and significantly reduced the activation of caspase 3.	NAD	65-69	poly (ADP-ribose) polymerase 1	Rattus norvegicus	14-18
21478153-1	2011	CD157, a member of the CD38 gene family, is an NAD-metabolizing ectoenzyme and a signaling molecule whose role in polarization, migration, and diapedesis of human granulocytes has been documented; however, the molecular events underpinning this role remain to be elucidated.	NAD	47-50	CD38 molecule	Homo sapiens	23-27
21499261-3	2011	Here we report that the NAD(+)-dependent deacetylase SIRT1 acts as an intrinsic negative modulator of Notch signalling in endothelial cells.	NAD	24-30	sirtuin 1	Mus musculus	53-58
21531334-5	2011	Consequently, there is a marked decrease in NADH/NAD(+), oxidative phosphorylation, and ATP levels, which results in AMPK activation, p27(kip1) phosphorylation, and autophagy.	NAD	44-48	cyclin dependent kinase inhibitor 1B	Homo sapiens	138-142
21531334-5	2011	Consequently, there is a marked decrease in NADH/NAD(+), oxidative phosphorylation, and ATP levels, which results in AMPK activation, p27(kip1) phosphorylation, and autophagy.	NAD	49-55	cyclin dependent kinase inhibitor 1B	Homo sapiens	138-142
21333409-6	2011	Furthermore, the ligand-binding site (LBS) volume was calculated to be 845 A(3), which suggests that the LBS of 11betaHSD2 is sufficiently large to contain cofactors and substrates (ligands), such as NAD(+) and cortisol.	NAD	200-206	hydroxysteroid 11-beta dehydrogenase 2	Homo sapiens	112-122
21401809-5	2011	Furthermore, we show that in the absence of other proteins Hst3 and Hst4 can deacetylate nucleosomal histone H3-K56 in a nicotinamide adenine dinucleotide(NAD)(+) -dependent manner.	NAD	121-154	NAD-dependent histone deacetylase HST3	Saccharomyces cerevisiae S288C	59-63
21401809-5	2011	Furthermore, we show that in the absence of other proteins Hst3 and Hst4 can deacetylate nucleosomal histone H3-K56 in a nicotinamide adenine dinucleotide(NAD)(+) -dependent manner.	NAD	155-158	NAD-dependent histone deacetylase HST3	Saccharomyces cerevisiae S288C	59-63
21245135-10	2011	We conclude that TLR4 stimulation and human sepsis activate pathways that couple NAD(+) and its sensor SIRT1 with epigenetic reprogramming.	NAD	81-87	toll like receptor 4	Homo sapiens	17-21
21166653-7	2011	Activity of ALDH3H1 was NAD+-dependent, whereas ALDH3I1 was able to use NAD+ and NADP+.	NAD	24-28	aldehyde dehydrogenase 3H1	Arabidopsis thaliana	12-19
21166653-7	2011	Activity of ALDH3H1 was NAD+-dependent, whereas ALDH3I1 was able to use NAD+ and NADP+.	NAD	72-76	aldehyde dehydrogenase 3H1	Arabidopsis thaliana	12-19
21166653-8	2011	An unusual isoleucine residue within the coenzyme-binding cleft was responsible for the NAD+-dependence of ALDH3H1.	NAD	88-92	aldehyde dehydrogenase 3H1	Arabidopsis thaliana	107-114
32594513-1	2020	Nicotinamide adenine dinucleotide (NAD+ ) is an essential metabolite in energy metabolism as well as a co-substrate in biochemical reactions such as protein deacylation, protein ADP-ribosylation, and cyclic ADP-ribose synthesis mediated by sirtuins, poly ADP-ribose polymerases (PARPs), and CD38.	NAD	0-33	CD38 molecule	Homo sapiens	291-295
21349442-11	2011	: The specific inhibition of Abeta generation by SIRT1 coupled with the potential link between aerobic glycolysis, NAD(+) depletion, and amyloidogenesis through the sirtuin pathway has translational implications.	NAD	115-121	sirtuin 1	Mus musculus	49-54
32594513-1	2020	Nicotinamide adenine dinucleotide (NAD+ ) is an essential metabolite in energy metabolism as well as a co-substrate in biochemical reactions such as protein deacylation, protein ADP-ribosylation, and cyclic ADP-ribose synthesis mediated by sirtuins, poly ADP-ribose polymerases (PARPs), and CD38.	NAD	35-39	CD38 molecule	Homo sapiens	291-295
32526680-7	2020	Quantitative acetyl-proteomics and cardiac metabolomics analysis revealed that loss of Sirt3 led to hyper-acetylation of critical enzymes within cardiac tricarboxylic acid (TCA) cycle and generation of lactate and NADH, subsequently promotion of cardiac dysfunction after sepsis.	NAD	214-218	sirtuin 3	Mus musculus	87-92
20823277-11	2011	Inhibition of nicotinamide phosphoribosyltransferase (Nampt, an important enzyme which regulates SIRT1 activity by maintaining availability of the substrate NAD(+)) also blocked both IPC-induced deacetylation and cardioprotection.	NAD	157-164	sirtuin 1	Mus musculus	97-102
20823277-13	2011	Inhibition of SIRT1, either directly or by restricting the availability of its substrate NAD(+), inhibits IPC.	NAD	89-95	sirtuin 1	Mus musculus	14-19
32831651-16	2020	Expression of p33ING1b was found to be inversely correlated to the NAD-dependent deacetylase silent information regulator 2 (SIR2).	NAD	67-70	inhibitor of growth family member 1	Homo sapiens	14-22
21131518-8	2011	Consistently, cytosolic relocalization of the native Mae1p, which can use both NADH and NADPH, in a pyc1,2Delta pdc2Delta strain grown under a CO(2) atmosphere, also enabled slow-growth on glucose.	NAD	79-83	malate dehydrogenase (oxaloacetate-decarboxylating)	Saccharomyces cerevisiae S288C	53-58
32831651-16	2020	Expression of p33ING1b was found to be inversely correlated to the NAD-dependent deacetylase silent information regulator 2 (SIR2).	NAD	67-70	sirtuin 2	Homo sapiens	93-123
32831651-16	2020	Expression of p33ING1b was found to be inversely correlated to the NAD-dependent deacetylase silent information regulator 2 (SIR2).	NAD	67-70	sirtuin 2	Homo sapiens	125-129
32389638-8	2020	Surprisingly, intracellular NAD concentration increased in HAEC stimulated by IL1beta or TNFalpha and this effect was associated with upregulation of NAMPT and CD73, whereas changes in CD38 expression were less pronounced.	NAD	28-31	interleukin 1 alpha	Mus musculus	78-85
20736960-4	2011	Tissue P(2) measurements, obtained simultaneously with NADH imaging in area CA1 in hippocampal slices, reveal that during prolonged train stimulation (ST) in 95% O(2), a persistent NADH oxidation is coupled with increased metabolic demand and oxygen utilization, for the duration of the stimulation.	NAD	55-59	carbonic anhydrase 1	Rattus norvegicus	76-79
20736960-4	2011	Tissue P(2) measurements, obtained simultaneously with NADH imaging in area CA1 in hippocampal slices, reveal that during prolonged train stimulation (ST) in 95% O(2), a persistent NADH oxidation is coupled with increased metabolic demand and oxygen utilization, for the duration of the stimulation.	NAD	181-185	carbonic anhydrase 1	Rattus norvegicus	76-79
32389638-8	2020	Surprisingly, intracellular NAD concentration increased in HAEC stimulated by IL1beta or TNFalpha and this effect was associated with upregulation of NAMPT and CD73, whereas changes in CD38 expression were less pronounced.	NAD	28-31	5' nucleotidase, ecto	Mus musculus	160-164
32389638-9	2020	NMN and NR further increased NAD in IL1beta-stimulated HAECs and AOPCP diminished NMN-induced increase in NAD, without an effect on NR-induced response.	NAD	29-32	interleukin 1 alpha	Mus musculus	36-43
32389638-14	2020	Extracellular conversion of NMN to NR by CD73 localized in the luminal surface of endothelial cells represent important vasoprotective mechanisms to maintain intracellular NAD.	NAD	172-175	5' nucleotidase, ecto	Mus musculus	41-45
32535108-9	2020	Interestingly, these enzymes are synergistically modulated by CD38, an NAD-consuming NAD-glycohydrolase.	NAD	71-74	CD38 molecule	Homo sapiens	62-66
21170645-4	2011	In fungi, the IDO homologue is thought to be expressed constitutively and supply NAD(+), as TDO is absent from their genomes.	NAD	81-87	indoleamine 2,3-dioxygenase 1	Homo sapiens	14-17
32697192-2	2020	Here, we show that Mtb upregulates one of the key epigenetic modulators, NAD+ dependent histone deacetylase Sirtuin 2 (SIRT2), which upon infection translocate to the nucleus and deacetylates histone H3K18, thus modulating the host transcriptome leading to enhanced macrophage activation.	NAD	73-76	sirtuin 2	Mus musculus	119-124
21461238-4	2011	CCL2 release by NAD(+) and NADP(+) was inhibited by a concentration dependent manner by suramin, an antagonist of P2-purinergic receptors.	NAD	16-22	C-C motif chemokine ligand 2	Homo sapiens	0-4
21461238-6	2011	NAD(+)- and NADP(+)-mediated CCL2 release was significantly attenuated by SP6001250, U0126, LY294002, Akt inhibitor IV, RO318220, GF109203X, and diphenyleneiodium chloride.	NAD	0-6	C-C motif chemokine ligand 2	Homo sapiens	29-33
32709019-3	2020	CD38, a major mammalian NAD+ glycohydrolase (NADase), expresses on T cells following activation and appears to be an essential modulator of intracellular NAD+ levels.	NAD	24-28	CD38 molecule	Homo sapiens	0-4
21785227-6	2011	TRPM channels (TRPM2, TRPM4 and TRPM5) control insulin secretion levels by sensing intracellular Ca2+ increase, NAD metabolites, or hormone receptor activation.	NAD	112-115	transient receptor potential cation channel subfamily M member 4	Homo sapiens	22-27
32709019-4	2020	The enzymatic activity of CD38 in the process of generating the second messenger cADPR utilizes intracellular NAD+, and thus limits its availability to different NAD+ consuming enzymes (PARP, ART, and sirtuins) inside the cells.	NAD	110-114	CD38 molecule	Homo sapiens	26-30
21750730-9	2011	In addition, we showed that SIRT1 was required for both exogenous NAD and Wld(S)-mediated cellular protection against paraquat.	NAD	66-69	sirtuin 1	Mus musculus	28-33
32709019-4	2020	The enzymatic activity of CD38 in the process of generating the second messenger cADPR utilizes intracellular NAD+, and thus limits its availability to different NAD+ consuming enzymes (PARP, ART, and sirtuins) inside the cells.	NAD	162-166	CD38 molecule	Homo sapiens	26-30
32709019-5	2020	The present review discusses how the CD38-NAD+ axis affects T cell activation and differentiation through interfering with their signaling and metabolic processes.	NAD	42-46	CD38 molecule	Homo sapiens	37-41
32709019-6	2020	We also describe the pivotal role of the CD38-NAD+ axis in influencing the chromatin remodeling and rewiring T cell response.	NAD	46-50	CD38 molecule	Homo sapiens	41-45
32709019-7	2020	Overall, this review emphasizes the crucial contribution of the CD38-NAD+ axis in altering T cell response in various pathophysiological conditions.	NAD	69-73	CD38 molecule	Homo sapiens	64-68
21655185-9	2011	Moreover, MDH1, the target of several deregulated microRNAs, is repressed in glioblastomas, making an intramitochondrial-NAD reduction mediated by the mitochondrial aspartate-malate shuttle unlikely.	NAD	121-124	malate dehydrogenase 1	Homo sapiens	10-14
33040724-10	2020	Simultaneously, the activities of NAD+-dependent IDH, mitochondrial aspartate aminotransferase, and two malate dehydrogenase isoenzymes, whose genes were not predicted to have the p53-binding sequences near the transcription starting points, were upregulated by cisplatin.	NAD	34-37	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	49-52
21212461-3	2010	Here we report that the NAD+-dependent deacetylase SIRT3 deacetylates the regulatory component of the mPTP, cyclophilin D (CypD) on lysine 166, adjacent to the binding site of cyclosporine A, a CypD inhibitor.	NAD	24-28	sirtuin 3	Mus musculus	51-56
32527005-4	2020	Methods and Results: Both the amount and activity of mitochondrial Complex I (nicotinamide adenine dinucleotide -reduced form, NADH, dehydrogenase) were upregulated in HCM vs. CTRL, whilst the activity of Complex V (ATP synthase) was not reduced and ATP levels were significantly higher in HCM vs. CTRL.	NAD	78-111	chymotrypsin like	Homo sapiens	176-180
20477789-1	2010	NAMPT encodes an enzyme catalysing the rate-limiting step in NAD biosynthesis.	NAD	61-64	nicotinamide phosphoribosyltransferase	Sus scrofa	0-5
20697932-0	2010	The simultaneous determination of NAD(H) and NADP(H) utilization by glutamate dehydrogenase.	NAD	34-40	glutamate dehydrogenase 1	Homo sapiens	68-91
20697932-1	2010	Glutamate dehydrogenase (GDH) from vertebrates is unusual among NAD(P)H-dependent dehydrogenases in that it can use either NAD(H) or NADP(H) as cofactor.	NAD	123-129	glutamate dehydrogenase 1	Homo sapiens	0-23
20697932-1	2010	Glutamate dehydrogenase (GDH) from vertebrates is unusual among NAD(P)H-dependent dehydrogenases in that it can use either NAD(H) or NADP(H) as cofactor.	NAD	123-129	glutamate dehydrogenase 1	Homo sapiens	25-28
20697932-3	2010	Methods for both reaction directions were developed, and for the first time, to our knowledge, the GDH activity has been simultaneously studied in the presence of both NAD(H) and NADP(H).	NAD	168-174	glutamate dehydrogenase 1	Homo sapiens	99-102
20697932-4	2010	Our data indicate that NADP(H) has inhibitory effects on the rate of NAD(H) utilization by GDH, a characteristic of GDH not previously recognized.	NAD	69-75	glutamate dehydrogenase 1	Homo sapiens	91-94
20697932-4	2010	Our data indicate that NADP(H) has inhibitory effects on the rate of NAD(H) utilization by GDH, a characteristic of GDH not previously recognized.	NAD	69-75	glutamate dehydrogenase 1	Homo sapiens	116-119
32655590-4	2020	We determined in this work that the mitochondrial AtGDH1 isozyme from A. thaliana is NAD+-specific.	NAD	85-89	glutamate dehydrogenase 1	Arabidopsis thaliana	50-56
20697932-5	2010	The response of GDH to allosteric activators in the presence of NAD(H) and NADP(H) suggests that ADP and leucine moderate much of the inhibitory effect of NADP(H) on the utilization of NAD(H).	NAD	64-70	glutamate dehydrogenase 1	Homo sapiens	16-19
20697932-5	2010	The response of GDH to allosteric activators in the presence of NAD(H) and NADP(H) suggests that ADP and leucine moderate much of the inhibitory effect of NADP(H) on the utilization of NAD(H).	NAD	185-191	glutamate dehydrogenase 1	Homo sapiens	16-19
20940411-3	2010	beta-Lap killed prostate cancer cells by NAD(P)H:quinone oxidoreductase 1 (NQO1) metabolic bioactivation, triggering a massive induction of reactive oxygen species, irreversible DNA single-strand breaks (SSB), poly(ADP-ribose) polymerase-1 (PARP-1) hyperactivation, NAD(+)/ATP depletion, and mu-calpain-induced programmed necrosis.	NAD	266-272	LAP	Homo sapiens	5-8
32655590-8	2020	We solved the crystal structure of recombinant AtGDH1 in the apo-form and in complex with NAD+ at 2.59 and 2.03 A resolution, respectively.	NAD	90-94	glutamate dehydrogenase 1	Arabidopsis thaliana	47-53
32369735-4	2020	In old mice, dampened BMAL1 chromatin binding, transcriptional oscillations, mitochondrial respiration rhythms, and late evening activity are restored by NAD+ repletion to youthful levels with NR.	NAD	154-158	aryl hydrocarbon receptor nuclear translocator-like	Mus musculus	22-27
20944228-2	2010	The crystal structure of the prephenate dehydrogenase component (HinfPDH) of the TyrA protein from H. influenzae Rd KW20 in complex with the inhibitor tyrosine and cofactor NAD(+) has been determined to 2.0 A resolution.	NAD	173-179	bifunctional chorismate mutase/prephenate dehydrogenase	Haemophilus influenzae Rd KW20	81-85
32278117-3	2020	This study aims to identify changes of specific components of NAD+/SIRTs system in white adipose tissue (WAT) and brown adipose tissue (BAT) of mice upon energy imbalance, focusing on key enzymes in NAD+ salvage (Nampt, Nmnat1, Nrk1), clearance (Nnmt, Aox1, Cyp2e1) and consumption pathways (Sirt1, Sirt2, Sirt3, Sirt6, Parp1).	NAD	62-66	cytochrome P450, family 2, subfamily e, polypeptide 1	Mus musculus	258-264
20595677-1	2010	Sirtuins (silent information regulator 2 [Sir2] proteins) belong to an ancient family of evolutionary conserved nicotinamide adenine dinucleotide (NAD)(+)-dependent enzymes with deacetylase and/or mono-ADP-ribosyltransferase activity.	NAD	112-145	sirtuin 2	Homo sapiens	10-40
32278117-3	2020	This study aims to identify changes of specific components of NAD+/SIRTs system in white adipose tissue (WAT) and brown adipose tissue (BAT) of mice upon energy imbalance, focusing on key enzymes in NAD+ salvage (Nampt, Nmnat1, Nrk1), clearance (Nnmt, Aox1, Cyp2e1) and consumption pathways (Sirt1, Sirt2, Sirt3, Sirt6, Parp1).	NAD	62-66	sirtuin 1	Mus musculus	292-297
20595677-1	2010	Sirtuins (silent information regulator 2 [Sir2] proteins) belong to an ancient family of evolutionary conserved nicotinamide adenine dinucleotide (NAD)(+)-dependent enzymes with deacetylase and/or mono-ADP-ribosyltransferase activity.	NAD	112-145	sirtuin 2	Homo sapiens	42-46
20595677-1	2010	Sirtuins (silent information regulator 2 [Sir2] proteins) belong to an ancient family of evolutionary conserved nicotinamide adenine dinucleotide (NAD)(+)-dependent enzymes with deacetylase and/or mono-ADP-ribosyltransferase activity.	NAD	147-154	sirtuin 2	Homo sapiens	10-40
32278117-3	2020	This study aims to identify changes of specific components of NAD+/SIRTs system in white adipose tissue (WAT) and brown adipose tissue (BAT) of mice upon energy imbalance, focusing on key enzymes in NAD+ salvage (Nampt, Nmnat1, Nrk1), clearance (Nnmt, Aox1, Cyp2e1) and consumption pathways (Sirt1, Sirt2, Sirt3, Sirt6, Parp1).	NAD	62-66	sirtuin 2	Mus musculus	299-304
20595677-1	2010	Sirtuins (silent information regulator 2 [Sir2] proteins) belong to an ancient family of evolutionary conserved nicotinamide adenine dinucleotide (NAD)(+)-dependent enzymes with deacetylase and/or mono-ADP-ribosyltransferase activity.	NAD	147-154	sirtuin 2	Homo sapiens	42-46
32278117-3	2020	This study aims to identify changes of specific components of NAD+/SIRTs system in white adipose tissue (WAT) and brown adipose tissue (BAT) of mice upon energy imbalance, focusing on key enzymes in NAD+ salvage (Nampt, Nmnat1, Nrk1), clearance (Nnmt, Aox1, Cyp2e1) and consumption pathways (Sirt1, Sirt2, Sirt3, Sirt6, Parp1).	NAD	62-66	sirtuin 3	Mus musculus	306-311
20528775-1	2010	The Arabidopsis thaliana genome contains two genes encoding NAD-MEs [NAD-dependent malic enzymes; NAD-ME1 (TAIR accession number At4G13560) and NAD-ME2 (TAIR accession number At4G00570)].	NAD	60-63	NAD-dependent malic enzyme 1	Arabidopsis thaliana	98-105
32278117-3	2020	This study aims to identify changes of specific components of NAD+/SIRTs system in white adipose tissue (WAT) and brown adipose tissue (BAT) of mice upon energy imbalance, focusing on key enzymes in NAD+ salvage (Nampt, Nmnat1, Nrk1), clearance (Nnmt, Aox1, Cyp2e1) and consumption pathways (Sirt1, Sirt2, Sirt3, Sirt6, Parp1).	NAD	199-203	cytochrome P450, family 2, subfamily e, polypeptide 1	Mus musculus	258-264
20528775-10	2010	The different kinetic mechanism of each NAD-ME entity suggests that, for a metabolic condition in which the mitochondrial NAD level is low and the L-malate level is high, the activity of NAD-ME2 and/or -MEH would be preferred over that of NAD-ME1.	NAD	40-43	NAD-dependent malic enzyme 1	Arabidopsis thaliana	239-246
32278117-3	2020	This study aims to identify changes of specific components of NAD+/SIRTs system in white adipose tissue (WAT) and brown adipose tissue (BAT) of mice upon energy imbalance, focusing on key enzymes in NAD+ salvage (Nampt, Nmnat1, Nrk1), clearance (Nnmt, Aox1, Cyp2e1) and consumption pathways (Sirt1, Sirt2, Sirt3, Sirt6, Parp1).	NAD	199-203	sirtuin 1	Mus musculus	292-297
32278117-3	2020	This study aims to identify changes of specific components of NAD+/SIRTs system in white adipose tissue (WAT) and brown adipose tissue (BAT) of mice upon energy imbalance, focusing on key enzymes in NAD+ salvage (Nampt, Nmnat1, Nrk1), clearance (Nnmt, Aox1, Cyp2e1) and consumption pathways (Sirt1, Sirt2, Sirt3, Sirt6, Parp1).	NAD	199-203	sirtuin 2	Mus musculus	299-304
32278117-3	2020	This study aims to identify changes of specific components of NAD+/SIRTs system in white adipose tissue (WAT) and brown adipose tissue (BAT) of mice upon energy imbalance, focusing on key enzymes in NAD+ salvage (Nampt, Nmnat1, Nrk1), clearance (Nnmt, Aox1, Cyp2e1) and consumption pathways (Sirt1, Sirt2, Sirt3, Sirt6, Parp1).	NAD	199-203	sirtuin 3	Mus musculus	306-311
20558724-0	2010	Localization and function of the membrane-bound riboflavin in the Na+-translocating NADH:quinone oxidoreductase (Na+-NQR) from Vibrio cholerae.	NAD	84-88	crystallin zeta	Homo sapiens	89-111
32428157-3	2020	Among them, the nicotinamide adenine dinucleotide phosphate-oxidase (NADPH) oxidase (NOX5) enzymes have been explored.	NAD	16-49	NADPH oxidase 5	Homo sapiens	85-89
20558724-1	2010	The sodium ion-translocating NADH:quinone oxidoreductase (Na(+)-NQR) from the human pathogen Vibrio cholerae is a respiratory membrane protein complex that couples the oxidation of NADH to the transport of Na(+) across the bacterial membrane.	NAD	29-33	crystallin zeta	Homo sapiens	34-56
20558724-1	2010	The sodium ion-translocating NADH:quinone oxidoreductase (Na(+)-NQR) from the human pathogen Vibrio cholerae is a respiratory membrane protein complex that couples the oxidation of NADH to the transport of Na(+) across the bacterial membrane.	NAD	181-185	crystallin zeta	Homo sapiens	34-56
20566368-12	2010	Furthermore, these data suggest that Nrk2b-mediated synthesis of NAD+ is functionally upstream of Laminin adhesion and Paxillin subcellular localization during MTJ development.	NAD	65-69	paxillin	Homo sapiens	119-127
32426286-0	2020	Sirtuin 1 Inhibiting Thiocyanates (S1th)-A New Class of Isotype Selective Inhibitors of NAD+ Dependent Lysine Deacetylases.	NAD	88-91	sirtuin 1	Mus musculus	0-9
32426286-1	2020	Sirtuin 1 (Sirt1) is a NAD+ dependent lysine deacetylase associated with the pathogenesis of various diseases including cancer.	NAD	23-26	sirtuin 1	Mus musculus	0-9
32426286-1	2020	Sirtuin 1 (Sirt1) is a NAD+ dependent lysine deacetylase associated with the pathogenesis of various diseases including cancer.	NAD	23-26	sirtuin 1	Mus musculus	11-16
31692222-1	2020	We have discovered the sirtuin rearranging ligands (SirReals) as highly potent and selective inhibitors of the NAD+-dependent lysine deacetylase Sirt2.	NAD	111-114	sirtuin 2	Homo sapiens	145-150
32250733-6	2020	Our work uncovers a dedicated chaperone of pTau and suggests NMNAT as a key node between NAD+ metabolism and Tau homeostasis in aging and neurodegeneration.	NAD	89-93	Nicotinamide mononucleotide adenylyltransferase	Drosophila melanogaster	61-66
20655472-3	2010	Here we show that production of beta-amyloid and plaques in a mouse model of AD are reduced by overexpressing the NAD-dependent deacetylase SIRT1 in brain, and are increased by knocking out SIRT1 in brain.	NAD	114-117	sirtuin 1	Mus musculus	140-145
20620997-3	2010	Here we show that lack of nicotinamide adenine dinucleotide (NAD(+))-dependent deacetylase SIRT1 in pro-opiomelanocortin (POMC) neurons causes hypersensitivity to diet-induced obesity due to reduced energy expenditure.	NAD	26-59	sirtuin 1	Mus musculus	91-96
20620997-3	2010	Here we show that lack of nicotinamide adenine dinucleotide (NAD(+))-dependent deacetylase SIRT1 in pro-opiomelanocortin (POMC) neurons causes hypersensitivity to diet-induced obesity due to reduced energy expenditure.	NAD	61-68	sirtuin 1	Mus musculus	91-96
20634564-2	2010	SIRT1 expression is regulated transcriptionally and post-transcriptionally, and its enzymatic activity is controlled by NAD+ levels and interacting proteins.	NAD	120-124	sirtuin 1	Mus musculus	0-5
20132901-9	2010	Using biotinylated NAD+ it was revealed that PARP activity was present ipsilateral to the KA injection site, and labeling was blocked by incubation with excess unlabeled NAD+ or PARP inhibitors.	NAD	19-23	poly (ADP-ribose) polymerase 1	Rattus norvegicus	45-49
20132901-9	2010	Using biotinylated NAD+ it was revealed that PARP activity was present ipsilateral to the KA injection site, and labeling was blocked by incubation with excess unlabeled NAD+ or PARP inhibitors.	NAD	19-23	poly (ADP-ribose) polymerase 1	Rattus norvegicus	178-182
20132901-9	2010	Using biotinylated NAD+ it was revealed that PARP activity was present ipsilateral to the KA injection site, and labeling was blocked by incubation with excess unlabeled NAD+ or PARP inhibitors.	NAD	170-174	poly (ADP-ribose) polymerase 1	Rattus norvegicus	45-49
20139070-1	2010	Sirt1, a NAD-dependent protein deacetylase, is reported to regulate intracellular metabolism and attenuate reactive oxidative species (ROS)-induced apoptosis leading to longevity and acute stress resistance.	NAD	9-12	sirtuin 1	Mus musculus	0-5
20975668-5	2010	SCO2-/- cells have increased intracellular oxygen and nicotinamide adenine dinucleotide (NADH) levels, which result in increased ROS and oxidative DNA damage.	NAD	54-87	synthesis of cytochrome C oxidase 2	Homo sapiens	0-4
20975668-5	2010	SCO2-/- cells have increased intracellular oxygen and nicotinamide adenine dinucleotide (NADH) levels, which result in increased ROS and oxidative DNA damage.	NAD	89-93	synthesis of cytochrome C oxidase 2	Homo sapiens	0-4
20054824-2	2010	Recently, beta-NAD was identified as an agonist for P2Y1 and P2Y11 purinergic receptors.	NAD	10-18	purinergic receptor P2Y1	Homo sapiens	52-56
20054824-2	2010	Recently, beta-NAD was identified as an agonist for P2Y1 and P2Y11 purinergic receptors.	NAD	10-18	purinergic receptor P2Y11	Homo sapiens	61-66
20335657-3	2010	Here, we investigated in mice the mechanisms underlying CR-mediated protection against hypoxia in aged kidney, with a special focus on the role of the NAD-dependent deacetylase sirtuin 1 (Sirt1), which is linked to CR-related longevity in model organisms, on mitochondrial autophagy.	NAD	151-154	sirtuin 1	Mus musculus	188-193
32209328-0	2020	Modulation of the cardiac sodium channel NaV1.5 peak and late currents by NAD+ precursors.	NAD	74-78	sodium voltage-gated channel alpha subunit 5	Homo sapiens	41-47
32209328-4	2020	In addition, NAD+-dependent deacetylation of NaV1.5 at K1479 by Sirtuin 1 increases NaV1.5 membrane trafficking and INa.	NAD	13-17	sodium voltage-gated channel alpha subunit 5	Homo sapiens	45-51
20093281-7	2010	SIRT1 was increased through an AMP-activated protein kinase-mediated increase in gene expression of nicotinamide phosphoribosyltransferase, the rate-limiting enzyme of the salvage pathway for NAD(+).	NAD	192-198	sirtuin 1	Mus musculus	0-5
32209328-4	2020	In addition, NAD+-dependent deacetylation of NaV1.5 at K1479 by Sirtuin 1 increases NaV1.5 membrane trafficking and INa.	NAD	13-17	sodium voltage-gated channel alpha subunit 5	Homo sapiens	84-90
32280711-1	2020	Objective: To explore the effects of N1-methylnicotinamide (MNAM) on insulin resistance and glucose metabolism in obese type 2 diabetes mellitus (T2DM) mice and regulatory mechanisms of the NAD-dependent deacetylase sirtuin-1 (SIRT1)/forkhead box protein O1 (FOXO1) pathway.	NAD	190-193	sirtuin 1	Mus musculus	227-232
20042612-3	2010	Ribosome-associated SIRT3 was found to be responsible for deacetylation of MRPL10 in an NAD(+)-dependent manner.	NAD	88-94	sirtuin 3	Mus musculus	20-25
32280711-1	2020	Objective: To explore the effects of N1-methylnicotinamide (MNAM) on insulin resistance and glucose metabolism in obese type 2 diabetes mellitus (T2DM) mice and regulatory mechanisms of the NAD-dependent deacetylase sirtuin-1 (SIRT1)/forkhead box protein O1 (FOXO1) pathway.	NAD	190-193	forkhead box O1	Mus musculus	234-257
32280711-1	2020	Objective: To explore the effects of N1-methylnicotinamide (MNAM) on insulin resistance and glucose metabolism in obese type 2 diabetes mellitus (T2DM) mice and regulatory mechanisms of the NAD-dependent deacetylase sirtuin-1 (SIRT1)/forkhead box protein O1 (FOXO1) pathway.	NAD	190-193	forkhead box O1	Mus musculus	259-264
32032542-3	2020	Here, we show that NLRP3, a pattern recognition receptor, is modified by acetylation in macrophages and is deacetylated by SIRT2, an NAD+-dependent deacetylase and a metabolic sensor.	NAD	133-136	NLR family, pyrin domain containing 3	Mus musculus	19-24
32032542-3	2020	Here, we show that NLRP3, a pattern recognition receptor, is modified by acetylation in macrophages and is deacetylated by SIRT2, an NAD+-dependent deacetylase and a metabolic sensor.	NAD	133-136	sirtuin 2	Mus musculus	123-128
31987812-7	2020	The mitochondrial uncoupling effects of embelin leading to increased NAD/NADH levels followed by enhanced SIRT1, PGC1alpha and mitochondrial biogenesis were found to confer embelin mediated protection as treatment of cells with SIRT1 inhibitor or siRNA nullified this effect.	NAD	73-77	sirtuin 1	Mus musculus	228-233
31837320-0	2020	NAD+ precursor modulates post-ischemic mitochondrial fragmentation and reactive oxygen species generation via SIRT3 dependent mechanisms.	NAD	0-4	sirtuin 3	Mus musculus	110-115
32003501-6	2020	Our data show that the NAD+ -dependent deacetylase silent information regulator 1 (Sirt1) mediates Res-induced browning and fat reduction of adipocytes, as well as other Res-improved metabolic phenotypes including hyperglycemina and hyperlipidemia in mice.	NAD	23-26	sirtuin 1	Mus musculus	51-81
32003501-6	2020	Our data show that the NAD+ -dependent deacetylase silent information regulator 1 (Sirt1) mediates Res-induced browning and fat reduction of adipocytes, as well as other Res-improved metabolic phenotypes including hyperglycemina and hyperlipidemia in mice.	NAD	23-26	sirtuin 1	Mus musculus	83-88
32081881-9	2020	In parallel, laminar flow led to the increased expression of SIRT1 protein, a NAD+-dependent deacetylase.	NAD	78-81	sirtuin 1	Mus musculus	61-66
32059481-16	2020	Consistently, the inhibition of both PARP-1 and SIRT-1 increased the NAD+/NADH-ratio in BAFs.	NAD	69-72	sirtuin 1	Mus musculus	48-54
32059481-16	2020	Consistently, the inhibition of both PARP-1 and SIRT-1 increased the NAD+/NADH-ratio in BAFs.	NAD	74-78	sirtuin 1	Mus musculus	48-54
32059481-17	2020	This suggests that cellular NAD+/NADH ratios control the complex interactions of PARP-1, H1 and SIRT-1 and regulate the interplay of parylation and acetylation/de-acetylation events with low NAD+/NADH ratios (reverse Warburg effect), promoting PARP-1 activation and estrogen synthesis in BAFs.	NAD	28-31	sirtuin 1	Mus musculus	96-102
32059481-17	2020	This suggests that cellular NAD+/NADH ratios control the complex interactions of PARP-1, H1 and SIRT-1 and regulate the interplay of parylation and acetylation/de-acetylation events with low NAD+/NADH ratios (reverse Warburg effect), promoting PARP-1 activation and estrogen synthesis in BAFs.	NAD	33-37	sirtuin 1	Mus musculus	96-102
32059481-17	2020	This suggests that cellular NAD+/NADH ratios control the complex interactions of PARP-1, H1 and SIRT-1 and regulate the interplay of parylation and acetylation/de-acetylation events with low NAD+/NADH ratios (reverse Warburg effect), promoting PARP-1 activation and estrogen synthesis in BAFs.	NAD	33-36	sirtuin 1	Mus musculus	96-102
32059481-17	2020	This suggests that cellular NAD+/NADH ratios control the complex interactions of PARP-1, H1 and SIRT-1 and regulate the interplay of parylation and acetylation/de-acetylation events with low NAD+/NADH ratios (reverse Warburg effect), promoting PARP-1 activation and estrogen synthesis in BAFs.	NAD	196-200	sirtuin 1	Mus musculus	96-102
32049001-3	2020	Treatment with the NAD+ metabolic precursor nicotinamide mononucleotide (NMN) rejuvenates oocyte quality in aged animals, leading to restoration in fertility, and this can be recapitulated by transgenic overexpression of the NAD+-dependent deacylase SIRT2, though deletion of this enzyme does not impair oocyte quality.	NAD	19-22	sirtuin 2	Homo sapiens	250-255
32049001-3	2020	Treatment with the NAD+ metabolic precursor nicotinamide mononucleotide (NMN) rejuvenates oocyte quality in aged animals, leading to restoration in fertility, and this can be recapitulated by transgenic overexpression of the NAD+-dependent deacylase SIRT2, though deletion of this enzyme does not impair oocyte quality.	NAD	225-228	sirtuin 2	Homo sapiens	250-255
32046066-3	2020	It has been shown that TRPM2 cation channels and CD38, a type II or type III transmembrane protein with ADP-ribosyl cyclase activity, simultaneously play a role in heat-sensitive and NAD+ metabolite-dependent intracellular free Ca2+ concentration increases in hypothalamic oxytocinergic neurons.	NAD	183-186	CD38 molecule	Homo sapiens	49-53
31952989-0	2020	Aifm2, a NADH Oxidase, Supports Robust Glycolysis and Is Required for Cold- and Diet-Induced Thermogenesis.	NAD	9-13	apoptosis inducing factor mitochondria associated 2	Homo sapiens	0-5
31952989-6	2020	As a unique BAT-specific first mammalian NDE (external NADH dehydrogenase)-like enzyme, Aifm2 oxidizes NADH to maintain high cytosolic NAD levels in supporting robust glycolysis and to transfer electrons to the electron transport chain (ETC) for fueling thermogenesis.	NAD	55-59	apoptosis inducing factor mitochondria associated 2	Homo sapiens	88-93
31952989-6	2020	As a unique BAT-specific first mammalian NDE (external NADH dehydrogenase)-like enzyme, Aifm2 oxidizes NADH to maintain high cytosolic NAD levels in supporting robust glycolysis and to transfer electrons to the electron transport chain (ETC) for fueling thermogenesis.	NAD	103-107	apoptosis inducing factor mitochondria associated 2	Homo sapiens	88-93
31952989-6	2020	As a unique BAT-specific first mammalian NDE (external NADH dehydrogenase)-like enzyme, Aifm2 oxidizes NADH to maintain high cytosolic NAD levels in supporting robust glycolysis and to transfer electrons to the electron transport chain (ETC) for fueling thermogenesis.	NAD	55-58	apoptosis inducing factor mitochondria associated 2	Homo sapiens	88-93
32110174-10	2020	Moreover, PSPC activated Sirt1 by boosting NAD+ level in HFD-treated mouse livers.	NAD	43-47	sirtuin 1	Mus musculus	25-30
31816398-6	2020	Mitochondrial content and membrane potential were significantly reduced in response to H2O2 treatment, whereas activated NRF2-PPARalpha/AMPKalpha pathway by NAMPT overexpression rescued the mitochondrial membrane potential and content, suggesting that maintained mitochondrial content and integrity by NAMPT overexpression might be one of the key mechanisms to maintain mitochondrial NAD+ level and subsequently dictate cell survival under oxidative stress.	NAD	384-387	peroxisome proliferator activated receptor alpha	Homo sapiens	126-135
31241768-8	2020	These data show that SCD1 is involved in nucleotide (ATP and NAD+ ) metabolism and suggest that the SCD1-dependent regulation of muscle steatosis and insulin sensitivity are mediated by cooperation between AMPK- and SIRT1-regulated pathways.	NAD	61-65	sirtuin 1	Mus musculus	216-221
31995750-3	2020	During the onset of acute inflammation, CD38 levels are increased, leading to the production of Ca2+-signaling messengers, nicotinic acid adenine dinucleotide phosphate (NAADP), ADP ribose (ADPR), and cyclic ADPR (cADPR) from NAD(P)+.	NAD	226-233	CD38 molecule	Homo sapiens	40-44
31618623-2	2020	Recent accumulating evidences suggest that Sirtuin 1 (SIRT1), an NAD+-dependent deacetylase, plays a key role in mood regulation, yet its role in the polarization of microglia acting on depressive behaviors remains unknown.	NAD	65-68	sirtuin 1	Mus musculus	43-52
31618623-2	2020	Recent accumulating evidences suggest that Sirtuin 1 (SIRT1), an NAD+-dependent deacetylase, plays a key role in mood regulation, yet its role in the polarization of microglia acting on depressive behaviors remains unknown.	NAD	65-68	sirtuin 1	Mus musculus	54-59
31777937-3	2020	Mouse DXO catalyzes the elimination of incomplete 5"-end caps (including pyrophosphate) and the non-canonical NAD+ cap on mRNAs, and possesses distributive 5"-3" exoribonuclease activity toward 5"-monophosphate (5"-PO4) RNA.	NAD	110-113	decapping exoribonuclease	Mus musculus	6-9
32922930-2	2020	Sirtuin3 (SIRT3) is a NAD+ dependent deacetylase which mainly located in mitochondria.	NAD	22-25	sirtuin 3	Mus musculus	0-8
32922930-2	2020	Sirtuin3 (SIRT3) is a NAD+ dependent deacetylase which mainly located in mitochondria.	NAD	22-25	sirtuin 3	Mus musculus	10-15
31604073-7	2020	Importantly, treatment with ER beta agonist DPN (5 nM) significantly decreased the inhibitory effect of a PTEN knockdown on tamoxifen response of both cell lines (p&lt;0.05).	NAD	44-47	phosphatase and tensin homolog	Homo sapiens	106-110
31952784-0	2020	Targeting NAD+ Synthesis to Potentiate CD38-Based Immunotherapy of Multiple Myeloma.	NAD	10-13	CD38 molecule	Homo sapiens	39-43
31952784-1	2020	Antibodies targeting CD38, a NAD+-degrading enzyme, have emerged as a promising immunotherapy against multiple myeloma (MM).	NAD	29-32	CD38 molecule	Homo sapiens	21-25
31952784-3	2020	Here, we advocate for the depletion of NAD+ to enhance the efficacy of anti-CD38-based immunotherapies in MM.	NAD	39-42	CD38 molecule	Homo sapiens	76-80
31599159-3	2019	Here, we report that ARH1, ARH3 and macrodomain proteins i.e. MacroD1, MacroD2, C6orf130 (TARG1), Af1521, hydrolyzed alpha-NAD+ but not beta-NAD+.	NAD	117-126	ADP-ribosylserine hydrolase	Homo sapiens	27-31
31804482-3	2019	Aurora-A-mediated phosphorylation of LDHB serine 162 significantly increases its activity in reducing pyruvate to lactate, which efficiently promotes NAD+ regeneration, glycolytic flux, lactate production and bio-synthesis with glycolytic intermediates.	NAD	150-153	lactate dehydrogenase B	Homo sapiens	37-41
31804482-4	2019	Mechanistically, LDHB serine 162 phosphorylation relieves its substrate inhibition effect by pyruvate, resulting in remarkable elevation in the conversions of pyruvate and NADH to lactate and NAD+.	NAD	172-176	lactate dehydrogenase B	Homo sapiens	17-21
31804482-4	2019	Mechanistically, LDHB serine 162 phosphorylation relieves its substrate inhibition effect by pyruvate, resulting in remarkable elevation in the conversions of pyruvate and NADH to lactate and NAD+.	NAD	172-175	lactate dehydrogenase B	Homo sapiens	17-21
31611261-7	2019	Mechanistically, hresistin promoted HMGB1 posttranslational lysine acetylation by preserving the NAD+-dependent deacetylase sirtuin (Sirt) 1 in human macrophages.	NAD	97-100	resistin	Homo sapiens	17-26
31702813-7	2019	Administration of NAD+ may also increase the expression of the key protein NAMPT and its related protein sirtuin 1 as well as the synthesis of NAD+.	NAD	18-22	sirtuin 1	Mus musculus	105-114
19934007-10	2010	In addition, resveratrol increased the NAD-to-NADH ratio in an AMPK-dependent manner, which may explain how resveratrol may activate Sirt1 indirectly.	NAD	39-42	sirtuin 1	Mus musculus	133-138
31610054-0	2019	Allosteric Discrimination at the NADH/ADP Regulatory Site of Glutamate Dehydrogenase.	NAD	33-37	glutamate dehydrogenase 1	Homo sapiens	61-84
19934007-10	2010	In addition, resveratrol increased the NAD-to-NADH ratio in an AMPK-dependent manner, which may explain how resveratrol may activate Sirt1 indirectly.	NAD	46-50	sirtuin 1	Mus musculus	133-138
31610054-3	2019	Our computational investigation of the NADH/ADP site presented in this paper provides insight into the opposite allosteric effects induced at a single site of binding inhibitor NADH versus activator ADP to GDH.	NAD	39-43	glutamate dehydrogenase 1	Homo sapiens	206-209
31610054-3	2019	Our computational investigation of the NADH/ADP site presented in this paper provides insight into the opposite allosteric effects induced at a single site of binding inhibitor NADH versus activator ADP to GDH.	NAD	177-181	glutamate dehydrogenase 1	Homo sapiens	206-209
20097174-1	2010	SIR2 protein, an NAD-dependent deacetylase, is localized to nucleus and is involved in life span extension by calorie restriction in yeast.	NAD	17-20	sirtuin 1	Mus musculus	0-4
31610054-5	2019	Our simulations show an interesting model of ADP with dissimilar binding conformations at each NADH/ADP site in the GDH trimer, which explains the poorly understood strong binding but weak activation shown in experimental studies.	NAD	95-99	glutamate dehydrogenase 1	Homo sapiens	116-119
19370397-0	2010	Nicotinamide adenine dinucleotide extends the lifespan of Caenorhabditis elegans mediated by sir-2.1 and daf-16.	NAD	0-33	Fork-head domain-containing protein;Forkhead box protein O	Caenorhabditis elegans	105-111
31788622-6	2019	In the absence of NAD+, this substrate is specific for HDAC11.	NAD	18-21	histone deacetylase 11	Homo sapiens	55-61
19370397-4	2010	We aimed here to elucidate the correlation between life extension in nematodes and NAD-dependent activation of sirtuin by analyzing the relationship between NAD and DAF-16.	NAD	83-86	Fork-head domain-containing protein;Forkhead box protein O	Caenorhabditis elegans	165-171
19370397-4	2010	We aimed here to elucidate the correlation between life extension in nematodes and NAD-dependent activation of sirtuin by analyzing the relationship between NAD and DAF-16.	NAD	157-160	Fork-head domain-containing protein;Forkhead box protein O	Caenorhabditis elegans	165-171
19370397-7	2010	However, life extension by NAD did not occur in daf-16-RNAi nematodes, suggesting that NAD-dependent longevity requires daf-16.	NAD	87-90	Fork-head domain-containing protein;Forkhead box protein O	Caenorhabditis elegans	120-126
19370397-9	2010	Expression of sod-3, a target gene of daf-16, and increased oxidative-stress resistance and adiposity were observed in response to NAD addition, indicating that NAD activated daf-16 in each phenotype.	NAD	131-134	Fork-head domain-containing protein;Forkhead box protein O	Caenorhabditis elegans	38-44
19370397-9	2010	Expression of sod-3, a target gene of daf-16, and increased oxidative-stress resistance and adiposity were observed in response to NAD addition, indicating that NAD activated daf-16 in each phenotype.	NAD	131-134	Fork-head domain-containing protein;Forkhead box protein O	Caenorhabditis elegans	175-181
19370397-9	2010	Expression of sod-3, a target gene of daf-16, and increased oxidative-stress resistance and adiposity were observed in response to NAD addition, indicating that NAD activated daf-16 in each phenotype.	NAD	161-164	Fork-head domain-containing protein;Forkhead box protein O	Caenorhabditis elegans	38-44
31563556-5	2019	Meanwhile, PPARalpha activation also increased significantly the expression of NADH dehydrogenase [ubiquinone] 1alpha subcomplex subunit 9 (NDUFA9, complex I) and mitochondrial cytochrome c oxidase 1 (MTCO1, complex IV).	NAD	79-83	peroxisome proliferator-activated receptor alpha	Oreochromis niloticus	11-20
19370397-9	2010	Expression of sod-3, a target gene of daf-16, and increased oxidative-stress resistance and adiposity were observed in response to NAD addition, indicating that NAD activated daf-16 in each phenotype.	NAD	161-164	Fork-head domain-containing protein;Forkhead box protein O	Caenorhabditis elegans	175-181
19941855-1	2010	2,3-butanediol dehydrogenase (BDH) catalyzes the NAD-dependent redox reaction between acetoin and 2,3-butanediol.	NAD	49-52	3-hydroxybutyrate dehydrogenase 1	Homo sapiens	0-28
19941855-1	2010	2,3-butanediol dehydrogenase (BDH) catalyzes the NAD-dependent redox reaction between acetoin and 2,3-butanediol.	NAD	49-52	3-hydroxybutyrate dehydrogenase 1	Homo sapiens	30-33
31563556-5	2019	Meanwhile, PPARalpha activation also increased significantly the expression of NADH dehydrogenase [ubiquinone] 1alpha subcomplex subunit 9 (NDUFA9, complex I) and mitochondrial cytochrome c oxidase 1 (MTCO1, complex IV).	NAD	79-83	NADH dehydrogenase [ubiquinone] 1 alpha subcomplex subunit 9, mitochondrial	Oreochromis niloticus	140-146
31604796-1	2019	Sirtuin 2 (SIRT2) is an NAD-dependent sirtuin deacetylase that regulates microtubule and chromatin dynamics, gene expression and cell cycle progression, as well as nuclear envelope reassembly.	NAD	24-27	sirtuin 2	Homo sapiens	0-9
19915031-5	2010	Consistent with earlier studies, deletion of the two genes encoding NAD-dependent glycerol-3-phosphate dehydrogenase (GPD1 and GPD2) led to elimination of glycerol production and an inability to grow anaerobically.	NAD	68-71	glycerol-3-phosphate dehydrogenase (NAD(+)) GPD2	Saccharomyces cerevisiae S288C	127-131
31604796-1	2019	Sirtuin 2 (SIRT2) is an NAD-dependent sirtuin deacetylase that regulates microtubule and chromatin dynamics, gene expression and cell cycle progression, as well as nuclear envelope reassembly.	NAD	24-27	sirtuin 2	Homo sapiens	11-16
31634899-10	2019	In conclusion, FSP1/CoQ10/NAD(P)H exists as a stand-alone parallel system, which co-operates with GPX4 and glutathione (GSH) to suppress phospholipid peroxidation (pLPO) and ferroptosis.	NAD	26-33	glutathione peroxidase 4	Homo sapiens	98-102
20228936-4	2009	Here we review the activities of a redox enzyme (NQR1 in yeast and CYB5R3 in mammals) that also influences the NAD(+)/NADH ratio and may play a regulatory role that connects aerobic metabolism with aging.	NAD	111-117	cytochrome-b5 reductase	Saccharomyces cerevisiae S288C	49-53
20228936-4	2009	Here we review the activities of a redox enzyme (NQR1 in yeast and CYB5R3 in mammals) that also influences the NAD(+)/NADH ratio and may play a regulatory role that connects aerobic metabolism with aging.	NAD	118-122	cytochrome-b5 reductase	Saccharomyces cerevisiae S288C	49-53
19764902-0	2009	Silencing of the mitochondrial NADH shuttle component aspartate-glutamate carrier AGC1/Aralar1 in INS-1E cells and rat islets.	NAD	31-35	solute carrier family 25 member 12	Rattus norvegicus	87-94
20228935-4	2009	In the murine heart, moderate overexpression of the NAD(+)-dependent deacetylase SirT1 was reported to mitigate oxidative stress.	NAD	52-58	sirtuin 1	Mus musculus	81-86
31278825-0	2019	The mitochondrial NAD+ transporter (NDT1) plays important roles in cellular NAD+ homeostasis in Arabidopsis thaliana.	NAD	18-22	NAD+ transporter 1	Arabidopsis thaliana	36-40
31278825-11	2019	These results are discussed in the context of the mitochondrial localization of AtNDT1 and its important role in the cellular NAD+ homeostasis for both metabolic and developmental processes in plants.	NAD	126-130	NAD+ transporter 1	Arabidopsis thaliana	80-86
31657440-8	2019	Inactivation of renalase and of PNPO in mammalian cells and of Ygr017w in yeasts led to the accumulation of a reduced form of 6-NADH, tentatively identified as 4,5,6-NADH3, which can also be produced in vitro by reduction of 6-NADH by glyceraldehyde-3-phosphate dehydrogenase or glucose-6-phosphate dehydrogenase.	NAD	126-132	renalase, FAD dependent amine oxidase	Homo sapiens	16-24
19640843-0	2009	Mechanism of cyclizing NAD to cyclic ADP-ribose by ADP-ribosyl cyclase and CD38.	NAD	23-26	CD38 molecule	Homo sapiens	75-79
31657440-8	2019	Inactivation of renalase and of PNPO in mammalian cells and of Ygr017w in yeasts led to the accumulation of a reduced form of 6-NADH, tentatively identified as 4,5,6-NADH3, which can also be produced in vitro by reduction of 6-NADH by glyceraldehyde-3-phosphate dehydrogenase or glucose-6-phosphate dehydrogenase.	NAD	126-132	glucose-6-phosphate dehydrogenase	Saccharomyces cerevisiae S288C	279-312
31657440-8	2019	Inactivation of renalase and of PNPO in mammalian cells and of Ygr017w in yeasts led to the accumulation of a reduced form of 6-NADH, tentatively identified as 4,5,6-NADH3, which can also be produced in vitro by reduction of 6-NADH by glyceraldehyde-3-phosphate dehydrogenase or glucose-6-phosphate dehydrogenase.	NAD	160-171	renalase, FAD dependent amine oxidase	Homo sapiens	16-24
31657440-8	2019	Inactivation of renalase and of PNPO in mammalian cells and of Ygr017w in yeasts led to the accumulation of a reduced form of 6-NADH, tentatively identified as 4,5,6-NADH3, which can also be produced in vitro by reduction of 6-NADH by glyceraldehyde-3-phosphate dehydrogenase or glucose-6-phosphate dehydrogenase.	NAD	160-171	glucose-6-phosphate dehydrogenase	Saccharomyces cerevisiae S288C	279-312
19748117-0	2009	Extracellular NAD(+) induces a rise in [Ca(2+)](i) in activated human monocytes via engagement of P2Y(1) and P2Y(11) receptors.	NAD	14-20	purinergic receptor P2Y1	Homo sapiens	98-104
31657440-8	2019	Inactivation of renalase and of PNPO in mammalian cells and of Ygr017w in yeasts led to the accumulation of a reduced form of 6-NADH, tentatively identified as 4,5,6-NADH3, which can also be produced in vitro by reduction of 6-NADH by glyceraldehyde-3-phosphate dehydrogenase or glucose-6-phosphate dehydrogenase.	NAD	164-170	renalase, FAD dependent amine oxidase	Homo sapiens	16-24
19748117-0	2009	Extracellular NAD(+) induces a rise in [Ca(2+)](i) in activated human monocytes via engagement of P2Y(1) and P2Y(11) receptors.	NAD	14-20	purinergic receptor P2Y11	Homo sapiens	109-116
31657440-10	2019	These findings indicate that two different classes of enzymes using either FAD (renalase) or FMN (PNPOs and PNPO-RPs) as a cofactor play an as yet unsuspected role in removing damaged forms of NAD(P).	NAD	193-196	renalase, FAD dependent amine oxidase	Homo sapiens	80-88
19748117-5	2009	The identification of P2Y(1) and P2Y(11) as receptor subtypes responsible for the NAD(+)-triggered increase in [Ca(2+)](i) was supported by several lines of evidence.	NAD	82-88	purinergic receptor P2Y1	Homo sapiens	22-28
31645480-0	2019	CD38-NAD+-Sirt1 axis In T cell immunotherapy.	NAD	5-8	CD38 molecule	Homo sapiens	0-4
19748117-5	2009	The identification of P2Y(1) and P2Y(11) as receptor subtypes responsible for the NAD(+)-triggered increase in [Ca(2+)](i) was supported by several lines of evidence.	NAD	82-88	purinergic receptor P2Y11	Homo sapiens	33-40
19748117-6	2009	First, specific P2Y(1) and P2Y(11) receptor antagonists inhibited the NAD(+)-induced increase in [Ca(2+)](i).	NAD	70-76	purinergic receptor P2Y1	Homo sapiens	16-22
19748117-6	2009	First, specific P2Y(1) and P2Y(11) receptor antagonists inhibited the NAD(+)-induced increase in [Ca(2+)](i).	NAD	70-76	purinergic receptor P2Y11	Homo sapiens	27-34
19748117-8	2009	Third, NAD(+) caused an increase in [cAMP](i), prevented by the P2Y(11) receptor-specific antagonist NF157.	NAD	7-13	purinergic receptor P2Y11	Homo sapiens	64-71
31749697-3	2019	Electron transfer in POR occurs from NADH to FAD to FMN, and the flexible hinge region in POR is essential for domain movements to bring the FAD and FMN close together for electron transfer.	NAD	37-41	formin 1	Homo sapiens	52-55
19796237-10	2009	Since CN patients respond to G-CSF treatment even in the absence of LEF-1 and C/EBPalpha, we conclude that treatment of CN patients with pharmacological doses of G-CSF activates NAMPT/NAD(+)/SIRT1-dependent "emergency" granulopoiesis via C/EBPbeta.	NAD	184-190	colony stimulating factor 3	Homo sapiens	162-167
19531481-4	2009	Here we identify PARP1, a DNA-binding protein with an NAD+-dependent enzymatic activity, as a cofactor of Oct4 and Sox2 to regulate expression of their target gene FGF4.	NAD	54-58	POU class 5 homeobox 1	Homo sapiens	106-110
31749697-3	2019	Electron transfer in POR occurs from NADH to FAD to FMN, and the flexible hinge region in POR is essential for domain movements to bring the FAD and FMN close together for electron transfer.	NAD	37-41	formin 1	Homo sapiens	149-152
31575956-7	2019	Antioxidant enzymes transcriptionally regulated by Nrf2 and involved in GSH, NADPH, and NADH generation were significantly lower including PRX1 and PRX3, GPX4, GSTP1, GCLC, and MTHFD2.	NAD	88-92	glutathione S-transferase pi 1	Homo sapiens	160-165
31576091-13	2019	Parp1 and Sirt1 are two NAD+-dependent enzymes which play major roles in the decision of a cell to live or die in the context of stress .	NAD	24-27	sirtuin 1	Mus musculus	10-15
19268440-5	2009	The isotypes responsible for tubulin deacetylation are HDAC6 and the NAD(+)-dependent histone deacetylase (sirtuin) Sirt2.	NAD	69-75	sirtuin 2	Homo sapiens	116-121
31576091-14	2019	We showed that NAD+ depletion attributed to Parp1 activation after DNA damage was caused by oxidative stress in hepatocytes and resulted in Sirt1 activity inhibition.	NAD	15-18	sirtuin 1	Mus musculus	140-145
31484760-5	2019	Importantly, nicotinamide mononucleotide adenylyltransferase (NMNAT), an evolutionarily conserved nicotinamide adenine dinucleotide (NAD+) synthase and neuroprotective factor, significantly mitigates mutant Htt-induced neurodegeneration by reducing mutant Htt aggregation through promoting autophagic clearance.	NAD	98-131	Nicotinamide mononucleotide adenylyltransferase	Drosophila melanogaster	13-60
19470756-1	2009	Poly(ADP-ribose) polymerase 1 (PARP1) and SIRT1 deacetylase are two NAD-dependent enzymes which play major roles in the decision of a cell to live or to die in a stress situation.	NAD	68-71	sirtuin 1	Mus musculus	42-47
31484760-5	2019	Importantly, nicotinamide mononucleotide adenylyltransferase (NMNAT), an evolutionarily conserved nicotinamide adenine dinucleotide (NAD+) synthase and neuroprotective factor, significantly mitigates mutant Htt-induced neurodegeneration by reducing mutant Htt aggregation through promoting autophagic clearance.	NAD	98-131	Nicotinamide mononucleotide adenylyltransferase	Drosophila melanogaster	62-67
31484760-5	2019	Importantly, nicotinamide mononucleotide adenylyltransferase (NMNAT), an evolutionarily conserved nicotinamide adenine dinucleotide (NAD+) synthase and neuroprotective factor, significantly mitigates mutant Htt-induced neurodegeneration by reducing mutant Htt aggregation through promoting autophagic clearance.	NAD	98-131	huntingtin	Drosophila melanogaster	207-210
19491102-5	2009	Here we demonstrate that the NAD(+)-dependent deacetylase sirtuin 1 (Sirt1) functionally and physically interacts with Dot1 to enhance the distributive activity of Dot1 on H3K79 methylation and thereby represses alpha-ENaC transcription in mIMCD3 cells.	NAD	29-35	sirtuin 1	Mus musculus	58-67
19491102-5	2009	Here we demonstrate that the NAD(+)-dependent deacetylase sirtuin 1 (Sirt1) functionally and physically interacts with Dot1 to enhance the distributive activity of Dot1 on H3K79 methylation and thereby represses alpha-ENaC transcription in mIMCD3 cells.	NAD	29-35	sirtuin 1	Mus musculus	69-74
31484760-5	2019	Importantly, nicotinamide mononucleotide adenylyltransferase (NMNAT), an evolutionarily conserved nicotinamide adenine dinucleotide (NAD+) synthase and neuroprotective factor, significantly mitigates mutant Htt-induced neurodegeneration by reducing mutant Htt aggregation through promoting autophagic clearance.	NAD	133-137	Nicotinamide mononucleotide adenylyltransferase	Drosophila melanogaster	13-60
31484760-5	2019	Importantly, nicotinamide mononucleotide adenylyltransferase (NMNAT), an evolutionarily conserved nicotinamide adenine dinucleotide (NAD+) synthase and neuroprotective factor, significantly mitigates mutant Htt-induced neurodegeneration by reducing mutant Htt aggregation through promoting autophagic clearance.	NAD	133-137	Nicotinamide mononucleotide adenylyltransferase	Drosophila melanogaster	62-67
31484760-5	2019	Importantly, nicotinamide mononucleotide adenylyltransferase (NMNAT), an evolutionarily conserved nicotinamide adenine dinucleotide (NAD+) synthase and neuroprotective factor, significantly mitigates mutant Htt-induced neurodegeneration by reducing mutant Htt aggregation through promoting autophagic clearance.	NAD	133-137	huntingtin	Drosophila melanogaster	207-210
31484760-5	2019	Importantly, nicotinamide mononucleotide adenylyltransferase (NMNAT), an evolutionarily conserved nicotinamide adenine dinucleotide (NAD+) synthase and neuroprotective factor, significantly mitigates mutant Htt-induced neurodegeneration by reducing mutant Htt aggregation through promoting autophagic clearance.	NAD	133-137	huntingtin	Drosophila melanogaster	256-259
31645844-11	2019	miR-494 significantly down-regulated NAMPT mRNA and protein expression and was also able to reduce the cellular NAD content.	NAD	112-115	microRNA 494	Homo sapiens	0-7
19645667-1	2009	Three forms of horse heart cytochrome c with specific substitutions of heme cleft surface located amino acid residues involved in specific interactions with ubiquinol:cytochrome c reductase (complex III) and cytochrome c oxidase (complex IV) were constructed, and their reactions with superoxide radical produced by NADH:ubiquinone reductase (complex I) were studied.	NAD	316-320	cytochrome c, somatic	Equus caballus	167-179
19645667-1	2009	Three forms of horse heart cytochrome c with specific substitutions of heme cleft surface located amino acid residues involved in specific interactions with ubiquinol:cytochrome c reductase (complex III) and cytochrome c oxidase (complex IV) were constructed, and their reactions with superoxide radical produced by NADH:ubiquinone reductase (complex I) were studied.	NAD	316-320	cytochrome c, somatic	Equus caballus	167-179
31145821-4	2019	IDO1 is required to maintain pluripotency by suppressing mitochondria activity and promoting glycolysis through the increase of NAD+ /NADH ratio.	NAD	128-132	indoleamine 2,3-dioxygenase 1	Homo sapiens	0-4
20183598-3	2009	Systematic kinetic and thermodynamic studies on association and dissociation of cofactor NAD/H for Tc-SAHH and Hs-SAHH provide a rationale for the design of anti-parasitic drugs directed toward cofactor-binding sites.	NAD	89-92	adenosylhomocysteinase	Homo sapiens	102-106
20183598-3	2009	Systematic kinetic and thermodynamic studies on association and dissociation of cofactor NAD/H for Tc-SAHH and Hs-SAHH provide a rationale for the design of anti-parasitic drugs directed toward cofactor-binding sites.	NAD	89-92	adenosylhomocysteinase	Homo sapiens	114-118
31145821-4	2019	IDO1 is required to maintain pluripotency by suppressing mitochondria activity and promoting glycolysis through the increase of NAD+ /NADH ratio.	NAD	134-138	indoleamine 2,3-dioxygenase 1	Homo sapiens	0-4
20183598-4	2009	Analogues of NAD and their reduced forms show significant selective inactivation of Tc-SAHH, confirming that this design approach is rational.	NAD	13-16	adenosylhomocysteinase	Homo sapiens	87-91
31302001-1	2019	Sirt3, as a major mitochondrial nicotinamide adenine dinucleotide (NAD)-dependent deacetylase, is required for mitochondrial metabolic adaption to various stresses.	NAD	32-65	sirtuin 3	Mus musculus	0-5
18926807-9	2009	As release of NADH can be a rate-limiting step for ALDH activity, NADH binding was evaluated for R166wt and R166H enzymes.	NAD	14-18	aldehyde dehydrogenase 5 family, member A1	Rattus norvegicus	51-55
18926807-9	2009	As release of NADH can be a rate-limiting step for ALDH activity, NADH binding was evaluated for R166wt and R166H enzymes.	NAD	66-70	aldehyde dehydrogenase 5 family, member A1	Rattus norvegicus	51-55
31302001-1	2019	Sirt3, as a major mitochondrial nicotinamide adenine dinucleotide (NAD)-dependent deacetylase, is required for mitochondrial metabolic adaption to various stresses.	NAD	67-70	sirtuin 3	Mus musculus	0-5
31097541-4	2019	Despite impaired fat utilization, Cpt1bM-/- mice have increased acetyl-CoA (14-fold) and NADH (2-fold), indicating metabolic shifts yield sufficient precursors to meet energy demand; however, this does not translate to enhance energy status as Cpt1bM-/- mice have low ATP and high AMP levels, signifying energy deficit.	NAD	89-93	carnitine palmitoyltransferase 1b, muscle	Mus musculus	34-38
19234185-8	2009	We further show that the routine preparation of primary lymph node and spleen cells induces the release of NAD(+) in sufficient concentrations for ART2.2 to ADP-ribosylate P2X(7), even at 4 degrees C. Gating of P2X(7) occurs when T cells are returned to 37 degrees C, rapidly inducing CD62L-shedding and PS-externalization by a substantial fraction of the cells.	NAD	107-113	ADP-ribosyltransferase 2b	Mus musculus	147-153
19052657-1	2009	Nicotinamide adenine dinucleotide (NAD(+)), a precursor of molecules involved in cell regulatory processes, is released in extra-cellular compartments after stress or inflammation.This study investigates the expression in the human cornea of CD38 and CD157, two NAD(+)-consuming ectoenzymes and surface receptors.	NAD	0-33	CD38 molecule	Homo sapiens	242-246
19052657-1	2009	Nicotinamide adenine dinucleotide (NAD(+)), a precursor of molecules involved in cell regulatory processes, is released in extra-cellular compartments after stress or inflammation.This study investigates the expression in the human cornea of CD38 and CD157, two NAD(+)-consuming ectoenzymes and surface receptors.	NAD	35-41	CD38 molecule	Homo sapiens	242-246
19052657-1	2009	Nicotinamide adenine dinucleotide (NAD(+)), a precursor of molecules involved in cell regulatory processes, is released in extra-cellular compartments after stress or inflammation.This study investigates the expression in the human cornea of CD38 and CD157, two NAD(+)-consuming ectoenzymes and surface receptors.	NAD	262-268	CD38 molecule	Homo sapiens	242-246
31393939-4	2019	The protective effects of NAD+ on microtubule loss have been shown to be indirect in some systems, for example through the sirtuin-3 pathway.	NAD	26-30	sirtuin 3	Bos taurus	123-132
19273055-8	2009	A potential crosstalk between PARP1, PARP2 and other NAD+-dependent ADP-ribosyling enzymes such as Sirtuins and CD38 in cell death and survival pathways is discussed.	NAD	53-57	CD38 molecule	Homo sapiens	112-116
19288225-0	2009	Nicotinamide prevents NAD+ depletion and protects neurons against excitotoxicity and cerebral ischemia: NAD+ consumption by SIRT1 may endanger energetically compromised neurons.	NAD	104-108	sirtuin 1	Mus musculus	124-129
19288225-2	2009	Here we studied the roles of NAD(+) bioenergetic state, and the NAD(+)-dependent enzymes SIRT1 and PARP-1, in excitotoxic neuronal death in cultured neurons and in a mouse model of focal ischemic stroke.	NAD	64-70	sirtuin 1	Mus musculus	89-94
19288225-12	2009	Our data further suggest that, SIRT1 is linked to bioenergetic state and stress responses in neurons, and that under conditions of reduced cellular energy levels SIRT1 enzyme activity may consume sufficient NAD(+) to nullify any cell survival-promoting effects of its deacetylase action on protein substrates.	NAD	207-213	sirtuin 1	Mus musculus	162-167
31680596-1	2019	Context: Sirtuin-3 (Sirt3), a NAD-dependent deacetylase, has been reported to be involved in many biological processes.Objective: The present study aimed to investigate the effect and mechanism of Sirt3 on diabetic mice and human umbilical vein endothelial cells (HUVECs) under high glucose (HG) condition.Materials and methods: HUVECs were cultured under HG and inflammation pathway was determined via qPCR, western blots, and immunofluorescence.Results: Sirt3 expression was reduced in the progression of diabetic nephropathy.	NAD	30-33	sirtuin 3	Mus musculus	9-18
31680596-1	2019	Context: Sirtuin-3 (Sirt3), a NAD-dependent deacetylase, has been reported to be involved in many biological processes.Objective: The present study aimed to investigate the effect and mechanism of Sirt3 on diabetic mice and human umbilical vein endothelial cells (HUVECs) under high glucose (HG) condition.Materials and methods: HUVECs were cultured under HG and inflammation pathway was determined via qPCR, western blots, and immunofluorescence.Results: Sirt3 expression was reduced in the progression of diabetic nephropathy.	NAD	30-33	sirtuin 3	Mus musculus	20-25
31680596-1	2019	Context: Sirtuin-3 (Sirt3), a NAD-dependent deacetylase, has been reported to be involved in many biological processes.Objective: The present study aimed to investigate the effect and mechanism of Sirt3 on diabetic mice and human umbilical vein endothelial cells (HUVECs) under high glucose (HG) condition.Materials and methods: HUVECs were cultured under HG and inflammation pathway was determined via qPCR, western blots, and immunofluorescence.Results: Sirt3 expression was reduced in the progression of diabetic nephropathy.	NAD	30-33	sirtuin 3	Mus musculus	197-202
19049465-1	2008	Sir2 enzymes catalyze the NAD+-dependent protein deacetylation and play critical roles in epigenetics, cell death, and lifespan regulation.	NAD	26-30	Sirtuin 1	Drosophila melanogaster	0-4
31019096-3	2019	An attractive prospect is that Tpt1 enzymes might catalyze reactions other than internal RNA 2"-PO4 removal, via their unique NAD+-dependent transferase mechanism.	NAD	126-129	tumor protein, translationally-controlled 1	Homo sapiens	31-35
30841754-4	2019	We now show that increasing total NAD+ content in astrocytes leads to the activation of the transcription factor nuclear factor, erythroid-derived 2, like 2 (Nfe2l2 or Nrf2) and up-regulation of the antioxidant proteins heme oxygenase 1 (HO-1) and sulfiredoxin 1 (SRXN1).	NAD	34-38	heme oxygenase 1	Homo sapiens	220-236
19076449-5	2008	The NAD(+)-dependent histone deacetylase sirtulin 1 (SIRT1) and glucose transporter 1 (GLUT1) mRNA are upregulated mouse brain under caloric restriction.	NAD	4-10	solute carrier family 2 (facilitated glucose transporter), member 1	Mus musculus	64-85
19076449-5	2008	The NAD(+)-dependent histone deacetylase sirtulin 1 (SIRT1) and glucose transporter 1 (GLUT1) mRNA are upregulated mouse brain under caloric restriction.	NAD	4-10	solute carrier family 2 (facilitated glucose transporter), member 1	Mus musculus	87-92
30879903-3	2019	Identified via complementary biochemical, organellar, and cellular approaches, we report that MDM2 negatively regulates NADH:ubiquinone oxidoreductase 75 kDa Fe-S protein 1 (NDUFS1), leading to decreased mitochondrial respiration, marked oxidative stress, and commitment to the mitochondrial pathway of apoptosis.	NAD	120-124	transformed mouse 3T3 cell double minute 2	Mus musculus	94-98
30665027-1	2019	The activity of NAD+-dependent deacetylase Sir2, originally discovered in yeast, is known to be essential for effective longevity.	NAD	16-19	sirtuin 1	Mus musculus	43-47
18815415-2	2008	We report the first prokaryotic crystal structure of SAHH, from Mycobacterium tuberculosis (Mtb), in complex with adenosine (ADO) and nicotinamide adenine dinucleotide.	NAD	134-167	adenosylhomocysteinase	Homo sapiens	53-57
18995842-3	2008	We found that the NAD(+)-dependent histone deacetylase SIRT2 deacetylates p300 in vitro and in cells.	NAD	18-24	sirtuin 2	Homo sapiens	55-60
30665027-4	2019	The three-domain structure of Sir2 has a distinct crevice that plays an important regulatory role in the binding of NAD+.	NAD	116-120	sirtuin 1	Mus musculus	30-34
19046567-1	2008	The NAD(+)-dependent deacetylase SIRT1 controls metabolic processes in response to low nutrient availability.	NAD	4-10	sirtuin 1	Mus musculus	33-38
30801870-9	2019	ABSTRACT: Nicotinamide adenine dinucleotide phosphate (NADPH) oxidases (Nox), comprise seven family members (Nox1-Nox5 and dual oxidase 1 and 2) and are major producers of reactive oxygen species in mammalian cells.	NAD	10-43	NADPH oxidase 5	Homo sapiens	114-118
31035592-3	2019	LDHA has a higher affinity for pyruvate, preferentially converting pyruvate to lactate, and NADH to NAD+ in anaerobic conditions, whereas LDHB possess a higher affinity for lactate, preferentially converting lactate to pyruvate, and NAD+ to NADH, when oxygen is abundant.	NAD	233-237	lactate dehydrogenase B	Homo sapiens	138-142
31035592-3	2019	LDHA has a higher affinity for pyruvate, preferentially converting pyruvate to lactate, and NADH to NAD+ in anaerobic conditions, whereas LDHB possess a higher affinity for lactate, preferentially converting lactate to pyruvate, and NAD+ to NADH, when oxygen is abundant.	NAD	241-245	lactate dehydrogenase B	Homo sapiens	138-142
30979096-0	2019	Studies on the Interaction between Poly-Phosphane Gold(I) Complexes and Dihydrofolate Reductase: An Interplay with Nicotinamide Adenine Dinucleotide Cofactor.	NAD	115-148	Dihydrofolate reductase	Escherichia coli	40-95
18502113-6	2008	Furthermore, we found the photovoltaic effect of CNTs/CdS/GDH can trigger the dehydrogenase enzymatic reaction in the absence of the NAD(+) or NADP(+) cofactors.	NAD	133-139	CDP-diacylglycerol synthase 1	Homo sapiens	54-57
18502113-6	2008	Furthermore, we found the photovoltaic effect of CNTs/CdS/GDH can trigger the dehydrogenase enzymatic reaction in the absence of the NAD(+) or NADP(+) cofactors.	NAD	133-139	glutamate dehydrogenase 1	Homo sapiens	58-61
18682386-0	2008	Histone 2B (H2B) expression is confined to a proper NAD+/NADH redox status.	NAD	52-56	H2B clustered histone 21	Homo sapiens	0-10
18682386-0	2008	Histone 2B (H2B) expression is confined to a proper NAD+/NADH redox status.	NAD	52-56	H2B clustered histone 21	Homo sapiens	12-15
30666558-6	2019	We show that while transient activation of the KP promotes synthesis of the essential co-enzyme nicotinamide adenine dinucleotide (NAD+), allowing cells to meet short-term increased energy demands, chronic KMO activation induces production of reactive oxygen species (ROS), mitochondrial damage and decreases spare-respiratory capacity (SRC).	NAD	131-135	kynurenine 3-monooxygenase	Homo sapiens	206-209
18682386-0	2008	Histone 2B (H2B) expression is confined to a proper NAD+/NADH redox status.	NAD	57-61	H2B clustered histone 21	Homo sapiens	0-10
18682386-0	2008	Histone 2B (H2B) expression is confined to a proper NAD+/NADH redox status.	NAD	57-61	H2B clustered histone 21	Homo sapiens	12-15
18682386-2	2008	H2B transcription in vitro is modulated by NAD(H).	NAD	43-49	H2B clustered histone 21	Homo sapiens	0-3
18682386-4	2008	Here, we show that H2B transcription requires a proper NAD(+)/NADH redox status in vitro and in vivo.	NAD	55-61	H2B clustered histone 21	Homo sapiens	19-22
18682386-4	2008	Here, we show that H2B transcription requires a proper NAD(+)/NADH redox status in vitro and in vivo.	NAD	62-66	H2B clustered histone 21	Homo sapiens	19-22
30877853-1	2019	Sirtuin-1 (SirT1) catalyzes NAD+-dependent protein lysine deacetylation and is a critical regulator of energy and lipid metabolism, mitochondrial biogenesis, apoptosis, and senescence.	NAD	28-31	sirtuin 1	Mus musculus	0-9
30877853-1	2019	Sirtuin-1 (SirT1) catalyzes NAD+-dependent protein lysine deacetylation and is a critical regulator of energy and lipid metabolism, mitochondrial biogenesis, apoptosis, and senescence.	NAD	28-31	sirtuin 1	Mus musculus	11-16
30949164-10	2019	Genetic testing of blood mtDNA revealed a heteroplasmic base exchange mutation in the mitochondrially encoded NADH:ubiquinone oxidoreductase core subunit 4 (MT-ND4) gene (m.12015T&gt;C; p.Leu419Pro; heteroplasmy level in blood 12%, in muscle tissue: 15%).	NAD	110-114	mitochondrially encoded NADH dehydrogenase 4	Homo sapiens	157-163
18498245-9	2008	TD lymphoblasts showed increased expression of CD38, which hydrolyses NAD(+) into ADP-ribose, a trigger of Ca(2+) release from the endoplasmic reticulum that, in turn, facilitated CD20-induced apoptosis.	NAD	70-76	CD38 molecule	Homo sapiens	47-51
30898999-6	2019	Moreover, inhibition of PARP1 protects against tachypacing-induced NAD+ depletion, oxidative stress, DNA damage and contractile dysfunction in atrial cardiomyocytes and Drosophila.	NAD	67-71	Poly-(ADP-ribose) polymerase	Drosophila melanogaster	24-29
30860478-4	2019	First, adenine depletion promotes transcriptional upregulation of the de novo NAD+ biosynthesis genes by a mechanism requiring the key-purine intermediates ZMP/SZMP and the Bas1/Pho2 transcription factors.	NAD	78-82	Pho2p	Saccharomyces cerevisiae S288C	178-182
18794531-1	2008	Here, we demonstrate a role for the mitochondrial NAD-dependent deacetylase Sirt3 in the maintenance of basal ATP levels and as a regulator of mitochondrial electron transport.	NAD	50-53	sirtuin 3	Mus musculus	76-81
30152543-2	2019	C-terminal binding protein 1 (CTBP1) is a transcriptional co-repressor of tumor suppressor genes that is activated by low NAD+ /NADH ratio.	NAD	122-126	C-terminal binding protein 1	Mus musculus	0-28
18563446-1	2008	With more than 40 subunits, one FMN co-factor and eight FeS clusters, complex I or NADH:ubiquinone oxidoreductase is the largest multimeric respiratory enzyme in the mitochondria.	NAD	83-87	formin 1	Homo sapiens	32-35
30152543-2	2019	C-terminal binding protein 1 (CTBP1) is a transcriptional co-repressor of tumor suppressor genes that is activated by low NAD+ /NADH ratio.	NAD	122-126	C-terminal binding protein 1	Mus musculus	30-35
30152543-2	2019	C-terminal binding protein 1 (CTBP1) is a transcriptional co-repressor of tumor suppressor genes that is activated by low NAD+ /NADH ratio.	NAD	128-132	C-terminal binding protein 1	Mus musculus	0-28
30152543-2	2019	C-terminal binding protein 1 (CTBP1) is a transcriptional co-repressor of tumor suppressor genes that is activated by low NAD+ /NADH ratio.	NAD	128-132	C-terminal binding protein 1	Mus musculus	30-35
30443978-1	2019	Lactate dehydrogenase B (LDHB) is a glycolytic enzyme that catalyses the conversion of lactate and NAD+ to pyruvate, NADH and H+ .	NAD	99-103	lactate dehydrogenase B	Homo sapiens	0-23
30443978-1	2019	Lactate dehydrogenase B (LDHB) is a glycolytic enzyme that catalyses the conversion of lactate and NAD+ to pyruvate, NADH and H+ .	NAD	99-103	lactate dehydrogenase B	Homo sapiens	25-29
30443978-1	2019	Lactate dehydrogenase B (LDHB) is a glycolytic enzyme that catalyses the conversion of lactate and NAD+ to pyruvate, NADH and H+ .	NAD	117-121	lactate dehydrogenase B	Homo sapiens	0-23
30443978-1	2019	Lactate dehydrogenase B (LDHB) is a glycolytic enzyme that catalyses the conversion of lactate and NAD+ to pyruvate, NADH and H+ .	NAD	117-121	lactate dehydrogenase B	Homo sapiens	25-29
29550257-4	2019	On the other hand, the non-canonical pathway metabolizes NAD+ to ADPR, through the action of CD38.	NAD	57-61	CD38 molecule	Homo sapiens	93-97
17701280-0	2008	Isolation and characterization of an NAD+-degrading bacterium PTX1 and its role in chromium biogeochemical cycle.	NAD	37-41	paired like homeodomain 1	Homo sapiens	62-66
29958894-3	2019	Among the host responses to the release of ATP, NAD+ and related small molecules is their breakdown on behalf of a panel of leukocyte ectonucleotidases - CD38, CD39, CD73, CD157, CD203a and CD203c -, whose activities are concatenated to form two nucleotide-catabolizing channels defined as the canonical and non-canonical adenosinergic pathways.	NAD	48-52	CD38 molecule	Homo sapiens	154-158
17701280-7	2008	PTX1 grew slowly on NAD(+) with a doubling time of 17 h, and even more slowly on the NAD(+)-Cr(III) complex with an estimated doubling time of 35 days.	NAD	20-26	paired like homeodomain 1	Homo sapiens	0-4
29958894-3	2019	Among the host responses to the release of ATP, NAD+ and related small molecules is their breakdown on behalf of a panel of leukocyte ectonucleotidases - CD38, CD39, CD73, CD157, CD203a and CD203c -, whose activities are concatenated to form two nucleotide-catabolizing channels defined as the canonical and non-canonical adenosinergic pathways.	NAD	48-52	ectonucleoside triphosphate diphosphohydrolase 1	Homo sapiens	160-164
17701280-8	2008	The slow growth suggests that PTX1 passively grew on trace NAD(+) dissociated from the NAD(+)-Cr(III) complex, facilitating further dissociation of the complex and formation of Cr(III) precipitates.	NAD	59-65	paired like homeodomain 1	Homo sapiens	30-34
30746504-1	2019	Sirt1 is an NAD-dependent, class III deacetylase that functions as a cellular energy sensor.	NAD	12-15	sirtuin 1	Mus musculus	0-5
18174234-5	2008	15-Hydroxyprostaglandin dehydrogenase [NAD(+)] (15-PGDH), a key enzyme in prostaglandin degradation, was identified as an upregulated protein in SGC7901 cells transfected with the COX-2siRNA plasmid.	NAD	39-45	15-hydroxyprostaglandin dehydrogenase	Homo sapiens	51-55
18485875-4	2008	Here we find that GzmA accesses the mitochondrial matrix to cleave the complex I protein NDUFS3, an iron-sulfur subunit of the NADH:ubiquinone oxidoreductase complex I, after Lys56 to interfere with NADH oxidation and generate superoxide anions.	NAD	127-131	NADH:ubiquinone oxidoreductase core subunit S3	Homo sapiens	89-95
18485875-4	2008	Here we find that GzmA accesses the mitochondrial matrix to cleave the complex I protein NDUFS3, an iron-sulfur subunit of the NADH:ubiquinone oxidoreductase complex I, after Lys56 to interfere with NADH oxidation and generate superoxide anions.	NAD	199-203	NADH:ubiquinone oxidoreductase core subunit S3	Homo sapiens	89-95
30540938-0	2018	Dual Inhibition of the Lactate Transporters MCT1 and MCT4 Is Synthetic Lethal with Metformin due to NAD+ Depletion in Cancer Cells.	NAD	100-104	solute carrier family 16 member 3	Homo sapiens	53-57
18646549-5	2008	Later investigations indicated the possibility of the participation in electron transport for reticular CYP isoenzymes, alternative NADH-dependent reticular system composed of cytochrome b5 reductase (CBR) and cytochrome b5.	NAD	132-136	peptidylprolyl isomerase G	Homo sapiens	104-107
30460421-1	2018	We have recently identified a positive feedback loop in which c-MYC increases silent information regulator 1 (SIRT1) protein level and activity through transcriptional activation of nicotinamide phosphoribosyltransferase (NAMPT) and NAD+ increase.	NAD	233-237	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	62-67
18391451-0	2008	Structure and function of NAD kinase and NADP phosphatase: key enzymes that regulate the intracellular balance of NAD(H) and NADP(H).	NAD	114-120	NAD kinase	Homo sapiens	26-36
18381895-3	2008	Here we show that the mitochondrial components of the malate-aspartate NADH shuttle (Mdh1 [malate dehydrogenase] and Aat1 [aspartate amino transferase]) and the glycerol-3-phosphate shuttle (Gut2, glycerol-3-phosphate dehydrogenase) are novel longevity factors in the CR pathway in yeast.	NAD	71-75	aspartate transaminase AAT1	Saccharomyces cerevisiae S288C	117-121
18364004-1	2008	Indoleamine 2, 3-dioxygenase (IDO) degrades the essential amino acid tryptophan in mammals, catalyzing the initial and rate-limiting step in the de novo biosynthesis nicotinamide adenine dinucleotide (NAD).	NAD	166-199	indoleamine 2,3-dioxygenase 1	Homo sapiens	0-28
30459772-1	2018	The NAD+-metabolizing ectoenzyme CD38 is an established therapeutic target in multiple myeloma.	NAD	4-8	CD38 molecule	Homo sapiens	33-37
30309657-4	2018	SIRT6 expression was up-regulated by PHH via increasing NAD+/NADH ratio in the prefrontal cortex.	NAD	56-60	sirtuin 6	Rattus norvegicus	0-5
18364004-1	2008	Indoleamine 2, 3-dioxygenase (IDO) degrades the essential amino acid tryptophan in mammals, catalyzing the initial and rate-limiting step in the de novo biosynthesis nicotinamide adenine dinucleotide (NAD).	NAD	166-199	indoleamine 2,3-dioxygenase 1	Homo sapiens	30-33
18364004-1	2008	Indoleamine 2, 3-dioxygenase (IDO) degrades the essential amino acid tryptophan in mammals, catalyzing the initial and rate-limiting step in the de novo biosynthesis nicotinamide adenine dinucleotide (NAD).	NAD	201-204	indoleamine 2,3-dioxygenase 1	Homo sapiens	0-28
18364004-1	2008	Indoleamine 2, 3-dioxygenase (IDO) degrades the essential amino acid tryptophan in mammals, catalyzing the initial and rate-limiting step in the de novo biosynthesis nicotinamide adenine dinucleotide (NAD).	NAD	201-204	indoleamine 2,3-dioxygenase 1	Homo sapiens	30-33
30309657-4	2018	SIRT6 expression was up-regulated by PHH via increasing NAD+/NADH ratio in the prefrontal cortex.	NAD	61-65	sirtuin 6	Rattus norvegicus	0-5
30389922-3	2018	Previous studies had shown that NAD-dependent deacetylase sirtuin-1 (SIRT1) in part influences the health-promoting effects of caloric restriction by boosting fat use in peripheral tissues.	NAD	32-35	sirtuin 1	Mus musculus	69-74
18317592-9	2008	DPN treatment increased BDNF expression in ARKO mice.	NAD	0-3	brain derived neurotrophic factor	Mus musculus	24-28
30401461-2	2018	ADP-ribosyltransferases transfer ADP-ribose from NAD+ to the target protein, and ADP-ribosylhydrolases, such as ADPRHL2, reverse the reaction.	NAD	49-53	ADP-ribosylserine hydrolase	Homo sapiens	112-119
18272180-6	2008	We performed NMR titrations of both free CTA1 and an active CTA1:ARF6-GTP complex with NAD(+), which revealed that the formation of the complex does not significantly enhance NAD(+) binding.	NAD	87-93	ADP ribosylation factor 6	Homo sapiens	65-69
30159648-6	2018	In shake-flask experiments, the total NAD(H) concentration positively correlated with conversion of xylitol to L-xylulose by xylitol 4-dehydrogenase, and the greatest conversion (80%) was observed using MG1655 nadR nudC mazG/pZE12-xdh/pCS27-nox.	NAD	38-44	RNA decapping hydrolase	Escherichia coli str. K-12 substr. MG1655	215-219
18199125-4	2008	We encountered that nrc mutants of denitrifying strains show a decrease in anaerobic growth rates not only with nitrate, but also with nitrite, NO and N(2)O, which is concomitant to their lower NADH oxidation activities in vitro.	NAD	194-198	nuclear receptor coactivator 6	Homo sapiens	20-23
30076241-0	2018	CD38 Inhibits Prostate Cancer Metabolism and Proliferation by Reducing Cellular NAD+ Pools.	NAD	80-84	CD38 molecule	Homo sapiens	0-4
30076241-5	2018	This study demonstrates a novel connection between CD38, modulation of NAD+, and tumor cell metabolism in prostate cancer.	NAD	71-75	CD38 molecule	Homo sapiens	51-55
18005249-8	2008	These findings provide insight into the age-dependent regulation of Sirt1 activity and suggest that enhancement of systemic NAD biosynthesis and Sirt1 activity in tissues such as beta cells may be an effective therapeutic intervention for age-associated metabolic disorders such as type 2 diabetes.	NAD	124-127	sirtuin 1	Mus musculus	68-73
30076241-7	2018	Expressing CD38 in prostate cancer cells lowered intracellular NAD+, resulting in cell-cycle arrest and expression of p21Cip1 (CDKNA1).	NAD	63-67	CD38 molecule	Homo sapiens	11-15
30076241-10	2018	Modulation of NAD+ by CD38 also induces significant differential expression of the transcriptome, producing a gene expression signature indicative of a nonproliferative phenotype.	NAD	14-18	CD38 molecule	Homo sapiens	22-26
30076241-11	2018	Altogether, in the context of prostate cancer, the data establish a novel role for the CD38-NAD+ axis in the regulation of cell metabolism and development.Implications: This research establishes a mechanistic connection between CD38 and metabolic control.	NAD	92-96	CD38 molecule	Homo sapiens	87-91
30076241-11	2018	Altogether, in the context of prostate cancer, the data establish a novel role for the CD38-NAD+ axis in the regulation of cell metabolism and development.Implications: This research establishes a mechanistic connection between CD38 and metabolic control.	NAD	92-96	CD38 molecule	Homo sapiens	228-232
18974062-3	2008	Reverse transcription-PCR analysis was used here to investigate further the expression patterns of the three CP12 Arabidopsis genes together with the genes encoding plastid GAPDH (GAPA-1 and GAPB), PRK (PRK), and plastid NAD-dependent GAPDH (GAPCp1 and GAPCp2) during development, in response to changes in light, temperature, and anaerobic conditions.	NAD	221-224	CP12 domain-containing protein 2	Arabidopsis thaliana	109-113
30078073-4	2018	We present evidence for C4-specific paralogs of NAD-malic enzyme 2, MPC1 and MPC2 (mitochondrial pyruvate carriers) via increased transcript abundance and associated rates of evolution, implicating them as genes recruited to perform C4 photosynthesis within NAD-ME and PEPCK subtypes.	NAD	48-51	mitochondrial pyruvate carrier 1	Homo sapiens	68-72
30078073-4	2018	We present evidence for C4-specific paralogs of NAD-malic enzyme 2, MPC1 and MPC2 (mitochondrial pyruvate carriers) via increased transcript abundance and associated rates of evolution, implicating them as genes recruited to perform C4 photosynthesis within NAD-ME and PEPCK subtypes.	NAD	48-51	mitochondrial pyruvate carrier 2	Homo sapiens	77-81
17954559-5	2008	Expression of the group 2 genes is selectively repressed by the NAD-dependent deacetylase SIRT1 in mature 3T3-L1 adipocytes, since knockdown of SIRT1 through the constitutive expression of a corresponding RNA interference enhances their expression without affecting the expression of classic adipogenic genes, such as adiponectin and FABP4/aP2.	NAD	64-67	fatty acid binding protein 4	Homo sapiens	334-339
17954559-5	2008	Expression of the group 2 genes is selectively repressed by the NAD-dependent deacetylase SIRT1 in mature 3T3-L1 adipocytes, since knockdown of SIRT1 through the constitutive expression of a corresponding RNA interference enhances their expression without affecting the expression of classic adipogenic genes, such as adiponectin and FABP4/aP2.	NAD	64-67	fatty acid binding protein 4	Homo sapiens	340-343
30510631-1	2018	We previously showed that treatment with resveratrol (3,5,4"-trihydroxy-trans-stilbene), an activator of the NAD+-dependent deacetylase SIRT1 at 4 g/kg food for 32 weeks, significantly decreased the muscular reactive oxygen species (ROS) levels and ameliorated the pathology of mdx mice, an animal model of Duchenne muscular dystrophy (DMD).	NAD	109-113	sirtuin 1	Mus musculus	136-141
18221243-6	2008	The protein implicated in this protective process is the silent information regulator 2 (SIR2, SIRT1 in mammals), an enzyme that belongs to a nicotinamide adenine dinucleotide (NAD)+-dependent protein deacetylases.	NAD	142-175	sirtuin 2	Homo sapiens	57-87
18221243-6	2008	The protein implicated in this protective process is the silent information regulator 2 (SIR2, SIRT1 in mammals), an enzyme that belongs to a nicotinamide adenine dinucleotide (NAD)+-dependent protein deacetylases.	NAD	142-175	sirtuin 2	Homo sapiens	89-93
30568770-4	2018	Substrate activity assays indicated the resulting S-NAD+ is chemically inert to human CD38 and sirtuin 2 enzymes, but capable of participating in redox reactions in a manner similar to NAD+.	NAD	52-56	CD38 molecule	Homo sapiens	86-90
30568770-4	2018	Substrate activity assays indicated the resulting S-NAD+ is chemically inert to human CD38 and sirtuin 2 enzymes, but capable of participating in redox reactions in a manner similar to NAD+.	NAD	52-56	sirtuin 2	Homo sapiens	95-104
30568770-5	2018	X-ray crystallographic analysis revealed binding of S-NAD+ to the active site of human CD38 and critical residues involved in leaving group activation and catalysis.	NAD	52-58	CD38 molecule	Homo sapiens	87-91
17977840-2	2007	We find that Hst3 has NAD-dependent histone deacetylase activity in vitro and that it functions during S phase to deacetylate the core domain of histone H3 at lysine 56 (H3K56).	NAD	22-25	NAD-dependent histone deacetylase HST3	Saccharomyces cerevisiae S288C	13-17
30405740-10	2018	MAN induced declines of both HMGB1/TLR4/p-p65 and TNF-alpha were substantially reversed by cotreatment with nicotinamide mononucleotide or NAD.	NAD	139-142	toll like receptor 4	Homo sapiens	35-39
30405740-11	2018	These results suggest that downregulation of NAMPT/NAD by MAN treatments contributes to the alleviation of TLR4/NF-kappaB-mediated inflammations in macrophage, which is essential for amelioration of ALI in rats.	NAD	51-54	toll like receptor 4	Homo sapiens	107-111
30356715-3	2018	We have recently shown in Arabidopsis thaliana that exogenous NAD induces defense responses, that pathogen infection leads to release of NAD into the extracellular space at concentrations sufficient for defense activation, and that depletion of extracellular NAD (eNAD) by transgenic expression of the human NAD-hydrolyzing ectoenzyme CD38 inhibits plant immunity.	NAD	62-65	CD38 molecule	Homo sapiens	335-339
17939663-2	2007	In the complex formed between morphinone reductase (MR) and the NADH analogue 1,4,5,6-tetrahydro-NADH (NADH4) the nicotinamide moiety is restrained close to the FMN isoalloxazine ring by hydrogen bonds from Asn-189 and His-186 as determined from the X-ray crystal structure.	NAD	64-68	formin 1	Homo sapiens	161-164
17939663-4	2007	Using stopped-flow spectroscopy, we show that reduction of the FMN cofactor by NADH in N189A MR is multiphasic, identifying at least four different reactive configurations of the MR-NADH complex.	NAD	79-83	formin 1	Homo sapiens	63-66
17939663-4	2007	Using stopped-flow spectroscopy, we show that reduction of the FMN cofactor by NADH in N189A MR is multiphasic, identifying at least four different reactive configurations of the MR-NADH complex.	NAD	182-186	formin 1	Homo sapiens	63-66
29980616-4	2018	In the present study, cellular NAD levels were decreased by overexpression of CD38, a NAD hydrolase, or by treating cells with FK866, an inhibitor of nicotinamide phosphoribosyltransferase (NAMPT).	NAD	31-34	CD38 molecule	Homo sapiens	78-82
17913880-7	2007	beta-NAD is an agonist for P2Y1 receptors, as demonstrated by receptor-mediated responses in HEK293 cells expressing P2Y1 receptors.	NAD	0-8	purinergic receptor P2Y1	Homo sapiens	27-31
29980616-8	2018	Secretomic analysis also showed that decreased NAD triggered interleukin-6 and transforming growth factor beta (TGFbeta) secretion, which activated integrin-beta-catenin, TGFbeta-MAPK, and inflammation signaling pathways to sustain the signaling required for EMT.	NAD	47-50	catenin beta 1	Homo sapiens	157-169
17913880-7	2007	beta-NAD is an agonist for P2Y1 receptors, as demonstrated by receptor-mediated responses in HEK293 cells expressing P2Y1 receptors.	NAD	0-8	purinergic receptor P2Y1	Homo sapiens	117-121
30275764-1	2018	Sirtuin 2 (SIRT2) is a nicotinamide adenine dinucleotide (NAD +)-dependent class III histone deacetylase.	NAD	23-56	sirtuin 2	Homo sapiens	0-9
17628866-7	2007	We tested a diverse set of suramin analogues to elucidate the inhibition of the NAD(+)-dependent histone deacetylases SIRT1 and SIRT2 and discovered selective inhibitors of human sirtuins with potency in the two-digit nanomolar range.	NAD	80-86	sirtuin 2	Homo sapiens	128-133
30275764-1	2018	Sirtuin 2 (SIRT2) is a nicotinamide adenine dinucleotide (NAD +)-dependent class III histone deacetylase.	NAD	23-56	sirtuin 2	Homo sapiens	11-16
30275764-1	2018	Sirtuin 2 (SIRT2) is a nicotinamide adenine dinucleotide (NAD +)-dependent class III histone deacetylase.	NAD	58-63	sirtuin 2	Homo sapiens	0-9
17463062-1	2007	Throughout gestation, the chorion laeve controls the levels of biologically active prostaglandins (PGs) by its high level of nicotinamide adenine dinucleotide-dependent 15-hydroxy PG dehydrogenase (PGDH).	NAD	125-158	15-hydroxyprostaglandin dehydrogenase	Homo sapiens	180-196
30275764-1	2018	Sirtuin 2 (SIRT2) is a nicotinamide adenine dinucleotide (NAD +)-dependent class III histone deacetylase.	NAD	58-63	sirtuin 2	Homo sapiens	11-16
17463062-1	2007	Throughout gestation, the chorion laeve controls the levels of biologically active prostaglandins (PGs) by its high level of nicotinamide adenine dinucleotide-dependent 15-hydroxy PG dehydrogenase (PGDH).	NAD	125-158	15-hydroxyprostaglandin dehydrogenase	Homo sapiens	198-202
30021836-1	2018	The NAD+-dependent deacetylase SIRT1 can be oncogenic or tumor suppressive depending on the tissue.	NAD	4-8	sirtuin 1	Mus musculus	31-36
30230244-7	2018	The effect of NAD treatment on the clock gene Period 1 (PER1) transcription was also studied.	NAD	14-17	period circadian clock 1	Mus musculus	46-54
17456799-1	2007	Sirtuins or Sir2 (silent information regulator 2)-related enzymes have originally been defined as a family of nicotinamide adenine dinucleotide-dependent enzymes that deacetylate lysine residue on various proteins.	NAD	110-143	sirtuin 2	Homo sapiens	12-16
17456799-1	2007	Sirtuins or Sir2 (silent information regulator 2)-related enzymes have originally been defined as a family of nicotinamide adenine dinucleotide-dependent enzymes that deacetylate lysine residue on various proteins.	NAD	110-143	sirtuin 2	Homo sapiens	18-48
30214397-5	2018	NAD+ is a marker of cellular health and a substrate for enzymes implicated in longevity and DNA damage repair such as sirtuins and poly-ADP ribose polymerase-1 (PARP-1).	NAD	0-4	poly (ADP-ribose) polymerase 1	Rattus norvegicus	131-159
17499714-5	2007	In this study we show that some PPAR ligands impair mitochondrial oxidative metabolism in human liver cell line mainly by deranging NADH oxidation.	NAD	132-136	peroxisome proliferator activated receptor alpha	Homo sapiens	32-36
30214397-5	2018	NAD+ is a marker of cellular health and a substrate for enzymes implicated in longevity and DNA damage repair such as sirtuins and poly-ADP ribose polymerase-1 (PARP-1).	NAD	0-4	poly (ADP-ribose) polymerase 1	Rattus norvegicus	161-167
29870726-4	2018	Here, to elucidate the coupled enzymatic reaction of NAD+ hydrolysis and ADP-ribosylation of ubiquitin in SdeA, we characterized the mono-ADP-ribosyltransferase domain of SdeA and show that it consists of two sub-domains termed mART-N and mART-C.	NAD	53-57	ADP-ribosyltransferase 2b	Mus musculus	228-232
17447732-4	2007	The equilibrium and kinetic properties of the association and dissociation of the cofactor NAD+ from the enzymes of Homo sapiens (Hs-SAHH) and Trypanosoma cruzi (Tc-SAHH) are qualitatively similar but quantitatively distinct.	NAD	91-95	adenosylhomocysteinase	Homo sapiens	133-137
17447732-4	2007	The equilibrium and kinetic properties of the association and dissociation of the cofactor NAD+ from the enzymes of Homo sapiens (Hs-SAHH) and Trypanosoma cruzi (Tc-SAHH) are qualitatively similar but quantitatively distinct.	NAD	91-95	adenosylhomocysteinase	Homo sapiens	165-169
17447732-9	2007	In the case of Tc-SAHH, the final affinity for NAD+ is roughly micromolar and this affinity persists as the equilibrium affinity.	NAD	47-51	adenosylhomocysteinase	Homo sapiens	18-22
17447732-11	2007	The slow binding of NAD+ by both enzymes exhibits saturation kinetics with respect to the cofactor concentration; however, binding to Hs-SAHH has a maximum rate constant around 0.06 s-1, while the rate constant for binding to Tc-SAHH levels out at 0.006 s-1.	NAD	20-24	adenosylhomocysteinase	Homo sapiens	137-141
29870726-4	2018	Here, to elucidate the coupled enzymatic reaction of NAD+ hydrolysis and ADP-ribosylation of ubiquitin in SdeA, we characterized the mono-ADP-ribosyltransferase domain of SdeA and show that it consists of two sub-domains termed mART-N and mART-C.	NAD	53-57	ADP-ribosyltransferase 2b	Mus musculus	239-243
29870726-5	2018	The crystal structure of the mART-C domain of SdeA was also determined in free form and in complex with NAD+ at high resolution.	NAD	104-108	ADP-ribosyltransferase 2b	Mus musculus	29-33
30038627-6	2018	Injection of the ARTC2.2-blocking nanobody s+16a 30 min prior to organ harvesting effectively prevented ADP-ribosylation of P2X7 during cell preparation and thereby prevented NAD-induced cell death of the isolated Trm upon subsequent incubation at 37 C. Consequently, preserving Trm vitality by s+16a injection enabled a highly sensitive in vitro cytokine expression profile analyses of FACS sorted liver Trm.	NAD	175-178	tremor	Mus musculus	214-217
30038627-6	2018	Injection of the ARTC2.2-blocking nanobody s+16a 30 min prior to organ harvesting effectively prevented ADP-ribosylation of P2X7 during cell preparation and thereby prevented NAD-induced cell death of the isolated Trm upon subsequent incubation at 37 C. Consequently, preserving Trm vitality by s+16a injection enabled a highly sensitive in vitro cytokine expression profile analyses of FACS sorted liver Trm.	NAD	175-178	tremor	Mus musculus	279-282
17447732-11	2007	The slow binding of NAD+ by both enzymes exhibits saturation kinetics with respect to the cofactor concentration; however, binding to Hs-SAHH has a maximum rate constant around 0.06 s-1, while the rate constant for binding to Tc-SAHH levels out at 0.006 s-1.	NAD	20-24	adenosylhomocysteinase	Homo sapiens	229-233
30038627-6	2018	Injection of the ARTC2.2-blocking nanobody s+16a 30 min prior to organ harvesting effectively prevented ADP-ribosylation of P2X7 during cell preparation and thereby prevented NAD-induced cell death of the isolated Trm upon subsequent incubation at 37 C. Consequently, preserving Trm vitality by s+16a injection enabled a highly sensitive in vitro cytokine expression profile analyses of FACS sorted liver Trm.	NAD	175-178	tremor	Mus musculus	279-282
17447732-13	2007	The equilibrium affinities of both Hs-SAHH and Tc-SAHH for NADH are in the nanomolar range.	NAD	59-63	adenosylhomocysteinase	Homo sapiens	38-42
17447732-13	2007	The equilibrium affinities of both Hs-SAHH and Tc-SAHH for NADH are in the nanomolar range.	NAD	59-63	adenosylhomocysteinase	Homo sapiens	50-54
28987935-7	2018	We present three examples validated with inhibitor sensitivity: (i) Complex I-mediated oxygen consumption driven by NADH, (ii) ATP hydrolysis by the F1FO complex measuring pH changes in an Agilent Seahorse XF Analyzer, and (iii) Mitochondrial glutaminase (GLS1) activity in a coupled reaction monitoring NADH fluorescence in a plate reader.	NAD	304-308	glutaminase	Homo sapiens	256-260
17447732-14	2007	The dissociation rate constants and the slow-binding association rate constants for NAD+ show a complex temperature dependence with both enzymes; however, the cofactor always dissociates more rapidly from Tc-SAHH than from Hs-SAHH, the ratio being around 80-fold at 37 degrees C, and the cofactor binds more rapidly to Hs-SAHH than to Tc-SAHH above approximately 16 degrees C. These features present an opening for selective inhibition of Tc-SAHH over Hs-SAHH, demonstrated with the thioamide analogues of NAD+ and NADH.	NAD	84-88	adenosylhomocysteinase	Homo sapiens	208-212
17447732-14	2007	The dissociation rate constants and the slow-binding association rate constants for NAD+ show a complex temperature dependence with both enzymes; however, the cofactor always dissociates more rapidly from Tc-SAHH than from Hs-SAHH, the ratio being around 80-fold at 37 degrees C, and the cofactor binds more rapidly to Hs-SAHH than to Tc-SAHH above approximately 16 degrees C. These features present an opening for selective inhibition of Tc-SAHH over Hs-SAHH, demonstrated with the thioamide analogues of NAD+ and NADH.	NAD	84-88	adenosylhomocysteinase	Homo sapiens	226-230
17447732-14	2007	The dissociation rate constants and the slow-binding association rate constants for NAD+ show a complex temperature dependence with both enzymes; however, the cofactor always dissociates more rapidly from Tc-SAHH than from Hs-SAHH, the ratio being around 80-fold at 37 degrees C, and the cofactor binds more rapidly to Hs-SAHH than to Tc-SAHH above approximately 16 degrees C. These features present an opening for selective inhibition of Tc-SAHH over Hs-SAHH, demonstrated with the thioamide analogues of NAD+ and NADH.	NAD	84-88	adenosylhomocysteinase	Homo sapiens	226-230
17447732-14	2007	The dissociation rate constants and the slow-binding association rate constants for NAD+ show a complex temperature dependence with both enzymes; however, the cofactor always dissociates more rapidly from Tc-SAHH than from Hs-SAHH, the ratio being around 80-fold at 37 degrees C, and the cofactor binds more rapidly to Hs-SAHH than to Tc-SAHH above approximately 16 degrees C. These features present an opening for selective inhibition of Tc-SAHH over Hs-SAHH, demonstrated with the thioamide analogues of NAD+ and NADH.	NAD	84-88	adenosylhomocysteinase	Homo sapiens	226-230
17447732-14	2007	The dissociation rate constants and the slow-binding association rate constants for NAD+ show a complex temperature dependence with both enzymes; however, the cofactor always dissociates more rapidly from Tc-SAHH than from Hs-SAHH, the ratio being around 80-fold at 37 degrees C, and the cofactor binds more rapidly to Hs-SAHH than to Tc-SAHH above approximately 16 degrees C. These features present an opening for selective inhibition of Tc-SAHH over Hs-SAHH, demonstrated with the thioamide analogues of NAD+ and NADH.	NAD	84-88	adenosylhomocysteinase	Homo sapiens	226-230
17447732-14	2007	The dissociation rate constants and the slow-binding association rate constants for NAD+ show a complex temperature dependence with both enzymes; however, the cofactor always dissociates more rapidly from Tc-SAHH than from Hs-SAHH, the ratio being around 80-fold at 37 degrees C, and the cofactor binds more rapidly to Hs-SAHH than to Tc-SAHH above approximately 16 degrees C. These features present an opening for selective inhibition of Tc-SAHH over Hs-SAHH, demonstrated with the thioamide analogues of NAD+ and NADH.	NAD	84-88	adenosylhomocysteinase	Homo sapiens	226-230
29648801-5	2018	PRODH is a flavin-dependent enzyme that couples proline oxidation with reduction of membrane-bound quinone, while GSALDH catalyzes the NAD+-dependent oxidation of GSAL to glutamate.	NAD	135-139	proline dehydrogenase 1	Homo sapiens	0-5
17432878-5	2007	The alpha-D181N IDH mutant exhibits a 2000-fold decrease in Vmax, with increases of 15-fold in the Kms for Mn(II) and NAD and a much smaller change in the Km for isocitrate.	NAD	118-121	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	16-19
29704621-4	2018	We find that the mitoNEET [2Fe-2S] clusters are rapidly reduced by a catalytic amount of FMNH2 which is reduced by flavin reductase and an equivalent amount of NADH under anaerobic conditions.	NAD	160-164	CDGSH iron sulfur domain 1	Homo sapiens	17-25
17482543-0	2007	Nicotinamide riboside promotes Sir2 silencing and extends lifespan via Nrk and Urh1/Pnp1/Meu1 pathways to NAD+.	NAD	106-110	purine-nucleoside phosphorylase	Mus musculus	84-88
17482543-1	2007	Although NAD(+) biosynthesis is required for Sir2 functions and replicative lifespan in yeast, alterations in NAD(+) precursors have been reported to accelerate aging but not to extend lifespan.	NAD	9-15	sirtuin 1	Mus musculus	45-49
17430113-13	2007	Chronic elevation of TNFalpha leading to necrotic events by NAD depletion in autoimmune disease likely occurs via combination of persistent IDO activation and iNOS-peroxynitrate activation of PARP1 both of which deplete NAD.	NAD	60-63	indoleamine 2,3-dioxygenase 1	Homo sapiens	140-143
17430113-16	2007	Thus pharmacological doses of NAD precursors (nicotinic acid/niacin, nicotinamide/niacinamide, or nicotinamide riboside) should be considered as potentially essential to the therapeutic success of any IDO-inducing regimen for treating autoimmune diseases.	NAD	30-33	indoleamine 2,3-dioxygenase 1	Homo sapiens	201-204
17067289-4	2007	In vitro, DHRS10 converts NAD+ into NADH in the presence of oestradiol, testosterone and 5-androstene-3beta,17beta-diol.	NAD	26-30	hydroxysteroid 17-beta dehydrogenase 14	Homo sapiens	10-16
17067289-4	2007	In vitro, DHRS10 converts NAD+ into NADH in the presence of oestradiol, testosterone and 5-androstene-3beta,17beta-diol.	NAD	36-40	hydroxysteroid 17-beta dehydrogenase 14	Homo sapiens	10-16
17489100-4	2007	To avoid the accumulation of metHb, reductive pathways mediated by cytochrome b5 or flavin, coupled with NADH-dependent or NADPH-dependent metHb reductases, respectively, keep the level of metHb in erythrocytes at less than 1% of the total hemoglobin under normal conditions.	NAD	105-109	cytochrome b5 type A	Homo sapiens	67-80
17489100-8	2007	In contrast, the cytochrome b5-NADH pathway becomes dominant under conditions of excess metHb accumulation, only after the capacity of the flavin-NADPH pathway has reached its limit.	NAD	31-35	cytochrome b5 type A	Homo sapiens	17-30
18404420-3	2007	ATP and its metabolites signal through purinergic P2 and P1 receptors, whereas extracellular NAD exerts its effects by serving as a substrate for ADP-ribosyltransferases (ARTs) and NAD glycohydrolases/ADPR cyclases like CD38 and CD157.	NAD	93-96	CD38 molecule	Homo sapiens	220-224
17269701-5	2007	Direct electrochemical regenerations of NADH were coupled to the synthesis of l-glutamate from alpha-ketoglutarate catalyzed by glutamate dehydrogenases (GDH).	NAD	40-44	glutamate dehydrogenase 1	Homo sapiens	128-152
17269701-5	2007	Direct electrochemical regenerations of NADH were coupled to the synthesis of l-glutamate from alpha-ketoglutarate catalyzed by glutamate dehydrogenases (GDH).	NAD	40-44	glutamate dehydrogenase 1	Homo sapiens	154-157
17269701-7	2007	When GDH were entrapped in "nonconductive" silica gels, synthesized using only TMOS, in the control experiment, the initial supply of NADH exhausted quickly and a final conversion of 30% was obtained.	NAD	134-138	glutamate dehydrogenase 1	Homo sapiens	5-8
17222174-10	2007	Semidehydroascorbate, a major oxidation product of vitamin C, is reconverted to ascorbate in the cytosol by cytochrome b(5) reductase and thioredoxin reductase in reactions involving NADH and NADPH, respectively.	NAD	183-187	peroxiredoxin 5	Homo sapiens	138-159
17127373-6	2007	Consequently, a dual mechanism, NADH-driven MMPT and CD95-mediated apoptosis, involving in both cases acetaldehyde metabolism and ROS production, operates in ethanol-induced apoptosis.	NAD	32-36	Fas cell surface death receptor	Homo sapiens	53-57
17083911-4	2006	The product, oxidized nicotinamide adenine dinucleotide phosphate (NADP(+)), formed following the reaction of NADK with NAD(+) and adenosine 5"-triphosphate was detected with the aid of glucose-6-phosphate dehydrogenase or NADP(+)-isocitrate dehydrogenase, iodonitrotetrazolium chloride, and phenazine methosulfate.	NAD	120-126	NAD kinase	Homo sapiens	110-114
29704621-7	2018	Under aerobic conditions, the mitoNEET [2Fe-2S] clusters can still be reduced by FMNH2 in the presence of flavin reductase and excess NADH.	NAD	134-138	CDGSH iron sulfur domain 1	Homo sapiens	30-38
29704621-8	2018	However, when NADH is completely consumed, the reduced mitoNEET [2Fe-2S] clusters are gradually oxidized by oxygen.	NAD	14-18	CDGSH iron sulfur domain 1	Homo sapiens	55-63
29477240-3	2018	SIRT1 encodes an NAD-dependent deacetylase that modifies the activity of key transcriptional regulators affected in diabetic kidneys, including NF-kappaB, STAT3, p53, FOXO4, and PGC1-alpha.	NAD	17-20	sirtuin 1	Mus musculus	0-5
29782205-6	2018	We linked this lack of therapeutic effect to NAD+-independent activation of SIRT-1 and -3 via AMPK and cAMP signaling related to the starvation-like metabolic state of Bcs1lp.S78G mice.	NAD	45-49	sirtuin 1	Mus musculus	76-89
29550483-9	2018	GR24 upregulated SIRT1 and enhanced the production of NAD+, an essential SIRT1 substrate.	NAD	54-58	sirtuin 1	Mus musculus	73-78
29409011-14	2018	Conclusions: Cardiac SIRT1 mediates AMPK activation via LKB1 deacetylation, and AMPK modulates SIRT1 activity via regulation of NAD+ level during ischaemia.	NAD	128-132	sirtuin 1	Mus musculus	95-100
29642888-3	2018	RESULTS: A new metabolic module was established here, in which, permease Gap1p for L-phenylalanine transportation, catalytic enzymes Aro8p, Aro10p and Adh2p in Ehrlich pathway respectively responsible for transamination, decarboxylation and reduction were assembled, besides, glutamate dehydrogenase Gdh2p was harbored for re-supplying another substrate 2-oxoglutarate, relieving product glutamate repression and regenerating cofactor NADH.	NAD	435-439	alcohol dehydrogenase ADH2	Saccharomyces cerevisiae S288C	151-156
29642888-3	2018	RESULTS: A new metabolic module was established here, in which, permease Gap1p for L-phenylalanine transportation, catalytic enzymes Aro8p, Aro10p and Adh2p in Ehrlich pathway respectively responsible for transamination, decarboxylation and reduction were assembled, besides, glutamate dehydrogenase Gdh2p was harbored for re-supplying another substrate 2-oxoglutarate, relieving product glutamate repression and regenerating cofactor NADH.	NAD	435-439	glutamate dehydrogenase (NAD(+))	Saccharomyces cerevisiae S288C	300-305
29440391-3	2018	Sirtuin 2 (SIRT2) is a cytoplasmic protein in the family of sirtuins that are NAD+-dependent class III histone deacetylases.	NAD	78-82	sirtuin 2	Mus musculus	0-9
29440391-3	2018	Sirtuin 2 (SIRT2) is a cytoplasmic protein in the family of sirtuins that are NAD+-dependent class III histone deacetylases.	NAD	78-82	sirtuin 2	Mus musculus	11-16
29349500-2	2018	Sirtuin 3 (SIRT3) is a NAD + -dependent deacetylase that regulates mitochondrial energy metabolism.	NAD	23-26	sirtuin 3	Mus musculus	0-9
29349500-2	2018	Sirtuin 3 (SIRT3) is a NAD + -dependent deacetylase that regulates mitochondrial energy metabolism.	NAD	23-26	sirtuin 3	Mus musculus	11-16
29349500-7	2018	Exogenous H2S restored the expression of NAMPT and the ratio of NAD+/NADH enhanced the expression and activity of SIRT3.	NAD	64-68	sirtuin 3	Mus musculus	114-119
17174885-1	2006	Resveratrol increases life span in lower organisms by activating the NAD(+)-dependent histone deacetylase Sirt1.	NAD	69-75	sirtuin 1	Mus musculus	106-111
29349500-7	2018	Exogenous H2S restored the expression of NAMPT and the ratio of NAD+/NADH enhanced the expression and activity of SIRT3.	NAD	69-73	sirtuin 3	Mus musculus	114-119
29636685-5	2018	NAD+ is converted by CD38, CD203 and other ecto-enzymes to the Ca2+ mobilizing messengers cyclic ADP-ribose and ADP-ribose, and to adenosine.	NAD	0-4	CD38 molecule	Homo sapiens	21-25
29307841-1	2018	Nicotinamide adenine dinucleotide (NAD) levels decrease with aging as a result of aging-associated CD38 upregulation.	NAD	0-33	CD38 molecule	Homo sapiens	99-103
17031400-3	2006	NRH:quinone oxidoreductase 2 catalysed the reduction of MMC at pH 5.8 with NADH as a co-factor.	NAD	75-79	N-ribosyldihydronicotinamide:quinone reductase 2	Homo sapiens	0-28
29307841-1	2018	Nicotinamide adenine dinucleotide (NAD) levels decrease with aging as a result of aging-associated CD38 upregulation.	NAD	35-38	CD38 molecule	Homo sapiens	99-103
29307841-2	2018	Here, we established a cell model with decreased cellular NAD levels by overexpressing CD38 or treating cells with FK866, an inhibitor of nicotinamide phosphoribosyltransferase.	NAD	58-61	CD38 molecule	Homo sapiens	87-91
29408361-3	2018	Molecular dynamic simulations predicted the binding of alpha-synuclein to the positively charged groove comprising NAD+-binding pocket of GAPDH.	NAD	115-119	synuclein alpha	Homo sapiens	55-70
17075046-1	2006	The silent information regulator 2 (Sir2) family of NAD-dependent N-acetyl-protein deacetylases participates in the regulation of gene silencing, chromatin structure, and longevity.	NAD	52-55	sirtuin 2	Homo sapiens	4-34
17075046-1	2006	The silent information regulator 2 (Sir2) family of NAD-dependent N-acetyl-protein deacetylases participates in the regulation of gene silencing, chromatin structure, and longevity.	NAD	52-55	sirtuin 2	Homo sapiens	36-40
17075046-2	2006	In the Sir2-catalyzed reaction, the acetyl moiety of N-acetyl-histone is transferred to the ADP-ribose of NAD, yielding O-acetyl-ADP-ribose and nicotinamide.	NAD	106-109	sirtuin 2	Homo sapiens	7-11
29371109-3	2018	SIRT2, a member of NAD(+)-dependent class III deacetylases, is involved in genomic stability, metabolism, inflammation, oxidative stress and autophagy.	NAD	19-25	sirtuin 2	Homo sapiens	0-5
17132048-9	2006	Our data indicate an NAD-independent requirement of NMNAT for maintaining neuronal integrity that can be exploited to protect neurons from neuronal activity-induced degeneration by overexpression of the protein.	NAD	21-24	Nicotinamide mononucleotide adenylyltransferase	Drosophila melanogaster	52-57
29309612-2	2018	Methods: We studied NAD biosynthesis in BRAF inhibitor (BRAFi)-resistant (BiR) melanoma cell lines.	NAD	20-23	Braf transforming gene	Mus musculus	40-44
29317496-9	2018	We showed that decreased nicotinamide mononucleotide adenylyltransferase (Nma1/Nma2) levels probably caused the NAD+ defects, and NMA1-oe was sufficient to restore NAD+ NatB-mediated N-terminal acetylation of Nma1 and Nma2 appears essential for maintaining NAD+ levels.	NAD	112-116	nicotinamide-nucleotide adenylyltransferase NMA1	Saccharomyces cerevisiae S288C	74-83
29317496-9	2018	We showed that decreased nicotinamide mononucleotide adenylyltransferase (Nma1/Nma2) levels probably caused the NAD+ defects, and NMA1-oe was sufficient to restore NAD+ NatB-mediated N-terminal acetylation of Nma1 and Nma2 appears essential for maintaining NAD+ levels.	NAD	112-116	nicotinamide-nucleotide adenylyltransferase NMA1	Saccharomyces cerevisiae S288C	74-78
16951430-3	2006	Human CD38 is an ectoenzyme that can use NAD(+) to synthesize two calcium-mobilizing molecules.	NAD	41-47	CD38 molecule	Homo sapiens	6-10
29402742-1	2018	The NAD+-dependent deacetylase SIRT1, which is associated with the improvement of metabolic syndromes, such as type 2 diabetes, is a well-known longevity-related gene.	NAD	4-8	sirtuin 1	Mus musculus	31-36
28970254-0	2018	Silybin inhibits NLRP3 inflammasome assembly through the NAD+/SIRT2 pathway in mice with nonalcoholic fatty liver disease.	NAD	57-61	NLR family, pyrin domain containing 3	Mus musculus	17-22
16935261-0	2006	Regulation of SIRT 1 mediated NAD dependent deacetylation: a novel role for the multifunctional enzyme CD38.	NAD	30-33	sirtuin 1	Mus musculus	14-20
16935261-7	2006	We propose that by modulating availability of NAD to the SIRT1 enzyme, CD38 may regulate SIRT1 enzymatic activity.	NAD	46-49	sirtuin 1	Mus musculus	57-62
16935261-7	2006	We propose that by modulating availability of NAD to the SIRT1 enzyme, CD38 may regulate SIRT1 enzymatic activity.	NAD	46-49	sirtuin 1	Mus musculus	89-94
28844085-8	2018	Nicotinamide, a PARP-1 inhibitor, protects against the metabolic cascade elicited by the primary stage, avoiding NAD+ exhaustion and the energetic crisis.	NAD	113-117	poly (ADP-ribose) polymerase 1	Rattus norvegicus	16-22
16632544-9	2006	This type of cell death was blocked by repletion of cellular NAD levels as well as by activation of the longevity factor Sir2alpha deacetylase, indicating that PARP induction and subsequent depletion of NAD levels are the sequence of events causing angiotensin II-mediated cardiomyocyte cell death.	NAD	203-206	sirtuin 1	Mus musculus	121-130
29416562-9	2018	Additional deletion of GPD2, which encodes an isoenzyme of NAD+-dependent glycerol-3-phosphate dehydrogenase, combined with overexpression of the structural genes for enzymes of the non-oxidative pentose-phosphate pathway, yielded a CO2-reducing strain that grew at the same rate as a non-engineered reference strain in anaerobic bioreactor batch cultures, while exhibiting a 86% lower glycerol yield and a 15% higher ethanol yield.	NAD	59-63	glycerol-3-phosphate dehydrogenase (NAD(+)) GPD2	Saccharomyces cerevisiae S288C	23-27
29320709-3	2018	(2018) demonstrate that intratumoral CD4+ T cell functions and memory can be improved by targeting a CD38-NAD+-Sirt1-Foxo1 metabolic circuit.	NAD	106-110	CD38 molecule	Homo sapiens	101-105
29343967-0	2018	Indoleamine 2,3-Dioxygenase Activity Increases NAD+ Production in IFN-gamma-Stimulated Human Primary Mononuclear Cells.	NAD	47-51	indoleamine 2,3-dioxygenase 1	Homo sapiens	0-27
29343967-7	2018	This study provides evidence for the first time that an immune-mediated increase in IDO activity increases NAD+ biosynthesis concomitantly with an increase in NAD+ catabolism in primary human macrophages.	NAD	107-111	indoleamine 2,3-dioxygenase 1	Homo sapiens	84-87
29343967-7	2018	This study provides evidence for the first time that an immune-mediated increase in IDO activity increases NAD+ biosynthesis concomitantly with an increase in NAD+ catabolism in primary human macrophages.	NAD	159-163	indoleamine 2,3-dioxygenase 1	Homo sapiens	84-87
29074724-3	2018	We demonstrate here that glucose deprivation or hypoxia results in the AMPK-mediated phosphorylation of phosphoribosyl pyrophosphate synthetase 1 (PRPS1) S180 and PRPS2 S183, leading to conversion of PRPS hexamers to monomers and thereby inhibiting PRPS1/2 activity, nucleotide synthesis, and nicotinamide adenine dinucleotide (NAD) production.	NAD	293-326	phosphoribosyl pyrophosphate synthetase 1	Homo sapiens	104-145
29074724-3	2018	We demonstrate here that glucose deprivation or hypoxia results in the AMPK-mediated phosphorylation of phosphoribosyl pyrophosphate synthetase 1 (PRPS1) S180 and PRPS2 S183, leading to conversion of PRPS hexamers to monomers and thereby inhibiting PRPS1/2 activity, nucleotide synthesis, and nicotinamide adenine dinucleotide (NAD) production.	NAD	293-326	phosphoribosyl pyrophosphate synthetase 1	Homo sapiens	147-152
29074724-3	2018	We demonstrate here that glucose deprivation or hypoxia results in the AMPK-mediated phosphorylation of phosphoribosyl pyrophosphate synthetase 1 (PRPS1) S180 and PRPS2 S183, leading to conversion of PRPS hexamers to monomers and thereby inhibiting PRPS1/2 activity, nucleotide synthesis, and nicotinamide adenine dinucleotide (NAD) production.	NAD	328-331	phosphoribosyl pyrophosphate synthetase 1	Homo sapiens	104-145
29074724-3	2018	We demonstrate here that glucose deprivation or hypoxia results in the AMPK-mediated phosphorylation of phosphoribosyl pyrophosphate synthetase 1 (PRPS1) S180 and PRPS2 S183, leading to conversion of PRPS hexamers to monomers and thereby inhibiting PRPS1/2 activity, nucleotide synthesis, and nicotinamide adenine dinucleotide (NAD) production.	NAD	328-331	phosphoribosyl pyrophosphate synthetase 1	Homo sapiens	147-152
29433736-5	2018	Deacetylation of FoxOs by the NAD-dependent histone deacetylase Sirt1 in both osteoblasts and osteoclasts stimulates bone formation and inhibits bone resorption, making Sirt1 activators promising therapeutic agents for diseases of low bone mass.	NAD	30-33	sirtuin 1	Mus musculus	64-69
29433736-5	2018	Deacetylation of FoxOs by the NAD-dependent histone deacetylase Sirt1 in both osteoblasts and osteoclasts stimulates bone formation and inhibits bone resorption, making Sirt1 activators promising therapeutic agents for diseases of low bone mass.	NAD	30-33	sirtuin 1	Mus musculus	169-174
29275294-5	2018	The gene expression of growth differentiation factor 9 (Gdf9), Mullerian-inhibiting substance, steroidogenic factor 1 (Sf1) and steroidogenic acute regulatory protein (Star) in the ovary was significantly increased in the mice neonatally exposed to 40 mug DPN compared to oil-treated mice.	NAD	256-259	growth differentiation factor 9	Mus musculus	23-54
29275294-6	2018	CONCLUSION: Since SF1 is an important transcription factor of several genes involved in ovarian function, up-regulation of Sf1 expression by neonatal exposure to DPN, through ERbeta, might affect expression of Gdf9, Mis and Star, resulting in increased PFs in mouse ovary.	NAD	162-165	growth differentiation factor 9	Mus musculus	210-214
30097862-1	2018	Nicotinamide adenine dinucleotide (NAD+) is an essential redox cofactor and signaling molecule that controls the activity of enzymes involved in metabolism, DNA repair, and cellular survival, such as the PARPs, CD38, and the sirtuins.	NAD	0-33	CD38 molecule	Homo sapiens	211-215
30097862-1	2018	Nicotinamide adenine dinucleotide (NAD+) is an essential redox cofactor and signaling molecule that controls the activity of enzymes involved in metabolism, DNA repair, and cellular survival, such as the PARPs, CD38, and the sirtuins.	NAD	35-39	CD38 molecule	Homo sapiens	211-215
29213065-2	2017	The disordered microtubule associated Tubulin Polymerization Promoting Protein (TPPP/p25) and the NAD+-dependent tubulin deacetylase sirtuin-2 (SIRT2) play key roles in oligodendrocyte differentiation by acting as dominant factors in the organization of myelin proteome.	NAD	98-102	sirtuin 2	Homo sapiens	133-142
29213065-2	2017	The disordered microtubule associated Tubulin Polymerization Promoting Protein (TPPP/p25) and the NAD+-dependent tubulin deacetylase sirtuin-2 (SIRT2) play key roles in oligodendrocyte differentiation by acting as dominant factors in the organization of myelin proteome.	NAD	98-102	sirtuin 2	Homo sapiens	144-149
28973657-0	2017	In vitro characterization of mitochondrial function and structure in rat and human cells with a deficiency of the NADH: ubiquinone oxidoreductase Ndufc2 subunit.	NAD	114-118	NADH:ubiquinone oxidoreductase subunit C2	Homo sapiens	146-152
28973657-1	2017	Ndufc2, a subunit of the NADH: ubiquinone oxidoreductase, plays a key role in the assembly and activity of complex I within the mitochondrial OXPHOS chain.	NAD	25-29	NADH:ubiquinone oxidoreductase subunit C2	Homo sapiens	0-6
28860121-3	2017	Vulnerability for NAD+ depletion has been reported for IDH1/2-mutant cells.	NAD	18-22	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	55-59
28544355-1	2017	AIMS: Activation of the NAD+ dependent protein deacetylase SIRT1 has been proposed as a therapeutic strategy to treat mitochondrial dysfunction and insulin resistance in skeletal muscle.	NAD	24-27	sirtuin 1	Mus musculus	59-64
28819816-4	2017	DHS catalyzes a complex reaction that occurs in two stages, first, the NAD-dependent cleavage of spermidine to form an enzyme-butylimine intermediate and enzyme-bound NADH, and second, the transfer of the butylimine moiety from the enzyme intermediate to the eIF5A precursor and subsequent reduction of the eIF5A-butylimine intermediate by enzyme-bound NADH to form deoxyhypusine [N epsilon -4-aminobutyl(lysine)].	NAD	71-74	eukaryotic translation initiation factor 5A	Homo sapiens	259-264
28819816-4	2017	DHS catalyzes a complex reaction that occurs in two stages, first, the NAD-dependent cleavage of spermidine to form an enzyme-butylimine intermediate and enzyme-bound NADH, and second, the transfer of the butylimine moiety from the enzyme intermediate to the eIF5A precursor and subsequent reduction of the eIF5A-butylimine intermediate by enzyme-bound NADH to form deoxyhypusine [N epsilon -4-aminobutyl(lysine)].	NAD	71-74	eukaryotic translation initiation factor 5A	Homo sapiens	307-312
28973648-0	2017	The NAD+-dependent deacetylase SIRT2 attenuates oxidative stress and mitochondrial dysfunction and improves insulin sensitivity in hepatocytes.	NAD	4-8	sirtuin 2	Homo sapiens	31-36
31966440-2	2017	The aim of the present study was to investigate whether the protective effects of propofol on the liver are related to Sirt1, an NAD+-dependent deacetylase with anti-inflammatory and antioxidant properties.	NAD	129-132	sirtuin 1	Mus musculus	119-124
27796760-0	2017	Downregulation of NAD-Dependent Deacetylase SIRT2 Protects Mouse Brain Against Ischemic Stroke.	NAD	18-21	sirtuin 2	Mus musculus	44-49
29072685-2	2017	SIRT3, a member of NAD+-dependent deacetylases, is mainly localized in mitochondria.	NAD	19-22	sirtuin 3	Mus musculus	0-5
29074993-1	2017	Sirtuins (SIRT1-7) are NAD-dependent proteins with the enzymatic activity of deacetylases and ADP ribosyltransferases.	NAD	23-26	sirtuin 1	Mus musculus	10-15
16965620-14	2006	The ERbeta agonist DPN caused a decrease of the PR mRNA levels, which was also found for PRAB and PRB immunostaining in the GE.	NAD	19-22	estrogen receptor 2	Rattus norvegicus	4-10
16965620-17	2006	The ERbeta agonist DPN decreased the mRNA levels of PRAB and PRB, as well as the PRAB protein level in GE.	NAD	19-22	estrogen receptor 2	Rattus norvegicus	4-10
16961761-7	2006	(2) Non-drinker rats carry a previously unreported allele of aldehyde dehydrogenase-2 (Aldh2) that encodes an enzyme with a low affinity for Nicotinamide-adenine-dinuclectide (NAD+) (Aldh2(2)), while drinker rats present two Aldh2 alleles (Aldh2(1) and Aldh2(3)) with four- to fivefold higher affinities for NAD+.	NAD	176-180	aldehyde dehydrogenase 2 family member	Rattus norvegicus	183-188
16961761-7	2006	(2) Non-drinker rats carry a previously unreported allele of aldehyde dehydrogenase-2 (Aldh2) that encodes an enzyme with a low affinity for Nicotinamide-adenine-dinuclectide (NAD+) (Aldh2(2)), while drinker rats present two Aldh2 alleles (Aldh2(1) and Aldh2(3)) with four- to fivefold higher affinities for NAD+.	NAD	176-180	aldehyde dehydrogenase 2 family member	Rattus norvegicus	183-188
16917544-6	2006	Importantly, mutagenesis of the LXXLL motif eliminated FoxO1 interaction with the nicotinamide adenine dinucleotide-dependent (NAD-dependent) deacetylase sirtuin 1 (Sirt1), sustained the acetylated state of FoxO1, and made FoxO1 nicotinamide and resveratrol insensitive, supporting a role for this motif in Sirt1 binding.	NAD	82-115	forkhead box O1	Mus musculus	55-60
16917544-6	2006	Importantly, mutagenesis of the LXXLL motif eliminated FoxO1 interaction with the nicotinamide adenine dinucleotide-dependent (NAD-dependent) deacetylase sirtuin 1 (Sirt1), sustained the acetylated state of FoxO1, and made FoxO1 nicotinamide and resveratrol insensitive, supporting a role for this motif in Sirt1 binding.	NAD	82-115	sirtuin 1	Mus musculus	154-163
16917544-6	2006	Importantly, mutagenesis of the LXXLL motif eliminated FoxO1 interaction with the nicotinamide adenine dinucleotide-dependent (NAD-dependent) deacetylase sirtuin 1 (Sirt1), sustained the acetylated state of FoxO1, and made FoxO1 nicotinamide and resveratrol insensitive, supporting a role for this motif in Sirt1 binding.	NAD	82-115	sirtuin 1	Mus musculus	165-170
16917544-6	2006	Importantly, mutagenesis of the LXXLL motif eliminated FoxO1 interaction with the nicotinamide adenine dinucleotide-dependent (NAD-dependent) deacetylase sirtuin 1 (Sirt1), sustained the acetylated state of FoxO1, and made FoxO1 nicotinamide and resveratrol insensitive, supporting a role for this motif in Sirt1 binding.	NAD	82-115	forkhead box O1	Mus musculus	207-212
16917544-6	2006	Importantly, mutagenesis of the LXXLL motif eliminated FoxO1 interaction with the nicotinamide adenine dinucleotide-dependent (NAD-dependent) deacetylase sirtuin 1 (Sirt1), sustained the acetylated state of FoxO1, and made FoxO1 nicotinamide and resveratrol insensitive, supporting a role for this motif in Sirt1 binding.	NAD	82-115	forkhead box O1	Mus musculus	207-212
16917544-6	2006	Importantly, mutagenesis of the LXXLL motif eliminated FoxO1 interaction with the nicotinamide adenine dinucleotide-dependent (NAD-dependent) deacetylase sirtuin 1 (Sirt1), sustained the acetylated state of FoxO1, and made FoxO1 nicotinamide and resveratrol insensitive, supporting a role for this motif in Sirt1 binding.	NAD	82-115	sirtuin 1	Mus musculus	307-312
16917544-6	2006	Importantly, mutagenesis of the LXXLL motif eliminated FoxO1 interaction with the nicotinamide adenine dinucleotide-dependent (NAD-dependent) deacetylase sirtuin 1 (Sirt1), sustained the acetylated state of FoxO1, and made FoxO1 nicotinamide and resveratrol insensitive, supporting a role for this motif in Sirt1 binding.	NAD	127-130	forkhead box O1	Mus musculus	55-60
16917544-6	2006	Importantly, mutagenesis of the LXXLL motif eliminated FoxO1 interaction with the nicotinamide adenine dinucleotide-dependent (NAD-dependent) deacetylase sirtuin 1 (Sirt1), sustained the acetylated state of FoxO1, and made FoxO1 nicotinamide and resveratrol insensitive, supporting a role for this motif in Sirt1 binding.	NAD	127-130	sirtuin 1	Mus musculus	154-163
16917544-6	2006	Importantly, mutagenesis of the LXXLL motif eliminated FoxO1 interaction with the nicotinamide adenine dinucleotide-dependent (NAD-dependent) deacetylase sirtuin 1 (Sirt1), sustained the acetylated state of FoxO1, and made FoxO1 nicotinamide and resveratrol insensitive, supporting a role for this motif in Sirt1 binding.	NAD	127-130	forkhead box O1	Mus musculus	207-212
16917544-6	2006	Importantly, mutagenesis of the LXXLL motif eliminated FoxO1 interaction with the nicotinamide adenine dinucleotide-dependent (NAD-dependent) deacetylase sirtuin 1 (Sirt1), sustained the acetylated state of FoxO1, and made FoxO1 nicotinamide and resveratrol insensitive, supporting a role for this motif in Sirt1 binding.	NAD	127-130	forkhead box O1	Mus musculus	207-212
16917544-6	2006	Importantly, mutagenesis of the LXXLL motif eliminated FoxO1 interaction with the nicotinamide adenine dinucleotide-dependent (NAD-dependent) deacetylase sirtuin 1 (Sirt1), sustained the acetylated state of FoxO1, and made FoxO1 nicotinamide and resveratrol insensitive, supporting a role for this motif in Sirt1 binding.	NAD	127-130	sirtuin 1	Mus musculus	307-312
16814740-1	2006	Cytochrome b5 reductase (cb5r), a member of the flavoprotein transhydrogenase family of oxidoreductase enzymes, catalyzes the transfer of reducing equivalents from the physiological electron donor, NADH, to two molecules of cytochrome b5.	NAD	198-202	cytochrome b5 type A	Homo sapiens	224-237
16764994-3	2006	Although the sit4 mutant failed to grow on respiratory substrates, in the exponential growth, phase respiration was de-repressed; active respiration was confirmed by measuring oxygen consumption and NADH generation.	NAD	199-203	type 2A-related serine/threonine-protein phosphatase SIT4	Saccharomyces cerevisiae S288C	13-17
16878501-2	2006	During the acute and subacute exposure of bone marrow cells to Doxorubicin in vivo, expression of CD38 is decreased corresponding to elevation of intracellular and extracellular NAD+ concentrations.	NAD	178-182	CD38 molecule	Homo sapiens	98-102
16041576-8	2006	In addition, genes involved in NAD metabolism, i.e. BNA2, BNA3, BNA4 and BNA6, or those involved in the TCA cycle and glutamate metabolism, i.e. MEU1, CIT1, CIT2, KDG1 and KDG2, displayed significant changes in expression.	NAD	31-34	kynurenine--oxoglutarate transaminase	Saccharomyces cerevisiae S288C	58-62
16041576-8	2006	In addition, genes involved in NAD metabolism, i.e. BNA2, BNA3, BNA4 and BNA6, or those involved in the TCA cycle and glutamate metabolism, i.e. MEU1, CIT1, CIT2, KDG1 and KDG2, displayed significant changes in expression.	NAD	31-34	nicotinate-nucleotide diphosphorylase (carboxylating)	Saccharomyces cerevisiae S288C	73-77
16502325-2	2006	1985 Biochim Pharmacol 34, 2605-2609], the interaction resulting in a stimulatory effect on the ceruloplasmin catalyzed oxidation of catecholamines and NADH; the latter used as substrate in the present study.	NAD	152-156	ceruloplasmin	Homo sapiens	96-109
28736243-2	2017	Cyclic ADP-ribose, a potent Ca2+ mobilizing second messenger synthesized from NAD+ by CD38, regulates the opening of ryanodine receptor.	NAD	78-82	CD38 molecule	Homo sapiens	86-90
29031725-3	2017	METHODS: Using the cre-loxP system, we overexpressed the mitochondrial NAD+ dependent protein deacetylase SIRT3 in enterocytes of mice (iSIRT3 mice).	NAD	71-74	sirtuin 3	Mus musculus	106-111
28989670-0	2017	Potent mechanism-based sirtuin-2-selective inhibition by an in situ-generated occupant of the substrate-binding site, "selectivity pocket" and NAD+-binding site.	NAD	143-147	sirtuin 2	Homo sapiens	23-32
28989670-1	2017	Sirtuin 2 (SIRT2), a member of the NAD+-dependent histone deacetylase family, has recently received increasing attention due to its potential involvement in neurodegenerative diseases and the progression of cancer.	NAD	35-38	sirtuin 2	Homo sapiens	0-9
28989670-1	2017	Sirtuin 2 (SIRT2), a member of the NAD+-dependent histone deacetylase family, has recently received increasing attention due to its potential involvement in neurodegenerative diseases and the progression of cancer.	NAD	35-38	sirtuin 2	Homo sapiens	11-16
28989670-4	2017	Compound 36 engages in a nucleophilic attack toward NAD+ at the active site of SIRT2, which affords a stable 36-ADP-ribose conjugate that simultaneously occupies the substrate-binding site, the "selectivity pocket" and the NAD+-binding site.	NAD	52-56	sirtuin 2	Homo sapiens	79-84
16211212-0	2005	FISH-mapping and genomic organization of the NAD-dependent histone deacetylase gene, Sirtuin 2 (Sirt2).	NAD	45-48	sirtuin 2	Homo sapiens	85-94
28989670-4	2017	Compound 36 engages in a nucleophilic attack toward NAD+ at the active site of SIRT2, which affords a stable 36-ADP-ribose conjugate that simultaneously occupies the substrate-binding site, the "selectivity pocket" and the NAD+-binding site.	NAD	223-227	sirtuin 2	Homo sapiens	79-84
16211212-0	2005	FISH-mapping and genomic organization of the NAD-dependent histone deacetylase gene, Sirtuin 2 (Sirt2).	NAD	45-48	sirtuin 2	Homo sapiens	96-101
28714002-13	2017	Stochastic perturbation analysis revealed that NADH:ubiquinone oxidoreductase subunit B2 (NDUFB2), NDUFB8 and ubiquinol-cytochrome c reductase hinge protein (UQCRH) were associated with cellular respiration in Gram-negative samples, whereas large tumor suppressor kinase 2 (LATS2) was associated with G1/S transition of the mitotic cell cycle in Gram-positive samples.	NAD	47-51	ubiquinol-cytochrome c reductase hinge protein	Homo sapiens	110-156
16211212-1	2005	Sirtuin 2 (SIRT2) is a nicotinamide adenine dinucleotide (NAD(+))-dependent deacetylase, which belongs to the Silent information regulator 2 (Sir2) family of sirtuin histone deacetylases (HDACs).	NAD	23-56	sirtuin 2	Homo sapiens	0-9
16211212-1	2005	Sirtuin 2 (SIRT2) is a nicotinamide adenine dinucleotide (NAD(+))-dependent deacetylase, which belongs to the Silent information regulator 2 (Sir2) family of sirtuin histone deacetylases (HDACs).	NAD	23-56	sirtuin 2	Homo sapiens	11-16
16211212-1	2005	Sirtuin 2 (SIRT2) is a nicotinamide adenine dinucleotide (NAD(+))-dependent deacetylase, which belongs to the Silent information regulator 2 (Sir2) family of sirtuin histone deacetylases (HDACs).	NAD	23-56	sirtuin 2	Homo sapiens	110-140
16211212-1	2005	Sirtuin 2 (SIRT2) is a nicotinamide adenine dinucleotide (NAD(+))-dependent deacetylase, which belongs to the Silent information regulator 2 (Sir2) family of sirtuin histone deacetylases (HDACs).	NAD	23-56	sirtuin 2	Homo sapiens	142-146
15935693-2	2005	Inhibition of AFMID by organophosphorus insecticides in developing chicken embryos is correlated with lowered NAD levels and severe teratogenesis.	NAD	110-113	arylformamidase	Gallus gallus	14-19
28714002-13	2017	Stochastic perturbation analysis revealed that NADH:ubiquinone oxidoreductase subunit B2 (NDUFB2), NDUFB8 and ubiquinol-cytochrome c reductase hinge protein (UQCRH) were associated with cellular respiration in Gram-negative samples, whereas large tumor suppressor kinase 2 (LATS2) was associated with G1/S transition of the mitotic cell cycle in Gram-positive samples.	NAD	47-51	ubiquinol-cytochrome c reductase hinge protein	Homo sapiens	158-163
27344330-7	2017	Significantly enhanced NAD production and Sirt2 expression were also found in the CNS of mice treated with LINGO-1-Fc-producing NSC.	NAD	23-26	leucine rich repeat and Ig domain containing 1	Mus musculus	107-114
16157265-3	2005	The results indicated that apart from the two subunits of cellular RNA polymerase complex, BTF3 and ATF5, this nsp10 protein was also able to interact specifically with the NADH 4L subunit and cytochrome oxidase II.	NAD	173-177	basic transcription factor 3	Homo sapiens	91-95
28804544-3	2017	SIRT3, as a mitochondrial NAD+-dependent histone deacetylase, has been demonstrated beneficial in many cardiovascular diseases.	NAD	26-29	sirtuin 3	Mus musculus	0-5
16177185-5	2005	This function of GPX1 is associated with attenuating the prooxidant-induced oxidation of NADPH, NADH, lipid, and protein in various tissues.	NAD	96-100	glutathione peroxidase 1	Mus musculus	17-21
28683272-2	2017	Axotomy activates an intrinsic pro-degenerative axon death signaling cascade involving loss of the NAD+ biosynthetic enzyme Nmnat/Nmnat2 in axons, activation of dSarm/Sarm1, and subsequent Sarm-dependent depletion of NAD+.	NAD	99-103	Nicotinamide mononucleotide adenylyltransferase	Drosophila melanogaster	124-129
16154090-7	2005	The analysis of the CD38 substrate binding models revealed two key residues that may be critical in controlling CD38"s multifunctionality of NAD hydrolysis, ADP-ribosyl cyclase, and cADPR hydrolysis activities.	NAD	141-144	CD38 molecule	Homo sapiens	20-24
16154090-7	2005	The analysis of the CD38 substrate binding models revealed two key residues that may be critical in controlling CD38"s multifunctionality of NAD hydrolysis, ADP-ribosyl cyclase, and cADPR hydrolysis activities.	NAD	141-144	CD38 molecule	Homo sapiens	112-116
28683272-2	2017	Axotomy activates an intrinsic pro-degenerative axon death signaling cascade involving loss of the NAD+ biosynthetic enzyme Nmnat/Nmnat2 in axons, activation of dSarm/Sarm1, and subsequent Sarm-dependent depletion of NAD+.	NAD	217-221	Nicotinamide mononucleotide adenylyltransferase	Drosophila melanogaster	124-129
15836437-7	2005	After the addition of catalase that removes the H2O2 necessary for NADH oxidation by apoplastic peroxidases, mitochondrial oxygen consumption could be measured in permeabilized cells.	NAD	67-71	catalase isozyme 1	Nicotiana tabacum	22-30
28476317-0	2017	Evolution, structure and membrane association of NDUFAF6, an assembly factor for NADH:ubiquinone oxidoreductase (Complex I).	NAD	81-85	NADH:ubiquinone oxidoreductase complex assembly factor 6	Homo sapiens	49-56
15855156-1	2005	NAD kinase phosphorylates NAD+ to form NADP+ and is strictly specific to NAD+, whereas NADH kinase phosphorylates both NAD+ and NADH, thereby showing relaxed substrate specificity.	NAD	26-30	NAD kinase	Homo sapiens	0-10
28476317-2	2017	Its FMN cofactor accepts two electrons from NADH and transfers them to ubiquinone via a chain of iron-sulphur centers.	NAD	44-48	formin 1	Homo sapiens	4-7
15855156-1	2005	NAD kinase phosphorylates NAD+ to form NADP+ and is strictly specific to NAD+, whereas NADH kinase phosphorylates both NAD+ and NADH, thereby showing relaxed substrate specificity.	NAD	73-77	NAD kinase	Homo sapiens	0-10
15855156-1	2005	NAD kinase phosphorylates NAD+ to form NADP+ and is strictly specific to NAD+, whereas NADH kinase phosphorylates both NAD+ and NADH, thereby showing relaxed substrate specificity.	NAD	73-77	NAD kinase	Homo sapiens	0-10
28375741-2	2017	The three IDH isoforms (nicotinamide adenine dinucleotide phosphate-dependent IDH1 and IDH2, and nicotinamide adenine dinucleotide-dependent IDH3) contribute to regulating the circuitry of central metabolism.	NAD	24-57	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	10-13
15924421-5	2005	The lack of a Mg(2+) ion effect on hydride transfer was further demonstrated with an E399Q mutant of ALDH1 whose rate-limiting step had been changed from NADH dissociation to hydride transfer.	NAD	154-158	aldehyde dehydrogenase 1 family member A1	Homo sapiens	101-106
15924421-11	2005	In contrast, the metal ions affected only the NAD(+) activation of ALDH1.	NAD	46-52	aldehyde dehydrogenase 1 family member A1	Homo sapiens	67-72
28375741-2	2017	The three IDH isoforms (nicotinamide adenine dinucleotide phosphate-dependent IDH1 and IDH2, and nicotinamide adenine dinucleotide-dependent IDH3) contribute to regulating the circuitry of central metabolism.	NAD	24-57	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	78-82
28461337-6	2017	In the presence of FMN, NADH, and flavin reductase, which reduces FMN to FMNH2 using NADH as the electron donor, mitoNEET mediates oxidation of NADH with a concomitant reduction of oxygen.	NAD	85-89	CDGSH iron sulfur domain 1	Homo sapiens	113-121
28461337-6	2017	In the presence of FMN, NADH, and flavin reductase, which reduces FMN to FMNH2 using NADH as the electron donor, mitoNEET mediates oxidation of NADH with a concomitant reduction of oxygen.	NAD	85-89	CDGSH iron sulfur domain 1	Homo sapiens	113-121
16038606-2	2005	It was found that: 1) the native tetrameric form of this enzyme catalyzes all types of studied reactions; 2) hydrogenase dimer, HoxHY, is a minimal structural unit catalyzing hydrogenase reaction with an artificial electron donor, reduced methyl viologen; 3) all structural fragments containing FMN and NAD+/NADH-binding sites exhibit catalytic activity in diaphorase reactions with one- and two-electron acceptors; 4) small subunits, HoxY and HoxU also exhibit activity in diaphorase reactions with artificial acceptors.	NAD	303-307	formin 1	Homo sapiens	295-298
28461337-9	2017	Pioglitazone or its analog NL-1 appears to inhibit the electron transfer activity of mitoNEET by forming a unique complex with mitoNEET and FMNH2 The results suggest that mitoNEET is a redox enzyme that may promote oxidation of NADH to facilitate enhanced glycolysis in the cytosol and that pioglitazone may regulate energy metabolism in mitochondria by inhibiting the electron transfer activity of mitoNEET.	NAD	228-232	CDGSH iron sulfur domain 1	Homo sapiens	85-93
16038606-2	2005	It was found that: 1) the native tetrameric form of this enzyme catalyzes all types of studied reactions; 2) hydrogenase dimer, HoxHY, is a minimal structural unit catalyzing hydrogenase reaction with an artificial electron donor, reduced methyl viologen; 3) all structural fragments containing FMN and NAD+/NADH-binding sites exhibit catalytic activity in diaphorase reactions with one- and two-electron acceptors; 4) small subunits, HoxY and HoxU also exhibit activity in diaphorase reactions with artificial acceptors.	NAD	308-312	formin 1	Homo sapiens	295-298
28461337-9	2017	Pioglitazone or its analog NL-1 appears to inhibit the electron transfer activity of mitoNEET by forming a unique complex with mitoNEET and FMNH2 The results suggest that mitoNEET is a redox enzyme that may promote oxidation of NADH to facilitate enhanced glycolysis in the cytosol and that pioglitazone may regulate energy metabolism in mitochondria by inhibiting the electron transfer activity of mitoNEET.	NAD	228-232	CDGSH iron sulfur domain 1	Homo sapiens	127-135
28461337-9	2017	Pioglitazone or its analog NL-1 appears to inhibit the electron transfer activity of mitoNEET by forming a unique complex with mitoNEET and FMNH2 The results suggest that mitoNEET is a redox enzyme that may promote oxidation of NADH to facilitate enhanced glycolysis in the cytosol and that pioglitazone may regulate energy metabolism in mitochondria by inhibiting the electron transfer activity of mitoNEET.	NAD	228-232	CDGSH iron sulfur domain 1	Homo sapiens	127-135
28461337-9	2017	Pioglitazone or its analog NL-1 appears to inhibit the electron transfer activity of mitoNEET by forming a unique complex with mitoNEET and FMNH2 The results suggest that mitoNEET is a redox enzyme that may promote oxidation of NADH to facilitate enhanced glycolysis in the cytosol and that pioglitazone may regulate energy metabolism in mitochondria by inhibiting the electron transfer activity of mitoNEET.	NAD	228-232	CDGSH iron sulfur domain 1	Homo sapiens	127-135
28659716-6	2017	More importantly, the immunoregulatory properties of NAD+ are strongly related to the overexpression of tryptophan hydroxylase 1 (Tph1).	NAD	53-57	tryptophan hydroxylase 1	Homo sapiens	104-128
15890622-0	2005	Pyruvate but not lactate prevents NADH-induced myoglobin oxidation.	NAD	34-38	myoglobin	Homo sapiens	47-56
15890622-1	2005	In this work, we investigated the influence of NADH on the redox state of myoglobin and the roles of pyruvate and lactate in this process.	NAD	47-51	myoglobin	Homo sapiens	74-83
28659716-6	2017	More importantly, the immunoregulatory properties of NAD+ are strongly related to the overexpression of tryptophan hydroxylase 1 (Tph1).	NAD	53-57	tryptophan hydroxylase 1	Homo sapiens	130-134
15890622-2	2005	NADH increased the autoxidation rate of myoglobin.	NAD	0-4	myoglobin	Homo sapiens	40-49
28752046-5	2017	RESULTS: Skeletal muscle cells primarily rely on nicotinamide phosphoribosyltransferase (NAMPT), NRK1, and NRK2 for salvage biosynthesis of NAD+.	NAD	140-144	nicotinamide riboside kinase 2	Mus musculus	107-111
15773895-0	2005	Role of NAD-dependent deacetylases SIRT1 and SIRT2 in radiation and cisplatin-induced cell death in vertebrate cells.	NAD	8-11	sirtuin 2	Gallus gallus	45-50
28752046-6	2017	NAMPT inhibition depletes muscle NAD+ availability and can be rescued by NR and NMN as the preferred precursors for elevating muscle cell NAD+ in a pathway that depends on NRK1 and NRK2.	NAD	138-142	nicotinamide riboside kinase 2	Mus musculus	181-185
28752046-7	2017	Nrk2 knockout mice develop normally and show subtle alterations to their NAD+ metabolome and expression of related genes.	NAD	73-77	nicotinamide riboside kinase 2	Mus musculus	0-4
28525742-5	2017	We show that the Dtx3L/Parp9 heterodimer mediates NAD+-dependent mono-ADP-ribosylation of ubiquitin, exclusively in the context of ubiquitin processing by E1 and E2 enzymes.	NAD	50-54	poly(ADP-ribose) polymerase family member 9	Homo sapiens	23-28
15949352-1	2005	OBJECTIVE: To study the differential expression and possible role of MLRQ subunit gene of nicotinamide adenine dinucleotide reduced (NADH) oxidoreductase in malignant tumors of digestive system.	NAD	90-123	NDUFA4 mitochondrial complex associated	Homo sapiens	69-73
28525742-9	2017	Mutation of the NAD+ binding site in Parp9 increases the DNA repair activity of the heterodimer.	NAD	16-20	poly(ADP-ribose) polymerase family member 9	Homo sapiens	37-42
28525742-11	2017	Dtx3L heterodimerization with Parp9 enables NAD+ and poly(ADP-ribose) regulation of E3 activity.	NAD	44-48	poly(ADP-ribose) polymerase family member 9	Homo sapiens	30-35
28434941-3	2017	Here, we report that a spectrum of environmental stresses, including oxidative stress, starvation, and DNA damage, profoundly activate SIRT1, an NAD+-dependent lysine deacetylase.	NAD	145-149	sirtuin 1	Mus musculus	135-140
15549291-6	2005	The resulting two-fold recombinant strain exhibited an in vitro catalytic alcohol dehydrogenase activity of 6.5 units mg-1 protein in reducing methyl acetoacetate to methyl (R)-3-hydroxy butanoate with NADPH as the cofactor and 0.7 units mg-1 protein with NADH.	NAD	256-260	Alcohol dehydrogenase	Escherichia coli	74-95
15549291-11	2005	Thus, the functional overexpression of alcohol dehydrogenase in the presence of formate dehydrogenase was sufficient to enable and sustain the desired reduction reaction via the relatively low specific activity of alcohol dehydrogenase with NADH, instead of NADPH, as a cofactor.	NAD	241-245	Alcohol dehydrogenase	Escherichia coli	39-60
15549291-11	2005	Thus, the functional overexpression of alcohol dehydrogenase in the presence of formate dehydrogenase was sufficient to enable and sustain the desired reduction reaction via the relatively low specific activity of alcohol dehydrogenase with NADH, instead of NADPH, as a cofactor.	NAD	241-245	Alcohol dehydrogenase	Escherichia coli	214-235
28239158-10	2017	Further studies revealed that treatment with 6014 did not affect the expression levels of PARP-1, but dose-dependently inhibited the activity of PARP-1 and subsequently restored the activity of SIRT-1 in heart tissues due to the decreased consumption of NAD+ and attenuated Poly-ADP-ribosylation (PARylation) of SIRT-1.	NAD	254-258	sirtuin 1	Mus musculus	194-200
15565635-1	2005	Human cyotsolic malate dehydrogenase (MDH1) is important in transporting NADH equivalents across the mitochondrial membrane, controlling tricarboxylic acid (TCA) cycle pool size and providing contractile function.	NAD	73-77	malate dehydrogenase 1	Homo sapiens	38-42
15565635-3	2005	The observed MDH1 localizations reflect the role of NADH in the support of a variety of functions in different organs.	NAD	52-56	malate dehydrogenase 1	Homo sapiens	13-17
28301150-1	2017	SIRT2, which is a NAD+ (nicotinamide adenine dinucleotide) dependent deacetylase, has been demonstrated to play an important role in the occurrence and development of a variety of diseases such as cancer, ischemia-reperfusion, and neurodegenerative diseases.	NAD	18-22	sirtuin 2	Homo sapiens	0-5
15680246-5	2005	Pre-incubation of DTx with a 2000-fold excess of NAD, the natural substrate for the toxin"s ADP-ribosyltransferase (ADPrT) activity, inhibited the transfer of radiolabeled ADP-ribose to elongation factor 2 but had no effect on the degradation of radiolabeled DNA.	NAD	49-52	eukaryotic translation elongation factor 2	Homo sapiens	186-205
28377411-4	2017	We showed that Sirtuin 1 (Sirt1), which is an NAD+ (nicotinamide adenine dinucleotide)-dependent lysine deacetylase that inhibits NIC-dependent gene transcription, stabilized NIC proximal to the plasma membrane to promote the survival and function of activated Treg cells.	NAD	46-50	sirtuin 1	Mus musculus	15-24
15644062-6	2005	A 2 : 1 and 3 : 1 ratio were obtained for isocitrate dehydrogenase (IDH)-NADP/NAD and malate dehydrogenase (MDH)-NADP/NAD activities respectively.	NAD	73-76	isocitrate dehydrogenase (NADP(+)) 2	Bos taurus	68-71
15522934-4	2005	Ovarian expression of the NAD+-dependent 15-hydroxy PG dehydrogenase (PGDH) was assessed by RT-PCR, Western blotting, and immunohistochemistry.	NAD	26-29	15-hydroxyprostaglandin dehydrogenase	Homo sapiens	52-68
15522934-4	2005	Ovarian expression of the NAD+-dependent 15-hydroxy PG dehydrogenase (PGDH) was assessed by RT-PCR, Western blotting, and immunohistochemistry.	NAD	26-29	15-hydroxyprostaglandin dehydrogenase	Homo sapiens	70-74
28377411-4	2017	We showed that Sirtuin 1 (Sirt1), which is an NAD+ (nicotinamide adenine dinucleotide)-dependent lysine deacetylase that inhibits NIC-dependent gene transcription, stabilized NIC proximal to the plasma membrane to promote the survival and function of activated Treg cells.	NAD	46-50	sirtuin 1	Mus musculus	26-31
28377411-4	2017	We showed that Sirtuin 1 (Sirt1), which is an NAD+ (nicotinamide adenine dinucleotide)-dependent lysine deacetylase that inhibits NIC-dependent gene transcription, stabilized NIC proximal to the plasma membrane to promote the survival and function of activated Treg cells.	NAD	52-85	sirtuin 1	Mus musculus	15-24
28377411-4	2017	We showed that Sirtuin 1 (Sirt1), which is an NAD+ (nicotinamide adenine dinucleotide)-dependent lysine deacetylase that inhibits NIC-dependent gene transcription, stabilized NIC proximal to the plasma membrane to promote the survival and function of activated Treg cells.	NAD	52-85	sirtuin 1	Mus musculus	26-31
27979739-1	2017	Sirtuin 3 (SIRT3) is a mitochondrial nicotinamide adenine dinucleotide (NAD)-dependent deacetylase.	NAD	37-70	sirtuin 3	Bos taurus	0-9
15616050-8	2005	Both this NADH increase and the cardioprotection by APC on reperfusion were prevented by superoxide dismutase, catalase, and glutathione and by N(G)-nitro-L-arginine-methyl-ester.	NAD	10-14	catalase	Cavia porcellus	111-119
27979739-1	2017	Sirtuin 3 (SIRT3) is a mitochondrial nicotinamide adenine dinucleotide (NAD)-dependent deacetylase.	NAD	37-70	sirtuin 3	Bos taurus	11-16
27979739-1	2017	Sirtuin 3 (SIRT3) is a mitochondrial nicotinamide adenine dinucleotide (NAD)-dependent deacetylase.	NAD	72-75	sirtuin 3	Bos taurus	0-9
27979739-1	2017	Sirtuin 3 (SIRT3) is a mitochondrial nicotinamide adenine dinucleotide (NAD)-dependent deacetylase.	NAD	72-75	sirtuin 3	Bos taurus	11-16
15947887-3	2005	In epithelial tissues the enzyme 11beta hydroxysteroid dehydrogenase Type 2 (11betaHSD2) allows aldosterone to selectively activate MR, by converting cortisol to cortisone and NAD to NADH.	NAD	176-179	hydroxysteroid 11-beta dehydrogenase 2	Homo sapiens	33-75
27888691-7	2017	We also measured the protein content of NAD+ dependent enzymes such as sirtuin3 (sirt3) and NAD(P)H: quinone oxidoreductase 1 (NQO1).	NAD	40-44	sirtuin 3	Rattus norvegicus	71-79
15947887-3	2005	In epithelial tissues the enzyme 11beta hydroxysteroid dehydrogenase Type 2 (11betaHSD2) allows aldosterone to selectively activate MR, by converting cortisol to cortisone and NAD to NADH.	NAD	183-187	hydroxysteroid 11-beta dehydrogenase 2	Homo sapiens	33-75
27888691-7	2017	We also measured the protein content of NAD+ dependent enzymes such as sirtuin3 (sirt3) and NAD(P)H: quinone oxidoreductase 1 (NQO1).	NAD	40-44	sirtuin 3	Rattus norvegicus	81-86
28130107-3	2017	In neurons, overactivation of PARP-1 during oxidative stress induces robust PAR formation, which depletes nicotinamide adenine dinucleotide levels and leads to cell death.	NAD	106-139	poly (ADP-ribose) polymerase 1	Rattus norvegicus	30-36
15763667-6	2005	The results showed that Ca(2+) presented an inhibitory effect on AOX pathway in potato mitochondria energized with NADH or succinate, which was only now observed when the cytochrome pathway was inhibited by cyanide.	NAD	115-119	ubiquinol oxidase 1, mitochondrial-like	Solanum tuberosum	65-68
15606760-2	2004	We identified two residues of GAPDH involved in protein-protein interactions in this complex, by changing residues K128 and R197 into A or E. K128A/E mutants had a Km for NADH that was twice that of the wild type and a lower catalytic constant, whatever the cofactor.	NAD	171-175	uncharacterized protein	Chlamydomonas reinhardtii	30-35
28228259-2	2017	Here, we show that the nicotinamide adenine dinucleotide (NAD)-dependent deacetylase, Sirt1, selectively prevents abnormal DNA methylation of some developmental genes in murine ESCs by antagonizing Dnmt3l.	NAD	23-56	sirtuin 1	Mus musculus	86-91
15301953-5	2004	Using this method, the kinetics of the reaction of the cosubstrate nicotinamide adenine dinucleotide and the competitive inhibitor nicotinamide with SIRT1 and SIRT2 has been analyzed.	NAD	67-100	sirtuin 2	Homo sapiens	159-164
28228259-2	2017	Here, we show that the nicotinamide adenine dinucleotide (NAD)-dependent deacetylase, Sirt1, selectively prevents abnormal DNA methylation of some developmental genes in murine ESCs by antagonizing Dnmt3l.	NAD	58-61	sirtuin 1	Mus musculus	86-91
27929731-8	2017	Collectively, these results uncover the link between the NAD+ biosynthesis pathway, CSC transcription factor POU5F1 and pluripotency, and further identify autophagy as a novel regulator of pluripotency of CSCs.	NAD	57-61	POU class 5 homeobox 1	Homo sapiens	109-115
27911441-3	2017	Here, we tested whether sirtuin-1 (SIRT1), a NAD+-dependent deacetylase, participates in modulating ER stress response in the heart.	NAD	45-48	sirtuin 1	Mus musculus	24-33
15241181-0	2004	The NAD+ precursor nicotinamide governs neuronal survival during oxidative stress through protein kinase B coupled to FOXO3a and mitochondrial membrane potential.	NAD	4-8	protein tyrosine kinase 2 beta	Homo sapiens	90-106
15111611-7	2004	In vitro studies showed that 15 minutes of exposure to 300 to 500 microM zinc resulted in the death of a substantial number of retinal cells in culture, and that this death was preceded by poly(ADP-ribose) polymerase (PARP)-mediated depletion of nicotinamide-adenine dinucleotide (NAD+) and adenosine triphosphate (ATP).	NAD	246-279	poly (ADP-ribose) polymerase 1	Rattus norvegicus	189-216
15111611-7	2004	In vitro studies showed that 15 minutes of exposure to 300 to 500 microM zinc resulted in the death of a substantial number of retinal cells in culture, and that this death was preceded by poly(ADP-ribose) polymerase (PARP)-mediated depletion of nicotinamide-adenine dinucleotide (NAD+) and adenosine triphosphate (ATP).	NAD	246-279	poly (ADP-ribose) polymerase 1	Rattus norvegicus	218-222
15111611-7	2004	In vitro studies showed that 15 minutes of exposure to 300 to 500 microM zinc resulted in the death of a substantial number of retinal cells in culture, and that this death was preceded by poly(ADP-ribose) polymerase (PARP)-mediated depletion of nicotinamide-adenine dinucleotide (NAD+) and adenosine triphosphate (ATP).	NAD	281-285	poly (ADP-ribose) polymerase 1	Rattus norvegicus	189-216
15111611-7	2004	In vitro studies showed that 15 minutes of exposure to 300 to 500 microM zinc resulted in the death of a substantial number of retinal cells in culture, and that this death was preceded by poly(ADP-ribose) polymerase (PARP)-mediated depletion of nicotinamide-adenine dinucleotide (NAD+) and adenosine triphosphate (ATP).	NAD	281-285	poly (ADP-ribose) polymerase 1	Rattus norvegicus	218-222
14680476-7	2004	Furthermore we find that GCY1, encoding a putative glycerol dehydrogenase, GPP2, encoding a NAD-dependent glycerol-3-phosphate phosphatase, and DCS2, a homologue to a decapping enzyme, have decreased mRNA levels in the yap4 -deleted strain.	NAD	92-95	5'-(N(7)-methyl 5'-triphosphoguanosine)-(mRNA) diphosphatase	Saccharomyces cerevisiae S288C	144-148
15030411-2	2004	It is started in astrocytes by ectocellular, CD38-catalysed conversion of NAD(+) to the calcium mobilizer cyclic ADP-ribose (cADPR).	NAD	74-80	CD38 molecule	Homo sapiens	45-49
14622413-10	2003	On the other, the Agc1p, as an aspartate-glutamate exchanger, plays a role within the malate-aspartate NADH shuttle which is critical for the growth of yeast on acetate and fatty acids as carbon sources.	NAD	103-107	citrin	Saccharomyces cerevisiae S288C	18-23
14525525-2	2003	To date, two isoforms of 11 beta HSD have been cloned: 11 beta HSD1 acts predominantly as an NADP(H)-dependent reductase to generate active cortisol or corticosterone, and 11 beta HSD2 is a high affinity NAD(+)-dependent enzyme that catalyses the enzymatic inactivation of glucocorticoids.	NAD	204-210	hydroxysteroid 11-beta dehydrogenase 2	Homo sapiens	180-184
12788913-5	2003	When eIF5A([3H]Dhp), radiolabeled in the 4-aminobutyl portion of its deoxyhypusine residue, was incubated with human deoxyhypusine synthase, NAD, and 1,3-diaminopropane, [3H]spermidine was formed by a rapid transfer of the radiolabeled 4-aminobutyl side chain of the [3H]deoxyhypusine residue to 1,3-diaminopropane.	NAD	141-144	eukaryotic translation initiation factor 5A	Homo sapiens	5-10
12901862-5	2003	The sulfhydryl protecting reagent dithiothreitol blocked thiram-induced inhibition and NAD+ partially protected 11 beta-HSD2 activity, indicating that DTCs act at the cofactor-binding site.	NAD	87-91	hydroxysteroid 11-beta dehydrogenase 2	Homo sapiens	112-124
12901862-6	2003	A 3D-model of 11 beta-HSD2 identified Cys90 in the NAD(+)-binding site as a likely target of DTCs, which was supported by a 99% reduced activity of mutant Cys90 to serine.	NAD	51-57	hydroxysteroid 11-beta dehydrogenase 2	Homo sapiens	14-26
12919668-1	2003	A new report reveals a role for the mammalian NAD-dependent deacetylase Sir2 in repressing the muscle cell differentiation program and implicates the cellular redox state as a critical determinant of transcriptional activity of differentiation-specific genes.	NAD	46-49	sirtuin 2	Homo sapiens	72-76
12824290-1	2003	We hypothesize that poly (ADP-ribosyl)ation, that is, poly (ADP-ribose) polymerase (PARP)-dependent transfer of ADP-ribose moieties from NAD to nuclear proteins, plays a role in diabetic nephropathy.	NAD	137-140	poly (ADP-ribose) polymerase 1	Rattus norvegicus	54-82
12805226-3	2003	Here, we report the crystal structures of rat CtBP/BARS in a binary complex with NAD(H), and in a ternary complex with a PIDLSKK peptide mimicking the consensus motif (PXDLS) recognized in CtBP/BARS cellular partners.	NAD	81-87	C-terminal binding protein 1	Rattus norvegicus	51-55
12805226-4	2003	The structural data show CtBP/BARS in a NAD(H)-bound dimeric form; the peptide binding maps the recognition site for DNA-binding proteins and histone deacetylases to an N-terminal region of the protein.	NAD	40-46	C-terminal binding protein 1	Rattus norvegicus	30-34
12763579-1	2003	Aralar1 and citrin are two isoforms of the mitochondrial carrier of aspartate-glutamate (AGC), a calcium regulated carrier, which is important in the malate-aspartate NADH shuttle.	NAD	167-171	solute carrier family 25 (mitochondrial carrier, adenine nucleotide translocator), member 13	Mus musculus	12-18
12697818-0	2003	Role for human SIRT2 NAD-dependent deacetylase activity in control of mitotic exit in the cell cycle.	NAD	21-24	sirtuin 2	Homo sapiens	15-20
12697818-3	2003	The SIRT2 protein is a NAD-dependent deacetylase (NDAC), the abundance of which increases dramatically during mitosis and is multiply phosphorylated at the G(2)/M transition of the cell cycle.	NAD	23-26	sirtuin 2	Homo sapiens	4-9
12702242-1	2003	Under anaerobic conditions, Saccharomyces cerevisiae uses NADH-dependent glycerol-3-phosphate dehydrogenase (Gpd1p and Gpd2p) to re-oxidize excess NADH, yielding substantial amounts of glycerol.	NAD	58-62	glycerol-3-phosphate dehydrogenase (NAD(+)) GPD2	Saccharomyces cerevisiae S288C	119-124
12702242-1	2003	Under anaerobic conditions, Saccharomyces cerevisiae uses NADH-dependent glycerol-3-phosphate dehydrogenase (Gpd1p and Gpd2p) to re-oxidize excess NADH, yielding substantial amounts of glycerol.	NAD	147-151	glycerol-3-phosphate dehydrogenase (NAD(+)) GPD2	Saccharomyces cerevisiae S288C	119-124
12605868-3	2003	A relatively rapid continuous spectrophotometric assay which uses 15-hydroxyprostaglandin dehydrogenase (PGDH) to couple the oxidation of the 15-hydroxy group of PGE(2) to the formation of NADH was developed.	NAD	189-193	15-hydroxyprostaglandin dehydrogenase	Homo sapiens	105-109
12535671-2	2003	Recently, it was shown that the Drosophila bHLH repressor proteins, Hairy and Deadpan, bind to and function with the NAD(+)-dependent histone deacetylase, Sir2.	NAD	117-123	Sirtuin 1	Drosophila melanogaster	155-159
14562752-0	2003	Effect of myoglobin inactivation on intracellular gradients of NADH fluorescence at critical mitochondrial oxygen supply.	NAD	63-67	myoglobin	Homo sapiens	10-19
12766354-2	2003	Nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d) reactivity was markedly reduced in the hippocampal CA1, CA2 and CA3 sectors as well as in the dentate gyrus, suggesting a suppression of NO production in these areas.	NAD	0-33	carbonic anhydrase 1	Rattus norvegicus	116-119
15051959-8	2003	The oxidation of reduced NAD with the conversion of pyruvate to lactate by LDH provides ATP necessary for protein kinase A (PKA) activity.	NAD	25-28	lactate dehydrogenase C	Homo sapiens	75-78
12524341-6	2002	We found that dSir2 expression is developmentally regulated and that dSir2 has an intrinsic NAD(+)-dependent histone deacetylase activity.	NAD	92-98	Sirtuin 1	Drosophila melanogaster	69-74
12270928-5	2002	The lack of requirement for NAD(+) to produce the toxin-eEF-2 complex demonstrates that the catalytic process is a random order mechanism, thereby disputing the current model.	NAD	28-34	eukaryotic translation elongation factor 2	Homo sapiens	56-61
27911441-3	2017	Here, we tested whether sirtuin-1 (SIRT1), a NAD+-dependent deacetylase, participates in modulating ER stress response in the heart.	NAD	45-48	sirtuin 1	Mus musculus	35-40
27345396-5	2017	Here, we show that the regulation of cancer invasion by OGT is dependent on the NAD+-dependent deacetylase SIRT1.	NAD	80-83	O-linked N-acetylglucosamine (GlcNAc) transferase	Homo sapiens	56-59
12193607-3	2002	Photoaffinity labeling with a specific probe, [(32)P]nicotinamide 2-azidoadenosine dinucleotide, was used to identify the NAD(+) binding site within human GDH encoded by the synthetic human GDH gene and expressed in Escherichia coli as a soluble protein.	NAD	122-128	glutamate dehydrogenase 1	Homo sapiens	155-158
12193607-3	2002	Photoaffinity labeling with a specific probe, [(32)P]nicotinamide 2-azidoadenosine dinucleotide, was used to identify the NAD(+) binding site within human GDH encoded by the synthetic human GDH gene and expressed in Escherichia coli as a soluble protein.	NAD	122-128	glutamate dehydrogenase 1	Homo sapiens	190-193
12193607-6	2002	Amino acid sequencing and compositional analysis identified Glu(279) as the site of photoinsertion into human GDH, suggesting that Glu(279) is located at or near the NAD(+) binding site.	NAD	166-172	glutamate dehydrogenase 1	Homo sapiens	110-113
29261224-4	2017	Therefore, the purpose of this study was to characterize the expression of mitochondrial sirtuins (Sirt3-5) in individual compartments of rat adrenal cortex, their developmental regulation and to demonstrate whether their expression is dependent on adrenocorticotrophic hormone (ACTH) and Nampt (nicotinamide phosphoribosyltransferase also known as visfatin/PBEF), the rate-limiting enzyme in the regulation of mammalian NAD synthesis.	NAD	421-424	sirtuin 3	Rattus norvegicus	99-106
12193607-9	2002	The K(m) values for NAD(+) were 10-14-fold greater for the mutant GDHs than for wild-type GDH, whereas the V(max) values were similar for wild-type and mutant GDHs.	NAD	20-26	glutamate dehydrogenase 1	Homo sapiens	66-69
12193607-14	2002	The results with photoaffinity labeling and cassette mutagenesis studies suggest that Glu(279) plays an important role for efficient binding of NAD(+) to human GDH.	NAD	144-150	glutamate dehydrogenase 1	Homo sapiens	160-163
12392591-6	2002	In addition, hydroxycelecoxib oxidation by different variants of recombinant human alcohol dehydrogenase (ADH1-3) was analysed by spectrophotometric monitoring of NADH generation from NAD+.	NAD	163-167	alcohol dehydrogenase 1A (class I), alpha polypeptide	Homo sapiens	106-112
12392591-6	2002	In addition, hydroxycelecoxib oxidation by different variants of recombinant human alcohol dehydrogenase (ADH1-3) was analysed by spectrophotometric monitoring of NADH generation from NAD+.	NAD	184-188	alcohol dehydrogenase 1A (class I), alpha polypeptide	Homo sapiens	106-112
29104317-8	2017	Two BaP-derived DNA adducts were generated by the CYP1A1-Supersomes, both in the presence of NADPH and NADH, whereas NADPH but not NADH was able to support this reaction in the CYP1A1-Bactosomes.	NAD	103-107	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	50-56
28656112-12	2017	CONCLUSIONS: Nicotinamide administration improves remyelination after stroke via the NAD+/BDNF/TrkB pathway.	NAD	85-89	brain derived neurotrophic factor	Mus musculus	90-94
28058510-3	2017	Mammalian isocitrate dehydrogenase (IDH) 3 is a heterotetramer of 2alfa, 1beta, and 1gamma subunits, and IDH3A encodes the alfa subunit of the mitochondrial NAD+-dependent IDH.	NAD	157-161	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	10-34
12203397-4	2002	The cellular mechanism that supports internal mobilization of calcium appears to depend on a complex multifunctional ectoenzyme, CD38, which converts NAD(+) into the intracellular Ca(2+)-mobilizing second-messenger cyclic ADP-ribose (cADPR) and could function as a detector for extracellular NAD(+), thus providing a novel signal detection system for evaluating the extracellular environment.	NAD	150-156	CD38 molecule	Homo sapiens	129-133
12203397-4	2002	The cellular mechanism that supports internal mobilization of calcium appears to depend on a complex multifunctional ectoenzyme, CD38, which converts NAD(+) into the intracellular Ca(2+)-mobilizing second-messenger cyclic ADP-ribose (cADPR) and could function as a detector for extracellular NAD(+), thus providing a novel signal detection system for evaluating the extracellular environment.	NAD	292-298	CD38 molecule	Homo sapiens	129-133
12203397-5	2002	Our results are consistent with a model of intracellular Ca(2+) mobilization in which membrane-bound CD38 binds extracellular NAD(+) and triggers intracellular Ca(2+) waves either by direct conversion of NAD(+) to cADPR or by activating intracellular cADPR synthesis.	NAD	126-132	CD38 molecule	Homo sapiens	101-105
12203397-5	2002	Our results are consistent with a model of intracellular Ca(2+) mobilization in which membrane-bound CD38 binds extracellular NAD(+) and triggers intracellular Ca(2+) waves either by direct conversion of NAD(+) to cADPR or by activating intracellular cADPR synthesis.	NAD	204-210	CD38 molecule	Homo sapiens	101-105
12203397-7	2002	Because NAD(+) is likely to be enhanced when cells are stress or damaged, CD38 could enable Muller cells to detect NAD(+) under these circumstances and respond appropriately.	NAD	8-14	CD38 molecule	Homo sapiens	74-78
12203397-7	2002	Because NAD(+) is likely to be enhanced when cells are stress or damaged, CD38 could enable Muller cells to detect NAD(+) under these circumstances and respond appropriately.	NAD	115-121	CD38 molecule	Homo sapiens	74-78
28058510-3	2017	Mammalian isocitrate dehydrogenase (IDH) 3 is a heterotetramer of 2alfa, 1beta, and 1gamma subunits, and IDH3A encodes the alfa subunit of the mitochondrial NAD+-dependent IDH.	NAD	157-161	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	36-39
28058510-3	2017	Mammalian isocitrate dehydrogenase (IDH) 3 is a heterotetramer of 2alfa, 1beta, and 1gamma subunits, and IDH3A encodes the alfa subunit of the mitochondrial NAD+-dependent IDH.	NAD	157-161	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	105-108
27793057-2	2016	HIC1 is a transcriptional repressor that directly binds to the promoter region of NAD-dependent deacetylase sirtuin-1 (SIRT1).	NAD	82-85	HIC ZBTB transcriptional repressor 1	Homo sapiens	0-4
27374990-2	2016	The study of NAD+ has become reinvigorated by new understandings that dynamics within NAD+ metabolism trigger major signaling processes coupled to effectors (sirtuins, PARPs, and CD38) that reprogram cellular metabolism using NAD+ as an effector substrate.	NAD	13-17	CD38 molecule	Homo sapiens	179-183
27374990-2	2016	The study of NAD+ has become reinvigorated by new understandings that dynamics within NAD+ metabolism trigger major signaling processes coupled to effectors (sirtuins, PARPs, and CD38) that reprogram cellular metabolism using NAD+ as an effector substrate.	NAD	86-90	CD38 molecule	Homo sapiens	179-183
27374990-2	2016	The study of NAD+ has become reinvigorated by new understandings that dynamics within NAD+ metabolism trigger major signaling processes coupled to effectors (sirtuins, PARPs, and CD38) that reprogram cellular metabolism using NAD+ as an effector substrate.	NAD	86-90	CD38 molecule	Homo sapiens	179-183
27240865-8	2016	Promoter truncation of GPD1 and gene deletion of GPD2 coding for glycerol-3-phosphate dehydrogenase to produce surplus NADH also did not lead to improved acetate consumption.	NAD	119-123	glycerol-3-phosphate dehydrogenase (NAD(+)) GPD2	Saccharomyces cerevisiae S288C	49-53
27372904-4	2016	We performed co-immunoprecipitation experiments to examine whether VILIP-3 can interact with reduced nicotine adenine dinucleotide (NADH)-cytochrome b 5 reductase.	NAD	132-136	cytochrome b5 type A	Homo sapiens	138-152
27694803-2	2016	Here, using a proteomic approach, we identified Saccharomyces cerevisiae cytochrome b5 reductase (Cbr1) as a NADH-dependent reductase for Dph3.	NAD	109-113	cytochrome-b5 reductase	Saccharomyces cerevisiae S288C	98-102
29442004-2	2016	Sirt-1, an NAD+ dependent deacetylase, regulates a variety of cellular processes, including aging, lifespan extension and glucose and lipid metabolism.	NAD	11-14	sirtuin 1	Mus musculus	0-6
27846305-7	2016	We unexpectedly uncover intermediate "partial" yet stable states lying between the tip and stalk cell fates, and identify that internal cellular factors, such as NAD-dependent deacetylase sirtuin-1 (Sirt1) and Lunatic fringe 1 (Lfng1), can specifically determine the length of time a cell spends in these newly identified partial tip/stalk states.	NAD	162-165	TOR signaling pathway regulator	Homo sapiens	330-333
27332042-11	2016	Transaldolase-deficient mice showed increased oxygen consumption, depletion of Drp1, activation of mTORC1, and elevated expression of NADH:ubiquinone oxidoreductase core subunit S3 (NDUFS3), a pro-oxidant subunit of ETC complex I, as well as increased production of aCL and anti-beta2 GPI autoantibodies.	NAD	134-138	transaldolase 1	Mus musculus	0-13
27582489-1	2016	NAD+ kinase (NADK) catalyzes the phosphorylation of nicotinamide adenine dinucleotide (NAD+) to nicotinamide adenine dinucleotide phosphate (NADP+) using ATP as the phosphate donor.	NAD	52-85	NAD kinase	Homo sapiens	0-11
27582489-1	2016	NAD+ kinase (NADK) catalyzes the phosphorylation of nicotinamide adenine dinucleotide (NAD+) to nicotinamide adenine dinucleotide phosphate (NADP+) using ATP as the phosphate donor.	NAD	52-85	NAD kinase	Homo sapiens	13-17
27582489-1	2016	NAD+ kinase (NADK) catalyzes the phosphorylation of nicotinamide adenine dinucleotide (NAD+) to nicotinamide adenine dinucleotide phosphate (NADP+) using ATP as the phosphate donor.	NAD	52-85	NAD kinase	Homo sapiens	0-3
27594441-2	2016	In experiment 1, dose response curves for PPT and DPN (ERalpha and ERbeta agonists, respectively) facilitation of lordosis behavior (lordosis quotient and lordosis score) were established by infusing these agonists into the right lateral ventricle (icv) in female rats injected 40h previously with 5mug of E2 benzoate.	NAD	50-53	estrogen receptor 1	Rattus norvegicus	55-62
12220851-1	2002	Members of the evolutionarily conserved silent information regulator 2 (Sir2) protein family are nicotinamide adenine dinucleotide (NAD(+))-dependent histone deacetylases.	NAD	97-130	sirtuin 2	Homo sapiens	40-70
12220851-1	2002	Members of the evolutionarily conserved silent information regulator 2 (Sir2) protein family are nicotinamide adenine dinucleotide (NAD(+))-dependent histone deacetylases.	NAD	97-130	sirtuin 2	Homo sapiens	72-76
12220851-1	2002	Members of the evolutionarily conserved silent information regulator 2 (Sir2) protein family are nicotinamide adenine dinucleotide (NAD(+))-dependent histone deacetylases.	NAD	132-139	sirtuin 2	Homo sapiens	40-70
12220851-1	2002	Members of the evolutionarily conserved silent information regulator 2 (Sir2) protein family are nicotinamide adenine dinucleotide (NAD(+))-dependent histone deacetylases.	NAD	132-139	sirtuin 2	Homo sapiens	72-76
12196144-4	2002	Met8p, from Saccharomyces cerevisiae, catalyses ferrochelation during the synthesis of sirohaem, and the structure reveals a novel chelatase architecture whereby both ferrochelation and NAD(+)-dependent dehydrogenation take place in a single bifunctional active site.	NAD	186-192	bifunctional precorrin-2 dehydrogenase/sirohydrochlorin ferrochelatase MET8	Saccharomyces cerevisiae S288C	0-5
12432938-1	2002	The primary catabolic pathway of prostaglandins and related eicosanoids is initiated by the oxidation of 15(S)-hydroxyl group catalyzed by NAD+-dependent 15-hydroxyprostaglandin dehydrogenase (15-PGDH) followed by the reduction of delta13 double bond catalyzed by NADPH/NADH dependent delta13-15-ketoprostaglandin reductase (13-PGR).	NAD	270-274	15-hydroxyprostaglandin dehydrogenase	Homo sapiens	139-191
12432938-1	2002	The primary catabolic pathway of prostaglandins and related eicosanoids is initiated by the oxidation of 15(S)-hydroxyl group catalyzed by NAD+-dependent 15-hydroxyprostaglandin dehydrogenase (15-PGDH) followed by the reduction of delta13 double bond catalyzed by NADPH/NADH dependent delta13-15-ketoprostaglandin reductase (13-PGR).	NAD	270-274	15-hydroxyprostaglandin dehydrogenase	Homo sapiens	193-200
11927587-11	2002	A detailed catalytic mechanism of AdoHcyase has been revealed based on the oxidation states of the bound NAD and the re-refined crystal structures of WT and D244E.Ado*.	NAD	105-108	adenosylhomocysteinase	Homo sapiens	34-43
11925444-1	2002	Previously we have demonstrated that activation of p38 mitogen-activated protein kinase (MAPK) and induction of DNA synthesis in response to receptor tyrosine kinase (RTK) and G protein-coupled receptor (GPCR) agonists require NADH/NADPH-like oxidase activity in vascular smooth muscle cells (VSMC).	NAD	227-231	ret proto-oncogene	Homo sapiens	141-165
11925444-1	2002	Previously we have demonstrated that activation of p38 mitogen-activated protein kinase (MAPK) and induction of DNA synthesis in response to receptor tyrosine kinase (RTK) and G protein-coupled receptor (GPCR) agonists require NADH/NADPH-like oxidase activity in vascular smooth muscle cells (VSMC).	NAD	227-231	ret proto-oncogene	Homo sapiens	167-170
11925444-1	2002	Previously we have demonstrated that activation of p38 mitogen-activated protein kinase (MAPK) and induction of DNA synthesis in response to receptor tyrosine kinase (RTK) and G protein-coupled receptor (GPCR) agonists require NADH/NADPH-like oxidase activity in vascular smooth muscle cells (VSMC).	NAD	227-231	C-X-C motif chemokine receptor 6	Homo sapiens	176-202
11925444-1	2002	Previously we have demonstrated that activation of p38 mitogen-activated protein kinase (MAPK) and induction of DNA synthesis in response to receptor tyrosine kinase (RTK) and G protein-coupled receptor (GPCR) agonists require NADH/NADPH-like oxidase activity in vascular smooth muscle cells (VSMC).	NAD	227-231	C-X-C motif chemokine receptor 6	Homo sapiens	204-208
11893743-3	2002	Sir2 enzymes have been shown to couple substrate deacetylation and beta-NAD(+) cleavage to the formation of O-acetyl-ADP-ribose, a newly described metabolite.	NAD	67-78	sirtuin 2	Homo sapiens	0-4
12144871-3	2002	A relatively conserved threonine residue corresponding to threonine 11 of 15-PGDH is proposed to be involved in the interaction with NAD(+).	NAD	133-139	15-hydroxyprostaglandin dehydrogenase	Homo sapiens	74-81
12144871-9	2002	These results suggest that threonine 11 may be involved in the interaction with NAD(+) either directly or indirectly and contributes to the full catalytic activity of 15-PGDH.	NAD	80-86	15-hydroxyprostaglandin dehydrogenase	Homo sapiens	167-174
27594441-2	2016	In experiment 1, dose response curves for PPT and DPN (ERalpha and ERbeta agonists, respectively) facilitation of lordosis behavior (lordosis quotient and lordosis score) were established by infusing these agonists into the right lateral ventricle (icv) in female rats injected 40h previously with 5mug of E2 benzoate.	NAD	50-53	estrogen receptor 2	Rattus norvegicus	67-73
27592202-6	2016	Regulation of the SIRT/NAD system was associated with early (SIRT4, SIRT7, NAPRT1 and NMNAT2) and late phases (NMNAT3, NMRK2, ABCA1 and CD38) of glucose intolerance.	NAD	23-26	sirtuin 4	Mus musculus	61-66
27592202-6	2016	Regulation of the SIRT/NAD system was associated with early (SIRT4, SIRT7, NAPRT1 and NMNAT2) and late phases (NMNAT3, NMRK2, ABCA1 and CD38) of glucose intolerance.	NAD	23-26	nicotinamide riboside kinase 2	Mus musculus	119-124
27456392-1	2016	BACKGROUND: We have previously shown leucine (Leu) to activate Sirt1 by lowering its KM for NAD+, thereby amplifying the effects of other sirtuin activators and improving insulin sensitivity.	NAD	92-96	sirtuin 1	Mus musculus	63-68
27456392-6	2016	RESULTS: Leu (0.5mmol/L)+Met (50-100mumol/L) synergistically activated Sirt1 (p&lt;0.001) at low (&lt;=100mumol/L) NAD+ levels while Met exerted no independent effect.	NAD	115-119	sirtuin 1	Mus musculus	71-76
27456392-12	2016	CONCLUSION: Thus, Leu and Met synergize to enable Sirt1 activation at low NAD+ concentrations (typical of energy replete states).	NAD	74-78	sirtuin 1	Mus musculus	50-55
27764779-4	2016	In this study, we investigated the effect of MSCs overexpressing an NAD-dependent deacetylase sirtuin 1 (MSCs-Sirt1) on prostate tumor growth, and we analyzed the underlying mechanisms.	NAD	68-71	sirtuin 1	Mus musculus	110-115
27759097-1	2016	The aldehyde dehydrogenase family 1 member A3 (ALDH1A3) catalyzes the oxidation of retinal to the pleiotropic factor retinoic acid using NAD+.	NAD	137-141	aldehyde dehydrogenase 1 family member A3	Homo sapiens	4-45
27759097-1	2016	The aldehyde dehydrogenase family 1 member A3 (ALDH1A3) catalyzes the oxidation of retinal to the pleiotropic factor retinoic acid using NAD+.	NAD	137-141	aldehyde dehydrogenase 1 family member A3	Homo sapiens	47-54
27759097-4	2016	Here we report the first crystal structure of human ALDH1A3 complexed with NAD+ and the product all-trans retinoic acid (REA).	NAD	75-79	aldehyde dehydrogenase 1 family member A3	Homo sapiens	52-59
27732834-0	2016	Overcoming ATM Deficiency by Activating the NAD+/SIRT1 Axis.	NAD	44-48	sirtuin 1	Mus musculus	49-54
27732834-3	2016	This broad suppression by activating the NAD+/SIRT1 axis may generally apply to diseases and aging maladies.	NAD	41-45	sirtuin 1	Mus musculus	46-51
27732853-4	2016	We demonstrate that Skp1a regulates the protein level of the nicotinamide adenine dinucleotide (NAD)+ synthesizing enzyme nicotinamide mononucleotide adenylyltransferase 2 (Nmnat2) in axons.	NAD	61-94	S-phase kinase associated protein 1	Homo sapiens	20-25
27732853-4	2016	We demonstrate that Skp1a regulates the protein level of the nicotinamide adenine dinucleotide (NAD)+ synthesizing enzyme nicotinamide mononucleotide adenylyltransferase 2 (Nmnat2) in axons.	NAD	96-99	S-phase kinase associated protein 1	Homo sapiens	20-25
27732856-4	2016	Maintenance of the naive state requires the NAD-dependent deacetylase, SirT1, which deacetylates Oct4.	NAD	44-47	POU class 5 homeobox 1	Homo sapiens	97-101
27423420-7	2016	Mechanistically, we identified NMNAT3 (nicotinamide mononucleotide adenylyltransferase 3), the rate-limiting enzyme for mitochondrial NAD biosynthesis, as a new target and binding partner of SIRT3.	NAD	134-137	sirtuin 3	Mus musculus	191-196
27500459-0	2016	Treatment with NAD(+) inhibited experimental autoimmune encephalomyelitis by activating AMPK/SIRT1 signaling pathway and modulating Th1/Th17 immune responses in mice.	NAD	15-21	sirtuin 1	Mus musculus	93-98
27500459-7	2016	We also found that the AMP-activated protein kinase (AMPK)/silent mating-type information regulation 2 homolog 1(SIRT1) pathway was activated in the NAD(+)-treated mice and NAD(+) treatment suppressed pro-inflammatory T cell responses.	NAD	149-155	sirtuin 1	Mus musculus	113-118
27500459-7	2016	We also found that the AMP-activated protein kinase (AMPK)/silent mating-type information regulation 2 homolog 1(SIRT1) pathway was activated in the NAD(+)-treated mice and NAD(+) treatment suppressed pro-inflammatory T cell responses.	NAD	173-179	sirtuin 1	Mus musculus	113-118
27431412-6	2016	The 11beta-HSD2 isoform, which catalyzes nicotinamide adenine dinucleotide+-dependent inactivation of cortisol/corticosterone to cortisone/11-DHC, is highly expressed in distal nephrons, the colon, sweat glands, and the placenta.	NAD	41-75	hydroxysteroid 11-beta dehydrogenase 2	Homo sapiens	4-15
27481895-1	2016	In vascular plants, the chloroplast NADH dehydrogenase-like (NDH) complex, a homolog of respiratory NADH:quinone oxidoreductase (Complex I), mediates plastoquinone reduction using ferredoxin as an electron donor in cyclic electron transport around PSI in the thylakoid membrane.	NAD	36-40	GLIS family zinc finger 3	Homo sapiens	61-64
11815615-2	2002	We show here that phosphoribulokinase exerts an imprinting on glyceraldehyde 3-phosphate dehydrogenase, which affects its catalysis by decreasing the energy barrier of the reactions with NADH or NADPH by 3.8 +/- 0.5 and 1.3 +/- 0.3 kJ.mol(-1).	NAD	187-191	uncharacterized protein	Chlamydomonas reinhardtii	62-102
11815615-3	2002	Phosphoribulokinase and glyceraldehyde 3-phosphate dehydrogenase within the complex are regulated by NADP(H) but not by NAD(H).	NAD	120-126	uncharacterized protein	Chlamydomonas reinhardtii	24-64
11815615-5	2002	NADP(H) increases phosphoribulokinase and NADPH-glyceraldehyde 3-phosphate dehydrogenase activities with a (~)K(0.5 (NADP)) of 0.68 +/- 0.16 mm and a (~)K(0.5 (NADPH)) of 2.93 +/- 0.87 mm and decreases NADH-dependent activity.	NAD	202-206	uncharacterized protein	Chlamydomonas reinhardtii	48-88
11872167-2	2002	Here, we isolated the cDNAs for the monkey homologues of NAD+- and NADP+-dependent types of 15-hydroxy PG dehydrogenase (PGDH) from lung and eye, respectively, and investigated the distribution of their mRNAs in the monkey eye.	NAD	57-61	15-hydroxyprostaglandin dehydrogenase	Homo sapiens	103-119
11872167-2	2002	Here, we isolated the cDNAs for the monkey homologues of NAD+- and NADP+-dependent types of 15-hydroxy PG dehydrogenase (PGDH) from lung and eye, respectively, and investigated the distribution of their mRNAs in the monkey eye.	NAD	57-61	15-hydroxyprostaglandin dehydrogenase	Homo sapiens	121-125
11872167-3	2002	The cDNAs for the NAD+- and NADP+-dependent types of PGDH contained an open reading frame of 798 and 831 bp encoding 266 and 277 amino acid residues with calculated molecular masses of 28.9 and 30.5 kDa, respectively.	NAD	18-22	15-hydroxyprostaglandin dehydrogenase	Homo sapiens	53-57
11904232-8	2002	In addition, prior incubation of human placental microsomes with NAD(+) (cofactor) but not cortisol (substrate) resulted in a concentration-dependent increase (EC(50)=8 microM) in 11 beta-HSD2 activity, indicating that binding of NAD(+) to the microsomal 11 beta-HSD2 facilitated the conversion of cortisol to cortisone.	NAD	65-71	hydroxysteroid 11-beta dehydrogenase 2	Homo sapiens	180-192
11904232-8	2002	In addition, prior incubation of human placental microsomes with NAD(+) (cofactor) but not cortisol (substrate) resulted in a concentration-dependent increase (EC(50)=8 microM) in 11 beta-HSD2 activity, indicating that binding of NAD(+) to the microsomal 11 beta-HSD2 facilitated the conversion of cortisol to cortisone.	NAD	65-71	hydroxysteroid 11-beta dehydrogenase 2	Homo sapiens	244-267
11795879-4	2002	Finally, NADH/NADPH inhibitors prevent the p66(Shc) Ser-phosphorylation induced by serum and by phorbol 12-myristate-13-acetate, which suggests that the direct target(s) of reactive oxygen species is(are) located upstream from the machinery connecting growth factor receptors to Ras.	NAD	9-13	DNA polymerase delta 3, accessory subunit	Homo sapiens	43-46
11694507-5	2002	In an in vitro system based on purified recombinant proteins and NAD, caspase-3 prevented the inhibition of DNAS1L3 endonuclease activity by wild-type PARP-1 but not that induced by a caspase-3-resistant PARP-1 mutant.	NAD	65-68	deoxyribonuclease 1 like 3	Homo sapiens	108-115
12168349-18	2002	A significant correlation was recorded between CBF and NADH redox state during changes in blood pressure, papaverine injection, spontaneous drop in blood supply to the brain or during releasing of high ICP levels.	NAD	55-59	CCAAT enhancer binding protein zeta	Homo sapiens	47-50
11752025-9	2002	GM-CSF release was also induced when internal ROS production was triggered with NADH, whereas H2O2 had only a small effect.	NAD	80-84	colony stimulating factor 2	Homo sapiens	0-6
11746417-1	2001	Glutamate dehydrogenase (GDH) catalyzes the oxidative deamination of glutamate to alpha-ketoglutarate using NAD or NADP as cofactors.	NAD	108-111	glutamate dehydrogenase 1	Homo sapiens	0-23
11746417-1	2001	Glutamate dehydrogenase (GDH) catalyzes the oxidative deamination of glutamate to alpha-ketoglutarate using NAD or NADP as cofactors.	NAD	108-111	glutamate dehydrogenase 1	Homo sapiens	25-28
11695905-0	2001	The structure and biochemistry of NADH-dependent cytochrome b5 reductase are now consistent.	NAD	34-38	cytochrome b5 type A	Homo sapiens	49-62
11695905-1	2001	Cytochrome b5 reductase (cb5r) (EC 1.6.6.2) catalyzes the reduction of two molecules of cytochrome b5 using NADH as the physiological electron donor.	NAD	108-112	cytochrome b5 type A	Homo sapiens	0-13
11695905-1	2001	Cytochrome b5 reductase (cb5r) (EC 1.6.6.2) catalyzes the reduction of two molecules of cytochrome b5 using NADH as the physiological electron donor.	NAD	108-112	cytochrome b5 type A	Homo sapiens	88-101
11410594-4	2001	The nuo-1 gene encodes the NADH- and FMN-binding subunit of complex I, the NADH-ubiquinone oxidoreductase.	NAD	27-31	NADH dehydrogenase [ubiquinone] flavoprotein 1, mitochondrial	Caenorhabditis elegans	4-9
11418649-7	2001	Further analyses revealed that natural knockout mice for Art2.a (C57BL/6) or Art2.b (NZW) were resistant to NAD-mediated apoptosis.	NAD	108-111	ADP-ribosyltransferase 2b	Mus musculus	77-83
11274198-7	2001	The co-purified cRDH showed marked substrate preference to 11-cis-retinal and preferred NADH rather than NADPH as the cofactor in reduction reactions.	NAD	88-92	retinol dehydrogenase 5	Bos taurus	16-20
11375511-3	2001	In Saccharomyces cerevisiae, the last step in the biosynthesis of sirohaem involves Met8p, a bifunctional enzyme responsible for both the NAD(+)-dependent dehydrogenation of the corrin ring and ferrochelation.	NAD	138-144	bifunctional precorrin-2 dehydrogenase/sirohydrochlorin ferrochelatase MET8	Saccharomyces cerevisiae S288C	84-89
11350048-5	2001	Moreover, the Ca2+-induced inhibition does not appear to involve altered cofactor (NAD+) binding since the inhibition of microsomal 11beta-HSD2 activity by a sub-maximal concentration of free Ca2+ was not overcome by increasing the concentration of NAD+.	NAD	249-253	hydroxysteroid 11-beta dehydrogenase 2	Homo sapiens	132-143
11424356-2	2001	We investigated 23 patients who had both DPN and sufficient ADPN innervation to the EDB on the intramuscular distribution of DPN and ADPN innervation to the medial and lateral side of the EDB.	NAD	61-64	patatin like phospholipase domain containing 3	Homo sapiens	133-137
11279298-6	2001	Enzyme activity studies confirmed the presence of a high-affinity, NAD-dependent dehydrogenase activity (K(m) 137 nmol/l and V(max) 128 pmol E/h/mg protein), indicative of the 11 beta-HSD2 isoform.	NAD	67-70	hydroxysteroid 11-beta dehydrogenase 2	Homo sapiens	176-188
11160087-6	2001	The transposon inserted into the coding sequences of hbdA, coding for S-(+)-beta-hydroxybutyryl-coenzyme A dehydrogenase and catalyzing an NAD-dependent reaction.	NAD	139-142	3-hydroxybutyryl-CoA dehydrogenase	Rhodobacter sphaeroides 2.4.1	53-57
11060293-11	2001	The K(m) of recombinant AKR1C1 for nicotinamide cofactors (K(m) NADPH approximately 6 microm, K(m)(app) NADH &gt;6 mm) suggested that it is primed for reductive metabolism of HNE.	NAD	104-108	aldo-keto reductase family 1 member C1	Homo sapiens	24-30
11136248-3	2001	Of the mutations made, the substitution of Trp-676 with alanine (W676A) resulted in a functional NADH-dependent enzyme, which catalyzed the reduction of cytochrome c and ferricyanide as well as facilitated the metabolism of 7-ethoxyresorufin by CYP1A2.	NAD	97-101	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	245-251
11501263-4	2001	However, for several pathological situations, which include massive DNA injury (brain ischemia for example), excessive activation of PARP can deplete stores of nicotinamide adenine dinucleotide (NAD+), the PARP substrate, which, with the subsequent ATP depletion, leads to cell death.	NAD	160-193	poly (ADP-ribose) polymerase 1	Rattus norvegicus	133-137
11106374-0	2000	Silent information regulator 2 family of NAD- dependent histone/protein deacetylases generates a unique product, 1-O-acetyl-ADP-ribose.	NAD	41-44	sirtuin 2	Homo sapiens	0-30
11106374-1	2000	Conflicting reports have suggested that the silent information regulator 2 (SIR2) protein family employs NAD(+) to ADP-ribosylate histones [Tanny, J. C., Dowd, G. J., Huang, J., Hilz, H. &amp; Moazed, D. (1999) Cell 99, 735-745; Frye, R. A.	NAD	105-111	sirtuin 2	Homo sapiens	44-74
11106374-1	2000	Conflicting reports have suggested that the silent information regulator 2 (SIR2) protein family employs NAD(+) to ADP-ribosylate histones [Tanny, J. C., Dowd, G. J., Huang, J., Hilz, H. &amp; Moazed, D. (1999) Cell 99, 735-745; Frye, R. A.	NAD	105-111	sirtuin 2	Homo sapiens	76-80
11095969-0	2000	Role of NAD(+) in the deacetylase activity of the SIR2-like proteins.	NAD	8-14	sirtuin 2	Homo sapiens	50-54
27575721-0	2016	Correction to NADH:Cytochrome b5 Reductase and Cytochrome b5 Can Act as Sole Electron Donors to Human Cytochrome P450 1A1-Mediated Oxidation and DNA Adduct Formation by Benzo[a]pyrene.	NAD	14-18	cytochrome b5 type A	Homo sapiens	19-32
11095969-1	2000	In this report we describe the role of NAD(+) in the deacetylation reaction catalyzed by the SIR2 family of enzymes.	NAD	39-45	sirtuin 2	Homo sapiens	93-97
27575721-0	2016	Correction to NADH:Cytochrome b5 Reductase and Cytochrome b5 Can Act as Sole Electron Donors to Human Cytochrome P450 1A1-Mediated Oxidation and DNA Adduct Formation by Benzo[a]pyrene.	NAD	14-18	cytochrome b5 type A	Homo sapiens	47-60
27575721-0	2016	Correction to NADH:Cytochrome b5 Reductase and Cytochrome b5 Can Act as Sole Electron Donors to Human Cytochrome P450 1A1-Mediated Oxidation and DNA Adduct Formation by Benzo[a]pyrene.	NAD	14-18	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	102-121
27076630-4	2016	EXPERIMENTAL DESIGN: The glycolytic dependency of Myc-driven glioblastoma was tested using (13)C metabolic flux analysis, glucose-limiting culture assays, and glycolysis inhibitors, including inhibitors of the NAD(+) salvage enzyme nicotinamide phosphoribosyl-transferase (NAMPT), in MYC and MYCN shRNA knockdown and lentivirus overexpression systems and in patient-derived glioblastoma tumorspheres with and without MYC/MYCN amplification.	NAD	210-216	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	50-53
11006082-9	2000	Poly(P)/ATP-NAD kinases of M. flavus and Ppnk of M. tuberculosis H37Rv specifically and completely phosphorylated NAD by utilizing commercially available poly(P)s and nucleoside triphosphates as phosphoryl donors.	NAD	12-15	inorganic polyphosphate/ATP-NAD kinase	Mycobacterium tuberculosis H37Rv	41-45
10737622-5	2000	PARP enzymatic activity was investigated by measuring nuclear [3H]NAD incorporation.	NAD	66-69	poly (ADP-ribose) polymerase 1	Rattus norvegicus	0-4
10693811-5	2000	Here we show that yeast and mouse Sir2 proteins are nicotinamide adenine dinucleotide (NAD)-dependent histone deacetylases, which deacetylate lysines 9 and 14 of H3 and specifically lysine 16 of H4.	NAD	52-85	sirtuin 1	Mus musculus	34-38
10693811-5	2000	Here we show that yeast and mouse Sir2 proteins are nicotinamide adenine dinucleotide (NAD)-dependent histone deacetylases, which deacetylate lysines 9 and 14 of H3 and specifically lysine 16 of H4.	NAD	87-90	sirtuin 1	Mus musculus	34-38
10984085-6	2000	Therefore, the putrescine enhancing LDH-5 activity appeared to be capable of stimulating NAD-mediated rhodopsin regeneration.	NAD	89-92	rhodopsin	Bos taurus	102-111
10939283-3	2000	However, the activity of indoleamine 2,3-dioxygenase (IDO), the rate limiting enzyme for de novo NAD synthesis, is also markedly increased in astrocytes during inflammation.	NAD	97-100	indoleamine 2,3-dioxygenase 1	Homo sapiens	25-52
10939283-3	2000	However, the activity of indoleamine 2,3-dioxygenase (IDO), the rate limiting enzyme for de novo NAD synthesis, is also markedly increased in astrocytes during inflammation.	NAD	97-100	indoleamine 2,3-dioxygenase 1	Homo sapiens	54-57
10939283-4	2000	This study investigated the role of IDO induction in the maintenance of intracellular NAD and its relationship to improved cell viability under conditions of increased oxidative stress in the human astroglioma cell line, HTB-138.	NAD	86-89	indoleamine 2,3-dioxygenase 1	Homo sapiens	36-39
10939283-8	2000	These results suggest that induction of IDO and subsequent de novo NAD synthesis may contribute to the maintenance of intracellular NAD levels and cell viability under conditions of increased oxidative stress.	NAD	132-135	indoleamine 2,3-dioxygenase 1	Homo sapiens	40-43
10585740-5	1999	Six factors influenced CYP1A2-mediated MROD rates: buffer type, pH, temperature, Mg/EDTA, NADH, and glycerol.	NAD	90-94	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	23-29
10567213-14	1999	Hence the function of YSA1H might be to remove free ADP-ribose arising from NAD(+) and protein-bound poly- and mono-(ADP-ribose) turnover to prevent the occurrence of non-enzymic protein glycation.	NAD	76-82	nudix hydrolase 5	Homo sapiens	22-27
10542202-5	1999	ART5 was found to be primarily an NADase at 10 microM NAD, whereas at higher NAD concentrations (1 mM), after some delay, transferase activity increased, whereas NADase activity fell.	NAD	34-37	ADP-ribosyltransferase 5	Homo sapiens	0-4
10542202-5	1999	ART5 was found to be primarily an NADase at 10 microM NAD, whereas at higher NAD concentrations (1 mM), after some delay, transferase activity increased, whereas NADase activity fell.	NAD	54-57	ADP-ribosyltransferase 5	Homo sapiens	0-4
10542202-8	1999	Auto-ADP-ribosylated ART5 isolated after incubation with NAD was primarily a transferase.	NAD	57-60	ADP-ribosyltransferase 5	Homo sapiens	21-25
10553576-2	1999	CD38 exists in beta-cells and has both ADP-ribosyl cyclase, which catalyzes the formation of cyclic ADP-ribose (cADPR) from NAD+, and cADPR hydrolase, which converts cADPR to ADP-ribose.	NAD	124-128	CD38 molecule	Homo sapiens	0-4
27648125-6	2016	We further found that the injection of NAD(+) can significantly decrease I/R-induced apoptotic damage in the heart: NAD(+) administration can both decrease the TUNEL signals, Bax, cleaved caspase-3 levels and increase the Bcl-XL levels in the rats that are subjected to myocardial I/R injury.	NAD	39-45	BCL2 associated X, apoptosis regulator	Rattus norvegicus	175-178
27648125-6	2016	We further found that the injection of NAD(+) can significantly decrease I/R-induced apoptotic damage in the heart: NAD(+) administration can both decrease the TUNEL signals, Bax, cleaved caspase-3 levels and increase the Bcl-XL levels in the rats that are subjected to myocardial I/R injury.	NAD	116-122	BCL2 associated X, apoptosis regulator	Rattus norvegicus	175-178
27060251-3	2016	In response to physiological glutamate signals, cytosolic Ca(2+) activates respiration by stimulation of the NADH malate-aspartate shuttle through Ca(2+)-binding to the mitochondrial aspartate/glutamate carrier (Aralar/AGC1/Slc25a12), and by stimulation of adenine nucleotide uptake through Ca(2+) binding to the mitochondrial ATP-Mg/Pi carrier (SCaMC-3/Slc25a23).	NAD	109-113	aggrecan	Mus musculus	219-223
27060251-3	2016	In response to physiological glutamate signals, cytosolic Ca(2+) activates respiration by stimulation of the NADH malate-aspartate shuttle through Ca(2+)-binding to the mitochondrial aspartate/glutamate carrier (Aralar/AGC1/Slc25a12), and by stimulation of adenine nucleotide uptake through Ca(2+) binding to the mitochondrial ATP-Mg/Pi carrier (SCaMC-3/Slc25a23).	NAD	109-113	solute carrier family 25 (mitochondrial carrier; phosphate carrier), member 23	Mus musculus	346-353
27060251-3	2016	In response to physiological glutamate signals, cytosolic Ca(2+) activates respiration by stimulation of the NADH malate-aspartate shuttle through Ca(2+)-binding to the mitochondrial aspartate/glutamate carrier (Aralar/AGC1/Slc25a12), and by stimulation of adenine nucleotide uptake through Ca(2+) binding to the mitochondrial ATP-Mg/Pi carrier (SCaMC-3/Slc25a23).	NAD	109-113	solute carrier family 25 (mitochondrial carrier; phosphate carrier), member 23	Mus musculus	354-362
29450127-3	2016	The current case control study aimed to investigate the possible relationship between mitochondrial NAD+-IDH activity in human seminal plasma and sperm motility among asthenozoospermic cellular phone users.	NAD	100-104	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	105-108
29450127-5	2016	NAD+-IDH activity was measured in human seminal plasma by spectrophotometer.	NAD	0-4	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	5-8
27128560-1	2016	RATIONALE: Sirtuin (SIRT3), a major nicotinamide adenine dinucleotide (NAD(+))-dependent deacetylase in mitochondria, declines with aging and its ablation is associated with accelerated development of cardiovascular diseases.	NAD	36-69	sirtuin 3	Mus musculus	20-25
27208243-3	2016	We previously identified a peroxisomal transport protein in Arabidopsis (Arabidopsis thaliana) called the peroxisomal NAD carrier (PXN).	NAD	118-121	Mitochondrial substrate carrier family protein	Arabidopsis thaliana	131-134
27208243-10	2016	These studies provided strong evidences that PXN was not able to function as a CoA transporter or a redox shuttle by mediating a NAD/NADH exchange, but instead catalyzed the import of NAD into peroxisomes against AMP in intact yeast cells.	NAD	129-132	Mitochondrial substrate carrier family protein	Arabidopsis thaliana	45-48
27208243-10	2016	These studies provided strong evidences that PXN was not able to function as a CoA transporter or a redox shuttle by mediating a NAD/NADH exchange, but instead catalyzed the import of NAD into peroxisomes against AMP in intact yeast cells.	NAD	133-137	Mitochondrial substrate carrier family protein	Arabidopsis thaliana	45-48
27208243-10	2016	These studies provided strong evidences that PXN was not able to function as a CoA transporter or a redox shuttle by mediating a NAD/NADH exchange, but instead catalyzed the import of NAD into peroxisomes against AMP in intact yeast cells.	NAD	133-136	Mitochondrial substrate carrier family protein	Arabidopsis thaliana	45-48
27291931-1	2016	SIRT2 is a member of the NAD+ dependent deacetylases.	NAD	25-28	sirtuin 2	Homo sapiens	0-5
26987957-9	2016	Application of nonspecific ER antagonist, ICI 182,780 and selective ERalpha and ERbeta agonists, PPT and DPN, respectively, demonstrated the involvement of both receptor subtypes in observed actions.	NAD	105-108	estrogen receptor 1	Rattus norvegicus	68-75
26987957-9	2016	Application of nonspecific ER antagonist, ICI 182,780 and selective ERalpha and ERbeta agonists, PPT and DPN, respectively, demonstrated the involvement of both receptor subtypes in observed actions.	NAD	105-108	estrogen receptor 2	Rattus norvegicus	80-86
26987957-10	2016	Selective ERalpha receptor agonist, PPT, induced upregulation of both the protein level and activity of eN, while application of selective ERbeta receptor agonist, DPN, increased only the activity of eN.	NAD	164-167	estrogen receptor 2	Rattus norvegicus	139-145
27173464-11	2016	Enhancing NAD pool rescued the impaired modulations of stromal cell-derived factor-1alpha (SDF-1alpha) and endothelial nitric oxide synthase (eNOS) protein levels in db/db mice BM upon hind-limb ischemia.	NAD	10-13	nitric oxide synthase 3, endothelial cell	Mus musculus	107-140
10493573-5	1999	This structure offers the first crystallographic evidence of a folded NAD with ring stacking, and it is the first enzyme structure containing an FMN cofactor interacting with NAD(P).	NAD	70-73	formin 1	Homo sapiens	145-148
27258319-10	2016	Pyruvate produced by the reverse reaction of alanine aminotransferase is funneled to the TCA cycle, while deaminating glutamate dehydrogenase regenerates, reducing equivalent (NADH) and 2-oxoglutarate to maintain the cycle function.	NAD	176-180	glutamate dehydrogenase 1	Homo sapiens	118-141
26926998-7	2016	Furthermore, mutations in genes encoding the other five Arabidopsis Elongator subunits (ELO2/AtELP1, AtELP2, ELO1/AtELP4, AtELP5, and AtELP6) also compromise exogenous NAD(+)-induced PR gene expression and resistance to P. syringae pv.	NAD	168-174	elongator protein 2	Arabidopsis thaliana	101-107
10437804-1	1999	CD38 is a multifunctional cell surface ectoenzyme that catalyzes both the synthesis of cyclic ADP-ribose from NAD+ and its hydrolysis to ADP-ribose.	NAD	110-114	CD38 molecule	Homo sapiens	0-4
27110715-6	2016	We found that the oxidation of NADH and mitochondrial membrane potential (Deltapsim) were significantly reduced in ND5 mutant cybrids.	NAD	31-35	mitochondrially encoded NADH dehydrogenase 5	Homo sapiens	115-118
10437804-9	1999	These results indicate that CD38, which is a multifunctional enzyme towards NAD+, displays exclusively a NADP+ glycohydrolase activity and is unable to catalyze both the synthesis and the hydrolysis of cyclic ADP-ribose 2"-phosphate.	NAD	76-80	CD38 molecule	Homo sapiens	28-32
10381378-0	1999	Characterization of five human cDNAs with homology to the yeast SIR2 gene: Sir2-like proteins (sirtuins) metabolize NAD and may have protein ADP-ribosyltransferase activity.	NAD	116-119	sirtuin 2	Homo sapiens	64-68
10381378-0	1999	Characterization of five human cDNAs with homology to the yeast SIR2 gene: Sir2-like proteins (sirtuins) metabolize NAD and may have protein ADP-ribosyltransferase activity.	NAD	116-119	sirtuin 2	Homo sapiens	75-79
10381378-8	1999	Recombinant E. coli cobB and human SIRT2 sirtuin proteins were able to cause radioactivity to be transferred from [32P]NAD to bovine serum albumin (BSA).	NAD	119-122	sirtuin 2	Homo sapiens	35-40
27127721-1	2016	BACKGROUND: PLA2G6-associated neurodegeneration (PLAN) is a recessive neurodegenerative disorder characterized by three distinct phenotypes: infantile neuroaxonal dystrophy (INAD), atypical neuroaxonal dystrophy (atypical NAD), and PLA2G6-related dystonia-parkinsonism.	NAD	175-178	85/88 kDa calcium-independent phospholipase A2	Meleagris gallopavo	12-18
10198228-0	1999	Threonine 188 is critical for interaction with NAD+ in human NAD+-dependent 15-hydroxyprostaglandin dehydrogenase.	NAD	47-51	15-hydroxyprostaglandin dehydrogenase	Homo sapiens	61-113
10198228-3	1999	A relatively conserved threonine residue corresponding to threonine 188 of 15-PGDH is proposed to be involved in the interaction with the carboxamide group of NAD+.	NAD	159-163	15-hydroxyprostaglandin dehydrogenase	Homo sapiens	75-82
10198228-9	1999	These results suggest that threonine 188 is critical for interaction with NAD+ and contributes to the full catalytic activity of 15-PGDH.	NAD	74-78	15-hydroxyprostaglandin dehydrogenase	Homo sapiens	129-136
10380010-1	1999	CD38 is expressed on a variety of hematopoietic cells and has a unique enzymatic activity that converts nicotinamide adenine dinucleotide (NAD) into cyclic ADP-ribose (cADPR) and then into ADPR.	NAD	104-137	CD38 molecule	Homo sapiens	0-4
10380010-1	1999	CD38 is expressed on a variety of hematopoietic cells and has a unique enzymatic activity that converts nicotinamide adenine dinucleotide (NAD) into cyclic ADP-ribose (cADPR) and then into ADPR.	NAD	139-142	CD38 molecule	Homo sapiens	0-4
10331645-8	1999	The expression of these two forms of PARP in E. coli demonstrated that while PARP II has the catalytic NAD-binding domain and DNA-binding domain it is enzymatically inactive.	NAD	103-106	Poly-(ADP-ribose) polymerase	Drosophila melanogaster	37-41
10331645-8	1999	The expression of these two forms of PARP in E. coli demonstrated that while PARP II has the catalytic NAD-binding domain and DNA-binding domain it is enzymatically inactive.	NAD	103-106	Poly-(ADP-ribose) polymerase	Drosophila melanogaster	77-81
10331647-2	1999	CD38 occurs in beta-cells and has both ADP-ribosyl cyclase, which catalyzes the formation of cyclic ADP-ribose (cADPR) from NAD+, and cADPR hydrolase, which converts cADPR to ADP-ribose.	NAD	124-128	CD38 molecule	Homo sapiens	0-4
9989216-5	1999	Their ability to mediate electron transfer between spinach NADH:ferredoxin oxidoreductase and horse heart cytochrome c was assessed.	NAD	59-63	cytochrome c, somatic	Equus caballus	106-118
27389650-0	1999	Coenzyme Activity of NAD Analogs for 3-Isopropylmalate Dehydrogenase from Thermus thermophilus HB8.	NAD	21-24	3-isopropylmalate dehydrogenase	Thermus thermophilus HB8	37-68
27389650-1	1999	In order to elucidate the enzyme-substrate-cofactor interaction in 3-isopropylmalate dehydrogenase, the coenzyme activity of NAD analogs which have a 3-substituted pyridine ring was examined.	NAD	125-128	3-isopropylmalate dehydrogenase	Thermus thermophilus HB8	67-98
10453439-9	1999	Niacin supplementation elevated skin NAD content, which is known to modulate the function of DNA strand scission surveillance proteins p53 and poly(ADP-ribose) polymerase, two proteins critical in cellular responses to UV-induced DNA damage.	NAD	37-40	transformation related protein 53, pseudogene	Mus musculus	135-138
10232052-3	1999	11 beta-HSD2 is a high affinity NAD-dependent dehydrogenase that protects the mineralocorticoid receptor from glucocorticoid excess; mutations in the HSD11B2 gene explain an inherited form of hypertension, the syndrome of apparent mineralocorticoid excess in which cortisol acts as a potent mineralocorticoid.	NAD	32-35	hydroxysteroid 11-beta dehydrogenase 2	Homo sapiens	150-157
9828181-5	1998	The 11beta-HSD activity in the placenta was characteristic of 11beta-HSD2 in that it possessed only dehydrogenase activity that was NAD-dependent and had a high affinity for cortisol (Km = 134 nM).	NAD	132-135	hydroxysteroid 11-beta dehydrogenase 2	Homo sapiens	62-73
9664081-1	1998	Cyclic ADP-ribose (cADPR) has been shown to be a mediator for intracellular Ca2+ mobilization for insulin secretion by glucose in pancreatic beta cells, and CD38 shows both ADP-ribosyl cyclase to synthesize cADPR from NAD+ and cADPR hydrolase to hydrolyze cADPR to ADP-ribose.	NAD	218-222	CD38 molecule	Homo sapiens	157-161
9588172-1	1998	To identify the cytochrome b5 residues responsible for the electrostatic interaction with NADH-cytochrome b5 reductase (b5R), we prepared and characterized the cytochrome b5 mutants in which Glu41, Glu42, Glu63, Asp70, and Glu73 were replaced by Ala, utilizing site-directed mutagenesis and the expression system for cytochrome b5 in Escherichia coli.	NAD	90-94	cytochrome b5 type A	Homo sapiens	16-29
9588172-1	1998	To identify the cytochrome b5 residues responsible for the electrostatic interaction with NADH-cytochrome b5 reductase (b5R), we prepared and characterized the cytochrome b5 mutants in which Glu41, Glu42, Glu63, Asp70, and Glu73 were replaced by Ala, utilizing site-directed mutagenesis and the expression system for cytochrome b5 in Escherichia coli.	NAD	90-94	cytochrome b5 type A	Homo sapiens	95-108
9588172-1	1998	To identify the cytochrome b5 residues responsible for the electrostatic interaction with NADH-cytochrome b5 reductase (b5R), we prepared and characterized the cytochrome b5 mutants in which Glu41, Glu42, Glu63, Asp70, and Glu73 were replaced by Ala, utilizing site-directed mutagenesis and the expression system for cytochrome b5 in Escherichia coli.	NAD	90-94	cytochrome b5 type A	Homo sapiens	95-108
9588172-1	1998	To identify the cytochrome b5 residues responsible for the electrostatic interaction with NADH-cytochrome b5 reductase (b5R), we prepared and characterized the cytochrome b5 mutants in which Glu41, Glu42, Glu63, Asp70, and Glu73 were replaced by Ala, utilizing site-directed mutagenesis and the expression system for cytochrome b5 in Escherichia coli.	NAD	90-94	cytochrome b5 type A	Homo sapiens	95-108
9525901-4	1998	Here we demonstrate that ectocellular expression of human CD38 in CD38(-) HeLa and 3T3 cells results in intracellular CD38 substrate (NAD+ + NADH) consumption and product (cADPR) accumulation.	NAD	134-138	CD38 molecule	Homo sapiens	58-62
9525901-4	1998	Here we demonstrate that ectocellular expression of human CD38 in CD38(-) HeLa and 3T3 cells results in intracellular CD38 substrate (NAD+ + NADH) consumption and product (cADPR) accumulation.	NAD	134-138	CD38 molecule	Homo sapiens	66-70
9525901-4	1998	Here we demonstrate that ectocellular expression of human CD38 in CD38(-) HeLa and 3T3 cells results in intracellular CD38 substrate (NAD+ + NADH) consumption and product (cADPR) accumulation.	NAD	141-145	CD38 molecule	Homo sapiens	58-62
9525901-4	1998	Here we demonstrate that ectocellular expression of human CD38 in CD38(-) HeLa and 3T3 cells results in intracellular CD38 substrate (NAD+ + NADH) consumption and product (cADPR) accumulation.	NAD	141-145	CD38 molecule	Homo sapiens	66-70
9386892-2	1998	Although classified as an orphan receptor, CD38 is also a bifunctional ectoenzyme that catalyzes both the conversion of NAD+ to nicotinamide and cyclic ADP-ribose (cADPR), via an ADP-ribosyl cyclase reaction, and also the hydrolysis of cADPR to ADP-ribose (hydrolase).	NAD	120-124	CD38 molecule	Homo sapiens	43-47
9386892-6	1998	On the other hand, in the CD38+ human Namalwa B lymphoid cells, NAD+ (and thiol compounds as well) induced a two-step process of self-aggregation followed by endocytosis of CD38, which resulted in a shift of cADPR metabolism from the cell surface to the cytosol.	NAD	64-68	CD38 molecule	Homo sapiens	26-30
9386892-6	1998	On the other hand, in the CD38+ human Namalwa B lymphoid cells, NAD+ (and thiol compounds as well) induced a two-step process of self-aggregation followed by endocytosis of CD38, which resulted in a shift of cADPR metabolism from the cell surface to the cytosol.	NAD	64-68	CD38 molecule	Homo sapiens	173-177
9893217-11	1998	At the end of 60 days, SBP in NADH-treated SHR was 184 mm Hg +/- 2.8 (SEM) compared to 201 mm Hg +/- 2.1 (SEM) in control SHR (p &lt; 0.001).	NAD	30-34	spermine binding protein	Rattus norvegicus	23-26
9426159-5	1997	Stably transfected CHO cell lines expressed high, NAD-dependent, unidirectional 11 beta-HSD2 activity.	NAD	50-53	hydroxysteroid 11-beta dehydrogenase 2	Homo sapiens	80-92
9389415-5	1997	One of the characteristic features of pseudohypoxia due to hyperglycaemia is an increase in the ratio of NADH/NAD+, so in the present study the changes in NADH - induced glucose 6-phosphatase activity were investigated as related to the release of inorganic phosphate (Pi) derived from glucose 6-phosphate.	NAD	105-109	glucose-6-phosphatase catalytic subunit 1	Rattus norvegicus	170-191
9389415-5	1997	One of the characteristic features of pseudohypoxia due to hyperglycaemia is an increase in the ratio of NADH/NAD+, so in the present study the changes in NADH - induced glucose 6-phosphatase activity were investigated as related to the release of inorganic phosphate (Pi) derived from glucose 6-phosphate.	NAD	110-114	glucose-6-phosphatase catalytic subunit 1	Rattus norvegicus	170-191
9389415-5	1997	One of the characteristic features of pseudohypoxia due to hyperglycaemia is an increase in the ratio of NADH/NAD+, so in the present study the changes in NADH - induced glucose 6-phosphatase activity were investigated as related to the release of inorganic phosphate (Pi) derived from glucose 6-phosphate.	NAD	155-159	glucose-6-phosphatase catalytic subunit 1	Rattus norvegicus	170-191
9389415-7	1997	The decrease in the activity of glucose 6-phosphatase generated by NADH was prevented by using desferrioxamine, an irreversible ferric chelator, butylated hydroxytoluene and Trolox, two agents which inhibit lipid peroxidation, and reduced glutathione, a non-specific radical scavenger.	NAD	67-71	glucose-6-phosphatase catalytic subunit 1	Rattus norvegicus	32-53
9378973-2	1997	CD38 can transmit positive or negative signals regulating T and B lymphocyte proliferation and differentiation and can enzymatically convert nicotinamide adenine dinucleotide to cyclic ADP-ribose, a potent intracellular calcium releaser.	NAD	141-174	CD38 molecule	Homo sapiens	0-4
9188485-3	1997	However, in the absence of the eIF-5A precursor, catalysis involves only the NAD-dependent cleavage of spermidine to generate 1,3-diaminopropane and a putative 4-carbon amine intermediate that gives rise to Delta1-pyrroline.	NAD	77-80	eukaryotic translation initiation factor 5A	Homo sapiens	31-37
9425751-4	1997	NAD+, NADH, pyruvate and lactate quench the relative fluorescence intensities of LDH-C4 in a concentration dependent manner.	NAD	0-4	lactate dehydrogenase C	Homo sapiens	81-87
9425751-4	1997	NAD+, NADH, pyruvate and lactate quench the relative fluorescence intensities of LDH-C4 in a concentration dependent manner.	NAD	6-10	lactate dehydrogenase C	Homo sapiens	81-87
26681113-4	2016	The origin of NF-kappaB activation was related to the age-dependent Bmal1/Clock/RORalpha/Rev-Erbalpha loop disruption, which lowers NAD(+) levels, reducing the SIRT1 deacetylase ability to inactivate NF-kappaB.	NAD	132-138	aryl hydrocarbon receptor nuclear translocator-like	Mus musculus	68-88
26660500-2	2016	It is one of the products produced from the catalysis of NAD(+) by the multifunctional CD38/ADP-ribosyl cyclase superfamily.	NAD	57-63	CD38 molecule	Homo sapiens	87-91
26879378-6	2016	RESULTS: A series of active whole-cell biocatalysts were constructed by over-expressing the (S)-selective omega-transaminase (VAMT) from Capsicum chinense together with the NADH-dependent (S)-selective alcohol dehydrogenase (SADH) originating from Rhodococcus erythropolis in strains with or without deletion of glycerol-3-phosphate dehydrogenases 1 and 2 (GPD1 and GPD2).	NAD	173-177	glycerol-3-phosphate dehydrogenase (NAD(+)) GPD2	Saccharomyces cerevisiae S288C	366-370
26414199-1	2016	The nicotinamide adenine dinucleotide-dependent protein deacetylase silent information regulator 2 (Sir2) regulates cellular lifespan in several organisms.	NAD	4-37	sirtuin 2	Homo sapiens	100-104
26307000-13	2016	In conclusion, our results suggest that the altered function and expression of P2X7 and ART1 in the human CD39+ Treg or CD39- Treg cells could participate in the resistance against cell death induced by ATP or NAD.	NAD	210-213	ectonucleoside triphosphate diphosphohydrolase 1	Homo sapiens	106-110
26307000-13	2016	In conclusion, our results suggest that the altered function and expression of P2X7 and ART1 in the human CD39+ Treg or CD39- Treg cells could participate in the resistance against cell death induced by ATP or NAD.	NAD	210-213	ectonucleoside triphosphate diphosphohydrolase 1	Homo sapiens	120-124
26397183-7	2016	Fittingly, in rat wounds treated with the ER-beta agonist (DPN), epidermal regeneration was accelerated.	NAD	59-62	estrogen receptor 2	Rattus norvegicus	42-49
27313401-6	2016	AMPK activation increased the NAD(+)/NADH ratio and activated Sirtuin 1 (SIRT1), a NAD(+)-dependent deacetylating enzyme and negative regulator of inflammation.	NAD	83-89	sirtuin 1	Mus musculus	62-71
27313401-6	2016	AMPK activation increased the NAD(+)/NADH ratio and activated Sirtuin 1 (SIRT1), a NAD(+)-dependent deacetylating enzyme and negative regulator of inflammation.	NAD	83-89	sirtuin 1	Mus musculus	73-78
27110038-7	2016	In the presence of either of the reductase cofactors tested, NADPH or NADH, cytochrome b5 stimulated CYP1A1-mediated formation of both BaP-DNA adducts.	NAD	70-74	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	101-107
27110038-8	2016	The results demonstrate that NADH can act as a sole electron donor for both the first and the second reduction of CYP1A1 during its reaction cycle catalyzing oxidation of BaP, and suggest that the NADH:cytochrome b5 reductase as the NADH-dependent reductase might substitute POR in this enzymatic system.	NAD	29-33	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	114-120
27110038-8	2016	The results demonstrate that NADH can act as a sole electron donor for both the first and the second reduction of CYP1A1 during its reaction cycle catalyzing oxidation of BaP, and suggest that the NADH:cytochrome b5 reductase as the NADH-dependent reductase might substitute POR in this enzymatic system.	NAD	197-201	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	114-120
26678339-0	2015	Extreme Vulnerability of IDH1 Mutant Cancers to NAD+ Depletion.	NAD	48-52	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	25-29
26678339-3	2015	To identify other metabolic therapeutic targets, we systematically profiled metabolites in endogenous IDH1 mutant cancer cells after mutant IDH1 inhibition and discovered a profound vulnerability to depletion of the coenzyme NAD+.	NAD	225-229	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	102-106
26678339-4	2015	Mutant IDH1 lowered NAD+ levels by downregulating the NAD+ salvage pathway enzyme nicotinate phosphoribosyltransferase (Naprt1), sensitizing to NAD+ depletion via concomitant nicotinamide phosphoribosyltransferase (NAMPT) inhibition.	NAD	20-24	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	7-11
26678339-4	2015	Mutant IDH1 lowered NAD+ levels by downregulating the NAD+ salvage pathway enzyme nicotinate phosphoribosyltransferase (Naprt1), sensitizing to NAD+ depletion via concomitant nicotinamide phosphoribosyltransferase (NAMPT) inhibition.	NAD	54-58	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	7-11
26678339-4	2015	Mutant IDH1 lowered NAD+ levels by downregulating the NAD+ salvage pathway enzyme nicotinate phosphoribosyltransferase (Naprt1), sensitizing to NAD+ depletion via concomitant nicotinamide phosphoribosyltransferase (NAMPT) inhibition.	NAD	54-58	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	7-11
26678339-6	2015	Thus, we identify NAD+ depletion as a metabolic susceptibility of IDH1 mutant cancers.	NAD	18-22	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	66-70
26282612-7	2015	Also, the ERbeta activation by its agonist DPN changed the subcellular localization of p21, inducing an increase in the p21 nuclear expression, where it acts as a tumoral suppressor.	NAD	43-46	estrogen receptor 2	Rattus norvegicus	10-16
26350462-3	2015	Using LC/MS we demonstrate that pnc-1 mutants do not salvage the nicotinamide released by NAD(+) consumers to resynthesize NAD(+), resulting in a reduction in global NAD(+) bioavailability.	NAD	123-129	Isochorismatase domain-containing protein	Caenorhabditis elegans	32-37
26350462-3	2015	Using LC/MS we demonstrate that pnc-1 mutants do not salvage the nicotinamide released by NAD(+) consumers to resynthesize NAD(+), resulting in a reduction in global NAD(+) bioavailability.	NAD	123-129	Isochorismatase domain-containing protein	Caenorhabditis elegans	32-37
26290368-5	2015	Mitochondria from hyperleptinemic LoxTB MC4R-/- mice kidneys respired NADH-generating substrates (including palmitate) at lower rates due to an apparent decrease in complex I activity, and these mitochondria showed oxidative damage.	NAD	70-74	melanocortin 4 receptor	Mus musculus	40-44
26325079-1	2015	Homoisocitrate dehydrogenase (HIcDH) catalyzes the NAD(+)-dependent oxidative decarboxylation of HIc to alpha-ketoadipate, the fourth step in the alpha-aminoadipate pathway responsible for the de novo synthesis of l-lysine in fungi.	NAD	51-57	homoisocitrate dehydrogenase	Saccharomyces cerevisiae S288C	0-28
26325079-1	2015	Homoisocitrate dehydrogenase (HIcDH) catalyzes the NAD(+)-dependent oxidative decarboxylation of HIc to alpha-ketoadipate, the fourth step in the alpha-aminoadipate pathway responsible for the de novo synthesis of l-lysine in fungi.	NAD	51-57	homoisocitrate dehydrogenase	Saccharomyces cerevisiae S288C	30-35
26466337-11	2015	The higher NADH-dependent cytochrome c reductase activity together with the higher transcript levels of CBR.1 and CYB5 in the crtR- mutant as well as the lower NADH-dependent activity in CBS-cbr.1- strongly suggest that CBR.1-CYB5 via participates as an alternative electron donor pathway for P450 enzymes involved in ergosterol biosynthesis in X. dendrorhous.	NAD	11-15	cytochrome b5 type A	Homo sapiens	114-118
26466337-11	2015	The higher NADH-dependent cytochrome c reductase activity together with the higher transcript levels of CBR.1 and CYB5 in the crtR- mutant as well as the lower NADH-dependent activity in CBS-cbr.1- strongly suggest that CBR.1-CYB5 via participates as an alternative electron donor pathway for P450 enzymes involved in ergosterol biosynthesis in X. dendrorhous.	NAD	11-15	cytochrome b5 type A	Homo sapiens	226-230
26462257-5	2015	ss-Lap is an NADPH:quinone oxidoreductase (NQO1)-bioactivatable drug that leads to NADPH depletion through high levels of reactive oxygen species (ROS) from the futile redox cycling of the drug and subsequently nicotinamide adenine dinucleotide (NAD)+ depletion through poly(ADP ribose) polymerase (PARP) hyperactivation.	NAD	13-16	poly (ADP-ribose) polymerase 1	Rattus norvegicus	270-297
26218637-8	2015	NAD(+) consumption by PARP-1 also undermined the recovery processes, and PARP inhibition significantly improved the metabolism and increased cellular ATP levels in cardiomyocytes.	NAD	0-6	poly (ADP-ribose) polymerase 1	Rattus norvegicus	22-28
26172206-0	2015	Type-II NADH:quinone oxidoreductase from Staphylococcus aureus has two distinct binding sites and is rate limited by quinone reduction.	NAD	8-12	AT695_RS05530	Staphylococcus aureus	13-35
26068950-3	2015	We identify the hydroxyprostaglandin dehydrogenase 15-(nicotinamide adenine dinucleotide) (HPGD/15-PGDH) tumor suppressor gene as a direct miR-620 target, which results in increased prostaglandin E2 (PGE2) levels.	NAD	55-88	15-hydroxyprostaglandin dehydrogenase	Homo sapiens	96-103
26068950-3	2015	We identify the hydroxyprostaglandin dehydrogenase 15-(nicotinamide adenine dinucleotide) (HPGD/15-PGDH) tumor suppressor gene as a direct miR-620 target, which results in increased prostaglandin E2 (PGE2) levels.	NAD	55-88	microRNA 620	Homo sapiens	139-146
26170451-6	2015	Using (32)P-labeled NAD(+) and immunoblotting, we also demonstrate that both subunits of the XPC-RAD23B are poly(ADP-ribosyl)ated by PARP1.	NAD	20-26	RAD23 homolog B, nucleotide excision repair protein	Homo sapiens	97-103
25447548-1	2015	CD38 catalyzes the synthesis of two structurally distinct messengers for Ca2+-mobilization, cyclic ADP-ribose (cADPR) and nicotinic acid adenine dinucleotide phosphate (NAADP), from cytosolic substrates, NAD and NADP, respectively.	NAD	204-207	CD38 molecule	Homo sapiens	0-4
26101264-6	2015	Both mitochondrial fatty acid oxidation and Complex I defect are responsible for increased protein lysine acetylation despite an unchanged amount of the NAD(+)-dependent mitochondrial deacetylase sirt3.	NAD	153-159	sirtuin 3	Rattus norvegicus	196-201
26209623-2	2015	In response to NAD(+) released from damaged cells during inflammation, ARTC2.2 ADP-ribosylates and thereby gates the P2X7 ion channel.	NAD	15-21	ADP-ribosyltransferase 2b	Mus musculus	71-76
26209623-6	2015	Intravenous injection of NAD(+) increased the level of enzymatically active ARTC2.2 in serum, indicating that this mechanism is operative also under inflammatory conditions in vivo.	NAD	25-31	ADP-ribosyltransferase 2b	Mus musculus	76-81
26037610-2	2015	An X-ray crystal structure of AdoHcyase with NAD(+) and 18a showed a novel open form co-crystal structure.	NAD	45-51	adenosylhomocysteinase	Homo sapiens	30-39
25909344-3	2015	We recently reported that TBT inhibits cell growth and the ATP content in the human embryonic carcinoma cell line NT2/D1 via a non-genomic pathway involving NAD(+)-dependent isocitrate dehydrogenase (NAD-IDH), which metabolizes isocitrate to alpha-ketoglutarate.	NAD	157-163	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	204-207
26156706-4	2015	RESULTS: Recombinant strains of S. cerevisiae modified for increased NADPH- and NADH-dependent Gdh1 and Gdh2 activity were tested for growth at low temperature.	NAD	80-84	glutamate dehydrogenase (NADP(+)) GDH1	Saccharomyces cerevisiae S288C	95-99
26156706-4	2015	RESULTS: Recombinant strains of S. cerevisiae modified for increased NADPH- and NADH-dependent Gdh1 and Gdh2 activity were tested for growth at low temperature.	NAD	80-84	glutamate dehydrogenase (NAD(+))	Saccharomyces cerevisiae S288C	104-108
26156706-8	2015	We also demonstrated that decreased capacity of glycerol production impairs growth at 15 but not at 30 C and that 15 C-grown baker"s yeast cells display higher fermentative capacity than those cultivated at 30 C. Thus, increasing NADH oxidation by overexpression of GDH2 would help to avoid perturbations in the redox metabolism induced by a higher fermentative/oxidative balance at low temperature.	NAD	230-234	glutamate dehydrogenase (NAD(+))	Saccharomyces cerevisiae S288C	266-270
25858853-2	2015	Leucine (Leu) activates Sirt1 by lowering its Km for NAD(+) and potentiates other sirtuin/AMPK-activators, resulting in improvement of insulin sensitivity.	NAD	53-59	sirtuin 1	Mus musculus	24-29
26098879-3	2015	Sirtuin1 (SIRT1) belongs to the family of NAD-dependent de-acyetylases and is modulated by cellular redox.	NAD	42-45	sirtuin 1	Mus musculus	0-8
28626720-2	2015	In this study, the possibility to steer the activity of the GPD2 promoter was investigated by placing it in strains with different ability to reoxidise NADH, and applying different environmental conditions.	NAD	152-156	glycerol-3-phosphate dehydrogenase (NAD(+)) GPD2	Saccharomyces cerevisiae S288C	60-64
25713058-0	2015	NADH fluorescence lifetime is an endogenous reporter of alpha-synuclein aggregation in live cells.	NAD	0-4	synuclein alpha	Homo sapiens	56-71
25980580-3	2015	IDH1 R132H/+ and isogenic IDH1 +/+ parental cells were screened for their ability to generate energy-rich NADH when cultured in a standardized high-throughput Phenotype MicroArrayplatform comprising &gt;300 nutrients.	NAD	106-110	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	0-4
25915406-2	2015	The NAD+-dependent protein deacetylase Sirtuin-3 (SIRT3) has been implicated in Type 2 diabetes.	NAD	4-7	sirtuin 3	Mus musculus	39-48
25915406-2	2015	The NAD+-dependent protein deacetylase Sirtuin-3 (SIRT3) has been implicated in Type 2 diabetes.	NAD	4-7	sirtuin 3	Mus musculus	50-55
25755250-0	2015	SIRT3-dependent GOT2 acetylation status affects the malate-aspartate NADH shuttle activity and pancreatic tumor growth.	NAD	69-73	glutamic-oxaloacetic transaminase 2	Homo sapiens	16-20
25755250-5	2015	The GOT2 acetylation at these three residues promotes the net transfer of cytosolic NADH into mitochondria and changes the mitochondrial NADH/NAD(+) redox state to support ATP production.	NAD	84-88	glutamic-oxaloacetic transaminase 2	Homo sapiens	4-8
25755250-5	2015	The GOT2 acetylation at these three residues promotes the net transfer of cytosolic NADH into mitochondria and changes the mitochondrial NADH/NAD(+) redox state to support ATP production.	NAD	137-141	glutamic-oxaloacetic transaminase 2	Homo sapiens	4-8
25755250-5	2015	The GOT2 acetylation at these three residues promotes the net transfer of cytosolic NADH into mitochondria and changes the mitochondrial NADH/NAD(+) redox state to support ATP production.	NAD	142-148	glutamic-oxaloacetic transaminase 2	Homo sapiens	4-8
25755250-9	2015	Our study uncovers a previously unknown mechanism by which GOT2 acetylation stimulates the malate-aspartate NADH shuttle activity and oxidative protection.	NAD	108-112	glutamic-oxaloacetic transaminase 2	Homo sapiens	59-63
25868125-1	2015	MP-124, a novel poly(ADP-ribose) polymerase-1 (PARP-1) inhibitor that competes with the binding of the PARP substrate nicotinamide adenine dinucleotide (NAD), is being developed as a neuroprotective agent against acute ischemic stroke.	NAD	118-151	poly (ADP-ribose) polymerase 1	Rattus norvegicus	16-45
25868125-1	2015	MP-124, a novel poly(ADP-ribose) polymerase-1 (PARP-1) inhibitor that competes with the binding of the PARP substrate nicotinamide adenine dinucleotide (NAD), is being developed as a neuroprotective agent against acute ischemic stroke.	NAD	118-151	poly (ADP-ribose) polymerase 1	Rattus norvegicus	47-53
25868125-1	2015	MP-124, a novel poly(ADP-ribose) polymerase-1 (PARP-1) inhibitor that competes with the binding of the PARP substrate nicotinamide adenine dinucleotide (NAD), is being developed as a neuroprotective agent against acute ischemic stroke.	NAD	153-156	poly (ADP-ribose) polymerase 1	Rattus norvegicus	16-45
25868125-1	2015	MP-124, a novel poly(ADP-ribose) polymerase-1 (PARP-1) inhibitor that competes with the binding of the PARP substrate nicotinamide adenine dinucleotide (NAD), is being developed as a neuroprotective agent against acute ischemic stroke.	NAD	153-156	poly (ADP-ribose) polymerase 1	Rattus norvegicus	47-53
25751424-0	2015	NAD(+)-SIRT1 control of H3K4 trimethylation through circadian deacetylation of MLL1.	NAD	0-6	lysine methyltransferase 2A	Homo sapiens	79-83
25751424-7	2015	Finally, levels of MLL1 acetylation and H3K4 trimethylation at circadian gene promoters depend on NAD(+) circadian levels.	NAD	98-104	lysine methyltransferase 2A	Homo sapiens	19-23
25666612-6	2015	Residues that line the propofol binding site on SIRT2 contact the sirtuin co-substrate NAD(+) during enzymatic catalysis, and assays that measured SIRT2 deacetylation of acetylated alpha-tubulin revealed that propofol inhibits enzymatic function.	NAD	87-93	sirtuin 2	Homo sapiens	48-53
25533949-5	2015	Downstream activation of key stress signalling pathways are causally connected to TyrRS-PARP1-NAD(+) collaboration.	NAD	94-100	tyrosyl-tRNA synthetase 2	Homo sapiens	82-87
25533949-7	2015	In contrast to functionally diverse tRNA synthetase catalytic nulls created by alternative splicing events that ablate active sites, here a non-spliced TyrRS catalytic null reveals a new PARP1- and NAD(+)-dependent dimension to the physiological mechanism of resveratrol.	NAD	198-204	tyrosyl-tRNA synthetase 2	Homo sapiens	152-157
25517228-8	2015	By utilizing an NAD(+)-based mechanism, PARP1 inhibition increases the activity of SIRT1.	NAD	16-22	sirtuin 1	Mus musculus	83-88
25890336-6	2015	Following initial validation, pathways that include NAD synthetase 1 (NADSYN1) and protein kinase B (AKT2) were hypothesized and experimentally tested to provide a mechanistic basis for AMPK regulation of cell migration and maintenance of cellular NAD(+) concentrations during catabolic processes.	NAD	248-254	protein tyrosine kinase 2 beta	Homo sapiens	83-99
25890336-6	2015	Following initial validation, pathways that include NAD synthetase 1 (NADSYN1) and protein kinase B (AKT2) were hypothesized and experimentally tested to provide a mechanistic basis for AMPK regulation of cell migration and maintenance of cellular NAD(+) concentrations during catabolic processes.	NAD	248-254	AKT serine/threonine kinase 2	Homo sapiens	101-105
25870619-5	2015	In comparison, class III HDACs (also known as the sirtuins) are composed of a family of NAD(+)-dependent protein-modifying enzymes related to the Sir2 gene.	NAD	88-94	sirtuin 2	Homo sapiens	146-150
25596911-6	2015	The rate of synthesis of NAD and niacin from tryptophan oxidation depends on the induction of the enzyme indoleamine 2,3-dioxygenase (IDO) by pro-inflammatory cytokines such as interferon-gamma.	NAD	25-28	indoleamine 2,3-dioxygenase 1	Homo sapiens	134-137
25531177-17	2015	The pure preparations of these molecules induce rapid reduction of the renalase flavin cofactor (230 s(-1) for 6-dihydroNAD, 850 s(-1) for 2-dihydroNAD) but bind only a few fold more tightly than beta-NADH.	NAD	196-205	renalase, FAD dependent amine oxidase	Homo sapiens	71-79
25619262-1	2015	BACKGROUND: A growing number of studies on the associations between nicotinamide adenine dinucleotide phosphate (NADPH) oxidase p22phox C242T polymorphism and risk of ischemic cerebrovascular disease have recently been published, but the results remain inconsistent.	NAD	68-101	calcineurin like EF-hand protein 1	Homo sapiens	128-131
25411385-1	2015	Renalase is a recently identified FAD/NADH-dependent amine oxidase mainly expressed in kidney that is secreted into blood and urine where it was suggested to metabolize catecholamines.	NAD	38-42	renalase, FAD-dependent amine oxidase	Mus musculus	0-8
25590809-3	2015	beta-Lap is bioactivated by NADPH:quinone oxidoreductase 1 (NQO1) in a futile redox cycle that consumes oxygen and generates high levels of reactive oxygen species (ROS) that cause extensive DNA damage and rapid PARP1-mediated NAD(+) consumption.	NAD	227-233	LAP	Homo sapiens	5-8
25590809-8	2015	Non-overlapping specificities of FK866 for PDA tumors that rely heavily on NAMPT-catalyzed NAD(+) synthesis and beta-lap for cancer cells with elevated NQO1 levels affords high tumor-selectivity.	NAD	91-97	LAP	Homo sapiens	8-11
25590809-9	2015	The concept of reducing NAD(+) pools in cancer cells to sensitize them to ROS-mediated cell death by beta-lap is a novel strategy with potential application for pancreatic and other types of NQO1+ solid tumors.	NAD	24-30	LAP	Homo sapiens	106-109
26303485-9	2015	Also the effect of 2-APB on hypoxia and/or anoxia were investigated on NADH and mitochondria (MT) membrane potential.	NAD	71-75	arginyl aminopeptidase	Rattus norvegicus	21-24
10072900-4	1997	The activities of GPI and GAPDH in the cysts were measured by the formation of NADH or NADPH.	NAD	79-83	glyceraldehyde-3-phosphate dehydrogenase	Mus musculus	26-31
8938450-1	1996	The cDNA for the PSST subunit of human mitochondrial nicotinamide adenine dinucleotide (NADH): ubiquinone oxidoreductase [complex I; NADH dehydrogenase (ubiquinone), Fe-S (20 kDa); EC 1.6.5.3] was generated by polymerase chain reaction (PCR) amplification of human cDNA.	NAD	53-86	NADH:ubiquinone oxidoreductase core subunit S7	Homo sapiens	17-21
26558285-5	2015	Finally, low sirtuin-1 and sirtuin-3 gene expressions due to higher NADH/NAD in Cmah-null mice decreased Foxo-1 and MnSOD gene expression, suggesting that oxidative stress may result in mitochondrial dysfunction in Cmah-null mouse.	NAD	68-72	sirtuin 1	Mus musculus	13-22
26558285-5	2015	Finally, low sirtuin-1 and sirtuin-3 gene expressions due to higher NADH/NAD in Cmah-null mice decreased Foxo-1 and MnSOD gene expression, suggesting that oxidative stress may result in mitochondrial dysfunction in Cmah-null mouse.	NAD	68-72	sirtuin 3	Mus musculus	27-36
26558285-5	2015	Finally, low sirtuin-1 and sirtuin-3 gene expressions due to higher NADH/NAD in Cmah-null mice decreased Foxo-1 and MnSOD gene expression, suggesting that oxidative stress may result in mitochondrial dysfunction in Cmah-null mouse.	NAD	68-72	forkhead box O1	Mus musculus	105-111
25996069-1	2015	The sirtuins form a superfamily of evolutionarily conserved NAD(+)-dependent protein N-epsilon-acyl-lysine (AcK) deacylases with roles in a variety of key cellular processes.	NAD	60-63	tyrosine kinase non receptor 2	Homo sapiens	108-111
8938450-1	1996	The cDNA for the PSST subunit of human mitochondrial nicotinamide adenine dinucleotide (NADH): ubiquinone oxidoreductase [complex I; NADH dehydrogenase (ubiquinone), Fe-S (20 kDa); EC 1.6.5.3] was generated by polymerase chain reaction (PCR) amplification of human cDNA.	NAD	88-92	NADH:ubiquinone oxidoreductase core subunit S7	Homo sapiens	17-21
25408220-5	2015	The endostatin/amyloid-beta1-42 ratio was significantly increased in patients with AD (257%, p < 0.0001) and nAD/nFTD (140%, p < 0.0001) compared to controls.	NAD	109-112	collagen type XVIII alpha 1 chain	Homo sapiens	4-14
8836136-0	1996	Regulation of NAD+ glycohydrolase activity by NAD(+)-dependent auto-ADP-ribosylation.	NAD	46-52	NAD glycohydrolase	Oryctolagus cuniculus	14-33
9425719-1	1996	A mixture of NADH, cytochrome-C-reductase and methylene blue was employed to antagonize ferri(met)-Hb formation during oximetries of dilute samples of human Hb-A.	NAD	13-17	keratin 90, pseudogene	Homo sapiens	157-161
25408220-8	2015	The measurement of endostatin in CSF and the calculation of its ratio relative to well-established AD markers improve the diagnosis of bvFTD patients and the discrimination of patients with AD from those with bvFTD and nAD/nFTD.	NAD	219-222	collagen type XVIII alpha 1 chain	Homo sapiens	19-29
24999994-1	2014	A novel electrochemical biosensing platform for nicotinamide adenine dinucleotide (NAD(+))-dependent dehydrogenase catalysis was designed using the nitrogen-doped graphene (NG), which had properties similar to NADH dehydrogenase (CoI).	NAD	48-81	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	230-233
24999994-1	2014	A novel electrochemical biosensing platform for nicotinamide adenine dinucleotide (NAD(+))-dependent dehydrogenase catalysis was designed using the nitrogen-doped graphene (NG), which had properties similar to NADH dehydrogenase (CoI).	NAD	83-90	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	230-233
8812833-6	1996	The recombinant domain retained both NADH:ferricyanide and NADH:cytochrome b5 reductase activities with Vmax of 48 and 26 micromol NADH consumed/min/nmol FAD, respectively, and Km of 6, 7, and 11 microM for NADH, ferricyanide, and cytochrome b5.	NAD	59-63	cytochrome b5 type A	Rattus norvegicus	64-77
8812833-6	1996	The recombinant domain retained both NADH:ferricyanide and NADH:cytochrome b5 reductase activities with Vmax of 48 and 26 micromol NADH consumed/min/nmol FAD, respectively, and Km of 6, 7, and 11 microM for NADH, ferricyanide, and cytochrome b5.	NAD	59-63	cytochrome b5 type A	Rattus norvegicus	231-244
24999994-4	2014	In comparison with a bare gold electrode, an 800 mV decrease in the overpotential for NADH oxidation and CoI-like behavior were observed at NG-modified electrode, which is the largest decrease in overpotential for NADH oxidation reported to date.	NAD	214-218	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	105-108
8812833-6	1996	The recombinant domain retained both NADH:ferricyanide and NADH:cytochrome b5 reductase activities with Vmax of 48 and 26 micromol NADH consumed/min/nmol FAD, respectively, and Km of 6, 7, and 11 microM for NADH, ferricyanide, and cytochrome b5.	NAD	59-63	cytochrome b5 type A	Rattus norvegicus	64-77
8812833-6	1996	The recombinant domain retained both NADH:ferricyanide and NADH:cytochrome b5 reductase activities with Vmax of 48 and 26 micromol NADH consumed/min/nmol FAD, respectively, and Km of 6, 7, and 11 microM for NADH, ferricyanide, and cytochrome b5.	NAD	59-63	cytochrome b5 type A	Rattus norvegicus	231-244
25470550-0	2014	Activation of SIRT3 by the NAD+ precursor nicotinamide riboside protects from noise-induced hearing loss.	NAD	27-31	sirtuin 3	Mus musculus	14-19
8812833-6	1996	The recombinant domain retained both NADH:ferricyanide and NADH:cytochrome b5 reductase activities with Vmax of 48 and 26 micromol NADH consumed/min/nmol FAD, respectively, and Km of 6, 7, and 11 microM for NADH, ferricyanide, and cytochrome b5.	NAD	59-63	cytochrome b5 type A	Rattus norvegicus	64-77
8812833-6	1996	The recombinant domain retained both NADH:ferricyanide and NADH:cytochrome b5 reductase activities with Vmax of 48 and 26 micromol NADH consumed/min/nmol FAD, respectively, and Km of 6, 7, and 11 microM for NADH, ferricyanide, and cytochrome b5.	NAD	59-63	cytochrome b5 type A	Rattus norvegicus	231-244
25470550-5	2014	These effects are mediated by the NAD(+)-dependent mitochondrial sirtuin, SIRT3, since SIRT3-overexpressing mice are resistant to NIHL and SIRT3 deletion abrogates the protective effects of NR and expression of NAD(+) biosynthetic enzymes.	NAD	34-40	sirtuin 3	Mus musculus	74-79
8663185-2	1996	The NAD(P)H:flavin oxidoreductase from Escherichia coli, Fre, is a monomer of 26.1 kDa which catalyzes the reduction of free flavins by NADPH or NADH.	NAD	145-149	oxidoreductase	Escherichia coli	19-33
25470550-5	2014	These effects are mediated by the NAD(+)-dependent mitochondrial sirtuin, SIRT3, since SIRT3-overexpressing mice are resistant to NIHL and SIRT3 deletion abrogates the protective effects of NR and expression of NAD(+) biosynthetic enzymes.	NAD	34-40	sirtuin 3	Mus musculus	87-92
8706705-1	1996	The lymphocyte cell surface antigen, CD38, which has an amino acid sequence similar to Aplysia ADP-ribosyl cyclase, catalyzes not only the hydrolysis of NAD+ and 1-(5-phospho-beta-D-ribosyl) adenosine 5"-phosphate cyclic anhydride (cyclic ADP-ribose) but also the formation of cyclic ADP-ribose from NAD+.	NAD	153-157	CD53 molecule	Homo sapiens	15-35
8706705-1	1996	The lymphocyte cell surface antigen, CD38, which has an amino acid sequence similar to Aplysia ADP-ribosyl cyclase, catalyzes not only the hydrolysis of NAD+ and 1-(5-phospho-beta-D-ribosyl) adenosine 5"-phosphate cyclic anhydride (cyclic ADP-ribose) but also the formation of cyclic ADP-ribose from NAD+.	NAD	300-304	CD53 molecule	Homo sapiens	15-35
25470550-5	2014	These effects are mediated by the NAD(+)-dependent mitochondrial sirtuin, SIRT3, since SIRT3-overexpressing mice are resistant to NIHL and SIRT3 deletion abrogates the protective effects of NR and expression of NAD(+) biosynthetic enzymes.	NAD	34-40	sirtuin 3	Mus musculus	87-92
25470550-5	2014	These effects are mediated by the NAD(+)-dependent mitochondrial sirtuin, SIRT3, since SIRT3-overexpressing mice are resistant to NIHL and SIRT3 deletion abrogates the protective effects of NR and expression of NAD(+) biosynthetic enzymes.	NAD	211-217	sirtuin 3	Mus musculus	74-79
25470550-6	2014	These findings reveal that administration of NR activates a NAD(+)-SIRT3 pathway that reduces neurite degeneration caused by noise exposure.	NAD	60-66	sirtuin 3	Mus musculus	67-72
25341895-0	2014	Intracellular NAMPT-NAD+-SIRT1 cascade improves post-ischaemic vascular repair by modulating Notch signalling in endothelial progenitors.	NAD	20-24	sirtuin 1	Mus musculus	25-30
25341895-0	2014	Intracellular NAMPT-NAD+-SIRT1 cascade improves post-ischaemic vascular repair by modulating Notch signalling in endothelial progenitors.	NAD	20-24	notch 1	Mus musculus	93-98
8687015-15	1996	DNA repair requires high levels of NAD in the nucleus for the activity of poly(ADP-ribose) polymerase.	NAD	35-38	poly (ADP-ribose) polymerase family, member 1	Mus musculus	74-101
25341895-11	2014	CONCLUSIONS: These results demonstrate that intracellular NAMPT-NAD(+)-SIRT1 cascade improves post-ischaemic neovascularization.	NAD	64-70	sirtuin 1	Mus musculus	71-76
25491822-3	2014	Compared to common carbon paste electrode, the electrochemical response was greatly improved for NADH electrooxidation at a surface of CdO/NP modified ionic liquid carbon paste electrode (IL/CdO/NP/CPE).	NAD	97-101	carboxypeptidase E	Homo sapiens	198-201
25199460-6	2014	SIRT1, a NAD(+)-dependent histone/non-histone protein deacetylase, has been reported to inhibit intracellular signaling mediated by SREBP-1 through deacetylation of this transcription factor.	NAD	9-15	sterol regulatory element binding transcription factor 1	Homo sapiens	132-139
25401080-1	2014	A reporter system was constructed to measure perturbations in the NADH/NAD(+) co-factor balance in yeast, by using the green fluorescent protein gene under the control of the GPD2 promoter that is induced under conditions of excess of NADH.	NAD	66-70	glycerol-3-phosphate dehydrogenase (NAD(+)) GPD2	Saccharomyces cerevisiae S288C	175-179
25401080-1	2014	A reporter system was constructed to measure perturbations in the NADH/NAD(+) co-factor balance in yeast, by using the green fluorescent protein gene under the control of the GPD2 promoter that is induced under conditions of excess of NADH.	NAD	71-77	glycerol-3-phosphate dehydrogenase (NAD(+)) GPD2	Saccharomyces cerevisiae S288C	175-179
25401080-1	2014	A reporter system was constructed to measure perturbations in the NADH/NAD(+) co-factor balance in yeast, by using the green fluorescent protein gene under the control of the GPD2 promoter that is induced under conditions of excess of NADH.	NAD	235-239	glycerol-3-phosphate dehydrogenase (NAD(+)) GPD2	Saccharomyces cerevisiae S288C	175-179
25356557-12	2014	This role of the NAD+-dependent Sir2 is supported by our finding that supplementing NAD+ precursors improves Hsf1 heat shock response in stationary-phase yeast, especially when combined with expression of excess Sir2.	NAD	17-21	stress-responsive transcription factor HSF1	Saccharomyces cerevisiae S288C	109-113
25356557-12	2014	This role of the NAD+-dependent Sir2 is supported by our finding that supplementing NAD+ precursors improves Hsf1 heat shock response in stationary-phase yeast, especially when combined with expression of excess Sir2.	NAD	84-88	stress-responsive transcription factor HSF1	Saccharomyces cerevisiae S288C	109-113
24814870-4	2014	provide evidence that sirtuin-2 (SIRT2), a NAD+-dependent deacetylase, inhibits the expression of keratin 15 and keratin 19, epidermal stem cell markers, while it stimulates the expression of loricrin, a marker of terminal keratinocyte differentiation.	NAD	43-46	sirtuin 2	Homo sapiens	22-31
24814870-4	2014	provide evidence that sirtuin-2 (SIRT2), a NAD+-dependent deacetylase, inhibits the expression of keratin 15 and keratin 19, epidermal stem cell markers, while it stimulates the expression of loricrin, a marker of terminal keratinocyte differentiation.	NAD	43-46	sirtuin 2	Homo sapiens	33-38
25088223-3	2014	A new concept supports that sepsis is an immunometabolic disease and that loss of control of nuclear epigenetic regulator sirtuin 1 (SIRT-1), a NAD(+) sensor directs immune and metabolic pathways during sepsis.	NAD	144-150	sirtuin 1	Mus musculus	122-131
25088223-3	2014	A new concept supports that sepsis is an immunometabolic disease and that loss of control of nuclear epigenetic regulator sirtuin 1 (SIRT-1), a NAD(+) sensor directs immune and metabolic pathways during sepsis.	NAD	144-150	sirtuin 1	Mus musculus	133-139
24753121-2	2014	Specifically, loss-of-function of the C. elegans NAD(+) salvage biosynthesis gene PNC-1 results in an array of developmental phenotypes.	NAD	49-55	Isochorismatase domain-containing protein	Caenorhabditis elegans	82-87
24753121-10	2014	Our work suggests a model where PNC-1 function is provided cell non-autonomously by a mix of intra and extracellular activity, most likely requiring NAD(+) salvage metabolite transport between tissues.	NAD	149-155	Isochorismatase domain-containing protein	Caenorhabditis elegans	32-37
24880091-6	2014	We show here that extracellular-signal-regulated kinase-5 regulates the transcription of the NADH(+)-dependent histone deacetylase silent mating type information regulation 2 homolog 1 (Sirtuin 1) in leukemic Jurkat T cells.	NAD	93-97	mitogen-activated protein kinase 7	Homo sapiens	18-57
25052842-1	2014	The Na(+)-translocating NADH:quinone oxidoreductase (Na(+)-NQR) is a unique Na(+) pumping respiratory complex found only in prokaryotes, that plays a key role in the metabolism of marine and pathogenic bacteria, including Vibrio cholerae and other human pathogens.	NAD	24-28	crystallin zeta	Homo sapiens	29-51
25083875-2	2014	Specifically, the NAD(+)-dependent deacetylase SIRT1, the founding member of the sirtuin family, contributes to clock function.	NAD	18-24	sirtuin 1	Mus musculus	47-52
25147754-4	2014	In the present study, we evaluated the effects of overexpressing genes encoding the transcription factor (YAP1) and the mitochondrial NADH-cytochrome b5 reductase (MCR1), either alone or in combination, in an already robust and xylose-consuming industrial strain of S. cerevisiae and evaluated the effect during the fermentation of undiluted and undetoxified spruce hydrolysate.	NAD	134-138	cytochrome-b5 reductase	Saccharomyces cerevisiae S288C	164-168
25057336-1	2014	CD38 is an ecto-enzyme that consumes NAD(+) to produce cyclic ADP-ribose (cADPR) --- a potent agonist of ryanodine receptors.	NAD	37-43	CD38 molecule	Homo sapiens	0-4
24796879-3	2014	Our most recent study found that DPN, an estrogen receptor (ER) beta-specific agonist, activated the Ndrg2 promoter and elevated endogenous NDRG2 protein expression in MCF7, HSG and T-47D cells.	NAD	33-36	NDRG family member 2	Homo sapiens	101-106
24796879-3	2014	Our most recent study found that DPN, an estrogen receptor (ER) beta-specific agonist, activated the Ndrg2 promoter and elevated endogenous NDRG2 protein expression in MCF7, HSG and T-47D cells.	NAD	33-36	NDRG family member 2	Homo sapiens	140-145
24796879-8	2014	After the OVX mice received continuous subcutaneous injections of 50mug/kg E2, 100mug/kg E2 or the ERbeta agonist DPN for 10 days, the Ndrg2 expression significantly increased compared with that of the OVX mice.	NAD	114-117	N-myc downstream regulated gene 2	Mus musculus	135-140
23113554-4	2014	Cytochrome b5 reductase is involved in the transfer of reducing equivalents from the physiological electron donor, NADH, via an FAD domain to the small molecules of cytochrome b5.	NAD	115-119	cytochrome b5 type A	Homo sapiens	0-13
24699315-6	2014	The NAD(+)-linked 15-hydroxyprostaglandin dehydrogenase (15-PGDH/HPGD), a key enzyme that converts the protumorigenic prostaglandin E2 (PGE2) to its biologically inactive metabolite, was identified as a direct target of miR-21 in cholangiocarcinoma cells.	NAD	4-10	15-hydroxyprostaglandin dehydrogenase	Homo sapiens	57-64
8809203-9	1996	After pre-incubation with NAD+ (10 microM), 11 alpha-BA-5 alpha-P inactivated 3 beta-HSD rapidly and specifically (t1/2 = 3.7 min).	NAD	26-30	hydroxy-delta-5-steroid dehydrogenase, 3 beta- and steroid delta-isomerase 1	Homo sapiens	78-88
24699315-6	2014	The NAD(+)-linked 15-hydroxyprostaglandin dehydrogenase (15-PGDH/HPGD), a key enzyme that converts the protumorigenic prostaglandin E2 (PGE2) to its biologically inactive metabolite, was identified as a direct target of miR-21 in cholangiocarcinoma cells.	NAD	4-10	microRNA 21	Homo sapiens	220-226
24722990-4	2014	We hypothesized that nicotinamide nucleotide transhydrogenase (Nnt), which utilizes the proton gradient to generate NADPH from NADH and NADP(+), provides the link between mitochondrial respiration and H2O2 detoxification through the thioredoxin/peroxiredoxin system.	NAD	127-131	thioredoxin	Homo sapiens	233-244
24784564-6	2014	Antisense reduction of IDO decreased NAD+ in human tumor cells.	NAD	37-41	indoleamine 2,3-dioxygenase 1	Homo sapiens	23-26
8609401-6	1996	Concomitant to suppression of the kinase by NAD, CD8 mediated transmembrane signaling and p56lck kinase activation are inhibited.	NAD	44-47	CD8a molecule	Homo sapiens	49-52
24784564-7	2014	NAD+ is essential for PARP activity and these data suggest that IDO mediates treatment resistance independent of immunity and at least partially due to a previously unrecognized role for IDO in DNA repair.	NAD	0-4	indoleamine 2,3-dioxygenase 1	Homo sapiens	64-67
24784564-7	2014	NAD+ is essential for PARP activity and these data suggest that IDO mediates treatment resistance independent of immunity and at least partially due to a previously unrecognized role for IDO in DNA repair.	NAD	0-4	indoleamine 2,3-dioxygenase 1	Homo sapiens	187-190
24423185-6	2014	Estradiol- or DPN-induced slowing of 5-HT clearance mediated by ERbeta was blocked after inhibition of MAPK/ERK1/2 but not of PI3K/Akt signaling pathways.	NAD	14-17	estrogen receptor 2	Rattus norvegicus	64-70
8833160-0	1996	Assignment of the human mitochondrial NAD+ -specific isocitrate dehydrogenase alpha subunit (IDH3A) gene to 15q25.1--&gt;q25.2by in situ hybridization.	NAD	38-41	isocitrate dehydrogenase (NAD(+)) 3 catalytic subunit alpha	Homo sapiens	93-98
24939540-1	2014	Sirtuin 2 (SIRT2) is an NAD(+) (nicotinamide adenine dinucleotide)-dependent deacetylase.	NAD	24-30	sirtuin 2	Homo sapiens	0-9
8963661-0	1996	NADH in the pyramidal cell layer of hippocampal regions CA1 and CA3 upon selective inhibition and uncoupling of oxidative phosphorylation.	NAD	0-4	carbonic anhydrase 3	Rattus norvegicus	64-67
8963661-6	1996	The CA1/CA3 ratio of NADH fluorescence mildly decreased to 0.92 +/- 0.04 (mean +/- S.D.)	NAD	21-25	carbonic anhydrase 3	Rattus norvegicus	8-11
24939540-1	2014	Sirtuin 2 (SIRT2) is an NAD(+) (nicotinamide adenine dinucleotide)-dependent deacetylase.	NAD	24-30	sirtuin 2	Homo sapiens	11-16
8742498-2	1996	The present study investigates the effects of a diet free of precursors of NAD, the substrate on which PARP acts, in female NMRI mice with AAP hepatitis and evaluates the influence of simultaneous ethanol consumption in these animals.	NAD	75-78	poly (ADP-ribose) polymerase family, member 1	Mus musculus	103-107
24939540-1	2014	Sirtuin 2 (SIRT2) is an NAD(+) (nicotinamide adenine dinucleotide)-dependent deacetylase.	NAD	32-65	sirtuin 2	Homo sapiens	0-9
24939540-1	2014	Sirtuin 2 (SIRT2) is an NAD(+) (nicotinamide adenine dinucleotide)-dependent deacetylase.	NAD	32-65	sirtuin 2	Homo sapiens	11-16
8521845-10	1995	Purified recombinant S. solfataricus PGK and GraP-DH showed half lives of 39 min and 17 h, respectively, at 80 degrees C. Unlike bacterial GraP-DH enzymes, S. solfataricus GraP-DH was able to use both NAD+ and NADP+ as cofactors, but exhibited a marked preference for NADP+.	NAD	201-205	hypothetical protein	Saccharolobus solfataricus	37-40
24717514-13	2014	Thus, NNMT is a novel regulator of histone methylation, polyamine flux and NAD(+)-dependent SIRT1 signalling, and is a unique and attractive target for treating obesity and type 2 diabetes.	NAD	75-81	sirtuin 1	Mus musculus	92-97
7557122-3	1995	Mn SOD is colocalized with reduced nicotinamide adenine dinucleotide (NADH) diaphorase in some tissues.	NAD	35-68	superoxide dismutase 2	Rattus norvegicus	0-6
7557122-3	1995	Mn SOD is colocalized with reduced nicotinamide adenine dinucleotide (NADH) diaphorase in some tissues.	NAD	70-74	superoxide dismutase 2	Rattus norvegicus	0-6
23384296-0	2014	Exogenous NAD(+) supplementation protects H9c2 cardiac myoblasts against hypoxia/reoxygenation injury via Sirt1-p53 pathway.	NAD	10-16	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	112-115
23384296-9	2014	NAD(+) replenishment restored Sirt1 activity, reduced the acetylation level of p53 (Lys373 &amp; 382), and attenuated cell apoptosis in HR-stressed H9c2 cells, whereas inhibition of Sirt1 activity alleviated the effects of NAD(+) replenishment.	NAD	0-6	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	79-82
23384296-10	2014	These results indicated that exogenous NAD(+) supplementation attenuated HR-induced cell apoptosis, which was at least partly mediated by restoring Sirt1 activity and subsequently inhibiting p53 activity via deacetylating p53 at lysine 373 and 382.	NAD	39-45	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	191-194
7673125-12	1995	This combination of affinity labeling and biophysical data using nucleotide derivatives supports our model for the sequential reaction mechanism; the cofactor product of the 3 beta-HSD reaction, NADH, activates isomerase by inducing a conformational change in the single, bifunctional enzyme protein.	NAD	195-199	hydroxy-delta-5-steroid dehydrogenase, 3 beta- and steroid delta-isomerase 1	Homo sapiens	174-184
23384296-10	2014	These results indicated that exogenous NAD(+) supplementation attenuated HR-induced cell apoptosis, which was at least partly mediated by restoring Sirt1 activity and subsequently inhibiting p53 activity via deacetylating p53 at lysine 373 and 382.	NAD	39-45	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	222-225
24586272-1	2014	Poly(ADP-ribose)polymerase and sirtuin 1 are both NAD(+)-dependent enzymes.	NAD	50-56	poly (ADP-ribose) polymerase 1	Rattus norvegicus	0-26
7608265-13	1995	Moreover, the mutant N100S protein had an apparent decreased affinity for NAD+, with a Km value of 650 +/- 66 mumol/L compared with 20 +/- 2 mumol/L for normal type II 3 beta HSD.	NAD	74-78	hydroxy-delta-5-steroid dehydrogenase, 3 beta- and steroid delta-isomerase 1	Homo sapiens	168-178
7476212-1	1995	We have cloned and characterized a homologue of the previously isolated GPD1 gene, encoding sn-glycerol 3-phosphate dehydrogenase (NAD+) in Saccharomyces cerevisiae.	NAD	131-135	glycerol-3-phosphate dehydrogenase (NAD(+)) GPD1	Saccharomyces cerevisiae S288C	72-76
24586272-4	2014	In addition, poly(ADP-ribose)polymerase inhibition restores NAD(+) level and sirtuin 1 activity in vitro.	NAD	60-66	poly (ADP-ribose) polymerase 1	Rattus norvegicus	13-39
24184811-2	2014	The nicotinamide adenine dinucleotide-dependent deacetylase SIRT1 regulates fatty acid metabolism through multiple nutrient sensors.	NAD	4-37	sirtuin 1	Mus musculus	60-65
7767940-11	1995	Metabolic activation of TNT by liver microsomes required NADPH but not NADH as the cofactor.	NAD	71-75	troponin T3, fast skeletal type	Rattus norvegicus	24-27
7744749-2	1995	Excessive poly-(ADP-ribose) formation by PARP has been assumed to deplete cellular NAD+ pools and to induce the death of several cell types, including the loss of insulin-producing islet cells in type I diabetes.	NAD	83-87	poly (ADP-ribose) polymerase family, member 1	Mus musculus	41-45
7744749-3	1995	In the present study we used cells from mice with a disrupted and thus inactivated PARP gene to provide direct evidence for a causal relationship between PARP activation, NAD+ depletion, and cell death.	NAD	171-175	poly (ADP-ribose) polymerase family, member 1	Mus musculus	83-87
7744749-3	1995	In the present study we used cells from mice with a disrupted and thus inactivated PARP gene to provide direct evidence for a causal relationship between PARP activation, NAD+ depletion, and cell death.	NAD	171-175	poly (ADP-ribose) polymerase family, member 1	Mus musculus	154-158
7744749-5	1995	These findings directly prove that PARP activation is responsible for most of the loss of NAD+ following such treatment.	NAD	90-94	poly (ADP-ribose) polymerase family, member 1	Mus musculus	35-39
18623311-4	1995	D-Lactate dehydrogenase, nicotinamide adenine dinucleotide (NAD(+)), a synthetic redox polymer containing covalently attached toluidine blue O as mediator, graphite powder, and paraffin oil were used for the construction of the modified carbon paste electrode.	NAD	60-66	lactate dehydrogenase D	Homo sapiens	0-23
7774637-1	1995	CD38 is a 42-kDa membrane associated enzyme which converts NAD into cyclic ADP-ribose (cADPR), a Ca(2+)-mobilizing second messenger, and ADP-ribose (ADPR).	NAD	59-62	CD38 antigen	Mus musculus	0-4
7774637-7	1995	CD38 immunoprecipitated from these B cell populations was normal in size and effectively hydrolyzed NAD, suggesting that the defect in CD38 signaling likely occurs downstream of CD38 itself.	NAD	100-103	CD38 antigen	Mus musculus	0-4
7774637-7	1995	CD38 immunoprecipitated from these B cell populations was normal in size and effectively hydrolyzed NAD, suggesting that the defect in CD38 signaling likely occurs downstream of CD38 itself.	NAD	100-103	CD38 antigen	Mus musculus	135-139
7774637-7	1995	CD38 immunoprecipitated from these B cell populations was normal in size and effectively hydrolyzed NAD, suggesting that the defect in CD38 signaling likely occurs downstream of CD38 itself.	NAD	100-103	CD38 antigen	Mus musculus	135-139
7893703-0	1995	Identification and characterization of the G15D mutation found in a male patient with 3 beta-hydroxysteroid dehydrogenase (3 beta-HSD) deficiency: alteration of the putative NAD-binding domain of type II 3 beta-HSD.	NAD	174-177	hydroxy-delta-5-steroid dehydrogenase, 3 beta- and steroid delta-isomerase 1	Homo sapiens	123-133
8527493-7	1995	After VP-16 administration, we have observed that the level of NAD is not heavily decreased.	NAD	63-66	host cell factor C1	Homo sapiens	6-11
7769961-5	1995	RESULTS: Significant changes in LF intensity were detected after injection of collagens I and III, cholesterol and elastin in thoracic aorta (P &lt; 0.001), but not with triglyceride or NADH.	NAD	186-190	elastin	Canis lupus familiaris	115-122
7734152-6	1994	These advantages should facilitate further studies elucidating NADH channelling to complex I from MDH and other dehydrogenases.	NAD	63-67	malic enzyme 1	Homo sapiens	98-101
8003469-9	1994	This result, coupled to the three-dimensional model built for Drosophila alcohol dehydrogenase, suggests a binding mechanism for the cofactor NAD different from that found for 3 alpha,20 beta-dehydroxysteroid dehydrogenase and similar to that found in the crystal structure of rat liver dihydropteridine reductase.	NAD	142-145	quinoid dihydropteridine reductase	Rattus norvegicus	287-313
8055187-1	1994	Spectrophotometric assay of microsomal cytochrome b5 in house-flies produces different results depending on whether sodium dithionite or NADH is used as the reducing agent and whether or not detergent is present.	NAD	137-141	cytochrome b5	Musca domestica	39-52
8053547-3	1994	More convenient and reliable photometric detection of the preferred labeling enzyme, glucose-6-phosphate dehydrogenase (G6PDH), is accomplished by monitoring the rate of generation of reduced thio-NAD (from thio-NAD) at 405 nm instead of NADH (from NAD) at 340 nm.	NAD	238-242	glucose-6-phosphate dehydrogenase	Homo sapiens	85-118
8053547-3	1994	More convenient and reliable photometric detection of the preferred labeling enzyme, glucose-6-phosphate dehydrogenase (G6PDH), is accomplished by monitoring the rate of generation of reduced thio-NAD (from thio-NAD) at 405 nm instead of NADH (from NAD) at 340 nm.	NAD	238-242	glucose-6-phosphate dehydrogenase	Homo sapiens	120-125
8053547-3	1994	More convenient and reliable photometric detection of the preferred labeling enzyme, glucose-6-phosphate dehydrogenase (G6PDH), is accomplished by monitoring the rate of generation of reduced thio-NAD (from thio-NAD) at 405 nm instead of NADH (from NAD) at 340 nm.	NAD	197-200	glucose-6-phosphate dehydrogenase	Homo sapiens	85-118
8053547-3	1994	More convenient and reliable photometric detection of the preferred labeling enzyme, glucose-6-phosphate dehydrogenase (G6PDH), is accomplished by monitoring the rate of generation of reduced thio-NAD (from thio-NAD) at 405 nm instead of NADH (from NAD) at 340 nm.	NAD	197-200	glucose-6-phosphate dehydrogenase	Homo sapiens	120-125
8302274-4	1994	NADH-dependent rates were about 25 to 30% of the NADPH-dependent rates.	NAD	0-4	2,4-dienoyl-CoA reductase 1	Homo sapiens	49-54
8299962-4	1993	Comparison of the PARP aa sequences among these species showed conservation of two zinc-finger motifs in the DNA-binding domain, and an NAD-binding motif and a Rossmann fold in the catalytic domain.	NAD	136-139	poly(ADP-ribose) polymerase 1 L homeolog	Xenopus laevis	18-22
7902582-3	1993	Koningic acid inhibited basal and sodium nitroprusside-stimulated NAD-dependent covalent modification of purified rabbit muscle GAPDH in a dose-dependent manner.	NAD	66-69	glyceraldehyde-3-phosphate dehydrogenase	Oryctolagus cuniculus	128-133
8235624-5	1993	Soluble CD38 catalyzed the formation and hydrolysis of cADPR when added to NAD+.	NAD	75-79	CD38 antigen	Mus musculus	8-12
8219401-6	1993	Some of the hepatotoxicity was found to result from the metabolic disturbances associated with the oxidation of ethanol via the liver alcohol dehydrogenase (ADH) pathway and the redox changes produced by the generated NADH, which in turn affects the metabolism of lipids, carbohydrates, proteins and purines.	NAD	218-222	aldo-keto reductase family 1 member A1	Homo sapiens	157-160
24241058-2	2014	Adenosine 5"-monophosphate-activated protein kinase (AMPK) is crucial for GTPCH-1 preservation, and tumor suppressor kinase liver kinase B1 (LKB1), an upstream kinase of AMPK, is activated by NAD-dependent class III histone deacetylase sirtuin 1 (SIRT1)-mediated deacetylation.	NAD	192-195	serine/threonine kinase 11	Rattus norvegicus	124-139
24241058-2	2014	Adenosine 5"-monophosphate-activated protein kinase (AMPK) is crucial for GTPCH-1 preservation, and tumor suppressor kinase liver kinase B1 (LKB1), an upstream kinase of AMPK, is activated by NAD-dependent class III histone deacetylase sirtuin 1 (SIRT1)-mediated deacetylation.	NAD	192-195	serine/threonine kinase 11	Rattus norvegicus	141-145
24026637-5	2014	Enteric neurons exposed to alpha-syn can also lead to impaired mitochondrial complex I activity, reduced mitochondrial function, and NAD(+) depletion culminating in cell death via energy restriction.	NAD	133-139	synuclein alpha	Homo sapiens	27-36
8454867-5	1993	In parallel, SNP induced endogenous ADP-ribosylation of GAPDH measured by a decreased incorporation of [32P]ADP-ribose from [32P]NAD+ in the cytosol of the SNP-treated cells.	NAD	129-133	glyceraldehyde-3-phosphate dehydrogenase	Rattus norvegicus	56-61
24231740-7	2014	Pretreatment of cells with PJ34, a PARP1 inhibitor prevented the cells from undergoing cell death and preserved intracellular NAD and ATP levels.	NAD	126-129	poly (ADP-ribose) polymerase 1	Rattus norvegicus	35-40
1281150-6	1992	Reduced nicotinamide adenine dinucleotide and dithiothreitol are required for the S-nitrosylation of GAPDH caused by the NO-generating compound sodium nitroprusside.	NAD	8-41	glyceraldehyde-3-phosphate dehydrogenase	Rattus norvegicus	101-106
25567503-1	2014	Renalase was described in 2005 as a new flavoprotein expressed mainly in the kidney that functions as a flavin adenine dinucleotide (FAD)- and nicotinamide adenine dinucleotide (NADH)-dependent amine oxidase.	NAD	143-176	renalase, FAD dependent amine oxidase	Homo sapiens	0-8
25567503-1	2014	Renalase was described in 2005 as a new flavoprotein expressed mainly in the kidney that functions as a flavin adenine dinucleotide (FAD)- and nicotinamide adenine dinucleotide (NADH)-dependent amine oxidase.	NAD	178-182	renalase, FAD dependent amine oxidase	Homo sapiens	0-8
22217852-5	1992	The protein expressed in bacteria was highly active in androsterone oxidation in the presence of NAD as cofactor and this activity was inhibited by indomethacin, a potent inhibitor of 3alpha-hydroxysteroid dehydrogenase.	NAD	97-100	aldo-keto reductase family 1, member C14	Rattus norvegicus	184-219
24266457-7	2013	As such, it appears that the root purpose of renalase is to return alpha-anomers of nicotinamide dinucleotides to the beta-anomer pool.	NAD	84-110	renalase, FAD dependent amine oxidase	Homo sapiens	45-53
1488820-4	1992	The inhibition of alcohol dehydrogenase by thiochrome is concurrent to NAD.	NAD	71-74	aldo-keto reductase family 1 member A1	Homo sapiens	18-39
23290998-2	2013	PARPs use NAD(+) as substrate and upon cleaving off nicotinamide they transfer the ADP-ribosyl moiety covalently to suitable acceptor proteins and elongate the chain by adding further ADP-ribose units to create a branched polymer, termed poly(ADP-ribose) (PAR), which is rapidly degraded by poly(ADP-ribose) glycohydrolase (PARG) and ADP-ribosylhydrolase 3 (ARH3).	NAD	10-16	ADP-ribosylserine hydrolase	Homo sapiens	334-356
1740142-6	1992	Km values for NAD were calculated to be 30 microM with beta/gamma-actin, 35 microM with alpha-actin and 20 microM with gamma-actin.	NAD	14-17	actin, alpha 2, smooth muscle, aorta	Gallus gallus	88-99
23290998-2	2013	PARPs use NAD(+) as substrate and upon cleaving off nicotinamide they transfer the ADP-ribosyl moiety covalently to suitable acceptor proteins and elongate the chain by adding further ADP-ribose units to create a branched polymer, termed poly(ADP-ribose) (PAR), which is rapidly degraded by poly(ADP-ribose) glycohydrolase (PARG) and ADP-ribosylhydrolase 3 (ARH3).	NAD	10-16	ADP-ribosylserine hydrolase	Homo sapiens	358-362
23954493-5	2013	We found that the ERalpha agonist PPT reproduced the actions of the low E2 dose on NMDAR-EPSCs and NMDAR-LTP, while the ERbeta agonist DPN reproduced the actions of the high E2 dose.	NAD	135-138	estrogen receptor 2	Rattus norvegicus	120-126
1334741-5	1992	RBP-retinol circulation supplies target cells, which then activate retinol into retinoic acid (RA) if they possess the NAD-dependent enzymatic oxidation system.	NAD	119-122	retinol binding protein 4	Homo sapiens	0-3
23831226-1	2013	NADH-Cytochrome b5 reductase (b5R), a flavoprotein consisting of NADH and flavin adenine dinucleotide (FAD) binding domains, catalyzes electron transfer from the two-electron carrier NADH to the one-electron carrier cytochrome b5 (Cb5).	NAD	65-69	cytochrome b5 type A	Homo sapiens	5-18
23831226-1	2013	NADH-Cytochrome b5 reductase (b5R), a flavoprotein consisting of NADH and flavin adenine dinucleotide (FAD) binding domains, catalyzes electron transfer from the two-electron carrier NADH to the one-electron carrier cytochrome b5 (Cb5).	NAD	65-69	cytochrome b5 type A	Homo sapiens	216-229
23831226-1	2013	NADH-Cytochrome b5 reductase (b5R), a flavoprotein consisting of NADH and flavin adenine dinucleotide (FAD) binding domains, catalyzes electron transfer from the two-electron carrier NADH to the one-electron carrier cytochrome b5 (Cb5).	NAD	65-69	cytochrome b5 type A	Homo sapiens	231-234
1747374-9	1991	Ligands that compete for the active site of 3 alpha-HSD (NAD+ and indomethacin) afforded protection against inactivation, and the inactivators could demonstrate competitive kinetics against 3 alpha-hydroxysteroid substrates by forming an E.NAD+.I complex.	NAD	57-61	aldo-keto reductase family 1, member C14	Rattus norvegicus	44-55
1747374-9	1991	Ligands that compete for the active site of 3 alpha-HSD (NAD+ and indomethacin) afforded protection against inactivation, and the inactivators could demonstrate competitive kinetics against 3 alpha-hydroxysteroid substrates by forming an E.NAD+.I complex.	NAD	240-244	aldo-keto reductase family 1, member C14	Rattus norvegicus	44-55
24089531-3	2013	The extrinsic arm contains binding sites for NADH and the primary electron acceptor FMN, and it provides a scaffold for seven iron-sulfur clusters that form an electron pathway linking FMN to the terminal electron acceptor, ubiquinone, which is bound in the region of the junction between the arms.	NAD	45-49	formin 1	Homo sapiens	84-87
1898363-4	1991	Both forms catalysed the rapid fixation of [14C]bicarbonate to the carboxy group atom of glycine during the exchange reaction, whereas the reversible exchange of electrons between NADH and lipoamide bound to the H-protein in the presence of 5,5"-dithiobis-(2-nitrobenzoic acid) was seen only with the form eluted at 350 mM-KCl.	NAD	180-184	myosin binding protein H	Homo sapiens	212-221
24089531-3	2013	The extrinsic arm contains binding sites for NADH and the primary electron acceptor FMN, and it provides a scaffold for seven iron-sulfur clusters that form an electron pathway linking FMN to the terminal electron acceptor, ubiquinone, which is bound in the region of the junction between the arms.	NAD	45-49	formin 1	Homo sapiens	185-188
24093018-1	2013	Silent information regulator 2 proteins (sirtuins or SIRTs) are a group of deacetylases (or deacylases) whose activities are dependent on and regulated by nicotinamide adenine dinucleotide (NAD(+)).	NAD	155-188	sirtuin 2	Homo sapiens	0-30
1888740-5	1991	A strong hydrogen bond is postulated to exist between amide carbonyl group of NAD+ and the enzyme in the binary complexes with both mMDH and sMDH on the basis of a sizable decrease in the frequency of the carbonyl double bond.	NAD	78-82	malate dehydrogenase 2, NAD (mitochondrial)	Mus musculus	132-136
1944309-7	1991	In vitro incubation with NAD+ and 3H-labeled pregnenolone or dehydroepiandrosterone shows that the type I protein possesses a 3 beta HSD/delta 5-delta 4 isomerase activity higher than type II, with respective Km values of 0.24 vs. 1.2 microM for pregnenolone and 0.18 vs. 1.6 microM for dihydroepiandrosterone, while the specific activity of both types is equivalent.	NAD	25-29	hydroxy-delta-5-steroid dehydrogenase, 3 beta- and steroid delta-isomerase 1	Homo sapiens	126-136
1944309-8	1991	Moreover, incubation in the presence of NADH of homogenates from cells transfected with type I or type II 3 beta HSD indicates that dihydrotestosterone is converted into 5 alpha-androstane-3 beta, 17 beta-diol, with Km values of 0.26 and 2.7 microM, respectively.	NAD	40-44	hydroxy-delta-5-steroid dehydrogenase, 3 beta- and steroid delta-isomerase 1	Homo sapiens	106-116
24093018-1	2013	Silent information regulator 2 proteins (sirtuins or SIRTs) are a group of deacetylases (or deacylases) whose activities are dependent on and regulated by nicotinamide adenine dinucleotide (NAD(+)).	NAD	190-196	sirtuin 2	Homo sapiens	0-30
23964689-5	2013	We have identified the catalytic activity of renalase as an alpha-NAD(P)H oxidase/anomerase, whereby low equilibrium concentrations of the alpha-anomer of NADPH and NADH initiate rapid reduction of the renalase flavin cofactor.	NAD	165-169	renalase, FAD dependent amine oxidase	Homo sapiens	45-53
1830494-0	1991	ADP-ribosyl cyclase: an enzyme that cyclizes NAD+ into a calcium-mobilizing metabolite.	NAD	45-49	ADP-ribosyl cyclase/cyclic ADP-ribose hydrolase	Aplysia californica	0-19
1854438-5	1991	On the other hand, the difference spectra of reduced minus oxidized forms of cytochromes were investigated to identify the inhibitory site, suggesting that alkylthiolated 2,3-dicyano-1,4-benzoquinones inhibit at sites between the substrates (succinate and NADH) and cytochrome b, and at the site after cytochrome a + a3 in the respiratory chain.	NAD	256-260	mitochondrially encoded cytochrome b	Homo sapiens	266-278
23964689-5	2013	We have identified the catalytic activity of renalase as an alpha-NAD(P)H oxidase/anomerase, whereby low equilibrium concentrations of the alpha-anomer of NADPH and NADH initiate rapid reduction of the renalase flavin cofactor.	NAD	165-169	renalase, FAD dependent amine oxidase	Homo sapiens	60-91
23964689-5	2013	We have identified the catalytic activity of renalase as an alpha-NAD(P)H oxidase/anomerase, whereby low equilibrium concentrations of the alpha-anomer of NADPH and NADH initiate rapid reduction of the renalase flavin cofactor.	NAD	165-169	renalase, FAD dependent amine oxidase	Homo sapiens	202-210
23880765-6	2013	In this study, we investigated the roles of CD38 and CD73 in providing ectocellular NAD(+) precursors for NAD(+) biosynthesis and in modulating cell susceptibility to FK866.	NAD	84-90	CD38 molecule	Homo sapiens	44-48
23880765-7	2013	By specifically silencing or overexpressing CD38 and CD73, we demonstrated that endogenous CD73 enables, whereas CD38 impairs, the conversion of extracellular NMN to NR as a precursor for intracellular NAD(+) biosynthesis in human cells.	NAD	202-208	CD38 molecule	Homo sapiens	44-48
23880765-7	2013	By specifically silencing or overexpressing CD38 and CD73, we demonstrated that endogenous CD73 enables, whereas CD38 impairs, the conversion of extracellular NMN to NR as a precursor for intracellular NAD(+) biosynthesis in human cells.	NAD	202-208	CD38 molecule	Homo sapiens	113-117
23767918-1	2013	Sirt3 (sirtuin 3) is an NAD-dependent deacetylase localized to mitochondria.	NAD	24-27	sirtuin 3	Mus musculus	0-5
1832811-14	1991	It was found that mitochondrial NAD-dependent aldehyde dehydrogenase, glucokinase, and CoASH were directly attacked and inactivated by the incorporated secondary products in the liver.	NAD	32-35	glucokinase	Homo sapiens	70-81
23767918-1	2013	Sirt3 (sirtuin 3) is an NAD-dependent deacetylase localized to mitochondria.	NAD	24-27	sirtuin 3	Mus musculus	7-16
16667858-1	1990	By probing total RNA blots with an NADH-dependent hydroxypyruvate reductase (HPR) cDNA clone, we have found that HPR transcript abundance is highly regulated in developing cucumber (Cucumis sativus) seedlings.	NAD	35-39	glycerate dehydrogenase	Cucumis sativus	77-80
16667858-1	1990	By probing total RNA blots with an NADH-dependent hydroxypyruvate reductase (HPR) cDNA clone, we have found that HPR transcript abundance is highly regulated in developing cucumber (Cucumis sativus) seedlings.	NAD	35-39	glycerate dehydrogenase	Cucumis sativus	113-116
23222413-4	2013	We investigated whether consumption of 2.0 g ginger daily regulated the level of two key enzymes that control prostaglandin E2 production, COX-1 and NAD(+)-dependent 15-hydroxyprostaglandin dehydrogenase (15-PGDH).	NAD	149-155	15-hydroxyprostaglandin dehydrogenase	Homo sapiens	205-212
2096889-3	1990	The binary complex formed between LDH and NADH was characterized by analytical affinity chromatography using both CPG/immobilized LDH and immobilized Cibacron Blue.	NAD	42-46	LDH	Bos taurus	34-37
2096889-3	1990	The binary complex formed between LDH and NADH was characterized by analytical affinity chromatography using both CPG/immobilized LDH and immobilized Cibacron Blue.	NAD	42-46	LDH	Bos taurus	130-133
2096889-4	1990	Since the dye competes with NADH in binding to the active site of LDH, competitive elution chromatography using the immobilized dye allows determination of the dissociation constant of the soluble LDH.NADH complex.	NAD	28-32	LDH	Bos taurus	66-69
2096889-4	1990	Since the dye competes with NADH in binding to the active site of LDH, competitive elution chromatography using the immobilized dye allows determination of the dissociation constant of the soluble LDH.NADH complex.	NAD	28-32	LDH	Bos taurus	197-200
2096889-4	1990	Since the dye competes with NADH in binding to the active site of LDH, competitive elution chromatography using the immobilized dye allows determination of the dissociation constant of the soluble LDH.NADH complex.	NAD	201-205	LDH	Bos taurus	66-69
2096889-4	1990	Since the dye competes with NADH in binding to the active site of LDH, competitive elution chromatography using the immobilized dye allows determination of the dissociation constant of the soluble LDH.NADH complex.	NAD	201-205	LDH	Bos taurus	197-200
2096889-5	1990	Agreement between the dissociation constants determined by direct chromatography of NADH on immobilized LDH (KD = 1.4 microM) and that determined for the soluble complex (KD = 2.4 microM) indicates that immobilization of LDH did not affect the interaction.	NAD	84-88	LDH	Bos taurus	104-107
23764826-6	2013	The calculated redox tuning of Co(I)H interactions on the reduction potential of Co(II)/Co(I) couple (60-800 mV vs standard hydrogen electrode (SHE)), irrespective of the beta-axial ligand considered, is significantly higher than the biological redox gap between the reduction potential of Co(II)/Co(I) couple and that of the biological reducing agents (50 mV vs SHE).	NAD	31-36	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	88-93
2223838-1	1990	Salicylate hydroxylase from Pseudomonas putida (EC 1.14.13.1, salicylate, NADH:oxygen oxidoreductase) is an FAD-containing monooxygenase, which catalyzes decarboxylative hydroxylation of salicylate to produce catechol in the presence of NADH and O2.	NAD	74-78	salicylate hydroxylase	Pseudomonas putida	0-22
23764826-6	2013	The calculated redox tuning of Co(I)H interactions on the reduction potential of Co(II)/Co(I) couple (60-800 mV vs standard hydrogen electrode (SHE)), irrespective of the beta-axial ligand considered, is significantly higher than the biological redox gap between the reduction potential of Co(II)/Co(I) couple and that of the biological reducing agents (50 mV vs SHE).	NAD	31-36	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	88-93
23798679-5	2013	There is also evidence that metabolites such as NAD(+) (acting via deacetylases such as SIRT1 and SIRT2) and succinate (which regulates hypoxia-inducible factor 1alpha) are signals that regulate innate immunity.	NAD	48-54	sirtuin 2	Homo sapiens	98-103
23708132-10	2013	A sad deletion mutant accumulated DHOPDCA, and expression in Escherichia coli revealed that sad encodes an aldehyde dehydrogenase for oxidizing DHOPDCA to the corresponding acid 7alpha,12alpha-dihydroxy-3-oxopregna-1,4-diene-20-carboxylate (DHOPDC) with NAD(+) as the electron acceptor.	NAD	254-260	Aldehyde dehydrogenase	Escherichia coli	107-129
2393709-0	1990	Impaired erythrocyte methemoglobin reduction in sickle cell disease: dependence of methemoglobin reduction on reduced nicotinamide adenine dinucleotide content.	NAD	118-151	hemoglobin subunit gamma 2	Homo sapiens	83-96
2143421-6	1990	Poly(ADP-ribose)polymerase (poly-ADPRP) was assayed by the DNAse-I-induced incorporation of [14C]NAD in nuclei of permeabilized L1210 cells.	NAD	97-100	poly (ADP-ribose) polymerase family, member 1	Mus musculus	0-26
23852118-2	2013	We sought to characterize the roles of the NAD(+)-dependent deacetylase SIRT1 in the neuronal response to DNA double-strand breaks (DSBs).	NAD	43-49	sirtuin 1	Mus musculus	72-77
2143421-6	1990	Poly(ADP-ribose)polymerase (poly-ADPRP) was assayed by the DNAse-I-induced incorporation of [14C]NAD in nuclei of permeabilized L1210 cells.	NAD	97-100	poly (ADP-ribose) polymerase family, member 1	Mus musculus	28-38
2143421-6	1990	Poly(ADP-ribose)polymerase (poly-ADPRP) was assayed by the DNAse-I-induced incorporation of [14C]NAD in nuclei of permeabilized L1210 cells.	NAD	97-100	deoxyribonuclease I	Mus musculus	59-66
2171815-3	1990	The N/T value measuring system, which is adaptable for autoanalysis and allows simultaneous determination of activities depending on NAD and thionicotinamide adenine dinucleotide (thio-NAD), yields both the total activity of MDH and the N/T value which was correlated significantly with MDHm/MDH (r = 0.748).	NAD	133-136	malic enzyme 1	Homo sapiens	225-228
23894440-10	2013	Remarkably, treating RC mutant fibroblasts with nicotinic acid to enhance sirtuin and PPAR activity also normalized mTORC1 and AMPK signaling, restored NADH/NAD(+) redox balance, and improved cellular respiratory capacity.	NAD	152-156	peroxisome proliferator activated receptor alpha	Homo sapiens	86-90
23894440-10	2013	Remarkably, treating RC mutant fibroblasts with nicotinic acid to enhance sirtuin and PPAR activity also normalized mTORC1 and AMPK signaling, restored NADH/NAD(+) redox balance, and improved cellular respiratory capacity.	NAD	157-163	peroxisome proliferator activated receptor alpha	Homo sapiens	86-90
23876775-5	2013	Recent studies have shown that sirtuin 1 (Sirt1), a nicotinamide adenine dinucleotide (NAD)-dependent histone deacetylase, is a critical negative regulator of both the innate and adaptive immune response in mice, and its altered functions are likely to be involved in autoimmune diseases.	NAD	52-85	sirtuin 1	Mus musculus	31-40
2115121-4	1990	Disruption of the chromosomal copy of KGD2 in a respiratory-competent haploid yeast strain elicited a growth phenotype similar to that of G104 mutants and abolished the ability to mitochondria to catalyze the reduction of NAD+ by alpha-ketoglutarate.	NAD	222-226	alpha-ketoglutarate dehydrogenase KGD2	Saccharomyces cerevisiae S288C	38-42
23876775-5	2013	Recent studies have shown that sirtuin 1 (Sirt1), a nicotinamide adenine dinucleotide (NAD)-dependent histone deacetylase, is a critical negative regulator of both the innate and adaptive immune response in mice, and its altered functions are likely to be involved in autoimmune diseases.	NAD	52-85	sirtuin 1	Mus musculus	42-47
1976062-10	1990	Increasing the ratio of NADH to NADPH in incubations containing lung microsomes and (S)-nicotine decreased the yield of the iminium ion, confirming the inhibitory effect of cytochrome b5 on the P-450 2-catalyzed alpha-carbon oxidation reaction.	NAD	24-28	cytochrome b5	Oryctolagus cuniculus	173-186
23744286-12	2013	Thus, it was concluded that the overexpression of GRE2 together with ADH1 restores glycolaldehyde tolerance by augmenting the NADPH-dependent reduction pathway in addition to NADH-dependent reduction pathway.	NAD	175-179	methylglyoxal reductase (NADPH-dependent) GRE2	Saccharomyces cerevisiae S288C	50-54
2365066-0	1990	Effect of NAD coenzyme on the inactivation of glyceraldehyde-3-phosphate dehydrogenase by anionic phospholipids.	NAD	10-13	LOC786101	Bos taurus	46-86
23766555-0	2013	Electron Paramagnetic Resonance and Electron Spin Echo Studies of Co2+ Coordination by Nicotinamide Adenine Dinucleotide (NAD+) in Water Solution.	NAD	87-120	complement C2	Homo sapiens	66-69
2350175-1	1990	A polyclonal antibody was produced in guinea pig against the lung NAD(+)-dependent 15-hydroxyprostaglandin dehydrogenase (PGDH) purified from pregnant rabbits.	NAD	66-72	15-hydroxyprostaglandin dehydrogenase [NAD(+)]	Cavia porcellus	122-126
23766555-0	2013	Electron Paramagnetic Resonance and Electron Spin Echo Studies of Co2+ Coordination by Nicotinamide Adenine Dinucleotide (NAD+) in Water Solution.	NAD	122-126	complement C2	Homo sapiens	66-69
23766555-1	2013	Co2+ binding to the nicotinamide adenine dinucleotide (NAD+) molecule in water solution was studied by electron paramagnetic resonance (EPR) and electron spin echo at low temperatures.	NAD	20-53	complement C2	Homo sapiens	0-3
23766555-1	2013	Co2+ binding to the nicotinamide adenine dinucleotide (NAD+) molecule in water solution was studied by electron paramagnetic resonance (EPR) and electron spin echo at low temperatures.	NAD	55-59	complement C2	Homo sapiens	0-3
23766555-6	2013	Thus, Co2+ ion is coordinated in pseudo-tetrahedral geometry by four nitrogen atoms of adenine rings of two NAD+ molecules.	NAD	108-112	complement C2	Homo sapiens	6-9
2161619-1	1990	Many of the toxic metabolic actions of ethanol on the liver have been ascribed to the enhanced cellular production of NADH, which arises as a consequence of the oxidation of ethanol by alcohol dehydrogenase (ADH).	NAD	118-122	aldo-keto reductase family 1 member A1	Homo sapiens	185-206
2161619-2	1990	Experiments were conducted to evaluate whether NADH generated from a reconstituted system containing ethanol plus NAD+ plus ADH could interact with ferric chelates to promote microsomal lipid peroxidation and generation of a hydroxyl radical (OH)-like species.	NAD	114-118	aldo-keto reductase family 1 member A1	Homo sapiens	48-51
23673559-1	2013	Sirtuin 5 (SIRT5) is a nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase, belonging to the silent information regulator 2 (Sir2) family of sirtuin histone deacetylases (sirtuins).	NAD	23-56	sirtuin 1	Mus musculus	104-134
23673559-1	2013	Sirtuin 5 (SIRT5) is a nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase, belonging to the silent information regulator 2 (Sir2) family of sirtuin histone deacetylases (sirtuins).	NAD	23-56	sirtuin 1	Mus musculus	136-140
23778143-2	2013	Here, we used Pkd1 mutant mouse models to demonstrate that the nicotinamide adenine dinucleotide-dependent (NAD-dependent) protein deacetylase sirtuin 1 (SIRT1) is involved in the pathophysiology of ADPKD.	NAD	63-96	polycystin 1, transient receptor potential channel interacting	Mus musculus	14-18
2345545-2	1990	The NADH reduced cytochrome b5 (cyt b5)4 spectrum of these cells was similar to rat liver cyt b5.	NAD	4-8	cytochrome b5 type A	Rattus norvegicus	17-30
2345545-2	1990	The NADH reduced cytochrome b5 (cyt b5)4 spectrum of these cells was similar to rat liver cyt b5.	NAD	4-8	cytochrome b5 type A	Rattus norvegicus	32-38
2337593-0	1990	Purification and structural characterization of placental NAD(+)-linked 15-hydroxyprostaglandin dehydrogenase.	NAD	58-64	carbonyl reductase 1	Homo sapiens	72-109
23778143-2	2013	Here, we used Pkd1 mutant mouse models to demonstrate that the nicotinamide adenine dinucleotide-dependent (NAD-dependent) protein deacetylase sirtuin 1 (SIRT1) is involved in the pathophysiology of ADPKD.	NAD	63-96	sirtuin 1	Mus musculus	143-152
2337593-2	1990	Human placental NAD(+)-linked 15-hydroxyprostaglandin dehydrogenase was purified to homogeneity according to a five-step method, with chromatography on DEAE-Sepharose, Blue Sepharose, and Mono-Q FPLC as principal steps.	NAD	16-22	carbonyl reductase 1	Homo sapiens	30-67
23778143-2	2013	Here, we used Pkd1 mutant mouse models to demonstrate that the nicotinamide adenine dinucleotide-dependent (NAD-dependent) protein deacetylase sirtuin 1 (SIRT1) is involved in the pathophysiology of ADPKD.	NAD	63-96	sirtuin 1	Mus musculus	154-159
23778143-2	2013	Here, we used Pkd1 mutant mouse models to demonstrate that the nicotinamide adenine dinucleotide-dependent (NAD-dependent) protein deacetylase sirtuin 1 (SIRT1) is involved in the pathophysiology of ADPKD.	NAD	108-111	polycystin 1, transient receptor potential channel interacting	Mus musculus	14-18
23778143-2	2013	Here, we used Pkd1 mutant mouse models to demonstrate that the nicotinamide adenine dinucleotide-dependent (NAD-dependent) protein deacetylase sirtuin 1 (SIRT1) is involved in the pathophysiology of ADPKD.	NAD	108-111	sirtuin 1	Mus musculus	143-152
1690278-3	1990	The activity of the enzyme marker system, glucose-6-phosphate dehydrogenase covalently conjugated to desipramine, is monitored by colorimetric detection of the rate of NADH formation at 340 nM.	NAD	168-172	glucose-6-phosphate dehydrogenase	Homo sapiens	42-75
23778143-2	2013	Here, we used Pkd1 mutant mouse models to demonstrate that the nicotinamide adenine dinucleotide-dependent (NAD-dependent) protein deacetylase sirtuin 1 (SIRT1) is involved in the pathophysiology of ADPKD.	NAD	108-111	sirtuin 1	Mus musculus	154-159
23567315-1	2013	The microsomal NADH-dependent electron transport system consisting of cytochrome b5 reductase and cytochrome b5 participates in a number of physiologically important processes including lipid metabolism as well as is involved in the metabolism of various drug and xenobiotics.	NAD	15-19	cytochrome b5 type A	Homo sapiens	70-83
26389889-1	2015	Nicotinamide phosphoribosyltransferase (NAMPT) has crucial roles for myocardial development, cardiomyocyte energy metabolism and cell death/survival by regulating NAD+-dependent sirtuin-1 (SIRT1) deacetylase.	NAD	163-167	sirtuin 1	Homo sapiens	178-187
26389889-1	2015	Nicotinamide phosphoribosyltransferase (NAMPT) has crucial roles for myocardial development, cardiomyocyte energy metabolism and cell death/survival by regulating NAD+-dependent sirtuin-1 (SIRT1) deacetylase.	NAD	163-167	sirtuin 1	Homo sapiens	189-194
23567315-1	2013	The microsomal NADH-dependent electron transport system consisting of cytochrome b5 reductase and cytochrome b5 participates in a number of physiologically important processes including lipid metabolism as well as is involved in the metabolism of various drug and xenobiotics.	NAD	15-19	cytochrome b5 type A	Homo sapiens	98-111
34843934-10	2022	Moreover, compared with M3 and M5 groups, the higher NAD+/NADH ratio in the liver of M1 group activated SIRT1, which stimulated the AMPK signaling associated pathways by up-regulating the LKB1 gene.	NAD	53-57	sirtuin 1	Sus scrofa	104-109
23734017-5	2013	These enzyme activities can be determined by incubating the substrates NAD or cADPR with either crude membranes, purified proteins, or intact cells expressing CD38; the latter is possible because the catalytic site of CD38 is on the cell surface.	NAD	71-74	CD38 molecule	Homo sapiens	159-163
34843934-10	2022	Moreover, compared with M3 and M5 groups, the higher NAD+/NADH ratio in the liver of M1 group activated SIRT1, which stimulated the AMPK signaling associated pathways by up-regulating the LKB1 gene.	NAD	58-62	sirtuin 1	Sus scrofa	104-109
23734017-5	2013	These enzyme activities can be determined by incubating the substrates NAD or cADPR with either crude membranes, purified proteins, or intact cells expressing CD38; the latter is possible because the catalytic site of CD38 is on the cell surface.	NAD	71-74	CD38 molecule	Homo sapiens	218-222
23312803-1	2013	Nicotinamide adenine dinucleotide (NAD)(+), a coenzyme involved in redox activities in the mitochondrial electron transport chain, has been identified as a key regulator of the lifespan-extending effects, and the activation of NAD(+) expression has been linked with a decrease in beta-amyloid (Abeta) toxicity in Alzheimer"s disease (AD).	NAD	0-33	amyloid beta (A4) precursor protein	Mus musculus	294-299
23312803-1	2013	Nicotinamide adenine dinucleotide (NAD)(+), a coenzyme involved in redox activities in the mitochondrial electron transport chain, has been identified as a key regulator of the lifespan-extending effects, and the activation of NAD(+) expression has been linked with a decrease in beta-amyloid (Abeta) toxicity in Alzheimer"s disease (AD).	NAD	35-39	amyloid beta (A4) precursor protein	Mus musculus	294-299
23312803-1	2013	Nicotinamide adenine dinucleotide (NAD)(+), a coenzyme involved in redox activities in the mitochondrial electron transport chain, has been identified as a key regulator of the lifespan-extending effects, and the activation of NAD(+) expression has been linked with a decrease in beta-amyloid (Abeta) toxicity in Alzheimer"s disease (AD).	NAD	227-233	amyloid beta (A4) precursor protein	Mus musculus	294-299
23798621-7	2013	DACH1 binding to p53 was inhibited by NAD-dependent deacetylation via DACH1 K628.	NAD	38-41	dachshund family transcription factor 1	Homo sapiens	0-5
23798621-7	2013	DACH1 binding to p53 was inhibited by NAD-dependent deacetylation via DACH1 K628.	NAD	38-41	dachshund family transcription factor 1	Homo sapiens	70-75
23798621-9	2013	DACH1 inhibits breast cancer cellular growth in an NAD and p53-dependent manner through direct protein-protein association.	NAD	51-54	dachshund family transcription factor 1	Homo sapiens	0-5
23335597-4	2013	Unexpectedly, overexpression of other genes in the salvage pathway for NAD(+) biosynthesis, including QNS1, NPT1 and PNC1 also protected against proteotoxicity.	NAD	71-77	nicotinate phosphoribosyltransferase	Saccharomyces cerevisiae S288C	108-112
23547115-2	2013	This suggested that activators of SIRT1, a highly conserved NAD-dependent protein deacetylase, might have immune-modulating or neuroprotective therapeutic effects in EAE.	NAD	60-63	sirtuin 1	Mus musculus	34-39
23547115-7	2013	Significant neuroprotective effects were observed, with fewer apoptotic cells found in the spinal cords of SIRT1-overexpressing EAE mice associated with increased brain-derived neurotrophic factor and NAD levels.	NAD	201-204	sirtuin 1	Mus musculus	107-112
23502856-4	2013	Inducers of the NLRP3 inflammasome caused aberrant mitochondrial homeostasis to diminish the concentration of the coenzyme NAD(+), which in turn inactivated the NAD(+)-dependent alpha-tubulin deacetylase sirtuin 2; this resulted in the accumulation of acetylated alpha-tubulin.	NAD	123-129	sirtuin 2	Homo sapiens	204-213
23502856-4	2013	Inducers of the NLRP3 inflammasome caused aberrant mitochondrial homeostasis to diminish the concentration of the coenzyme NAD(+), which in turn inactivated the NAD(+)-dependent alpha-tubulin deacetylase sirtuin 2; this resulted in the accumulation of acetylated alpha-tubulin.	NAD	161-167	sirtuin 2	Homo sapiens	204-213
23646183-6	2013	The activation of these clock genes in vitro was not observed when we used mutated dCtBP which carries amino acid substitutions in NAD+ domain.	NAD	131-135	C-terminal Binding Protein	Drosophila melanogaster	83-88
23457303-1	2013	Sirt1 is a NAD(+)-dependent class III deacetylase that functions as a cellular energy sensor.	NAD	11-17	sirtuin 1	Mus musculus	0-5
23271118-9	2013	Diphteria toxin is the part which has the FA enzymatic activity corresponding the N-terminal section of the toxin, which inhibits the protein synthesis by ADP-ribosylating the elongation factor 2 in the presence of NAD.	NAD	215-218	eukaryotic translation elongation factor 2	Homo sapiens	176-195
23478437-1	2013	The NAD+-dependent deacetylases Sirt1 and Sirt2 mediate cellular stress responses and are highly expressed in vascular endothelial cells.	NAD	4-7	sirtuin 2	Homo sapiens	42-47
23616928-13	2013	Identification of MNADK immediately suggests a model in which NADK and MNADK are responsible for de novo synthesis of NADP(+) in cytosol and mitochondria, respectively, and therefore provides novel insights into understanding the sources and mechanisms of mitochondrial NADP(+) and NADH production in human cells.	NAD	282-286	NAD kinase	Homo sapiens	19-23
23295229-2	2013	Physiologic levels of Mg(2+) ions decrease ALDH1 activity in part by increasing NADH binding affinity to the enzyme.	NAD	80-84	aldehyde dehydrogenase 1 family member A1	Homo sapiens	43-48
23295229-4	2013	We used this technique to investigate the effects of Mg(2+) ions on the ALDH1A1-NADH binding characteristics and enzyme catalysis.	NAD	80-84	aldehyde dehydrogenase 1 family member A1	Homo sapiens	72-79
23295229-5	2013	From the resolved free and bound NADH fluorescence signatures, the KD values for both NADH conformations in ALDH1A1 ranged from about 24 muM to 1 muM for Mg(2+) ion concentrations of 0-6000 muM, respectively.	NAD	33-37	aldehyde dehydrogenase 1 family member A1	Homo sapiens	108-115
23295229-5	2013	From the resolved free and bound NADH fluorescence signatures, the KD values for both NADH conformations in ALDH1A1 ranged from about 24 muM to 1 muM for Mg(2+) ion concentrations of 0-6000 muM, respectively.	NAD	86-90	aldehyde dehydrogenase 1 family member A1	Homo sapiens	108-115
23295229-9	2013	This shift in conformational population at higher Mg(2+) ion concentrations and to lower enzyme activity may be due to longer residence time of the NADH in the ALDH1 pocket.	NAD	148-152	aldehyde dehydrogenase 1 family member A1	Homo sapiens	160-165
23295229-10	2013	The results from monitoring enzyme catalysis in the absence of magnesium suggests that the ALDH1-NADH complex with the shorter fluorescence lifetime is the form initially produced, and the complex with the longer fluorescence lifetime is produced through isomerization.	NAD	97-101	aldehyde dehydrogenase 1 family member A1	Homo sapiens	91-96
23235157-2	2013	A novel metabolic analysis that measures the real-time oxidation state of NAD(H) and the hemes of the electron transport chain and oxygen consumption within intact, living cells found that structurally distinct MEK1/2 inhibitors had an immediate, dose-dependent effect on mitochondrial metabolism.	NAD	74-80	mitogen-activated protein kinase kinase 1	Homo sapiens	211-217
23146569-2	2013	Resveratrol has been reported to be an activator of NAD+-dependent deacetylase sirtuin 1 (SIRT1), which may regulate liver X receptor (LXR) activity, thereby upregulating the expression of genes crucial in reverse cholesterol transport (RCT).	NAD	52-55	sirtuin 1	Mus musculus	90-95
23832361-2	2013	We investigated in this study the effect of phytol, a phytochemical known as a peroxisome proliferator-activated receptor alpha (PPARalpha) ligand, on NAD synthesis and ACMSD expression in rats.	NAD	151-154	peroxisome proliferator activated receptor alpha	Rattus norvegicus	129-138
23055259-4	2013	Using yeast two-hybrid screening assays, we found that beta- but not alpha-hOGG1 directly interacts with the mitochondrial protein NADH:ubiquinone oxidoreductase 1 beta subcomplex 10 (NDUFB10), an integral factor in Complex 1 on the mitochondrial inner membrane.	NAD	131-135	8-oxoguanine DNA glycosylase	Homo sapiens	75-80
23042952-2	2013	RSV targets and activates the NAD(+)-dependent protein deacetylase SIRT1; in turn, SIRT1 induces an intracellular antioxidative mechanism by inducing mitochondrial superoxide dismutase (SOD2).	NAD	30-36	sirtuin 1	Mus musculus	67-72
23042952-2	2013	RSV targets and activates the NAD(+)-dependent protein deacetylase SIRT1; in turn, SIRT1 induces an intracellular antioxidative mechanism by inducing mitochondrial superoxide dismutase (SOD2).	NAD	30-36	sirtuin 1	Mus musculus	83-88
23460888-0	2013	Inhibition of the NAD-dependent protein deacetylase SIRT2 induces granulocytic differentiation in human leukemia cells.	NAD	18-21	sirtuin 2	Homo sapiens	52-57
23409188-1	2013	BACKGROUND: Epidemiological studies have evaluated the association between nicotinamide adenine dinucleotide phosphate (NADPH) oxidase p22(phox) C242T polymorphism and risk of ischemic cerebrovascular disease (ICVD), but the results remain inconclusive.	NAD	75-108	calcineurin like EF-hand protein 1	Homo sapiens	135-138
34523242-11	2022	CONCLUSIONS: Imeglimin may activate TRPM2 channels in beta-cells via the production of NAD+ /cADPR, leading to the potentiation of GSIS.	NAD	87-91	transient receptor potential cation channel, subfamily M, member 2	Mus musculus	36-41
34322899-5	2021	Activity of SIRT1 was regulated by presence of NAD+ in CCA cells.	NAD	47-51	sirtuin 1	Homo sapiens	12-17
34322899-6	2021	Inhibition of NAD+ producing enzyme Nicotinamide phosphoribosyl transferase (NAMPT) increased ciliary length and frequency in CCA cells and in SIRT1 overexpressed H69 cells.	NAD	14-18	sirtuin 1	Homo sapiens	143-148
23064253-3	2012	An extensive analysis of these mutants showed that the NAD(+)(H)/NADP(+)(H)-dependent cytosolic alcohol (ADH) and aldehyde (ALD) dehydrogenase balance affects the expression of the G6PDH activity pattern.	NAD	55-64	glucose-6-phosphate dehydrogenase	Saccharomyces cerevisiae S288C	181-186
34826187-1	2022	Sirtuin 1 (SIRT1), an NAD+ -dependent histone/protein deacetylase, has multifaceted functions in various biological events such as inflammation, aging and energy metabolism.	NAD	22-25	sirtuin 1	Homo sapiens	0-9
34826187-1	2022	Sirtuin 1 (SIRT1), an NAD+ -dependent histone/protein deacetylase, has multifaceted functions in various biological events such as inflammation, aging and energy metabolism.	NAD	22-25	sirtuin 1	Homo sapiens	11-16
22992735-6	2012	Substitution of catalytic residues shows that the mART function is responsible for the toxicity, and it binds NAD(+) with high affinity (K(D) = 52.3 +- 12.2 muM).	NAD	110-116	ADP-ribosyltransferase 2b	Mus musculus	50-54
34808628-1	2022	SIRT1 (silent information regulator 1), a NAD+-dependent III class histone deacetylase, plays crucial roles in cell proliferation, apoptosis, senescence, metabolism, and stress responses.	NAD	42-45	sirtuin 1	Homo sapiens	0-5
34873458-5	2021	Sirtuin1 (SIRT1) is a type of the Class III histone deacetylase family that is distinctively dependent on nicotinamide adenine dinucleotide (NAD+) for catalysis reaction.	NAD	106-139	sirtuin 1	Homo sapiens	0-8
23137106-7	2012	Moreover, in vitro treatment with telmisartan led to increased expression of Sirt1 mRNA in C2C12 skeletal muscle cells; the increase in Sirt1 mRNA in telmisartan-treated C2C12 myoblasts occurred concomitantly with an increase in AMPK phosphorylation, an increase in NAD+/NADH ratio, and increases in the mRNA levels of PGC1alpha, FATP1, ACO, and GLUT4.	NAD	266-270	sirtuin 1	Mus musculus	136-141
34873458-5	2021	Sirtuin1 (SIRT1) is a type of the Class III histone deacetylase family that is distinctively dependent on nicotinamide adenine dinucleotide (NAD+) for catalysis reaction.	NAD	106-139	sirtuin 1	Homo sapiens	10-15
34873458-5	2021	Sirtuin1 (SIRT1) is a type of the Class III histone deacetylase family that is distinctively dependent on nicotinamide adenine dinucleotide (NAD+) for catalysis reaction.	NAD	141-145	sirtuin 1	Homo sapiens	0-8
23137106-7	2012	Moreover, in vitro treatment with telmisartan led to increased expression of Sirt1 mRNA in C2C12 skeletal muscle cells; the increase in Sirt1 mRNA in telmisartan-treated C2C12 myoblasts occurred concomitantly with an increase in AMPK phosphorylation, an increase in NAD+/NADH ratio, and increases in the mRNA levels of PGC1alpha, FATP1, ACO, and GLUT4.	NAD	271-275	sirtuin 1	Mus musculus	136-141
34873458-5	2021	Sirtuin1 (SIRT1) is a type of the Class III histone deacetylase family that is distinctively dependent on nicotinamide adenine dinucleotide (NAD+) for catalysis reaction.	NAD	141-145	sirtuin 1	Homo sapiens	10-15
23107895-1	2012	Renalase is a novel flavoprotein, highly expressed in kidney and heart, which metabolizes catecholamines and catecholamine-like substances via a superoxide (O2(-))-dependent mechanism using nicotinamide adenine dinucleotide (NADH) as a cofactor.	NAD	190-223	renalase, FAD dependent amine oxidase	Homo sapiens	0-8
34750509-3	2021	In order to assess whether other genes implicated in NAD+ metabolism were synthetic lethal with BRCA1 or BRCA2 gene defects, we carried out a genetic screen, which identified a synthetic lethality between BRCA1 and genetic inhibition of either of two sirtuin (SIRT) enzymes, SIRT1 or SIRT6.	NAD	53-57	BRCA2 DNA repair associated	Homo sapiens	105-110
34750509-3	2021	In order to assess whether other genes implicated in NAD+ metabolism were synthetic lethal with BRCA1 or BRCA2 gene defects, we carried out a genetic screen, which identified a synthetic lethality between BRCA1 and genetic inhibition of either of two sirtuin (SIRT) enzymes, SIRT1 or SIRT6.	NAD	53-57	BRCA1 DNA repair associated	Homo sapiens	205-210
34750509-3	2021	In order to assess whether other genes implicated in NAD+ metabolism were synthetic lethal with BRCA1 or BRCA2 gene defects, we carried out a genetic screen, which identified a synthetic lethality between BRCA1 and genetic inhibition of either of two sirtuin (SIRT) enzymes, SIRT1 or SIRT6.	NAD	53-57	sirtuin 1	Homo sapiens	275-280
34750622-1	2022	Mutations in NMNAT1, a key enzyme involved in the synthesis of NAD+ in the nucleus, lead to an early onset severe inherited retinal degeneration (IRD).	NAD	63-67	nicotinamide nucleotide adenylyltransferase 1	Mus musculus	13-19
34750622-2	2022	We aimed to understand the role of nuclear NAD+ in the retina and to identify the molecular mechanisms underlying NMNAT1-associated disease, using a mouse model that harbors the p.V9M mutation in Nmnat1 (Nmnat1V9M/V9M).	NAD	43-47	nicotinamide nucleotide adenylyltransferase 1	Mus musculus	196-202
23107895-1	2012	Renalase is a novel flavoprotein, highly expressed in kidney and heart, which metabolizes catecholamines and catecholamine-like substances via a superoxide (O2(-))-dependent mechanism using nicotinamide adenine dinucleotide (NADH) as a cofactor.	NAD	225-229	renalase, FAD dependent amine oxidase	Homo sapiens	0-8
22818888-3	2012	The SlscADH1 recombinant protein produced in Escherichia coli exhibited dehydrogenase-reductase activity towards several volatile compounds present in tomato flavour with a strong preference for the NAD/NADH co-factors.	NAD	199-202	short-chain dehydrogenase-reductase	Solanum lycopersicum	4-12
34750622-2	2022	We aimed to understand the role of nuclear NAD+ in the retina and to identify the molecular mechanisms underlying NMNAT1-associated disease, using a mouse model that harbors the p.V9M mutation in Nmnat1 (Nmnat1V9M/V9M).	NAD	43-47	nicotinamide nucleotide adenylyltransferase 1	Mus musculus	204-217
34750622-4	2022	Expression of the primary consumer of NAD+ in the nucleus, PARP1, an enzyme involved in DNA damage repair and transcriptional regulation, as well as 7 other PARP family enzymes, was elevated in the retinas of Nmnat1V9M/V9M.	NAD	38-42	poly (ADP-ribose) polymerase family, member 1	Mus musculus	59-64
34750622-4	2022	Expression of the primary consumer of NAD+ in the nucleus, PARP1, an enzyme involved in DNA damage repair and transcriptional regulation, as well as 7 other PARP family enzymes, was elevated in the retinas of Nmnat1V9M/V9M.	NAD	38-42	poly (ADP-ribose) polymerase family, member 1	Mus musculus	157-161
22818888-3	2012	The SlscADH1 recombinant protein produced in Escherichia coli exhibited dehydrogenase-reductase activity towards several volatile compounds present in tomato flavour with a strong preference for the NAD/NADH co-factors.	NAD	203-207	short-chain dehydrogenase-reductase	Solanum lycopersicum	4-12
34750622-4	2022	Expression of the primary consumer of NAD+ in the nucleus, PARP1, an enzyme involved in DNA damage repair and transcriptional regulation, as well as 7 other PARP family enzymes, was elevated in the retinas of Nmnat1V9M/V9M.	NAD	38-42	nicotinamide nucleotide adenylyltransferase 1	Mus musculus	209-222
22971926-2	2012	Cytosolic malate dehydrogenase (MDH1) catalyzes the reversible reduction of oxaloacetate to malate at the expense of reduced nicotinamide adenine dinucleotide (NADH).	NAD	125-158	malate dehydrogenase 1	Homo sapiens	0-30
34750622-5	2022	This was associated with elevated levels of DNA damage, PARP-mediated NAD+ consumption, and migration of Iba1+/CD45+ microglia/macrophages to the subretinal space in the retinas of Nmnat1V9M/V9M mice.	NAD	70-74	poly (ADP-ribose) polymerase family, member 1	Mus musculus	56-60
34750622-5	2022	This was associated with elevated levels of DNA damage, PARP-mediated NAD+ consumption, and migration of Iba1+/CD45+ microglia/macrophages to the subretinal space in the retinas of Nmnat1V9M/V9M mice.	NAD	70-74	nicotinamide nucleotide adenylyltransferase 1	Mus musculus	181-194
22971926-2	2012	Cytosolic malate dehydrogenase (MDH1) catalyzes the reversible reduction of oxaloacetate to malate at the expense of reduced nicotinamide adenine dinucleotide (NADH).	NAD	125-158	malate dehydrogenase 1	Homo sapiens	32-36
34831209-4	2021	We demonstrate that impairment of DNMT1 enzymatic activity by NAD-promoted ADP-ribosylation leads to demethylation and transcriptional activation of the CEBPA gene, suggesting the existence of an unknown NAD-controlled region within the locus.	NAD	62-65	DNA methyltransferase 1	Homo sapiens	34-39
22971926-2	2012	Cytosolic malate dehydrogenase (MDH1) catalyzes the reversible reduction of oxaloacetate to malate at the expense of reduced nicotinamide adenine dinucleotide (NADH).	NAD	160-164	malate dehydrogenase 1	Homo sapiens	0-30
34831209-4	2021	We demonstrate that impairment of DNMT1 enzymatic activity by NAD-promoted ADP-ribosylation leads to demethylation and transcriptional activation of the CEBPA gene, suggesting the existence of an unknown NAD-controlled region within the locus.	NAD	204-207	DNA methyltransferase 1	Homo sapiens	34-39
22971926-2	2012	Cytosolic malate dehydrogenase (MDH1) catalyzes the reversible reduction of oxaloacetate to malate at the expense of reduced nicotinamide adenine dinucleotide (NADH).	NAD	160-164	malate dehydrogenase 1	Homo sapiens	32-36
22700872-3	2012	We also show that either DPN or Tam treatment increases QR levels and results in a decrease in ductal hyperplasia, proliferation, oxidative DNA damage (ODD), and an increase in apoptosis.	NAD	25-28	crystallin, zeta	Mus musculus	56-58
22700872-5	2012	Overall, we provide evidence that up-regulation of QR through induction by Tam or DPN can inhibit estrogen-induced ODD and mammary cell tumorigenesis, representing a novel mechanism of prevention against breast cancer.	NAD	82-85	crystallin, zeta	Mus musculus	51-53
34373353-9	2021	Subsequently, molecular modelling was used to demonstrate that CC-292 can be docked into both the NAD and retinal binding pockets of the analogous human ALDH1A2 enzyme.	NAD	98-101	aldehyde dehydrogenase 1 family member A2	Homo sapiens	153-160
22735644-1	2012	Human DBC1 (deleted in breast cancer-1; KIAA1967) is a nuclear protein that, in response to DNA damage, competitively inhibits the NAD(+)-dependent deacetylase SIRT1, a regulator of p53 apoptotic functions in response to genotoxic stress.	NAD	131-137	cell cycle and apoptosis regulator 2	Homo sapiens	6-10
34603081-14	2021	In conclusion, NAD+ biosynthesis was significantly impaired in CKD, which may attribute to downregulation of QPRT and NMNAT 1/3.	NAD	15-19	nicotinamide nucleotide adenylyltransferase 1	Rattus norvegicus	118-127
22700429-7	2012	Knockdown of different VDAC isoforms, especially of the least abundant isoform, VDAC3, also decreases DeltaPsi(m), cellular ATP, and NADH/NAD+, suggesting that VDAC1 and VDAC2 are most inhibited by free tubulin.	NAD	133-137	voltage dependent anion channel 3	Homo sapiens	80-85
34116043-2	2021	Silence information regulator 1 (SIRT1) is a member of the third class of nicotinamide adenine dinucleotide (NAD+)-dependent sirtuins.	NAD	74-107	sirtuin 1	Homo sapiens	0-31
34116043-2	2021	Silence information regulator 1 (SIRT1) is a member of the third class of nicotinamide adenine dinucleotide (NAD+)-dependent sirtuins.	NAD	74-107	sirtuin 1	Homo sapiens	33-38
22700429-7	2012	Knockdown of different VDAC isoforms, especially of the least abundant isoform, VDAC3, also decreases DeltaPsi(m), cellular ATP, and NADH/NAD+, suggesting that VDAC1 and VDAC2 are most inhibited by free tubulin.	NAD	138-142	voltage dependent anion channel 3	Homo sapiens	80-85
34116043-2	2021	Silence information regulator 1 (SIRT1) is a member of the third class of nicotinamide adenine dinucleotide (NAD+)-dependent sirtuins.	NAD	109-113	sirtuin 1	Homo sapiens	0-31
34116043-2	2021	Silence information regulator 1 (SIRT1) is a member of the third class of nicotinamide adenine dinucleotide (NAD+)-dependent sirtuins.	NAD	109-113	sirtuin 1	Homo sapiens	33-38
34314389-5	2021	Furthermore, LSD1 regulates gene expression and protein methylation of nicotinamide mononucleotide adenylyltransferase 1 (NMNAT1), which controls the final step of NAD+ synthesis and limits NAD+ availability in nucleus.	NAD	164-168	nicotinamide nucleotide adenylyltransferase 1	Mus musculus	71-120
34314389-5	2021	Furthermore, LSD1 regulates gene expression and protein methylation of nicotinamide mononucleotide adenylyltransferase 1 (NMNAT1), which controls the final step of NAD+ synthesis and limits NAD+ availability in nucleus.	NAD	164-168	nicotinamide nucleotide adenylyltransferase 1	Mus musculus	122-128
34314389-5	2021	Furthermore, LSD1 regulates gene expression and protein methylation of nicotinamide mononucleotide adenylyltransferase 1 (NMNAT1), which controls the final step of NAD+ synthesis and limits NAD+ availability in nucleus.	NAD	190-194	nicotinamide nucleotide adenylyltransferase 1	Mus musculus	71-120
34314389-5	2021	Furthermore, LSD1 regulates gene expression and protein methylation of nicotinamide mononucleotide adenylyltransferase 1 (NMNAT1), which controls the final step of NAD+ synthesis and limits NAD+ availability in nucleus.	NAD	190-194	nicotinamide nucleotide adenylyltransferase 1	Mus musculus	122-128
34314389-6	2021	Lsd1 knockout reduces NAD+-dependent SIRT1 and SIRT7 deacetylase activity, leading to hyperacetylation and hypofunctioning of GABPbeta and PGC-1alpha, the major transcriptional factor/cofactor for nuclear-encoded mitochondrial genes.	NAD	22-25	sirtuin 7	Mus musculus	47-52
34539634-1	2021	CD38 is the major NAD+-hydrolyzing ecto-enzyme in most mammals.	NAD	18-22	CD38 antigen	Mus musculus	0-4
34119539-1	2021	AIMS: Silent information regulator 1 (SIRT1) is a NAD+-dependent protein-modifying enzyme involved in regulating gene expression, DNA damage repair, cell metabolism, and mitochondrial functions.	NAD	50-53	sirtuin 1	Homo sapiens	6-36
34119539-1	2021	AIMS: Silent information regulator 1 (SIRT1) is a NAD+-dependent protein-modifying enzyme involved in regulating gene expression, DNA damage repair, cell metabolism, and mitochondrial functions.	NAD	50-53	sirtuin 1	Homo sapiens	38-43
34116746-4	2021	In this study, a stable and efficient NADH oxidase from Bacillus cereus (bcNOX) was found to be more compatible with mMDH to recycle NAD+ in E. coli cells for l-gulose biosynthesis.	NAD	133-137	malate dehydrogenase 2, NAD (mitochondrial)	Mus musculus	117-121
34130091-9	2021	Moreover, the NAMPT inhibitor abrogated the sirtuin-1 (SIRT1)-mediated deacetylation of p53 and significantly inhibited the proliferation of UVA/B-irradiated cells, suggesting that the NAMPT-NAD+-SIRT1 axis regulates p53 functions upon UVA/B stress.	NAD	191-195	sirtuin 1	Homo sapiens	44-53
34130091-9	2021	Moreover, the NAMPT inhibitor abrogated the sirtuin-1 (SIRT1)-mediated deacetylation of p53 and significantly inhibited the proliferation of UVA/B-irradiated cells, suggesting that the NAMPT-NAD+-SIRT1 axis regulates p53 functions upon UVA/B stress.	NAD	191-195	sirtuin 1	Homo sapiens	55-60
34130091-9	2021	Moreover, the NAMPT inhibitor abrogated the sirtuin-1 (SIRT1)-mediated deacetylation of p53 and significantly inhibited the proliferation of UVA/B-irradiated cells, suggesting that the NAMPT-NAD+-SIRT1 axis regulates p53 functions upon UVA/B stress.	NAD	191-195	sirtuin 1	Homo sapiens	196-201
34142751-5	2021	In stenotic valves (n = 50), due to reduced CD73 activity, NAD+ was degraded predominantly by CD38 and additionally by ALP and eNPP1.	NAD	59-63	ATHS	Homo sapiens	119-122
34117073-2	2021	AIFM1 encodes a mitochondrial flavin adenine dinucleotide (FAD)-dependent nicotinamide adenine dinucleotide (NADH) oxidoreductase, with roles in the regulation of respiratory complex assembly and function, production of reactive oxygen species, and the coordination of a caspase-independent type of apoptosis known as parthanatos.	NAD	74-107	apoptosis inducing factor mitochondria associated 1	Homo sapiens	0-5
34117073-2	2021	AIFM1 encodes a mitochondrial flavin adenine dinucleotide (FAD)-dependent nicotinamide adenine dinucleotide (NADH) oxidoreductase, with roles in the regulation of respiratory complex assembly and function, production of reactive oxygen species, and the coordination of a caspase-independent type of apoptosis known as parthanatos.	NAD	109-113	apoptosis inducing factor mitochondria associated 1	Homo sapiens	0-5
34208136-2	2021	SARS-CoV-2 infection occurs through the interaction of the viral protein Spike with the angiotensin II receptor (ACE 2), leading to an increase of angiotensin II and activation of nicotinamide adenine dinucleotide phosphate oxidase2 (NOX2), resulting in the release of both reactive oxygen species (ROS) and inflammatory molecules.	NAD	180-213	cytochrome b-245 beta chain	Homo sapiens	234-238
34199982-4	2021	Furthermore, the influence of the mitochondrial status on cytosolic NAD+ availability affecting the activity of cytosolic SIRT5 iso1 and iso4-in turn regulating cytosolic protein lysine succinylations-is presented.	NAD	68-72	eukaryotic translation initiation factor 1	Homo sapiens	128-132
34070758-7	2021	In vitro data confirmed that SFRP2 promotes NFATc3, CD38 and PD-1 expression in T-cells, while hSFRP2 mAb treatment counteracts these effects and increases NAD+ levels.	NAD	156-160	secreted frizzled related protein 2	Sus scrofa	29-34
34103440-2	2021	Nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase class III SIRT1 regulates the polarization of macrophages, controlling the inhibition of the M1 subpopulation and stimulating the activation of M2 macrophages.	NAD	0-33	sirtuin 1	Homo sapiens	73-78
34103440-2	2021	Nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase class III SIRT1 regulates the polarization of macrophages, controlling the inhibition of the M1 subpopulation and stimulating the activation of M2 macrophages.	NAD	35-39	sirtuin 1	Homo sapiens	73-78
35490494-5	2022	Sirtuins (SIRT1-7) is a family of seven proteins with NAD+-dependent type III histone deacetylase activity.	NAD	54-57	sirtuin 1	Homo sapiens	10-17
35334034-8	2022	This review provides detailed insights into the roles of NAD+ along with molecular mechanisms during aging and disease conditions, such as the impacts of age-related NAD+ deficiencies on NAD+-dependent enzymes, including poly (ADP-ribose) polymerase (PARPs), CD38, and sirtuins within skeletal muscle, and the most recent studies on the potential of nutritional supplementation and distinct modes of exercise to replenish the NAD+ pool.	NAD	187-191	poly (ADP-ribose) polymerase family, member 1	Mus musculus	221-249
35617143-5	2022	Nrx-1-null Drosophila also exhibit diminished levels of nicotinamide adenine dinucleotide (NAD+), an important coenzyme in major energy metabolism pathways.	NAD	56-89	Neurexin 1	Drosophila melanogaster	0-5
35617143-5	2022	Nrx-1-null Drosophila also exhibit diminished levels of nicotinamide adenine dinucleotide (NAD+), an important coenzyme in major energy metabolism pathways.	NAD	91-95	Neurexin 1	Drosophila melanogaster	0-5
35602958-5	2022	Therefore, our results suggest that decreased NAD+ are correlated with T cell dysfunction, but deficiency of CD38 is not enough for rescuing NAD+ in tumor infiltrated CD8+ T cells and fails to increase the efficacy of antitumor T cell therapy.	NAD	141-145	CD8a molecule	Homo sapiens	167-170
35491967-1	2022	Congenital nicotinamide adenine dinucleotide (NAD) deficiency disorders are associated with pathogenic variants in the genes NADSYN1, HAAO, and KYNU.	NAD	11-44	NAD synthetase 1	Homo sapiens	125-132
35441488-1	2022	OBJECTIVE: To observe expression of CD38, a key modulator of nicotinamide dinucleotide (NAD+) metabolism in mice with knee osteoarthritis, and protective effect of CD38 inhibition during the osteoarthritis (OA) development.	NAD	88-92	CD38 antigen	Mus musculus	36-40
35289490-7	2022	Acox1 and Idh3a control lipid oxidation and NADH generation in the TCA cycle, respectively, and Col6a1 comprises part of type VI collagen with reported profibrotic functions, suggesting influential roles in cachexia.	NAD	44-48	acyl-Coenzyme A oxidase 1, palmitoyl	Mus musculus	0-5
35289490-7	2022	Acox1 and Idh3a control lipid oxidation and NADH generation in the TCA cycle, respectively, and Col6a1 comprises part of type VI collagen with reported profibrotic functions, suggesting influential roles in cachexia.	NAD	44-48	isocitrate dehydrogenase 3 (NAD+) alpha	Mus musculus	10-15
35289490-7	2022	Acox1 and Idh3a control lipid oxidation and NADH generation in the TCA cycle, respectively, and Col6a1 comprises part of type VI collagen with reported profibrotic functions, suggesting influential roles in cachexia.	NAD	44-48	collagen, type VI, alpha 1	Mus musculus	96-102
35566069-1	2022	SIRT1, an NAD+-dependent deacetylase, catalyzes the deacetylation of proteins coupled with the breakdown of NAD+ into nicotinamide and 2"-O-acetyl-ADP-ribose (OAADPr).	NAD	10-13	sirtuin 1	Homo sapiens	0-5
35566069-1	2022	SIRT1, an NAD+-dependent deacetylase, catalyzes the deacetylation of proteins coupled with the breakdown of NAD+ into nicotinamide and 2"-O-acetyl-ADP-ribose (OAADPr).	NAD	108-112	sirtuin 1	Homo sapiens	0-5
35582109-3	2022	Sirtuins are a family of nicotinamide adenine dinucleotide (NAD+)-dependent proteins consisting of seven members (SIRT1-7).	NAD	25-58	sirtuin 1	Homo sapiens	114-121
35582109-3	2022	Sirtuins are a family of nicotinamide adenine dinucleotide (NAD+)-dependent proteins consisting of seven members (SIRT1-7).	NAD	60-63	sirtuin 1	Homo sapiens	114-121
35263032-2	2022	The NADase CD38 plays a key role in age-related NAD decline.	NAD	48-51	CD38 antigen	Mus musculus	11-15
35251333-0	2022	Sirtuin 1 participates in intervertebral disc degeneration via the nicotinamide phosphoribosyl transferase/nicotinamide adenine dinucleotide/sirtuin 1 pathway responsible for regulating autophagy of nucleus pulposus cells.	NAD	107-140	sirtuin 1	Homo sapiens	0-9
22510730-8	2012	On the other hand, DPN induced basal ERbeta translocalization into nucleus of anastrozole-treated cells.	NAD	19-22	estrogen receptor 2	Rattus norvegicus	37-43
35251333-0	2022	Sirtuin 1 participates in intervertebral disc degeneration via the nicotinamide phosphoribosyl transferase/nicotinamide adenine dinucleotide/sirtuin 1 pathway responsible for regulating autophagy of nucleus pulposus cells.	NAD	107-140	sirtuin 1	Homo sapiens	141-150
35251333-14	2022	SIRT1 serves a role in the process of IVDD through Nampt/NAD+/SIRT1 pathway that regulates autophagy of nucleus pulposus cells.	NAD	57-61	sirtuin 1	Homo sapiens	0-5
22539348-4	2012	In Saccharomyces cerevisiae, the nicotinamidase Pnc1 converts NAM to nicotinic acid (NA), which is then used as a substrate by the NAD(+) salvage pathway enzyme NA phosphoribosyltransferase (Npt1).	NAD	131-137	nicotinate phosphoribosyltransferase	Saccharomyces cerevisiae S288C	191-195
35251333-14	2022	SIRT1 serves a role in the process of IVDD through Nampt/NAD+/SIRT1 pathway that regulates autophagy of nucleus pulposus cells.	NAD	57-61	sirtuin 1	Homo sapiens	62-67
22539348-9	2012	The INAM-induced increase in NAD(+) was strongly dependent on Pnc1 and Npt1, suggesting that INAM increases flux through the NAD(+) salvage pathway.	NAD	29-35	nicotinate phosphoribosyltransferase	Saccharomyces cerevisiae S288C	71-75
35137552-7	2022	Inhibition of SIRT1 blunted the protective effect of NAD+ and up-regulated the activity of glycogen synthase kinase-3beta (GSK-3beta) that was concomitant with mitigated Nrf2 nuclear accumulation, thereby exacerbates AKI.	NAD	53-57	sirtuin 1	Homo sapiens	14-19
22539348-9	2012	The INAM-induced increase in NAD(+) was strongly dependent on Pnc1 and Npt1, suggesting that INAM increases flux through the NAD(+) salvage pathway.	NAD	125-131	nicotinate phosphoribosyltransferase	Saccharomyces cerevisiae S288C	71-75
22682224-2	2012	In line with this premise, decreased activity of PARP-1 or CD38-both NAD(+) consumers-increases NAD(+) bioavailability, resulting in SIRT1 activation and protection against metabolic disease.	NAD	69-75	CD38 molecule	Homo sapiens	59-63
22691943-1	2012	Locally acting insulin growth factor isoform (mIGF-1) and the NAD+-dependent protein deacetylase SIRT1 are implicated in life and health span.	NAD	62-65	sirtuin 1	Mus musculus	97-102
35399501-7	2022	In addition to known tumor-promoting genes, e.g., c-MYC, YAP1, RAD51B, TRIB3, SLC17A9, JADE1, we found that NAPRT, encoding a key enzyme for NAD+ biosynthesis from nicotinic acid, was also suppressed in HCC cells by the BRD4 inhibitor.	NAD	141-145	nicotinate phosphoribosyltransferase	Homo sapiens	108-113
35408818-4	2022	Here our study found that the disruption of NAD+ anabolism homeostasis caused an elevation in both oxidative stress and fibronectin expression, along with a decrease in Sirt1 and an increase in both NF-kappaB P65 expression and acetylation, culminating in extracellular matrix deposition and globular fibrosis in DN.	NAD	44-48	sirtuin 1	Homo sapiens	169-174
35408818-5	2022	More importantly, through constitutively overexpressing NMNAT1 or NAMPT in human mesangial cells, we revealed NAD+ levels altered inversely with NMN levels in the context of DN and, further, their changes affect Sirt1/NF-kappaB P65, thus playing a crucial role in the pathogenesis of DN.	NAD	110-114	sirtuin 1	Homo sapiens	212-217
22555559-1	2012	The peroxisomal protein PXN encoded by the Arabidopsis gene At2g39970 has very recently been found to transport NAD+, NADH, AMP and ADP.	NAD	112-116	Mitochondrial substrate carrier family protein	Arabidopsis thaliana	24-27
35297126-1	2022	Sirtuins (SIRT1-7) are distinct histone deacetylases (HDACs) whose activity is determined by cellular metabolic status andnicotinamide adenine dinucleotide (NAD+ ) levels.	NAD	157-161	sirtuin 1	Homo sapiens	10-17
35294260-6	2022	In vitro, P2X7R+ CD8 T cells were susceptible to ART1-mediated ADP-ribosylation and NICD, which was exacerbated upon blockade of the NAD+-degrading ADP-ribosyl cyclase CD38.	NAD	133-137	CD8a molecule	Homo sapiens	17-20
35138178-11	2022	In diseases in which CD38 appears to play a role, CD38-dependent NAD decline is often a common denominator of pathophysiology.	NAD	65-68	CD38 antigen	Mus musculus	21-25
22555559-1	2012	The peroxisomal protein PXN encoded by the Arabidopsis gene At2g39970 has very recently been found to transport NAD+, NADH, AMP and ADP.	NAD	118-122	Mitochondrial substrate carrier family protein	Arabidopsis thaliana	24-27
35138178-11	2022	In diseases in which CD38 appears to play a role, CD38-dependent NAD decline is often a common denominator of pathophysiology.	NAD	65-68	CD38 antigen	Mus musculus	50-54
22555559-6	2012	The physiological role of PXN is probably to provide the peroxisomes with the essential coenzymes NAD+ and CoA.	NAD	98-102	Mitochondrial substrate carrier family protein	Arabidopsis thaliana	26-29
35195252-5	2022	Specifically, FoxOs regulate mitochondrial biogenesis by dampening NRF1-Tfam and c-Myc-Tfam cascades directly, and inhibiting NAD-Sirt1-Pgc1alpha cascade indirectly by inducing Hmox1 or repressing Fxn and Urod.	NAD	126-129	sirtuin 1	Homo sapiens	130-135
23565341-7	2012	RESULTS: 1) sirtuin pathway inhibition or SIRT1 knockdown attenuated Zn2+-, STZ-, and cytokine-mediated toxicity and NAD+ loss in beta-cells, 2) SIRT1 overexpression potentiated these toxicities, 3) young SIRT1 beta-cell transgenic mice have improved glucose tolerance under basal conditions, but upon aging showed increased sensitivity to streptozotocin compared to SIRT1 +/- mice, and 4) SIRT1 +/- mice in an NOD background or exposed to streptozotocin trended toward reduced diabetic incidence and mortality compared to wildtype.	NAD	117-121	sirtuin 1	Mus musculus	42-47
35135596-12	2022	CONCLUSION: MTHFD2, as a NAD + -dependent enzyme, accelerated tumor progression by up-regulating MBO1A, suggesting that this protein may be an independent prognostic factor and a potential therapeutic target for future ovarian cancer treatments.	NAD	25-28	methylenetetrahydrofolate dehydrogenase (NADP+ dependent) 2, methenyltetrahydrofolate cyclohydrolase	Homo sapiens	12-18
23565341-8	2012	CONCLUSIONS: These results have implicated SIRT1-mediated NAD+ loss in Zn2+, STZ, or cytokine toxicities of MIN6, and in NOD or streptozotocin T1DM animal models.	NAD	58-62	sirtuin 1	Mus musculus	43-48
22155497-9	2012	The abundance of NAD-dependent deacetylase sirtuin-3 (Sirt3), a mitochondrial deacetylase was reduced in SS and SHHF failing hearts.	NAD	17-20	sirtuin 3	Rattus norvegicus	54-59
22234649-5	2012	RESULTS: Incubation of MIN6 and INS-1 832/3 insulinoma cell cultures with GKA significantly reduced cell death and impairment of intracellular NADH production caused by exposure to hydrogen peroxide.	NAD	143-147	insulin 1	Rattus norvegicus	32-37
35277012-1	2022	SIRT1 is an NAD+-dependent class III histone deacetylase that is abundantly expressed in the kidney, where it modulates gene expression, apoptosis, energy homeostasis, autophagy, acute stress responses, and mitochondrial biogenesis.	NAD	12-15	sirtuin 1	Homo sapiens	0-5
34699038-1	2022	Nicotinamide N-methyltransferase (NNMT) is a novel regulator, shown recently to regulate adipose tissue energy expenditure partly through changing NAD + content, which is essential for mitochondrial.	NAD	147-152	nicotinamide N-methyltransferase	Mus musculus	0-32
34699038-1	2022	Nicotinamide N-methyltransferase (NNMT) is a novel regulator, shown recently to regulate adipose tissue energy expenditure partly through changing NAD + content, which is essential for mitochondrial.	NAD	147-152	nicotinamide N-methyltransferase	Mus musculus	34-38
34699038-6	2022	A combination of NNMT and its related genetic (Nmnat1, Nampt, Cyp2e1, Nrk1, Cd38) and proteic analyses and also the NAD + levels demonstrated the dynamical and depot-specific remodeling of NAD metabolism in different adipose tissues in response to cold exposure.	NAD	189-192	nicotinamide N-methyltransferase	Mus musculus	17-21
34699038-6	2022	A combination of NNMT and its related genetic (Nmnat1, Nampt, Cyp2e1, Nrk1, Cd38) and proteic analyses and also the NAD + levels demonstrated the dynamical and depot-specific remodeling of NAD metabolism in different adipose tissues in response to cold exposure.	NAD	189-192	nicotinamide nucleotide adenylyltransferase 1	Mus musculus	47-53
35087020-0	2022	Transfer of the longevity-associated variant of BPIFB4 gene rejuvenates immune system and vasculature by a reduction of CD38+ macrophages and NAD+ decline.	NAD	142-146	BPI fold containing family B, member 4	Mus musculus	48-54
35087020-9	2022	At the functional level, the reduction of senescence-associated inflammation ensured sustained NAD+ levels in the plasma of AAV-LAV-BPIFB4 old mice by preventing the NADase CD38 increase in F4/80+ tissue-resident macrophages and Ly6Chigh pro-inflammatory monocytes of the spleen and bone marrow.	NAD	95-99	BPI fold containing family B, member 4	Mus musculus	132-138
35087020-9	2022	At the functional level, the reduction of senescence-associated inflammation ensured sustained NAD+ levels in the plasma of AAV-LAV-BPIFB4 old mice by preventing the NADase CD38 increase in F4/80+ tissue-resident macrophages and Ly6Chigh pro-inflammatory monocytes of the spleen and bone marrow.	NAD	95-99	CD38 antigen	Mus musculus	173-177
35087020-9	2022	At the functional level, the reduction of senescence-associated inflammation ensured sustained NAD+ levels in the plasma of AAV-LAV-BPIFB4 old mice by preventing the NADase CD38 increase in F4/80+ tissue-resident macrophages and Ly6Chigh pro-inflammatory monocytes of the spleen and bone marrow.	NAD	95-99	adhesion G protein-coupled receptor E1	Mus musculus	190-195
34997120-9	2022	Sirtuin1 (SIRT1) as an NAD+-dependent protein deacetylase that seems to play a potential protective role in this process.	NAD	23-26	sirtuin 1	Homo sapiens	0-8
34997120-9	2022	Sirtuin1 (SIRT1) as an NAD+-dependent protein deacetylase that seems to play a potential protective role in this process.	NAD	23-26	sirtuin 1	Homo sapiens	10-15
35392250-9	2022	Metabolite studies by NMR and flux analyses by LC-MS support a mechanism, wherein DeltaPsi effects on the production of reactive oxygen alters the NADH/NAD+ ratio affecting OAA accumulation and, hence, OAA inhibition of SDH.	NAD	147-151	succinate dehydrogenase complex iron sulfur subunit B	Homo sapiens	220-223
35392250-9	2022	Metabolite studies by NMR and flux analyses by LC-MS support a mechanism, wherein DeltaPsi effects on the production of reactive oxygen alters the NADH/NAD+ ratio affecting OAA accumulation and, hence, OAA inhibition of SDH.	NAD	152-156	succinate dehydrogenase complex iron sulfur subunit B	Homo sapiens	220-223
2510723-1	1989	NADPH-cytochrome P-450 reductase (FP1) and NADH-cytochrome b5 reductase (FP2) involved in the microsomal fraction of rat liver have been modified chemically by periodate-oxidized NADP+ and NAD+ (o-NAD(P].	NAD	189-193	cytochrome p450 oxidoreductase	Rattus norvegicus	0-32
2640566-2	1989	Both of these compounds inactivate homogeneous 3 alpha-HSD in a time- and concentration-dependent manner only in the presence of NAD+.	NAD	129-133	aldo-keto reductase family 1, member C14	Rattus norvegicus	47-58
2640566-14	1989	The Michael acceptors III and IV inactivate the 3 alpha-HSD in the absence of NAD+ at a rate too high to accurately measure and titrate the enzyme in a stoichiometric manner.	NAD	78-82	aldo-keto reductase family 1, member C14	Rattus norvegicus	48-59
2519111-1	1989	A full-length cDNA encoding NADH-dependent hydroxypyruvate reductase (HPR), a photorespiratory enzyme localized in leaf peroxisomes, was isolated from a lambda gt11 cDNA library made by reverse transcription of poly(A)+ RNA from cucumber cotyledons.	NAD	28-32	glycerate dehydrogenase	Cucumis sativus	43-68
2519111-1	1989	A full-length cDNA encoding NADH-dependent hydroxypyruvate reductase (HPR), a photorespiratory enzyme localized in leaf peroxisomes, was isolated from a lambda gt11 cDNA library made by reverse transcription of poly(A)+ RNA from cucumber cotyledons.	NAD	28-32	glycerate dehydrogenase	Cucumis sativus	70-73
2519111-10	1989	The derived amino acid sequence for HPR also contains the characteristics of an NAD-binding domain.	NAD	80-83	glycerate dehydrogenase	Cucumis sativus	36-39
2815153-1	1989	In all subcellular pituitary fractions, 3 alpha-hydroxysteroid dehydrogenase (3 alpha-ol dehydrogenase) activity is high (1 to 3 pmol/mg/h) with NADH or NADPH as cofactor, and 3 beta-hydroxysteroid dehydrogenase (3 beta-ol dehydrogenase) activity much lower.	NAD	145-149	aldo-keto reductase family 1, member C14	Rattus norvegicus	40-76
2812907-0	1989	[Cyanosis in children caused by inherited methemoglobinemia due to deficiency of NADH-dependent methemoglobin reductase in erythrocytes].	NAD	81-85	hemoglobin subunit gamma 2	Homo sapiens	42-55
2812907-1	1989	Two cases of the congenital methemoglobinemia in children due to the deficiency of NADH-dependent methemoglobin reductase in erythrocytes.	NAD	83-87	hemoglobin subunit gamma 2	Homo sapiens	28-41
2812907-3	1989	Cardiological examinations excluded heart defect but an increased blood methemoglobin level and decreased activity of NADH-dependent methemoglobin reductase were found, that caused methemoglobinemia.	NAD	118-122	hemoglobin subunit gamma 2	Homo sapiens	133-146
3062940-2	1988	ADH is an enzyme of the cytosol, requires NAD+ as cofactor and exhibits a pH optimum in the alkaline range.	NAD	42-46	aldo-keto reductase family 1 member A1	Homo sapiens	0-3
3218146-3	1988	These data suggest that reduced NAD- and NADP-containing oxidoreductases alpha-GPD and G6PD are donors of H+ used in biosynthesis of H2O2 catalyzed by SOD.	NAD	32-35	glucose-6-phosphate dehydrogenase	Homo sapiens	87-91
3262717-10	1988	Among the NAD+-linked dehydrogenases in the tricarboxylic acid cycle, alpha-ketoglutarate dehydrogenase complex was significantly inhibited by MPP+.	NAD	10-13	oxoglutarate (alpha-ketoglutarate) dehydrogenase (lipoamide)	Mus musculus	70-103
2844232-9	1988	NADH binding is clearly shown to involve a trapped inorganic phosphate at the position normally occupied by the 2"-phosphate of NADPH.	NAD	0-4	2,4-dienoyl-CoA reductase 1	Homo sapiens	128-133
3360015-7	1988	From measurements of NADPH, NADH, oxidized and reduced glutathione contents of mitochondria incubated under a variety of conditions, evidence has been obtained indicating that the mitochondrial NADH supply represents an important factor in the regulation of pyruvate carboxylase activity.	NAD	194-198	pyruvate carboxylase	Rattus norvegicus	258-278
3348868-1	1988	New inhibitor or inhibitors of nicotinamide-adenine dinucleotide-dependent 15-hydroxyprostaglandin dehydrogenase (PGDH) activity were found in breast milk but not in powdered milk.	NAD	31-64	carbonyl reductase 1	Homo sapiens	75-112
3258785-3	1988	Incubation of rat striatal slices with MPP+ (1 microM) produced a time-dependent oxidation of Cytochrome-b in a manner consistent with the concept of a block in electron transport in the intramitochondrial respiratory chain between nicotinamide adenine dinucleotide (NAD) and Cytochrome-b.	NAD	232-265	cytochrome b, mitochondrial	Rattus norvegicus	94-106
3258785-3	1988	Incubation of rat striatal slices with MPP+ (1 microM) produced a time-dependent oxidation of Cytochrome-b in a manner consistent with the concept of a block in electron transport in the intramitochondrial respiratory chain between nicotinamide adenine dinucleotide (NAD) and Cytochrome-b.	NAD	267-270	cytochrome b, mitochondrial	Rattus norvegicus	94-106
22339434-6	2012	Formation of adducts of ALDH1A1 and ALDH2 with acrolein increased their K(d) values for NAD(+) by 2- and 3-fold, respectively.	NAD	88-94	aldehyde dehydrogenase 1 family member A1	Homo sapiens	24-31
22139586-1	2012	Diphtheria toxin (DT) and its N-terminal fragment A (FA) catalyse the transfer of the ADP-ribose moiety of nicotinamide adenine dinucleotide (NAD) into a covalent linkage with eukaryotic elongation factor 2 (eEF2).	NAD	107-140	eukaryotic translation elongation factor 2	Homo sapiens	176-206
18964484-5	1988	Alcohol dehydrogenase is the enzyme and the rate of production of reduced nicotinamide adenine dinucleotide is measured.	NAD	74-107	aldo-keto reductase family 1 member A1	Homo sapiens	0-21
22139586-1	2012	Diphtheria toxin (DT) and its N-terminal fragment A (FA) catalyse the transfer of the ADP-ribose moiety of nicotinamide adenine dinucleotide (NAD) into a covalent linkage with eukaryotic elongation factor 2 (eEF2).	NAD	107-140	eukaryotic translation elongation factor 2	Homo sapiens	208-212
22139586-1	2012	Diphtheria toxin (DT) and its N-terminal fragment A (FA) catalyse the transfer of the ADP-ribose moiety of nicotinamide adenine dinucleotide (NAD) into a covalent linkage with eukaryotic elongation factor 2 (eEF2).	NAD	142-145	eukaryotic translation elongation factor 2	Homo sapiens	176-206
22139586-1	2012	Diphtheria toxin (DT) and its N-terminal fragment A (FA) catalyse the transfer of the ADP-ribose moiety of nicotinamide adenine dinucleotide (NAD) into a covalent linkage with eukaryotic elongation factor 2 (eEF2).	NAD	142-145	eukaryotic translation elongation factor 2	Homo sapiens	208-212
21667072-0	2012	Molecular docking and structural analysis of cofactor-protein interaction between NAD+ and 11beta-hydroxysteroid dehydrogenase type 2.	NAD	82-86	hydroxysteroid 11-beta dehydrogenase 2	Homo sapiens	91-133
2832095-6	1988	The effect on the steady-state of cytochrome b, as well as, the inhibitory effect on state III of respiration with NAD+-linked substrates, offers a reasonable possibility to suggesting that the inhibition site of MTX could be in a place anterior to cytochrome b region, and not linked to respiratory chain.	NAD	115-119	mitochondrially encoded cytochrome b	Homo sapiens	249-261
21667072-4	2012	Our present study also revealed that Asp91, Phe94, Tyr232 and Thr267 could be of importance in the interaction between NAD(+) and 11betaHSD2.	NAD	119-125	hydroxysteroid 11-beta dehydrogenase 2	Homo sapiens	130-140
2828773-6	1987	Large differences were also observed between corresponding spectra when the binding sites were saturated with NAD+, reflecting the development of marked conformational changes in both young and old GPDH species upon coenzyme binding.	NAD	110-114	glyceraldehyde-3-phosphate dehydrogenase	Rattus norvegicus	198-202
21667072-6	2012	The present study proposes the latest models for 11betaHSD2 and its cofactor NAD(+), and to the best of our knowledge, this is the first report of a m11betaHSD2 model with NAD(+).	NAD	77-83	hydroxysteroid 11-beta dehydrogenase 2	Homo sapiens	49-59
21667072-6	2012	The present study proposes the latest models for 11betaHSD2 and its cofactor NAD(+), and to the best of our knowledge, this is the first report of a m11betaHSD2 model with NAD(+).	NAD	172-178	hydroxysteroid 11-beta dehydrogenase 2	Homo sapiens	49-59
3542971-3	1987	Anaerobically, L-lactaldehyde serves as an electron acceptor to regenerate NAD from NADH by the action of an oxidoreductase; the reduced product, L-12-propanediol, is excreted.	NAD	75-78	oxidoreductase	Escherichia coli	109-123
22316301-2	2012	NAD-dependent deacetylase sirtuin-1(SIRT1) is an important hub which links lipid metabolism with circadian clock by its deacetylation activity depends on intracellular NAD+/NADH content ratio.	NAD	0-3	sirtuin 1	Mus musculus	36-41
3542971-3	1987	Anaerobically, L-lactaldehyde serves as an electron acceptor to regenerate NAD from NADH by the action of an oxidoreductase; the reduced product, L-12-propanediol, is excreted.	NAD	84-88	oxidoreductase	Escherichia coli	109-123
22316301-2	2012	NAD-dependent deacetylase sirtuin-1(SIRT1) is an important hub which links lipid metabolism with circadian clock by its deacetylation activity depends on intracellular NAD+/NADH content ratio.	NAD	168-172	sirtuin 1	Mus musculus	36-41
22316301-2	2012	NAD-dependent deacetylase sirtuin-1(SIRT1) is an important hub which links lipid metabolism with circadian clock by its deacetylation activity depends on intracellular NAD+/NADH content ratio.	NAD	173-177	sirtuin 1	Mus musculus	36-41
3482476-2	1987	The stability of this SFHS containing Methemoglobin Reductase, can be improved by addition of NADH.	NAD	94-98	hemoglobin subunit gamma 2	Homo sapiens	38-51
22204321-5	2012	For examples, the key NAD(+)-dependent enzymes SIRT1 and SIRT2 have been indicated to strongly affect the pathological changes of PD and AD; PARP-1 inhibition can profoundly reduce the brain injury in the animal models of multiple neurological diseases; and administration of either NAD(+) or nicotinamide can also decrease ischemic brain damage.	NAD	22-28	sirtuin 2	Homo sapiens	57-62
22302938-0	2012	Dietary obesity-associated Hif1alpha activation in adipocytes restricts fatty acid oxidation and energy expenditure via suppression of the Sirt2-NAD+ system.	NAD	145-149	sirtuin 2	Homo sapiens	139-144
3778866-2	1986	This NAD+ photoaffinity analogue has been previously demonstrated to modify glyceraldehyde-3-phosphate dehydrogenase in a very specific manner and probably at the active site of the enzyme [Chen, S., Davis, H., Vierra, J. R., &amp; Guillory, R. J.	NAD	5-9	glyceraldehyde-3-phosphate dehydrogenase	Oryctolagus cuniculus	76-116
3777430-3	1986	Using a new reflectometry technique based on measurement of the polarization change of light reflected upon the biochip, continuous monitoring of the affinity binding and subsequent desorption of alcohol dehydrogenase and lactate dehydrogenase from the NAD surface were possible; allowing repeated use of the same NAD chip--an advantage when the assay was carried out in a continuous reflectometer.	NAD	253-256	aldo-keto reductase family 1 member A1	Homo sapiens	196-217
3777430-3	1986	Using a new reflectometry technique based on measurement of the polarization change of light reflected upon the biochip, continuous monitoring of the affinity binding and subsequent desorption of alcohol dehydrogenase and lactate dehydrogenase from the NAD surface were possible; allowing repeated use of the same NAD chip--an advantage when the assay was carried out in a continuous reflectometer.	NAD	314-317	aldo-keto reductase family 1 member A1	Homo sapiens	196-217
22157016-1	2012	SIRT1 is one of seven mammalian sirtuin (silent information regulator 2-related) proteins that harbor NAD(+)-dependent protein deacetylase activity and is implicated in multiple metabolic and age-associated pathways and disorders.	NAD	102-108	sirtuin 2	Homo sapiens	41-71
22339640-1	2012	Poly(ADP-ribose) polymerase-1 (PARP-1), a chromatin-associated enzyme that catalyzes the NAD+-dependent addition of ADP-ribose polymers onto a variety of nuclear proteins, has been shown to be associated with the nuclear matrix.	NAD	89-93	poly (ADP-ribose) polymerase 1	Rattus norvegicus	0-29
3013300-6	1986	Strikingly, in inside-out vesicles, NADH oxidation generates a H+ electrochemical gradient that is very significantly greater than that produced by either D-lactate or ubiquinol 1; furthermore, NADH/ubiquinone 1 and NADH/ferricyanide oxidoreductase activities are electrogenic.	NAD	36-40	oxidoreductase	Escherichia coli	234-248
22339640-1	2012	Poly(ADP-ribose) polymerase-1 (PARP-1), a chromatin-associated enzyme that catalyzes the NAD+-dependent addition of ADP-ribose polymers onto a variety of nuclear proteins, has been shown to be associated with the nuclear matrix.	NAD	89-93	poly (ADP-ribose) polymerase 1	Rattus norvegicus	31-37
22105513-1	2012	The NAD-dependent histone deacetylase sirtuin (Sirt)1 is implicated in a wide variety of physiological processes, ranging from tumorigenesis to mitochondrial biogenesis to neuronal development.	NAD	4-7	sirtuin 1	Mus musculus	47-53
2937805-10	1986	H2O2 at 40 microM or higher inhibited DNA synthesis, and induced SSB within less than 30 s. These results suggest that DNA damage induced within seconds after addition of oxidant may lead to stimulation of poly-ADP-ribose polymerase, and a consequent fall in NAD.	NAD	259-262	poly (ADP-ribose) polymerase family, member 1	Mus musculus	206-232
2937805-11	1986	Excessive stimulation of poly-ADP-ribose polymerase leads to a fall in NAD sufficient to interfere with ATP synthesis.	NAD	71-74	poly (ADP-ribose) polymerase family, member 1	Mus musculus	25-51
3935115-1	1985	This study compared the NADH- and NADPH-supported p-nitrophenetole (NP) O-deethylase, ethylmorphine (EM) O-deethylase and EM N-demethylase activities of rat hepatic microsomes with respect to dioxygen requirement, inhibition by carbon monoxide, inhibition by classical inhibitors of cytochrome P-450 systems, and the involvement of NADH-cytochrome b5, cytochrome b5 reductase and NADPH-cytochrome P-450 reductase.	NAD	24-28	cytochrome b5 type A	Rattus norvegicus	337-350
3935115-1	1985	This study compared the NADH- and NADPH-supported p-nitrophenetole (NP) O-deethylase, ethylmorphine (EM) O-deethylase and EM N-demethylase activities of rat hepatic microsomes with respect to dioxygen requirement, inhibition by carbon monoxide, inhibition by classical inhibitors of cytochrome P-450 systems, and the involvement of NADH-cytochrome b5, cytochrome b5 reductase and NADPH-cytochrome P-450 reductase.	NAD	24-28	cytochrome b5 type A	Rattus norvegicus	352-365
21895810-9	2012	Hence, At2g39970 was named PXN for peroxisomal NAD(+)  carrier.	NAD	47-53	Mitochondrial substrate carrier family protein	Arabidopsis thaliana	27-30
3935115-1	1985	This study compared the NADH- and NADPH-supported p-nitrophenetole (NP) O-deethylase, ethylmorphine (EM) O-deethylase and EM N-demethylase activities of rat hepatic microsomes with respect to dioxygen requirement, inhibition by carbon monoxide, inhibition by classical inhibitors of cytochrome P-450 systems, and the involvement of NADH-cytochrome b5, cytochrome b5 reductase and NADPH-cytochrome P-450 reductase.	NAD	24-28	cytochrome p450 oxidoreductase	Rattus norvegicus	380-412
3935115-5	1985	The use of antibodies against NADPH-cytochrome P-450 reductase, NADH-cytochrome b5 reductase and cytochrome b5 demonstrated that both the NADH- and the NADPH-supported reactions depend on established components of cytochrome P-450 systems.	NAD	64-68	cytochrome b5 type A	Rattus norvegicus	69-82
21895810-10	2012	The loss of PXN in Arabidopsis causes defects in NAD(+) -dependent beta-oxidation during seedling establishment.	NAD	49-55	Mitochondrial substrate carrier family protein	Arabidopsis thaliana	12-15
4062295-3	1985	Although NADPH, NADH, and GSH have no direct methemoglobin-reducing activity in vitro, they convert oxidized divicine to the reduced hydroquinone species, which is responsible for the electron transfer to methemoglobin.	NAD	16-20	hemoglobin subunit gamma 2	Homo sapiens	205-218
21895810-12	2012	Based on our results, we propose that PXN delivers NAD(+)  for optimal fatty acid degradation during storage oil mobilization.	NAD	51-57	Mitochondrial substrate carrier family protein	Arabidopsis thaliana	38-41
23284917-10	2012	However, during aging, the MRL/lpr T-cell population exhibits a drastically reduced sensitivity to ATP- or NAD-mediated stimulation of P2X7R, which parallels the increase in B220(+) DN T-cell numbers in lymphoid organs.	NAD	107-110	protein tyrosine phosphatase, receptor type, C	Mus musculus	174-178
3932085-10	1985	At 0.1 microM NAD as substrate pmol quantities of monomeric ADP-ribose adducts per mg DNA were formed and the main acceptors were sharply discernable on the basis of molecular mass as histones, high mobility non-histone proteins, two protein groups of a mass of 66 and 44 kD respectively, and the poly(ADP-ribose) polymerase enzyme protein of 119 kD mass.	NAD	14-17	poly (ADP-ribose) polymerase family, member 1	Mus musculus	297-324
23284917-12	2012	The few B220(+) T cells observed in normal MRL(+/+) and C57BL/6 mice are also resistant to ATP or NAD treatment.	NAD	98-101	protein tyrosine phosphatase, receptor type, C	Mus musculus	8-12
23240497-0	2012	[NAD+-converting enzymes in neuronal and glial cells: CD38 as a novel target for neuroprotection].	NAD	1-5	CD38 molecule	Homo sapiens	54-58
2992639-6	1985	The purified enzyme was characterized by a high specificity for NADH as electron donor (Km = 6.4 mumol/L v Km greater than 1.6 mmol/L for NADPH) and exhibited a maximal turnover of ca.	NAD	64-68	2,4-dienoyl-CoA reductase 1	Homo sapiens	138-143
23240497-3	2012	Special attention is paid to involvement of CD38 into regulation of NAD+ levels in brain cells in normal and pathological conditions.	NAD	68-72	CD38 molecule	Homo sapiens	44-48
21998399-13	2011	CONCLUSIONS: Our results demonstrate that Wld(S) combines an insulinotropic effect with protection against beta-cell failure and suggest that enhancing NAD biosynthesis in beta-cells to increase SIRT1 activity could be a potential therapeutic approach for diabetes.	NAD	152-155	sirtuin 1	Mus musculus	195-200
21890893-7	2011	Nicotinamide phosphoribosyltransferase (NAMPT) that synthesizes NAD(+) required for SIRT1 activation exerts similar effects on CIITA activity.	NAD	64-70	class II major histocompatibility complex transactivator	Homo sapiens	127-132
21840382-1	2011	Sirt3 is a NAD+-dependent protein deacetylase mainly localized in mitochondria.	NAD	11-14	sirtuin 3	Mus musculus	0-5
21949390-2	2011	We previously used global expression profiling to examine peripheral nerve myelination and identified the NAD(+)-dependent deacetylase Sir-two-homolog 2 (Sirt2) as a protein likely to be involved in myelination.	NAD	106-112	sirtuin 2	Mus musculus	135-152
21949390-2	2011	We previously used global expression profiling to examine peripheral nerve myelination and identified the NAD(+)-dependent deacetylase Sir-two-homolog 2 (Sirt2) as a protein likely to be involved in myelination.	NAD	106-112	sirtuin 2	Mus musculus	154-159
21242068-2	2011	In yeast, NADP-dependent enzymes, encoded by GDH1 and GDH3, are reported to synthesize glutamate from alpha-ketoglutarate, while an NAD-dependent enzyme, encoded by GDH2, catalyzes the reverse.	NAD	10-13	glutamate dehydrogenase (NADP(+)) GDH1	Saccharomyces cerevisiae S288C	45-49
21242068-2	2011	In yeast, NADP-dependent enzymes, encoded by GDH1 and GDH3, are reported to synthesize glutamate from alpha-ketoglutarate, while an NAD-dependent enzyme, encoded by GDH2, catalyzes the reverse.	NAD	10-13	glutamate dehydrogenase (NAD(+))	Saccharomyces cerevisiae S288C	165-169
21242068-4	2011	In YNAceRaf the doubling time of wild type, gdh2Delta, and gdh3Delta cells was comparable at ~4 h. NADP-dependent GDH activity (Gdh1p+Gdh3p) in wild type, gdh2Delta, and gdh3Delta was decreased ~80% and NAD-dependent activity (Gdh2p) in wild type and gdh3Delta was increased ~20-fold in YNAceRaf as compared to glucose.	NAD	99-102	glutamate dehydrogenase (NADP(+)) GDH1	Saccharomyces cerevisiae S288C	128-133
21242068-4	2011	In YNAceRaf the doubling time of wild type, gdh2Delta, and gdh3Delta cells was comparable at ~4 h. NADP-dependent GDH activity (Gdh1p+Gdh3p) in wild type, gdh2Delta, and gdh3Delta was decreased ~80% and NAD-dependent activity (Gdh2p) in wild type and gdh3Delta was increased ~20-fold in YNAceRaf as compared to glucose.	NAD	99-102	glutamate dehydrogenase (NAD(+))	Saccharomyces cerevisiae S288C	227-232
21689736-5	2011	In mammals, IDO activity plays a significant role in the immune system while in fungal species, IDO is constitutively expressed and supplies NAD(+), like mammalian TDO.	NAD	141-147	indoleamine 2,3-dioxygenase 1	Homo sapiens	12-15
21689736-5	2011	In mammals, IDO activity plays a significant role in the immune system while in fungal species, IDO is constitutively expressed and supplies NAD(+), like mammalian TDO.	NAD	141-147	indoleamine 2,3-dioxygenase 1	Homo sapiens	96-99
21689736-15	2011	Although the G. aurantiaca also has NadA and NadB to synthesize a quinolinic acid (a precursor of NAD(+)) via the aspartate pathway, the high activity of the G. aurantiaca IDO flanking the kynU gene suggests its IDO has a function similar to eukaryotic enzymes.	NAD	98-104	indoleamine 2,3-dioxygenase 1	Homo sapiens	172-175
21873234-5	2011	BATF, together with c-Jun, transcriptionally inhibited expression of the nicotinamide adenine dinucleotide (NAD(+))-dependent deacetylase Sirt1, resulting in increased histone acetylation of the T-bet locus and increased cellular NAD(+), which increased ATP production.	NAD	73-106	T-box transcription factor 21	Homo sapiens	195-200
21873234-5	2011	BATF, together with c-Jun, transcriptionally inhibited expression of the nicotinamide adenine dinucleotide (NAD(+))-dependent deacetylase Sirt1, resulting in increased histone acetylation of the T-bet locus and increased cellular NAD(+), which increased ATP production.	NAD	108-114	T-box transcription factor 21	Homo sapiens	195-200
21873234-5	2011	BATF, together with c-Jun, transcriptionally inhibited expression of the nicotinamide adenine dinucleotide (NAD(+))-dependent deacetylase Sirt1, resulting in increased histone acetylation of the T-bet locus and increased cellular NAD(+), which increased ATP production.	NAD	230-236	T-box transcription factor 21	Homo sapiens	195-200
21526340-1	2011	NAD kinase (NADK, EC 2.7.1.23) is the sole NADP(+)-biosynthetic enzyme that catalyzes phosphorylation of NAD(+) to yield NADP(+) using ATP as a phosphoryl donor, and thus, plays a vital role in the cell and represents a potentially powerful antimicrobial drug target.	NAD	105-111	NAD kinase	Homo sapiens	0-10
21526340-1	2011	NAD kinase (NADK, EC 2.7.1.23) is the sole NADP(+)-biosynthetic enzyme that catalyzes phosphorylation of NAD(+) to yield NADP(+) using ATP as a phosphoryl donor, and thus, plays a vital role in the cell and represents a potentially powerful antimicrobial drug target.	NAD	105-111	NAD kinase	Homo sapiens	12-16
21526340-5	2011	Using the purified human NADK, we revealed a sigmoidal kinetic behavior toward ATP and the inhibitory effects of NADPH and NADH, but not of NADP(+), on the catalytic activity of the enzyme.	NAD	123-127	NAD kinase	Homo sapiens	25-29
21641039-0	2011	Transgenic overexpression of toxin-related ecto-ADP-ribosyltransferase ART2.2 sensitizes T cells but not B cells to NAD-induced cell death.	NAD	116-119	ADP-ribosyltransferase 2b	Mus musculus	71-77
21641039-2	2011	In inflammatory settings, cells release NAD, the substrate for ART2.2.	NAD	40-43	ADP-ribosyltransferase 2b	Mus musculus	63-69
21641039-8	2011	Exposure of ART2.2-transgenic T cells to low, submicromolar concentrations of NAD caused cell membrane alterations including uptake of propidium iodide, externalization of phosphatidylserine, and shedding of CD62L, while ART2.2-transgenic B cells were resistant to NAD.	NAD	78-81	ADP-ribosyltransferase 2b	Mus musculus	12-18
21641039-8	2011	Exposure of ART2.2-transgenic T cells to low, submicromolar concentrations of NAD caused cell membrane alterations including uptake of propidium iodide, externalization of phosphatidylserine, and shedding of CD62L, while ART2.2-transgenic B cells were resistant to NAD.	NAD	78-81	ADP-ribosyltransferase 2b	Mus musculus	221-227
21641039-8	2011	Exposure of ART2.2-transgenic T cells to low, submicromolar concentrations of NAD caused cell membrane alterations including uptake of propidium iodide, externalization of phosphatidylserine, and shedding of CD62L, while ART2.2-transgenic B cells were resistant to NAD.	NAD	265-268	ADP-ribosyltransferase 2b	Mus musculus	12-18
21641039-9	2011	The ART2.2-overexpressing animals described here confirm that ART2.2 is an essential component for the regulation of T-cell functions by extracellular NAD and provide a useful tool to further elucidate the function of ART2.2 in vivo.	NAD	151-154	ADP-ribosyltransferase 2b	Mus musculus	4-10
21641039-9	2011	The ART2.2-overexpressing animals described here confirm that ART2.2 is an essential component for the regulation of T-cell functions by extracellular NAD and provide a useful tool to further elucidate the function of ART2.2 in vivo.	NAD	151-154	ADP-ribosyltransferase 2b	Mus musculus	62-68
21641039-9	2011	The ART2.2-overexpressing animals described here confirm that ART2.2 is an essential component for the regulation of T-cell functions by extracellular NAD and provide a useful tool to further elucidate the function of ART2.2 in vivo.	NAD	151-154	ADP-ribosyltransferase 2b	Mus musculus	62-68
21600947-4	2011	Indeed, GDH directly depends on the provision of the co-factor NADH/NAD(+), rendering the enzyme sensitive to the redox status of the cell.	NAD	63-67	glutamate dehydrogenase 1	Homo sapiens	8-11
21600947-4	2011	Indeed, GDH directly depends on the provision of the co-factor NADH/NAD(+), rendering the enzyme sensitive to the redox status of the cell.	NAD	68-74	glutamate dehydrogenase 1	Homo sapiens	8-11
21695322-2	2011	A thorough comparison of their effectiveness towards NAD(+) (expressed as TOF) revealed that the Rh(III) complexes were much more potent catalysts than the Ru(II) complexes.	NAD	53-59	FEZ family zinc finger 2	Homo sapiens	74-77
6238571-3	1984	The steady-state redox segregation (1.36 log NAD+/NADH ratio out vs NAD+/NADH in the mitochondrial matrix) was maximally about 3 kcal, and declined together with the membrane potential (delta psi) and log ATP/ADP, which obtain on imposing an increasing energy load on the system.	NAD	45-49	seminal vesicle secretory protein 4	Rattus norvegicus	205-212
20824484-1	2011	The GPD2 gene, encoding NAD(+)-dependent glycerol-3-phosphate dehydrogenase in an industrial ethanol-producing strain of Saccharomyces cerevisiae, was deleted.	NAD	24-30	glycerol-3-phosphate dehydrogenase (NAD(+)) GPD2	Saccharomyces cerevisiae S288C	4-8
21554883-4	2011	DPN had a greater adverse impact than PPT on reproductive behavior, suggesting a functional role for ERbeta in the organization of these male-specific behaviors.	NAD	0-3	estrogen receptor 2	Rattus norvegicus	101-107
6238571-3	1984	The steady-state redox segregation (1.36 log NAD+/NADH ratio out vs NAD+/NADH in the mitochondrial matrix) was maximally about 3 kcal, and declined together with the membrane potential (delta psi) and log ATP/ADP, which obtain on imposing an increasing energy load on the system.	NAD	50-54	seminal vesicle secretory protein 4	Rattus norvegicus	205-212
21399558-3	2011	Poly(ADP-ribose) polymerase-1 (PARP-1) is a critical enzyme activated to facilitate DNA repair using nicotinamide adenine dinucleotide (NAD+) as a substrate.	NAD	101-134	poly (ADP-ribose) polymerase 1	Rattus norvegicus	0-29
6595051-4	1984	3 beta-HSD was assayed by measuring the conversion of tritiated dehydroepiandrosterone (DHEA) to androstenedione in the presence of NAD+.	NAD	132-136	hydroxy-delta-5-steroid dehydrogenase, 3 beta- and steroid delta-isomerase 1	Homo sapiens	0-10
6086644-0	1984	Interactions and spatial arrangement of spin-labeled NAD+ bound to glyceraldehyde-3-phosphate dehydrogenase.	NAD	53-57	glyceraldehyde-3-phosphate dehydrogenase	Oryctolagus cuniculus	67-107
6086644-2	1984	The spatial arrangement of coenzyme NAD+ in remote and adjacent binding sites in various stoichiometric complexes with tetrameric glyceraldehyde-3-phosphate dehydrogenase from rabbit muscle was examined via EPR spectroscopy.	NAD	36-40	glyceraldehyde-3-phosphate dehydrogenase	Oryctolagus cuniculus	130-170
21399558-3	2011	Poly(ADP-ribose) polymerase-1 (PARP-1) is a critical enzyme activated to facilitate DNA repair using nicotinamide adenine dinucleotide (NAD+) as a substrate.	NAD	101-134	poly (ADP-ribose) polymerase 1	Rattus norvegicus	31-37
21399558-3	2011	Poly(ADP-ribose) polymerase-1 (PARP-1) is a critical enzyme activated to facilitate DNA repair using nicotinamide adenine dinucleotide (NAD+) as a substrate.	NAD	136-140	poly (ADP-ribose) polymerase 1	Rattus norvegicus	0-29
21399558-3	2011	Poly(ADP-ribose) polymerase-1 (PARP-1) is a critical enzyme activated to facilitate DNA repair using nicotinamide adenine dinucleotide (NAD+) as a substrate.	NAD	136-140	poly (ADP-ribose) polymerase 1	Rattus norvegicus	31-37
21399558-4	2011	However, in the presence of severe oxidative stress and DNA damage, PARP-1 overactivation may ensue, depleting cells of NAD+ and ATP, killing them by metabolic catastrophe.	NAD	120-124	poly (ADP-ribose) polymerase 1	Rattus norvegicus	68-74
6431905-1	1984	Four protein components of the hepatic microsomal electron transfer system, NADPH-cytochrome P-450 reductase, cytochrome P-450, NADH-cytochrome b5 reductase, and cytochrome b5, all purified from liver microsomes of phenobarbital-pretreated rabbits, were co-reconstituted into liposomes of egg yolk phosphatidylcholine.	NAD	128-132	cytochrome b5	Oryctolagus cuniculus	133-146
21596603-2	2011	The NAD(+)-dependent deacetylase and gene repressor SIRT1 removes histone H4K16 acetylation marks and facilitates heterochromatin formation.	NAD	4-10	Sirtuin 1	Drosophila melanogaster	52-57
6589599-6	1984	The binding sites have the relative affinities NADPH greater than NADH greater than NADP+ greater than NAD+.	NAD	103-107	2,4-dienoyl-CoA reductase 1	Homo sapiens	47-52
21514298-5	2011	CD38 is the main mammalian enzyme that hydrolyzes NAD(+), generating Ca(2+)-active metabolites.	NAD	50-56	CD38 molecule	Homo sapiens	0-4
6372432-1	1984	A new commercially available homogeneous enzyme immunoassay, using the glucose-6-phosphate dehydrogenase (G6PDH) catalyzed conversion of NAD to NADH, has been evaluated and applied to the determination of acetaminophen in serum.	NAD	137-140	glucose-6-phosphate dehydrogenase	Homo sapiens	71-104
6372432-1	1984	A new commercially available homogeneous enzyme immunoassay, using the glucose-6-phosphate dehydrogenase (G6PDH) catalyzed conversion of NAD to NADH, has been evaluated and applied to the determination of acetaminophen in serum.	NAD	137-140	glucose-6-phosphate dehydrogenase	Homo sapiens	106-111
21431168-1	2011	Human CD38 is a novel multi-functional protein that acts not only as an antigen for B-lymphocyte activation, but also as an enzyme catalyzing the synthesis of a Ca(2+) messenger molecule, cyclic ADP-ribose, from NAD(+).	NAD	212-218	CD38 molecule	Homo sapiens	6-10
6372432-1	1984	A new commercially available homogeneous enzyme immunoassay, using the glucose-6-phosphate dehydrogenase (G6PDH) catalyzed conversion of NAD to NADH, has been evaluated and applied to the determination of acetaminophen in serum.	NAD	144-148	glucose-6-phosphate dehydrogenase	Homo sapiens	71-104
6372432-1	1984	A new commercially available homogeneous enzyme immunoassay, using the glucose-6-phosphate dehydrogenase (G6PDH) catalyzed conversion of NAD to NADH, has been evaluated and applied to the determination of acetaminophen in serum.	NAD	144-148	glucose-6-phosphate dehydrogenase	Homo sapiens	106-111
6714231-11	1984	Ethanol metabolism elevates NADH in both periportal and pericentral regions of the liver lobule causing redox inhibition of glyceraldehyde-3-phosphate dehydrogenase and decreased rates of glycolytic ATP synthesis.	NAD	28-32	glyceraldehyde-3-phosphate dehydrogenase	Rattus norvegicus	124-164
21431168-3	2011	Based on the crystal structure of the CD38/NAD(+) complex, we synthesized a series of simplified N-substituted nicotinamide derivatives (Compound 1-14).	NAD	43-49	CD38 molecule	Homo sapiens	38-42
21431168-4	2011	A number of these compounds exhibited moderate inhibition of the NAD(+) utilizing activity of CD38, with Compound 4 showing the highest potency.	NAD	65-71	CD38 molecule	Homo sapiens	94-98
6425273-5	1984	When dehydroepiandrosterone and NAD+ were added as substrates for 3 beta-hydroxy-delta 5-steroid dehydrogenase in order to synthesize NADH by enzymatic reaction, the NADPH-supported activities of steroid 17 alpha-hydroxylase and C-17-C-20 lyase were further stimulated as compared with the addition of NADH, and this stimulation was suppressed by the antibody against cytochrome b5.	NAD	32-36	cytochrome b5 type A	Rattus norvegicus	368-381
21541336-2	2011	Apart from its role as an important redox carrier, NAD+ also serves as the sole substrate for NAD-dependent enzymes, including poly(ADP-ribose) polymerase (PARP), an important DNA nick sensor, and NAD-dependent histone deacetylases, Sirtuins which play an important role in a wide variety of processes, including senescence, apoptosis, differentiation, and aging.	NAD	51-55	poly (ADP-ribose) polymerase 1	Rattus norvegicus	127-154
6425273-5	1984	When dehydroepiandrosterone and NAD+ were added as substrates for 3 beta-hydroxy-delta 5-steroid dehydrogenase in order to synthesize NADH by enzymatic reaction, the NADPH-supported activities of steroid 17 alpha-hydroxylase and C-17-C-20 lyase were further stimulated as compared with the addition of NADH, and this stimulation was suppressed by the antibody against cytochrome b5.	NAD	134-138	cytochrome b5 type A	Rattus norvegicus	368-381
6317018-0	1983	Poly(ADP-ribose) Polymerase inhibitors preserve nicotinamide adenine dinucleotide and adenosine 5"-triphosphate pools in DNA-damaged cells: mechanism of stimulation of unscheduled DNA synthesis.	NAD	48-81	poly (ADP-ribose) polymerase family, member 1	Mus musculus	0-27
6317018-3	1983	When the L1210 cells were exposed to 136 microM N-methyl-N"-nitro-N-nitrosoguanidine, the activation of poly(ADP-ribose) polymerase resulted in the rapid depletion of oxidized nicotinamide adenine dinucleotide (NAD+) levels and subsequent depletion of adenosine 5"-triphosphate (ATP) pools.	NAD	176-209	poly (ADP-ribose) polymerase family, member 1	Mus musculus	104-131
6317018-3	1983	When the L1210 cells were exposed to 136 microM N-methyl-N"-nitro-N-nitrosoguanidine, the activation of poly(ADP-ribose) polymerase resulted in the rapid depletion of oxidized nicotinamide adenine dinucleotide (NAD+) levels and subsequent depletion of adenosine 5"-triphosphate (ATP) pools.	NAD	211-215	poly (ADP-ribose) polymerase family, member 1	Mus musculus	104-131
6317018-5	1983	Poly(ADP-ribose) polymerase inhibitors prevented the rapid fall in NAD+ and ATP pools.	NAD	67-71	poly (ADP-ribose) polymerase family, member 1	Mus musculus	0-27
6317018-7	1983	Thus, the mechanism by which poly(ADP-ribose) polymerase inhibitors stimulate DNA, RNA, and protein synthesis in DNA-damaged cells appears to be mediated by their ability to prevent the drastic depletion of NAD+ pools that occurs in heavily damaged cells, thereby preserving the cells" ability to generate ATP and maintain energy-dependent processes.	NAD	207-211	poly (ADP-ribose) polymerase family, member 1	Mus musculus	29-56
21541336-2	2011	Apart from its role as an important redox carrier, NAD+ also serves as the sole substrate for NAD-dependent enzymes, including poly(ADP-ribose) polymerase (PARP), an important DNA nick sensor, and NAD-dependent histone deacetylases, Sirtuins which play an important role in a wide variety of processes, including senescence, apoptosis, differentiation, and aging.	NAD	51-55	poly (ADP-ribose) polymerase 1	Rattus norvegicus	156-160
21541336-2	2011	Apart from its role as an important redox carrier, NAD+ also serves as the sole substrate for NAD-dependent enzymes, including poly(ADP-ribose) polymerase (PARP), an important DNA nick sensor, and NAD-dependent histone deacetylases, Sirtuins which play an important role in a wide variety of processes, including senescence, apoptosis, differentiation, and aging.	NAD	51-54	poly (ADP-ribose) polymerase 1	Rattus norvegicus	127-154
21541336-2	2011	Apart from its role as an important redox carrier, NAD+ also serves as the sole substrate for NAD-dependent enzymes, including poly(ADP-ribose) polymerase (PARP), an important DNA nick sensor, and NAD-dependent histone deacetylases, Sirtuins which play an important role in a wide variety of processes, including senescence, apoptosis, differentiation, and aging.	NAD	51-54	poly (ADP-ribose) polymerase 1	Rattus norvegicus	156-160
21541336-2	2011	Apart from its role as an important redox carrier, NAD+ also serves as the sole substrate for NAD-dependent enzymes, including poly(ADP-ribose) polymerase (PARP), an important DNA nick sensor, and NAD-dependent histone deacetylases, Sirtuins which play an important role in a wide variety of processes, including senescence, apoptosis, differentiation, and aging.	NAD	94-97	poly (ADP-ribose) polymerase 1	Rattus norvegicus	127-154
6830827-4	1983	Also, we find that a fragment of rat liver NADH-cytochrome b5 reductase can restore NADH-dependent cytochrome b5 reduction to Tetrahymena microsomes which have been treated with N-ethylmaleimide to eliminate endogenous reductase activity.	NAD	43-47	cytochrome b5 type A	Rattus norvegicus	48-61
21541336-2	2011	Apart from its role as an important redox carrier, NAD+ also serves as the sole substrate for NAD-dependent enzymes, including poly(ADP-ribose) polymerase (PARP), an important DNA nick sensor, and NAD-dependent histone deacetylases, Sirtuins which play an important role in a wide variety of processes, including senescence, apoptosis, differentiation, and aging.	NAD	94-97	poly (ADP-ribose) polymerase 1	Rattus norvegicus	156-160
6830827-4	1983	Also, we find that a fragment of rat liver NADH-cytochrome b5 reductase can restore NADH-dependent cytochrome b5 reduction to Tetrahymena microsomes which have been treated with N-ethylmaleimide to eliminate endogenous reductase activity.	NAD	43-47	cytochrome b5 type A	Rattus norvegicus	99-112
21541336-7	2011	Decreased Sirt1 activity and increased acetylated p53 were observed in organ tissues in parallel with the drop in NAD+ and moderate over-expression of Sirt1 protein.	NAD	114-118	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	50-53
6340103-4	1983	By using a third enzyme, lipoamide dehydrogenase (NADH:lipoamide oxidoreductase, EC 1.6.4.3), which was also coupled to the same beads and which competes with lactate dehydrogenase for the NADH produced by alcohol dehydrogenase, the effect of site-to-site directed immobilization was studied.	NAD	50-54	aldo-keto reductase family 1 member A1	Homo sapiens	206-227
6830592-2	1983	Light emission with low decay rates was obtained by regulating the conversion of NADH to NAD+ by controlling oxidoreductase activity.	NAD	81-85	thioredoxin reductase 1	Homo sapiens	109-123
21459317-3	2011	This metabolic phenotype is achieved, in part, through SIRT1 activation, either by increasing NAD(+) levels or by promoting SIRT1 expression.	NAD	94-100	sirtuin 1	Mus musculus	55-60
6830592-2	1983	Light emission with low decay rates was obtained by regulating the conversion of NADH to NAD+ by controlling oxidoreductase activity.	NAD	89-93	thioredoxin reductase 1	Homo sapiens	109-123
6830592-6	1983	The Michaelis constants of bacterial luciferase for FMNH2 and decanal were 3 X 10(-6) M and 8 X 10(-7) M, respectively, and those of oxidoreductase for FMN and NADH were 6.1 X 10(-6) M and 1.6 X 10(-5) M, respectively.	NAD	160-164	thioredoxin reductase 1	Homo sapiens	133-147
21176092-1	2011	Silent information regulator 2 (Sir2) orthologs are an evolutionarily conserved family of NAD-dependent protein deacetylases that regulate aging and longevity in model organisms.	NAD	90-93	sirtuin 2	Homo sapiens	0-30
6572036-3	1983	A microsomal fraction was prepared from each of 14 follicular-phase follicles, and 3 beta-HSD enzyme activity was estimated by the amount of androstenedione synthesized in the presence of excess substrate (dehydroepiandrosterone) and cofactor (nicotinamide adenine dinucleotide).	NAD	244-277	hydroxy-delta-5-steroid dehydrogenase, 3 beta- and steroid delta-isomerase 1	Homo sapiens	83-93
6218154-5	1983	In addition, precipitation lines were found for hydrogenase, cytochrome oxidase, the membrane-bound ATPase, and the dehydrogenases for succinate, malate, dihydroorotate, D-lactate, 6-phosphogluconate, and NADH.	NAD	205-209	ATPase	Escherichia coli	100-106
21176092-1	2011	Silent information regulator 2 (Sir2) orthologs are an evolutionarily conserved family of NAD-dependent protein deacetylases that regulate aging and longevity in model organisms.	NAD	90-93	sirtuin 2	Homo sapiens	32-36
20388721-4	2011	With respect to their immunological relevance, the importance and function of the major NAD+ metabolizing enzymes, namely CD38/CD157, ADP-ribosyltransferases (ARTs), poly-ADP-ribose-polymerases (PARPs), and sirtuins are summarized and roles of NAD+ and its main degradation product adenosine 5"-diphosphoribose (ADPR) in cell signaling are discussed.	NAD	88-92	CD38 molecule	Homo sapiens	122-126
6342464-5	1983	When the NADH had been measured, the NAD+ present in the extract was enzymatically converted to NADH by the addition of alcohol dehydrogenase, after which the second increase in light level was recorded.	NAD	9-13	aldo-keto reductase family 1 member A1	Homo sapiens	120-141
6342464-5	1983	When the NADH had been measured, the NAD+ present in the extract was enzymatically converted to NADH by the addition of alcohol dehydrogenase, after which the second increase in light level was recorded.	NAD	37-41	aldo-keto reductase family 1 member A1	Homo sapiens	120-141
6342464-5	1983	When the NADH had been measured, the NAD+ present in the extract was enzymatically converted to NADH by the addition of alcohol dehydrogenase, after which the second increase in light level was recorded.	NAD	96-100	aldo-keto reductase family 1 member A1	Homo sapiens	120-141
21178975-8	2011	The ratio of oxidized (NAD) to reduced (NADH) nicotinamide adenine dinucleotide in cardiac tissue, however, was significantly decreased in the hearts of renalase knockout mice, as was plasma NADH oxidase activity.	NAD	23-26	renalase, FAD-dependent amine oxidase	Mus musculus	153-161
6634835-3	1983	The changed ratio between the rates indicated that the ratio of NAD+ to NADH bound to alcohol dehydrogenase decreased several hundred times.	NAD	64-68	aldo-keto reductase family 1 member A1	Homo sapiens	86-107
21178975-8	2011	The ratio of oxidized (NAD) to reduced (NADH) nicotinamide adenine dinucleotide in cardiac tissue, however, was significantly decreased in the hearts of renalase knockout mice, as was plasma NADH oxidase activity.	NAD	40-44	renalase, FAD-dependent amine oxidase	Mus musculus	153-161
6634835-3	1983	The changed ratio between the rates indicated that the ratio of NAD+ to NADH bound to alcohol dehydrogenase decreased several hundred times.	NAD	72-76	aldo-keto reductase family 1 member A1	Homo sapiens	86-107
21178975-8	2011	The ratio of oxidized (NAD) to reduced (NADH) nicotinamide adenine dinucleotide in cardiac tissue, however, was significantly decreased in the hearts of renalase knockout mice, as was plasma NADH oxidase activity.	NAD	46-79	renalase, FAD-dependent amine oxidase	Mus musculus	153-161
21178975-9	2011	In vitro studies confirmed that renalase metabolizes NADH and catecholamines.	NAD	53-57	renalase, FAD-dependent amine oxidase	Mus musculus	32-40
21246601-9	2011	In neurons, Nampt positively modulated NAD(+) levels and thereby controlled SIRT1 activity.	NAD	39-45	sirtuin 1	Mus musculus	76-81
7165731-9	1982	The extent of reduction of cytochrome b in an anaerobic neutrophil homogenate containing NADH increased from 30% to 70% on illumination.	NAD	89-93	mitochondrially encoded cytochrome b	Homo sapiens	27-39
21134381-0	2011	Dynamic conformations of the CD38-mediated NAD cyclization captured in a single crystal.	NAD	43-46	CD38 molecule	Homo sapiens	29-33
7142187-11	1982	These findings suggest that regulation of glycolysis in round spermatids by glyceraldehyde-3-phosphate dehydrogenase is most likely and that glyceraldehyde-3-phosphate dehydrogenase is inhibited by the adenine nucleotides, particularly by 5"-AMP and ADP as inhibitors competitive with NAD.	NAD	285-288	glyceraldehyde-3-phosphate dehydrogenase	Rattus norvegicus	141-181
7142202-0	1982	Rat liver cytosolic malate dehydrogenase: purification, kinetic properties, role in control of free cytosolic NADH concentration.	NAD	110-114	malate dehydrogenase 1	Rattus norvegicus	10-40
7138916-2	1982	The NAD-dependent conversion of malate to lactate in human erythrocytes was studied by spin echo proton NMR.	NAD	4-7	spindlin 1	Homo sapiens	87-91
7295782-1	1981	Native and modified methemoglobin (beta-93-SH groups blocked) were reduced by NADH-dependent methemoglobin reductase in the absence and the presence of organic phosphate (inositol hexaphosphate).	NAD	78-82	hemoglobin subunit gamma 2	Homo sapiens	20-33
7295782-1	1981	Native and modified methemoglobin (beta-93-SH groups blocked) were reduced by NADH-dependent methemoglobin reductase in the absence and the presence of organic phosphate (inositol hexaphosphate).	NAD	78-82	hemoglobin subunit gamma 2	Homo sapiens	93-106
7228857-10	1981	These results strongly support the suggestion that membrane-bound cytochrome b5 of rat liver microsomes is an obligatory electron carrier from NADH to 4-methyl sterol oxidase.	NAD	143-147	cytochrome b5 type A	Rattus norvegicus	66-79
7225094-0	1981	Genetic variation in erythrocyte NAD levels in the mouse and its effect on glyceraldehyde phosphate dehydrogenase activity and stability.	NAD	33-36	glyceraldehyde-3-phosphate dehydrogenase	Mus musculus	75-113
7449761-2	1980	Methemoglobin reduction in human red cells involves successively an electron transport from NADH to a soluble form of cytochrome b5 (step 1) and from cytochrome b5 to methemoglobin (step 2).	NAD	92-96	hemoglobin subunit gamma 2	Homo sapiens	0-13
7403570-3	1980	It catalyzes oxidoreduction of prostaglandins at both the C-15 and C-9 positions, is more active with NADP than NAD, is inhibited by indomethacin and ethacrynic acid, and migrates as three bands on disc gel electrophoresis.	NAD	102-105	complement component C9	Oryctolagus cuniculus	67-70
7390994-0	1980	NADH- and NADPH-dependent reconstituted p-nitroanisole O-demethylation system containing cytochrome P-450 with high affinity for cytochrome b5.	NAD	0-4	cytochrome b5	Oryctolagus cuniculus	129-142
6161446-0	1980	Use of nicotinamide adenine dinucleotide (NAD)-dependent glucose-6-phosphate dehydrogenase in enzyme staining procedures.	NAD	7-40	glucose-6-phosphate dehydrogenase	Homo sapiens	57-90
6161446-0	1980	Use of nicotinamide adenine dinucleotide (NAD)-dependent glucose-6-phosphate dehydrogenase in enzyme staining procedures.	NAD	42-45	glucose-6-phosphate dehydrogenase	Homo sapiens	57-90
6161446-1	1980	Substitution of nicotinamide adenine dinucleotide dependent glucose-6-phosphate dehydrogenase for the nicotinamide adenine dinucleotide phosphate dependent enzyme has produced identical results in a number of enzyme-linked electrophoretic staining procedures.	NAD	16-49	glucose-6-phosphate dehydrogenase	Homo sapiens	60-93
20940012-6	2011	Increased nicotinamide adenine dinucleotide phosphate (NADHP) oxidase activity and apoptosis induction, regulated by mitochondrial signal pathway through an increased pro-apoptotic Bax/BcL(2) ratio and caspase 3 activity, were demonstrated.	NAD	10-43	BCL2 associated X, apoptosis regulator	Rattus norvegicus	181-184
21078873-4	2011	CtBP contains a central NAD(H) binding core domain that is homologous to D2 hydroxy acid dehydrogenase enzymes, as well as an unstructured C-terminal domain.	NAD	24-30	C-terminal Binding Protein	Drosophila melanogaster	0-4
21078873-5	2011	NAD(H) binding is important for CtBP function, but the significance of its intrinsic dehydrogenase activity, as well as that of the unstructured C terminus, is poorly understood.	NAD	0-6	C-terminal Binding Protein	Drosophila melanogaster	32-36
21858060-6	2011	SDHA is hyperacetylated in SIRT3 KO mice and SIRT3 directly deacetylates SDHA in a NAD-dependent manner.	NAD	83-86	sirtuin 3	Mus musculus	45-50
21179242-4	2010	Retinal pigment epithelial (RPE) cells were shown to be sensitive to oxidative stress, and zinc, causing loss of nicotinamide adenine dinucleotide (NAD+) and adenine triphosphate (ATP), which was prevented by pyruvate and nicotinamide.	NAD	113-146	ribulose-5-phosphate-3-epimerase	Rattus norvegicus	28-31
21179242-4	2010	Retinal pigment epithelial (RPE) cells were shown to be sensitive to oxidative stress, and zinc, causing loss of nicotinamide adenine dinucleotide (NAD+) and adenine triphosphate (ATP), which was prevented by pyruvate and nicotinamide.	NAD	148-152	ribulose-5-phosphate-3-epimerase	Rattus norvegicus	28-31
20940631-5	2010	Pharmacological inhibition of kynurenine 3-hydroxylase and kynureninase led to decreased cellular NAD levels and increased apoptosis in the hippocampus.	NAD	98-101	kynurenine 3-monooxygenase	Homo sapiens	30-54
20798610-4	2010	In response to stress, FoxO1 dissociated from an NAD(+)-dependent histone deacetylase SIRT2 and FoxO1 thus became acetylated and in turn bound to Atg7, an E1-like protein, to influence the autophagic process leading to cell death.	NAD	49-55	sirtuin 2	Homo sapiens	86-91
20543840-5	2010	In response to stress, FoxO1 was acetylated by dissociation from sirtuin-2 (SIRT2), a NAD(+)-dependent histone deacetylase, and the acetylated FoxO1 bound to Atg7, an E1-like protein, to influence the autophagic process leading to cell death.	NAD	86-92	sirtuin 2	Homo sapiens	65-74
20543840-5	2010	In response to stress, FoxO1 was acetylated by dissociation from sirtuin-2 (SIRT2), a NAD(+)-dependent histone deacetylase, and the acetylated FoxO1 bound to Atg7, an E1-like protein, to influence the autophagic process leading to cell death.	NAD	86-92	sirtuin 2	Homo sapiens	76-81
20620956-5	2010	During hypoxia, SIRT1 was downregulated due to decreased NAD(+) levels, which allowed the acetylation and activation of HIF-1alpha.	NAD	57-63	sirtuin 1	Mus musculus	16-21
20620956-5	2010	During hypoxia, SIRT1 was downregulated due to decreased NAD(+) levels, which allowed the acetylation and activation of HIF-1alpha.	NAD	57-63	hypoxia inducible factor 1, alpha subunit	Mus musculus	120-130
20056102-0	2010	Sodium-translocating NADH:quinone oxidoreductase as a redox-driven ion pump.	NAD	21-25	crystallin zeta	Homo sapiens	26-48
7370273-0	1980	Characterization of a NADH:flavin oxidoreductase induced by cholic acid in a 7 alpha-dehydroxylating intestinal Eubacterium species.	NAD	22-26	thioredoxin reductase 1	Homo sapiens	34-48
7370273-7	1980	NADH:flavin oxidoreductase showed an absolute specificity for NADH as electron donor.	NAD	0-4	thioredoxin reductase 1	Homo sapiens	12-26
6999874-4	1980	Seven different cell lines have been studied and found to contain an enzymatic activity identified as alcohol dehydrogenase by the following criteria: it is NAD+-dependent, the Km for ethanol is like human liver, it is completely inhibited by 25 microM 4-pentylpyrazole.	NAD	157-161	aldo-keto reductase family 1 member A1	Homo sapiens	102-123
488057-7	1979	The NADH or NADPH production is measured and utilized for the calculation of the guanase activity.	NAD	4-8	guanine deaminase	Homo sapiens	81-88
697732-3	1978	Steady-state kinetic studies of methylated liver alcohol dehydrogenase over a wide range of alcohol concentrations suggest that alcohol oxidation proceeds via a random addition of coenzyme and substrate with a pathway for the formation of the productive enzyme-NADH-alcohol complex.	NAD	261-265	aldo-keto reductase family 1 member A1	Homo sapiens	49-70
259500-5	1978	A stereospecific assay was used to measure D-lactate in human plasma; it involved the spectrophotometric analysis of NADH at 340 nm catalysed by D-lactate dehydrogenase (D-lactate:NAD+ oxidoreductase; EC 1.1.1.28) from Lactobacillus leichmannii.	NAD	117-121	lactate dehydrogenase D	Homo sapiens	145-168
926709-3	1977	Under physiological conditions ascorbic acid induced methemoglobin reduction is far less important than reduction by the NADH dependent methemoglobin reductase system.	NAD	121-125	hemoglobin subunit gamma 2	Homo sapiens	136-149
195838-0	1977	8-Spin-label nicotinamide adenine dinucleotide, synthesis and properties of a new spin-labelled coenzyme.	NAD	13-46	spindlin 1	Homo sapiens	2-6
195838-0	1977	8-Spin-label nicotinamide adenine dinucleotide, synthesis and properties of a new spin-labelled coenzyme.	NAD	13-46	spindlin 1	Homo sapiens	82-86
184819-1	1976	The stereospecificity of swine renal NAD+-dependent 15-hydroxyprostaglandin dehydrogenase has been determined.	NAD	37-40	carbonyl reductase [NADPH] 1	Sus scrofa	52-89
182529-2	1976	In a second step LDH-X is bound to the same matrix at lower NADH and NaCl concentrations and the pure enzyme can subsequently be eluted.	NAD	60-64	lactate dehydrogenase C	Mus musculus	17-22
181253-3	1976	The rate constants for NADH binding and dissociation for carboxymethylated alcohol dehydrogenase have been determined and compared to those for the native enzyme.	NAD	23-27	aldo-keto reductase family 1 member A1	Homo sapiens	75-96
132427-2	1976	Reduced nicotinamide adenine dinucleotide (NADH) oxidase (reduced NAD: oxidoreductase, EC 1.6.99.3) and Mg2+-Ca2+-activated adenosine triphosphatase (ATP phosphohydrolase, EC 3.6.1.3), which are normally localized to the inner surface of the cytoplasmic membrane, were 50% acceesible to their polar substrates in these vesicles.	NAD	8-41	oxidoreductase	Escherichia coli	71-85
179563-0	1976	Cooperativity and noncooperativity in the binding of NAD analogues to rabbit muscle glyceraldehyde-3-phosphate dehydrogenase.	NAD	53-56	glyceraldehyde-3-phosphate dehydrogenase	Oryctolagus cuniculus	84-124
188292-1	1976	Binding of four molecules of NAD to pig muscle glyceraldehyde-3-phosphate dehydrogenase decreases the apparent reactivity of Cys-153 -- a residue exposed only temporarily -- towards PMB in all four subunits of the enzyme.	NAD	29-32	glyceraldehyde-3-phosphate dehydrogenase	Sus scrofa	47-87
1194829-6	1975	The opposite was found for the relative weights of uterus and seminal vesicles and renal NADH-dependent 3alpha-HSD activities.	NAD	89-93	aldo-keto reductase family 1, member C14	Rattus norvegicus	104-114
1194829-9	1975	But whereas intact male rats had higher NADH-dependent 3alpha-HSD activities than female rats the opposite was found after gonadectomy.	NAD	40-44	aldo-keto reductase family 1, member C14	Rattus norvegicus	55-65
1175656-7	1975	On the other hand, the oxidation of cytochrome b5 by hydroperoxides is readily demonstrable in microsomal fractions in presence of NADH.	NAD	131-135	cytochrome b5 type A	Rattus norvegicus	36-49
171213-2	1975	A complete initial rate analysis of the forward reaction catalyzed by 15-hydroxyprostaglandin dehydrogenase from human term placenta was carried out at pH 7.4 (100mM triethanolamine) with the substrates NAD, and the prostaglandins E1, E2 and F2alpha.	NAD	203-206	carbonyl reductase 1	Homo sapiens	70-107
170765-1	1975	Alcohol dehydrogenase from horse (isoenzyme SS and ES, but not EE), rat and human liver were found to catalyze the NAD-dependent oxidation of 3beta-hydroxy groups in 5alpha- and 5beta-steroids of the C19, C21, and C24 series.	NAD	115-118	aldo-keto reductase family 1 member A1	Homo sapiens	0-21
20230777-3	2010	There are several possible electrons pathways but we show that most of them take the route defined by the successive sites and redox centres: NADH+ site-FMN-N3-N1b-N4-N5-N6a-N6b-N2-Q site.	NAD	142-146	formin 1	Homo sapiens	153-156
1083207-4	1975	A.LOx possesses two different mechanisms for the oxidation of formate: (1) the constitutive formate oxidase which is present in the particulate fraction of oxalate-grown and succinate-plus-formate-grown cells; (2) the inducible NAD-linked formate dehydrogenase present in the 100 000 x g supernatant fraction of the cell-free extracts of oxalate-grown cells alone.	NAD	228-231	lysyl oxidase	Homo sapiens	2-5
4355308-0	1973	Chemical and structural relationships of NAD+ and platinum binding to malate dehydrogenase.	NAD	41-45	malic enzyme 1	Homo sapiens	70-90
20463219-0	2010	Nicotinamide adenine dinucleotide-dependent binding of the neuronal Ca2+ sensor protein GCAP2 to photoreceptor synaptic ribbons.	NAD	0-33	guanylate cyclase activator 1B	Homo sapiens	88-93
4348919-2	1973	Evidence that the proposed control of glucose 6-phosphate dehydrogenase by reduced diphosphopyridine nucleotide is an instrumental artifact.	NAD	83-111	glucose-6-phosphate dehydrogenase	Homo sapiens	38-71
20354108-1	2010	Sirtuin 1 (SirT1) is the largest of the seven members of the sirtuin family of class III nicotinamide adenine dinucleotide (NAD(+))-dependent protein deacetylases, whose activation is beneficial for metabolic, neurodegenerative, inflammatory and neoplastic diseases, and augments life span in model organisms (Finkel et al., 2009; Lavu et al., 2008).	NAD	89-122	sirtuin 1	Mus musculus	0-9
5544661-0	1971	Temperature-jump study of the interaction of malate dehydrogenase with reduced nicotinamide-adenine dinucleotide and D-malate.	NAD	79-112	malic enzyme 1	Homo sapiens	45-65
20354108-1	2010	Sirtuin 1 (SirT1) is the largest of the seven members of the sirtuin family of class III nicotinamide adenine dinucleotide (NAD(+))-dependent protein deacetylases, whose activation is beneficial for metabolic, neurodegenerative, inflammatory and neoplastic diseases, and augments life span in model organisms (Finkel et al., 2009; Lavu et al., 2008).	NAD	89-122	sirtuin 1	Mus musculus	11-16
20354108-1	2010	Sirtuin 1 (SirT1) is the largest of the seven members of the sirtuin family of class III nicotinamide adenine dinucleotide (NAD(+))-dependent protein deacetylases, whose activation is beneficial for metabolic, neurodegenerative, inflammatory and neoplastic diseases, and augments life span in model organisms (Finkel et al., 2009; Lavu et al., 2008).	NAD	124-129	sirtuin 1	Mus musculus	0-9
20354108-1	2010	Sirtuin 1 (SirT1) is the largest of the seven members of the sirtuin family of class III nicotinamide adenine dinucleotide (NAD(+))-dependent protein deacetylases, whose activation is beneficial for metabolic, neurodegenerative, inflammatory and neoplastic diseases, and augments life span in model organisms (Finkel et al., 2009; Lavu et al., 2008).	NAD	124-129	sirtuin 1	Mus musculus	11-16
20226541-0	2010	Ten years of NAD-dependent SIR2 family deacetylases: implications for metabolic diseases.	NAD	13-16	sirtuin 2	Homo sapiens	27-31
5277094-2	1971	Since the former pathway utilizes NADH for reduction of the C-2 carbonyl, while the latter requires NADPH, we were able to compare the relative participation of the two pathways for phospholipid synthesis by measuring the incorporation of radioactivity from tritiumlabeled NADH and NADPH into C-2 of lipid glycerol.	NAD	34-38	complement component 2 (within H-2S)	Mus musculus	60-63
4316548-1	1970	By competition with lactate dehydrogenase (LDH) for nicotinamide adenine dinucleotide (NAD), commonly occurring intracellular proteins, such as glyceraldehyde-3-phosphate dehydrogenase, malate dehydrogenase, and albumin, can protect LDH-1 and LDH-5 from inhibition and ternary complex formation with NAD and pyruvate.	NAD	87-90	malic enzyme 1	Homo sapiens	186-206
4316548-1	1970	By competition with lactate dehydrogenase (LDH) for nicotinamide adenine dinucleotide (NAD), commonly occurring intracellular proteins, such as glyceraldehyde-3-phosphate dehydrogenase, malate dehydrogenase, and albumin, can protect LDH-1 and LDH-5 from inhibition and ternary complex formation with NAD and pyruvate.	NAD	300-303	malic enzyme 1	Homo sapiens	186-206
20226541-1	2010	Since the discovery of NAD-dependent deacetylase activity of the silent information regulator-2 (SIR2) family ("sirtuins"), many exciting connections between protein deacetylation and energy metabolism have been revealed.	NAD	23-26	sirtuin 2	Homo sapiens	65-95
20226541-1	2010	Since the discovery of NAD-dependent deacetylase activity of the silent information regulator-2 (SIR2) family ("sirtuins"), many exciting connections between protein deacetylation and energy metabolism have been revealed.	NAD	23-26	sirtuin 2	Homo sapiens	97-101
4313530-0	1970	The effect of NAD+ on the catalytic efficiency of glyceraldehyde-3-phosphate dehydrogenase from rabbit muscle.	NAD	14-18	glyceraldehyde-3-phosphate dehydrogenase	Oryctolagus cuniculus	50-90
20185821-1	2010	Sirtuin 1 (SIRT1) is a NAD-dependent deacetylase that is critically involved in diverse cellular processes including metabolic disease, cancer, and possibly aging.	NAD	23-26	sirtuin 1	Mus musculus	0-9
5411644-0	1970	NADH diaphorase: an inherited variant associated with normal methemoglobin reduction.	NAD	0-4	hemoglobin subunit gamma 2	Homo sapiens	61-74
20185821-1	2010	Sirtuin 1 (SIRT1) is a NAD-dependent deacetylase that is critically involved in diverse cellular processes including metabolic disease, cancer, and possibly aging.	NAD	23-26	sirtuin 1	Mus musculus	11-16
20127344-7	2010	NADP+-dependent IDH activity was determined in comparison with activity of NAD+-dependent IDH and all other NADPH-producing dehydrogenases, glucose-6-phosphate dehydrogenase, 6-phosphogluconate dehydrogenase, malate dehydrogenase, and hexose-6-phosphate dehydrogenase.	NAD	0-3	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	16-19
14114510-0	1964	CHEMICAL RELAXATION OF THE REACTION OF MALATE DEHYDROGENASE WITH REDUCED NICOTINAMIDE ADENINE DINUCLEOTIDE DETERMINED BY FLUORESCENCE DETECTION.	NAD	73-106	malic enzyme 1	Homo sapiens	39-59
20127344-9	2010	twofold diminished NADP+-dependent IDH activity, whereas activity of NAD+-dependent IDH and the other NADP+-dependent dehydrogenases was not affected in situ in glioblastoma.	NAD	69-73	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	84-87
20300811-11	2010	The production of ROS during reverse electron transport can be prevented either by rotenone or by the oxidation of NADH by complex I.	NAD	115-119	ros	Drosophila melanogaster	18-21
14067907-6	1963	It was shown first that both nicotinamide and diphosphopyridine nucleotide (DPN), compounds along the pathway initiated by TP, are each as effective as cortisone in protecting mice against lethality of different amounts of endotoxin.	NAD	46-74	tryptophan 2,3-dioxygenase	Mus musculus	123-125
14067907-6	1963	It was shown first that both nicotinamide and diphosphopyridine nucleotide (DPN), compounds along the pathway initiated by TP, are each as effective as cortisone in protecting mice against lethality of different amounts of endotoxin.	NAD	76-79	tryptophan 2,3-dioxygenase	Mus musculus	123-125
20054824-8	2010	Interestingly, inhibitory analysis (pharmacological antagonists and receptor sequence specific siRNAs) indicates the participation of both P2Y1 and P2Y11 receptors in beta-NAD-induced TER increase.	NAD	167-175	purinergic receptor P2Y1	Homo sapiens	139-143
13436414-1	1957	V.  Diphosphopyridine nucleotide ion binding abilities of alcohol dehydrogenase and its zinc complex].	NAD	4-32	aldo-keto reductase family 1 member A1	Homo sapiens	58-79
20054824-8	2010	Interestingly, inhibitory analysis (pharmacological antagonists and receptor sequence specific siRNAs) indicates the participation of both P2Y1 and P2Y11 receptors in beta-NAD-induced TER increase.	NAD	167-175	purinergic receptor P2Y11	Homo sapiens	148-153
19796917-3	2010	Diminished activity of the CD38 ectoenzyme that normally represents a counter-regulatory competitor for the NAD substrate represents one mechanism enhancing ART2.2 activity.	NAD	108-111	ADP-ribosyltransferase 2b	Mus musculus	157-163
33862368-7	2021	Increase in expression levels of proteins related to oxidative phosphorylation such as NADH:ubiquinone oxidoreductase core subunit V1 (Ndufv1) was observed in LXRbeta-knockdown Dami cells.	NAD	87-91	NADH:ubiquinone oxidoreductase core subunit V1	Homo sapiens	135-141
20070122-3	2010	Using a proteomic approach and validation by coexpression analysis, we illustrate that overexpression of FADD-DED in E. coli invokes protein expression changes that facilitate conversion of pro-oxidant NADH into antioxidant NADPH.	NAD	202-206	Fas associated via death domain	Homo sapiens	105-109
34049472-0	2021	Apigenin Alleviates Oxidative Stress-Induced Cellular Senescence via Modulation of the SIRT1-NAD[Formula: see text]-CD38 Axis.	NAD	93-96	sirtuin 1	Homo sapiens	87-92
34029951-0	2021	Notoginsenoside R1 activates the NAMPT-NAD+-SIRT1 cascade to promote postischemic angiogenesis by modulating Notch signaling.	NAD	39-43	sirtuin 1	Homo sapiens	44-49
34029951-14	2021	The promotion of R1 on angiogenesis were associated with the NAMPT-NAD+-SIRT1 cascade and Notch/VEGFR-2 signaling pathway, which was partially eliminated by inhibitors of NAMPT and SIRT1.	NAD	67-71	sirtuin 1	Homo sapiens	72-77
33528041-8	2021	Nmnat3 gene expression is suppressed by HIF1alpha, a transcription factor that is stabilized by mitochondrial translation dysfunction, suggesting that HIF1alpha-Nmnat3-mediated NAD+ production is important for lysosomal function.	NAD	177-181	nicotinamide nucleotide adenylyltransferase 3	Mus musculus	0-6
33528041-8	2021	Nmnat3 gene expression is suppressed by HIF1alpha, a transcription factor that is stabilized by mitochondrial translation dysfunction, suggesting that HIF1alpha-Nmnat3-mediated NAD+ production is important for lysosomal function.	NAD	177-181	nicotinamide nucleotide adenylyltransferase 3	Mus musculus	161-167
20060806-1	2010	Sirtuin1 (SIRT1) deacetylase and poly(ADP-ribose)-polymerase-1 (PARP-1) respond to environmental cues, and both require NAD(+) cofactor for their enzymatic activities.	NAD	120-126	sirtuin 1	Mus musculus	0-8
33795658-4	2021	The NAD+-dependent Sirtuin1 (Sirt1) deacetylates FoxOs and beta-catenin in osteoblast progenitors and, thereby, increases bone mass.	NAD	4-8	catenin (cadherin associated protein), beta 1	Mus musculus	59-71
20060806-1	2010	Sirtuin1 (SIRT1) deacetylase and poly(ADP-ribose)-polymerase-1 (PARP-1) respond to environmental cues, and both require NAD(+) cofactor for their enzymatic activities.	NAD	120-126	sirtuin 1	Mus musculus	10-15
33795658-7	2021	The NAD+ precursor nicotinamide riboside (NR) abrogated FoxO1 and beta-catenin acetylation and several marker of cellular senescence, and increased the osteoblastogenic capacity of cells from old mice.	NAD	4-8	catenin (cadherin associated protein), beta 1	Mus musculus	66-78
20060806-2	2010	However, the functional link between environmental/oxidative stress-mediated activation of PARP-1 and SIRT1 through NAD(+) cofactor availability is not known.	NAD	116-122	sirtuin 1	Mus musculus	102-107
33597293-3	2021	Here, we show that IFN signaling, present in a subset of PDAC tumors, substantially lowers NAD(H) levels through up-regulating the expression of NAD-consuming enzymes PARP9, PARP10, and PARP14.	NAD	91-94	poly(ADP-ribose) polymerase family member 14	Homo sapiens	186-192
20060806-3	2010	We investigated whether NAD(+) depletion by PARP-1 activation plays a role in environmental stimuli/oxidant-induced reduction in SIRT1 activity.	NAD	24-30	sirtuin 1	Mus musculus	129-134
19370397-10	2010	These results suggest that NAD affected lifespan through the activation of SIR-2.1 and DAF-16 along a signaling pathway, namely insulin-like signalling pathway (at least parts of it), different from that associated with caloric restriction.	NAD	27-30	Fork-head domain-containing protein;Forkhead box protein O	Caenorhabditis elegans	87-93
33503437-5	2021	Disruption of one of these Fos/AP-1 targets, NAD(+)-consuming mono-ADP-ribosyl-transferase 1 (Art1), in SCs delays cell cycle entry and impedes progenitor cell expansion and muscle regeneration.	NAD	45-51	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	27-30
33503437-5	2021	Disruption of one of these Fos/AP-1 targets, NAD(+)-consuming mono-ADP-ribosyl-transferase 1 (Art1), in SCs delays cell cycle entry and impedes progenitor cell expansion and muscle regeneration.	NAD	45-51	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	31-35
19711072-2	2010	Overexpression of the genes coding for NAD(+)-specific glutamate dehydrogenase (GDH2) of S. cerevisiae or NADPH-utilising glyceraldehyde-3-phosphate dehydrogenase (gapB) of Bacillus subtilis enabled growth of the pgi1 mutant strains on D-glucose.	NAD	39-45	glutamate dehydrogenase (NAD(+))	Saccharomyces cerevisiae S288C	80-84
19568269-5	2009	We detected two novel homozygous mutations in HPGD in these families: a missense mutation affecting the NAD(+) binding motif and a frameshift mutation.	NAD	104-110	15-hydroxyprostaglandin dehydrogenase	Homo sapiens	46-50
33537003-3	2020	Sirtuin 1 (SIRT1), a nicotinamide adenosine dinucleotide (NAD+)-dependent deacetylase, has been reported to not only deacetylate histones to modulate chromatin function but also deacetylate numerous transcription factors to regulate the expression of target genes, both positively and negatively.	NAD	58-61	sirtuin 1	Homo sapiens	0-9
33537003-3	2020	Sirtuin 1 (SIRT1), a nicotinamide adenosine dinucleotide (NAD+)-dependent deacetylase, has been reported to not only deacetylate histones to modulate chromatin function but also deacetylate numerous transcription factors to regulate the expression of target genes, both positively and negatively.	NAD	58-61	sirtuin 1	Homo sapiens	11-16
33290962-9	2021	Treatment with NAD + also inhibited the expressions of NLRP3 and modulated the differentiation of Th1 and Th17 cells, reduced the expressions of the pro-inflammatory factors IL-1beta, IL-2, IL-18, IFN-gamma and IL-17, and increased the expression of anti-inflammatory IL-10.	NAD	15-20	interleukin 17A	Mus musculus	211-216
19820182-9	2009	We demonstrate that nicotinamide phosphoribosyltransferase (Nampt), the equivalent enzyme in nicotinamide recycling to NAD(+) in vertebrates, can functionally substitute for PNC-1.	NAD	119-125	Isochorismatase domain-containing protein	Caenorhabditis elegans	174-179
33371997-5	2021	Augmentation of SIRT1 may be carried out using dietary means such as nicotinamide adenine dinucleotide (NAD) supplementation and/or ketogenic diet.	NAD	69-102	sirtuin 1	Homo sapiens	16-21
33371997-5	2021	Augmentation of SIRT1 may be carried out using dietary means such as nicotinamide adenine dinucleotide (NAD) supplementation and/or ketogenic diet.	NAD	104-107	sirtuin 1	Homo sapiens	16-21
33392072-3	2020	Here we demonstrated that DGUOK regulated NAD+ biogenesis.	NAD	42-46	deoxyguanosine kinase	Homo sapiens	26-31
33392072-4	2020	Depletion of the DGUOK significantly decreased NAD+ level.	NAD	47-51	deoxyguanosine kinase	Homo sapiens	17-22
33392072-5	2020	Furthermore, knockout of the DGUOK considerably reduced expression of the NMNAT2, a key molecule controlling NAD+ synthesis, at both mRNA and protein levels.	NAD	109-113	deoxyguanosine kinase	Homo sapiens	29-34
33392072-6	2020	Ectopic expression of the NMNAT2 abrogated the effect of knockdown of DGUOK on NAD+.	NAD	79-83	deoxyguanosine kinase	Homo sapiens	70-75
33392072-9	2020	Our study suggested that DGUOK regulates NAD+ in a NMNAT2 dependent manner and DGUOK-NMNAT2-NAD+ axis could be a potential therapeutic target in lung adenocarcinoma.	NAD	41-45	deoxyguanosine kinase	Homo sapiens	25-30
33392072-9	2020	Our study suggested that DGUOK regulates NAD+ in a NMNAT2 dependent manner and DGUOK-NMNAT2-NAD+ axis could be a potential therapeutic target in lung adenocarcinoma.	NAD	92-96	deoxyguanosine kinase	Homo sapiens	79-84
33326496-1	2020	The ability of CD38 and CD157 to utilize nicotinamide adenine dinucleotide (NAD) has received much attention because the aging-induced elevation of CD38 expression plays a role in the senescence-related decline in NAD levels.	NAD	41-74	CD38 antigen	Mus musculus	15-19
19838201-5	2009	The expression of several forkhead box O1 (Foxo1) target genes increased in the DKO liver, including heme oxygenase-1 (Hmox1), which disrupts complex III and IV of the respiratory chain and lowers the NAD(+)/NADH ratio and ATP production.	NAD	201-207	forkhead box O1	Mus musculus	43-48
33326496-1	2020	The ability of CD38 and CD157 to utilize nicotinamide adenine dinucleotide (NAD) has received much attention because the aging-induced elevation of CD38 expression plays a role in the senescence-related decline in NAD levels.	NAD	41-74	CD38 antigen	Mus musculus	148-152
33326496-1	2020	The ability of CD38 and CD157 to utilize nicotinamide adenine dinucleotide (NAD) has received much attention because the aging-induced elevation of CD38 expression plays a role in the senescence-related decline in NAD levels.	NAD	76-79	CD38 antigen	Mus musculus	15-19
33326496-1	2020	The ability of CD38 and CD157 to utilize nicotinamide adenine dinucleotide (NAD) has received much attention because the aging-induced elevation of CD38 expression plays a role in the senescence-related decline in NAD levels.	NAD	76-79	CD38 antigen	Mus musculus	148-152
33326496-1	2020	The ability of CD38 and CD157 to utilize nicotinamide adenine dinucleotide (NAD) has received much attention because the aging-induced elevation of CD38 expression plays a role in the senescence-related decline in NAD levels.	NAD	214-217	CD38 antigen	Mus musculus	15-19
33326496-1	2020	The ability of CD38 and CD157 to utilize nicotinamide adenine dinucleotide (NAD) has received much attention because the aging-induced elevation of CD38 expression plays a role in the senescence-related decline in NAD levels.	NAD	214-217	CD38 antigen	Mus musculus	148-152
19838201-5	2009	The expression of several forkhead box O1 (Foxo1) target genes increased in the DKO liver, including heme oxygenase-1 (Hmox1), which disrupts complex III and IV of the respiratory chain and lowers the NAD(+)/NADH ratio and ATP production.	NAD	208-212	forkhead box O1	Mus musculus	43-48
19838201-7	2009	Deletion of hepatic Foxo1 in DKO liver normalized the expression of Hmox1 and the NAD(+)/NADH ratio, reduced Ppargc-1alpha acetylation and restored mitochondrial oxidative metabolism and biogenesis.	NAD	82-88	forkhead box O1	Mus musculus	20-25
19838201-7	2009	Deletion of hepatic Foxo1 in DKO liver normalized the expression of Hmox1 and the NAD(+)/NADH ratio, reduced Ppargc-1alpha acetylation and restored mitochondrial oxidative metabolism and biogenesis.	NAD	89-93	forkhead box O1	Mus musculus	20-25
19640846-3	2009	Although ADPRC and CD38 share a common evolutionary ancestor, their enzymatic functions toward NAD and cADPR homeostasis have evolved divergently.	NAD	95-98	CD38 molecule	Homo sapiens	19-23
33326496-9	2020	We discuss the distinct differences in aging effects from the perspective of inhibition of NAD metabolism in CD157 and CD38 KO mice, which may contribute to differential behavioral changes during aging.	NAD	91-94	CD38 antigen	Mus musculus	119-123
19672559-1	2009	Poly(ADP-ribose) polymerase-1 (Parp-1) and the protein deacetylase SirT1 are two of the most effective NAD(+)-consuming enzymes in the cell with key functions in genome integrity and chromatin-based pathways.	NAD	103-109	sirtuin 1	Mus musculus	67-72
33319867-5	2020	Treatment with NAD + precursor nicotinamide increases the intracellular NAD + level and re-balances the NAD + /NADH ratio, with enhanced Sirt-1 activity in hMSCs at high passage, partially restores mitochondrial fitness and rejuvenates senescent hMSCs.	NAD	15-20	sirtuin 1	Homo sapiens	137-143
19596275-6	2009	DPN also increased GluR2 expression in the other lamina of the CA1.	NAD	0-3	carbonic anhydrase 1	Rattus norvegicus	63-66
19661458-1	2009	RATIONALE: NAD+ acts not only as a cofactor for cellular respiration but also as a substrate for NAD(+)-dependent enzymes, such as Sirt1.	NAD	11-15	sirtuin 1	Mus musculus	131-136
19661458-1	2009	RATIONALE: NAD+ acts not only as a cofactor for cellular respiration but also as a substrate for NAD(+)-dependent enzymes, such as Sirt1.	NAD	97-103	sirtuin 1	Mus musculus	131-136
33098904-1	2020	NAD synthetase (NadE) catalyzes the last step in NAD biosynthesis, transforming deamido-NAD+ into NAD+ by a two-step reaction with co-substrates ATP and amide donor ammonia.	NAD	0-3	AT695_RS07645	Staphylococcus aureus	16-20
33098904-1	2020	NAD synthetase (NadE) catalyzes the last step in NAD biosynthesis, transforming deamido-NAD+ into NAD+ by a two-step reaction with co-substrates ATP and amide donor ammonia.	NAD	88-92	AT695_RS07645	Staphylococcus aureus	0-14
19680552-1	2009	SIRT1, an NAD(+) (nicotinamide adenine dinucleotide)-dependent deacetylase, protects cells from stress-induced apoptosis, and its orthologues delay aging in lower eukaryotes.	NAD	10-16	sirtuin 1	Mus musculus	0-5
33098904-1	2020	NAD synthetase (NadE) catalyzes the last step in NAD biosynthesis, transforming deamido-NAD+ into NAD+ by a two-step reaction with co-substrates ATP and amide donor ammonia.	NAD	88-92	AT695_RS07645	Staphylococcus aureus	16-20
33199755-3	2020	The PARP substrate NAD+ is synthesized from 5-phosphoribose-1-pyrophosphate (PRPP), and we found that treating cells for 6 h with cisplatin reduced intracellular PRPP availability.	NAD	19-23	poly (ADP-ribose) polymerase family, member 1	Mus musculus	4-8
19530703-1	2009	Homoisocitrate dehydrogenase (HIcDH) catalyzes the Mg2+- and K+-dependent oxidative decarboxylation of homoisocitrate to alpha-ketoadipate using NAD as the oxidant.	NAD	145-148	homoisocitrate dehydrogenase	Saccharomyces cerevisiae S288C	0-28
33152110-5	2021	RESULTS: Our study found sirtuin1 (SIRT1), an NAD-dependent deacetylase, to be a direct target of miR-211 - the most significantly downregulated miRNA in lesional epidermis.	NAD	46-49	sirtuin 1	Homo sapiens	25-33
33152110-5	2021	RESULTS: Our study found sirtuin1 (SIRT1), an NAD-dependent deacetylase, to be a direct target of miR-211 - the most significantly downregulated miRNA in lesional epidermis.	NAD	46-49	sirtuin 1	Homo sapiens	35-40
33152110-5	2021	RESULTS: Our study found sirtuin1 (SIRT1), an NAD-dependent deacetylase, to be a direct target of miR-211 - the most significantly downregulated miRNA in lesional epidermis.	NAD	46-49	microRNA 211	Homo sapiens	98-105
19530703-1	2009	Homoisocitrate dehydrogenase (HIcDH) catalyzes the Mg2+- and K+-dependent oxidative decarboxylation of homoisocitrate to alpha-ketoadipate using NAD as the oxidant.	NAD	145-148	homoisocitrate dehydrogenase	Saccharomyces cerevisiae S288C	30-35
32697331-3	2020	The CYB5R3 gene encodes cytochrome b5 reductase 3, which converts methemoglobin to hemoglobin through oxidation of NADH.	NAD	115-119	hemoglobin subunit gamma 2	Homo sapiens	66-79
18932012-5	2009	The products NAD(+) and NADPH are required in many critical biological processes, e.g., NAD(+) is used by histone deacetylase Sir2 which regulates longevity in different species.	NAD	13-19	sirtuin 1	Mus musculus	126-130
32890737-6	2020	A primary determinant of the cellular redox state is nicotinamide adenine dinucleotide (NAD+), whose levels drive an inverse relationship between xanthine oxidase and sirtuin-1 (SIRT1), a nutrient deprivation sensor that exerts important antioxidant and cardioprotective effects.	NAD	53-86	sirtuin 1	Homo sapiens	167-176
32890737-6	2020	A primary determinant of the cellular redox state is nicotinamide adenine dinucleotide (NAD+), whose levels drive an inverse relationship between xanthine oxidase and sirtuin-1 (SIRT1), a nutrient deprivation sensor that exerts important antioxidant and cardioprotective effects.	NAD	53-86	sirtuin 1	Homo sapiens	178-183
18932012-5	2009	The products NAD(+) and NADPH are required in many critical biological processes, e.g., NAD(+) is used by histone deacetylase Sir2 which regulates longevity in different species.	NAD	88-94	sirtuin 1	Mus musculus	126-130
32890737-6	2020	A primary determinant of the cellular redox state is nicotinamide adenine dinucleotide (NAD+), whose levels drive an inverse relationship between xanthine oxidase and sirtuin-1 (SIRT1), a nutrient deprivation sensor that exerts important antioxidant and cardioprotective effects.	NAD	88-92	sirtuin 1	Homo sapiens	167-176
32890737-6	2020	A primary determinant of the cellular redox state is nicotinamide adenine dinucleotide (NAD+), whose levels drive an inverse relationship between xanthine oxidase and sirtuin-1 (SIRT1), a nutrient deprivation sensor that exerts important antioxidant and cardioprotective effects.	NAD	88-92	sirtuin 1	Homo sapiens	178-183
19491102-5	2009	Here we demonstrate that the NAD(+)-dependent deacetylase sirtuin 1 (Sirt1) functionally and physically interacts with Dot1 to enhance the distributive activity of Dot1 on H3K79 methylation and thereby represses alpha-ENaC transcription in mIMCD3 cells.	NAD	29-35	sodium channel, nonvoltage-gated 1 alpha	Mus musculus	212-222
32758884-5	2020	Further consumption of NAD+ in a pre-existent depleted state is more likely to cause progression to the hyperinflammatory stage of the disease through its limiting effects on the production of SIRT1.	NAD	23-27	sirtuin 1	Homo sapiens	193-198
19211805-6	2009	In contrast to E2, acute treatment of superovulating rats with a high dose of CC or the ESR2-selective agonist 2,3-bis (4-hydroxyphenyl)-propionitrile (DPN) significantly delayed the transport of oocyte-cumulus complexes through the fallopian tube.	NAD	152-155	estrogen receptor 2	Rattus norvegicus	88-92
33063092-9	2020	It conserves NAD+ and prevents ATP depletion by PARP 1 and Sirtuin 1 (silent mating type information regulation 2 homologue 1) inhibition, enhances NAD+ synthesis, and hence that of NADP+ which is a stronger PARP inhibitor, reverses lung injury caused by ischaemia/reperfusion, inhibits proinflammatory cytokines and is effective against HIV infection.	NAD	13-17	sirtuin 1	Homo sapiens	59-68
19319672-4	2009	In the current studies, NAD metabolism was evaluated in HPRT gene knock-out mice.	NAD	24-27	hypoxanthine guanine phosphoribosyl transferase	Mus musculus	56-60
33063092-9	2020	It conserves NAD+ and prevents ATP depletion by PARP 1 and Sirtuin 1 (silent mating type information regulation 2 homologue 1) inhibition, enhances NAD+ synthesis, and hence that of NADP+ which is a stronger PARP inhibitor, reverses lung injury caused by ischaemia/reperfusion, inhibits proinflammatory cytokines and is effective against HIV infection.	NAD	148-152	sirtuin 1	Homo sapiens	59-68
33092205-3	2020	Herein, we summarize the regulation of the most common calcium channels (TRPM2, TPCs, RyRs, and TRPML1) by NAD+ and its metabolites, with a particular focus on their roles in cancers.	NAD	107-111	transient receptor potential cation channel subfamily M member 2	Homo sapiens	73-78
19306844-1	2009	The sirtuins (SIRT1-7), also being referred to as class III HDACs, exert NAD-dependent deacetylase and/or ADP-ribosyltransferase activities in various cellular compartments including the cell nucleus, the cytoplasm and the mitochondria.	NAD	73-76	sirtuin 1	Mus musculus	14-19
32389809-1	2020	BACKGROUND & AIM: Abundantly expressed in the metabolically active cells including hepatocytes, N-nicotinamide methyltransferase (NNMT) catalyzes S-adenosylmethionine (SAM)-dependent methylation/degradation of nicotinamide, the predominant precursor for intracellular nicotinamide adenine dinucleotide (NAD+) regeneration via the salvage pathway.	NAD	303-307	nicotinamide N-methyltransferase	Mus musculus	130-134
32389809-11	2020	Further investigations revealed that NNMT inhibition-induced lipogenic pathway activation was independent of its NAD+-enhancing action; however, incremental cellular NAD+ contents due to NNMT inhibition was associated with marked liver AMPK activation.	NAD	166-170	nicotinamide N-methyltransferase	Mus musculus	187-191
19428988-11	2009	Both PPT, a specific ERalpha agonist, and DPN, a specific ERbeta agonist, inhibited GnRH gene expression in GN11 cells, but only DPN inhibited GnRH gene expression in GT1-7 cells, consistent with their undetectable levels of ERalpha expression.	NAD	42-45	gonadotropin releasing hormone 1	Mus musculus	84-88
19428988-11	2009	Both PPT, a specific ERalpha agonist, and DPN, a specific ERbeta agonist, inhibited GnRH gene expression in GN11 cells, but only DPN inhibited GnRH gene expression in GT1-7 cells, consistent with their undetectable levels of ERalpha expression.	NAD	42-45	estrogen receptor 1 (alpha)	Mus musculus	225-232
19428988-11	2009	Both PPT, a specific ERalpha agonist, and DPN, a specific ERbeta agonist, inhibited GnRH gene expression in GN11 cells, but only DPN inhibited GnRH gene expression in GT1-7 cells, consistent with their undetectable levels of ERalpha expression.	NAD	129-132	gonadotropin releasing hormone 1	Mus musculus	143-147
32886247-5	2020	By virtues of the outstanding electrocatalytic activity, PtAg/rGO exhibits effective amperometric detection of NADH at 0.15 V within a wide linear concentration range of 2-2378 muM, a high sensitivity of 92.62 muA mM-1 cm-2, low detection limit of 0.2 muM, and long-term detection over 2500 s. Moreover, the as-constructed biosensors can achieve accurate NADH detection in human serum samples, indicating its promising application feasibility in fundamental and clinic research.	NAD	111-115	Mix1 homeobox-like 1 (Xenopus laevis)	Mus musculus	214-223
19430699-1	2009	NAD kinase catalyzes the phosphorylation of NAD(H) to form NADP(H), using ATP as phosphoryl donor.	NAD	44-50	NAD kinase	Homo sapiens	0-10
19430699-4	2009	Recent studies have partially demonstrated that NAD kinase plays a crucial role in the regulation of NAD(H)/NADP(H) conversion.	NAD	101-107	NAD kinase	Homo sapiens	48-58
19262508-5	2009	Here we demonstrate that AMPK controls the expression of genes involved in energy metabolism in mouse skeletal muscle by acting in coordination with another metabolic sensor, the NAD+-dependent type III deacetylase SIRT1.	NAD	179-183	sirtuin 1	Mus musculus	215-220
19262508-6	2009	AMPK enhances SIRT1 activity by increasing cellular NAD+ levels, resulting in the deacetylation and modulation of the activity of downstream SIRT1 targets that include the peroxisome proliferator-activated receptor-gamma coactivator 1alpha and the forkhead box O1 (FOXO1) and O3 (FOXO3a) transcription factors.	NAD	52-56	sirtuin 1	Mus musculus	14-19
19262508-6	2009	AMPK enhances SIRT1 activity by increasing cellular NAD+ levels, resulting in the deacetylation and modulation of the activity of downstream SIRT1 targets that include the peroxisome proliferator-activated receptor-gamma coactivator 1alpha and the forkhead box O1 (FOXO1) and O3 (FOXO3a) transcription factors.	NAD	52-56	forkhead box O1	Mus musculus	248-263
19262508-6	2009	AMPK enhances SIRT1 activity by increasing cellular NAD+ levels, resulting in the deacetylation and modulation of the activity of downstream SIRT1 targets that include the peroxisome proliferator-activated receptor-gamma coactivator 1alpha and the forkhead box O1 (FOXO1) and O3 (FOXO3a) transcription factors.	NAD	52-56	forkhead box O1	Mus musculus	265-270
19007763-6	2009	A common aldo-keto reductase substrate, 1-acenaphthenol, was used to monitor the NAD(+)-dependent oxidation catalyzed by AKR1C1.	NAD	81-87	aldo-keto reductase family 1 member C1	Homo sapiens	121-127
19199480-1	2009	A series of imidazo[1,2-b]thiazole derivatives is shown to activate the NAD(+)-dependent deacetylase SIRT1, a potential new therapeutic target to treat various metabolic disorders.	NAD	72-78	sirtuin 1	Mus musculus	101-106
19234185-3	2009	Although ATP acts as a soluble ligand to activate P2X(7), gating of P2X(7) by NAD(+) requires ecto-ADP-ribosyltransferase ART2.2-catalyzed transfer of the ADP-ribose moiety from NAD(+) onto Arg125 of P2X(7).	NAD	78-84	ADP-ribosyltransferase 2b	Mus musculus	122-128
19234185-3	2009	Although ATP acts as a soluble ligand to activate P2X(7), gating of P2X(7) by NAD(+) requires ecto-ADP-ribosyltransferase ART2.2-catalyzed transfer of the ADP-ribose moiety from NAD(+) onto Arg125 of P2X(7).	NAD	178-184	ADP-ribosyltransferase 2b	Mus musculus	122-128
19276158-6	2009	Because lactate dehydrogenase-A (LDH-A), also a HIF-1alpha target, promotes fermentative glycolysis (conversion of pyruvate to lactate), a step essential for regenerating NAD+, we asked whether FH-deficient cells would be exquisitely sensitive to LDH-A blockade.	NAD	171-175	hypoxia inducible factor 1, alpha subunit	Mus musculus	48-58
19241369-6	2009	In addition, we determined the inhibition constants and mechanism of action for nicotinamide and a small molecule SIRT3 inhibitor against active mouse SIRT3 and show that the mechanisms are different for the two compounds with respect to peptide substrate and NAD(+).	NAD	260-266	sirtuin 3	Mus musculus	114-119
19178345-7	2009	This may be due to the activation of the DNA repair enzyme, poly(ADP-ribose) polymerase, in response to the oxidative damage imposed on DNA, since pretreatment of the cells with an inhibitor of these enzymes prevented the reduction of cellular NAD(+) and NADH levels.	NAD	244-250	poly (ADP-ribose) polymerase 1	Rattus norvegicus	60-87
19178345-7	2009	This may be due to the activation of the DNA repair enzyme, poly(ADP-ribose) polymerase, in response to the oxidative damage imposed on DNA, since pretreatment of the cells with an inhibitor of these enzymes prevented the reduction of cellular NAD(+) and NADH levels.	NAD	255-259	poly (ADP-ribose) polymerase 1	Rattus norvegicus	60-87
19169615-5	2009	These data are evidence that CD38 is involved in the regulation of both NAD(+) and calcium-mobilizing agents, the concentration resulting in an essential enzyme that plays a key role in cellular energy and signal-transduction systems.	NAD	72-78	CD38 molecule	Bos taurus	29-33
19149603-0	2009	CD38 as a regulator of cellular NAD: a novel potential pharmacological target for metabolic conditions.	NAD	32-35	CD38 molecule	Homo sapiens	0-4
19149603-1	2009	CD38 is a multifunctional enzyme that uses nicotinamide adenine dinucleotide (NAD) as a substrate to generate second messengers.	NAD	43-76	CD38 molecule	Homo sapiens	0-4
19149603-1	2009	CD38 is a multifunctional enzyme that uses nicotinamide adenine dinucleotide (NAD) as a substrate to generate second messengers.	NAD	78-81	CD38 molecule	Homo sapiens	0-4
19149603-2	2009	Recently, CD38 was also identified as one of the main cellular NADases in mammalian tissues and appears to regulate cellular levels of NAD in multiple tissues and cells.	NAD	63-66	CD38 molecule	Homo sapiens	10-14
19149603-5	2009	The discovery of CD38 as the main cellular NADase in mammalian tissues, and the characterization of its role on the control of cellular NAD levels indicate that CD38 may serve as a pharmacological target for multiple conditions.	NAD	43-46	CD38 molecule	Homo sapiens	17-21
19149603-5	2009	The discovery of CD38 as the main cellular NADase in mammalian tissues, and the characterization of its role on the control of cellular NAD levels indicate that CD38 may serve as a pharmacological target for multiple conditions.	NAD	43-46	CD38 molecule	Homo sapiens	161-165
19296407-4	2009	The purified recombinant human lens ALDH1A1 exhibited optimal catalytic activity at pH 8 and preferred NAD(+) as cofactor and specifically catalyzed the oxidation of toxic lipid aldehydes such as 4-hydroxynonenal (HNE; K(m) = 4.8 microM) and malonaldehyde (K(m) MDA = 3.5 microM).	NAD	103-109	aldehyde dehydrogenase 1 family member A1	Homo sapiens	36-43
19390637-5	2009	We found that Saccharomyces cerevisiae cells null for all GAPDH paralogues (Tdh1, Tdh2, and Tdh3) survived the counter-selection of a GAPDH-encoding plasmid when the NAD(+) metabolizing deacetylase Sir2 was overexpressed.	NAD	166-172	glyceraldehyde-3-phosphate dehydrogenase (phosphorylating) TDH2	Saccharomyces cerevisiae S288C	82-86
18980249-1	2008	tNOX (ENOX2), a cancer-specific and growth-related cell surface protein with protein disulfide-thiol interchange and hydroquinone (NADH) oxidase activities was overexpressed in a transgenic mouse model.	NAD	131-135	ecto-NOX disulfide-thiol exchanger 2	Mus musculus	0-4
18980249-1	2008	tNOX (ENOX2), a cancer-specific and growth-related cell surface protein with protein disulfide-thiol interchange and hydroquinone (NADH) oxidase activities was overexpressed in a transgenic mouse model.	NAD	131-135	ecto-NOX disulfide-thiol exchanger 2	Mus musculus	6-11
18835239-1	2008	ADP-ribosyl cyclase and NAD+ glycohydrolase (CD38, E.C.3.2.2.5) efficiently catalyze the exchange of the nicotinamidyl moiety of NAD+, nicotinamide adenine dinucleotide phosphate (NADP+) or nicotinamide mononucleotide (NMN+) with an alternative base.	NAD	24-28	CD38 molecule	Homo sapiens	45-49
18799617-4	2008	H3 K56 is acetylated by Rtt109p before its incorporation into chromatin during S phase, and this modification is then removed by the NAD(+)-dependent deacetylases Hst3p and Hst4p during G2/M phase.	NAD	133-139	NAD-dependent histone deacetylase HST3	Saccharomyces cerevisiae S288C	163-168
18759251-7	2008	The presence of nuclear CD38 during different stages of hematopoietic differentiation suggests that it may play a role in the control of nuclear Ca(2+) homeostasis and NAD levels.	NAD	168-171	CD38 molecule	Homo sapiens	24-28
32841544-4	2020	In addition, nicotinamide adenine dinucleotide is a crucially important redox-active substrate for multiple catabolic and anabolic reactions with the ratios of NAD+ /NADH and NADP+ /NADPH being suggested as indicators of the general intracellular redox potential and hence metabolic state.	NAD	13-46	2,4-dienoyl-CoA reductase 1	Homo sapiens	182-187
32442721-1	2020	Sirtuins (SIRTs), a class III histone deacetylases (HDACs) that require NAD+ as a cofactor and include SIRT1-7 proteins in mammals.	NAD	72-76	sirtuin 1	Homo sapiens	103-110
32396938-0	2020	MDH1-mediated malate-aspartate NADH shuttle maintains the activity levels of fetal liver hematopoietic stem cells.	NAD	31-35	malate dehydrogenase 1, NAD (soluble)	Mus musculus	0-4
32396938-6	2020	Mechanistically, STAT3 transactivates MDH1 to sustain the malate-aspartate NADH shuttle activity and the HSC self-renewal and differentiation.	NAD	75-79	malate dehydrogenase 1, NAD (soluble)	Mus musculus	38-42
32432680-5	2020	The NAD+-dependent protein SIRT1 deacetylates RECQL4 in vitro and in cells thereby controlling the interaction between OGG1 and RECQL4 after DNA repair and maintaining RECQL4 in a low acetylated state.	NAD	4-8	sirtuin 1	Homo sapiens	27-32
18328086-1	2008	NAD(+) dependent 15-hydroxyprostaglandin dehydrogenate (15-PGDH) catalyses oxidation of 15(S)-hydroxyl group of prostaglandins and as a result inactivates their physiological potential.	NAD	0-6	15-hydroxyprostaglandin dehydrogenase	Homo sapiens	56-63
18441094-1	2008	The enzymatic activity of CD38, ADP-ribosyl cyclase, synthesizes the calcium mobilizing molecule cyclic ADP-ribose from beta-NAD.	NAD	120-128	CD38 molecule	Homo sapiens	26-30
18626062-2	2008	Expressed in distinct patterns in most tissues, CD38 (and CD157) cleaves NAD(+) and NADP(+), generating cyclic ADP ribose (cADPR), NAADP, and ADPR.	NAD	73-79	CD38 molecule	Homo sapiens	48-52
19080518-3	2008	RESULTS: The expression rate of COP9 gene in group 1 was detected markedly lower than that in group 2 (39% vs 95%, P &lt; 0.01); whereas the expression rates of JAK2, HSP and NADH in group 1 were significantly higher that those in group 2 (91%, 97%, 94% vs 29%, 48%, 43%; all P &lt; 0.05).	NAD	175-179	COP9 signalosome subunit 8	Homo sapiens	32-36
18418069-0	2008	Analysis of DBC1 and its homologs suggests a potential mechanism for regulation of sirtuin domain deacetylases by NAD metabolites.	NAD	114-117	cell cycle and apoptosis regulator 2	Homo sapiens	12-16
32251643-7	2020	There is significantly decreased 15-hydroxyprostaglandin dehydrogenase [NAD(+)], which degrades eicosanoids.	NAD	72-75	carbonyl reductase 1	Homo sapiens	33-70
18418069-4	2008	Given that Nudix domains are known to bind nucleoside diphosphate sugars and NAD, we predict that this domain in DBC1 and its homologs binds NAD metabolites such as ADP-ribose.	NAD	77-80	cell cycle and apoptosis regulator 2	Homo sapiens	113-117
32637615-5	2020	By combining quantitative data-independent proteomics, 2D Blue native gel electrophoresis, and functional analysis of enriched respirasome fractions, we show that SCAF1 confers structural attachment between III2 and IV within the N-respirasome, increases NADH-dependent respiration, and reduces reactive oxygen species (ROS).	NAD	255-259	SR-related CTD-associated factor 1	Mus musculus	163-168
18418069-4	2008	Given that Nudix domains are known to bind nucleoside diphosphate sugars and NAD, we predict that this domain in DBC1 and its homologs binds NAD metabolites such as ADP-ribose.	NAD	141-144	cell cycle and apoptosis regulator 2	Homo sapiens	113-117
18418069-5	2008	Hence, we propose that DBC1 and its homologs are likely to regulate the activity of SIRT1 or related deacetylases by sensing the soluble products or substrates of the NAD-dependent deacetylation reaction.	NAD	167-170	cell cycle and apoptosis regulator 2	Homo sapiens	23-27
18418069-6	2008	The complex domain architectures of the members of the DBC1 family, which include fusions to the RNA-binding S1-like domain, the DNA-binding SAP domain and EF-hand domains, suggest that they are likely to function as integrators of distinct regulatory signals including chromatin protein modification, soluble compounds in NAD metabolism, apoptotic stimuli and RNA recognition.	NAD	323-326	cell cycle and apoptosis regulator 2	Homo sapiens	55-59
18239056-3	2008	The present study tests the hypothesis that activation of SREBP-1 by ethanol may be mediated by mammalian sirtuin 1 (SIRT1), a NAD(+)-dependent class III protein deacetylase.	NAD	127-133	sterol regulatory element binding transcription factor 1	Homo sapiens	58-65
18211827-10	2008	Mudd, I. Jurak, O. Vugrek, A single mutation at tyrosine 143 of human S-adenosylhomocysteine hydrolase renders the enzyme thermosensitive and effects the oxidation state of bound co-factor NAD, Biochem.	NAD	189-192	adenosylhomocysteinase	Homo sapiens	70-102
18332217-3	2008	We identify on protein expression arrays novel cyclin E-Cdk2 substrates, including SIRT2, a member of the Sirtuin family of NAD(+)-dependent deacetylases that targets alpha-tubulin.	NAD	124-130	sirtuin 2	Homo sapiens	83-88
18044719-1	2008	The mammalian silent information regulator 2 (SIRT2) is an NAD-dependent histone deacetylase with known roles in the regulation of the cell cycle.	NAD	59-62	sirtuin 2	Homo sapiens	14-44
18044719-1	2008	The mammalian silent information regulator 2 (SIRT2) is an NAD-dependent histone deacetylase with known roles in the regulation of the cell cycle.	NAD	59-62	sirtuin 2	Homo sapiens	46-51
18199125-2	2008	This process is carried out by two heterotetrameric enzymes that catalyse the oxidation of NADH (Nrc) and the reduction of nitrate (Nar), whose expression is activated by the NCE-encoded transcription factors DnrS and DnrT.	NAD	91-95	nuclear receptor coactivator 6	Homo sapiens	97-100
17936613-4	2008	The ERalpha agonist, PPT, is shown as estradiol to modulate hippocampal NMDA receptors and AMPA receptors in cortex and striatum of ovariectomized rats whereas the ERbeta agonist DPN is inactive.	NAD	179-182	estrogen receptor 1	Rattus norvegicus	4-11
17936613-4	2008	The ERalpha agonist, PPT, is shown as estradiol to modulate hippocampal NMDA receptors and AMPA receptors in cortex and striatum of ovariectomized rats whereas the ERbeta agonist DPN is inactive.	NAD	179-182	estrogen receptor 2	Rattus norvegicus	164-170
17936613-5	2008	Striatal DPN activity suggests implication of ERbeta in estradiol modulation of D2 receptors and transporters in ovariectomized rats and is supported by the lack of effect of estradiol in ERbeta knockout (ERKObeta) mice.	NAD	9-12	estrogen receptor 2	Rattus norvegicus	46-52
17947231-5	2008	In the presence of NAD, oxidized CP12-2 interacts with A(4)-GAPDH (K(D) = 0.18 microm) to form a binary complex of 170 kDa with (A(4)-GAPDH)-(CP12-2)(2) stoichiometry, as determined by isothermal titration calorimetry and multiangle light scattering analysis.	NAD	19-22	CP12 domain-containing protein 2	Arabidopsis thaliana	33-37
17947231-5	2008	In the presence of NAD, oxidized CP12-2 interacts with A(4)-GAPDH (K(D) = 0.18 microm) to form a binary complex of 170 kDa with (A(4)-GAPDH)-(CP12-2)(2) stoichiometry, as determined by isothermal titration calorimetry and multiangle light scattering analysis.	NAD	19-22	CP12 domain-containing protein 2	Arabidopsis thaliana	142-146
18336735-3	2008	CD38 acts as an ectocyclase that converts NAD+ to the Ca2+ -releasing second messenger cyclic ADP-ribose (cADPR).	NAD	42-46	CD38 molecule	Homo sapiens	0-4
17947500-9	2008	PDH kinase was unchanged in both trials, suggesting that the attenuation of PDHa activity with n-6 PUFA was a result of changes in the concentrations of intramitochondrial effectors, potentially intramitochondrial NADH or Ca(2+).	NAD	214-218	pyruvate dehydrogenase E1 subunit alpha 1	Homo sapiens	76-80
18296429-6	2008	The two isolated mutants, gdh1-2 and gdh2-1, were crossed to make a double knockout mutant, gdh1-2/gdh2-1, which contained negligible levels of NAD(H)-dependent GDH activity.	NAD	144-150	glutamate dehydrogenase 1	Arabidopsis thaliana	92-98
17951578-1	2007	Class III histone deacetylases (Sir2 or sirtuins) catalyze the NAD+-dependent conversion of acetyl-lysine residues to nicotinamide, 2"-O-acetyl-ADP-ribose (OAADPr), and deacetylated lysine.	NAD	63-67	sirtuin 2	Homo sapiens	32-36
18027980-1	2007	Sir2 protein deacetylases (or sirtuins) catalyze NAD+-dependent conversion of epsilon-amino-acetylated lysine residues to deacetylated lysine, nicotinamide, and 2"-O-acetyl-ADP-ribose.	NAD	49-53	sirtuin 2	Homo sapiens	0-4
17875315-2	2007	This lifespan extension was dependent on an NAD(+)-dependent histone deacetylase, Sir2 in Drosophila and SIR-2.1 in C. elegans.	NAD	44-50	Sirtuin 1	Drosophila melanogaster	82-86
32371394-1	2020	Sirtuins (e.g., human Sirt1-7) catalyze the removal of acyl groups from lysine residues in proteins in an NAD+-dependent manner, and loss of sirtuin deacylase activity correlates with the development of aging-related diseases.	NAD	106-110	sirtuin 1	Homo sapiens	22-29
17634366-8	2007	Because normal SIRT2 activity is controlled by the NAD+/NADH ratio, its function may be coupled to the axo-glial metabolism and the long-term support of axons by oligodendrocytes.	NAD	51-55	sirtuin 2	Mus musculus	15-20
32544883-6	2020	Collectively, this study revealed potential roles of miR-9 and miR-29a as contributors to DPN development through the SHH signaling pathway by binding to ISL1.	NAD	90-93	sonic hedgehog signaling molecule	Rattus norvegicus	118-121
32300965-3	2020	However, age-related DNA damage and increased SASP activate PARP-1 and CD38, the enzymes competing with SIRTs for NAD+.	NAD	114-118	poly (ADP-ribose) polymerase family, member 1	Mus musculus	60-66
17634366-8	2007	Because normal SIRT2 activity is controlled by the NAD+/NADH ratio, its function may be coupled to the axo-glial metabolism and the long-term support of axons by oligodendrocytes.	NAD	56-60	sirtuin 2	Mus musculus	15-20
32300965-3	2020	However, age-related DNA damage and increased SASP activate PARP-1 and CD38, the enzymes competing with SIRTs for NAD+.	NAD	114-118	CD38 antigen	Mus musculus	71-75
17664018-4	2007	We focus on ADP-ribosyl cyclase/CD38 which synthesizes cyclic ADP-ribose (cADPR), a universal Ca(2+) mobilizer from intracellular stores, from beta-NAD(+).	NAD	143-154	CD38 molecule	Homo sapiens	32-36
32278117-3	2020	This study aims to identify changes of specific components of NAD+/SIRTs system in white adipose tissue (WAT) and brown adipose tissue (BAT) of mice upon energy imbalance, focusing on key enzymes in NAD+ salvage (Nampt, Nmnat1, Nrk1), clearance (Nnmt, Aox1, Cyp2e1) and consumption pathways (Sirt1, Sirt2, Sirt3, Sirt6, Parp1).	NAD	199-203	poly (ADP-ribose) polymerase family, member 1	Mus musculus	320-325
17468208-1	2007	NAD-dependent isocitrate dehydrogenase (IDH) is a tricarboxylic acid cycle enzyme that produces 2-oxoglutarate, an organic acid required by the glutamine synthetase/glutamate synthase cycle to assimilate ammonium.	NAD	0-3	hypothetical protein	Arabidopsis thaliana	144-164
31833115-1	2020	As it forms water-filled channel in the mitochondria outer membrane and diffuses essential metabolites such as NADH and ATP, the voltage-dependent anion channel (VDAC) protein family plays a central role in all eukaryotic cells.	NAD	111-115	mitochondrial outer membrane protein porin of 34 kDa	Solanum tuberosum	129-160
31833115-1	2020	As it forms water-filled channel in the mitochondria outer membrane and diffuses essential metabolites such as NADH and ATP, the voltage-dependent anion channel (VDAC) protein family plays a central role in all eukaryotic cells.	NAD	111-115	mitochondrial outer membrane protein porin of 34 kDa	Solanum tuberosum	162-166
32371497-4	2020	NADH-free forms of CtBPs cooperated with the p53-binding partner HDM2 to suppress p53 function, and loss of these forms in highly glycolytic cells resulted in p53 accumulation.	NAD	0-4	MDM2 proto-oncogene	Homo sapiens	65-69
17384184-4	2007	NAD is regenerated by mixed acid and butanediol fermentation, as indicated by an elevated synthesis level of fermentation enzymes like lactate dehydrogenases (Ldh1 and Ldh2), alcohol dehydrogenases (AdhE and Adh), alpha-acetolactate decarboxylase (BudA1), acetolactate synthase (BudB), and acetoin reductase (SACOL0111) as well as an accumulation of fermentation products as lactate and acetate.	NAD	0-3	AT695_RS06395	Staphylococcus aureus	214-246
17416668-6	2007	The enzymatic properties and kinetic parameters of dimeric recombinant AruH were determined by a coupled reaction with NAD(+) and L-alanine dehydrogenase.	NAD	119-125	arginine:pyruvate transaminase AruH	Pseudomonas aeruginosa PAO1	71-75
17529993-2	2007	Here we uncover a positive role for SET in dislodging DEK and PARP1, which restrict access to chromatin in the absence of SET and the PARP1 substrate NAD(+).	NAD	150-156	DEK proto-oncogene	Homo sapiens	54-57
17529993-5	2007	In the presence of NAD(+), PARP1 poly(ADP-ribosyl)ates and evicts DEK (and itself) from chromatin to permit Mediator loading and transcription independent of SET.	NAD	19-25	DEK proto-oncogene	Homo sapiens	66-69
17447732-14	2007	The dissociation rate constants and the slow-binding association rate constants for NAD+ show a complex temperature dependence with both enzymes; however, the cofactor always dissociates more rapidly from Tc-SAHH than from Hs-SAHH, the ratio being around 80-fold at 37 degrees C, and the cofactor binds more rapidly to Hs-SAHH than to Tc-SAHH above approximately 16 degrees C. These features present an opening for selective inhibition of Tc-SAHH over Hs-SAHH, demonstrated with the thioamide analogues of NAD+ and NADH.	NAD	506-510	adenosylhomocysteinase	Homo sapiens	226-230
17447732-14	2007	The dissociation rate constants and the slow-binding association rate constants for NAD+ show a complex temperature dependence with both enzymes; however, the cofactor always dissociates more rapidly from Tc-SAHH than from Hs-SAHH, the ratio being around 80-fold at 37 degrees C, and the cofactor binds more rapidly to Hs-SAHH than to Tc-SAHH above approximately 16 degrees C. These features present an opening for selective inhibition of Tc-SAHH over Hs-SAHH, demonstrated with the thioamide analogues of NAD+ and NADH.	NAD	506-510	adenosylhomocysteinase	Homo sapiens	226-230
17447732-14	2007	The dissociation rate constants and the slow-binding association rate constants for NAD+ show a complex temperature dependence with both enzymes; however, the cofactor always dissociates more rapidly from Tc-SAHH than from Hs-SAHH, the ratio being around 80-fold at 37 degrees C, and the cofactor binds more rapidly to Hs-SAHH than to Tc-SAHH above approximately 16 degrees C. These features present an opening for selective inhibition of Tc-SAHH over Hs-SAHH, demonstrated with the thioamide analogues of NAD+ and NADH.	NAD	506-510	adenosylhomocysteinase	Homo sapiens	226-230
17447732-14	2007	The dissociation rate constants and the slow-binding association rate constants for NAD+ show a complex temperature dependence with both enzymes; however, the cofactor always dissociates more rapidly from Tc-SAHH than from Hs-SAHH, the ratio being around 80-fold at 37 degrees C, and the cofactor binds more rapidly to Hs-SAHH than to Tc-SAHH above approximately 16 degrees C. These features present an opening for selective inhibition of Tc-SAHH over Hs-SAHH, demonstrated with the thioamide analogues of NAD+ and NADH.	NAD	506-510	adenosylhomocysteinase	Homo sapiens	226-230
17447732-14	2007	The dissociation rate constants and the slow-binding association rate constants for NAD+ show a complex temperature dependence with both enzymes; however, the cofactor always dissociates more rapidly from Tc-SAHH than from Hs-SAHH, the ratio being around 80-fold at 37 degrees C, and the cofactor binds more rapidly to Hs-SAHH than to Tc-SAHH above approximately 16 degrees C. These features present an opening for selective inhibition of Tc-SAHH over Hs-SAHH, demonstrated with the thioamide analogues of NAD+ and NADH.	NAD	506-510	adenosylhomocysteinase	Homo sapiens	226-230
17447732-14	2007	The dissociation rate constants and the slow-binding association rate constants for NAD+ show a complex temperature dependence with both enzymes; however, the cofactor always dissociates more rapidly from Tc-SAHH than from Hs-SAHH, the ratio being around 80-fold at 37 degrees C, and the cofactor binds more rapidly to Hs-SAHH than to Tc-SAHH above approximately 16 degrees C. These features present an opening for selective inhibition of Tc-SAHH over Hs-SAHH, demonstrated with the thioamide analogues of NAD+ and NADH.	NAD	515-519	adenosylhomocysteinase	Homo sapiens	226-230
17447732-14	2007	The dissociation rate constants and the slow-binding association rate constants for NAD+ show a complex temperature dependence with both enzymes; however, the cofactor always dissociates more rapidly from Tc-SAHH than from Hs-SAHH, the ratio being around 80-fold at 37 degrees C, and the cofactor binds more rapidly to Hs-SAHH than to Tc-SAHH above approximately 16 degrees C. These features present an opening for selective inhibition of Tc-SAHH over Hs-SAHH, demonstrated with the thioamide analogues of NAD+ and NADH.	NAD	515-519	adenosylhomocysteinase	Homo sapiens	226-230
17447732-14	2007	The dissociation rate constants and the slow-binding association rate constants for NAD+ show a complex temperature dependence with both enzymes; however, the cofactor always dissociates more rapidly from Tc-SAHH than from Hs-SAHH, the ratio being around 80-fold at 37 degrees C, and the cofactor binds more rapidly to Hs-SAHH than to Tc-SAHH above approximately 16 degrees C. These features present an opening for selective inhibition of Tc-SAHH over Hs-SAHH, demonstrated with the thioamide analogues of NAD+ and NADH.	NAD	515-519	adenosylhomocysteinase	Homo sapiens	226-230
17447732-14	2007	The dissociation rate constants and the slow-binding association rate constants for NAD+ show a complex temperature dependence with both enzymes; however, the cofactor always dissociates more rapidly from Tc-SAHH than from Hs-SAHH, the ratio being around 80-fold at 37 degrees C, and the cofactor binds more rapidly to Hs-SAHH than to Tc-SAHH above approximately 16 degrees C. These features present an opening for selective inhibition of Tc-SAHH over Hs-SAHH, demonstrated with the thioamide analogues of NAD+ and NADH.	NAD	515-519	adenosylhomocysteinase	Homo sapiens	226-230
17447732-14	2007	The dissociation rate constants and the slow-binding association rate constants for NAD+ show a complex temperature dependence with both enzymes; however, the cofactor always dissociates more rapidly from Tc-SAHH than from Hs-SAHH, the ratio being around 80-fold at 37 degrees C, and the cofactor binds more rapidly to Hs-SAHH than to Tc-SAHH above approximately 16 degrees C. These features present an opening for selective inhibition of Tc-SAHH over Hs-SAHH, demonstrated with the thioamide analogues of NAD+ and NADH.	NAD	515-519	adenosylhomocysteinase	Homo sapiens	226-230
17267199-6	2007	In connection with the oxidation of nicotinamide adenine dinucleotide (NADH), excellent electrocatalytic activities were observed at MB/CNT/GCE compared with MB/GP modified glassy carbon electrode (MB/GP/GCE).	NAD	36-69	aminomethyltransferase	Homo sapiens	158-207
17267199-6	2007	In connection with the oxidation of nicotinamide adenine dinucleotide (NADH), excellent electrocatalytic activities were observed at MB/CNT/GCE compared with MB/GP modified glassy carbon electrode (MB/GP/GCE).	NAD	71-75	aminomethyltransferase	Homo sapiens	140-143
17267199-6	2007	In connection with the oxidation of nicotinamide adenine dinucleotide (NADH), excellent electrocatalytic activities were observed at MB/CNT/GCE compared with MB/GP modified glassy carbon electrode (MB/GP/GCE).	NAD	71-75	aminomethyltransferase	Homo sapiens	158-207
17267199-7	2007	Based on the results, a new NADH sensor was successfully established using the MB/CNT/GCE.	NAD	28-32	aminomethyltransferase	Homo sapiens	86-89
17457050-1	2007	Sir2, an NAD+-dependent protein deacetylase, extends the lifespan in diverse species from yeast to flies.	NAD	9-12	sirtuin 2	Homo sapiens	0-4
17182614-1	2007	Human CD38 is a multifunctional ectoenzyme responsible for catalyzing the conversions from nicotinamide adenine dinucleotide (NAD) to cyclic ADP-ribose (cADPR) and from cADPR to ADP-ribose (ADPR).	NAD	91-124	CD38 molecule	Homo sapiens	6-10
17182614-1	2007	Human CD38 is a multifunctional ectoenzyme responsible for catalyzing the conversions from nicotinamide adenine dinucleotide (NAD) to cyclic ADP-ribose (cADPR) and from cADPR to ADP-ribose (ADPR).	NAD	126-129	CD38 molecule	Homo sapiens	6-10
17182614-3	2007	In this study, we determined three crystal structures of the human CD38 enzymatic domain complexed with cADPR at 1.5-A resolution, with its analog, cyclic GDP-ribose (cGDPR) (1.68 A) and with NGD (2.1 A) a substrate analog of NAD.	NAD	226-229	CD38 molecule	Homo sapiens	67-71
17214740-1	2007	Silent information regulator 2 (Sir2)-related proteins or sirtuins function as NAD(+)-dependent deacetylases or ADP ribosylases that target a range of substrates, thereby influencing chromatin structure and a diverse range of other biological functions.	NAD	79-85	sirtuin 2	Homo sapiens	0-30
17102138-3	2007	The cytosolic NADP(+)-specific isoform (ME1) was the most abundant, with the mitochondrial isoforms NAD(+)-preferred (ME2) expressed at approximately 50%, and the NADP(+)-specific (ME3) at approximately 10% compared with ME1.	NAD	100-106	malic enzyme 2	Rattus norvegicus	118-121
17665640-3	2007	Incubation of eEF-2 tryptic fragment 32/33 kDa (32F) with NAD was ADP-ribosylated and gave rise to the covalent binding of ADP-ribose to eEF-2.	NAD	58-61	eukaryotic translation elongation factor 2	Homo sapiens	14-19
17665640-3	2007	Incubation of eEF-2 tryptic fragment 32/33 kDa (32F) with NAD was ADP-ribosylated and gave rise to the covalent binding of ADP-ribose to eEF-2.	NAD	58-61	eukaryotic translation elongation factor 2	Homo sapiens	137-142
17127275-2	2007	Increasing evidence has supported the hypothesis that PARP-1 induces cell death by depleting intracellular NAD+.	NAD	107-111	poly (ADP-ribose) polymerase 1	Rattus norvegicus	54-60
32361710-1	2020	The NAD-dependent deacetylase sirtuin 1 (SIRT1), a member of the mammalian sirtuin family, plays a pivotal role in deacetylating histone and nonhistone proteins.	NAD	4-7	sirtuin 1	Homo sapiens	41-46
17127275-3	2007	Based on our in vitro finding that NAD+ treatment can abolish PARP-1-mediated cell death, we hypothesized that NAD+ administration may decrease ischemic brain injury.	NAD	35-39	poly (ADP-ribose) polymerase 1	Rattus norvegicus	62-68
17127275-3	2007	Based on our in vitro finding that NAD+ treatment can abolish PARP-1-mediated cell death, we hypothesized that NAD+ administration may decrease ischemic brain injury.	NAD	111-115	poly (ADP-ribose) polymerase 1	Rattus norvegicus	62-68
31697432-5	2020	Differential scanning fluorimetry demonstrates that YjhC binds N-acetylneuraminic acid and its lactone variant, along with NAD(H), which is consistent with its role as an oxidoreductase.	NAD	123-126	oxidoreductase	Escherichia coli	171-185
17127275-9	2007	These results provide the first in vivo evidence that NAD+ metabolism is a new target for treating brain ischemia, and that NAD+ administration may be a novel strategy for decreasing brain damage in cerebral ischemia and possibly other PARP-1-associated neurological diseases.	NAD	54-58	poly (ADP-ribose) polymerase 1	Rattus norvegicus	236-242
32301489-12	2020	Moreover, NAD+ treatment up-regulated the expressions of IL-13 and down-regulated the expression of IFN-gamma and IL-17.	NAD	10-14	interleukin 17A	Mus musculus	114-119
17127275-9	2007	These results provide the first in vivo evidence that NAD+ metabolism is a new target for treating brain ischemia, and that NAD+ administration may be a novel strategy for decreasing brain damage in cerebral ischemia and possibly other PARP-1-associated neurological diseases.	NAD	124-128	poly (ADP-ribose) polymerase 1	Rattus norvegicus	236-242
17158952-6	2006	The increase in NADH caused by respiratory deficiency inactivates PTEN through a redox modification mechanism, leading to Akt activation.	NAD	16-20	phosphatase and tensin homolog	Homo sapiens	66-70
16872278-0	2006	A single mutation at Tyr143 of human S-adenosylhomocysteine hydrolase renders the enzyme thermosensitive and affects the oxidation state of bound cofactor nicotinamide-adenine dinucleotide.	NAD	155-188	adenosylhomocysteinase	Homo sapiens	37-69
32133466-3	2020	In this study, we developed a biofluorometric gas-imaging system (sniff-cam) based on nicotinamide adenine dinucleotide (NAD)-dependent alcohol dehydrogenase (ADH) to visualize transcutaneous ethanol (EtOH) distribution.	NAD	86-119	aldo-keto reductase family 1 member A1	Homo sapiens	159-162
32133466-3	2020	In this study, we developed a biofluorometric gas-imaging system (sniff-cam) based on nicotinamide adenine dinucleotide (NAD)-dependent alcohol dehydrogenase (ADH) to visualize transcutaneous ethanol (EtOH) distribution.	NAD	121-124	aldo-keto reductase family 1 member A1	Homo sapiens	159-162
32133466-5	2020	First, we optimized the solution volume and concentration of the oxidized NAD, which was a coenzyme of ADH.	NAD	74-77	aldo-keto reductase family 1 member A1	Homo sapiens	103-106
16872278-16	2006	In summary, a single mutation in the AdoHcyase affecting both the oxidation state of bound co-factor NAD and enzyme stability is present in a human with AdoHcyase deficiency.	NAD	101-104	adenosylhomocysteinase	Homo sapiens	37-46
17125375-1	2006	A highly efficient photocatalytic system for hydrogen evolution with dihydronicotinamide coenzyme (NADH) as a sacrificial agent in an aqueous solution has been constructed by using water-soluble platinum clusters functionalized with methyl viologen-alkanethiol (MVA2+) and a simple electron-donor dyad, 9-mesityl-10-methylacridinium ion (Acr+-Mes), which is capable of fast photoinduced electron transfer but extremely slow back electron transfer.	NAD	99-103	acrosin	Homo sapiens	338-341
32321406-4	2021	A NAD + dependent histone deacetylase enzyme, Sirtuin 1 (SIRT1) is involved in a variety of human disorders such as type II diabetes, cancer, obesity, and aging.	NAD	2-5	sirtuin 1	Homo sapiens	46-55
17125375-5	2006	The decay of the absorbance due to NAD*, produced by the deprotonation from NADH*+, coincides with the appearance of the absorption band due to Acr*-Mes.	NAD	35-39	acrosin	Homo sapiens	144-147
32321406-4	2021	A NAD + dependent histone deacetylase enzyme, Sirtuin 1 (SIRT1) is involved in a variety of human disorders such as type II diabetes, cancer, obesity, and aging.	NAD	2-5	sirtuin 1	Homo sapiens	57-62
17125375-5	2006	The decay of the absorbance due to NAD*, produced by the deprotonation from NADH*+, coincides with the appearance of the absorption band due to Acr*-Mes.	NAD	76-80	acrosin	Homo sapiens	144-147
17125375-6	2006	This indicates electron transfer from NAD* to Acr+-Mes to give Acr*-Mes, which undergoes the electron-transfer reduction of MVA2+-PtC, leading to the efficient hydrogen evolution.	NAD	38-42	acrosin	Homo sapiens	46-49
17125375-6	2006	This indicates electron transfer from NAD* to Acr+-Mes to give Acr*-Mes, which undergoes the electron-transfer reduction of MVA2+-PtC, leading to the efficient hydrogen evolution.	NAD	38-42	acrosin	Homo sapiens	63-66
17031400-0	2006	Reduction of mitomycin C is catalysed by human recombinant NRH:quinone oxidoreductase 2 using reduced nicotinamide adenine dinucleotide as an electron donating co-factor.	NAD	102-135	N-ribosyldihydronicotinamide:quinone reductase 2	Homo sapiens	59-87
32059949-9	2020	Nudt3, Nudt16, and Nudt20 bound m7G capped RNA more tightly than RNA with NADH caps.	NAD	74-78	nudix hydrolase 16	Homo sapiens	7-13
17031400-1	2006	NRH:Quinone Oxidoreductase 2 (NQO2) has been described as having no enzymatic activity with nicotinamide adenine dinucleotide (NADH) or NADPH as electron donating cosubstrates.	NAD	92-125	N-ribosyldihydronicotinamide:quinone reductase 2	Homo sapiens	30-34
17172838-5	2006	Removal of K56 acetylation takes place in the G2/M phase of the cell cycle and is dependent upon Hst3 and Hst4, two proteins that are related to the NAD+-dependent histone deacetylase Sir2.	NAD	149-153	NAD-dependent histone deacetylase HST3	Saccharomyces cerevisiae S288C	97-101
32337346-6	2020	The 3 subjects shared a variant (c.1195G>A; p.Gly399Ser) in exon 12 of the AIFM1 gene, which is not reported in the exome/genome sequence databases, affecting a critical amino acid for protein function involved in NAD(H) binding and predicted to be pathogenic with very high probability by variant analysis programs.	NAD	214-220	apoptosis inducing factor mitochondria associated 1	Homo sapiens	75-80
17003133-3	2006	TAL(-/-) spermatozoa show loss of Deltapsi(m) and mitochondrial membrane integrity because of diminished NADPH, NADH, and GSH.	NAD	112-116	transaldolase 1	Mus musculus	0-3
31970414-1	2020	NAD+-dependent SIRT7 deacylase plays essential roles in ribosome biogenesis, stress response, genome integrity, metabolism and aging, while how it is transcriptionally regulated is still largely unclear.	NAD	0-3	sirtuin 7	Homo sapiens	15-20
30588784-6	2020	We were able to validate the underexpression of the mitochondrial complex subunits NADH:Ubiquinone Oxidoreductase Core Subunit S1 (NDUFS1) and ubiquinol-cytochrome C reductase core protein 2 (UQCRC2), as well as the underexpression of the testis-specific sodium/potassium-transporting ATPase subunit alpha-4 (ATP1A4) in the NSTC group.	NAD	83-87	NADH:ubiquinone oxidoreductase core subunit S1	Homo sapiens	131-137
30588784-6	2020	We were able to validate the underexpression of the mitochondrial complex subunits NADH:Ubiquinone Oxidoreductase Core Subunit S1 (NDUFS1) and ubiquinol-cytochrome C reductase core protein 2 (UQCRC2), as well as the underexpression of the testis-specific sodium/potassium-transporting ATPase subunit alpha-4 (ATP1A4) in the NSTC group.	NAD	83-87	immunoglobulin binding protein 1	Homo sapiens	300-307
32152092-4	2020	SIRT1, a NAD+-dependent deacetylase, is pivotal in regulating hepatic gene expression and has emerged as a key therapeutic target.	NAD	9-12	sirtuin 1	Homo sapiens	0-5
32245130-2	2020	Except for its role in the production of adenosine triphosphate (ATP), NAD+ acts as a substrate for several enzymes including sirtuin 1 (SIRT1) and poly ADP-ribose polymerase 1 (PARP1).	NAD	71-75	sirtuin 1	Homo sapiens	126-135
32245130-2	2020	Except for its role in the production of adenosine triphosphate (ATP), NAD+ acts as a substrate for several enzymes including sirtuin 1 (SIRT1) and poly ADP-ribose polymerase 1 (PARP1).	NAD	71-75	sirtuin 1	Homo sapiens	137-142
31988240-7	2020	These results indicate that by forming a complex with GAPDH, NAMPT can translocate to the nucleus and thereby sustain the stress-induced NMN/NAD+ salvage pathway.	NAD	141-144	glyceraldehyde-3-phosphate dehydrogenase	Mus musculus	54-59
32211535-7	2020	What is more, the protein levels of phosphorylated AMPK alpha (p-AMPKalpha) and nicotinamide adenine dinucleotide (NAD)-dependent protein deacetylase sirtuin-1 (SIRT1) were decreased by AA treatments in a time depending manner.	NAD	80-113	sirtuin 1	Homo sapiens	150-159
32211535-7	2020	What is more, the protein levels of phosphorylated AMPK alpha (p-AMPKalpha) and nicotinamide adenine dinucleotide (NAD)-dependent protein deacetylase sirtuin-1 (SIRT1) were decreased by AA treatments in a time depending manner.	NAD	80-113	sirtuin 1	Homo sapiens	161-166
32211535-7	2020	What is more, the protein levels of phosphorylated AMPK alpha (p-AMPKalpha) and nicotinamide adenine dinucleotide (NAD)-dependent protein deacetylase sirtuin-1 (SIRT1) were decreased by AA treatments in a time depending manner.	NAD	115-118	sirtuin 1	Homo sapiens	150-159
32211535-7	2020	What is more, the protein levels of phosphorylated AMPK alpha (p-AMPKalpha) and nicotinamide adenine dinucleotide (NAD)-dependent protein deacetylase sirtuin-1 (SIRT1) were decreased by AA treatments in a time depending manner.	NAD	115-118	sirtuin 1	Homo sapiens	161-166
31651049-4	2020	Consequently, CG amount, NADH, D-glucose-6-phosphate (G6P), phosphate buffer and the pH, and ionic strength of solution had important effects on the residual activity of CG-G6PD.	NAD	25-29	glucose-6-phosphate dehydrogenase	Homo sapiens	173-177
32066462-16	2020	PARP-1 detects DNA breaks and synthesizes PAR polymers to initiate the DNA repair system that consumes a large amount of cellular NAD+.	NAD	130-133	poly (ADP-ribose) polymerase family, member 1	Mus musculus	0-6
32029763-6	2020	Furthermore, MID1 is associated with other trans-factors involved in NICOTINAMIDE ADENINE DINUCLEOTIDE HYDROGEN (NADH) DEHYDROGENASE SUBUNIT 2 (nad2) intron 1 splicing, and interacts directly with itself and MITOCHONDRIAL STABILITY FACTOR 1 (MTSF1).	NAD	69-89	Tetratricopeptide repeat (TPR)-like superfamily protein	Arabidopsis thaliana	208-240
32029763-6	2020	Furthermore, MID1 is associated with other trans-factors involved in NICOTINAMIDE ADENINE DINUCLEOTIDE HYDROGEN (NADH) DEHYDROGENASE SUBUNIT 2 (nad2) intron 1 splicing, and interacts directly with itself and MITOCHONDRIAL STABILITY FACTOR 1 (MTSF1).	NAD	69-89	Tetratricopeptide repeat (TPR)-like superfamily protein	Arabidopsis thaliana	242-247
32005247-0	2020	Targeting the NAD+ salvage pathway suppresses APC mutation-driven colorectal cancer growth and Wnt/beta-catenin signaling via increasing Axin level.	NAD	14-17	axin 1	Homo sapiens	137-141
31914379-0	2020	The CD38/NAD/SIRTUIN1/EZH2 Axis Mitigates Cytotoxic CD8 T Cell Function and Identifies Patients with SLE Prone to Infections.	NAD	9-12	sirtuin 1	Homo sapiens	13-21
31914379-0	2020	The CD38/NAD/SIRTUIN1/EZH2 Axis Mitigates Cytotoxic CD8 T Cell Function and Identifies Patients with SLE Prone to Infections.	NAD	9-12	CD8a molecule	Homo sapiens	52-55
31883644-2	2020	Here we present five individuals from four unrelated families, individuals who share similar phenotypes with disease-causal bi-allelic variants in NADSYN1, encoding NAD synthetase 1, the final enzyme of the nicotinamide adenine dinucleotide (NAD) de novo synthesis pathway.	NAD	207-240	NAD synthetase 1	Homo sapiens	147-154
31883644-2	2020	Here we present five individuals from four unrelated families, individuals who share similar phenotypes with disease-causal bi-allelic variants in NADSYN1, encoding NAD synthetase 1, the final enzyme of the nicotinamide adenine dinucleotide (NAD) de novo synthesis pathway.	NAD	207-240	NAD synthetase 1	Homo sapiens	165-181
31883644-2	2020	Here we present five individuals from four unrelated families, individuals who share similar phenotypes with disease-causal bi-allelic variants in NADSYN1, encoding NAD synthetase 1, the final enzyme of the nicotinamide adenine dinucleotide (NAD) de novo synthesis pathway.	NAD	147-150	NAD synthetase 1	Homo sapiens	165-181
31883644-7	2020	Thus, NADSYN1 represents an additional gene required for NAD synthesis during embryogenesis, and NADSYN1 has bi-allelic missense variants that cause NAD deficiency-dependent malformations.	NAD	57-60	NAD synthetase 1	Homo sapiens	6-13
31914648-3	2020	We show that loss of SDH activity in a chromaffin cell model does not perturb complex I function, retaining the ability to oxidize NADH within the electron transport chain.	NAD	131-135	succinate dehydrogenase complex iron sulfur subunit B	Homo sapiens	21-24
33612619-3	2020	SIRT1, a NAD-dependent deacetylase gene, is responsible for upregulating lipolysis genes and is downregulated after acute high-fat meal consumption.	NAD	9-12	sirtuin 1	Homo sapiens	0-5
32270742-1	2020	BACKGROUND: The class III NAD-dependent histone deacetylase (HDAC) sirtuin 1 (SIRT1) is an important regulator of senescence, aging, and inflammation.	NAD	26-29	sirtuin 1	Homo sapiens	67-76
32270742-1	2020	BACKGROUND: The class III NAD-dependent histone deacetylase (HDAC) sirtuin 1 (SIRT1) is an important regulator of senescence, aging, and inflammation.	NAD	26-29	sirtuin 1	Homo sapiens	78-83
31864392-7	2019	The NAD-dependent transcriptional co-repressor C-terminal Binding Protein (CtBP) was discovered 25 years ago due to its high affinity binding to AdV E1A proteins, however, the role of this interaction in the viral life cycle remains unclear.	NAD	4-7	poly(rC) binding protein 2	Mus musculus	75-79
31864392-12	2019	We found differential expression of the NAD-dependent CtBP protein homologs between lymphocytes and epithelial cells, and inhibition of CtBP complexes upregulates AdV E1A expression in T lymphocyte cell lines but not in lytically-infected epithelial cells.	NAD	40-43	poly(rC) binding protein 2	Mus musculus	54-58
31864392-14	2019	In contrast, disrupting the NAD-dependent CtBP repressor complex interaction with PxDLS-containing binding partners paradoxically alters AdV gene expression.	NAD	28-31	poly(rC) binding protein 2	Mus musculus	42-46
31864392-15	2019	Our findings also indicate that CtBP activities on viral gene expression may be distinct from those occurring upon metabolic alterations in cellular NAD+/NADH ratios or those occurring after lymphocyte activation.	NAD	154-158	poly(rC) binding protein 2	Mus musculus	32-36
31888308-6	2019	This arsenate resistance system was potentially linked to two genes: orf69, encoding an organoarsenical efflux major facilitator superfamily (MFS) transporter-like protein related to ArsJ, and orf70, encoding nicotinamide adenine dinucleotide (NAD)-dependent glyceraldehyde-3-phosphate dehydrogenase.	NAD	209-242	hypothetical protein	Escherichia coli	69-74
31888308-6	2019	This arsenate resistance system was potentially linked to two genes: orf69, encoding an organoarsenical efflux major facilitator superfamily (MFS) transporter-like protein related to ArsJ, and orf70, encoding nicotinamide adenine dinucleotide (NAD)-dependent glyceraldehyde-3-phosphate dehydrogenase.	NAD	244-247	hypothetical protein	Escherichia coli	69-74
31614144-3	2019	We previously reported high expression of Sirtuin 1, a nicotinamide adenine dinucleotide (NAD+)-dependent histone/protein deacetylase, in primary acute-type ATL cells.	NAD	55-88	sirtuin 1	Homo sapiens	42-51
31614144-3	2019	We previously reported high expression of Sirtuin 1, a nicotinamide adenine dinucleotide (NAD+)-dependent histone/protein deacetylase, in primary acute-type ATL cells.	NAD	90-94	sirtuin 1	Homo sapiens	42-51
31614144-4	2019	NAD+ biosynthesis via nicotinamide phosphoribosyltransferase (NAMPT) modulates Sirtuin 1 activity.	NAD	0-3	sirtuin 1	Homo sapiens	79-88
31598701-0	2019	Exogenous pyruvate represses histone gene expression and inhibits cancer cell proliferation via the NAMPT-NAD+-SIRT1 pathway.	NAD	106-109	sirtuin 1	Homo sapiens	111-116
31598701-5	2019	Pyruvate represses histone gene expression by inducing the expression of NAD+ biosynthesis enzyme, nicotinamide phosphoribosyltransferase (NAMPT) via myocyte enhancer factor 2C (MEF2C), which then increases NAD+ levels and activates the histone deacetylase activity of SIRT1.	NAD	73-76	sirtuin 1	Homo sapiens	269-274
31754701-12	2019	In dorsal root ganglion protein extracts from nSIRT1OE mice, the NAD+-consuming enzyme PARP1 was deactivated and the major deacetylated protein was identified to be an E3 protein ligase, NEDD4-1, a protein required for axonal growth, regeneration and proteostasis in neurodegenerative diseases.	NAD	65-69	poly (ADP-ribose) polymerase family, member 1	Mus musculus	87-92
30996287-1	2019	Poly (ADP-ribose) polymerase (PARP)-1 and PARP-2 regulate the function of various DNA-interacting proteins by transferring ADP-ribose emerging from catalytic cleavage of cellular beta-NAD+.	NAD	179-188	poly (ADP-ribose) polymerase family, member 1	Mus musculus	0-37
31515847-1	2019	As a deacetylase relying on NAD, sirtuin 1 (SIRT1) has been proven to inhibit osteoclastogenesis directly by repressing reactive oxygen species (ROS) production and TRPV1 channel stimulation modulated by TNF-alpha.	NAD	28-31	sirtuin 1	Homo sapiens	33-42
16878979-10	2006	Using the structure of a sheep class 1 ALDH, it was possible to deduce that the interaction between the side chain of T244 and its neighboring residues with the nicotinamide ring of NAD(+) were an essential determinant in the catalytic action of ALDH1.	NAD	182-188	aldehyde dehydrogenase 1 family member A1	Homo sapiens	246-251
31515847-1	2019	As a deacetylase relying on NAD, sirtuin 1 (SIRT1) has been proven to inhibit osteoclastogenesis directly by repressing reactive oxygen species (ROS) production and TRPV1 channel stimulation modulated by TNF-alpha.	NAD	28-31	sirtuin 1	Homo sapiens	44-49
31993545-2	2019	It has been known that nicotinamide inhibits the enzymatic activity of SIRT1, an NAD+-dependent deacetylase.	NAD	81-84	sirtuin 1	Homo sapiens	71-76
16571104-12	2006	The findings of the present study indicate that the hydroxylation requires complex formation between Des2 and mb5 via their membrane-spanning domains and electron transfer from NADH to the substrate via the reduction of mb5 by b5R.	NAD	177-181	delta(4)-desaturase, sphingolipid 2	Mus musculus	101-105
31608530-10	2019	Treatment with DPN resulted in the up-regulation of CREB and BDNF expressions, while PPT up-regulated expression of CREB without affecting BDNF levels.	NAD	15-18	brain-derived neurotrophic factor	Rattus norvegicus	61-65
16762039-6	2006	Here, we show that HIC1 interacts with both CtBP1 and CtBP2 and that this interaction is stimulated by agents increasing NADH levels.	NAD	121-125	HIC ZBTB transcriptional repressor 1	Homo sapiens	19-23
31723053-5	2019	Ischemia-induced NADH elevation in the cortex indicated prolonged production of reactive oxygen species by xanthine oxidase (XOD).	NAD	17-21	xanthine dehydrogenase	Mus musculus	107-123
16897483-7	2006	Cm-ADH1 has strong preference for NAPDH as a co-factor, whereas Cm-ADH2 preferentially uses NADH.	NAD	92-96	alcohol dehydrogenase ADH2	Saccharomyces cerevisiae S288C	67-71
31282985-1	2019	SIRT1, a member of the sirtuin family, belongs to the NAD +-dependent class III histone deacetylase.	NAD	54-59	sirtuin 1	Homo sapiens	0-5
16940699-10	2006	U-II also activates nicotinamide adenine dinucleotide phosphate (NADPH) oxidase and plasminogen activator inhibitor-1 in human VSMCs, and stimulates VSMC proliferation with synergistic effects observed when combined with oxidized low-density lipoprotein, lysophosphatidylcholine, reactive oxygen species or serotonin.	NAD	20-53	urotensin 2	Homo sapiens	0-4
31390002-2	2019	Preclinical evidence suggests that the NAD+/SIRT1 axis may be implicated in modulating important gut-related aspects of glucose regulation.	NAD	39-43	sirtuin 1	Homo sapiens	44-49
31634899-8	2019	We further demonstrate that ferroptosis suppression by FSP1 is mediated via ubiquinone (CoQ10): its reduced form ubiquinol traps lipid peroxyl radicals that mediate lipid peroxidation, while FSP1 catalyses its regeneration by using NAD(P)H.	NAD	232-239	S100 calcium binding protein A4	Homo sapiens	55-59
16648462-1	2006	The mammalian cytoplasmic protein SirT2 is a member of the Sir2 family of NAD+-dependent protein deacetylases involved in caloric restriction-dependent life span extension.	NAD	74-77	sirtuin 2	Homo sapiens	34-39
16571778-1	2006	The transmembrane glycoprotein CD38 catalyzes the synthesis of the calcium mobilizing molecule cyclic ADP-ribose from NAD.	NAD	118-121	CD38 molecule	Homo sapiens	31-35
31651733-3	2019	We hypothesized that SIRT1 expression is decreased in proinflammatory lymphocytes following lung transplant and that treatment with SIRT1 activators (resveratrol, curcumin) and agents that prevent NAD depletion (theophylline) upregulate SIRT1 and reduce proinflammatory cytokine expression in these cells.	NAD	197-200	sirtuin 1	Homo sapiens	21-26
31651733-3	2019	We hypothesized that SIRT1 expression is decreased in proinflammatory lymphocytes following lung transplant and that treatment with SIRT1 activators (resveratrol, curcumin) and agents that prevent NAD depletion (theophylline) upregulate SIRT1 and reduce proinflammatory cytokine expression in these cells.	NAD	197-200	sirtuin 1	Homo sapiens	132-137
31651733-3	2019	We hypothesized that SIRT1 expression is decreased in proinflammatory lymphocytes following lung transplant and that treatment with SIRT1 activators (resveratrol, curcumin) and agents that prevent NAD depletion (theophylline) upregulate SIRT1 and reduce proinflammatory cytokine expression in these cells.	NAD	197-200	sirtuin 1	Homo sapiens	132-137
16618762-2	2006	Hereby, we describe the identification of a compound we named cambinol that inhibits NAD-dependent deacetylase activity of human SIRT1 and SIRT2.	NAD	85-88	sirtuin 2	Homo sapiens	139-144
31681271-0	2019	Switch of NAD Salvage to de novo Biosynthesis Sustains SIRT1-RelB-Dependent Inflammatory Tolerance.	NAD	10-13	sirtuin 1	Homo sapiens	55-60
31681271-6	2019	This is resulted from the IDO1-dependent expansion of nuclear NAD pool and nuclear NAD-dependent prolongation of sirtuin1 (SIRT1)-directed epigenetics of immune tolerance.	NAD	83-86	sirtuin 1	Homo sapiens	113-121
31681271-6	2019	This is resulted from the IDO1-dependent expansion of nuclear NAD pool and nuclear NAD-dependent prolongation of sirtuin1 (SIRT1)-directed epigenetics of immune tolerance.	NAD	83-86	sirtuin 1	Homo sapiens	123-128
31681271-7	2019	Inhibition of IDO1 activity predominantly decreased nuclear NAD level, which promoted sequential dissociations of immunosuppressive SIRT1 and RelB from the promoter of pro-inflammatory TNF-alpha gene and broke endotoxin tolerance.	NAD	60-63	sirtuin 1	Homo sapiens	132-137
16261579-2	2006	Our results suggest that CD38 is likely to recognize the two phosphate groups in NAD and the two carboxyl groups in tandem sialic acid residues of gangliosides.	NAD	81-84	CD38 molecule	Homo sapiens	25-29
31590397-13	2019	Rb1 provides an advantage during high glucose-induced cell damage by targeting the NAD-PARP-SIRT signaling pathway and modulating the redox state in RCECs.	NAD	83-86	RB transcriptional corepressor 1	Rattus norvegicus	0-3
31353811-0	2019	Augmentation of cellular NAD+ by NQO1 enzymatic action improves age-related hearing impairment.	NAD	25-29	NAD(P)H dehydrogenase, quinone 1	Mus musculus	33-37
31353811-3	2019	Recent studies suggest that NAD+ /NADH ratio may play a critical role in cellular senescence by regulating sirtuins, PARP-1, and PGC-1alpha.	NAD	28-32	poly (ADP-ribose) polymerase family, member 1	Mus musculus	117-123
31353811-3	2019	Recent studies suggest that NAD+ /NADH ratio may play a critical role in cellular senescence by regulating sirtuins, PARP-1, and PGC-1alpha.	NAD	34-38	poly (ADP-ribose) polymerase family, member 1	Mus musculus	117-123
16385446-8	2006	In an application to asthma case-control data from the Children"s Health Study, FITF identified a significant multilocus effect between the nicotinamide adenine dinucleotide (phosphate) reduced:quinone oxidoreductase gene (NQO1), myeloperoxidase gene (MPO), and catalase gene (CAT) (unadjusted P = .00026), three genes that are involved in the oxidative stress pathway.	NAD	140-173	crystallin zeta	Homo sapiens	194-216
31353811-5	2019	Herein, we investigated the effect of beta-lapachone (beta-lap), a known plant-derived metabolite that modulates cellular NAD+ by conversion of NADH to NAD+ via the enzymatic action of NADH: quinone oxidoreductase 1 (NQO1) on ARHL in C57BL/6 mice.	NAD	144-148	NAD(P)H dehydrogenase, quinone 1	Mus musculus	185-215
31353811-5	2019	Herein, we investigated the effect of beta-lapachone (beta-lap), a known plant-derived metabolite that modulates cellular NAD+ by conversion of NADH to NAD+ via the enzymatic action of NADH: quinone oxidoreductase 1 (NQO1) on ARHL in C57BL/6 mice.	NAD	152-156	NAD(P)H dehydrogenase, quinone 1	Mus musculus	185-215
16484774-1	2006	Sirtuin 5 (SIRT5) is a nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase and belongs to the Silent information regulator 2 (Sir2) family of sirtuin histone deacetylases (HDACs), which play a central role in epigenetic gene silencing, DNA repair and recombination, cell-cycle, microtubule organization, and in the regulation of aging.	NAD	23-56	sirtuin 2	Homo sapiens	137-141
16484774-1	2006	Sirtuin 5 (SIRT5) is a nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase and belongs to the Silent information regulator 2 (Sir2) family of sirtuin histone deacetylases (HDACs), which play a central role in epigenetic gene silencing, DNA repair and recombination, cell-cycle, microtubule organization, and in the regulation of aging.	NAD	58-61	sirtuin 2	Homo sapiens	137-141
16181422-5	2005	During the Reox, PARP-1 was much activated and autopoly(ADP-ribosyl)ated, consuming the substrate, NAD+.	NAD	99-103	poly (ADP-ribose) polymerase 1	Rattus norvegicus	17-23
30721374-1	2019	Silent information regulator 1 (SIRT1) is a nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase, and the function is linked to cellular metabolism including mitochondrial biogenesis.	NAD	44-77	sirtuin 1	Homo sapiens	0-30
30721374-1	2019	Silent information regulator 1 (SIRT1) is a nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase, and the function is linked to cellular metabolism including mitochondrial biogenesis.	NAD	44-77	sirtuin 1	Homo sapiens	32-37
30721374-1	2019	Silent information regulator 1 (SIRT1) is a nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase, and the function is linked to cellular metabolism including mitochondrial biogenesis.	NAD	79-83	sirtuin 1	Homo sapiens	0-30
30721374-1	2019	Silent information regulator 1 (SIRT1) is a nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase, and the function is linked to cellular metabolism including mitochondrial biogenesis.	NAD	79-83	sirtuin 1	Homo sapiens	32-37
30721374-4	2019	In this study, we hypothesized that the metabolic production of NAD+ from L-serine and thus activation of SIRT1 contribute to the action of L-serine.	NAD	64-68	sirtuin 1	Homo sapiens	106-111
30993413-6	2019	Mac1 appears to work with the Hst1-Sum1-Rfm1 complex to repress the expression of de novo NAD+ biosynthesis genes.	NAD	90-94	Sum1p	Saccharomyces cerevisiae S288C	35-39
30901096-8	2019	Mechanistically, the acetylation status of MRPS5 is directly regulated by NAD+ dependent deacetylase sirtuin-1 (SIRT1), which is abundant in liver CSCs and decreased during differentiation.	NAD	74-77	sirtuin 1	Homo sapiens	101-110
30901096-8	2019	Mechanistically, the acetylation status of MRPS5 is directly regulated by NAD+ dependent deacetylase sirtuin-1 (SIRT1), which is abundant in liver CSCs and decreased during differentiation.	NAD	74-77	sirtuin 1	Homo sapiens	112-117
16076959-2	2005	We previously reported that Foxo1, a member of the FOXO family, is regulated through reversible acetylation catalyzed by histone acetyltransferase cAMP-response element-binding protein (CREB)-binding protein (CBP) and NAD-dependent histone deacetylase silent information regulator 2, and that the acetylation at Lys-242, Lys-245, and Lys-262 of Foxo1 attenuates its transcriptional activity.	NAD	218-221	sirtuin 2	Homo sapiens	252-282
16023112-1	2005	When the influence of ADP-ribosylation on the activities of the purified human glutamate dehydrogenase isozymes (hGDH1 and hGDH2) was measured in the presence of 100 microM NAD+ for 60 min, hGDH isozymes were inhibited by up to 75%.	NAD	173-177	glutamate dehydrogenase 1	Homo sapiens	113-118
31292999-1	2019	Sirtuin-1 and -3 (SIRT1 and SIRT3) are important nicotinamide adenine dinucleotide (NAD+ )-dependent deacetylases known to regulate a variety of cellular functions.	NAD	49-82	sirtuin 1	Homo sapiens	0-16
31292999-1	2019	Sirtuin-1 and -3 (SIRT1 and SIRT3) are important nicotinamide adenine dinucleotide (NAD+ )-dependent deacetylases known to regulate a variety of cellular functions.	NAD	49-82	sirtuin 1	Homo sapiens	18-23
16006743-1	2005	Sir2 (silent information regulator 2) is an NAD-dependent deacetylase that is broadly conserved from bacteria to humans.	NAD	44-47	sirtuin 2	Homo sapiens	0-4
31292999-1	2019	Sirtuin-1 and -3 (SIRT1 and SIRT3) are important nicotinamide adenine dinucleotide (NAD+ )-dependent deacetylases known to regulate a variety of cellular functions.	NAD	84-87	sirtuin 1	Homo sapiens	0-16
31292999-1	2019	Sirtuin-1 and -3 (SIRT1 and SIRT3) are important nicotinamide adenine dinucleotide (NAD+ )-dependent deacetylases known to regulate a variety of cellular functions.	NAD	84-87	sirtuin 1	Homo sapiens	18-23
31575956-5	2019	In TRPM2 depleted cells, antioxidant cofactors glutathione, NADPH, and NADH were significantly reduced.	NAD	71-75	transient receptor potential cation channel subfamily M member 2	Homo sapiens	3-8
16006743-1	2005	Sir2 (silent information regulator 2) is an NAD-dependent deacetylase that is broadly conserved from bacteria to humans.	NAD	44-47	sirtuin 2	Homo sapiens	6-36
15911748-8	2005	A strong correlation between the Cyp-GRD peptide and mitochondrial NADH concentration suggests that the new molecule could also report on the metabolic status of cells ex vivo.	NAD	67-71	peptidylprolyl isomerase G	Homo sapiens	33-36
31557786-1	2019	Sirtuins (SIRTs) are seven nicotinamide adenine dinucleotide (NAD+)-dependent protein deacetylases enzymes (SIRT1-7) that play an important role in maintaining cellular homeostasis.	NAD	27-60	sirtuin 1	Homo sapiens	108-115
31557786-1	2019	Sirtuins (SIRTs) are seven nicotinamide adenine dinucleotide (NAD+)-dependent protein deacetylases enzymes (SIRT1-7) that play an important role in maintaining cellular homeostasis.	NAD	62-66	sirtuin 1	Homo sapiens	108-115
15838709-9	2005	These correlations were biased by the large response to fenofibrate compared to the other treatments; nevertheless the data do indicate a relationship between the tryptophan-NAD+ pathway and PPARalpha-dependent pathways, making this metabolite a potentially useful biomarker to detect PP.	NAD	174-178	peroxisome proliferator activated receptor alpha	Rattus norvegicus	191-200
31608282-3	2019	Sirtuin 1 (SIRT1) is a nicotinamide adenine dinucleotide-dependent enzyme that is frequently overexpressed in HCC, where it promotes tumorigenicity, metastasis, and chemoresistance.	NAD	23-56	sirtuin 1	Homo sapiens	0-9
31608282-3	2019	Sirtuin 1 (SIRT1) is a nicotinamide adenine dinucleotide-dependent enzyme that is frequently overexpressed in HCC, where it promotes tumorigenicity, metastasis, and chemoresistance.	NAD	23-56	sirtuin 1	Homo sapiens	11-16
15466246-3	2005	Among several NAD(+)-utilizing enzymes, DR2313 was specific for PARP but not selective between PARP-1 and PARP-2.	NAD	14-20	poly (ADP-ribose) polymerase 1	Rattus norvegicus	64-68
31513012-2	2019	TRPM2"s activation by Ca2+ and ADP ribose (ADPR), an NAD+-metabolite produced under oxidative stress and neurodegenerative conditions, suggests a role in neurological disorders.	NAD	53-57	transient receptor potential cation channel subfamily M member 2	Homo sapiens	0-5
23045123-1	2005	NADH cytochrome b(5) reductase (b(5)R; EC 1.6.2.2; Diaphorase I; NADH: ferricytochrome b(5) oxidoreductase) is an FAD-containing protein, which, along with the hemoprotein cytochrome b(5) (cyt b(5)), mediates electron transfer from NADH to fatty acid desaturases, P450 oxidases, methemoglobin, and ascorbyl free radical.	NAD	0-4	cytochrome b5 type A	Homo sapiens	5-20
23045123-1	2005	NADH cytochrome b(5) reductase (b(5)R; EC 1.6.2.2; Diaphorase I; NADH: ferricytochrome b(5) oxidoreductase) is an FAD-containing protein, which, along with the hemoprotein cytochrome b(5) (cyt b(5)), mediates electron transfer from NADH to fatty acid desaturases, P450 oxidases, methemoglobin, and ascorbyl free radical.	NAD	0-4	cytochrome b5 type A	Homo sapiens	76-91
23045123-1	2005	NADH cytochrome b(5) reductase (b(5)R; EC 1.6.2.2; Diaphorase I; NADH: ferricytochrome b(5) oxidoreductase) is an FAD-containing protein, which, along with the hemoprotein cytochrome b(5) (cyt b(5)), mediates electron transfer from NADH to fatty acid desaturases, P450 oxidases, methemoglobin, and ascorbyl free radical.	NAD	0-4	cytochrome b5 type A	Homo sapiens	189-197
31075303-1	2019	Sirtuin 7 (SIRT7) is an NAD+-dependent lysine deacetylase that regulates diverse biological processes.	NAD	24-27	sirtuin 7	Homo sapiens	0-9
31075303-1	2019	Sirtuin 7 (SIRT7) is an NAD+-dependent lysine deacetylase that regulates diverse biological processes.	NAD	24-27	sirtuin 7	Homo sapiens	11-16
15494407-0	2004	The malate-aspartate NADH shuttle member Aralar1 determines glucose metabolic fate, mitochondrial activity, and insulin secretion in beta cells.	NAD	21-25	solute carrier family 25 member 12	Rattus norvegicus	41-48
15381699-4	2004	In this study, we determined the kinetics of the NAD biosynthesis mediated by nicotinamide phosphoribosyltransferase (Nampt) and nicotinamide/nicotinic acid mononucleotide adenylyltransferase (Nmnat), and we examined its effects on the transcriptional regulatory function of the mouse Sir2 ortholog, Sir2alpha, in mouse fibroblasts.	NAD	49-52	sirtuin 1	Mus musculus	285-289
31304802-14	2019	RANKL -643 C/T was significantly associated with DPN alone while -693 C/G was significantly associated with both DPN and CN.	NAD	49-52	TNF superfamily member 11	Homo sapiens	0-5
15381699-4	2004	In this study, we determined the kinetics of the NAD biosynthesis mediated by nicotinamide phosphoribosyltransferase (Nampt) and nicotinamide/nicotinic acid mononucleotide adenylyltransferase (Nmnat), and we examined its effects on the transcriptional regulatory function of the mouse Sir2 ortholog, Sir2alpha, in mouse fibroblasts.	NAD	49-52	sirtuin 1	Mus musculus	300-309
15650244-2	2004	A topological paradox has long been recognized, as CD38 is an ectoenzyme, or an intravesicularly located enzyme in subcellular membrane vesicles, therefore apparently shielded from its substrate NAD+.	NAD	195-199	CD38 molecule	Homo sapiens	51-55
15650244-5	2004	Connexin 43 (Cx43) hemichannels mediate an equilibrative transport of NAD+ from the cytosol to the active site of CD38 (either ectocellular or intravesicular).	NAD	70-74	CD38 molecule	Homo sapiens	114-118
31317367-1	2019	Sirtuin1 (SIRT1) is a mammalian NAD+-dependent type III deacetylase that plays paramount roles in diverse cellular processes.	NAD	32-35	sirtuin 1	Homo sapiens	0-8
31317367-1	2019	Sirtuin1 (SIRT1) is a mammalian NAD+-dependent type III deacetylase that plays paramount roles in diverse cellular processes.	NAD	32-35	sirtuin 1	Homo sapiens	10-15
15465278-3	2004	Upon activation PARP-1 uses NAD(+) as a substrate to catalyze the transfer of ADP-ribose subunits to a host of nuclear proteins.	NAD	28-34	poly (ADP-ribose) polymerase 1	Rattus norvegicus	16-22
15450783-2	2004	Because mitochondrial dysfunction has been suggested in bipolar disorder, NDUFV2 at 18p11, encoding a subunit of the complex I, reduced nicotinamide adenine dinucleotide (NADH)ubiquinone oxidoreductase, is a candidate gene for this disorder.	NAD	136-169	NADH:ubiquinone oxidoreductase core subunit V2	Homo sapiens	74-80
31452603-4	2019	Furthermore, by supporting a new mother"s apparent higher demand for NAD precursors, we increased circulation of prolactin, superinduced mammary biosynthetic programs, increased her time of arched-back nursing, enhanced mammary production of brain-derived neurotrophic factor, promoted postgestational weight loss, advanced the neurobehavioral development of her offspring, and allowed them to mature as stronger and more resilient adults with advantages in hippocampal neurogenesis and body composition.	NAD	69-72	brain derived neurotrophic factor	Homo sapiens	242-275
31447857-9	2019	In conclusion, our data indicate that an AMPK-NAMPT-NAD+ signaling axis promotes P2Y11 receptor expression during M2 polarization of human macrophages in response to IL-10.	NAD	52-56	interleukin 10	Homo sapiens	166-171
15210723-3	2004	The growth inhibition of respiratory incompetent cox18Delta cells lacking GPD2 is reversed by the addition of acetoin, an alternative sink for NADH oxidation.	NAD	143-147	glycerol-3-phosphate dehydrogenase (NAD(+)) GPD2	Saccharomyces cerevisiae S288C	74-78
15233622-5	2004	Selective inhibition of CD38, an NAD-glycohydrolase that generates free ADPR from NAD(+), does not abolish the effect of NAD(+), excluding the possibility that NAD(+) might act via ADPR.	NAD	82-88	CD38 molecule	Homo sapiens	24-28
15075382-1	2004	The activation of poly(ADP-ribose) polymerase-1 (PARP-1) after exposure to nitric oxide or oxygen-free radicals can lead to cell injury via severe, irreversible depletion of NAD.	NAD	174-177	poly (ADP-ribose) polymerase 1	Rattus norvegicus	18-47
15075382-1	2004	The activation of poly(ADP-ribose) polymerase-1 (PARP-1) after exposure to nitric oxide or oxygen-free radicals can lead to cell injury via severe, irreversible depletion of NAD.	NAD	174-177	poly (ADP-ribose) polymerase 1	Rattus norvegicus	49-55
15075382-6	2004	In cell death model, treatment with FR247304 (10(-8)-10(-5) M) significantly reduced NAD depletion by PARP-1 inhibition and attenuated cell death after hydrogen peroxide (100 microM) exposure.	NAD	85-88	poly (ADP-ribose) polymerase 1	Rattus norvegicus	102-108
15266023-1	2004	Recent evidence suggests that CD38, an ectoenzyme that converts NAD(+) to cyclic ADP-ribose (cADPr), may play a role in cytokine-induced airway smooth muscle (ASM) cell hyper-responsiveness, a key feature associated with chronic asthma.	NAD	64-70	CD38 molecule	Homo sapiens	30-34
15505998-1	2004	Human CD38 is a protein which catalyzes the synthesis of nicotinic acid adenine dinucleotide (NAADP+) and the conversion of NAD+ to cADPR.	NAD	124-128	CD38 molecule	Homo sapiens	6-10
15199149-0	2004	CtBP contributes quantitatively to Knirps repression activity in an NAD binding-dependent manner.	NAD	68-71	C-terminal Binding Protein	Drosophila melanogaster	0-4
15199149-8	2004	CtBP mutant proteins unable to bind NAD fail to interact with DNA-bound factors.	NAD	36-39	C-terminal Binding Protein	Drosophila melanogaster	0-4
15199149-9	2004	We show that DNA-binding Gal4-CtBP fusion proteins also require NAD binding for activity, indicating that NAD plays a role in repression at a step subsequent to CtBP recruitment to the promoter.	NAD	64-67	C-terminal Binding Protein	Drosophila melanogaster	30-34
15199149-9	2004	We show that DNA-binding Gal4-CtBP fusion proteins also require NAD binding for activity, indicating that NAD plays a role in repression at a step subsequent to CtBP recruitment to the promoter.	NAD	106-109	C-terminal Binding Protein	Drosophila melanogaster	30-34
14754756-1	2004	Poly(ADP-ribose) polymerase 1 (PARP-1) is the predominant NAD-dependent modifying enzyme in DNA repair, transcription, and apoptosis; its involvement in development has not been defined.	NAD	58-61	poly (ADP-ribose) polymerase 1	Rattus norvegicus	0-29
14754756-1	2004	Poly(ADP-ribose) polymerase 1 (PARP-1) is the predominant NAD-dependent modifying enzyme in DNA repair, transcription, and apoptosis; its involvement in development has not been defined.	NAD	58-61	poly (ADP-ribose) polymerase 1	Rattus norvegicus	31-37
15101683-5	2004	To rationally design inhibitors it is critical to understand the mechanism(s) by which CD38 catalyzes the transformation of its substrate NAD+ into cyclic ADP-ribose.	NAD	138-142	CD38 molecule	Homo sapiens	87-91
14741735-2	2004	Using the natural substrate of the enzyme, NAD+, the ratio of ADP-ribosyl cyclase/NAD glycohydrolase of CD38 is about 1/100.	NAD	43-47	CD38 molecule	Homo sapiens	104-108
14652693-1	2004	A strain of Saccharomyces cerevisiae lacking the GPD2 gene, encoding one of the glycerol-3-phosphate dehydrogenases, grows slowly under anaerobic conditions, due to reductive stress caused by the accumulation of cytoplasmic NADH.	NAD	224-228	glycerol-3-phosphate dehydrogenase (NAD(+)) GPD2	Saccharomyces cerevisiae S288C	49-53
15047725-7	2004	The recombinant soluble cytochrome b(5) showed an asymmetrical absorption spectrum at 560 nm as is shown by mammalian cytochromes b(5) upon reduction with NADH and NADH-cytochrome b(5) reductase.	NAD	155-159	cytochrome b5 type A	Homo sapiens	24-39
14706864-0	2004	Predominant expression of Sir2alpha, an NAD-dependent histone deacetylase, in the embryonic mouse heart and brain.	NAD	40-43	sirtuin 1	Mus musculus	26-35
14522996-1	2003	Silent information regulator 2 (Sir2) enzymes catalyze NAD+-dependent protein/histone deacetylation, where the acetyl group from the lysine epsilon-amino group is transferred to the ADP-ribose moiety of NAD+, producing nicotinamide and the novel metabolite O-acetyl-ADP-ribose.	NAD	55-59	sirtuin 2	Homo sapiens	0-30
14522996-1	2003	Silent information regulator 2 (Sir2) enzymes catalyze NAD+-dependent protein/histone deacetylation, where the acetyl group from the lysine epsilon-amino group is transferred to the ADP-ribose moiety of NAD+, producing nicotinamide and the novel metabolite O-acetyl-ADP-ribose.	NAD	55-59	sirtuin 2	Homo sapiens	32-36
14522996-1	2003	Silent information regulator 2 (Sir2) enzymes catalyze NAD+-dependent protein/histone deacetylation, where the acetyl group from the lysine epsilon-amino group is transferred to the ADP-ribose moiety of NAD+, producing nicotinamide and the novel metabolite O-acetyl-ADP-ribose.	NAD	203-207	sirtuin 2	Homo sapiens	0-30
14522996-1	2003	Silent information regulator 2 (Sir2) enzymes catalyze NAD+-dependent protein/histone deacetylation, where the acetyl group from the lysine epsilon-amino group is transferred to the ADP-ribose moiety of NAD+, producing nicotinamide and the novel metabolite O-acetyl-ADP-ribose.	NAD	203-207	sirtuin 2	Homo sapiens	32-36
19087393-2	2003	On the other hand, ADP-ribosyl cyclase/cyclic ADP-ribose hydrolase (CD38) synthesizes cyclic ADP-ribose from NAD+, which acts as a second messenger, mobilizing intracellular Ca2+ for insulin secretion in response to glucose in beta-cells.	NAD	109-113	CD38 molecule	Homo sapiens	68-72
14580993-1	2003	The lymphoid surface antigen CD38 is a NAD(+)-glycohydrolase that also catalyzes the transformation of NAD(+) into cyclic ADP-ribose, a calcium mobilizing second messenger.	NAD	39-45	CD38 molecule	Homo sapiens	29-33
14580993-4	2003	We have now examined the molecular changes of this protein during its interaction with NAD(+) by measuring the intrinsic fluorescence of CD38.	NAD	87-93	CD38 molecule	Homo sapiens	137-141
12963490-0	2003	Inhibition of indoleamine 2,3-dioxygenase activity in IFN-gamma stimulated astroglioma cells decreases intracellular NAD levels.	NAD	117-120	indoleamine 2,3-dioxygenase 1	Homo sapiens	14-41
12943516-3	2003	In contrast, 11beta-HSD2 is a NAD-dependent dehydrogenase inactivating cortisol to cortisone, thereby protecting the mineralocorticoid receptor from occupation by cortisol.	NAD	30-33	hydroxysteroid 11-beta dehydrogenase 2	Homo sapiens	13-24
30697640-2	2019	Sirtuin 1 (SIRT1) is an NAD-dependent deacetylase enzyme that contributes in the regulation of metabolic processes and protects against lipid accumulation in hepatocytes.	NAD	24-27	sirtuin 1	Homo sapiens	0-9
30697640-2	2019	Sirtuin 1 (SIRT1) is an NAD-dependent deacetylase enzyme that contributes in the regulation of metabolic processes and protects against lipid accumulation in hepatocytes.	NAD	24-27	sirtuin 1	Homo sapiens	11-16
12950262-1	2003	The plastid terminal oxidase (PTOX) encoded by the Arabidopsis IMMUTANS gene was expressed in Escherichia coli cells and its quinone/oxygen oxidoreductase activity monitored in isolated bacterial membranes using NADH as an electron donor.	NAD	212-216	Alternative oxidase family protein	Arabidopsis thaliana	4-28
31142674-6	2019	The mammalian homologue of SIR2 is SIRT1, an NAD-dependent histone deacetylase.	NAD	45-48	sirtuin 1	Homo sapiens	27-31
31142674-6	2019	The mammalian homologue of SIR2 is SIRT1, an NAD-dependent histone deacetylase.	NAD	45-48	sirtuin 1	Homo sapiens	35-40
31142674-13	2019	The mammalian homologue of SIR2 is SIRT1, an NAD-dependent histone deacetylase.	NAD	45-48	sirtuin 1	Homo sapiens	27-31
12950262-1	2003	The plastid terminal oxidase (PTOX) encoded by the Arabidopsis IMMUTANS gene was expressed in Escherichia coli cells and its quinone/oxygen oxidoreductase activity monitored in isolated bacterial membranes using NADH as an electron donor.	NAD	212-216	Alternative oxidase family protein	Arabidopsis thaliana	30-34
31142674-13	2019	The mammalian homologue of SIR2 is SIRT1, an NAD-dependent histone deacetylase.	NAD	45-48	sirtuin 1	Homo sapiens	35-40
12969423-7	2003	AXS1 required NAD+ for enzymatic activity, and was strongly inhibited by UDP-d-galacturonate.	NAD	14-18	UDP-D-apiose/UDP-D-xylose synthase 1	Arabidopsis thaliana	0-4
30969017-5	2019	High-producing cell lines bear unique mutations in nicotinamide adenine dinucleotide (NADH) dehydrogenase (ND2 and ND4) and in peroxisomal acyl-CoA synthetase (ACSL4), involved in lipid metabolism.	NAD	86-90	NADH dehydrogenase subunit 4	Cricetulus griseus	115-118
12918120-8	2003	NADH could not only eliminate the apoptosis induced by X-ray irradiation, but also up-regulate expression of bcl-2 protein and down-regulate expression of p53, bax, fas and fasL proteins (P&lt;0.05).	NAD	0-4	Fas ligand	Homo sapiens	173-177
31108370-2	2019	Pyrroline-5-carboxylate reductase 1 (PYCR1) participates in proline synthesis process by catalyzing the reduction of P5C to proline with concomitant generation of NAD+ and NADP+.	NAD	163-167	pyrroline-5-carboxylate reductase 1	Homo sapiens	0-35
31108370-2	2019	Pyrroline-5-carboxylate reductase 1 (PYCR1) participates in proline synthesis process by catalyzing the reduction of P5C to proline with concomitant generation of NAD+ and NADP+.	NAD	163-167	pyrroline-5-carboxylate reductase 1	Homo sapiens	37-42
12918120-10	2003	CONCLUSION: NADH has marked anti-radiation effect, its mechanism may be associated with up-regulation of bcl-2 expression and down-regulation of p53, bax fas and fasL expression, as well as decline of intracellular ROS.	NAD	12-16	Fas ligand	Homo sapiens	162-166
31151734-1	2019	Various nutritional signals are transduced by two epigenetic pathways: NAD-dependent sirtuin Sirt1 (NAD+-Sirt1) deacetylase and flavin adenine dinucleotide-dependent lysine-specific demethylase 1 (FAD-LSD1).	NAD	71-74	sirtuin 1	Homo sapiens	93-98
12834903-1	2003	Poly(ADP-ribose) is synthesized from nicotinamide adenine dinucleotide (NAD(+)) by poly(ADP-ribose) polymerase (PARP) and degraded by poly(ADP-ribose) glycohydrolase (PARG).	NAD	72-78	poly (ADP-ribose) glycohydrolase	Rattus norvegicus	167-171
31151734-1	2019	Various nutritional signals are transduced by two epigenetic pathways: NAD-dependent sirtuin Sirt1 (NAD+-Sirt1) deacetylase and flavin adenine dinucleotide-dependent lysine-specific demethylase 1 (FAD-LSD1).	NAD	71-74	sirtuin 1	Homo sapiens	100-110
12805226-2	2003	Co-repressor activity is regulated by NAD(H) binding to CtBP/BARS, while membrane fission is associated with its acyl-CoA-dependent acyltransferase activity.	NAD	38-44	C-terminal binding protein 1	Rattus norvegicus	61-65
30450916-7	2019	We have identified new molecules that modulate the hAIF reduced nicotinamide adenine dinucleotide (NADH)/oxidized nicotinamide adenine dinucleotide (NAD+) association/dissociation equilibrium and regulate its catalytic efficiency.	NAD	64-97	apoptosis inducing factor mitochondria associated 1	Homo sapiens	51-55
12944176-5	2003	1H nuclear magnetic resonance spectroscopy and multivariate statistical data analysis of urinary spectra from animals given the PPARalpha and -delta agonists identified two new potential biomarkers of peroxisome proliferation--N-methylnicotinamide (NMN) and N-methyl-4-pyridone-3-carboxamide (4PY)--both endproducts of the tryptophan-nicotinamide adenine dinucleotide (NAD+) pathway.	NAD	334-367	peroxisome proliferator activated receptor alpha	Rattus norvegicus	128-137
30450916-7	2019	We have identified new molecules that modulate the hAIF reduced nicotinamide adenine dinucleotide (NADH)/oxidized nicotinamide adenine dinucleotide (NAD+) association/dissociation equilibrium and regulate its catalytic efficiency.	NAD	99-103	apoptosis inducing factor mitochondria associated 1	Homo sapiens	51-55
30450916-7	2019	We have identified new molecules that modulate the hAIF reduced nicotinamide adenine dinucleotide (NADH)/oxidized nicotinamide adenine dinucleotide (NAD+) association/dissociation equilibrium and regulate its catalytic efficiency.	NAD	114-147	apoptosis inducing factor mitochondria associated 1	Homo sapiens	51-55
30450916-7	2019	We have identified new molecules that modulate the hAIF reduced nicotinamide adenine dinucleotide (NADH)/oxidized nicotinamide adenine dinucleotide (NAD+) association/dissociation equilibrium and regulate its catalytic efficiency.	NAD	149-153	apoptosis inducing factor mitochondria associated 1	Homo sapiens	51-55
30450916-10	2019	NADH-redox-linked conformation changes course with strong NAD+ binding and protein dimerization, but they produce a negative impact in overall hAIF stability.	NAD	0-4	apoptosis inducing factor mitochondria associated 1	Homo sapiens	143-147
12944176-5	2003	1H nuclear magnetic resonance spectroscopy and multivariate statistical data analysis of urinary spectra from animals given the PPARalpha and -delta agonists identified two new potential biomarkers of peroxisome proliferation--N-methylnicotinamide (NMN) and N-methyl-4-pyridone-3-carboxamide (4PY)--both endproducts of the tryptophan-nicotinamide adenine dinucleotide (NAD+) pathway.	NAD	369-373	peroxisome proliferator activated receptor alpha	Rattus norvegicus	128-137
12681501-5	2003	The K(M) values for NADH and 2-oxoglutarate were 1.5-fold and 2.5-fold greater, respectively, for the mutant GDH than for wild-type GDH, indicating that substitution at position 454 had appreciable effects on the affinity of the enzyme for both NADH and 2-oxoglutarate.	NAD	20-24	glutamate dehydrogenase 1	Homo sapiens	109-112
31175267-0	2019	Nicotinamide phosphoribosyltransferase postpones rat bone marrow mesenchymal stem cell senescence by mediating NAD+-Sirt1 signaling.	NAD	111-115	nicotinamide phosphoribosyltransferase	Rattus norvegicus	0-38
31175267-2	2019	Previously, we found that MSC natural senescence is accompanied by altered intracellular nicotinamide adenine dinucleotide (NAD+) metabolism, in which Nampt plays a key role.	NAD	89-122	nicotinamide phosphoribosyltransferase	Rattus norvegicus	151-156
31175267-2	2019	Previously, we found that MSC natural senescence is accompanied by altered intracellular nicotinamide adenine dinucleotide (NAD+) metabolism, in which Nampt plays a key role.	NAD	124-128	nicotinamide phosphoribosyltransferase	Rattus norvegicus	151-156
31175267-7	2019	Further, Nampt inhibition resulted in reduced intracellular NAD+ content, NAD+/NADH ratio, and Sirt1 activity, whereas overexpression had the opposite effects.	NAD	60-64	nicotinamide phosphoribosyltransferase	Rattus norvegicus	9-14
31175267-7	2019	Further, Nampt inhibition resulted in reduced intracellular NAD+ content, NAD+/NADH ratio, and Sirt1 activity, whereas overexpression had the opposite effects.	NAD	74-78	nicotinamide phosphoribosyltransferase	Rattus norvegicus	9-14
12681501-5	2003	The K(M) values for NADH and 2-oxoglutarate were 1.5-fold and 2.5-fold greater, respectively, for the mutant GDH than for wild-type GDH, indicating that substitution at position 454 had appreciable effects on the affinity of the enzyme for both NADH and 2-oxoglutarate.	NAD	20-24	glutamate dehydrogenase 1	Homo sapiens	132-135
12681501-5	2003	The K(M) values for NADH and 2-oxoglutarate were 1.5-fold and 2.5-fold greater, respectively, for the mutant GDH than for wild-type GDH, indicating that substitution at position 454 had appreciable effects on the affinity of the enzyme for both NADH and 2-oxoglutarate.	NAD	245-249	glutamate dehydrogenase 1	Homo sapiens	109-112
12681501-5	2003	The K(M) values for NADH and 2-oxoglutarate were 1.5-fold and 2.5-fold greater, respectively, for the mutant GDH than for wild-type GDH, indicating that substitution at position 454 had appreciable effects on the affinity of the enzyme for both NADH and 2-oxoglutarate.	NAD	245-249	glutamate dehydrogenase 1	Homo sapiens	132-135
12646278-2	2003	To determine whether electron input via the NADH-dependent pathway was similarly functional in whole cells and necessary for the stimulation by cytochrome b(5), we constructed five plasmids designed to express human CYP2E1 in various combinations with cytochrome b(5) reductase, cytochrome b(5), and cytochrome P450 reductase.	NAD	44-48	cytochrome b5 type A	Homo sapiens	144-158
31175267-7	2019	Further, Nampt inhibition resulted in reduced intracellular NAD+ content, NAD+/NADH ratio, and Sirt1 activity, whereas overexpression had the opposite effects.	NAD	79-83	nicotinamide phosphoribosyltransferase	Rattus norvegicus	9-14
31175267-9	2019	Thus, Nampt suppresses MSC senescence via mediating NAD+-Sirt1 signaling.	NAD	52-56	nicotinamide phosphoribosyltransferase	Rattus norvegicus	6-11
12648681-3	2003	It has been shown that NAD affects longevity and transcriptional silencing through the regulation of the Sir2p family, which are NAD-dependent deacetylases.	NAD	23-26	sirtuin 2	Homo sapiens	105-110
31158122-1	2019	BACKGROUND Resveratrol has been shown to possess beneficial activities including antioxidant, anti-inflammatory, and cardioprotective effects through activating a nicotinamide adenine dinucleotide (NAD)-dependent histone deacetylase family member sirtuin-1 (SIRT1) protein.	NAD	163-196	sirtuin 1	Homo sapiens	247-256
31158122-1	2019	BACKGROUND Resveratrol has been shown to possess beneficial activities including antioxidant, anti-inflammatory, and cardioprotective effects through activating a nicotinamide adenine dinucleotide (NAD)-dependent histone deacetylase family member sirtuin-1 (SIRT1) protein.	NAD	163-196	sirtuin 1	Homo sapiens	258-263
12648681-4	2003	Many human diseases are associated with changes in NAD level and/or the NAD : NADH ratio, raising the possibility that the Sir2p family might play a role in these diseases.	NAD	51-54	sirtuin 2	Homo sapiens	123-128
31158122-1	2019	BACKGROUND Resveratrol has been shown to possess beneficial activities including antioxidant, anti-inflammatory, and cardioprotective effects through activating a nicotinamide adenine dinucleotide (NAD)-dependent histone deacetylase family member sirtuin-1 (SIRT1) protein.	NAD	198-201	sirtuin 1	Homo sapiens	247-256
31158122-1	2019	BACKGROUND Resveratrol has been shown to possess beneficial activities including antioxidant, anti-inflammatory, and cardioprotective effects through activating a nicotinamide adenine dinucleotide (NAD)-dependent histone deacetylase family member sirtuin-1 (SIRT1) protein.	NAD	198-201	sirtuin 1	Homo sapiens	258-263
12648681-4	2003	Many human diseases are associated with changes in NAD level and/or the NAD : NADH ratio, raising the possibility that the Sir2p family might play a role in these diseases.	NAD	72-75	sirtuin 2	Homo sapiens	123-128
12648681-4	2003	Many human diseases are associated with changes in NAD level and/or the NAD : NADH ratio, raising the possibility that the Sir2p family might play a role in these diseases.	NAD	78-82	sirtuin 2	Homo sapiens	123-128
12706305-0	2003	Glutamate-115 renders specificity of human 11beta-hydroxysteroid dehydrogenase type 2 for the cofactor NAD+.	NAD	103-107	hydroxysteroid 11-beta dehydrogenase 2	Homo sapiens	43-85
30771931-4	2019	The sniff-cam was based on the pH-dependent redox reactions of nicotinamide adenine dinucleotide (NAD)-dependent alcohol dehydrogenase (ADH).	NAD	63-96	aldo-keto reductase family 1 member A1	Homo sapiens	113-134
30771931-4	2019	The sniff-cam was based on the pH-dependent redox reactions of nicotinamide adenine dinucleotide (NAD)-dependent alcohol dehydrogenase (ADH).	NAD	63-96	aldo-keto reductase family 1 member A1	Homo sapiens	136-139
30771931-4	2019	The sniff-cam was based on the pH-dependent redox reactions of nicotinamide adenine dinucleotide (NAD)-dependent alcohol dehydrogenase (ADH).	NAD	98-101	aldo-keto reductase family 1 member A1	Homo sapiens	113-134
30771931-4	2019	The sniff-cam was based on the pH-dependent redox reactions of nicotinamide adenine dinucleotide (NAD)-dependent alcohol dehydrogenase (ADH).	NAD	98-101	aldo-keto reductase family 1 member A1	Homo sapiens	136-139
30771931-6	2019	The ADH-immobilized mesh containing a solution of the oxidized form of NAD (NAD+) or reduced form (NADH) was used as an EtOH-imaging mesh and an AcH-imaging mesh, respectively.	NAD	99-103	aldo-keto reductase family 1 member A1	Homo sapiens	4-7
12706305-8	2003	Thus, predictions using the 3D-model combined with analysis of mutants allowed the identification of residues critical for NAD(+)-dependent activity of 11beta-HSD2.	NAD	123-129	hydroxysteroid 11-beta dehydrogenase 2	Homo sapiens	152-163
12590576-1	2003	S-Adenosylhomocysteine hydrolase (AdoHcy hydrolase) crystallizes from solutions containing the intermediate analogue neplanocin A with the analogue bound in its 3"-keto form at the active sites of all of its four subunits and the four tightly bound cofactors in their reduced (NADH) state.	NAD	277-281	adenosylhomocysteinase	Homo sapiens	0-32
30982660-1	2019	The NAD+-dependent deacetylase Sirtuin 1 (SIRT1) is down-regulated in triple-negative breast cancer.	NAD	4-7	sirtuin 1	Homo sapiens	42-47
31019297-4	2019	If the rate-limiting enzyme of de novo NAD synthesis, NAPRT, is highly expressed in a normal tissue type, cancers that arise from that tissue will have a high frequency of NAPRT amplification and be completely and irreversibly dependent on NAPRT for survival.	NAD	39-42	nicotinate phosphoribosyltransferase	Homo sapiens	54-59
31019297-4	2019	If the rate-limiting enzyme of de novo NAD synthesis, NAPRT, is highly expressed in a normal tissue type, cancers that arise from that tissue will have a high frequency of NAPRT amplification and be completely and irreversibly dependent on NAPRT for survival.	NAD	39-42	nicotinate phosphoribosyltransferase	Homo sapiens	172-177
31019297-4	2019	If the rate-limiting enzyme of de novo NAD synthesis, NAPRT, is highly expressed in a normal tissue type, cancers that arise from that tissue will have a high frequency of NAPRT amplification and be completely and irreversibly dependent on NAPRT for survival.	NAD	39-42	nicotinate phosphoribosyltransferase	Homo sapiens	172-177
12591154-1	2003	High levels of neuropeptide Y (NPY) are found in basal ganglia where it is co-localised with somatostatin (SOM) and nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH/d) in a population of striatal GABA containing interneurones.	NAD	116-149	neuropeptide Y	Homo sapiens	15-29
12591154-1	2003	High levels of neuropeptide Y (NPY) are found in basal ganglia where it is co-localised with somatostatin (SOM) and nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH/d) in a population of striatal GABA containing interneurones.	NAD	116-149	neuropeptide Y	Homo sapiens	31-34
12620231-0	2003	The human Sir2 ortholog, SIRT2, is an NAD+-dependent tubulin deacetylase.	NAD	38-41	sirtuin 2	Homo sapiens	10-14
31110473-3	2019	Sirtuin 1 (SIRT1) is a nicotinamide adenine dinucleotide (NAD+)-dependent lysine deacetylase, regulating transcription, and critical for the cellular adaptations to metabolic stress.	NAD	23-56	sirtuin 1	Homo sapiens	0-9
31110473-3	2019	Sirtuin 1 (SIRT1) is a nicotinamide adenine dinucleotide (NAD+)-dependent lysine deacetylase, regulating transcription, and critical for the cellular adaptations to metabolic stress.	NAD	23-56	sirtuin 1	Homo sapiens	11-16
31110473-3	2019	Sirtuin 1 (SIRT1) is a nicotinamide adenine dinucleotide (NAD+)-dependent lysine deacetylase, regulating transcription, and critical for the cellular adaptations to metabolic stress.	NAD	58-62	sirtuin 1	Homo sapiens	0-9
31110473-3	2019	Sirtuin 1 (SIRT1) is a nicotinamide adenine dinucleotide (NAD+)-dependent lysine deacetylase, regulating transcription, and critical for the cellular adaptations to metabolic stress.	NAD	58-62	sirtuin 1	Homo sapiens	11-16
12620231-0	2003	The human Sir2 ortholog, SIRT2, is an NAD+-dependent tubulin deacetylase.	NAD	38-41	sirtuin 2	Homo sapiens	25-30
30777853-2	2019	We report that in tumor-bearing mice the macrophage colony-stimulating factor elevates the myeloid cell levels of nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme in the NAD salvage pathway, which acts as negative regulator of the CXCR4 retention axis of hematopoietic cells in the bone marrow.	NAD	194-197	chemokine (C-X-C motif) receptor 4	Mus musculus	255-260
15206786-4	2003	The gradual decrease of NAD observed in primary cultured hepatocytes, was partially inhibited by the addition of poly(ADP-ribose) polymerase and/or NAD glycohydrolase inhibitors.	NAD	24-27	poly (ADP-ribose) polymerase 1	Rattus norvegicus	113-140
30777853-3	2019	NAMPT inhibits CXCR4 through a NAD/Sirtuin 1-mediated inactivation of HIF1alpha-driven CXCR4 gene transcription, leading to mobilization of immature myeloid-derived suppressor cells (MDSC) and enhancing their production of suppressive nitric oxide.	NAD	31-34	chemokine (C-X-C motif) receptor 4	Mus musculus	15-20
30777853-3	2019	NAMPT inhibits CXCR4 through a NAD/Sirtuin 1-mediated inactivation of HIF1alpha-driven CXCR4 gene transcription, leading to mobilization of immature myeloid-derived suppressor cells (MDSC) and enhancing their production of suppressive nitric oxide.	NAD	31-34	sirtuin 1	Homo sapiens	35-44
12415565-5	2002	Both molecules are involved in the metabolism of NAD(+), and the CD157 gene is synthenic on 4p15 with CD38, with which it also shares a unique genomic organization.	NAD	49-55	CD38 molecule	Homo sapiens	102-106
30777853-3	2019	NAMPT inhibits CXCR4 through a NAD/Sirtuin 1-mediated inactivation of HIF1alpha-driven CXCR4 gene transcription, leading to mobilization of immature myeloid-derived suppressor cells (MDSC) and enhancing their production of suppressive nitric oxide.	NAD	31-34	chemokine (C-X-C motif) receptor 4	Mus musculus	87-92
30973934-1	2019	SIRT1, a NAD+-dependent deacetylase, protects neurons in a variety of in vitro and in vivo models of neurodegenerative disease.	NAD	9-12	sirtuin 1	Homo sapiens	0-5
12379464-1	2002	Poly(ADP-ribose) polymerase (PARP) binds to DNA single and double strand breaks and uses NAD in the synthesis of poly(ADP-ribose) (pADPr).	NAD	89-92	poly (ADP-ribose) polymerase 1	Rattus norvegicus	0-27
30707625-1	2019	The nicotinamide adenine dinucleotide-dependent deacetylase, sirtuin (SIRT)1, in skeletal muscle is reduced in insulin-resistant states.	NAD	4-37	sirtuin 1	Homo sapiens	70-76
12379464-1	2002	Poly(ADP-ribose) polymerase (PARP) binds to DNA single and double strand breaks and uses NAD in the synthesis of poly(ADP-ribose) (pADPr).	NAD	89-92	poly (ADP-ribose) polymerase 1	Rattus norvegicus	29-33
12220539-1	2002	NAD(+)-dependent 15-hydroxyprostaglandin dehydrogenase (15-PGDH) catalyzes NAD(+)-dependent oxidation of prostaglandins and other nonprostanoid compounds.	NAD	0-6	15-hydroxyprostaglandin dehydrogenase	Homo sapiens	56-63
30972029-6	2019	Sirtuin 1 (SIRT1), the mammalian homolog of Sir2, was originally identified as a nicotinamide adenine dinucleotide (NAD+)-dependent histone deacetylase.	NAD	81-114	sirtuin 1	Homo sapiens	0-9
30972029-6	2019	Sirtuin 1 (SIRT1), the mammalian homolog of Sir2, was originally identified as a nicotinamide adenine dinucleotide (NAD+)-dependent histone deacetylase.	NAD	81-114	sirtuin 1	Homo sapiens	11-16
12186850-1	2002	The yeast silent information regulator (Sir)2 protein links cellular metabolism and transcriptional silencing through its nicotinamide adenine dinucleotide (NAD)-dependent histone deacetylase activity.	NAD	122-155	sirtuin 2	Homo sapiens	40-45
30972029-6	2019	Sirtuin 1 (SIRT1), the mammalian homolog of Sir2, was originally identified as a nicotinamide adenine dinucleotide (NAD+)-dependent histone deacetylase.	NAD	81-114	sirtuin 1	Homo sapiens	44-48
30972029-6	2019	Sirtuin 1 (SIRT1), the mammalian homolog of Sir2, was originally identified as a nicotinamide adenine dinucleotide (NAD+)-dependent histone deacetylase.	NAD	116-120	sirtuin 1	Homo sapiens	0-9
30972029-6	2019	Sirtuin 1 (SIRT1), the mammalian homolog of Sir2, was originally identified as a nicotinamide adenine dinucleotide (NAD+)-dependent histone deacetylase.	NAD	116-120	sirtuin 1	Homo sapiens	11-16
30972029-6	2019	Sirtuin 1 (SIRT1), the mammalian homolog of Sir2, was originally identified as a nicotinamide adenine dinucleotide (NAD+)-dependent histone deacetylase.	NAD	116-120	sirtuin 1	Homo sapiens	44-48
12186850-1	2002	The yeast silent information regulator (Sir)2 protein links cellular metabolism and transcriptional silencing through its nicotinamide adenine dinucleotide (NAD)-dependent histone deacetylase activity.	NAD	157-160	sirtuin 2	Homo sapiens	40-45
12065597-4	2002	Cysteine is utilized by the cysteine desulfurase Nfs1p to release sulfan sulfur; ATP presumably reflects the function of the Hsp70 family chaperone Ssq1p; and NADH is used for reduction of the ferredoxin Yah1p involved in Fe/S protein biogenesis.	NAD	159-163	adrenodoxin	Saccharomyces cerevisiae S288C	204-209
30902968-3	2019	SIRT1, an NAD+-dependent deacetylase that regulates metabolism and aging, has been shown to protect cells from DDR.	NAD	10-13	sirtuin 1	Homo sapiens	0-5
30885209-8	2019	RESULTS: Our work demonstrates that GFPT2 is transcriptionally upregulated by NF-kappaB and repressed by the NAD+-dependent deacetylase SIRT6.	NAD	109-113	glutamine-fructose-6-phosphate transaminase 2	Homo sapiens	36-41
12183365-1	2002	Poly(ADP-ribose) polymerase (PARP) is a major NAD-dependent modifying enzyme that mediates important steps in DNA repair, transcription, and apoptosis, but its role during development is poorly understood.	NAD	46-49	Poly-(ADP-ribose) polymerase	Drosophila melanogaster	29-33
12036956-5	2002	We demonstrate that RalR1 exhibits an oxidoreductive catalytic activity toward retinoids, but not steroids, with at least an 800-fold lower apparent K(m) values for NADP+ and NADPH versus NAD+ and NADH as cofactors.	NAD	188-192	retinol dehydrogenase 11	Homo sapiens	20-25
30890936-4	2019	PARP14 takes advantage of nicotinamide adenine dinucleotide (NAD+) as a metabolic substrate to conduct mono-ADP-ribosylation modification on target proteins, taking part in cellular responses and signaling pathways in the immune system.	NAD	26-59	poly(ADP-ribose) polymerase family member 14	Homo sapiens	0-6
30890936-4	2019	PARP14 takes advantage of nicotinamide adenine dinucleotide (NAD+) as a metabolic substrate to conduct mono-ADP-ribosylation modification on target proteins, taking part in cellular responses and signaling pathways in the immune system.	NAD	61-65	poly(ADP-ribose) polymerase family member 14	Homo sapiens	0-6
30205735-0	2019	CERKL regulates autophagy via the NAD-dependent deacetylase SIRT1.	NAD	34-37	sirtuin 1	Homo sapiens	60-65
12036956-5	2002	We demonstrate that RalR1 exhibits an oxidoreductive catalytic activity toward retinoids, but not steroids, with at least an 800-fold lower apparent K(m) values for NADP+ and NADPH versus NAD+ and NADH as cofactors.	NAD	197-201	retinol dehydrogenase 11	Homo sapiens	20-25
30496552-4	2019	For NAD+-mediated ligation, the BRCA1 C-terminal (BRCT) domain of Ligase IV recognizes NAD+ and facilitates the adenylation of Ligase IV, the first step of ligation.	NAD	4-8	BRCA1 DNA repair associated	Homo sapiens	32-37
12236576-7	2002	Hematoporphyrin also increases the myoglobin-catalysed hydrogen peroxide-mediated oxidation of o-dianisidine and NADH.	NAD	113-117	myoglobin	Homo sapiens	35-44
30496552-4	2019	For NAD+-mediated ligation, the BRCA1 C-terminal (BRCT) domain of Ligase IV recognizes NAD+ and facilitates the adenylation of Ligase IV, the first step of ligation.	NAD	87-91	BRCA1 DNA repair associated	Homo sapiens	32-37
30638660-3	2019	To elucidate the enzymatic properties of MDH from M. sedula (MsMDH), we determined the crystal structure of MsMDH as a complex with NAD+ and a ternary complex with malate and NAD+.	NAD	132-136	NADP-dependent malic enzyme	Metallosphaera sedula	41-44
30638660-3	2019	To elucidate the enzymatic properties of MDH from M. sedula (MsMDH), we determined the crystal structure of MsMDH as a complex with NAD+ and a ternary complex with malate and NAD+.	NAD	175-179	NADP-dependent malic enzyme	Metallosphaera sedula	41-44
30595481-3	2019	Here we report the metabolome of activated macrophages during efferocytosis to reveal an interleukin-10 (IL-10) cytokine escalation that was independent of glycolysis yet bolstered by apoptotic cell fatty acids and mitochondrial beta-oxidation, the electron transport chain, and heightened coenzyme NAD+.	NAD	299-303	interleukin 10	Homo sapiens	89-103
30595481-3	2019	Here we report the metabolome of activated macrophages during efferocytosis to reveal an interleukin-10 (IL-10) cytokine escalation that was independent of glycolysis yet bolstered by apoptotic cell fatty acids and mitochondrial beta-oxidation, the electron transport chain, and heightened coenzyme NAD+.	NAD	299-303	interleukin 10	Homo sapiens	105-110
30595481-4	2019	Loss of IL-10 due to mitochondrial complex III defects was remarkably rescued by adding NAD+ precursors.	NAD	88-92	interleukin 10	Homo sapiens	8-13
31087296-1	2019	SIRT1 is an NAD+-dependent lysine deacetylase that promotes healthy aging and longevity in diverse organisms.	NAD	12-16	sirtuin 1	Homo sapiens	0-5
30414145-5	2019	Importantly, several of the cofactors that are known to regulate FOXO transcriptional activity are also sensitive to changes in the cellular redox status, in particular the deacetylase SirT1 is activated in response to reduced levels of reducing equivalents (increased NAD+/NADH+ ratio) and the coactivator PGC-1alpha is induced in response to increased cellular oxidative stress.	NAD	269-273	sirtuin 1	Homo sapiens	185-190
30414145-5	2019	Importantly, several of the cofactors that are known to regulate FOXO transcriptional activity are also sensitive to changes in the cellular redox status, in particular the deacetylase SirT1 is activated in response to reduced levels of reducing equivalents (increased NAD+/NADH+ ratio) and the coactivator PGC-1alpha is induced in response to increased cellular oxidative stress.	NAD	274-279	sirtuin 1	Homo sapiens	185-190
30655851-1	2019	Sirtuin-7 is an evolutionarily conserved NAD-dependent deacetylase, which serves an important role in carcinogenesis.	NAD	41-44	sirtuin 7	Homo sapiens	0-9
30591661-4	2018	The results of our study indicate a substantial increase in ATP production from mitochondria, through an elevation of mitochondrial biogenesis, mediated by SIRT1 activation that is driven by increased NAD+/NADH ratio.	NAD	201-205	sirtuin 1	Homo sapiens	156-161
30591661-4	2018	The results of our study indicate a substantial increase in ATP production from mitochondria, through an elevation of mitochondrial biogenesis, mediated by SIRT1 activation that is driven by increased NAD+/NADH ratio.	NAD	206-210	sirtuin 1	Homo sapiens	156-161
30619489-5	2018	In this paper, we investigated the effects of changes in the cellular content of NAD+ on CLS by altering the expression of mitochondrial NAD+ carriers, namely Ndt1 and Ndt2.	NAD	81-85	NAD+ transporter	Saccharomyces cerevisiae S288C	168-172
30619489-5	2018	In this paper, we investigated the effects of changes in the cellular content of NAD+ on CLS by altering the expression of mitochondrial NAD+ carriers, namely Ndt1 and Ndt2.	NAD	137-141	NAD+ transporter	Saccharomyces cerevisiae S288C	168-172
30567305-4	2018	In this work, we screened for association with MS 11 single nucleotide polymorphisms (SNPs) and two microsatellite markers in the five genes (NCF1, NCF2, NCF4, CYBA, and CYBB) of the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX2) system, the enzymatic pathway producing ROS in the brain and neural tissues, in 347 Finnish patients with MS and 714 unaffected family members.	NAD	183-216	cytochrome b-245 beta chain	Homo sapiens	244-248
30300564-1	2018	Sirtuin 5 (SIRT5) belongs to the mitochondrial sirtuin family, which constitutes a highly conserved family of nicotinamide adenine dinucleotide NAD+-dependent deacetylases and ADP-ribosyltransferases that play an important regulatory role in stress resistance and metabolic homeostasis.	NAD	110-143	sirtuin 5	Bos taurus	0-9
30300564-1	2018	Sirtuin 5 (SIRT5) belongs to the mitochondrial sirtuin family, which constitutes a highly conserved family of nicotinamide adenine dinucleotide NAD+-dependent deacetylases and ADP-ribosyltransferases that play an important regulatory role in stress resistance and metabolic homeostasis.	NAD	110-143	sirtuin 5	Bos taurus	11-16
30397317-4	2018	Visible light drives PSP efficiently into a long-lived triplet excited state (PSP*), which reacts rapidly with reduced nicotinamide adenine dinucleotide to generate a super-reducing radical (PSP ), which is strong enough to reduce many CO2-reducing catalysts.	NAD	119-152	microseminoprotein beta	Homo sapiens	21-24
30397317-4	2018	Visible light drives PSP efficiently into a long-lived triplet excited state (PSP*), which reacts rapidly with reduced nicotinamide adenine dinucleotide to generate a super-reducing radical (PSP ), which is strong enough to reduce many CO2-reducing catalysts.	NAD	119-152	microseminoprotein beta	Homo sapiens	78-81
30397317-4	2018	Visible light drives PSP efficiently into a long-lived triplet excited state (PSP*), which reacts rapidly with reduced nicotinamide adenine dinucleotide to generate a super-reducing radical (PSP ), which is strong enough to reduce many CO2-reducing catalysts.	NAD	119-152	microseminoprotein beta	Homo sapiens	78-81
30227304-1	2018	Sirtuin3 (SIRT3) is a member of the Sirtuin family of NAD+-dependent deacetylase.	NAD	54-57	NAD-dependent protein deacetylase sirtuin-3, mitochondrial	Capra hircus	0-8
30227304-1	2018	Sirtuin3 (SIRT3) is a member of the Sirtuin family of NAD+-dependent deacetylase.	NAD	54-57	NAD-dependent protein deacetylase sirtuin-3, mitochondrial	Capra hircus	10-15
30243136-9	2018	On the other hand, NAD-dependent isocitrate and malate dehydrogenase were not modified by hyaluronic acid induction.	NAD	19-22	malic enzyme 1	Homo sapiens	48-68
30448921-1	2018	The NAD+-dependent deacetylase SIRT1 plays important roles in several physiological processes such as transcription, genome stability, stress responses, and aging.	NAD	4-8	sirtuin 1	Homo sapiens	31-36
30448921-8	2018	Determination of the MM/PBSA free energy indicated that the binding of DHP-8 to SIRT1 significantly increased the binding affinity of SIRT1 to its substrate p53-W as well as to NAD+.	NAD	177-181	sirtuin 1	Homo sapiens	80-85
30448921-8	2018	Determination of the MM/PBSA free energy indicated that the binding of DHP-8 to SIRT1 significantly increased the binding affinity of SIRT1 to its substrate p53-W as well as to NAD+.	NAD	177-181	sirtuin 1	Homo sapiens	134-139
30416740-8	2018	We identified calcium/calmodulin-dependent serine protein kinase (Cask) as a potential downstream effector in response to age-associated NAD+ reduction in the hippocampus.	NAD	137-141	calcium/calmodulin-dependent serine protein kinase (MAGUK family)	Mus musculus	14-64
30416740-8	2018	We identified calcium/calmodulin-dependent serine protein kinase (Cask) as a potential downstream effector in response to age-associated NAD+ reduction in the hippocampus.	NAD	137-141	calcium/calmodulin-dependent serine protein kinase (MAGUK family)	Mus musculus	66-70
30416740-9	2018	Cask expression is responsive to NAD+ changes and also reduced in the hippocampus during aging.	NAD	33-37	calcium/calmodulin-dependent serine protein kinase (MAGUK family)	Mus musculus	0-4
30404003-4	2018	Nicotinamide adenine dinucleotide (NAD) was found to improve mitochondrial function in DGUOK-deficient hepatocyte-like cells by activating the peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC1alpha).	NAD	0-33	deoxyguanosine kinase	Homo sapiens	87-92
30404003-4	2018	Nicotinamide adenine dinucleotide (NAD) was found to improve mitochondrial function in DGUOK-deficient hepatocyte-like cells by activating the peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC1alpha).	NAD	35-38	deoxyguanosine kinase	Homo sapiens	87-92
30291911-0	2018	Augmentation of NAD+ levels by enzymatic action of NAD(P)H quinone oxidoreductase 1 attenuates adriamycin-induced cardiac dysfunction in mice.	NAD	16-20	NAD(P)H dehydrogenase, quinone 1	Mus musculus	51-83
30291911-5	2018	Therefore, we illustrate the role of NAD+/NADH modulation by NAD(P)H quinone oxidoreductase 1 (NQO1) enzymatic action on AIC.	NAD	37-41	NAD(P)H dehydrogenase, quinone 1	Mus musculus	61-93
30291911-5	2018	Therefore, we illustrate the role of NAD+/NADH modulation by NAD(P)H quinone oxidoreductase 1 (NQO1) enzymatic action on AIC.	NAD	37-41	NAD(P)H dehydrogenase, quinone 1	Mus musculus	95-99
30291911-5	2018	Therefore, we illustrate the role of NAD+/NADH modulation by NAD(P)H quinone oxidoreductase 1 (NQO1) enzymatic action on AIC.	NAD	42-46	NAD(P)H dehydrogenase, quinone 1	Mus musculus	61-93
30291911-5	2018	Therefore, we illustrate the role of NAD+/NADH modulation by NAD(P)H quinone oxidoreductase 1 (NQO1) enzymatic action on AIC.	NAD	42-46	NAD(P)H dehydrogenase, quinone 1	Mus musculus	95-99
30291911-11	2018	In addition, a decrease in SIRT1 activity due to a reduction in the NAD+/NADH ratio by PARP-1 hyperactivation was associated with AIC through increased nuclear factor (NF)-kappaB p65 and p53 acetylation in both WT and NQO1-/- mice.	NAD	68-72	poly (ADP-ribose) polymerase family, member 1	Mus musculus	87-93
30291911-11	2018	In addition, a decrease in SIRT1 activity due to a reduction in the NAD+/NADH ratio by PARP-1 hyperactivation was associated with AIC through increased nuclear factor (NF)-kappaB p65 and p53 acetylation in both WT and NQO1-/- mice.	NAD	73-77	poly (ADP-ribose) polymerase family, member 1	Mus musculus	87-93
30291911-12	2018	While an elevation in NAD+/NADH ratio via NQO1 enzymatic action using dunnione recovered SIRT1 activity and subsequently deacetylated NF-kappaB p65 and p53, however not in NQO1-/- mice, thereby attenuating AIC.	NAD	22-26	NAD(P)H dehydrogenase, quinone 1	Mus musculus	42-46
30291911-12	2018	While an elevation in NAD+/NADH ratio via NQO1 enzymatic action using dunnione recovered SIRT1 activity and subsequently deacetylated NF-kappaB p65 and p53, however not in NQO1-/- mice, thereby attenuating AIC.	NAD	27-31	NAD(P)H dehydrogenase, quinone 1	Mus musculus	42-46
12203899-5	2002	In both MG1363 and the gapA overexpressing strain the GAPDH activity was specific for NAD.	NAD	86-89	gapA	Lactococcus lactis subsp. lactis Il1403	23-27
30291911-13	2018	CONCLUSION: Thus, modulation of NAD+/NADH by NQO1 may be a novel therapeutic approach to prevent chemotherapy-associated heart failure, including AIC.	NAD	32-36	NAD(P)H dehydrogenase, quinone 1	Mus musculus	45-49
30291911-13	2018	CONCLUSION: Thus, modulation of NAD+/NADH by NQO1 may be a novel therapeutic approach to prevent chemotherapy-associated heart failure, including AIC.	NAD	37-41	NAD(P)H dehydrogenase, quinone 1	Mus musculus	45-49
12203899-5	2002	In both MG1363 and the gapA overexpressing strain the GAPDH activity was specific for NAD.	NAD	86-89	gapB	Lactococcus lactis subsp. lactis Il1403	54-59
30405528-4	2018	Sirtuin 1 (SIRT1) is a nicotinamide adenine dinucleotide (NAD)-dependent histone deacetylase that is activated in response to calorie restriction (CR).	NAD	23-56	sirtuin 1	Homo sapiens	0-9
30405528-4	2018	Sirtuin 1 (SIRT1) is a nicotinamide adenine dinucleotide (NAD)-dependent histone deacetylase that is activated in response to calorie restriction (CR).	NAD	23-56	sirtuin 1	Homo sapiens	11-16
12081495-1	2002	The soluble domain of human CD38 catalyzes the conversion of NAD(+) to cyclic ADP-ribose and to ADP-ribose via a common covalent intermediate [Sauve, A.	NAD	61-67	CD38 molecule	Homo sapiens	28-32
30405528-4	2018	Sirtuin 1 (SIRT1) is a nicotinamide adenine dinucleotide (NAD)-dependent histone deacetylase that is activated in response to calorie restriction (CR).	NAD	58-61	sirtuin 1	Homo sapiens	0-9
30405528-4	2018	Sirtuin 1 (SIRT1) is a nicotinamide adenine dinucleotide (NAD)-dependent histone deacetylase that is activated in response to calorie restriction (CR).	NAD	58-61	sirtuin 1	Homo sapiens	11-16
29763382-5	2018	Finally, stable KDM2B-knockdown cell lines exhibit displacement of NAD+-dependent deacetylase sirtuin-1 (SIRT1) from chromatin, with concomitant increases in H3K79 methylation and H4K16 acetylation.	NAD	67-70	sirtuin 1	Homo sapiens	94-103
29763382-5	2018	Finally, stable KDM2B-knockdown cell lines exhibit displacement of NAD+-dependent deacetylase sirtuin-1 (SIRT1) from chromatin, with concomitant increases in H3K79 methylation and H4K16 acetylation.	NAD	67-70	sirtuin 1	Homo sapiens	105-110
11884393-2	2002	Here we show that increased dosage of NPT1, encoding a nicotinate phosphoribosyltransferase critical for the NAD(+) salvage pathway, increases Sir2-dependent silencing, stabilizes the rDNA locus, and extends yeast replicative life span by up to 60%.	NAD	109-115	nicotinate phosphoribosyltransferase	Saccharomyces cerevisiae S288C	38-42
30184263-3	2018	Herein, we show that NAD+ -binding promotes assembly of the ALDH7A1 tetramer.	NAD	21-25	aldehyde dehydrogenase 7 family member A1	Homo sapiens	60-67
11884393-4	2002	We show that Npt1 and a previously uncharacterized salvage pathway enzyme, Nma2, are both concentrated in the nucleus, indicating that a significant amount of NAD(+) is regenerated in this organelle.	NAD	159-165	nicotinate phosphoribosyltransferase	Saccharomyces cerevisiae S288C	13-17
12054821-11	2002	These results support the previous proposal that purines regulate GDH activity by altering the dynamics of the NAD binding domain.	NAD	111-114	glutamate dehydrogenase 1	Homo sapiens	66-69
12062417-1	2002	In Saccharomyces cerevisiae the nicotinic acid moiety of NAD+ can be synthesized from tryptophan using the kynurenine pathway or incorporated directly using nicotinate phosphoribosyl transferase (NPT1).	NAD	57-61	nicotinate phosphoribosyltransferase	Saccharomyces cerevisiae S288C	196-200
28621566-1	2018	The enzyme glutamate dehydrogenase (GDH; Glud1) catalyzes the (reversible) oxidative deamination of glutamate to alpha-ketoglutarate accompanied by a reduction of NAD+ to NADH.	NAD	163-167	glutamate dehydrogenase 1	Mus musculus	41-46
28621566-1	2018	The enzyme glutamate dehydrogenase (GDH; Glud1) catalyzes the (reversible) oxidative deamination of glutamate to alpha-ketoglutarate accompanied by a reduction of NAD+ to NADH.	NAD	171-175	glutamate dehydrogenase 1	Mus musculus	41-46
11812773-5	2002	Kinetic studies revealed a K(m) NAD value of 45 microm for the processed 32-kDa MTX fragment, and a K(m) NAD value of 1300 microm for the processed holotoxin.	NAD	32-35	metaxin 1	Homo sapiens	80-83
29939337-8	2018	The incubation of ERalpha agonist PPT rather than ERbeta agonist DPN could increase the level of AVPV-kisspeptin expression, which was sensitive to the treatment with PFOS.	NAD	65-68	KiSS-1 metastasis-suppressor	Mus musculus	102-112
11862125-10	2002	The mitogenic effect of mox-LDL, ox-LDL, or LPC and their interaction with ET-1 were inhibited by defatted albumin (10 microg/ml), antioxidant N-acetylcysteine (400 microM), the reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase inhibitor diphenylene iodonium (1 microM).	NAD	186-219	monooxygenase DBH like 1	Homo sapiens	24-27
30093403-2	2018	AIF catalyzes the oxidation of NADH in vitro, yet the significance of this redox activity in cells remains unclear.	NAD	31-35	apoptosis inducing factor mitochondria associated 1	Homo sapiens	0-3
11904232-8	2002	In addition, prior incubation of human placental microsomes with NAD(+) (cofactor) but not cortisol (substrate) resulted in a concentration-dependent increase (EC(50)=8 microM) in 11 beta-HSD2 activity, indicating that binding of NAD(+) to the microsomal 11 beta-HSD2 facilitated the conversion of cortisol to cortisone.	NAD	230-236	hydroxysteroid 11-beta dehydrogenase 2	Homo sapiens	180-192
11904232-9	2002	Thus, this finding substantiates the previously proposed concept that a compulsorily ordered ternary complex mechanism may operate for 11 beta-HSD2, with NAD(+) binding first, followed by a conformational change allowing cortisol binding with high affinity.	NAD	154-160	hydroxysteroid 11-beta dehydrogenase 2	Homo sapiens	135-147
12503636-0	2002	Nad-299 antagonises 5-HT-stimulated and spiperone-inhibited [35S]GTPgammaS binding in cloned 5-HT1A receptors.	NAD	0-3	5-hydroxytryptamine receptor 1A	Homo sapiens	93-99
30090057-1	2018	Sirtuin enzymes are a family of highly seven conserved protein deacetylases, namely SIRT1 through SIRT7, whose enzymatic activities require the cofactor nicotinamide adenine dinucleotide (NAD+).	NAD	153-186	sirtuin 1	Homo sapiens	84-89
30090057-1	2018	Sirtuin enzymes are a family of highly seven conserved protein deacetylases, namely SIRT1 through SIRT7, whose enzymatic activities require the cofactor nicotinamide adenine dinucleotide (NAD+).	NAD	153-186	sirtuin 7	Homo sapiens	98-103
30090057-1	2018	Sirtuin enzymes are a family of highly seven conserved protein deacetylases, namely SIRT1 through SIRT7, whose enzymatic activities require the cofactor nicotinamide adenine dinucleotide (NAD+).	NAD	188-192	sirtuin 1	Homo sapiens	84-89
30090057-1	2018	Sirtuin enzymes are a family of highly seven conserved protein deacetylases, namely SIRT1 through SIRT7, whose enzymatic activities require the cofactor nicotinamide adenine dinucleotide (NAD+).	NAD	188-192	sirtuin 7	Homo sapiens	98-103
11741702-3	2002	The method most commonly employed to determine phosphofructokinase-1 activity is based on oxidation of NADH by the use of aldolase, triosephosphate isomerase, and alpha-glycerophosphate dehydrogenase.	NAD	103-107	phosphofructokinase, muscle	Homo sapiens	47-68
30029680-3	2018	We recently established that oxaliplatin also exert its anti-cancer activity in gastric cancer cell lines by targeting tumor-associated NADH oxidase (tNOX), attenuate NAD+ generation and reduce NAD+-dependent sirtuin 1 (SIRT1) deacetylase activity, which in turn enhances p53 acetylation and apoptosis.	NAD	194-198	sirtuin 1	Homo sapiens	209-218
12204198-5	2002	Fluorescence lifetime sensitive spectroscopy of NADH in the CA1 pyramidal cell layer (gate set for detection of protein-bound NADH) showed a wavelength maximum at 455.3+/-1.6 nm (mean+/-S.D.)	NAD	48-52	carbonic anhydrase 1	Mus musculus	60-63
29789426-1	2018	The type III NAD-dependent histone deacetylase Sirt1 plays important roles in a variety of pathobiological functions through targeting either the acetylated histones or transcription factors.	NAD	13-16	sirtuin 1	Homo sapiens	47-52
12204198-5	2002	Fluorescence lifetime sensitive spectroscopy of NADH in the CA1 pyramidal cell layer (gate set for detection of protein-bound NADH) showed a wavelength maximum at 455.3+/-1.6 nm (mean+/-S.D.)	NAD	126-130	carbonic anhydrase 1	Mus musculus	60-63
29996103-3	2018	Here, we show that NAD+ depletion by TNT activates RIPK3 and MLKL, key mediators of necroptosis.	NAD	19-23	receptor interacting serine/threonine kinase 3	Homo sapiens	51-56
11679254-3	2001	In the first reactor, alpha-ketoglutarate was converted to L-glutamate by GDH in the presence of ammonia and NADH.	NAD	109-113	glutamate dehydrogenase 1	Homo sapiens	74-77
29996103-7	2018	Surprisingly, NAD+ depletion itself was sufficient to trigger necroptosis in a RIPK3- and MLKL-dependent manner by inhibiting the NAD+ salvage pathway in THP-1 cells or by TNT expression in Jurkat T cells.	NAD	14-18	receptor interacting serine/threonine kinase 3	Homo sapiens	79-84
29996103-7	2018	Surprisingly, NAD+ depletion itself was sufficient to trigger necroptosis in a RIPK3- and MLKL-dependent manner by inhibiting the NAD+ salvage pathway in THP-1 cells or by TNT expression in Jurkat T cells.	NAD	130-134	receptor interacting serine/threonine kinase 3	Homo sapiens	79-84
30026729-6	2018	Elevated NAD+ levels induced by KL1333 triggered the activation of SIRT1 and AMPK, and subsequently activated PGC-1alpha in these cells.	NAD	9-13	sirtuin 1	Sus scrofa	67-72
11737057-1	2001	Autoantibodies directed against human CD38 (an enzyme catalysing the interconversion of NAD(+) and cyclic ADP-ribose) have been demonstrated recently in patients with type 2 diabetes.	NAD	88-94	CD38 molecule	Homo sapiens	38-42
29703752-7	2018	For the first time, the product of the semialdehyde oxidation by AMSDH is also revealed by NMR and high-resolution MS. We found that ALDH8A1 catalyzes the NAD+-dependent oxidation of 2-AMS with a catalytic efficiency equivalent to that of AMSDH from the bacterium Pseudomonas fluorescens Substitution of active-site residues required for substrate recognition, binding, and isomerization in the bacterial enzyme resulted in human ALDH8A1 variants with 160-fold increased Km or no detectable activity.	NAD	155-159	aldehyde dehydrogenase 8 family member A1	Homo sapiens	133-140
29703752-7	2018	For the first time, the product of the semialdehyde oxidation by AMSDH is also revealed by NMR and high-resolution MS. We found that ALDH8A1 catalyzes the NAD+-dependent oxidation of 2-AMS with a catalytic efficiency equivalent to that of AMSDH from the bacterium Pseudomonas fluorescens Substitution of active-site residues required for substrate recognition, binding, and isomerization in the bacterial enzyme resulted in human ALDH8A1 variants with 160-fold increased Km or no detectable activity.	NAD	155-159	aldehyde dehydrogenase 8 family member A1	Homo sapiens	430-437
29905535-4	2018	NAD+ levels declined with age and correlated directly with decreased nicotinamide phosphoribosyltransferase (NAMPT) expression, increased expression of senescence markers (p16INK4a, p21Waf/Cip1, ApoJ, CTGF and beta-galactosidase) and significant reductions in SIRT1 expression and activity.	NAD	0-4	cyclin-dependent kinase inhibitor 1A (P21)	Mus musculus	182-188
29905535-4	2018	NAD+ levels declined with age and correlated directly with decreased nicotinamide phosphoribosyltransferase (NAMPT) expression, increased expression of senescence markers (p16INK4a, p21Waf/Cip1, ApoJ, CTGF and beta-galactosidase) and significant reductions in SIRT1 expression and activity.	NAD	0-4	cyclin-dependent kinase inhibitor 1A (P21)	Mus musculus	189-193
11683883-4	2001	Expression of CD38, which has been identified as NAD+-glycohydrolase (EC 3.2.2.6) degrading NAD+ into nicotinamide and ADP-ribose, was determined on freshly isolated human monocytes by flow cytometry and RT-PCR.	NAD	49-53	CD38 molecule	Homo sapiens	14-18
29679549-7	2018	Our results indicated that CHM-1 increased the expression of SIRT2 protein, an NAD-dependent tubulin deacetylase.	NAD	79-82	chondromodulin	Homo sapiens	27-32
29852001-8	2018	The defects in these mutants were qualitatively similar to heterochromatin mutants lacking Swi6, the NAD+-dependent histone deacetylase Sir2, or the Clr4, Raf1 or Rik1 subunits of the histone H3 lysine 9 (H3K9) methyltransferase complex, albeit not as extreme.	NAD	101-105	sirtuin 1	Homo sapiens	136-140
29852001-10	2018	This was the case for mutants in the NAD+-independent deacetylase complex subunits Clr1, Clr2 and Clr3, the casein kinase CK2 subunit Ckb1, the ubiquitin ligase component Pof3, and the CENP-B homologue Cbp1, as well as for double mutants lacking Swi6 and Brl2, Pof3, or Cbp1.	NAD	37-41	forkhead box L2	Homo sapiens	171-175
29852001-10	2018	This was the case for mutants in the NAD+-independent deacetylase complex subunits Clr1, Clr2 and Clr3, the casein kinase CK2 subunit Ckb1, the ubiquitin ligase component Pof3, and the CENP-B homologue Cbp1, as well as for double mutants lacking Swi6 and Brl2, Pof3, or Cbp1.	NAD	37-41	serpin family H member 1	Homo sapiens	202-206
29852001-10	2018	This was the case for mutants in the NAD+-independent deacetylase complex subunits Clr1, Clr2 and Clr3, the casein kinase CK2 subunit Ckb1, the ubiquitin ligase component Pof3, and the CENP-B homologue Cbp1, as well as for double mutants lacking Swi6 and Brl2, Pof3, or Cbp1.	NAD	37-41	forkhead box L2	Homo sapiens	261-265
29852001-10	2018	This was the case for mutants in the NAD+-independent deacetylase complex subunits Clr1, Clr2 and Clr3, the casein kinase CK2 subunit Ckb1, the ubiquitin ligase component Pof3, and the CENP-B homologue Cbp1, as well as for double mutants lacking Swi6 and Brl2, Pof3, or Cbp1.	NAD	37-41	serpin family H member 1	Homo sapiens	270-274
29977153-8	2018	However, re-expression of CD38 in the knockdown clones reversed the effect on Sirt1/NF-kappaB/TLR2 signaling, which is NAD-dependent.	NAD	119-122	CD38 antigen	Mus musculus	26-30
29861836-2	2018	Expression of the NAD+-dependent deacetylase Sirtuin 1 (SIRT1), an antiaging molecule with a key role in oxidative stress response, has been described as decreased in the lung of COPD patients.	NAD	18-22	sirtuin 1	Homo sapiens	56-61
29719225-0	2018	A Potent and Specific CD38 Inhibitor Ameliorates Age-Related Metabolic Dysfunction by Reversing Tissue NAD+ Decline.	NAD	103-107	CD38 antigen	Mus musculus	22-26
29719225-3	2018	We recently demonstrated that the NADase CD38 has a central role in age-related NAD+ decline.	NAD	80-84	CD38 antigen	Mus musculus	41-45
29719225-4	2018	Here we show that a highly potent and specific thiazoloquin(az)olin(on)e CD38 inhibitor, 78c, reverses age-related NAD+ decline and improves several physiological and metabolic parameters of aging, including glucose tolerance, muscle function, exercise capacity, and cardiac function in mouse models of natural and accelerated aging.	NAD	115-119	CD38 antigen	Mus musculus	73-77
29752474-5	2018	Mechanistically, the interaction between CHES1 and ERalpha enhanced the recruitment of nicotinamide adenine dinucleotide (NAD+) deacetylase Sirtuin 1 (SIRT1), and it further induced SIRT1-mediated ERalpha deacetylation and repression on the promoter-binding enrichment of ERalpha.	NAD	87-120	sirtuin 1	Homo sapiens	140-149
29752474-5	2018	Mechanistically, the interaction between CHES1 and ERalpha enhanced the recruitment of nicotinamide adenine dinucleotide (NAD+) deacetylase Sirtuin 1 (SIRT1), and it further induced SIRT1-mediated ERalpha deacetylation and repression on the promoter-binding enrichment of ERalpha.	NAD	87-120	sirtuin 1	Homo sapiens	151-156
29752474-5	2018	Mechanistically, the interaction between CHES1 and ERalpha enhanced the recruitment of nicotinamide adenine dinucleotide (NAD+) deacetylase Sirtuin 1 (SIRT1), and it further induced SIRT1-mediated ERalpha deacetylation and repression on the promoter-binding enrichment of ERalpha.	NAD	87-120	sirtuin 1	Homo sapiens	182-187
29481647-1	2018	STUDY QUESTION: Are cohesins SA1/SA2 and the NAD-dependent deacetylase SIRT1 involved in telomere homeostasis of cumulus cells and thus eligible as biomarkers of follicular physiology and ovarian aging?	NAD	45-48	sirtuin 1	Homo sapiens	71-76
29481647-4	2018	The NAD+-dependent protein deacetylase Sirtuin 1 (SIRT1), which preserves DNA integrity from oxidative stress, may also modulate genome stability and telomere length.	NAD	4-7	sirtuin 1	Homo sapiens	39-48
29481647-4	2018	The NAD+-dependent protein deacetylase Sirtuin 1 (SIRT1), which preserves DNA integrity from oxidative stress, may also modulate genome stability and telomere length.	NAD	4-7	sirtuin 1	Homo sapiens	50-55
29306019-7	2018	SIRT1 can regulate monocyte function through NF-kappaB and PGC-1, accompanying an increased NAD+ level.	NAD	92-96	sirtuin 1	Homo sapiens	0-5
29306019-9	2018	For adaptive immune cells, SIRT1 can mediate the differentiation of inflammatory T cell subsets in a NAD+-dependent manner.	NAD	101-105	sirtuin 1	Homo sapiens	27-32
29562167-4	2018	By virtue of a change in cellular redox homeostasis, IDH1-mutated cells synthesize excess glutamine-derived proline through enhanced activity of pyrroline 5-carboxylate reductase 1 (PYCR1), coupled to NADH oxidation.	NAD	201-205	pyrroline-5-carboxylate reductase 1	Homo sapiens	182-187
29721150-6	2018	Sirt3 modulates age-associated mitochondrial biology and function via lysine deacetylation of target proteins, and we show that its regulation depends on its nitration status and is benefited by the improved NAD+/NADH ratio in aged p66Shc(-/-) brain mitochondria.	NAD	208-212	src homology 2 domain-containing transforming protein C1	Mus musculus	232-238
29721150-6	2018	Sirt3 modulates age-associated mitochondrial biology and function via lysine deacetylation of target proteins, and we show that its regulation depends on its nitration status and is benefited by the improved NAD+/NADH ratio in aged p66Shc(-/-) brain mitochondria.	NAD	213-217	src homology 2 domain-containing transforming protein C1	Mus musculus	232-238
29317476-1	2018	Poly(ADP-ribose) polymerase (PARP) is an NAD-consuming enzyme and its specific role in the pathogenesis of alcoholic fatty liver disease (AFLD) remains elusive.	NAD	41-44	poly (ADP-ribose) polymerase family, member 1	Mus musculus	0-27
29317476-1	2018	Poly(ADP-ribose) polymerase (PARP) is an NAD-consuming enzyme and its specific role in the pathogenesis of alcoholic fatty liver disease (AFLD) remains elusive.	NAD	41-44	poly (ADP-ribose) polymerase family, member 1	Mus musculus	29-33
29317476-9	2018	These data indicate that applying PARP-specific inhibitor PJ34 by intraperitoneal injection attenuated hepatic NAD+ depletion and TG accumulation in alcohol-fed mice and may be a potential candidate for use in AFLD therapy.	NAD	111-115	poly (ADP-ribose) polymerase family, member 1	Mus musculus	34-38
29380601-4	2018	In the AcH bio-sniffer, a reverse reaction of alcohol dehydrogenase (ADH) was employed for reducing AcH to ethanol and simultaneously consuming a coenzyme, reduced form of nicotinamide adenine dinucleotide (NADH).	NAD	172-205	aldo-keto reductase family 1 member A1	Homo sapiens	46-67
29380601-4	2018	In the AcH bio-sniffer, a reverse reaction of alcohol dehydrogenase (ADH) was employed for reducing AcH to ethanol and simultaneously consuming a coenzyme, reduced form of nicotinamide adenine dinucleotide (NADH).	NAD	172-205	aldo-keto reductase family 1 member A1	Homo sapiens	69-72
29380601-4	2018	In the AcH bio-sniffer, a reverse reaction of alcohol dehydrogenase (ADH) was employed for reducing AcH to ethanol and simultaneously consuming a coenzyme, reduced form of nicotinamide adenine dinucleotide (NADH).	NAD	207-211	aldo-keto reductase family 1 member A1	Homo sapiens	46-67
29380601-4	2018	In the AcH bio-sniffer, a reverse reaction of alcohol dehydrogenase (ADH) was employed for reducing AcH to ethanol and simultaneously consuming a coenzyme, reduced form of nicotinamide adenine dinucleotide (NADH).	NAD	207-211	aldo-keto reductase family 1 member A1	Homo sapiens	69-72
29495316-0	2018	Bioinspired Design of Alcohol Dehydrogenase@nano TiO2 Microreactors for Sustainable Cycling of NAD+/NADH Coenzyme.	NAD	95-99	aldo-keto reductase family 1 member A1	Homo sapiens	22-44
29495316-0	2018	Bioinspired Design of Alcohol Dehydrogenase@nano TiO2 Microreactors for Sustainable Cycling of NAD+/NADH Coenzyme.	NAD	100-104	aldo-keto reductase family 1 member A1	Homo sapiens	22-44
29317496-9	2018	We showed that decreased nicotinamide mononucleotide adenylyltransferase (Nma1/Nma2) levels probably caused the NAD+ defects, and NMA1-oe was sufficient to restore NAD+ NatB-mediated N-terminal acetylation of Nma1 and Nma2 appears essential for maintaining NAD+ levels.	NAD	112-116	nicotinamide-nucleotide adenylyltransferase NMA2	Saccharomyces cerevisiae S288C	79-83
29552083-11	2018	In addition, DHI treatment also elevated brain-derived neurotrophic factor (BDNF) level in sciatic nerve of DPN rat.	NAD	108-111	brain-derived neurotrophic factor	Rattus norvegicus	41-74
29552083-11	2018	In addition, DHI treatment also elevated brain-derived neurotrophic factor (BDNF) level in sciatic nerve of DPN rat.	NAD	108-111	brain-derived neurotrophic factor	Rattus norvegicus	76-80
29129787-3	2018	Using transcriptomics and metabolic profiling approaches, we showed that the enhanced anti-tumor property of Th1/17 cells was dependent on the increased NAD+-dependent activity of the histone deacetylase Sirt1.	NAD	153-157	negative elongation factor complex member C/D	Homo sapiens	109-112
29129787-3	2018	Using transcriptomics and metabolic profiling approaches, we showed that the enhanced anti-tumor property of Th1/17 cells was dependent on the increased NAD+-dependent activity of the histone deacetylase Sirt1.	NAD	153-157	sirtuin 1	Homo sapiens	204-209
29155147-10	2018	NNMT inhibitors reduced intracellular 1-MNA, increased intracellular NAD+ and S-(5"-adenosyl)-l-methionine (SAM), and suppressed lipogenesis in adipocytes.	NAD	69-73	nicotinamide N-methyltransferase	Mus musculus	0-4
29155147-14	2018	Increased flux of key cellular energy regulators, including NAD+ and SAM, may potentially define the therapeutic mechanism-of-action of NNMT inhibitors.	NAD	60-64	nicotinamide N-methyltransferase	Mus musculus	136-140
30114710-6	2018	RESULTS: Our results revealed that CD38 deficiency significantly elevated the intracellular glutathione (GSH) concentration and GSH/GSSG ratio, decreased the contents of free fatty acids and increased intracellular NAD+ level in heart from CD38-/- mice fed with HFD.	NAD	215-219	CD38 antigen	Mus musculus	35-39
30787047-2	2018	Mice carrying a triplication of the gene encoding the culminating enzyme in NAD+ salvage from nicotinamide, NMNAT, are protected from a variety of insults to axons.	NAD	76-80	nicotinamide nucleotide adenylyltransferase 1	Mus musculus	108-113
28935607-9	2017	S-glutathionylation results in loosening of the tertiary structure of GAPDH, decreases its affinity to NAD+ and thermal stability.	NAD	103-107	glyceraldehyde-3-phosphate dehydrogenase	Oryctolagus cuniculus	70-75
31966549-1	2017	BACKGROUND: Several members of the SIRT family (SIRT1-7), a highly conserved family of NAD+-dependent enzymes, play an important role in tumor formation.	NAD	87-90	sirtuin 1	Homo sapiens	48-53
29088536-3	2017	At the bioanode, multiplex enzymes including alcohol dehydrogenase, aldehyde dehydrogenase, and formate dehydrogenase are coimmobilized on CNDs electrode which is previously coated with in situ polymerized methylene blue as the electrocatalyst for oxidizing NADH to NAD+.	NAD	258-262	aldo-keto reductase family 1 member A1	Homo sapiens	45-66
29088536-3	2017	At the bioanode, multiplex enzymes including alcohol dehydrogenase, aldehyde dehydrogenase, and formate dehydrogenase are coimmobilized on CNDs electrode which is previously coated with in situ polymerized methylene blue as the electrocatalyst for oxidizing NADH to NAD+.	NAD	266-270	aldo-keto reductase family 1 member A1	Homo sapiens	45-66
29125463-4	2017	Daily treatment of rats with the first-in-class NAMPT stimulator, P7C3-A20, prevented behavioral and histologic indicators of peripheral neuropathy, stimulated tissue NAD recovery, improved general health, and abolished attrition produced by a near maximum-tolerated dose of PTX.	NAD	167-170	nicotinamide phosphoribosyltransferase	Rattus norvegicus	48-53
29118980-2	2017	The lysine residue K9 of histone H3 (H3K9) is a prime target of SIRT1, a member of NAD+-dependent histone deacetylase family of enzymes targeting both histone and non-histone substrates.	NAD	83-87	sirtuin 1	Homo sapiens	64-69
29029745-3	2017	In presence of NADH at aerobic conditions, SHL catalyzed the decarboxylative hydroxylation of SAF and released a redox reporter amino ferrocene (AF 6).	NAD	15-19	afadin, adherens junction formation factor	Homo sapiens	145-149
11500379-3	2001	The Sir4p-containing complex has an NAD-dependent histone deacetylase activity, while the Net1p-containing complex possesses deacetylase activity but only weak NAD-dependent histone deacetylase activity.	NAD	160-163	neuroepithelial cell transforming 1	Homo sapiens	90-95
28807785-6	2017	CD38 knockdown or 8-Br-cADPR treatment significantly reduced NAD+, cADPR and intracellular Ca2+ levels.	NAD	61-65	CD38 antigen	Mus musculus	0-4
28970491-0	2017	Rev1 contributes to proper mitochondrial function via the PARP-NAD+-SIRT1-PGC1alpha axis.	NAD	63-67	REV1, DNA directed polymerase	Mus musculus	0-4
28970491-0	2017	Rev1 contributes to proper mitochondrial function via the PARP-NAD+-SIRT1-PGC1alpha axis.	NAD	63-67	poly (ADP-ribose) polymerase family, member 1	Mus musculus	58-62
11336438-1	2001	The nuclear enzyme poly(ADP-ribose) polymerase (PARP), which has been shown to be activated following experimental traumatic brain injury (TBI), binds to DNA strand breaks and utilizes nicotinamide adenine dinucleotide (NAD) as a substrate.	NAD	185-218	poly (ADP-ribose) polymerase 1	Rattus norvegicus	19-46
28970491-6	2017	We conclude that replication stress via Rev1-deficiency contributes to metabolic stress caused by compromized mitochondrial function via the PARP-NAD+-SIRT1-PGC1alpha axis.	NAD	146-150	poly (ADP-ribose) polymerase family, member 1	Mus musculus	141-145
28545714-3	2017	Treatment of PKD-derived cells with this compound not only reduces PAK4 steady-state protein levels and regulates beta-catenin signaling, but also inhibits nicotinamide phosphoribosyl transferase, the rate-limiting enzyme in a key NAD salvage pathway.	NAD	231-234	protein kinase D1	Mus musculus	13-16
11336438-1	2001	The nuclear enzyme poly(ADP-ribose) polymerase (PARP), which has been shown to be activated following experimental traumatic brain injury (TBI), binds to DNA strand breaks and utilizes nicotinamide adenine dinucleotide (NAD) as a substrate.	NAD	185-218	poly (ADP-ribose) polymerase 1	Rattus norvegicus	48-52
11336438-1	2001	The nuclear enzyme poly(ADP-ribose) polymerase (PARP), which has been shown to be activated following experimental traumatic brain injury (TBI), binds to DNA strand breaks and utilizes nicotinamide adenine dinucleotide (NAD) as a substrate.	NAD	220-223	poly (ADP-ribose) polymerase 1	Rattus norvegicus	19-46
11336438-1	2001	The nuclear enzyme poly(ADP-ribose) polymerase (PARP), which has been shown to be activated following experimental traumatic brain injury (TBI), binds to DNA strand breaks and utilizes nicotinamide adenine dinucleotide (NAD) as a substrate.	NAD	220-223	poly (ADP-ribose) polymerase 1	Rattus norvegicus	48-52
11469811-3	2001	In contrast, 11beta-HSD2 acts exclusively as an NAD-dependent dehydrogenase inactivating cortisol to cortisone, thereby protecting the mineralocorticoid receptor from occupation by cortisol.	NAD	48-51	hydroxysteroid 11-beta dehydrogenase 2	Homo sapiens	13-24
11306077-7	2001	Unlike hAR the enzyme from C. tenuis has a dual coenzyme specificity and shows similar specificity constants for NADPH and NADH.	NAD	123-127	lymphatic vessel endothelial hyaluronan receptor 1	Homo sapiens	7-10
28863411-4	2017	Human serum nicotinamide adenine dinucleotide (NAD)-dependent deacetylase sirtuin-1 (SIRT1/SIRT2L1) levels were detected using a commercial colorimetric kit.	NAD	12-45	sirtuin 1	Homo sapiens	85-90
28863411-4	2017	Human serum nicotinamide adenine dinucleotide (NAD)-dependent deacetylase sirtuin-1 (SIRT1/SIRT2L1) levels were detected using a commercial colorimetric kit.	NAD	47-50	sirtuin 1	Homo sapiens	85-90
11136248-7	2001	Furthermore, NADPH was a potent inhibitor of the W676A NADH-dependent cytochrome c reduction and CYP1A2 activity.	NAD	55-59	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	97-103
11134896-6	2001	In contrast, the GSH precursor NAC at low concentrations was able to enhance the level of oxidative damage, as observed with NADH.	NAD	125-129	synuclein alpha	Homo sapiens	31-34
28815614-4	2017	The sirtuins (e.g., mammalian SIRT1) are deacetylases that link energy balance (NAD+ /NADH) to regulation of gene transcription.	NAD	80-84	sirtuin 1	Homo sapiens	30-35
28815614-4	2017	The sirtuins (e.g., mammalian SIRT1) are deacetylases that link energy balance (NAD+ /NADH) to regulation of gene transcription.	NAD	86-90	sirtuin 1	Homo sapiens	30-35
11113971-2	2000	NAD(+)-dependent glycerol-3-phosphate dehydrogenase in S. cerevisiae is present in two isoforms, coded for by two different genes, GPD1 and GPD2.	NAD	0-6	glycerol-3-phosphate dehydrogenase (NAD(+)) GPD2	Saccharomyces cerevisiae S288C	140-144
28625912-4	2017	The specific activity of the freshly purified hGAPDH constitutes 117 +- 5 mumol NADH/min per mg protein (pH 9.0, 22  C), which is close to the specific activity of rabbit muscle glyceraldehyde-3-phosphate dehydrogenase determined under the same conditions and several times exceeds the specific activity of his-tagged GAPDH preparations.	NAD	80-84	glyceraldehyde-3-phosphate dehydrogenase	Oryctolagus cuniculus	47-52
11113971-5	2000	At high demand for NADH reoxidation, a strong induction was seen not only of the GPD2 gene, but also of GPP1, encoding one of the molecular forms of glycerol-3-phosphatase.	NAD	19-23	glycerol-3-phosphate dehydrogenase (NAD(+)) GPD2	Saccharomyces cerevisiae S288C	81-85
11113971-7	2000	At low demand for NADH reoxidation via glycerol formation, the GPD1, GPD2, GPP1, and GPP2 genes were all expressed at basal levels.	NAD	18-22	glycerol-3-phosphate dehydrogenase (NAD(+)) GPD2	Saccharomyces cerevisiae S288C	69-73
28777558-2	2017	Treatment of (ArL)Fe with adamantyl azide or mesityl azide led to the formation of the high-spin (S = 5/2), three-coordinate imidos (ArL)Fe(NAd) and (ArL)Fe(NMes), respectively, as determined by EPR, zero-field 57Fe Mossbauer, magnetometry, and single crystal X-ray diffraction.	NAD	140-143	spindlin 1	Homo sapiens	92-96
10995836-4	2000	The PARP inhibitor 3-aminobenzamide (3AB) protects neurons against homocysteine-induced NAD depletion, loss of mitochondrial transmembrane potential, and cell death, demonstrating a requirement for PARP activation and/or NAD depletion in homocysteine-induced apoptosis.	NAD	88-91	poly (ADP-ribose) polymerase 1	Rattus norvegicus	4-8
28756945-3	2017	Here, we report that the nicotinamide adenine dinucleotide (NAD)-dependent deacetylase SIRT1 acts as an energy sensor and negatively regulates poly(A)RNA transport via deacetylating a poly(A)-binding protein, PABP1.	NAD	25-58	sirtuin 1	Homo sapiens	87-92
28756945-3	2017	Here, we report that the nicotinamide adenine dinucleotide (NAD)-dependent deacetylase SIRT1 acts as an energy sensor and negatively regulates poly(A)RNA transport via deacetylating a poly(A)-binding protein, PABP1.	NAD	60-63	sirtuin 1	Homo sapiens	87-92
10837478-6	2000	With NADH as a cofactor, 15-PGDH acted as a 15-carbonyl reductase and catalyzed the conversion of 13,14-dihydro-15-oxo-LXA(4) to 13, 14-dihydro-LXA(4).	NAD	5-9	15-hydroxyprostaglandin dehydrogenase	Homo sapiens	25-32
28845527-10	2017	In conclusion, the results show that extracellular visfatin produces NAD that causes upregulation of SIRT1 activity and p53 deacetylation.	NAD	69-72	sirtuin 1	Homo sapiens	101-106
10933785-5	2000	The HH-Histag-BDH-PC complex (and HH-BDH derived therefrom by enterokinase cleavage) has apparent Michaelis constants (K(m) values) for NAD(+), NADH, (R)-3-hydroxybutyrate (HOB), and acetoacetate (AcAc) similar to those for bovine heart or rat liver BDH.	NAD	144-148	3-hydroxybutyrate dehydrogenase 1	Homo sapiens	14-17
28723574-1	2017	Tankyrase 1 (TNKS) and tankyrase 2 (TNKS2) belong to the poly(ADP-ribose) polymerase family of proteins, which use nicotinamide adenine dinucleotide to modify substrate proteins with ADP-ribose modifications.	NAD	115-148	tankyrase 2	Homo sapiens	23-34
28723574-1	2017	Tankyrase 1 (TNKS) and tankyrase 2 (TNKS2) belong to the poly(ADP-ribose) polymerase family of proteins, which use nicotinamide adenine dinucleotide to modify substrate proteins with ADP-ribose modifications.	NAD	115-148	tankyrase 2	Homo sapiens	36-41
10933785-5	2000	The HH-Histag-BDH-PC complex (and HH-BDH derived therefrom by enterokinase cleavage) has apparent Michaelis constants (K(m) values) for NAD(+), NADH, (R)-3-hydroxybutyrate (HOB), and acetoacetate (AcAc) similar to those for bovine heart or rat liver BDH.	NAD	144-148	3-hydroxybutyrate dehydrogenase 1	Homo sapiens	37-40
10933785-6	2000	A computed structural model of HH-BDH predicts the two active center sulfhydryls to be C69 (near the adenosine moiety of NAD) and C242.	NAD	121-124	3-hydroxybutyrate dehydrogenase 1	Homo sapiens	34-37
10924711-9	2000	Since NADH fluorescence is absorbed by hemoglobin, the initial increase and subsequent decrease in fluorescence seem to have been induced by increases in NADH content and CBF, respectively.	NAD	6-10	CCAAT enhancer binding protein zeta	Homo sapiens	171-174
28597012-5	2017	Our electrochemical measurements have shown that the entrapped ADH exhibits high ability to exchange electrons in the presence of the NAD+/NADH cofactor and that the SWCNT-rGO nanohybrid significantly enhances the biocatalytic activity of the immobilized ADH and the electrochemical oxidation of NADH in comparison with either SWCNTs or rGO.	NAD	139-143	aldo-keto reductase family 1 member A1	Homo sapiens	63-66
28597012-5	2017	Our electrochemical measurements have shown that the entrapped ADH exhibits high ability to exchange electrons in the presence of the NAD+/NADH cofactor and that the SWCNT-rGO nanohybrid significantly enhances the biocatalytic activity of the immobilized ADH and the electrochemical oxidation of NADH in comparison with either SWCNTs or rGO.	NAD	296-300	aldo-keto reductase family 1 member A1	Homo sapiens	63-66
10771174-7	2000	Specific PARP inhibition with 10 mg/kg 3-aminobenzamide protected the rat energy state by preserving cortical phosphocreatine and NAD(+).	NAD	130-136	poly (ADP-ribose) polymerase 1	Rattus norvegicus	9-13
28526414-1	2017	The NAD+-dependent protein deacetylase SIRT1 has emerged as an important target for epigenetic therapeutics of colon cancer as its increased expression is associated with cancer progression.	NAD	4-7	sirtuin 1	Homo sapiens	39-44
28461090-5	2017	By screening the expression and function of NAD+ dependent type III deacetylase Sirtuin family members, we found that SIRT5 and SIRT1/2 had opposite expression patterns and functions in macrophages.	NAD	44-48	sirtuin 1	Homo sapiens	128-135
28537485-6	2017	DBC1-PARP1 complexes in old mice can be broken by increasing NAD+ levels through treatment with NMN, reducing DNA damage and restoring PARP activity to youthful levels.	NAD	61-65	poly (ADP-ribose) polymerase family, member 1	Mus musculus	5-10
28537485-6	2017	DBC1-PARP1 complexes in old mice can be broken by increasing NAD+ levels through treatment with NMN, reducing DNA damage and restoring PARP activity to youthful levels.	NAD	61-65	poly (ADP-ribose) polymerase family, member 1	Mus musculus	5-9
28537485-8	2017	There is a correlation of PARP activity with mammalian life span that suggests that NAD+/SIRT1/PARP1 may be more significant than the modest effects on life span observed for NR supplementation in old mice.	NAD	84-88	sirtuin 1	Homo sapiens	89-94
28537485-9	2017	The NAD+/PARP1/SIRT1 axis may link NAD+ levels and DNA damage with the apparent epigenomic DNA methylation clocks that have been described.	NAD	4-8	poly (ADP-ribose) polymerase family, member 1	Mus musculus	9-14
28537485-9	2017	The NAD+/PARP1/SIRT1 axis may link NAD+ levels and DNA damage with the apparent epigenomic DNA methylation clocks that have been described.	NAD	35-39	poly (ADP-ribose) polymerase family, member 1	Mus musculus	9-14
28416276-3	2017	Here we show that two enzymes committed to NAD biosynthesis, nicotinamide phosphoribosyltransferase (NAMPT) and nicotinate phosphoribosyltransferase (NAPT), can both catalyze the synthesis and degradation of Ap4 through their facultative ATPase activity.	NAD	43-46	nicotinate phosphoribosyltransferase	Mus musculus	112-148
28416276-3	2017	Here we show that two enzymes committed to NAD biosynthesis, nicotinamide phosphoribosyltransferase (NAMPT) and nicotinate phosphoribosyltransferase (NAPT), can both catalyze the synthesis and degradation of Ap4 through their facultative ATPase activity.	NAD	43-46	nicotinate phosphoribosyltransferase	Mus musculus	150-154
28416276-3	2017	Here we show that two enzymes committed to NAD biosynthesis, nicotinamide phosphoribosyltransferase (NAMPT) and nicotinate phosphoribosyltransferase (NAPT), can both catalyze the synthesis and degradation of Ap4 through their facultative ATPase activity.	NAD	43-46	transcription factor AP4	Mus musculus	208-211
28295415-2	2017	Over the past decade, NAMPT-mediated NAD+ biosynthesis, together with its key downstream mediator, namely the NAD+ -dependent protein deacetylase SIRT1, has been demonstrated to regulate glucose and lipid metabolism in a tissue-dependent manner.	NAD	37-41	sirtuin 1	Homo sapiens	146-151
28295415-2	2017	Over the past decade, NAMPT-mediated NAD+ biosynthesis, together with its key downstream mediator, namely the NAD+ -dependent protein deacetylase SIRT1, has been demonstrated to regulate glucose and lipid metabolism in a tissue-dependent manner.	NAD	37-40	sirtuin 1	Homo sapiens	146-151
30210557-6	2017	Furthermore, the NAD(+) - dependent protein deacetylase Sirt1 has been proposed to have a dual role in both control of circadian clock circuitry and promotion of cell survival by inhibiting apoptotic pathways in cancer.	NAD	17-21	sirtuin 1	Homo sapiens	56-61
28469414-5	2017	The model takes the synergistically acting light/dark cycles and feeding rhythms as inputs and incorporates the activity of sirtuin 1, a cellular energy sensor and a metabolic enzyme activated by nicotinamide adenine dinucleotide.	NAD	196-229	sirtuin 1	Homo sapiens	124-133
28095341-0	2017	Effect of the R119G mutation on human P5CR structure and its interactions with NAD: Insights derived from molecular dynamics simulation and free energy analysis.	NAD	79-82	pyrroline-5-carboxylate reductase 1	Homo sapiens	38-42
28095341-6	2017	Our study provides insight into the possible role of the R119G mutation during interactions between P5CR and NAD, thus bettering our understanding of how the mutation promotes cutis laxa.	NAD	109-112	pyrroline-5-carboxylate reductase 1	Homo sapiens	100-104
28216063-7	2017	Despite similar levels of p53 protein upregulation after irradiation, higher NAD+ concentrations led to reduced acetylation of this protein, suggesting enhanced SIRT1 activity.	NAD	77-81	sirtuin 1	Homo sapiens	161-166
28109694-1	2017	SIRT1, a NAD dependent histone and protein deacetylase, is a member of the histone deacetylase class III family.	NAD	9-12	sirtuin 1	Homo sapiens	0-5
28032259-7	2017	In vitro NADH-dependent O 2 - production at the plasma membrane in the presence of NQR was reduced upon addition of AIR12.	NAD	9-13	ARP protein (REF)	Arabidopsis thaliana	83-86
28355560-1	2017	The conserved NAD+-dependent deacylase SIRT1 plays pivotal, sometimes contrasting, roles in diverse physiological and pathophysiological conditions.	NAD	14-18	sirtuin 1	Homo sapiens	39-44
10705374-9	2000	Also, strain TN23 (gpd1-Delta1 gpd2-Delta1 YEp24-PGKp-cth-PGKt) was unable to grow anaerobically, leading to the conclusion that the NAD(+) pool became limiting in biomass synthesis before the nucleotide levels favoured a transhydrogenase reaction that could convert NADH and NADP(+) to NADPH and NAD(+).	NAD	133-139	glycerol-3-phosphate dehydrogenase (NAD(+)) GPD2	Saccharomyces cerevisiae S288C	31-35
10683447-2	2000	Electrochemical and fluorometric measurements both showed that NO is produced by corn NR in the presence of nitrite and NADH at pH 7.	NAD	120-124	nitrate reductase [NADH] 1	Zea mays	86-88
10672018-3	2000	Rec-K3H was shown to have an optimum pH at 7.5, to use NADPH more efficiently than NADH, and to contain one molecule of non-covalently bound FAD per molecule of enzyme.	NAD	83-87	kynurenine 3-monooxygenase	Homo sapiens	4-7
10623477-4	2000	The activation of the repair enzyme poly(ADP-ribose)polymerase (PARP) following DNA damage by tBOOH induced a dramatic drop in both NAD(+) and ATP.	NAD	132-138	poly (ADP-ribose) polymerase 1	Rattus norvegicus	36-62
10623477-4	2000	The activation of the repair enzyme poly(ADP-ribose)polymerase (PARP) following DNA damage by tBOOH induced a dramatic drop in both NAD(+) and ATP.	NAD	132-138	poly (ADP-ribose) polymerase 1	Rattus norvegicus	64-68
10623477-5	2000	The inhibition of PARP by 3-aminobenzamide enhanced DNA damage by tBOOH, restored NAD(+) and ATP levels, but did not result in better survival against cell killing by tBOOH.	NAD	82-88	poly (ADP-ribose) polymerase 1	Rattus norvegicus	18-22
10556812-5	1999	One of the suggested roles of the CD38 ectoenzyme is to degrade extra cellular NAD and thus recycle its permeable metabolites.	NAD	79-82	CD38 molecule	Homo sapiens	34-38
10460161-3	1999	A reductase, which contains FMN and a plant-type [2Fe-2S] ferredoxin domain, transfers electrons from NADH to the Rieske center.	NAD	102-106	formin 1	Homo sapiens	28-31
10211832-1	1999	NAD+ facilitates high-yield reactivation of clostridial glutamate dehydrogenase (GDH) after unfolding in urea.	NAD	0-4	glutamate dehydrogenase 1	Homo sapiens	56-79
10211832-1	1999	NAD+ facilitates high-yield reactivation of clostridial glutamate dehydrogenase (GDH) after unfolding in urea.	NAD	0-4	glutamate dehydrogenase 1	Homo sapiens	81-84
10051442-7	1999	After purification, the functions of the His-tagged Met8p were studied in vitro by assay with precorrin-2 in the presence of NAD+ and Co2+.	NAD	125-129	bifunctional precorrin-2 dehydrogenase/sirohydrochlorin ferrochelatase MET8	Saccharomyces cerevisiae S288C	52-57
10072513-4	1999	Interestingly, the extracellular domain of CD38 catalyzes the conversion of NAD+ into nicotinamide, ADP-ribose (ADPR), and cyclic ADPR (cADPR).	NAD	76-80	CD38 molecule	Homo sapiens	43-47
10088597-2	1999	CD38 is a member of a nascent eukaryotic gene family encoding cytosolic and membrane-bound enzymes whose substrate is NAD, a coenzyme ubiquitously distributed in nature.	NAD	118-121	CD38 molecule	Homo sapiens	0-4
28273448-0	2017	Mutations that Allow SIR2 Orthologs to Function in a NAD+-Depleted Environment.	NAD	53-57	sirtuin 1	Homo sapiens	21-25
28273448-3	2017	In this study, we used a genetic screen to identify two mutations in the catalytic domain of yeast Sir2 that allow the enzyme to function in an NAD+-depleted environment.	NAD	144-148	sirtuin 1	Homo sapiens	99-103
10406076-2	1999	Two different 11 beta-HSD isoforms exist: a low-affinity NADP-dependent dehydrogenase/oxoreductase (11 beta-HSD1) and a high-affinity NAD-dependent dehydrogenase (11 beta-HSD2).	NAD	57-60	hydroxysteroid 11-beta dehydrogenase 2	Homo sapiens	14-21
27984176-6	2017	RESULTS: PARP activity was increased in livers due to excessive alcohol intake, which was associated with decreased NAD+ content and SIRT1 activity.	NAD	116-120	poly (ADP-ribose) polymerase family, member 1	Mus musculus	9-13
27984176-7	2017	Pharmacological inhibition of PARP restored the hepatic NAD+ content, attenuated the decrease in SIRT1 activation and beneficially affected the metabolic-, inflammatory-, and oxidative stress-related alterations due to alcohol feeding in the liver.	NAD	56-60	poly (ADP-ribose) polymerase family, member 1	Mus musculus	30-34
28122359-5	2017	In AGS cells, we found that the oxaliplatin-inhibited tNOX effectively attenuated the NAD+/NADH ratio and reduced the deacetylase activity of an NAD+-dependent sirtuin 1, thereby enhancing p53 acetylation and apoptosis.	NAD	86-90	sirtuin 1	Homo sapiens	160-169
28122359-5	2017	In AGS cells, we found that the oxaliplatin-inhibited tNOX effectively attenuated the NAD+/NADH ratio and reduced the deacetylase activity of an NAD+-dependent sirtuin 1, thereby enhancing p53 acetylation and apoptosis.	NAD	91-95	sirtuin 1	Homo sapiens	160-169
28122359-5	2017	In AGS cells, we found that the oxaliplatin-inhibited tNOX effectively attenuated the NAD+/NADH ratio and reduced the deacetylase activity of an NAD+-dependent sirtuin 1, thereby enhancing p53 acetylation and apoptosis.	NAD	86-89	sirtuin 1	Homo sapiens	160-169
27899380-5	2017	We also disclose the first crystal structure of MTHFD2 in complex with a substrate-based inhibitor and the enzyme cofactors NAD+ and inorganic phosphate.	NAD	124-128	methylenetetrahydrofolate dehydrogenase (NADP+ dependent) 2, methenyltetrahydrofolate cyclohydrolase	Homo sapiens	48-54
27302189-7	2017	Activity of SIRT-1 and PAR modification of VEGF in turn, was found to be correlated to the cellular NAD+ levels.	NAD	100-104	sirtuin 1	Homo sapiens	12-18
27916733-1	2017	AIMS: Recent evidence indicates that sirtuin1 (SIRT1), an NAD+-dependent deacetylase, exerts a protective effect against inflammatory kidney injury by suppressing pro-inflammatory cytokines production.	NAD	58-61	sirtuin 1	Homo sapiens	37-45
27916733-1	2017	AIMS: Recent evidence indicates that sirtuin1 (SIRT1), an NAD+-dependent deacetylase, exerts a protective effect against inflammatory kidney injury by suppressing pro-inflammatory cytokines production.	NAD	58-61	sirtuin 1	Homo sapiens	47-52
28125705-3	2017	Nampt is a rate-limiting NAD biosynthetic enzyme that plays critical roles in energy metabolism, cell senescence and maintaining life spans.	NAD	25-28	nicotinamide phosphoribosyltransferase	Rattus norvegicus	0-5
28125705-7	2017	Reducing the level of Nampt in aged MSCs resulted in lower intracellular concentrations of NAD+ and downregulated Sirt1 expression and activity.	NAD	91-95	nicotinamide phosphoribosyltransferase	Rattus norvegicus	22-27
28095779-1	2017	BACKGROUND: Poly(ADP-ribose) polymerase 1 (PARP-1), which catalyzes poly(ADP-ribosyl)ation of proteins by using NAD+ as a substrate, plays a key role in several nuclear events, including DNA repair, replication, and transcription.	NAD	112-116	poly (ADP-ribose) polymerase family, member 1	Mus musculus	12-41
28095779-1	2017	BACKGROUND: Poly(ADP-ribose) polymerase 1 (PARP-1), which catalyzes poly(ADP-ribosyl)ation of proteins by using NAD+ as a substrate, plays a key role in several nuclear events, including DNA repair, replication, and transcription.	NAD	112-116	poly (ADP-ribose) polymerase family, member 1	Mus musculus	43-49
27388719-6	2017	We further clarified that NAD-dependent deacetylase SIRT1, a direct target of miR-34, is decreased by the treatment with AU-1.	NAD	26-29	sirtuin 1	Homo sapiens	52-57
27886975-4	2017	This pathway is comprised of glucose phosphorylation via polyphosphate glucokinase, NADH generation catalyzed by glucose 6-phosphate dehydrogenase (G6PDH) and 6-phosphogluconate dehydrogenase (6PGDH), electron transfer from NADH to the anode, and glucose 6-phosphate regeneration via the non-oxidative pentose phosphate pathway and gluconeogenesis.	NAD	84-88	glucose-6-phosphate dehydrogenase	Homo sapiens	113-146
27886975-4	2017	This pathway is comprised of glucose phosphorylation via polyphosphate glucokinase, NADH generation catalyzed by glucose 6-phosphate dehydrogenase (G6PDH) and 6-phosphogluconate dehydrogenase (6PGDH), electron transfer from NADH to the anode, and glucose 6-phosphate regeneration via the non-oxidative pentose phosphate pathway and gluconeogenesis.	NAD	84-88	glucose-6-phosphate dehydrogenase	Homo sapiens	148-153
27886975-4	2017	This pathway is comprised of glucose phosphorylation via polyphosphate glucokinase, NADH generation catalyzed by glucose 6-phosphate dehydrogenase (G6PDH) and 6-phosphogluconate dehydrogenase (6PGDH), electron transfer from NADH to the anode, and glucose 6-phosphate regeneration via the non-oxidative pentose phosphate pathway and gluconeogenesis.	NAD	224-228	glucose-6-phosphate dehydrogenase	Homo sapiens	113-146
27886975-4	2017	This pathway is comprised of glucose phosphorylation via polyphosphate glucokinase, NADH generation catalyzed by glucose 6-phosphate dehydrogenase (G6PDH) and 6-phosphogluconate dehydrogenase (6PGDH), electron transfer from NADH to the anode, and glucose 6-phosphate regeneration via the non-oxidative pentose phosphate pathway and gluconeogenesis.	NAD	224-228	glucose-6-phosphate dehydrogenase	Homo sapiens	148-153
27518087-2	2017	NAD+ depletion following ischemic insult can result in cell death and has been associated with over-activation of poly-ADP-ribose polymerase PARP1 as well as an increase in NAD+ consuming enzyme CD38.	NAD	0-4	CD38 antigen	Mus musculus	195-199
27518087-2	2017	NAD+ depletion following ischemic insult can result in cell death and has been associated with over-activation of poly-ADP-ribose polymerase PARP1 as well as an increase in NAD+ consuming enzyme CD38.	NAD	173-177	CD38 antigen	Mus musculus	195-199
27518087-6	2017	Decrease of hippocampal NAD+ levels detected during reperfusion in WT mice was only transient in CD38KO animals, suggesting that CD38 contributes to post-ischemic NAD+ catabolism.	NAD	24-28	CD38 antigen	Mus musculus	129-133
27518087-6	2017	Decrease of hippocampal NAD+ levels detected during reperfusion in WT mice was only transient in CD38KO animals, suggesting that CD38 contributes to post-ischemic NAD+ catabolism.	NAD	163-167	CD38 antigen	Mus musculus	129-133
27518087-9	2017	Thus, the absence of CD38 activity can not only directly affect inflammatory response, but also result in unpredicted alterations in the expression levels of enzymes participating in NAD+ metabolism.	NAD	183-187	CD38 antigen	Mus musculus	21-25
28028356-3	2016	SIRT1 and 3, the most studied sirtuins, use the product of cellular metabolism nicotinamide adenine dinucleotide as a cofactor to post-translationally deacetylate cellular proteins and consequently link the metabolic status of the cell to protein function.	NAD	79-112	sirtuin 1	Homo sapiens	0-11
27816507-5	2016	Additionally, depletion of NAD+ causes sensitization of cancer cells to oxidative damage by disruption of the anti-oxidant defense system, decreased cell proliferation, and initiation of cell death through manipulation of cell signaling pathways (e.g., SIRT1 and p53).	NAD	27-31	sirtuin 1	Homo sapiens	253-258
27687729-5	2016	The synergistic increase in nuclear p53 and FOXO3 by exercise can facilitate their known interaction in transactivating Sirtuin 1 (SIRT1), a NAD+-dependent histone deacetylase that mediates adaptation to various stresses.	NAD	141-145	forkhead box O3	Mus musculus	44-49
27645993-3	2016	Here we employed REX, a bacterial NADH-binding protein, fused to the VP16 activator to convert intracellular endogenous redox balance into transcriptional readouts by a reporter gene in mammalian cells.	NAD	34-38	host cell factor C1	Homo sapiens	69-73
27452907-5	2016	The NAD+-dependent histone deacetylase sirtuin (SIRT)1 amplified the pro-apoptotic effect by deacetylating FOXO3a, which induced EGR1 binding to the Bim promoter and activated Bim expression.	NAD	4-8	sirtuin 1	Homo sapiens	48-54
27783615-7	2016	For NADH oxidation without ferredoxin oxidation, increasing PH2 within the rumen physiological range decreased FT from unity to zero for different NAD+ to NADH ratios and pH of 6.2 and 7.0, which indicates thermodynamic control of PH2.	NAD	155-159	polyhomeotic homolog 2	Homo sapiens	60-63
27783615-8	2016	For NADH oxidation with ferredoxin oxidation, increasing PH2 within the rumen physiological range decreased FT from unity at pH of 7.0 only.	NAD	4-8	polyhomeotic homolog 2	Homo sapiens	57-60
27783615-12	2016	This theoretical investigation shows that thermodynamic control of PH2 on individual VFA produced and associated yield of hydrogen and methane cannot be explained without considering NADH oxidation.	NAD	183-187	polyhomeotic homolog 2	Homo sapiens	67-70
27767101-1	2016	Sirtuin-1 (SIRT1) and SIRT6, NAD+-dependent Class III protein deacetylases, are putative anti-aging enzymes, down-regulated in patients with chronic obstructive pulmonary disease (COPD), which is characterized by the accelerated ageing of the lung and associated with increased oxidative stress.	NAD	29-32	sirtuin 1	Homo sapiens	0-9
27767101-1	2016	Sirtuin-1 (SIRT1) and SIRT6, NAD+-dependent Class III protein deacetylases, are putative anti-aging enzymes, down-regulated in patients with chronic obstructive pulmonary disease (COPD), which is characterized by the accelerated ageing of the lung and associated with increased oxidative stress.	NAD	29-32	sirtuin 1	Homo sapiens	11-16
27798264-6	2016	The effects of NAD+ repletion in mdx mice relied on the improvement in mitochondrial function and structural protein expression (alpha-dystrobrevin and delta-sarcoglycan) and on the reductions in general poly(ADP)-ribosylation, inflammation, and fibrosis.	NAD	15-19	sarcoglycan, delta (dystrophin-associated glycoprotein)	Mus musculus	152-169
11717938-5	1998	After adding appropriate amount of NAD+ to mouse cardiac muscle specimen with hypoxia, PAGE showed the numbers of subbands of four kinds of isozymes (LDH2-LDH5) decreased even totally disappeared in the isozyme pattern.	NAD	35-39	lactate dehydrogenase B	Mus musculus	150-154
9844746-1	1998	Bovine spleen NAD+glycohydrolase, an ecto-enzyme closely related to CD38, catalyzes the conversion of NAD+ into ADP-ribose and cyclic ADP-ribose, a calcium-mobilizing metabolite.	NAD	14-18	CD38 molecule	Bos taurus	68-72
9748331-2	1998	Human recombinant CD38 catalyzes the formation of both cyclic ADP-ribose and ADP-ribose products from NAD+ and hydrolyzes cyclic ADP-ribose to ADP-ribose.	NAD	102-106	CD38 molecule	Homo sapiens	18-22
9748331-6	1998	The kcat for NMN+ was 5-fold higher than that of NAD+ and has the greatest reported kcat of any substrate for CD38.	NAD	49-53	CD38 molecule	Homo sapiens	110-114
9748331-9	1998	The ratio of methanolysis to hydrolysis for cADPR and NAD+ catalyzed by CD38 increases linearly with MeOH concentration.	NAD	54-58	CD38 molecule	Homo sapiens	72-76
9685604-0	1998	The nuoM arg368his mutation in NADH:ubiquinone oxidoreductase from Rhodobacter capsulatus: a model for the human nd4-11778 mtDNA mutation associated with Leber"s hereditary optic neuropathy.	NAD	31-35	mitochondrially encoded NADH dehydrogenase 4	Homo sapiens	113-116
9635141-2	1998	The rates of the flavocytochrome-catalyzed, H2O2-supported reactions far exceeded those of the appropriate NADH-dependent reactions and were comparable with the cytochrome P450 2B4-catalyzed, peroxide-mediated reaction rates.	NAD	107-111	CD244 molecule	Homo sapiens	177-180
9521775-8	1998	Since the amounts of G3PDH activity in INS-1 and hepatocyte extracts are similar, we suggest that flux through this step in INS-1 cells is limited by failure to regenerate NAD in the LDH reaction and that a fundamental difference between hepatocytes and islet beta-cells is the limited capacity of the latter to metabolize glycolytic intermediates beyond the G3PDH step.	NAD	172-175	insulin 1	Rattus norvegicus	124-129
9494110-4	1998	To classify CD38 among the enzymes that transfer the ADP-ribosyl moiety of NAD+ to a variety of acceptors, we have investigated its substrate specificity and some characteristics of its kinetic and molecular mechanisms.	NAD	75-79	CD38 molecule	Homo sapiens	12-16
9570746-10	1998	NADH and NADPH (5 mM) triggered sperm capacitation and phosphorylation of p105/p81, but these processes were not prevented by SOD or catalase, nor were they associated with an increased O2.- production.	NAD	0-4	ezrin	Homo sapiens	79-82
9409558-11	1997	However, when TRX reductase and nicotinamide adenine dinucleotide (NADPH) were added to the extracellular medium with TRX, more than 80% of E. coli TRX was found to be in a fully reduced state in human adenocarcinoma (A549) cells.	NAD	32-65	thioredoxin	Homo sapiens	118-121
9409558-11	1997	However, when TRX reductase and nicotinamide adenine dinucleotide (NADPH) were added to the extracellular medium with TRX, more than 80% of E. coli TRX was found to be in a fully reduced state in human adenocarcinoma (A549) cells.	NAD	32-65	thioredoxin	Homo sapiens	118-121
9352085-0	1997	Cloning of the human cDNA sequence encoding the NADH:ubiquinone oxidoreductase MLRQ subunit.	NAD	48-52	NDUFA4 mitochondrial complex associated	Homo sapiens	79-83
9352085-1	1997	A cDNA clone encoding human NADH:ubiquinone oxidoreductase (complex I of mitochondrial respiratory chain) MLRQ subunit was isolated from human fetal liver cDNA library.	NAD	28-32	NDUFA4 mitochondrial complex associated	Homo sapiens	106-110
9308897-1	1997	NADP-malic enzyme (NADP-ME, EC 1.1.1.40) was purified to near-homogeneity from leaves of the C4 dicot Flaveria bidentis and shown to possess intrinsic NAD-dependent malic enzyme activity.	NAD	0-3	malic enzyme 1	Gallus gallus	19-26
27744418-4	2016	Sirt1, an NAD+-dependent deacetylase, is considered an anti-aging molecule and is induced during CR.	NAD	10-13	sirtuin 1	Homo sapiens	0-5
27735788-0	2016	NMNAT1 inhibits axon degeneration via blockade of SARM1-mediated NAD+ depletion.	NAD	65-69	nicotinamide nucleotide adenylyltransferase 1	Mus musculus	0-6
27735788-1	2016	Overexpression of the NAD+ biosynthetic enzyme NMNAT1 leads to preservation of injured axons.	NAD	22-26	nicotinamide nucleotide adenylyltransferase 1	Mus musculus	47-53
27735788-3	2016	Using steady-state and flux analysis of NAD+ metabolites in healthy and injured mouse dorsal root ganglion axons, we find that rather than altering NAD+ synthesis, NMNAT1 instead blocks the injury-induced, SARM1-dependent NAD+ consumption that is central to axon degeneration.	NAD	40-44	nicotinamide nucleotide adenylyltransferase 1	Mus musculus	164-170
27562971-8	2016	Decreasing NADH pharmacologically with MTOB or genetically blocking CtBP1 with siRNA upregulated the cyclin-dependent genes (p15 and p21) and proapoptotic regulators (NOXA and PERP), attenuated proliferation, corrected the glycolytic reprogramming phenotype of PH-Fibs, and augmented transcription of the anti-inflammatory gene HMOX1.	NAD	11-15	p53 apoptosis effector related to PMP22	Homo sapiens	176-180
27566573-0	2016	De-novo NAD+ synthesis regulates SIRT1-FOXO1 apoptotic pathway in response to NQO1 substrates in lung cancer cells.	NAD	8-12	sirtuin 1	Homo sapiens	33-38
27566573-3	2016	Here, we establish a mechanistic link from L-type amino acid transporter 1 (LAT1) mediated transport of tryptophan and the subsequent de-novo NAD+ synthesis to SIRT1-FOXO1 regulated apoptotic signaling in A549 cells in response to NQO1 activation.	NAD	142-146	sirtuin 1	Homo sapiens	160-165
27566573-6	2016	Particularly, the LAT1-NAD+-SIRT1 signaling is activated in tumor tissues of patients with non-small cell lung cancer.	NAD	23-27	sirtuin 1	Homo sapiens	28-33
27153347-1	2016	Silent information regulator two homologue one (SIRT1) is the most widely studied member of the sirtuin family related to histone deacetylases class III super-family using nicotinamide adenine dinucleotide (NAD(+)) as its cofactor.	NAD	172-205	sirtuin 1	Homo sapiens	48-53
27153347-1	2016	Silent information regulator two homologue one (SIRT1) is the most widely studied member of the sirtuin family related to histone deacetylases class III super-family using nicotinamide adenine dinucleotide (NAD(+)) as its cofactor.	NAD	207-213	sirtuin 1	Homo sapiens	48-53
27153347-3	2016	SIRT1 specifically cleaves the nicotinamide ribosyl bond of NAD(+) and transfers the acetyl group from proteins to their co-substrate through an ADP- ribose-peptidyl imidate intermediate.	NAD	60-66	sirtuin 1	Homo sapiens	0-5
27404282-3	2016	We also studied the efficiencies of the coenzymes of these reductases, NADPH as a coenzyme of POR, and NADH as a coenzyme of CBR, to mediate BaP oxidation.	NAD	103-107	carbonyl reductase 1	Homo sapiens	125-128
26164272-4	2016	We show that the glycerol synthetic enzyme Gpd1 is involved in the post-translational modification of Tcp-1 (subunit of TRiC) by acetylation and glycation through the NAD(+)/NADH shuttle and the triose phosphate intermediate dihydroxyacetone phosphate, respectively.	NAD	167-173	glycerol-3-phosphate dehydrogenase (NAD(+)) GPD1	Saccharomyces cerevisiae S288C	43-47
26164272-4	2016	We show that the glycerol synthetic enzyme Gpd1 is involved in the post-translational modification of Tcp-1 (subunit of TRiC) by acetylation and glycation through the NAD(+)/NADH shuttle and the triose phosphate intermediate dihydroxyacetone phosphate, respectively.	NAD	167-173	chaperonin-containing T-complex alpha subunit TCP1	Saccharomyces cerevisiae S288C	102-107
26164272-4	2016	We show that the glycerol synthetic enzyme Gpd1 is involved in the post-translational modification of Tcp-1 (subunit of TRiC) by acetylation and glycation through the NAD(+)/NADH shuttle and the triose phosphate intermediate dihydroxyacetone phosphate, respectively.	NAD	174-178	glycerol-3-phosphate dehydrogenase (NAD(+)) GPD1	Saccharomyces cerevisiae S288C	43-47
26164272-4	2016	We show that the glycerol synthetic enzyme Gpd1 is involved in the post-translational modification of Tcp-1 (subunit of TRiC) by acetylation and glycation through the NAD(+)/NADH shuttle and the triose phosphate intermediate dihydroxyacetone phosphate, respectively.	NAD	174-178	chaperonin-containing T-complex alpha subunit TCP1	Saccharomyces cerevisiae S288C	102-107
27068062-4	2016	In the presence of inhibitor, both malate and glutamate were required to generate a high enough NADH/NAD(+) ratio to support ROS production through the coordinated activity of malate dehydrogenase (MDH) and aspartate aminotransferase (AST).	NAD	96-100	malic enzyme 1	Homo sapiens	176-196
27068062-4	2016	In the presence of inhibitor, both malate and glutamate were required to generate a high enough NADH/NAD(+) ratio to support ROS production through the coordinated activity of malate dehydrogenase (MDH) and aspartate aminotransferase (AST).	NAD	96-100	malic enzyme 1	Homo sapiens	198-201
27068062-4	2016	In the presence of inhibitor, both malate and glutamate were required to generate a high enough NADH/NAD(+) ratio to support ROS production through the coordinated activity of malate dehydrogenase (MDH) and aspartate aminotransferase (AST).	NAD	101-107	malic enzyme 1	Homo sapiens	176-196
27068062-4	2016	In the presence of inhibitor, both malate and glutamate were required to generate a high enough NADH/NAD(+) ratio to support ROS production through the coordinated activity of malate dehydrogenase (MDH) and aspartate aminotransferase (AST).	NAD	101-107	malic enzyme 1	Homo sapiens	198-201
27068062-6	2016	With malate alone, oxaloacetate accumulation limited NADH production by MDH unless glutamate was also added to promote oxaloacetate removal via AST.	NAD	53-57	malic enzyme 1	Homo sapiens	72-75
27068062-9	2016	CoA depletion decreased KG oxidation by alpha-ketoglutarate dehydrogenase (KGDH), such that the resulting increase in [KG] inhibited oxaloacetate removal by AST and NADH generation by MDH.	NAD	165-169	malic enzyme 1	Homo sapiens	184-187
27095738-1	2016	Arabidopsis Nudix hydrolases, AtNUDX6 and 7, exhibit pyrophosphohydrolase activities toward NADH and contribute to the modulation of various defense responses, such as the poly(ADP-ribosyl)ation (PAR) reaction and salicylic acid (SA)-induced Nonexpresser of Pathogenesis-Related genes 1 (NPR1)-dependent defense pathway, against biotic and abiotic stresses.	NAD	92-96	regulatory protein (NPR1)	Arabidopsis thaliana	288-292
27095738-5	2016	A transcriptome analysis using KO-nudx6, KO-nudx7 and double KO-nudx6/7 plants, in which intracellular NADH levels increased, identified genes (NADH-responsive genes, NRGs) whose expression levels positively and negatively correlated with NADH levels.	NAD	144-148	MutT/nudix family protein	Arabidopsis thaliana	44-49
27095738-5	2016	A transcriptome analysis using KO-nudx6, KO-nudx7 and double KO-nudx6/7 plants, in which intracellular NADH levels increased, identified genes (NADH-responsive genes, NRGs) whose expression levels positively and negatively correlated with NADH levels.	NAD	144-148	MutT/nudix family protein	Arabidopsis thaliana	44-49
26984186-6	2016	Both genetic deletion of Trpa1 (Trpa1(-/-)) and pharmacological blockade (HC-030031 and A-967079) abrogated pain-like behaviours (both P &lt; 0.001), which were abated by the antioxidant, alpha-lipoic acid, and the nicotinamide adenine dinucleotide phosphate oxidase inhibitor, apocynin (both P &lt; 0.001).	NAD	215-248	transient receptor potential cation channel, subfamily A, member 1	Mus musculus	25-30
26923291-4	2016	In this study, we elucidated that Sphk1/S1P upregulates sirtuin 1 (SIRT1), a NAD+ dependent deacetylases protease which exerts multiple cellular functions, to regulate the proliferation and migration of endothelial cells.	NAD	77-80	membrane bound transcription factor peptidase, site 1	Homo sapiens	40-43
26923291-4	2016	In this study, we elucidated that Sphk1/S1P upregulates sirtuin 1 (SIRT1), a NAD+ dependent deacetylases protease which exerts multiple cellular functions, to regulate the proliferation and migration of endothelial cells.	NAD	77-80	sirtuin 1	Homo sapiens	56-65
26923291-4	2016	In this study, we elucidated that Sphk1/S1P upregulates sirtuin 1 (SIRT1), a NAD+ dependent deacetylases protease which exerts multiple cellular functions, to regulate the proliferation and migration of endothelial cells.	NAD	77-80	sirtuin 1	Homo sapiens	67-72
26926998-5	2016	Mutations in the ELO3/AtELP3 gene compromise exogenous NAD(+)-induced expression of pathogenesis-related (PR) genes and resistance to the bacterial pathogen Pseudomonas syringae pv.	NAD	55-61	radical SAM domain-containing protein / GCN5-related N-acetyltransferase (GNAT) family protein	Arabidopsis thaliana	17-21
26926998-5	2016	Mutations in the ELO3/AtELP3 gene compromise exogenous NAD(+)-induced expression of pathogenesis-related (PR) genes and resistance to the bacterial pathogen Pseudomonas syringae pv.	NAD	55-61	radical SAM domain-containing protein / GCN5-related N-acetyltransferase (GNAT) family protein	Arabidopsis thaliana	22-28
26926998-6	2016	maculicola ES4326, and transgenic expression of the coding region of ELO3/AtELP3 in elo3/Atelp3 restores NAD(+) responsiveness to the mutant plants, demonstrating that ELO3/AtELP3 is required for exogenous NAD(+)-induced defense responses.	NAD	105-111	radical SAM domain-containing protein / GCN5-related N-acetyltransferase (GNAT) family protein	Arabidopsis thaliana	69-73
26926998-6	2016	maculicola ES4326, and transgenic expression of the coding region of ELO3/AtELP3 in elo3/Atelp3 restores NAD(+) responsiveness to the mutant plants, demonstrating that ELO3/AtELP3 is required for exogenous NAD(+)-induced defense responses.	NAD	105-111	radical SAM domain-containing protein / GCN5-related N-acetyltransferase (GNAT) family protein	Arabidopsis thaliana	74-80
26926998-6	2016	maculicola ES4326, and transgenic expression of the coding region of ELO3/AtELP3 in elo3/Atelp3 restores NAD(+) responsiveness to the mutant plants, demonstrating that ELO3/AtELP3 is required for exogenous NAD(+)-induced defense responses.	NAD	105-111	radical SAM domain-containing protein / GCN5-related N-acetyltransferase (GNAT) family protein	Arabidopsis thaliana	84-88
26926998-6	2016	maculicola ES4326, and transgenic expression of the coding region of ELO3/AtELP3 in elo3/Atelp3 restores NAD(+) responsiveness to the mutant plants, demonstrating that ELO3/AtELP3 is required for exogenous NAD(+)-induced defense responses.	NAD	105-111	radical SAM domain-containing protein / GCN5-related N-acetyltransferase (GNAT) family protein	Arabidopsis thaliana	89-95
26926998-6	2016	maculicola ES4326, and transgenic expression of the coding region of ELO3/AtELP3 in elo3/Atelp3 restores NAD(+) responsiveness to the mutant plants, demonstrating that ELO3/AtELP3 is required for exogenous NAD(+)-induced defense responses.	NAD	105-111	radical SAM domain-containing protein / GCN5-related N-acetyltransferase (GNAT) family protein	Arabidopsis thaliana	168-172
26926998-6	2016	maculicola ES4326, and transgenic expression of the coding region of ELO3/AtELP3 in elo3/Atelp3 restores NAD(+) responsiveness to the mutant plants, demonstrating that ELO3/AtELP3 is required for exogenous NAD(+)-induced defense responses.	NAD	105-111	radical SAM domain-containing protein / GCN5-related N-acetyltransferase (GNAT) family protein	Arabidopsis thaliana	173-179
26926998-6	2016	maculicola ES4326, and transgenic expression of the coding region of ELO3/AtELP3 in elo3/Atelp3 restores NAD(+) responsiveness to the mutant plants, demonstrating that ELO3/AtELP3 is required for exogenous NAD(+)-induced defense responses.	NAD	206-212	radical SAM domain-containing protein / GCN5-related N-acetyltransferase (GNAT) family protein	Arabidopsis thaliana	69-73
26926998-6	2016	maculicola ES4326, and transgenic expression of the coding region of ELO3/AtELP3 in elo3/Atelp3 restores NAD(+) responsiveness to the mutant plants, demonstrating that ELO3/AtELP3 is required for exogenous NAD(+)-induced defense responses.	NAD	206-212	radical SAM domain-containing protein / GCN5-related N-acetyltransferase (GNAT) family protein	Arabidopsis thaliana	74-80
27035562-2	2016	Nicotinamide phosphoribosyltransferase (NAMPT) catalyzes the first rate-limiting step in the nicotinamide adenine dinucleotide (NAD+) biosynthetic pathway in mammals, is a substrate for NAD+-dependent enzymes, such as sirtuin 1 (SIRT1), and contributes to cell fate decisions.	NAD	93-126	nicotinamide phosphoribosyltransferase	Rattus norvegicus	0-38
27035562-2	2016	Nicotinamide phosphoribosyltransferase (NAMPT) catalyzes the first rate-limiting step in the nicotinamide adenine dinucleotide (NAD+) biosynthetic pathway in mammals, is a substrate for NAD+-dependent enzymes, such as sirtuin 1 (SIRT1), and contributes to cell fate decisions.	NAD	93-126	nicotinamide phosphoribosyltransferase	Rattus norvegicus	40-45
27035562-2	2016	Nicotinamide phosphoribosyltransferase (NAMPT) catalyzes the first rate-limiting step in the nicotinamide adenine dinucleotide (NAD+) biosynthetic pathway in mammals, is a substrate for NAD+-dependent enzymes, such as sirtuin 1 (SIRT1), and contributes to cell fate decisions.	NAD	128-132	nicotinamide phosphoribosyltransferase	Rattus norvegicus	0-38
27035562-2	2016	Nicotinamide phosphoribosyltransferase (NAMPT) catalyzes the first rate-limiting step in the nicotinamide adenine dinucleotide (NAD+) biosynthetic pathway in mammals, is a substrate for NAD+-dependent enzymes, such as sirtuin 1 (SIRT1), and contributes to cell fate decisions.	NAD	128-132	nicotinamide phosphoribosyltransferase	Rattus norvegicus	40-45
27035562-2	2016	Nicotinamide phosphoribosyltransferase (NAMPT) catalyzes the first rate-limiting step in the nicotinamide adenine dinucleotide (NAD+) biosynthetic pathway in mammals, is a substrate for NAD+-dependent enzymes, such as sirtuin 1 (SIRT1), and contributes to cell fate decisions.	NAD	186-190	nicotinamide phosphoribosyltransferase	Rattus norvegicus	0-38
27035562-2	2016	Nicotinamide phosphoribosyltransferase (NAMPT) catalyzes the first rate-limiting step in the nicotinamide adenine dinucleotide (NAD+) biosynthetic pathway in mammals, is a substrate for NAD+-dependent enzymes, such as sirtuin 1 (SIRT1), and contributes to cell fate decisions.	NAD	186-190	nicotinamide phosphoribosyltransferase	Rattus norvegicus	40-45
26907567-1	2016	Mammalian sirtuins (SIRT1-7) are members of a highly conserved family of nicotinamide adenine dinucleotide (NAD(+))-dependent protein deacetylases that regulate many biological processes including metabolism, genome stability, and transcription.	NAD	73-106	sirtuin 1	Homo sapiens	20-25
26907567-1	2016	Mammalian sirtuins (SIRT1-7) are members of a highly conserved family of nicotinamide adenine dinucleotide (NAD(+))-dependent protein deacetylases that regulate many biological processes including metabolism, genome stability, and transcription.	NAD	108-114	sirtuin 1	Homo sapiens	20-25
27186285-4	2016	Hypomethylation in the BRCA1 promoter was associated with BRCA1 activation, significantly elevated SIRT1 levels, decreased nicotinamide adenine dinucleotide (NAD)-mediated SIRT1 activity, and decreased EGFR levels.	NAD	123-156	BRCA1 DNA repair associated	Homo sapiens	23-28
27186285-4	2016	Hypomethylation in the BRCA1 promoter was associated with BRCA1 activation, significantly elevated SIRT1 levels, decreased nicotinamide adenine dinucleotide (NAD)-mediated SIRT1 activity, and decreased EGFR levels.	NAD	123-156	sirtuin 1	Homo sapiens	172-177
27186285-4	2016	Hypomethylation in the BRCA1 promoter was associated with BRCA1 activation, significantly elevated SIRT1 levels, decreased nicotinamide adenine dinucleotide (NAD)-mediated SIRT1 activity, and decreased EGFR levels.	NAD	158-161	BRCA1 DNA repair associated	Homo sapiens	23-28
27186285-5	2016	Treatment with 5 and 10 mug/ml cisplatin induced a gradual increase in BRCA1 and SIRT1 levels and a gradual decrease in NAD levels and NAD-mediated SIRT1 activity, whereas EGFR levels were increased or decreased by treatment with 5 or 10 mug/ml cisplatin, respectively.	NAD	135-138	sirtuin 1	Homo sapiens	148-153
26840709-7	2016	These included ATP5D, UQCRC2, UQCR11 and genes encoding nicotinamide adenine dinucleotide (NADH), which are mainly associated with mitochondrial ATP synthesis coupled electron transport, and which were enriched in the oxidative phosphorylation pathway.	NAD	91-95	ATP synthase F1 subunit delta	Homo sapiens	15-20
26565538-1	2016	Here, we describe three cases of loss-of-function mutations in the nicotinamide adenine dinucleotide phosphate (NADPH)-oxidase (NOX) domain of dual oxidase 2 (DUOX2) occurring along with concurrent missense mutations in thyroid peroxidase (TPO), leading to transient congenital hypothyroidism (CH).	NAD	67-100	thyroid peroxidase	Homo sapiens	240-243
26856538-1	2016	BACKGROUND: We reported that zinc neurotoxicity, a key mechanism of ischemic neuronal death, was mediated by poly ADP-ribose polymerase (PARP) over-activation following NAD(+)/ATP depletion in cortical cultures.	NAD	169-175	poly (ADP-ribose) polymerase family, member 1	Mus musculus	109-135
9223549-17	1997	Its agonist actions at 5-HT1A autoreceptors underlie its ability to decrease extracellular levels of 5-HT in the FCX, and likely contribute to the increase in extracellular levels of DA and NAD evoked by S 15535 in this structure.	NAD	190-193	5-hydroxytryptamine receptor 1A	Homo sapiens	23-29
26856538-1	2016	BACKGROUND: We reported that zinc neurotoxicity, a key mechanism of ischemic neuronal death, was mediated by poly ADP-ribose polymerase (PARP) over-activation following NAD(+)/ATP depletion in cortical cultures.	NAD	169-175	poly (ADP-ribose) polymerase family, member 1	Mus musculus	137-141
26574517-9	2016	Additionally, we observed an increase in the total NAD(+)/NADH level and the ATP level in CM764-treated SK-N-SH cells compared with untreated cells.	NAD	51-57	hedgehog acyltransferase	Homo sapiens	104-108
9164864-5	1997	Covalent modification of TFIIF increased with time of incubation, with increasing TFIIF concentration and with increasing NAD+ concentration.	NAD	122-126	general transcription factor IIF subunit 1	Homo sapiens	25-30
26794150-0	2016	Functional characterization of NAD dependent de-acetylases SIRT1 and SIRT2 in B-Cell Chronic Lymphocytic Leukemia (CLL).	NAD	31-34	sirtuin 1	Homo sapiens	59-64
9135568-3	1997	We have developed a gas chromatographic mass spectrometric assay for dexamethasone and 11-dehydrodexamethasone and have confirmed in vitro that dexamethasone is a substrate for 11 beta-HSD2 but not 11 beta-HSD1 (conversion to 11-dehydrodexamethasone 0.6 +/- 0.3% in homogenates of rat liver with NADP+ for 11 beta-HSD1, and 29.4 +/- 10.3% and 40.0 +/- 2.0% in homogenates of rat and human kidney respectively with NAD+ for 11 beta-HSD2).	NAD	414-418	hydroxysteroid 11-beta dehydrogenase 2	Homo sapiens	177-184
26929388-9	2016	Nonetheless AKT inhibition in the context of loss of NAD-dependent SIRT1 deacetylase modulates FOXO3 localization in HSPCs.	NAD	53-56	sirtuin 1	Homo sapiens	67-72
27184051-4	2016	This study aims to investigate the role of Nmnat1, an enzyme which catalyzes a key step in the biosynthesis of nicotinamide adenine dinucleotide (NAD), in high glucose-induced RGC injury.	NAD	111-144	nicotinamide nucleotide adenylyltransferase 1	Mus musculus	43-49
27184051-4	2016	This study aims to investigate the role of Nmnat1, an enzyme which catalyzes a key step in the biosynthesis of nicotinamide adenine dinucleotide (NAD), in high glucose-induced RGC injury.	NAD	146-149	nicotinamide nucleotide adenylyltransferase 1	Mus musculus	43-49
26931472-1	2016	SIRT1 is an NAD-dependent deacetylase.	NAD	12-15	sirtuin 1	Homo sapiens	0-5
26574954-5	2016	RESULTS: SIRT1, SIRT3, SIRT5, NAMPT, NMNAT2, NMNAT3, and NRK1 expressions were significantly down-regulated and the activity of main cellular NAD(+) consumers, PARPs, trended to be higher in the SAT of heavier co-twins of body mass index-discordant pairs.	NAD	142-148	sirtuin 1	Homo sapiens	9-14
27118078-7	2016	The enzymatic characterization revealed that the intrinsic NAD(+)-dependent deacetylation activity of LpSirA (protein encoded by sirA) is comparable to human SIRT1.	NAD	59-65	sirtuin 1	Homo sapiens	158-163
27110038-3	2016	We also studied the effectiveness of coenzymes of two of the microsomal reductases, NADPH as a coenzyme of POR, and NADH as a coenzyme of NADH:cytochrome b5 reductase, to mediate BaP metabolism in these systems.	NAD	116-120	cytochrome b5 type A	Rattus norvegicus	143-156
27110038-3	2016	We also studied the effectiveness of coenzymes of two of the microsomal reductases, NADPH as a coenzyme of POR, and NADH as a coenzyme of NADH:cytochrome b5 reductase, to mediate BaP metabolism in these systems.	NAD	138-142	cytochrome b5 type A	Rattus norvegicus	143-156
26788256-8	2016	In the same way, manipulation of cellular NAD levels by pharmacological inhibition of other NAD-consuming enzymes results in activation of SIRT1 and protection against obesity-related pathologies.	NAD	42-45	sirtuin 1	Homo sapiens	139-144
26788256-8	2016	In the same way, manipulation of cellular NAD levels by pharmacological inhibition of other NAD-consuming enzymes results in activation of SIRT1 and protection against obesity-related pathologies.	NAD	92-95	sirtuin 1	Homo sapiens	139-144
26735933-9	2016	When cofactor NAD+ was used, MXC and HPTE were the noncompetitive inhibitors of HSD3B1.	NAD	14-18	hydroxy-delta-5-steroid dehydrogenase, 3 beta- and steroid delta-isomerase 1	Homo sapiens	80-86
26633734-0	2015	Synthesis and Characterization of 4,11-Diaminoanthra[2,3-b]furan-5,10-diones: Tumor Cell Apoptosis through tNOX-Modulated NAD(+)/NADH Ratio and SIRT1.	NAD	129-133	sirtuin 1	Homo sapiens	144-149
26633734-3	2015	Compounds 11-14 utilized multiple mechanisms of cytotoxicity including inhibition of Top1/Top2-mediated DNA relaxation, reduced NAD(+)/NADH ratio through tNOX inhibition, suppression of a NAD(+)-dependent sirtuin 1 (SIRT1) deacetylase activity, and activation of caspase-mediated apoptosis.	NAD	188-194	sirtuin 1	Homo sapiens	205-214
26626483-1	2015	Eukaryotes initiate autophagy to cope with the lack of external nutrients, which requires the activation of the nicotinamide adenine dinucleotide (NAD(+))-dependent deacetylase Sirtuin 1 (Sirt1).	NAD	112-145	sirtuin 1	Homo sapiens	188-193
26626483-1	2015	Eukaryotes initiate autophagy to cope with the lack of external nutrients, which requires the activation of the nicotinamide adenine dinucleotide (NAD(+))-dependent deacetylase Sirtuin 1 (Sirt1).	NAD	147-154	sirtuin 1	Homo sapiens	188-193
26481524-6	2015	Sirtuins 1-7 (SIRT1-7) belong to class III of histone deacetylase enzymes which are dependent on NAD(+) for activity.	NAD	97-103	sirtuin 1	Homo sapiens	0-12
26481524-6	2015	Sirtuins 1-7 (SIRT1-7) belong to class III of histone deacetylase enzymes which are dependent on NAD(+) for activity.	NAD	97-103	sirtuin 1	Homo sapiens	14-21
26463129-0	2015	Negishi cross-coupling enabled synthesis of novel NAD(+)-dependent DNA ligase inhibitors and SAR development.	NAD	50-56	sarcosine dehydrogenase	Homo sapiens	93-96
26542945-6	2015	Jurkat cells in which AMPK or LKB1 expression was silenced or in which a non-phosphorylatable EIF2A mutant was ectopically expressed showed enhanced sensitivity to the NAMPT inhibitor, confirming a key role for the LKB1-AMPK-EIF2A axis in cell fate determination in response to energetic stress via NAD(+) depletion.	NAD	299-305	eukaryotic translation initiation factor 2A	Homo sapiens	94-99
26306884-3	2015	Moreover, there is reason to suspect that ketones can activate Sirt1 in neurons, in part by increasing cytoplasmic and nuclear levels of Sirt1"s obligate cofactor NAD(+).	NAD	163-169	sirtuin 1	Homo sapiens	63-68
26306884-3	2015	Moreover, there is reason to suspect that ketones can activate Sirt1 in neurons, in part by increasing cytoplasmic and nuclear levels of Sirt1"s obligate cofactor NAD(+).	NAD	163-169	sirtuin 1	Homo sapiens	137-142
26089537-3	2015	BPZE1-DC induces CD4(+) and CD8(+) T lymphocytes to express 2 sets of ectoenzymes generating ADO: 1 set is part of the conventional CD39/CD73 pathway, which uses ATP as substrate, whereas the other is part of the CD38/CD203a/CD73 pathway and metabolizes NAD(+).	NAD	254-260	ectonucleoside triphosphate diphosphohydrolase 1	Mus musculus	132-136
26253470-0	2015	Genistein inhibits activities of methylenetetrahydrofolate reductase and lactate dehydrogenase, enzymes which use NADH as a substrate.	NAD	114-118	methylenetetrahydrofolate reductase	Homo sapiens	33-68
26253470-4	2015	Both enzymes use NADH as a substrate, and results of biochemical as well as molecular modeling studies with MetF suggest that genistein may interfere with binding of this dinucleotide to the enzyme.	NAD	17-21	methylenetetrahydrofolate reductase	Homo sapiens	108-112
26189030-2	2015	Using NAD(+) as a substrate, they poly(ADP-ribosyl)ate TRF1 (regulating lengths of telomeres), NuMA (facilitating mitosis) and axin (in wnt/beta-catenin signalling).	NAD	6-12	axin 1	Homo sapiens	127-131
26237213-3	2015	Upon reduction by NADH, hAIF dimerizes and produces very stable flavin/nicotinamide charge transfer complexes (CTC), by stacking of the oxidized nicotinamide moiety of the NAD(+) coenzyme against the re-face of the reduced flavin ring of its FAD cofactor.	NAD	18-22	apoptosis inducing factor mitochondria associated 1	Homo sapiens	24-28
26237213-3	2015	Upon reduction by NADH, hAIF dimerizes and produces very stable flavin/nicotinamide charge transfer complexes (CTC), by stacking of the oxidized nicotinamide moiety of the NAD(+) coenzyme against the re-face of the reduced flavin ring of its FAD cofactor.	NAD	172-178	apoptosis inducing factor mitochondria associated 1	Homo sapiens	24-28
26237213-5	2015	The molecular basis of the hAIF reductase activity is here investigated by analyzing the role played by residues contributing to the interaction of the FAD isoalloxazine ring and of the nicotinamide moiety of NADH at the active site.	NAD	209-213	apoptosis inducing factor mitochondria associated 1	Homo sapiens	27-31
26237213-7	2015	Characterization of P173G hAIF indicates that the stacking of P173 against the isoalloxazine ring is relevant to determine the flavin environment and to modulate the enzyme affinity for NADH.	NAD	186-190	apoptosis inducing factor mitochondria associated 1	Homo sapiens	26-30
26237213-8	2015	Finally, the properties of the F310G and H454S hAIF mutants indicate that these two positions contribute to form a compact active site essential for NADH binding, CTC stabilization, and NAD(+) affinity for the reduced state of hAIF.	NAD	149-153	apoptosis inducing factor mitochondria associated 1	Homo sapiens	47-51
26237213-8	2015	Finally, the properties of the F310G and H454S hAIF mutants indicate that these two positions contribute to form a compact active site essential for NADH binding, CTC stabilization, and NAD(+) affinity for the reduced state of hAIF.	NAD	149-153	apoptosis inducing factor mitochondria associated 1	Homo sapiens	227-231
26237213-8	2015	Finally, the properties of the F310G and H454S hAIF mutants indicate that these two positions contribute to form a compact active site essential for NADH binding, CTC stabilization, and NAD(+) affinity for the reduced state of hAIF.	NAD	186-192	apoptosis inducing factor mitochondria associated 1	Homo sapiens	47-51
26237213-8	2015	Finally, the properties of the F310G and H454S hAIF mutants indicate that these two positions contribute to form a compact active site essential for NADH binding, CTC stabilization, and NAD(+) affinity for the reduced state of hAIF.	NAD	186-192	apoptosis inducing factor mitochondria associated 1	Homo sapiens	227-231
26063804-6	2015	However, after reconstituting isolated AIF or AMID into bacterial or mitochondrial membranes, N-terminally tagged AIF and AMID displayed substantial NADH:O2 activities and supported NADH-linked proton pumping activities in the host membranes almost as efficiently as Ndi1.	NAD	149-153	apoptosis inducing factor mitochondria associated 1	Homo sapiens	39-42
26063804-6	2015	However, after reconstituting isolated AIF or AMID into bacterial or mitochondrial membranes, N-terminally tagged AIF and AMID displayed substantial NADH:O2 activities and supported NADH-linked proton pumping activities in the host membranes almost as efficiently as Ndi1.	NAD	149-153	apoptosis inducing factor mitochondria associated 1	Homo sapiens	114-117
26063804-6	2015	However, after reconstituting isolated AIF or AMID into bacterial or mitochondrial membranes, N-terminally tagged AIF and AMID displayed substantial NADH:O2 activities and supported NADH-linked proton pumping activities in the host membranes almost as efficiently as Ndi1.	NAD	182-186	apoptosis inducing factor mitochondria associated 1	Homo sapiens	39-42
26063804-6	2015	However, after reconstituting isolated AIF or AMID into bacterial or mitochondrial membranes, N-terminally tagged AIF and AMID displayed substantial NADH:O2 activities and supported NADH-linked proton pumping activities in the host membranes almost as efficiently as Ndi1.	NAD	182-186	apoptosis inducing factor mitochondria associated 1	Homo sapiens	114-117
26063804-9	2015	In contrast, C-terminally tagged AIF and NADH-binding site mutants of N-terminally tagged AIF and AMID failed to show both NADH:O2 activity and the growth-enhancing effect.	NAD	41-45	apoptosis inducing factor mitochondria associated 1	Homo sapiens	90-93
26063804-12	2015	We propose that AIF and AMID are previously unidentified mammalian NDH-2 enzymes, whose bioenergetic function could be supplemental NADH oxidation in cells.	NAD	132-136	apoptosis inducing factor mitochondria associated 1	Homo sapiens	16-19
9112779-12	1997	Likewise, the relative difference in the level of alpha or beta subunits was correlated with changes in the level of GDH1 or GDH2 transcript detected in each sample, suggesting that NAD(H)-GDH activity is controlled at least in part at the transcriptional level.	NAD	182-188	glutamate dehydrogenase 1	Arabidopsis thaliana	117-121
26176355-4	2015	For tyrosinase to act in this way, the Eox form (oxy-tyrosinase) must be present in the reaction medium, which can be brought about by (a) hydrogen peroxide, (b) ascorbic acid, or (c) catalytic concentrations of o-diphenol and a reductant (NADH) to maintain it constant.	NAD	240-244	tyrosinase	Homo sapiens	4-14
26176355-4	2015	For tyrosinase to act in this way, the Eox form (oxy-tyrosinase) must be present in the reaction medium, which can be brought about by (a) hydrogen peroxide, (b) ascorbic acid, or (c) catalytic concentrations of o-diphenol and a reductant (NADH) to maintain it constant.	NAD	240-244	tyrosinase	Homo sapiens	53-63
26056253-6	2015	Peritoneal CD49d(high)CD4(+) T cells were more resistant to irradiation and more sensitive to NAD-induced cell death than CD49d(low)CD4(+) T cells.	NAD	94-97	CD4 antigen	Mus musculus	11-14
26056253-6	2015	Peritoneal CD49d(high)CD4(+) T cells were more resistant to irradiation and more sensitive to NAD-induced cell death than CD49d(low)CD4(+) T cells.	NAD	94-97	CD4 antigen	Mus musculus	22-25
9027727-10	1997	In response to an external application of NADH (1 mM), the membrane bound cytochrome b558 produces two times more O2- than to the external NADPH (1 mM) application.	NAD	42-46	mitochondrially encoded cytochrome b	Homo sapiens	74-86
26051626-8	2015	NAD levels, which are controlled by Nampt and also exhibit circadian rhythm, decreased or increased according to Nampt expression.	NAD	0-3	nicotinamide phosphoribosyltransferase	Rattus norvegicus	36-41
26051626-8	2015	NAD levels, which are controlled by Nampt and also exhibit circadian rhythm, decreased or increased according to Nampt expression.	NAD	0-3	nicotinamide phosphoribosyltransferase	Rattus norvegicus	113-118
25926139-9	2015	Infecting VSMCs with an adenovirus encoding full-length Mfn-2 increased NADH level and reduced NAD(+) level, while infecting the cells with an adenovirus that silences the p21(ras) signature motif produced opposite effects.	NAD	72-76	mitofusin 2	Homo sapiens	56-61
25926139-9	2015	Infecting VSMCs with an adenovirus encoding full-length Mfn-2 increased NADH level and reduced NAD(+) level, while infecting the cells with an adenovirus that silences the p21(ras) signature motif produced opposite effects.	NAD	95-101	mitofusin 2	Homo sapiens	56-61
26057809-4	2015	NAD synthetase catalyzes the last step in the biosynthesis of nicotinamide adenine dinucleotide, making it a crucial intermediate enzyme linked to the biosynthesis of several amino acids, purine and pyrimidine nucleotides, coenzymes and antibiotics.	NAD	62-95	AT695_RS07645	Staphylococcus aureus	0-14
25841561-1	2015	Nicotinamide mononucleotide adenylyltransferase 1 (NMNAT1) is a nicotinamide adenine dinucleotide biosynthetic enzyme.	NAD	64-97	nicotinamide nucleotide adenylyltransferase 1	Mus musculus	0-49
25841561-1	2015	Nicotinamide mononucleotide adenylyltransferase 1 (NMNAT1) is a nicotinamide adenine dinucleotide biosynthetic enzyme.	NAD	64-97	nicotinamide nucleotide adenylyltransferase 1	Mus musculus	51-57
25926383-2	2015	SIRT1 (silent information regulator 1), a member of mammalian sirtuin family protein (SIRT1-SIRT7), functions as a conserved nicotinamide adenine dinucleotide (NAD)+-dependent deacetylase to implicate in the modulation of transcriptional silencing and cell survival.	NAD	125-158	sirtuin 1	Homo sapiens	0-5
25926383-2	2015	SIRT1 (silent information regulator 1), a member of mammalian sirtuin family protein (SIRT1-SIRT7), functions as a conserved nicotinamide adenine dinucleotide (NAD)+-dependent deacetylase to implicate in the modulation of transcriptional silencing and cell survival.	NAD	125-158	sirtuin 1	Homo sapiens	7-37
25926383-2	2015	SIRT1 (silent information regulator 1), a member of mammalian sirtuin family protein (SIRT1-SIRT7), functions as a conserved nicotinamide adenine dinucleotide (NAD)+-dependent deacetylase to implicate in the modulation of transcriptional silencing and cell survival.	NAD	160-163	sirtuin 1	Homo sapiens	0-5
25926383-2	2015	SIRT1 (silent information regulator 1), a member of mammalian sirtuin family protein (SIRT1-SIRT7), functions as a conserved nicotinamide adenine dinucleotide (NAD)+-dependent deacetylase to implicate in the modulation of transcriptional silencing and cell survival.	NAD	160-163	sirtuin 1	Homo sapiens	7-37
26023773-3	2015	Mitotic repression of Pol I transcription correlates with transient nucleolar enrichment of the NAD(+)-dependent deacetylase SIRT1, which deacetylates another subunit of SL1, TAFI68.	NAD	96-102	sirtuin 1	Homo sapiens	125-130
25825491-0	2015	Reduced Ssy1-Ptr3-Ssy5 (SPS) signaling extends replicative life span by enhancing NAD+ homeostasis in Saccharomyces cerevisiae.	NAD	82-86	Ssy1p	Saccharomyces cerevisiae S288C	8-22
25825491-5	2015	First, expression of the putative malate-pyruvate NADH shuttle increases in ssy5Delta cells, and deleting components of this shuttle, MAE1 and OAC1, largely abolishes RLS extension.	NAD	50-54	Ssy5p	Saccharomyces cerevisiae S288C	76-85
26042198-1	2015	Nicotinic acid phosphoribosyltransferase (EC 2.4.2.11) (NaPRTase) is the rate-limiting enzyme in the three-step Preiss-Handler pathway for the biosynthesis of NAD.	NAD	159-162	nicotinate phosphoribosyltransferase	Homo sapiens	56-64
26042198-3	2015	Several studies have underlined the importance of NaPRTase for NAD homeostasis in mammals, but no crystallographic data are available for this enzyme from higher eukaryotes.	NAD	63-66	nicotinate phosphoribosyltransferase	Homo sapiens	50-58
26042198-7	2015	Moreover, structural comparison of human NaPRTase with the other two human type II phosphoribosyltransferases involved in NAD biosynthesis, quinolinate phosphoribosyltransferase and nicotinamide phosphoribosyltransferase, reveals that while the three enzymes share a conserved overall structure, a few distinctive structural traits can be identified.	NAD	122-125	nicotinate phosphoribosyltransferase	Homo sapiens	41-49
25921090-3	2015	Here we demonstrate that deacetylation of iNAMPT by the mammalian NAD(+)-dependent deacetylase SIRT1 predisposes the protein to secretion in adipocytes.	NAD	66-72	sirtuin 1	Homo sapiens	95-100
25942624-6	2015	Expression of these proteins increases during nutrient stress through an NAD(+)/Sir2-dependent mechanism that in turn accelerates the downregulation of a broad range of cell-surface proteins.	NAD	73-79	sirtuin 1	Homo sapiens	80-84
25736100-1	2015	Silent information regulator 1 (SIRT1) is a nicotinamide adenine dinucleotide (NAD(+) )-dependent protein deacetylase.	NAD	44-77	sirtuin 1	Homo sapiens	0-30
25736100-1	2015	Silent information regulator 1 (SIRT1) is a nicotinamide adenine dinucleotide (NAD(+) )-dependent protein deacetylase.	NAD	44-77	sirtuin 1	Homo sapiens	32-37
25736100-1	2015	Silent information regulator 1 (SIRT1) is a nicotinamide adenine dinucleotide (NAD(+) )-dependent protein deacetylase.	NAD	79-87	sirtuin 1	Homo sapiens	0-30
25736100-1	2015	Silent information regulator 1 (SIRT1) is a nicotinamide adenine dinucleotide (NAD(+) )-dependent protein deacetylase.	NAD	79-87	sirtuin 1	Homo sapiens	32-37
25736100-5	2015	In the liver of hepatitis patients, decreased NAD(+) amounts and its regulatory enzyme nicotinamide phosphoribosyltransferase expression levels were observed, and this led to inhibition of SIRT1 activity.	NAD	46-52	sirtuin 1	Homo sapiens	189-194
25918360-2	2015	In addition, the pyridine dinucleotides nicotinamide-adenine-dinucleotide (NAD), nicotinic acid-adenine-dinucleotide (NAAD), and NAAD-2"-phosphate (NAADP) have been shown to activate TRPM2, or to enhance its activation by ADPR, when dialyzed into cells.	NAD	40-73	transient receptor potential cation channel subfamily M member 2	Homo sapiens	183-188
25918360-5	2015	Direct application of purified NAD, NAAD, or NAADP to the cytosolic face of TRPM2 channels in inside-out patches demonstrated that none of them stimulates gating, or affects channel activation by ADPR, indicating that none of these dinucleotides directly binds to TRPM2.	NAD	31-34	transient receptor potential cation channel subfamily M member 2	Homo sapiens	76-81
25933096-7	2015	Regarding hepatic lipid homeostasis, the ratio of NAD+ to NADH was dramatically increased in mouse liver replete with LRPPRC.	NAD	50-54	leucine-rich PPR-motif containing	Mus musculus	118-124
25933096-7	2015	Regarding hepatic lipid homeostasis, the ratio of NAD+ to NADH was dramatically increased in mouse liver replete with LRPPRC.	NAD	58-62	leucine-rich PPR-motif containing	Mus musculus	118-124
25924011-3	2015	Resveratrol"s anti-aging effects both in vitro and in vivo attributed to activation of a (NAD)-dependent histone deacetylase family member sirtuin-1 (SIRT1) protein.	NAD	89-94	sirtuin 1	Homo sapiens	139-148
25924011-3	2015	Resveratrol"s anti-aging effects both in vitro and in vivo attributed to activation of a (NAD)-dependent histone deacetylase family member sirtuin-1 (SIRT1) protein.	NAD	89-94	sirtuin 1	Homo sapiens	150-155
25923415-3	2015	These hubs are the pathway defined by the mammalian target of rapamycin (mTOR) and that defined by the NAD+-dependent deacetylase enzyme, SIRT1.	NAD	103-107	sirtuin 1	Homo sapiens	138-143
25860861-4	2015	Here we report that Sirt7, a NAD(+)-dependent class III histone deacetylase, is over-expressed in human gastric cancer tissues.	NAD	29-35	sirtuin 7	Homo sapiens	20-25
26005675-5	2015	Remarkably, the effects of ethanol on these regulators are mediated in whole or in part by inhibition of a central signaling molecule, sirtuin 1 (SIRT1), which is a nicotinamide adenine dinucleotide (NAD(+), NADH)-dependent class III protein deacetylase.	NAD	165-198	sirtuin 1	Homo sapiens	135-144
26005675-5	2015	Remarkably, the effects of ethanol on these regulators are mediated in whole or in part by inhibition of a central signaling molecule, sirtuin 1 (SIRT1), which is a nicotinamide adenine dinucleotide (NAD(+), NADH)-dependent class III protein deacetylase.	NAD	165-198	sirtuin 1	Homo sapiens	146-151
26005675-5	2015	Remarkably, the effects of ethanol on these regulators are mediated in whole or in part by inhibition of a central signaling molecule, sirtuin 1 (SIRT1), which is a nicotinamide adenine dinucleotide (NAD(+), NADH)-dependent class III protein deacetylase.	NAD	200-206	sirtuin 1	Homo sapiens	135-144
26005675-5	2015	Remarkably, the effects of ethanol on these regulators are mediated in whole or in part by inhibition of a central signaling molecule, sirtuin 1 (SIRT1), which is a nicotinamide adenine dinucleotide (NAD(+), NADH)-dependent class III protein deacetylase.	NAD	200-206	sirtuin 1	Homo sapiens	146-151
26005675-5	2015	Remarkably, the effects of ethanol on these regulators are mediated in whole or in part by inhibition of a central signaling molecule, sirtuin 1 (SIRT1), which is a nicotinamide adenine dinucleotide (NAD(+), NADH)-dependent class III protein deacetylase.	NAD	208-212	sirtuin 1	Homo sapiens	135-144
26005675-5	2015	Remarkably, the effects of ethanol on these regulators are mediated in whole or in part by inhibition of a central signaling molecule, sirtuin 1 (SIRT1), which is a nicotinamide adenine dinucleotide (NAD(+), NADH)-dependent class III protein deacetylase.	NAD	208-212	sirtuin 1	Homo sapiens	146-151
25813492-0	2015	NAD+ treatment can prevent rotenone-induced increases in DNA damage, Bax levels and nuclear translocation of apoptosis-inducing factor in differentiated PC12 cells.	NAD	0-4	apoptosis inducing factor, mitochondria associated 1	Rattus norvegicus	109-134
25813492-5	2015	We found that NAD(+) treatment can markedly attenuate the rotenone-induced increases in the levels of Bax and nuclear translocation of AIF in the cells.	NAD	14-20	apoptosis inducing factor, mitochondria associated 1	Rattus norvegicus	135-138
25837871-0	2015	Methylation gets into rhythm with NAD(+)-SIRT1.	NAD	34-40	sirtuin 1	Homo sapiens	41-46
25576955-1	2015	Silent information regulator 6 (SIRT6) belongs to the family of class III nicotinamide adenine dinucleotide (NAD)-dependent deacetylase and plays an essential role in DNA repair and metabolism.	NAD	74-107	sirtuin 6	Bos taurus	0-30
25576955-1	2015	Silent information regulator 6 (SIRT6) belongs to the family of class III nicotinamide adenine dinucleotide (NAD)-dependent deacetylase and plays an essential role in DNA repair and metabolism.	NAD	74-107	sirtuin 6	Bos taurus	32-37
25576955-1	2015	Silent information regulator 6 (SIRT6) belongs to the family of class III nicotinamide adenine dinucleotide (NAD)-dependent deacetylase and plays an essential role in DNA repair and metabolism.	NAD	109-112	sirtuin 6	Bos taurus	0-30
25576955-1	2015	Silent information regulator 6 (SIRT6) belongs to the family of class III nicotinamide adenine dinucleotide (NAD)-dependent deacetylase and plays an essential role in DNA repair and metabolism.	NAD	109-112	sirtuin 6	Bos taurus	32-37
26113881-6	2015	We report the direct electrochemical addressing of immobilized alcohol dehydrogenase for the reduction of butyraldehyde to butanol without consumption of NADH.	NAD	154-158	aldo-keto reductase family 1 member A1	Homo sapiens	63-84
25714130-9	2015	Knockdown of NDUFAF1 by siRNA caused mitochondrial respiration deficiency, accumulation of NADH and subsequent increase of glycolytic activity.	NAD	91-95	NADH:ubiquinone oxidoreductase complex assembly factor 1	Homo sapiens	13-20
26045998-4	2015	Here, we show that DNMT1 levels are upregulated, along with increased NAD levels in non-BRCA1-mutated ovarian cancer cells.	NAD	70-73	DNA methyltransferase 1	Homo sapiens	19-24
26045998-8	2015	Therefore, these results highlight a novel regulatory effect of NAD on DNMT1, and further correlate the physiological properties of NAD metabolism with DNMT1-mediated biological processes.	NAD	64-67	DNA methyltransferase 1	Homo sapiens	71-76
26045998-8	2015	Therefore, these results highlight a novel regulatory effect of NAD on DNMT1, and further correlate the physiological properties of NAD metabolism with DNMT1-mediated biological processes.	NAD	64-67	DNA methyltransferase 1	Homo sapiens	152-157
26045998-8	2015	Therefore, these results highlight a novel regulatory effect of NAD on DNMT1, and further correlate the physiological properties of NAD metabolism with DNMT1-mediated biological processes.	NAD	132-135	DNA methyltransferase 1	Homo sapiens	71-76
26045998-8	2015	Therefore, these results highlight a novel regulatory effect of NAD on DNMT1, and further correlate the physiological properties of NAD metabolism with DNMT1-mediated biological processes.	NAD	132-135	DNA methyltransferase 1	Homo sapiens	152-157
25212631-10	2015	Conversely, Npas2 controlled the circadian rhythm of Shp expression by binding rhythmically to the Shp promoter, which was enhanced by nicotinamide adenine dinucleotide, but not nicotinamide adenine dinucleotide phosphate.	NAD	135-168	neuronal PAS domain protein 2	Mus musculus	12-17
25212631-10	2015	Conversely, Npas2 controlled the circadian rhythm of Shp expression by binding rhythmically to the Shp promoter, which was enhanced by nicotinamide adenine dinucleotide, but not nicotinamide adenine dinucleotide phosphate.	NAD	135-168	nuclear receptor subfamily 0, group B, member 2	Mus musculus	53-56
25212631-10	2015	Conversely, Npas2 controlled the circadian rhythm of Shp expression by binding rhythmically to the Shp promoter, which was enhanced by nicotinamide adenine dinucleotide, but not nicotinamide adenine dinucleotide phosphate.	NAD	135-168	nuclear receptor subfamily 0, group B, member 2	Mus musculus	99-102
25785061-1	2015	SIRT1 is the homologue of sir2 in mammals, which is a nicotinamide adenine dinucleotide (NAD(+)) dependent histone deacetylase.	NAD	54-87	sirtuin 1	Homo sapiens	0-5
25785061-1	2015	SIRT1 is the homologue of sir2 in mammals, which is a nicotinamide adenine dinucleotide (NAD(+)) dependent histone deacetylase.	NAD	54-87	sirtuin 1	Homo sapiens	26-30
25785061-1	2015	SIRT1 is the homologue of sir2 in mammals, which is a nicotinamide adenine dinucleotide (NAD(+)) dependent histone deacetylase.	NAD	89-95	sirtuin 1	Homo sapiens	0-5
25785061-1	2015	SIRT1 is the homologue of sir2 in mammals, which is a nicotinamide adenine dinucleotide (NAD(+)) dependent histone deacetylase.	NAD	89-95	sirtuin 1	Homo sapiens	26-30
25587857-2	2015	SIRT1, as an intracellular energy sensor, detects the concentration of intracellular NAD(+) and uses this information to adapt cellular energy output to cellular energy requirements.	NAD	85-91	sirtuin 1	Homo sapiens	0-5
25404738-1	2015	We reported that NAD(+)-dependent SIRT1, RELB, and SIRT6 nuclear proteins in monocytes regulate a switch from the glycolysis-dependent acute inflammatory response to fatty acid oxidation-dependent sepsis adaptation.	NAD	17-23	sirtuin 1	Homo sapiens	34-39
25529796-8	2015	Thus, the NAD(+)-dependent inhibition of SOD2 activity and ROS by SIRT1 provides a gatekeeper function to reduce PARK2-mediated mitophagy and aberrant cell survival.	NAD	10-16	sirtuin 1	Homo sapiens	66-71
25921180-1	2015	BACKGROUND: Sirtuin7 (SIRT7) is a type of nicotinamide adenine dinucleotide oxidized form (NAD+)-dependent deacetylase and the least understood member of the sirtuins family; it is implicated in various processes, such as aging, DNA damage repair and cell signaling transduction.	NAD	42-75	sirtuin 7	Homo sapiens	12-20
25921180-1	2015	BACKGROUND: Sirtuin7 (SIRT7) is a type of nicotinamide adenine dinucleotide oxidized form (NAD+)-dependent deacetylase and the least understood member of the sirtuins family; it is implicated in various processes, such as aging, DNA damage repair and cell signaling transduction.	NAD	42-75	sirtuin 7	Homo sapiens	22-27
25666794-3	2015	Cumulating evidence has suggested that NAD(+) can produce its protective effects by multiple mechanisms, including preventing mitochondrial alterations, enhancing energy metabolism, preventing virtually all forms of cell death including apoptosis, necrosis and autophagy, inhibiting inflammation, directly increasing antioxidation capacity of cells and tissues, and activating SIRT1.	NAD	39-45	sirtuin 1	Homo sapiens	377-382
25500546-1	2014	SIRT1, a NAD(+) dependent class III deacetylase, takes part in many important biological processes.	NAD	9-15	sirtuin 1	Homo sapiens	0-5
25451262-5	2014	Finally, beta-lap activated Sirt1 by increasing the intracellular NAD(+)/NADH ratio, which was accompanied by increased mtDNA content.	NAD	66-72	sirtuin 1	Homo sapiens	28-33
25451262-5	2014	Finally, beta-lap activated Sirt1 by increasing the intracellular NAD(+)/NADH ratio, which was accompanied by increased mtDNA content.	NAD	73-77	sirtuin 1	Homo sapiens	28-33
25417168-3	2014	The seven mammalian sirtuins, SIRT1-7, share a highly conserved NAD+-binding catalytic core domain although they exhibit distinct expression patterns, catalytic activities, and biological functions.	NAD	64-68	sirtuin 1	Homo sapiens	30-37
25440052-3	2014	(2014) demonstrate that increasing NAD(+) levels may reverse the inactivation of Sirt1 and mitochondrial defects in Cockayne Syndrome B that stem from nuclear NAD(+) depletion by the DNA repair protein PARP.	NAD	35-41	sirtuin 1	Homo sapiens	81-86
25440052-3	2014	(2014) demonstrate that increasing NAD(+) levels may reverse the inactivation of Sirt1 and mitochondrial defects in Cockayne Syndrome B that stem from nuclear NAD(+) depletion by the DNA repair protein PARP.	NAD	159-165	sirtuin 1	Homo sapiens	81-86
25349818-9	2014	A number of molecular links, including nicotinamide adenine dinucleotide, nicotinamide, biotin, and related metabolites, are suggested to be the most important conduits mediating caloric restriction-induced Sir2/SIRT1 activation and lifespan extension.	NAD	39-72	sirtuin 1	Homo sapiens	212-217
25339333-7	2014	CONCLUSION: High dose of Vitamin B3 may play an important role in increasing absolute neutrophil count in healthy rat under steady state, and the mechanism may be dependent on NAMPT-NAD+-SIRT1 signaling pathways.	NAD	182-186	nicotinamide phosphoribosyltransferase	Rattus norvegicus	176-181
25193706-8	2014	NAD(+) (an essential cofactor of SIRT1) was also increased.	NAD	0-6	sirtuin 1	Homo sapiens	33-38
25250818-6	2014	miR-34a activity was validated by measuring the expression levels of one of its well described target: the NADH dependent sirtuin1 (SIRT1).	NAD	107-111	sirtuin 1	Homo sapiens	122-130
25250818-6	2014	miR-34a activity was validated by measuring the expression levels of one of its well described target: the NADH dependent sirtuin1 (SIRT1).	NAD	107-111	sirtuin 1	Homo sapiens	132-137
25324471-4	2014	Importantly, rapamycin treatment of Mandibuloacral dysplasia cells, which feature very low levels of the NAD-dependent sirtuin SIRT-1 in the nuclear matrix, restores SIRT-1 localization and distribution of chromatin markers, elicits release of the transcription factor Oct-1 and determines shortening of the prolonged S-phase.	NAD	105-108	sirtuin 1	Homo sapiens	127-133
24414799-1	2014	Tat transactivating activity regulated by NAD(+) -dependent histone deacetylase sirtuin1 (SIRT1) connects HIV transcription with the metabolic state of the cell.	NAD	42-48	sirtuin 1	Homo sapiens	80-88
24414799-1	2014	Tat transactivating activity regulated by NAD(+) -dependent histone deacetylase sirtuin1 (SIRT1) connects HIV transcription with the metabolic state of the cell.	NAD	42-48	sirtuin 1	Homo sapiens	90-95
25922660-1	2014	BACKGROUND: Sirtuin1 (SIRT1) is an NAD(+)-dependent type III histone deacetylase (HDAC).	NAD	35-41	sirtuin 1	Homo sapiens	12-20
25922660-1	2014	BACKGROUND: Sirtuin1 (SIRT1) is an NAD(+)-dependent type III histone deacetylase (HDAC).	NAD	35-41	sirtuin 1	Homo sapiens	22-27
24816293-4	2014	In this work, we have purified Cb5R from pig liver and we have experimentally shown that this enzyme catalyzed NADH-dependent production of superoxide anion, assayed with cytochrome c and nitroblue tetrazolium as detection reagents for this particular ROS.	NAD	111-115	cytochrome c	Sus scrofa	171-183
25117334-2	2014	In the present study, we replaced four amino acid residues in the Rossmann fold (betaB-alphaC) region of NADH-dependent ScMDH by site-directed mutagenesis with those of NADPH-dependent MDH (Glu42Gly, Ile43Ser, Pro45Arg, and Ala46Ser).	NAD	105-109	malic enzyme 1	Homo sapiens	122-125
24914854-3	2014	The crystal structure of the human AIF (hAIF):NAD(H)-bound dimer revealed one FAD and, unexpectedly, two NAD(H) molecules per protomer.	NAD	46-52	apoptosis inducing factor mitochondria associated 1	Homo sapiens	35-38
24914854-3	2014	The crystal structure of the human AIF (hAIF):NAD(H)-bound dimer revealed one FAD and, unexpectedly, two NAD(H) molecules per protomer.	NAD	46-52	apoptosis inducing factor mitochondria associated 1	Homo sapiens	40-44
24914854-3	2014	The crystal structure of the human AIF (hAIF):NAD(H)-bound dimer revealed one FAD and, unexpectedly, two NAD(H) molecules per protomer.	NAD	105-111	apoptosis inducing factor mitochondria associated 1	Homo sapiens	35-38
24914854-3	2014	The crystal structure of the human AIF (hAIF):NAD(H)-bound dimer revealed one FAD and, unexpectedly, two NAD(H) molecules per protomer.	NAD	105-111	apoptosis inducing factor mitochondria associated 1	Homo sapiens	40-44
24914854-4	2014	A 1:2 hAIF:NAD(H) binding stoichiometry was additionally confirmed in solution by using surface plasmon resonance.	NAD	11-17	apoptosis inducing factor mitochondria associated 1	Homo sapiens	6-10
24914854-5	2014	The here newly discovered NAD(H)-binding site includes residues mutated in human disorders, and accommodation of the coenzyme in it requires restructuring of a hAIF portion within the 509-560 apoptogenic segment.	NAD	26-32	apoptosis inducing factor mitochondria associated 1	Homo sapiens	160-164
24922076-5	2014	Here, we demonstrate for the first time that, in cisplatin-mediated ototoxicity, the levels and activities of SIRT1 are suppressed by the reduction of intracellular NAD(+) levels.	NAD	165-171	sirtuin 1	Homo sapiens	110-115
24959376-1	2014	SIRT1, a member of the NAD(+)-dependent histone/protein deacetylase family, is involved in chromatin remodeling, DNA repair, and stress response and is a potential drug target.	NAD	23-29	sirtuin 1	Homo sapiens	0-5
24739386-2	2014	Nicotinamide mononucleotide adenylyltransferase 3 (Nmnat3) is considered a mitochondria-localized NAD synthesis enzyme involved in de novo and salvage pathways.	NAD	98-101	nicotinamide nucleotide adenylyltransferase 3	Mus musculus	0-49
24739386-2	2014	Nicotinamide mononucleotide adenylyltransferase 3 (Nmnat3) is considered a mitochondria-localized NAD synthesis enzyme involved in de novo and salvage pathways.	NAD	98-101	nicotinamide nucleotide adenylyltransferase 3	Mus musculus	51-57
24739386-4	2014	In this study, we demonstrated that Nmnat3 was localized in the cytoplasm of mature erythrocytes and critically regulated their NAD pool.	NAD	128-131	nicotinamide nucleotide adenylyltransferase 3	Mus musculus	36-42
24739386-7	2014	LC-MS/MS-based metabolomics revealed that the glycolysis pathway in Nmnat3-deficient erythrocytes was blocked at a glyceraldehyde 3-phosphate dehydrogenase (GAPDH) step because of the shortage of the coenzyme NAD.	NAD	209-212	nicotinamide nucleotide adenylyltransferase 3	Mus musculus	68-74
24739386-7	2014	LC-MS/MS-based metabolomics revealed that the glycolysis pathway in Nmnat3-deficient erythrocytes was blocked at a glyceraldehyde 3-phosphate dehydrogenase (GAPDH) step because of the shortage of the coenzyme NAD.	NAD	209-212	glyceraldehyde-3-phosphate dehydrogenase	Mus musculus	157-162
24739386-9	2014	Our findings indicate the critical roles of Nmnat3 in maintenance of the NAD pool in mature erythrocytes and the physiological impacts at its absence in mice.	NAD	73-76	nicotinamide nucleotide adenylyltransferase 3	Mus musculus	44-50
24813611-4	2014	The mitochondrial abnormalities appear to be caused by decreased activation of the NAD(+)-SIRT1-PGC-1alpha axis triggered by hyperactivation of the DNA damage sensor PARP-1.	NAD	83-89	sirtuin 1	Homo sapiens	90-95
24557422-2	2014	It has been reported that the nicotinamide adenine dinucleotide-dependent deacetylase sirtuin 1 attenuates myocardial, cerebral, and renal ischemia/reperfusion damage.	NAD	30-63	sirtuin 1	Homo sapiens	86-95
24757201-5	2014	Interestingly, miR-149 inhibits poly(ADP-ribose) polymerase-2 (PARP-2) and so increased cellular NAD(+) levels and SIRT-1 activity that subsequently increases mitochondrial function and biogenesis via PGC-1alpha activation.	NAD	97-103	microRNA 149	Mus musculus	15-22
24548601-1	2014	BACKGROUND: Together with p53, the NAD-dependent lysine deacetylase SIRT1 and the microRNA miR-34a form a feedback loop which self-regulates SIRT1 expression and modulates p53-dependent responses.	NAD	35-38	sirtuin 1	Homo sapiens	68-73
24548601-1	2014	BACKGROUND: Together with p53, the NAD-dependent lysine deacetylase SIRT1 and the microRNA miR-34a form a feedback loop which self-regulates SIRT1 expression and modulates p53-dependent responses.	NAD	35-38	sirtuin 1	Homo sapiens	141-146
24743044-3	2014	SIRT1, a NAD(+)-dependent class III histone deacetylase, has been implicated in a variety of physiological processes and pathological conditions.	NAD	9-15	sirtuin 1	Homo sapiens	0-5
24491677-5	2014	The NAD(+) administration also attenuated the DOX-induced increases in the levels of double-strand DNA (dsDNA) damage, TUNEL signals, and active caspase-3.	NAD	4-10	caspase 3	Mus musculus	145-154
24536059-1	2014	SIRT7 belongs to the Sirtuin family of NAD-dependent enzymes, the members of which play diverse roles in aging, metabolism, and disease biology.	NAD	39-42	sirtuin 7	Homo sapiens	0-5
24451382-1	2014	Sirtuin-1 (SirT1), a member of the NAD(+)-dependent class III histone deacetylase family, is inactivated in vitro by oxidation of critical cysteine thiols.	NAD	35-41	sirtuin 1	Homo sapiens	0-9
24451382-1	2014	Sirtuin-1 (SirT1), a member of the NAD(+)-dependent class III histone deacetylase family, is inactivated in vitro by oxidation of critical cysteine thiols.	NAD	35-41	sirtuin 1	Homo sapiens	11-16
24557752-9	2014	A heat-shock protein (GrpE), a nicotinamide adenine dinucleotide-dependent glyceraldehyde 3-phosphate dehydrogenase (GAPN), and 4 proteins from paralogous gene families (PGFs) were identified as antigens by Western blot.	NAD	31-64	glyceraldehyde-3-phosphate dehydrogenase	Sus scrofa	75-115
9116490-2	1997	HPR, a homogenous side-fraction arising from this purification procedure, was identified after sequencing of three internal peptides which showed near 100% homology with the amino acid sequence deduced from the cDNA encoding the NADH-dependent HPR from cucumber.	NAD	229-233	glycerate dehydrogenase	Cucumis sativus	0-3
24025646-0	2014	Pharmacological activation of NQO1 increases NAD+ levels and attenuates cisplatin-mediated acute kidney injury in mice.	NAD	45-49	NAD(P)H dehydrogenase, quinone 1	Mus musculus	30-34
24025646-4	2014	As NAD(+) is a cofactor for various enzymes associated with cellular homeostasis, we studied the effects of increased NAD(+) levels by means of NAD(P)H: quinone oxidoreductase 1 (NQO1) activation using a known pharmacological activator (beta-lapachone) in wild-type and NQO1(-/-) mice on cisplatin-induced renal dysfunction in vivo.	NAD	3-9	NAD(P)H dehydrogenase, quinone 1	Mus musculus	179-183
9116490-2	1997	HPR, a homogenous side-fraction arising from this purification procedure, was identified after sequencing of three internal peptides which showed near 100% homology with the amino acid sequence deduced from the cDNA encoding the NADH-dependent HPR from cucumber.	NAD	229-233	glycerate dehydrogenase	Cucumis sativus	244-247
8920979-2	1996	As a result, S-adenosylmethionine synthetase activity increased 2.3-fold, an effect that was accompanied by increased S-adenosylmethionine, a depletion of ATP and NAD levels, elevation of the S-adenosylmethionine/S-adenosylhomocysteine ratio (the methylation ratio), increased DNA methylation and polyamine levels (spermidine and spermine), and normal GSH levels.	NAD	163-166	methionine adenosyltransferase 1A	Rattus norvegicus	13-44
8798532-6	1996	Here we report that the complete inhibition of p22(phox) mRNA expression by stable transfection of antisense p22(phox) cDNA into VSMCs results in a decrease in cytochrome b content, which is accompanied by a significant inhibition of angiotensin II-stimulated NADH/NADPH-dependent superoxide production, subsequent hydrogen peroxide production, and [3H]leucine incorporation.	NAD	260-264	cytochrome b, mitochondrial	Rattus norvegicus	160-172
8780571-6	1996	Neutrophil depletion or antibodies to either ICAM-1 or CD11/CD18 blunted the gut I/R-induced increases in NADH autofluorescence in the pericentral region, leukocyte adherence, and nonperfused sinusoids.	NAD	106-110	intercellular adhesion molecule 1	Rattus norvegicus	45-51
8984999-1	1996	The kinetics of glucose 6-phosphate oxidation by glucose 6-phosphate dehydrogenase from wheat seeds was studied at pH 6-11 within a broad interval of the glucose 6-phosphate and NADH concentrations.	NAD	178-182	glucose-6-phosphate 1-dehydrogenase, cytoplasmic isoform	Triticum aestivum	49-82
8984999-2	1996	A high substrate concentration (over 4-6 mM) activated the enzyme within the pH range studied; the excess of NADH inhibited glucose 6-phosphate dehydrogenase at pH 6.0-9.5.	NAD	109-113	glucose-6-phosphate 1-dehydrogenase, cytoplasmic isoform	Triticum aestivum	124-157
8812833-6	1996	The recombinant domain retained both NADH:ferricyanide and NADH:cytochrome b5 reductase activities with Vmax of 48 and 26 micromol NADH consumed/min/nmol FAD, respectively, and Km of 6, 7, and 11 microM for NADH, ferricyanide, and cytochrome b5.	NAD	37-41	cytochrome b5 type A	Rattus norvegicus	64-77
8812833-6	1996	The recombinant domain retained both NADH:ferricyanide and NADH:cytochrome b5 reductase activities with Vmax of 48 and 26 micromol NADH consumed/min/nmol FAD, respectively, and Km of 6, 7, and 11 microM for NADH, ferricyanide, and cytochrome b5.	NAD	37-41	cytochrome b5 type A	Rattus norvegicus	231-244
8733012-4	1996	11 beta-HSD2 is NAD-dependent, is present in tissues such as the kidney and placenta, and converts cortisol to cortisone (corticosterone to 11-dehydrocorticosterone in the rat).	NAD	16-19	hydroxysteroid 11-beta dehydrogenase 2	Rattus norvegicus	0-12
8848280-6	1996	This may prevent the critical depletion of NAD+ by poly(ADP-ribose) polymerase (PARP) and provide additional substrate during the repair of DNA.	NAD	43-47	poly (ADP-ribose) polymerase family, member 1	Mus musculus	51-78
8848280-6	1996	This may prevent the critical depletion of NAD+ by poly(ADP-ribose) polymerase (PARP) and provide additional substrate during the repair of DNA.	NAD	43-47	poly (ADP-ribose) polymerase family, member 1	Mus musculus	80-84
8881035-2	1996	The deduced amino acid sequence of Bp3 cDNA shares significant similarity to human and mouse CD38 and molluscan ADP-ribosyl cyclase, enzymes that generate the calcium mobilizing agent cyclic ADP-ribose from NAD.	NAD	207-210	CD38 antigen	Mus musculus	93-97
8628729-1	1996	ADP-ribosyl cyclase synthesizes the secondary messenger cyclic ADP-ribose from NAD+.	NAD	79-83	ADP-ribosyl cyclase/cyclic ADP-ribose hydrolase	Aplysia californica	0-19
7492598-6	1995	Changes in intrinsic protein fluorescence and in the 410 nm fluorescence of the NAD derivatives introduced at the active sites of both the glycated and non-glycated GAPDH from rabbit were compared on inactivation during denaturation in GuHCl.	NAD	80-83	glyceraldehyde-3-phosphate dehydrogenase	Oryctolagus cuniculus	165-170
7498471-1	1995	Incorporation of L-[35S]cysteine into rabbit muscle glyceraldehyde-3-phosphate dehydrogenase was detected following incubation of the enzyme in a mixture containing glyceraldehyde-3-phosphate, NAD+ and the labeled cysteine.	NAD	193-197	glyceraldehyde-3-phosphate dehydrogenase	Oryctolagus cuniculus	52-92
7547230-6	1995	Temozolomide treatment caused a decrease in cellular NAD levels, and this was abolished by the PADPRP inhibitors.	NAD	53-56	poly (ADP-ribose) polymerase family, member 1	Mus musculus	95-101
8777059-7	1995	Generation of either NADH or NADPH in solution by malate dehydrogenase or isocitrate dehydrogenase, respectively, was monitored by the MTS reduction reaction.	NAD	21-25	malic enzyme 1	Homo sapiens	50-70
7590113-7	1995	The Thal-induced exacerbation of AAP hepatotoxicity was completely inhibited by nicotinic acid amide, a selective inhibitor of poly(ADP-ribose) polymerase (PARP) (P &lt; 0.0001), suggesting a possible influence of Thal on the hepatic metabolism of NAD-adenoribosylation.	NAD	248-251	poly (ADP-ribose) polymerase family, member 1	Mus musculus	127-154
7590113-7	1995	The Thal-induced exacerbation of AAP hepatotoxicity was completely inhibited by nicotinic acid amide, a selective inhibitor of poly(ADP-ribose) polymerase (PARP) (P &lt; 0.0001), suggesting a possible influence of Thal on the hepatic metabolism of NAD-adenoribosylation.	NAD	248-251	poly (ADP-ribose) polymerase family, member 1	Mus musculus	156-160
7619054-4	1995	The enzymes alcohol dehydrogenase and diaphorase are used to cycle beta-NAD+ in the presence of ethanol and p-Iodonitrotetrazolium Violet.	NAD	67-76	aldo-keto reductase family 1 member A1	Homo sapiens	12-33
7556871-3	1995	Radiometric conversion assay using adrenal cortical tissues revealed extremely high levels of 11 beta-HSD activity which was characteristic of 11 beta-HSD2 in that it was NAD-dependent and displayed a Km for cortisol of 41 +/- 4 nM.	NAD	171-174	11-beta-hydroxysteroid dehydrogenase 1	Ovis aries	94-101
7755589-1	1995	A 0.6 kb cDNA fragment encoding the human NAD(+)-specific isocitrate dehydrogenase alpha-subunit (H-IDH alpha) was amplified by PCR using oligonucleotide primers synthesized on the basis of pig tryptic peptide sequences [Huang and Colman (1990) Biochemistry 29, 8266-8273].	NAD	42-48	isocitrate dehydrogenase (NAD(+)) 3 catalytic subunit alpha	Homo sapiens	98-109
7755589-5	1995	It is 55, 43 and 44% identical with yeast NAD(+)-specific IDH2, yeast NAD(+)-specific IDH1 and monkey NAD(+)-specific IDH gamma-subunit (IDH gamma) respectively.	NAD	42-48	isocitrate dehydrogenase (NAD(+)) IDH2	Saccharomyces cerevisiae S288C	58-62
24304867-5	2014	We found that NAD(+) can decrease both early-stage and late-stage apoptosis, as well as necrosis of rotenone-treated PC12 cells, as assessed by FACS-based Annexin V/AAD assay.	NAD	14-20	annexin A5	Rattus norvegicus	155-164
7755589-8	1995	Structural analysis of the deduced H-IDH alpha protein revealed that the amino acids responsible for the binding of isocitrate, Mg2+ and NAD+ are highly conserved.	NAD	137-141	isocitrate dehydrogenase (NAD(+)) 3 catalytic subunit alpha	Homo sapiens	35-46
7766894-6	1995	The RGA1 polypeptide expressed in Escherichia coli was, however, ADP-ribosylated by 10 microM [adenylate-32P] NAD and activated cholera toxin.	NAD	110-113	GRAS family transcription factor family protein	Arabidopsis thaliana	4-8
23873758-2	2014	COL2A1 gene expression is positively regulated by the NAD-dependent protein deacetylase Sirtuin 1 (SirT1), through its ability to bind chromatin regions of the COL2A1 promoter and enhancer.	NAD	54-57	sirtuin 1	Homo sapiens	88-97
7588400-3	1995	By contrast, 11 beta-HSD2 (the renal isoform) was unidirectional and NAD-dependent.	NAD	69-72	11-beta-hydroxysteroid dehydrogenase 1	Ovis aries	13-20
23873758-2	2014	COL2A1 gene expression is positively regulated by the NAD-dependent protein deacetylase Sirtuin 1 (SirT1), through its ability to bind chromatin regions of the COL2A1 promoter and enhancer.	NAD	54-57	sirtuin 1	Homo sapiens	99-104
23772790-2	2014	While many photosynthetic, photorespiratory and some respiratory enzymes, such as the rotenone-insensitive NADH and NADPH dehydrogenases and the alternative oxidase, are stimulated by light, succinate dehydrogenase, subunits of the pyruvate dehydrogenase complex, cytochrome oxidase and fumarase are inhibited via the phytochrome mechanism.	NAD	107-111	fumarate hydratase	Homo sapiens	287-295
7802659-3	1994	Purification of the enzymes indicated that the oxygen-dependent enzyme was a flavoenzyme, retinal oxidase (EC 1.2.3.11), composed of two 135 kDa subunits; and the NAD(+)-dependent enzyme was a basic pI retinal dehydrogenase composed of four 55-kDa subunits.	NAD	163-169	aldehyde oxidase 1	Oryctolagus cuniculus	90-105
24343700-1	2014	Silent information regulator type-1 (SIRT1) is the best-studied member of the Sirtuin (Sir2) family of nicotinamide dinucleotide (NAD)-dependent class III histone deacetylases (HDACs), but has not yet been explored in cutaneous T-cell lymphoma (CTCL).	NAD	103-128	sirtuin 1	Homo sapiens	0-35
24343700-1	2014	Silent information regulator type-1 (SIRT1) is the best-studied member of the Sirtuin (Sir2) family of nicotinamide dinucleotide (NAD)-dependent class III histone deacetylases (HDACs), but has not yet been explored in cutaneous T-cell lymphoma (CTCL).	NAD	103-128	sirtuin 1	Homo sapiens	37-42
24343700-1	2014	Silent information regulator type-1 (SIRT1) is the best-studied member of the Sirtuin (Sir2) family of nicotinamide dinucleotide (NAD)-dependent class III histone deacetylases (HDACs), but has not yet been explored in cutaneous T-cell lymphoma (CTCL).	NAD	130-133	sirtuin 1	Homo sapiens	0-35
24343700-1	2014	Silent information regulator type-1 (SIRT1) is the best-studied member of the Sirtuin (Sir2) family of nicotinamide dinucleotide (NAD)-dependent class III histone deacetylases (HDACs), but has not yet been explored in cutaneous T-cell lymphoma (CTCL).	NAD	130-133	sirtuin 1	Homo sapiens	37-42
7858221-5	1994	The level of MDH, ICL and MS mRNAs then declines, but then MDH mRNA increases again together with that of peroxisomal NAD(+)-dependent hydroxypyruvate reductase (HPR).	NAD	118-124	glycerate dehydrogenase	Cucumis sativus	135-160
23946338-3	2014	In this work, we studied whether nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme for nicotinamide adenine dinucleotide biosynthesis, plays a role in CR-induced beneficial metabolic effects using a specific inhibitor of NAMPT (FK866).	NAD	110-143	nicotinamide phosphoribosyltransferase	Rattus norvegicus	33-71
23946338-3	2014	In this work, we studied whether nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme for nicotinamide adenine dinucleotide biosynthesis, plays a role in CR-induced beneficial metabolic effects using a specific inhibitor of NAMPT (FK866).	NAD	110-143	nicotinamide phosphoribosyltransferase	Rattus norvegicus	73-78
24360018-2	2013	Both SIRT1 and PARP1 share a common co-factor nicotinamide adenine dinucleotide (NAD+) and several common substrates, including regulators of DNA damage response and circadian rhythms.	NAD	46-79	sirtuin 1	Homo sapiens	5-10
7858221-5	1994	The level of MDH, ICL and MS mRNAs then declines, but then MDH mRNA increases again together with that of peroxisomal NAD(+)-dependent hydroxypyruvate reductase (HPR).	NAD	118-124	glycerate dehydrogenase	Cucumis sativus	162-165
7961476-2	1994	DAR1 encodes an NADH-dependent dihydroxyacetone phosphate reductase (sn-glycerol-3-phosphate dehydrogenase [G3PDase; EC 1.1.1.8]) homologous to several other eukaryotic G3PDases.	NAD	16-20	glycerol-3-phosphate dehydrogenase (NAD(+)) GPD1	Saccharomyces cerevisiae S288C	0-4
24360018-2	2013	Both SIRT1 and PARP1 share a common co-factor nicotinamide adenine dinucleotide (NAD+) and several common substrates, including regulators of DNA damage response and circadian rhythms.	NAD	81-85	sirtuin 1	Homo sapiens	5-10
7961476-5	1994	Disruption of DAR1 in a haploid S. cerevisiae was not lethal but led to a decrease in cytoplasmic NADH-dependent G3PDase activity, an increase in osmotic sensitivity, and a 25% reduction in glycerol secretion from cells grown anaerobically on glucose.	NAD	98-102	glycerol-3-phosphate dehydrogenase (NAD(+)) GPD1	Saccharomyces cerevisiae S288C	14-18
7918597-0	1994	Superoxide generation by lipoxygenase in the presence of NADH and NADPH.	NAD	57-61	linoleate 9S-lipoxygenase-4	Glycine max	25-37
24323420-1	2013	Silent information regulator 1 (SIRT1) is a NAD+-dependent histone deacetylase that represses gene expression and plays a role in longevity.	NAD	44-47	sirtuin 1	Homo sapiens	0-30
24323420-1	2013	Silent information regulator 1 (SIRT1) is a NAD+-dependent histone deacetylase that represses gene expression and plays a role in longevity.	NAD	44-47	sirtuin 1	Homo sapiens	32-37
23860243-5	2013	One of these proteins was found to be the NADH-dependent hydroxypyruvate reductase (HPR).	NAD	42-46	hydroxypyruvate reductase	Arabidopsis thaliana	57-82
7918597-2	1994	At optimum pH of 8.3, lipoxygenase oxidized both NADH and NADPH in the presence of 700 microM linoleic acid.	NAD	49-53	linoleate 9S-lipoxygenase-4	Glycine max	22-34
23860243-5	2013	One of these proteins was found to be the NADH-dependent hydroxypyruvate reductase (HPR).	NAD	42-46	hydroxypyruvate reductase	Arabidopsis thaliana	84-87
23860243-11	2013	GENERAL SIGNIFICANCE: This is the first report demonstrating the peroxisomal NADH-dependent HPR activity involved in the photorespiration pathway is regulated by tyrosine nitration, indicating that peroxisomal NO metabolism may contribute to the regulation of physiological processes under no-stress conditions.	NAD	77-81	hydroxypyruvate reductase	Arabidopsis thaliana	92-95
8093047-5	1994	The cell surface antigen has an amino acid sequence homologous to Aplysia ADP-ribosyl cyclase that catalyzes the conversion of NAD to cyclic ADP-ribose with a calcium-mobilizing activity.	NAD	127-130	CD53 molecule	Homo sapiens	4-24
23994167-4	2013	3HBD is a member (AKR1C29) of the aldo-keto reductase (AKR) superfamily, and exhibited high preference for NADP(H) over NAD(H) at a physiological pH of 7.4.	NAD	120-126	prostaglandin-E(2) 9-reductase-like	Oryctolagus cuniculus	0-4
8027853-4	1994	By mixing both purified cytochrome b5-like hemoprotein (outer membrane-cytochrome b) and cytochrome b5 reductase, cob(II)alamin was formed from aquacobalamin and NADH.	NAD	162-166	cytochrome b, mitochondrial	Rattus norvegicus	24-36
23922380-9	2013	Finally, RelB also couples with bioenergy NAD(+) sensor SIRT1 to integrate acute inflammation with changes in metabolism and mitochondrial bioenergetics.	NAD	42-48	sirtuin 1	Homo sapiens	56-61
8027853-5	1994	These results provide evidence that the outer membrane-cytochrome b/cytochrome b5 reductase complex has the activity of the NADH-linked aquacobalamin reductase in rat liver mitochondria.	NAD	124-128	cytochrome b, mitochondrial	Rattus norvegicus	55-67
8196651-2	1994	We have cloned a gene encoding the key enzyme of glycerol synthesis, the NADH-dependent cytosolic glycerol-3-phosphate dehydrogenase, and we named it GPD1.	NAD	73-77	glycerol-3-phosphate dehydrogenase (NAD(+)) GPD1	Saccharomyces cerevisiae S288C	150-154
24331693-5	2013	Effects on SIRT1 protein activity were tested by measuring the levels of reactive oxygen species (ROS) and the nicotinamide adenine dinucleotide (NAD+)/beta-nicotinamide adenine dinucleotide, reduced (NADH) by flow cytometry and chromatometry, and the levels of triacylglycerol (TG), total cholesterol (TC), and fatty acid beta oxidation rate by enzymatic analysis and liquid scintillation counting.	NAD	111-144	sirtuin 1	Homo sapiens	11-16
24331693-5	2013	Effects on SIRT1 protein activity were tested by measuring the levels of reactive oxygen species (ROS) and the nicotinamide adenine dinucleotide (NAD+)/beta-nicotinamide adenine dinucleotide, reduced (NADH) by flow cytometry and chromatometry, and the levels of triacylglycerol (TG), total cholesterol (TC), and fatty acid beta oxidation rate by enzymatic analysis and liquid scintillation counting.	NAD	146-150	sirtuin 1	Homo sapiens	11-16
24331693-5	2013	Effects on SIRT1 protein activity were tested by measuring the levels of reactive oxygen species (ROS) and the nicotinamide adenine dinucleotide (NAD+)/beta-nicotinamide adenine dinucleotide, reduced (NADH) by flow cytometry and chromatometry, and the levels of triacylglycerol (TG), total cholesterol (TC), and fatty acid beta oxidation rate by enzymatic analysis and liquid scintillation counting.	NAD	152-190	sirtuin 1	Homo sapiens	11-16
24331693-5	2013	Effects on SIRT1 protein activity were tested by measuring the levels of reactive oxygen species (ROS) and the nicotinamide adenine dinucleotide (NAD+)/beta-nicotinamide adenine dinucleotide, reduced (NADH) by flow cytometry and chromatometry, and the levels of triacylglycerol (TG), total cholesterol (TC), and fatty acid beta oxidation rate by enzymatic analysis and liquid scintillation counting.	NAD	201-205	sirtuin 1	Homo sapiens	11-16
8175767-1	1994	A gene has been constructed coding for a chimeric flavocytochrome b5 protein that comprises the soluble domain of rat hepatic cytochrome b5 as the NH2-terminal portion of the chimera and the flavin-containing domain of spinach assimilatory NADH:nitrate reductase as the C terminus.	NAD	240-244	cytochrome b5 type A	Rattus norvegicus	55-68
23994215-4	2013	The results showed that PARP-1 over-activation caused by Mg2+-free stimuli led to cellular NAD depletion which could block AIF translocation from mitochondria to nucleus and attenuate neuronal death.	NAD	91-94	apoptosis inducing factor mitochondria associated 1	Homo sapiens	123-126
23994215-5	2013	Also, SIRT1 deacetylase activity was reduced by Mg2+-free treatment, accompanied by elevated ratio of neuronal death, which could be rescued by NAD repletion.	NAD	144-147	sirtuin 1	Homo sapiens	6-11
25309947-9	2013	Nuclear translocation of NAD-dependent histone deacetylase SIRT1 and global chromatin silencing lead to hESC cardiac fate determination, while silencing of pluripotence-associated hsa-miR-302 family and drastic up-regulation of neuroectodermal Hox miRNA hsa-miR-10 family lead to hESC neural fate determination.	NAD	25-28	sirtuin 1	Homo sapiens	59-64
23915912-1	2013	Seven Sirtuin family members (SIRT1-7), comprising a family of NAD+-dependent protein deacetylases and ADP-ribosyltransferases, are key proteins that regulate multiple physiological processes.	NAD	63-66	sirtuin 1	Homo sapiens	30-35
9419765-2	1994	METHODS: Purified human placental 3 beta-HSD/isomerase was affinity-radioalkylated by 2 alpha-bromo [2"-14C]acetoxyprogesterone (2 alpha-[14C]BAP) in the presence or absence of the reduced diphosphopyridine nucleotide, NADH.	NAD	189-217	hydroxy-delta-5-steroid dehydrogenase, 3 beta- and steroid delta-isomerase 1	Homo sapiens	34-44
23747282-2	2013	The first assay is based on the reduction of Delta(1)-pyrroline-5-carboxylate (P5C), generated from ornithine by OAT, using human pyrroline 5-carboxylate reductase 1 (PYCR1), which results in the concomitant oxidation of NADH (nicotinamide adenine dinucleotide, reduced form) to NAD+ (nicotinamide adenine dinucleotide, oxidized form).	NAD	221-225	pyrroline-5-carboxylate reductase 1	Homo sapiens	45-77
23747282-2	2013	The first assay is based on the reduction of Delta(1)-pyrroline-5-carboxylate (P5C), generated from ornithine by OAT, using human pyrroline 5-carboxylate reductase 1 (PYCR1), which results in the concomitant oxidation of NADH (nicotinamide adenine dinucleotide, reduced form) to NAD+ (nicotinamide adenine dinucleotide, oxidized form).	NAD	221-225	pyrroline-5-carboxylate reductase 1	Homo sapiens	79-82
23747282-2	2013	The first assay is based on the reduction of Delta(1)-pyrroline-5-carboxylate (P5C), generated from ornithine by OAT, using human pyrroline 5-carboxylate reductase 1 (PYCR1), which results in the concomitant oxidation of NADH (nicotinamide adenine dinucleotide, reduced form) to NAD+ (nicotinamide adenine dinucleotide, oxidized form).	NAD	221-225	pyrroline-5-carboxylate reductase 1	Homo sapiens	130-165
23747282-2	2013	The first assay is based on the reduction of Delta(1)-pyrroline-5-carboxylate (P5C), generated from ornithine by OAT, using human pyrroline 5-carboxylate reductase 1 (PYCR1), which results in the concomitant oxidation of NADH (nicotinamide adenine dinucleotide, reduced form) to NAD+ (nicotinamide adenine dinucleotide, oxidized form).	NAD	221-225	pyrroline-5-carboxylate reductase 1	Homo sapiens	167-172
9419765-2	1994	METHODS: Purified human placental 3 beta-HSD/isomerase was affinity-radioalkylated by 2 alpha-bromo [2"-14C]acetoxyprogesterone (2 alpha-[14C]BAP) in the presence or absence of the reduced diphosphopyridine nucleotide, NADH.	NAD	219-223	hydroxy-delta-5-steroid dehydrogenase, 3 beta- and steroid delta-isomerase 1	Homo sapiens	34-44
23747282-2	2013	The first assay is based on the reduction of Delta(1)-pyrroline-5-carboxylate (P5C), generated from ornithine by OAT, using human pyrroline 5-carboxylate reductase 1 (PYCR1), which results in the concomitant oxidation of NADH (nicotinamide adenine dinucleotide, reduced form) to NAD+ (nicotinamide adenine dinucleotide, oxidized form).	NAD	227-260	pyrroline-5-carboxylate reductase 1	Homo sapiens	45-77
23747282-2	2013	The first assay is based on the reduction of Delta(1)-pyrroline-5-carboxylate (P5C), generated from ornithine by OAT, using human pyrroline 5-carboxylate reductase 1 (PYCR1), which results in the concomitant oxidation of NADH (nicotinamide adenine dinucleotide, reduced form) to NAD+ (nicotinamide adenine dinucleotide, oxidized form).	NAD	227-260	pyrroline-5-carboxylate reductase 1	Homo sapiens	79-82
9419765-3	1994	NADH protected both 3 beta-HSD and isomerase from inactivation by 2 alpha-[14C]BAP.	NAD	0-4	hydroxy-delta-5-steroid dehydrogenase, 3 beta- and steroid delta-isomerase 1	Homo sapiens	20-30
8079379-3	1994	We constructed a multiple sequence alignment of these proteins, which, when combined with the recently determined tertiary structure of Streptomyces hydrogenans 3 alpha, 20 beta-hydroxysteroid dehydrogenase and a homologous enzyme, rat dihydropteridine reductase, identifies segments and residues that are likely to be structurally important in the functioning of these enzymes especially regarding specificity for NADPH and NADH.	NAD	425-429	quinoid dihydropteridine reductase	Rattus norvegicus	236-262
23726949-3	2013	SIRT1, a conserved nicotinamide adenine dinucleotide (NAD(+))-dependent deacetylase, has been implicated in modulating transcriptional silencing and cell survival and plays a key role in carcinogenesis through the deacetylation of important regulatory proteins.	NAD	19-52	sirtuin 1	Homo sapiens	0-5
23726949-3	2013	SIRT1, a conserved nicotinamide adenine dinucleotide (NAD(+))-dependent deacetylase, has been implicated in modulating transcriptional silencing and cell survival and plays a key role in carcinogenesis through the deacetylation of important regulatory proteins.	NAD	54-61	sirtuin 1	Homo sapiens	0-5
8206124-1	1994	Nitric oxide (NO) is known to inhibit glyceraldehyde-3-phosphate dehydrogenase enzyme activity caused by an NAD(+)-dependent posttranslational protein modification mechanism.	NAD	108-114	glyceraldehyde-3-phosphate dehydrogenase	Mus musculus	38-78
23797802-10	2013	LDH inhibition led to decreased NAD cellular levels, which resulted in sirtuin-1 inhibition.	NAD	32-35	sirtuin 1	Homo sapiens	71-80
24003918-2	2013	SIRT1, the mammalian nicotinamide adenine dinucleotide (NAD)-dependent protein deacetylase, and nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting NAD biosynthetic enzyme, together comprise a novel systemic regulatory network, named the "NAD World", that orchestrates physiological responses to internal and external perturbations and maintains the robustness of the physiological system in mammals.	NAD	162-165	sirtuin 1	Homo sapiens	0-5
24003918-2	2013	SIRT1, the mammalian nicotinamide adenine dinucleotide (NAD)-dependent protein deacetylase, and nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting NAD biosynthetic enzyme, together comprise a novel systemic regulatory network, named the "NAD World", that orchestrates physiological responses to internal and external perturbations and maintains the robustness of the physiological system in mammals.	NAD	162-165	sirtuin 1	Homo sapiens	0-5
8206124-5	1994	Employing the differential NAD(+)-dependent labelling method, glyceraldehyde-3-phosphate dehydrogenase in heart and spleen cytosol of the endotoxin-treated group, versus the control group, had been endogenously modified.	NAD	27-33	glyceraldehyde-3-phosphate dehydrogenase	Mus musculus	62-102
8206124-8	1994	Since an endogenously NAD(+)-modified glyceraldehyde-3-phosphate dehydrogenase occurred in endotoxin-treated mice, at least in some organs, this NO-stimulated posttranslational protein modification mechanism seems to function under in vivo conditions.	NAD	22-28	glyceraldehyde-3-phosphate dehydrogenase	Mus musculus	38-78
8032149-4	1994	Although H. pylori ADH was capable of utilizing both NADP and NAD as cofactors in alcohol oxidation, it showed a strong preference for NADP over NAD.	NAD	53-56	aldo-keto reductase family 1 member A1	Homo sapiens	19-22
8032149-4	1994	Although H. pylori ADH was capable of utilizing both NADP and NAD as cofactors in alcohol oxidation, it showed a strong preference for NADP over NAD.	NAD	62-65	aldo-keto reductase family 1 member A1	Homo sapiens	19-22
7934860-4	1993	The osg1-1 mutant, described in this work, is unable to grow at low water potential and shows a decreased capacity for glycerol production and a strongly reduced activity of NAD(+)-dependent sn-glycerol 3-phosphate dehydrogenase (GPD), an enzyme in the glycerol-producing pathway.	NAD	174-180	glycerol-3-phosphate dehydrogenase (NAD(+)) GPD1	Saccharomyces cerevisiae S288C	4-10
8251495-7	1993	Finally, results from equilibrium binding experiments are consistent with cytoplasmic malate dehydrogenase binding NADH in a negatively cooperative manner.	NAD	115-119	malic enzyme 1	Homo sapiens	86-106
8099357-2	1993	The two mitochondrial isozymes, IDH and IDP1, are NAD- and NADP-specific, respectively.	NAD	50-53	isocitrate dehydrogenase (NADP(+)) IDP1	Saccharomyces cerevisiae S288C	40-44
7763682-4	1993	The conjugation reaction of G6PDH and the electrochemical oxidation of NADH were confirmed by cyclic voltammetry and the constant potential electrochemical reaction.	NAD	71-75	glucose-6-phosphate dehydrogenase	Homo sapiens	28-33
8103766-1	1993	Partially purified glutamine synthetase from rat liver underwent rapid inactivation upon incubation with NADH and benzyl viologen, under aerobic conditions.	NAD	105-109	glutamate-ammonia ligase	Rattus norvegicus	19-39
8103766-3	1993	Similar inactivation was observed when the rat liver glutamine synthetase was preincubated, under anaerobic conditions, with NADH and benzyl viologen, and hydrogen peroxide was added to the reaction mixture.	NAD	125-129	glutamate-ammonia ligase	Rattus norvegicus	53-73
8486361-1	1993	The biosynthesis of steroid hormones in the gonads and adrenal glands requires the activities of the enzyme 3 beta-hydroxysteroid dehydrogenase/isomerase (3 beta HSD) which catalyzes the NAD(+)-dependent dehydrogenation and subsequent delta 5--&gt;delta 4 isomerization of delta 5-3 beta-hydroxysteroids to delta 4-3-ketosteroids.	NAD	187-193	hydroxy-delta-5-steroid dehydrogenase, 3 beta- and steroid delta-isomerase 1	Homo sapiens	155-165
1639779-1	1992	Kinetic constants for the interaction of NADH and NADPH with native rat dihydropteridine reductase (DHPR) and an Escherichia coli expressed mutant (D-37-I) have been determined.	NAD	41-45	quinoid dihydropteridine reductase	Rattus norvegicus	72-98
1639779-1	1992	Kinetic constants for the interaction of NADH and NADPH with native rat dihydropteridine reductase (DHPR) and an Escherichia coli expressed mutant (D-37-I) have been determined.	NAD	41-45	quinoid dihydropteridine reductase	Rattus norvegicus	100-104
1639779-8	1992	Examination of the rat DHPR sequence shows a typical dinucleotide binding fold with Asp-37 located precisely in the position predicted for the acidic residue that participates in hydrogen bond formation with the 2"-hydroxyl moiety of all known NAD-dependent dehydrogenases.	NAD	244-247	quinoid dihydropteridine reductase	Rattus norvegicus	23-27
1368798-8	1992	The NAD oxidation system of the rotating graphite disk electrode with PMS adsorbed was combined with glucose-6-phosphate dehydrogenase reaction, which reduced NAD with the consumption of glucose-6-phosphate.	NAD	4-7	glucose-6-phosphate dehydrogenase	Homo sapiens	101-134
1368798-8	1992	The NAD oxidation system of the rotating graphite disk electrode with PMS adsorbed was combined with glucose-6-phosphate dehydrogenase reaction, which reduced NAD with the consumption of glucose-6-phosphate.	NAD	159-162	glucose-6-phosphate dehydrogenase	Homo sapiens	101-134
1552368-2	1992	Microsomal NADH-linked aquacobalamin reductase, which was solubilized with 10 g/L sodium deoxycholate, showed identical elution behavior to NADH-cytochrome c reductase (cytochrome b5/cytochrome b5 reductase complex) on DEAE-Toyopearl 650 column chromatography.	NAD	11-15	cytochrome b5 type A	Rattus norvegicus	169-182
1552368-2	1992	Microsomal NADH-linked aquacobalamin reductase, which was solubilized with 10 g/L sodium deoxycholate, showed identical elution behavior to NADH-cytochrome c reductase (cytochrome b5/cytochrome b5 reductase complex) on DEAE-Toyopearl 650 column chromatography.	NAD	11-15	cytochrome b5 type A	Rattus norvegicus	183-196
1344194-0	1992	[Nonenzymatic reduction of methemoglobin by free radical forms of NADH and riboflavin].	NAD	66-70	hemoglobin subunit gamma 2	Homo sapiens	27-40
1344194-1	1992	Nonenzymatic reduction of methemoglobin (met-Hb) is effectively catalyzed by NADH and riboflavin (RF).	NAD	77-81	hemoglobin subunit gamma 2	Homo sapiens	26-39
1730148-5	1992	Catalytic concentrations of FMN greatly facilitated the NADH-induced reductive release of ferritin-bound iron.	NAD	56-60	formin 1	Mus musculus	28-31
1939242-7	1991	The disruption strain expressed no detectable IDH2, as determined by Western blot analysis, and was found to lack NAD(+)-dependent isocitrate dehydrogenase activity, indicating that IDH2 is essential for a functional enzyme.	NAD	114-120	isocitrate dehydrogenase (NAD(+)) IDH2	Saccharomyces cerevisiae S288C	182-186
1898363-7	1991	The methylamine bound to the lipoamide of the H-protein prevented the reversible exchange of electrons between NADH and lipoamide.	NAD	111-115	myosin binding protein H	Homo sapiens	46-55
1898374-11	1991	An examination of other kinetic models, developed to describe the LDH/GPDH/NADH system better, revealed that the experimental results may be best explained by assuming that free NADH, and not E1.NADH, is the sole substrate for GPDH.	NAD	75-79	E1 small nucleolar RNA	Oryctolagus cuniculus	192-199
1907200-6	1991	Aldose reductase had activity for aldo-sugars such as D-xylose, D-glucose and D-galactose as substrates and utilized both NADPH and NADH as coenzymes.	NAD	132-136	aldo-keto reductase family 1 member B1	Canis lupus familiaris	0-16
1885704-2	1991	It was first converted into the pyruvate hydrazone in the presence of D-lactate dehydrogenase, an NADH-reoxidation system using diaphorase, D,L-6,8-thioctamide and hydrazine.	NAD	98-102	lactate dehydrogenase D	Homo sapiens	70-93
1668635-3	1991	The flux control coefficients of carnitine palmitoyltransferase II, ETF:CoQ oxidoreductase and beta-hydroxybutyrate dehydrogenase were determined from elasticity coefficients obtained by measuring the flux dependencies of acyl-CoA and acetyl-CoA+CoASH concentrations, the electron transfer flavoprotein redox state, the CoQ redox state and the NAD redox state.	NAD	344-347	carnitine palmitoyltransferase 2	Rattus norvegicus	33-66
24009611-6	2013	Finally, adenosine diphosphoribose (ADPR) a breakdown product of both NAD and cADPR activates a plasma membrane cation channel termed TRPM2 thereby facilitating calcium (and sodium) entry into T cells.	NAD	70-73	transient receptor potential cation channel subfamily M member 2	Homo sapiens	134-139
23597856-3	2013	De-acetylation at this site is performed by sirtuin 1(SIRT1) and possibly other sirtuins in an NAD(+) dependent manner, such that SIRT1 inhibition promotes NF-kappaB transcriptional activity.	NAD	95-101	sirtuin 1	Homo sapiens	44-53
23597856-3	2013	De-acetylation at this site is performed by sirtuin 1(SIRT1) and possibly other sirtuins in an NAD(+) dependent manner, such that SIRT1 inhibition promotes NF-kappaB transcriptional activity.	NAD	95-101	sirtuin 1	Homo sapiens	54-59
1668635-3	1991	The flux control coefficients of carnitine palmitoyltransferase II, ETF:CoQ oxidoreductase and beta-hydroxybutyrate dehydrogenase were determined from elasticity coefficients obtained by measuring the flux dependencies of acyl-CoA and acetyl-CoA+CoASH concentrations, the electron transfer flavoprotein redox state, the CoQ redox state and the NAD redox state.	NAD	344-347	electron transfer flavoprotein subunit alpha	Rattus norvegicus	68-71
2266114-2	1990	In the oxidation process, the highest enthalpy of activation, 9.7 kcal/mol, occurs for the turnover of the liver alcohol dehydrogenase-NAD(+)-ethanol ternary complex.	NAD	135-141	aldo-keto reductase family 1 member A1	Homo sapiens	113-134
23562377-4	2013	Knockdown of the NAD+ salvage pathway enzymes such as nicotinamide phosphoribosyl transferase (NAMPT) or nicotinamide mononucleotide adenyltransferase (NMNAT) did not augment death.	NAD	17-21	nicotinamide phosphoribosyltransferase	Rattus norvegicus	54-93
23562377-4	2013	Knockdown of the NAD+ salvage pathway enzymes such as nicotinamide phosphoribosyl transferase (NAMPT) or nicotinamide mononucleotide adenyltransferase (NMNAT) did not augment death.	NAD	17-21	nicotinamide phosphoribosyltransferase	Rattus norvegicus	95-100
23575529-3	2013	Here, we show that in the presence of extracellular NAD(+) , ART2.2 caused ADP-ribosylation of CD8-beta on murine CD8(+) T cells in vitro and in vivo.	NAD	52-58	CD8 antigen, beta chain 1	Mus musculus	95-103
23575529-4	2013	Treatment with NAD(+) prevented binding of anti-CD8-beta mAb YTS156.7.7 but not of mAb H35-17.2, indicating that NAD(+) caused modification of certain epitopes and not a general loss of CD8-beta.	NAD	15-21	CD8 antigen, beta chain 1	Mus musculus	48-56
23575529-4	2013	Treatment with NAD(+) prevented binding of anti-CD8-beta mAb YTS156.7.7 but not of mAb H35-17.2, indicating that NAD(+) caused modification of certain epitopes and not a general loss of CD8-beta.	NAD	15-21	CD8 antigen, beta chain 1	Mus musculus	186-194
23575529-4	2013	Treatment with NAD(+) prevented binding of anti-CD8-beta mAb YTS156.7.7 but not of mAb H35-17.2, indicating that NAD(+) caused modification of certain epitopes and not a general loss of CD8-beta.	NAD	113-119	CD8 antigen, beta chain 1	Mus musculus	48-56
23575529-9	2013	We propose that ADP-ribosylation of CD8-beta can regulate the coreceptor function of CD8 in the presence of elevated levels of extracellular NAD(+) .	NAD	141-147	CD8 antigen, beta chain 1	Mus musculus	36-44
2099148-3	1990	The partially purified mu-alcohol dehydrogenase, specifically using NAD+ as cofactor, catalyzed the oxidation of aliphatic and aromatic alcohols with long chain alcohols being better substrates, indicating a barrel-shape hydrophobic binding pocket for substrate.	NAD	68-72	aldo-keto reductase family 1 member A1	Homo sapiens	26-47
2099148-4	1990	mu-Alcohol dehydrogenase stood out in high Km values for both ethanol (18 mM) and NAD+ (340 microM) as well as in high Ki value (320 microM) for 4-methylpyrazole, a competitive inhibitor for ethanol.	NAD	82-86	aldo-keto reductase family 1 member A1	Homo sapiens	3-24
2076453-3	1990	When a substrate (ethanol) in the oil phase of toluene or chloroform slowly migrated into the aqueous phase containing alcohol dehydrogenase and NAD+, oscillations were observed in the concentration of NADH produced.	NAD	202-206	aldo-keto reductase family 1 member A1	Homo sapiens	119-140
23796896-3	2013	Here we report microRNA-138 (miR-138) as a novel suppressor of axon regeneration and show that SIRT1, the NAD-dependent histone deacetylase, is the functional target of miR-138.	NAD	106-109	sirtuin 1	Homo sapiens	95-100
2275805-1	1990	A cytosolic fraction prepared from a mouse fibroblast cell line reduced secondary products of lipid peroxidation, including alkenals, alkanals, alk-2-enals, and alka-2,4-dienals, using NADH or NADPH.	NAD	185-189	activin A receptor, type 1	Mus musculus	144-149
23611872-0	2013	In vivo NADH fluorescence imaging indicates effect of aquaporin-4 deletion on oxygen microdistribution in cortical spreading depression.	NAD	8-12	aquaporin 4	Mus musculus	54-65
23611872-1	2013	Using in vivo two-photon imaging, we show that mice deficient in aquaporin-4 (AQP4) display increased fluorescence of nicotinamide adenine dinucleotide (NADH) when subjected to cortical spreading depression.	NAD	118-151	aquaporin 4	Mus musculus	65-76
23611872-1	2013	Using in vivo two-photon imaging, we show that mice deficient in aquaporin-4 (AQP4) display increased fluorescence of nicotinamide adenine dinucleotide (NADH) when subjected to cortical spreading depression.	NAD	118-151	aquaporin 4	Mus musculus	78-82
23611872-1	2013	Using in vivo two-photon imaging, we show that mice deficient in aquaporin-4 (AQP4) display increased fluorescence of nicotinamide adenine dinucleotide (NADH) when subjected to cortical spreading depression.	NAD	153-157	aquaporin 4	Mus musculus	65-76
23611872-1	2013	Using in vivo two-photon imaging, we show that mice deficient in aquaporin-4 (AQP4) display increased fluorescence of nicotinamide adenine dinucleotide (NADH) when subjected to cortical spreading depression.	NAD	153-157	aquaporin 4	Mus musculus	78-82
2150901-1	1990	It is shown that nicotinamide-induced in vivo stimulation of NAD biosynthesis in the liver nuclei of rats causes a decrease of the DNA sensitivity to treatment with DNAse I under conditions of weak hydrolysis.	NAD	61-64	deoxyribonuclease 1	Rattus norvegicus	165-172
23479127-1	2013	Sirtuin 1 (SIRT1), a NAD(+)-dependent class III histone deacetylase, participates in regulating cellular apoptosis, senescence and metabolism by deacetylating histones and multiple transcription factors.	NAD	21-27	sirtuin 1	Homo sapiens	0-9
23479127-1	2013	Sirtuin 1 (SIRT1), a NAD(+)-dependent class III histone deacetylase, participates in regulating cellular apoptosis, senescence and metabolism by deacetylating histones and multiple transcription factors.	NAD	21-27	sirtuin 1	Homo sapiens	11-16
2332415-1	1990	Lactate dehydrogenase (LDH) [EC 1.1.1.27] in a crude extract (40-80% ammonium sulfate fraction) of bovine brain was adsorbed on an immobilized colchicine column and specifically eluted by addition of 1 mM NADH.	NAD	205-209	LDH	Bos taurus	0-21
23703906-4	2013	In addition, loss of Miner1 caused a depletion of ER Ca(2+) stores, a dramatic increase in mitochondrial Ca(2+) load, increased reactive oxygen and nitrogen species, an increase in the GSSG/GSH and NAD(+)/NADH ratios, and an increase in the ADP/ATP ratio consistent with enhanced ATP utilization.	NAD	198-204	CDGSH iron sulfur domain 2	Mus musculus	21-27
23703906-4	2013	In addition, loss of Miner1 caused a depletion of ER Ca(2+) stores, a dramatic increase in mitochondrial Ca(2+) load, increased reactive oxygen and nitrogen species, an increase in the GSSG/GSH and NAD(+)/NADH ratios, and an increase in the ADP/ATP ratio consistent with enhanced ATP utilization.	NAD	205-209	CDGSH iron sulfur domain 2	Mus musculus	21-27
23435312-3	2013	The coenzyme nicotinamide adenine dinucleotide (NAD(+)) is not only essential for cellular metabolism; it also affects activity of NAD-dependent enzymes, such as PARP-1 and SIRT-1.	NAD	13-46	sirtuin 1	Homo sapiens	173-179
23435312-3	2013	The coenzyme nicotinamide adenine dinucleotide (NAD(+)) is not only essential for cellular metabolism; it also affects activity of NAD-dependent enzymes, such as PARP-1 and SIRT-1.	NAD	48-55	sirtuin 1	Homo sapiens	173-179
23435312-3	2013	The coenzyme nicotinamide adenine dinucleotide (NAD(+)) is not only essential for cellular metabolism; it also affects activity of NAD-dependent enzymes, such as PARP-1 and SIRT-1.	NAD	48-51	sirtuin 1	Homo sapiens	173-179
2332415-1	1990	Lactate dehydrogenase (LDH) [EC 1.1.1.27] in a crude extract (40-80% ammonium sulfate fraction) of bovine brain was adsorbed on an immobilized colchicine column and specifically eluted by addition of 1 mM NADH.	NAD	205-209	LDH	Bos taurus	23-26
2332415-6	1990	Kinetic studies revealed that colchicine apparently competed with cofactor NAD for the active site of LDH and the Ki values of colchicine decreased with an increase of NaCl concentration.	NAD	75-78	LDH	Bos taurus	102-105
33802063-8	2021	These results suggest that NAD+-mediated SIRT1 activation facilitates mitochondrial fission through activation of Drp1 by suppressing its phosphorylation and accelerating its dephosphorylation.	NAD	27-31	sirtuin 1	Homo sapiens	41-46
26201784-7	2013	RESULTS: In replicon cells, the level of ROS increased and the value of nicotinamide adenine dinucleotide (NAD(+))/NADH decreased, then the activity and expression level of mRNA and protein of SIRT1 decreased.	NAD	72-105	sirtuin 1	Homo sapiens	193-198
26201784-11	2013	CONCLUSIONS: HCV replication decreasing the NAD(+)/NADH ratio may downregulate the activity and expression of SIRT1, then change the expression profile of glucose metabolism-related genes, thereby causing glucose metabolism disorders of hepatocytes and promoting HCV replication.	NAD	44-50	sirtuin 1	Homo sapiens	110-115
26201784-11	2013	CONCLUSIONS: HCV replication decreasing the NAD(+)/NADH ratio may downregulate the activity and expression of SIRT1, then change the expression profile of glucose metabolism-related genes, thereby causing glucose metabolism disorders of hepatocytes and promoting HCV replication.	NAD	51-55	sirtuin 1	Homo sapiens	110-115
21492230-1	2011	The purpose of the study was to determine in human malignant lymphomas the expression patterns of nicotinamide phosphoribosyltransferase (NAMPT) and nicotinic acid phosphoribosyltransferase (NAPRT), the primary, rate-limiting enzymes in the synthesis of NAD+.	NAD	254-258	nicotinate phosphoribosyltransferase	Homo sapiens	149-189
23228600-5	2013	We also review the recently published finding that cyt-b(5) allosterically augments the activity of 3beta-hydroxysteroid dehydrogenase/Delta(5)-Delta(4) isomerase (3betaHSD), a non cytochrome P450 enzyme, by increasing the enzymes affinity for its cofactor, NAD(+).	NAD	258-264	hydroxy-delta-5-steroid dehydrogenase, 3 beta- and steroid delta-isomerase 1	Homo sapiens	100-162
34915296-6	2022	The catalytic mechanism of the NADH oxidase mimics is that O2 involves in the oxidation of NADH, to generate O2.- intermediate and finally turn to H2O2, while SuOx mimics comes from that MoS2 particles can effectively catalyze sulfite to reduce (Fe(CN)6)3-.	NAD	91-95	sulfite oxidase	Homo sapiens	159-163
23228600-5	2013	We also review the recently published finding that cyt-b(5) allosterically augments the activity of 3beta-hydroxysteroid dehydrogenase/Delta(5)-Delta(4) isomerase (3betaHSD), a non cytochrome P450 enzyme, by increasing the enzymes affinity for its cofactor, NAD(+).	NAD	258-264	hydroxy-delta-5-steroid dehydrogenase, 3 beta- and steroid delta-isomerase 1	Homo sapiens	164-172
23445365-6	2013	The binding of DMQn (n = 0 or 2) to GB1-hCLK-1 mediates reduction of the diiron center by nicotinamide adenine dinucleotide (NADH) and initiates O2 activation for subsequent DMQ hydroxylation.	NAD	90-123	gamma-aminobutyric acid type B receptor subunit 1	Homo sapiens	36-39
23445365-6	2013	The binding of DMQn (n = 0 or 2) to GB1-hCLK-1 mediates reduction of the diiron center by nicotinamide adenine dinucleotide (NADH) and initiates O2 activation for subsequent DMQ hydroxylation.	NAD	125-129	gamma-aminobutyric acid type B receptor subunit 1	Homo sapiens	36-39
23445365-7	2013	Deployment of DMQ to mediate reduction of the diiron center in GB1-hCLK-1 improves substrate specificity and diminishes consumption of NADH that is uncoupled from substrate oxidation.	NAD	135-139	gamma-aminobutyric acid type B receptor subunit 1	Homo sapiens	63-66
34678494-1	2022	Mammalian sirtuins (SIRT1-7) are members of the nicotine adenine dinucleotide (NAD+)-dependent family of enzymes critical for histone deacetylation and posttranslational modification of proteins.	NAD	79-83	sirtuin 1	Homo sapiens	20-27
23190689-5	2013	Vascular nicotinamide adenine dinucleotide phosphate (NADPH) oxidase subunit NOX1 gene expression was significantly attenuated in all therapeutic groups, and significantly greater attenuation was observed in the valsartan+cilnidipine-treated group than in the valsartan-treated group.	NAD	9-42	NADPH oxidase 1	Rattus norvegicus	77-81
34894601-9	2022	Raman and AFM analysis revealed that KLF6 reduces NADH level and increases cell Young"s modulus.	NAD	50-54	Kruppel like factor 6	Homo sapiens	37-41
34946971-1	2021	The nicotinate phosphoribosyltransferase (NAPRT) gene has gained relevance in the research of cancer therapeutic strategies due to its main role as a NAD biosynthetic enzyme.	NAD	150-153	nicotinate phosphoribosyltransferase	Homo sapiens	4-40
34946971-1	2021	The nicotinate phosphoribosyltransferase (NAPRT) gene has gained relevance in the research of cancer therapeutic strategies due to its main role as a NAD biosynthetic enzyme.	NAD	150-153	nicotinate phosphoribosyltransferase	Homo sapiens	42-47
34637964-1	2021	Cluster of differentiation (CD) 38, a major enzyme for nicotinamide adenine dinucleotide (NAD+) degradation, plays a key role in inflammation.	NAD	90-94	CD38 antigen	Mus musculus	0-34
34637964-7	2021	However, CD38 inhibition by 78c elevated intracellular NAD+ levels and suppressed IL-1beta release in MSU crystals-treated THP-1 macrophages and BMDMs.	NAD	55-59	CD38 antigen	Mus musculus	9-13
34637964-9	2021	In conclusion, the present study revealed that MSU crystals could activate CD38 with the ensuing intracellular NAD+ decline to promote inflammatory responses in THP-1 macrophages and BMDMs, while CD38 inhibition could suppress MSU crystals-triggered inflammatory responses, indicating that CD38 is a potential therapeutic target for gout.	NAD	111-115	CD38 antigen	Mus musculus	75-79
34637964-9	2021	In conclusion, the present study revealed that MSU crystals could activate CD38 with the ensuing intracellular NAD+ decline to promote inflammatory responses in THP-1 macrophages and BMDMs, while CD38 inhibition could suppress MSU crystals-triggered inflammatory responses, indicating that CD38 is a potential therapeutic target for gout.	NAD	111-115	CD38 antigen	Mus musculus	290-294
34531546-4	2021	Furthermore, ROF significantly enhanced the lysosomal function, as evidenced by the increased levels of mature cathepsin D (CTSD) and lysosomal-associated membrane protein 1 (LAMP1) through increasing NAD+/NADH and the expression of sirtuin 1 (SIRT1).	NAD	201-205	cathepsin D	Mus musculus	124-128
34531546-4	2021	Furthermore, ROF significantly enhanced the lysosomal function, as evidenced by the increased levels of mature cathepsin D (CTSD) and lysosomal-associated membrane protein 1 (LAMP1) through increasing NAD+/NADH and the expression of sirtuin 1 (SIRT1).	NAD	201-205	lysosomal-associated membrane protein 1	Mus musculus	134-173
34531546-4	2021	Furthermore, ROF significantly enhanced the lysosomal function, as evidenced by the increased levels of mature cathepsin D (CTSD) and lysosomal-associated membrane protein 1 (LAMP1) through increasing NAD+/NADH and the expression of sirtuin 1 (SIRT1).	NAD	201-205	lysosomal-associated membrane protein 1	Mus musculus	175-180
34291342-1	2021	Delta1-Pyrroline-5-carboxylate (P5C) reductase (PYCR or P5CR) catalyzes the conversion of P5C to L-proline (Pro) with concomitant oxidation of a cofactor, NADPH or NADH.	NAD	164-168	pyrroline-5-carboxylate reductase 1	Homo sapiens	0-30
34291342-1	2021	Delta1-Pyrroline-5-carboxylate (P5C) reductase (PYCR or P5CR) catalyzes the conversion of P5C to L-proline (Pro) with concomitant oxidation of a cofactor, NADPH or NADH.	NAD	164-168	pyrroline-5-carboxylate reductase 1	Homo sapiens	32-35
34752167-0	2021	NAMPT-mediated NAD+ biosynthesis suppresses activation of hepatic stellate cells and protects against CCl4-induced liver fibrosis in mice.	NAD	15-19	chemokine (C-C motif) ligand 4	Mus musculus	102-106
34752167-8	2021	Adenovirus-mediated NAMPT overexpression or nicotinamide mononucleotide (NMN) administration was carried out to study the effects of elevation of NAD+ levels on protecting CCl4-induced liver fibrosis in mice.	NAD	146-150	chemokine (C-C motif) ligand 4	Mus musculus	172-176
34752167-14	2021	Conclusions: NAMPT-mediated NAD+ biosynthesis inhibits HSC activation and protects against CCl4-induced liver fibrosis.	NAD	28-32	chemokine (C-C motif) ligand 4	Mus musculus	91-95
34769515-2	2021	NAD(P)H quinone oxidoreductase 1 (NQO1) increases the cellular nicotinamide adenine dinucleotide (NAD+) levels by accelerating the oxidation of NADH to NAD+, thus playing important roles in cellular homeostasis, energy metabolism, and inflammatory responses.	NAD	63-96	NAD(P)H dehydrogenase, quinone 1	Mus musculus	0-32
34769515-2	2021	NAD(P)H quinone oxidoreductase 1 (NQO1) increases the cellular nicotinamide adenine dinucleotide (NAD+) levels by accelerating the oxidation of NADH to NAD+, thus playing important roles in cellular homeostasis, energy metabolism, and inflammatory responses.	NAD	98-102	NAD(P)H dehydrogenase, quinone 1	Mus musculus	0-32
34769515-2	2021	NAD(P)H quinone oxidoreductase 1 (NQO1) increases the cellular nicotinamide adenine dinucleotide (NAD+) levels by accelerating the oxidation of NADH to NAD+, thus playing important roles in cellular homeostasis, energy metabolism, and inflammatory responses.	NAD	144-148	NAD(P)H dehydrogenase, quinone 1	Mus musculus	0-32
34769515-2	2021	NAD(P)H quinone oxidoreductase 1 (NQO1) increases the cellular nicotinamide adenine dinucleotide (NAD+) levels by accelerating the oxidation of NADH to NAD+, thus playing important roles in cellular homeostasis, energy metabolism, and inflammatory responses.	NAD	152-156	NAD(P)H dehydrogenase, quinone 1	Mus musculus	0-32
34374810-6	2021	This was confirmed in vitro, as the interaction of FhHDM-1 with the NOD-derived beta-cell line, NIT-1, resulted in increased levels of phosphorylated Akt, increased NADH and NADPH and reduced activity of the NAD-dependent DNA nick sensor, poly(ADP-ribose) polymerase (PARP-1).	NAD	165-169	nitrilase 1	Mus musculus	96-101
34213071-2	2021	Glycine betaine synthesis is catalyzed by the enzyme betaine aldehyde dehydrogenase (BADH) using NAD+ as coenzyme.	NAD	97-101	aldehyde dehydrogenase 7 family member A1	Homo sapiens	53-83
34803499-0	2021	CD38 Deficiency Protects Mice from High Fat Diet-Induced Nonalcoholic Fatty Liver Disease through Activating NAD+/Sirtuins Signaling Pathways-Mediated Inhibition of Lipid Accumulation and Oxidative Stress in Hepatocytes.	NAD	109-113	CD38 antigen	Mus musculus	0-4
34690807-1	2021	Sirtuin 1 (SIRT1) is a histone deacetylase belonging to the family of Sirtuins, a class of nicotinamide adenine dinucleotide (NAD+)-dependent enzymes with multiple metabolic functions.	NAD	91-124	sirtuin 1	Homo sapiens	0-9
34690807-1	2021	Sirtuin 1 (SIRT1) is a histone deacetylase belonging to the family of Sirtuins, a class of nicotinamide adenine dinucleotide (NAD+)-dependent enzymes with multiple metabolic functions.	NAD	91-124	sirtuin 1	Homo sapiens	11-16
34690807-1	2021	Sirtuin 1 (SIRT1) is a histone deacetylase belonging to the family of Sirtuins, a class of nicotinamide adenine dinucleotide (NAD+)-dependent enzymes with multiple metabolic functions.	NAD	126-130	sirtuin 1	Homo sapiens	0-9
34690807-1	2021	Sirtuin 1 (SIRT1) is a histone deacetylase belonging to the family of Sirtuins, a class of nicotinamide adenine dinucleotide (NAD+)-dependent enzymes with multiple metabolic functions.	NAD	126-130	sirtuin 1	Homo sapiens	11-16
34663976-5	2021	In the nucleus, the altered PHGDH activity restricts NAD+ level and compartmentally repressed NAD+-dependent PARP1 activity for poly(ADP-ribosyl)ation of c-Jun, thereby leading to impaired c-Jun transcriptional activity linked to cell growth inhibition.	NAD	53-57	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	154-159
34089817-3	2021	Nicotinamide adenine dinucleotide (NAD+), a co-substrate for the sirtuin family and PARPs, has emerged as a potent therapeutic molecular target in various diseases.	NAD	0-33	poly (ADP-ribose) polymerase family, member 1	Mus musculus	84-89
34089817-3	2021	Nicotinamide adenine dinucleotide (NAD+), a co-substrate for the sirtuin family and PARPs, has emerged as a potent therapeutic molecular target in various diseases.	NAD	35-39	poly (ADP-ribose) polymerase family, member 1	Mus musculus	84-89
34089817-5	2021	Supplementation of a specific inhibitor (TES-1025) of alpha-amino-beta-carboxymuconate-epsilon-semialdehyde decarboxylase (ACMSD), a rate-limiting enzyme of NAD+de novo synthesis pathway, promoted SIRT1 activity, increased mtDNA contents and enhanced AMPK expression, thus significantly reduced hair cells loss and deformation.	NAD	157-161	amino carboxymuconate semialdehyde decarboxylase	Mus musculus	123-128
34537933-5	2022	Silent information regulator 1 (SIRT1) is a NAD+-dependent HDAC (histone deacetylase) and plays a major role in biological processes, such as inflammation, apoptosis, and oxidative stress responses.	NAD	44-47	sirtuin 1	Homo sapiens	0-30
34537933-5	2022	Silent information regulator 1 (SIRT1) is a NAD+-dependent HDAC (histone deacetylase) and plays a major role in biological processes, such as inflammation, apoptosis, and oxidative stress responses.	NAD	44-47	sirtuin 1	Homo sapiens	32-37
34537933-5	2022	Silent information regulator 1 (SIRT1) is a NAD+-dependent HDAC (histone deacetylase) and plays a major role in biological processes, such as inflammation, apoptosis, and oxidative stress responses.	NAD	44-47	histone deacetylase 9	Homo sapiens	59-63
34537933-5	2022	Silent information regulator 1 (SIRT1) is a NAD+-dependent HDAC (histone deacetylase) and plays a major role in biological processes, such as inflammation, apoptosis, and oxidative stress responses.	NAD	44-47	histone deacetylase 9	Homo sapiens	65-84
34604215-2	2021	SIRT7 is a NAD+-dependent protein deacetylase.	NAD	11-14	sirtuin 7	Homo sapiens	0-5
34571983-0	2021	CAR T-Cells Depend on the Coupling of NADH Oxidation with ATP Production.	NAD	38-42	nuclear receptor subfamily 1 group I member 3	Homo sapiens	0-3
23442768-2	2013	Activity of the rate-limiting enzyme for PGE2 catabolism (15-hydroxyprostaglandin dehydrogenase [15-PGDH]) is dependent on availability of NAD+.	NAD	139-143	carbonyl reductase 1	Homo sapiens	58-95
23442768-2	2013	Activity of the rate-limiting enzyme for PGE2 catabolism (15-hydroxyprostaglandin dehydrogenase [15-PGDH]) is dependent on availability of NAD+.	NAD	139-143	carbonyl reductase 1	Homo sapiens	97-104
23358244-6	2013	The NAD-dependent deacetylase sirtuin 2 (SIRT2) associated with and deacetylated K8.	NAD	4-7	keratin 8	Homo sapiens	81-83
34183378-9	2021	In addition, silybin enhanced the intracellular NAD+ concentration by decreasing PARP1 expression.	NAD	48-52	poly (ADP-ribose) polymerase family, member 1	Mus musculus	81-86
34183378-11	2021	These findings indicate that the NAD+/SIRT2 pathway plays an important role in CYP3A regulation during NAFLD.	NAD	33-37	cytochrome P450, family 3, subfamily a, polypeptide 11	Mus musculus	79-84
34403696-6	2021	Pre-incubation of TRF1 with its regulator protein Tankyrase 1 and the cofactor NAD+ significantly reduced TRF1-TIN2 mediated DNA-DNA bridging, whereas TIN2 protected the disassembly of TRF1-TIN2 mediated DNA-DNA bridging upon Tankyrase 1 addition.	NAD	79-83	TERF1 interacting nuclear factor 2	Homo sapiens	111-115
23075334-5	2013	SIRT1 deacetylates target proteins using the coenzyme NAD+ and is therefore linked to cellular energy metabolism and the redox state through multiple signalling and survival pathways.	NAD	54-58	sirtuin 1	Homo sapiens	0-5
34403696-6	2021	Pre-incubation of TRF1 with its regulator protein Tankyrase 1 and the cofactor NAD+ significantly reduced TRF1-TIN2 mediated DNA-DNA bridging, whereas TIN2 protected the disassembly of TRF1-TIN2 mediated DNA-DNA bridging upon Tankyrase 1 addition.	NAD	79-83	TERF1 interacting nuclear factor 2	Homo sapiens	190-194
34296720-4	2021	Moreover, a Ru(iii) centre and an anthraquinone anion centre may be generated upon irradiation, which can further oxidize NADH/NADPH and generate O2 -, successfully eliciting photoredox catalysis and photodynamic therapy (PDT).	NAD	122-126	2,4-dienoyl-CoA reductase 1	Homo sapiens	127-132
32480969-5	2013	The GPD1 gene was used to overexpress G3PDH, a cytosolic NAD+-dependent key enzyme of cellular glycerol biosynthesis essential for growth of cells under abiotic stresses.	NAD	57-61	glycerol-3-phosphate dehydrogenase (NAD(+)) GPD1	Saccharomyces cerevisiae S288C	4-8
34407842-2	2021	Previous studies suggest that the NAD-dependent deacetylase sirtuin 1 (SIRT1) has a dual role in hematologic malignancies, acting as a tumor suppressor or tumor promoter depending on the tumor type.	NAD	34-37	sirtuin 1	Homo sapiens	71-76
22902533-3	2013	Alcohol dehydrogenase (ADH) and NAD(+)/NADH were immobilized with a gelatin hydrogel on an electrode that was modified with an electropolymerized ruthenium complex containing 5-amino-1,10-phenanthroline (pAPRu) as a mediator for NADH oxidation.	NAD	229-233	aldo-keto reductase family 1 member A1	Homo sapiens	0-21
22902533-3	2013	Alcohol dehydrogenase (ADH) and NAD(+)/NADH were immobilized with a gelatin hydrogel on an electrode that was modified with an electropolymerized ruthenium complex containing 5-amino-1,10-phenanthroline (pAPRu) as a mediator for NADH oxidation.	NAD	229-233	aldo-keto reductase family 1 member A1	Homo sapiens	23-26
22902533-4	2013	The (ADH, NAD(+))/pAPRu-immobilized electrode exhibited the electrocatalytic oxidation of ethanol in [C4mim][Tf(2)N].	NAD	10-17	aldo-keto reductase family 1 member A1	Homo sapiens	5-8
34380043-0	2021	NAD+ supplement potentiates tumor-killing function by rescuing defective TUB-mediated NAMPT transcription in tumor-infiltrated T cells.	NAD	0-4	tubby bipartite transcription factor	Mus musculus	73-76
34380043-6	2021	Excitingly, both adoptive CAR-T and anti-PD1 immune checkpoint blockade mouse models demonstrate that NAD+ supplementation enhanced the tumor-killing efficacy of T cells.	NAD	102-106	CART prepropeptide	Mus musculus	26-31
34380043-7	2021	Collectively, this study reveals that an impaired TCR-TUB-NAMPT-NAD+ axis leads to T cell dysfunction in the tumor microenvironment, and an over-the-counter nutrient supplement of NAD+ could boost T-cell-based immunotherapy.	NAD	64-68	tubby bipartite transcription factor	Mus musculus	54-57
34380043-7	2021	Collectively, this study reveals that an impaired TCR-TUB-NAMPT-NAD+ axis leads to T cell dysfunction in the tumor microenvironment, and an over-the-counter nutrient supplement of NAD+ could boost T-cell-based immunotherapy.	NAD	180-184	tubby bipartite transcription factor	Mus musculus	54-57
34356669-5	2021	VAD was readily generated by a base-exchange reaction, replacing the nicotinamide moiety of NAD by vacor, catalyzed by Aplysia californica ADP ribosyl cyclase.	NAD	92-95	ADP-ribosyl cyclase/cyclic ADP-ribose hydrolase	Aplysia californica	139-158
22616762-1	2013	AIM: SRT2104 is a novel, first-in-class, highly selective small molecule activator of the NAD + dependent deacetylase SIRT1.	NAD	90-93	sirtuin 1	Homo sapiens	118-123
23248098-1	2013	SIRT1 (mammalian ortholog of the yeast silent information regulator 2) is a NAD-dependent histone deacetylase belonging to the multigene family of sirtuins.	NAD	76-79	sirtuin 1	Homo sapiens	0-5
34128977-5	2021	SIRT7, as a NAD+-dependent histone desuccinylase, could bind to cccDNA through interaction with HBV core protein where it catalysed histone H3K122 desuccinylation.	NAD	12-15	sirtuin 7	Homo sapiens	0-5
23432678-11	2013	Resveratrol is known to activate cascades involving Wnt and NAD-dependent deacetylase sirtuin-1 (Sirt1).	NAD	60-63	sirtuin 1	Homo sapiens	97-102
23383098-8	2013	In the actin-activated ATPase activity assay, the rate of NADH oxidation was higher in the wild-type myosin VIIA, indicating that the ATPase activity in the p.R668H mutant myosin VIIA was significantly destroyed.	NAD	58-62	myosin VIIA	Homo sapiens	101-112
34108855-5	2021	We found that, among the core clock proteins, PER2 is mainly affected in its subcellular localization by NAD+ amount, and a higher cytoplasmic PER2 localization was observed under low NAD+ condition.	NAD	105-109	period circadian regulator 2	Homo sapiens	46-50
23383098-8	2013	In the actin-activated ATPase activity assay, the rate of NADH oxidation was higher in the wild-type myosin VIIA, indicating that the ATPase activity in the p.R668H mutant myosin VIIA was significantly destroyed.	NAD	58-62	myosin VIIA	Homo sapiens	172-183
23053940-4	2012	The NAD(+)-dependent modifications catalyzed by PARP-1 and SIRT1 liberate NAM, and NAM acts as feedback inhibitor of PARP-1 and SIRT1 through interacting with the enzymes at the binding site for NAD(+).	NAD	195-201	sirtuin 1	Homo sapiens	128-133
23079621-4	2012	Here we report that SIRT1, an NAD-dependent, class III deacetylase, forms a complex with RFX5.	NAD	30-33	sirtuin 1	Homo sapiens	20-25
23079621-5	2012	Over-expression of SIRT1 or NAMPT, which synthesizes NAD+ to activate SIRT1, or treatment with the SIRT1 agonist resveratrol decreases RFX5 acetylation and disrupts repression of the COL1A2 promoter activity by RFX5.	NAD	53-57	sirtuin 1	Homo sapiens	19-24
23079621-5	2012	Over-expression of SIRT1 or NAMPT, which synthesizes NAD+ to activate SIRT1, or treatment with the SIRT1 agonist resveratrol decreases RFX5 acetylation and disrupts repression of the COL1A2 promoter activity by RFX5.	NAD	53-57	sirtuin 1	Homo sapiens	70-75
23079621-5	2012	Over-expression of SIRT1 or NAMPT, which synthesizes NAD+ to activate SIRT1, or treatment with the SIRT1 agonist resveratrol decreases RFX5 acetylation and disrupts repression of the COL1A2 promoter activity by RFX5.	NAD	53-57	sirtuin 1	Homo sapiens	70-75
23086143-2	2012	The yeast NDH-2 (Ndi1) oxidizes NADH on the matrix side and reduces ubiquinone to maintain mitochondrial NADH/NAD(+) homeostasis.	NAD	32-36	NADH-ubiquinone reductase (H(+)-translocating) NDE2	Saccharomyces cerevisiae S288C	10-15
23086143-2	2012	The yeast NDH-2 (Ndi1) oxidizes NADH on the matrix side and reduces ubiquinone to maintain mitochondrial NADH/NAD(+) homeostasis.	NAD	105-109	NADH-ubiquinone reductase (H(+)-translocating) NDE2	Saccharomyces cerevisiae S288C	10-15
23086143-2	2012	The yeast NDH-2 (Ndi1) oxidizes NADH on the matrix side and reduces ubiquinone to maintain mitochondrial NADH/NAD(+) homeostasis.	NAD	110-116	NADH-ubiquinone reductase (H(+)-translocating) NDE2	Saccharomyces cerevisiae S288C	10-15
22322739-2	2012	SIRT1, a nicotinamide adenine dinucleotide(+)-dependent histone/protein deacetylase, plays a crucial role in various physiological processes, such as aging, metabolism, neurogenesis and apoptosis, owing to its ability to deacetylate numerous substrates, such as histone and NF-kappaB, which is implicated as an exacerbation factor in ATL.	NAD	9-42	sirtuin 1	Homo sapiens	0-5
22402365-10	2012	Nutrition restriction induced an increase in the level of the miR-140-3p target, NAD+-dependent SIRT1.	NAD	81-85	sirtuin 1	Homo sapiens	96-101
22249251-7	2012	NQO1 protection of C/EBPalpha required binding of NADH with NQO1.	NAD	50-54	NAD(P)H dehydrogenase, quinone 1	Mus musculus	0-4
22249251-7	2012	NQO1 protection of C/EBPalpha required binding of NADH with NQO1.	NAD	50-54	NAD(P)H dehydrogenase, quinone 1	Mus musculus	60-64
34108855-5	2021	We found that, among the core clock proteins, PER2 is mainly affected in its subcellular localization by NAD+ amount, and a higher cytoplasmic PER2 localization was observed under low NAD+ condition.	NAD	184-188	period circadian regulator 2	Homo sapiens	46-50
34108855-5	2021	We found that, among the core clock proteins, PER2 is mainly affected in its subcellular localization by NAD+ amount, and a higher cytoplasmic PER2 localization was observed under low NAD+ condition.	NAD	184-188	period circadian regulator 2	Homo sapiens	143-147
34108855-7	2021	Thus, we anticipate that the altered PER2 subcellular localization by low NAD+ is one of the complex changes that occurs in the aged circadian clock.	NAD	74-78	period circadian regulator 2	Homo sapiens	37-41
22858621-9	2012	The NAD(+)-to-NADH.H(+) ratio was reduced (by 24-fold) after the sprints, with a greater reduction in hypoxia than in normoxia (P &lt; 0.05), concomitant with 53% lower sirtuin 1 (SIRT1) protein levels after the sprint in hypoxia (P &lt; 0.05).	NAD	4-10	sirtuin 1	Homo sapiens	169-178
22858621-9	2012	The NAD(+)-to-NADH.H(+) ratio was reduced (by 24-fold) after the sprints, with a greater reduction in hypoxia than in normoxia (P &lt; 0.05), concomitant with 53% lower sirtuin 1 (SIRT1) protein levels after the sprint in hypoxia (P &lt; 0.05).	NAD	4-10	sirtuin 1	Homo sapiens	180-185
34082111-8	2021	However, alcohol induced NQO1 nuclear translocation was triggered by decreased cellular NAD+/NADH ratio rather than AhR activation.	NAD	88-92	NAD(P)H dehydrogenase, quinone 1	Mus musculus	25-29
34082111-8	2021	However, alcohol induced NQO1 nuclear translocation was triggered by decreased cellular NAD+/NADH ratio rather than AhR activation.	NAD	93-97	NAD(P)H dehydrogenase, quinone 1	Mus musculus	25-29
34082111-9	2021	Furthermore, both in vitro and in vivo overexpression NQO1 prevented alcohol-induced hepatic NAD+ depletion, thereby enhancing activities of NAD+-dependent enzymes and reversing alcohol-induced liver injury.	NAD	93-97	NAD(P)H dehydrogenase, quinone 1	Mus musculus	54-58
22773876-4	2012	EPO increases the Sirt1 level, a NAD(+)-dependent deacetylase, and also induces the NAD(+)/NADH ratio that further increases Sirt1 activity.	NAD	33-39	sirtuin 1	Homo sapiens	18-23
34082111-9	2021	Furthermore, both in vitro and in vivo overexpression NQO1 prevented alcohol-induced hepatic NAD+ depletion, thereby enhancing activities of NAD+-dependent enzymes and reversing alcohol-induced liver injury.	NAD	141-145	NAD(P)H dehydrogenase, quinone 1	Mus musculus	54-58
22773876-4	2012	EPO increases the Sirt1 level, a NAD(+)-dependent deacetylase, and also induces the NAD(+)/NADH ratio that further increases Sirt1 activity.	NAD	91-95	sirtuin 1	Homo sapiens	125-130
34082111-11	2021	CONCLUSION: This study demonstrated that AhR activation is a protective response to counteract alcohol-induced hepatic NAD+ depletion through induction of NQO1 and targeting hepatic AhR-NQO1 pathway may serve as a novel therapeutic approach for ALD.	NAD	119-123	NAD(P)H dehydrogenase, quinone 1	Mus musculus	155-159
22733276-7	2012	Together with two-photon imaging of NAD(P)H and confocal imaging of lipoamide dehydrogenase (LipDH) autofluorescence, we show that the ETC predominantly draws electrons from LipDH/NADH-dependent Complex I rather than from ETF/FADH(2)-dependent ETF:CoQ oxidoreductase (ETF-QO).	NAD	180-184	electron transfer flavoprotein dehydrogenase	Homo sapiens	268-274
35413388-0	2022	Inhibition of Nicotinamide adenine dinucleotide phosphate oxidase 4 attenuates cell apoptosis and oxidative stress in a rat model of polycystic ovary syndrome through the activation of Nrf-2/HO-1 signaling pathway.	NAD	14-47	heme oxygenase 1	Rattus norvegicus	191-195
22689570-0	2012	Intracellular beta-nicotinamide adenine dinucleotide inhibits the skeletal muscle ClC-1 chloride channel.	NAD	14-52	chloride voltage-gated channel 1	Homo sapiens	82-87
22689570-2	2012	Here we show that the coenzyme beta-nicotinamide adenine dinucleotide (NAD), an important metabolic regulator, robustly inhibits ClC-1 when included in the pipette solution in whole cell patch clamp experiments and when transiently applied to inside-out patches.	NAD	31-69	chloride voltage-gated channel 1	Homo sapiens	129-134
22689570-2	2012	Here we show that the coenzyme beta-nicotinamide adenine dinucleotide (NAD), an important metabolic regulator, robustly inhibits ClC-1 when included in the pipette solution in whole cell patch clamp experiments and when transiently applied to inside-out patches.	NAD	71-74	chloride voltage-gated channel 1	Homo sapiens	129-134
35451939-1	2022	Sirtuin 1 (SIRT1) is a nicotinamide adenine dinucleotide (NAD(Formula: see text)-dependent deacetylase involved in multiple glucose metabolism pathways and plays an important role in the pathogenesis of diabetes mellitus (DM).	NAD	23-56	sirtuin 1	Homo sapiens	0-9
22689570-4	2012	Molecular modeling, based on the structural coordinates of the homologous ClC-5 and CmClC proteins and in silico docking, suggest that NAD(+) binds with the adenine base deep in a cleft formed by ClC-1 intracellular cystathionine beta-synthase domains, and the nicotinamide base interacts with the membrane-embedded channel domain.	NAD	135-141	chloride voltage-gated channel 5	Homo sapiens	74-79
22689570-4	2012	Molecular modeling, based on the structural coordinates of the homologous ClC-5 and CmClC proteins and in silico docking, suggest that NAD(+) binds with the adenine base deep in a cleft formed by ClC-1 intracellular cystathionine beta-synthase domains, and the nicotinamide base interacts with the membrane-embedded channel domain.	NAD	135-141	chloride voltage-gated channel 1	Homo sapiens	196-201
22689570-7	2012	Our results identify a new biological role for NAD and suggest that the main physiological relevance may be the exquisite sensitivity to intracellular pH that NAD(+) inhibition imparts to ClC-1 gating.	NAD	47-50	chloride voltage-gated channel 1	Homo sapiens	188-193
22689570-7	2012	Our results identify a new biological role for NAD and suggest that the main physiological relevance may be the exquisite sensitivity to intracellular pH that NAD(+) inhibition imparts to ClC-1 gating.	NAD	159-165	chloride voltage-gated channel 1	Homo sapiens	188-193
35451939-1	2022	Sirtuin 1 (SIRT1) is a nicotinamide adenine dinucleotide (NAD(Formula: see text)-dependent deacetylase involved in multiple glucose metabolism pathways and plays an important role in the pathogenesis of diabetes mellitus (DM).	NAD	23-56	sirtuin 1	Homo sapiens	11-16
22689577-3	2012	Sirt-1, a nicotinamide adenine dinucleotide (NAD(+))-dependent deacetylase, has been linked to transcriptional silencing and appears to play a key role in inflammation.	NAD	10-43	sirtuin 1	Homo sapiens	0-6
35451939-1	2022	Sirtuin 1 (SIRT1) is a nicotinamide adenine dinucleotide (NAD(Formula: see text)-dependent deacetylase involved in multiple glucose metabolism pathways and plays an important role in the pathogenesis of diabetes mellitus (DM).	NAD	58-61	sirtuin 1	Homo sapiens	0-9
35451939-1	2022	Sirtuin 1 (SIRT1) is a nicotinamide adenine dinucleotide (NAD(Formula: see text)-dependent deacetylase involved in multiple glucose metabolism pathways and plays an important role in the pathogenesis of diabetes mellitus (DM).	NAD	58-61	sirtuin 1	Homo sapiens	11-16
35422087-5	2022	SHMT2 deficiency promoted the accumulation of intracellular reactive oxygen species (ROS) by decreasing the NADH/NAD+, NADPH/NADP+, and GSH/GSSG ratios, leading to a loss in mitochondrial membrane potential, release of cytochrome c, translocation of Bcl-2 family protein and activation of caspase-3.	NAD	108-112	serine hydroxymethyltransferase 2	Homo sapiens	0-5
22722849-3	2012	Here we show that SIRT7 is an NAD(+)-dependent H3K18Ac (acetylated lysine 18 of histone H3) deacetylase that stabilizes the transformed state of cancer cells.	NAD	30-36	sirtuin 7	Homo sapiens	18-23
22505229-4	2012	Quantitative change in ND2 (a subunit of NADH) and the methylation             status of the D-loop were observed during the initiation and progression of colorectal             cancer.	NAD	41-45	mitochondrially encoded NADH dehydrogenase 2	Homo sapiens	23-26
35422087-5	2022	SHMT2 deficiency promoted the accumulation of intracellular reactive oxygen species (ROS) by decreasing the NADH/NAD+, NADPH/NADP+, and GSH/GSSG ratios, leading to a loss in mitochondrial membrane potential, release of cytochrome c, translocation of Bcl-2 family protein and activation of caspase-3.	NAD	113-117	serine hydroxymethyltransferase 2	Homo sapiens	0-5
35114390-3	2022	Supplementation with NAD+ precursors and overexpression of NMNAT1, the key enzyme in the NAD+ biosynthetic process, have significant neuroprotective effects.	NAD	89-93	nicotinamide nucleotide adenylyltransferase 1	Mus musculus	59-65
35120937-1	2022	Ammonia dependent NAD+ synthetase from multi drug resistance Staphylococcus aureus catalyzes ATP dependent formation of NAD+ from deamido-NAD+ and ammonia at the synthetase active site.	NAD	120-124	AT695_RS07645	Staphylococcus aureus	18-33
22552445-1	2012	SIRT1 is the human orthologue of SIR2, a conserved NAD-dependent protein             deacetylase that regulates longevity in yeast and in Caenorhabditis elegans.	NAD	51-54	sirtuin 1	Homo sapiens	0-5
22552445-1	2012	SIRT1 is the human orthologue of SIR2, a conserved NAD-dependent protein             deacetylase that regulates longevity in yeast and in Caenorhabditis elegans.	NAD	51-54	sirtuin 1	Homo sapiens	33-37
35078249-5	2022	MdWRKY126 directly bound to the promoter of the cytoplasmic NAD-dependent malate dehydrogenase MdMDH5 and promoted its expression, thereby enhancing the malate content of apple fruit.	NAD	60-63	malate dehydrogenase	Malus domestica	74-94
35359990-5	2022	We also summarize factors that influence SIRT1 activity including the NAD+/NADH ratio, SIRT1 binding partners, and post-translational modifications.	NAD	75-79	sirtuin 1	Homo sapiens	41-46
22458729-5	2012	CymA is reduced with menadiol (E(m) = -80 mV) in the presence of NADH (E(m) = -320 mV) and an NADH-menadione (2-methyl-1,4-naphthoquinone) oxidoreductase, but not by menadiol alone.	NAD	65-69	cytochrome c	Shewanella oneidensis MR-1	0-4
22458729-6	2012	In cytoplasmic membranes reduction of CymA may then require the thermodynamic driving force from NADH, formate or H2 oxidation as the redox poise of the menaquinol pool in isolation is insufficient.	NAD	97-101	cytochrome c	Shewanella oneidensis MR-1	38-42
22547068-7	2012	The use of specific siRNA showed that the changes of Ca(2+) homeostasis induced by NAD(+) precursors are mediated by CD38 and the consequent ADPR-mediated TRPM2 gating.	NAD	83-89	transient receptor potential cation channel subfamily M member 2	Homo sapiens	155-160
22682224-2	2012	In line with this premise, decreased activity of PARP-1 or CD38-both NAD(+) consumers-increases NAD(+) bioavailability, resulting in SIRT1 activation and protection against metabolic disease.	NAD	96-102	sirtuin 1	Homo sapiens	133-138
35301252-7	2022	Ferulic acid also enhances the activation of AMP-activated kinase (AMPK) by increasing expression and activity of its activating kinase LKB1-whereas AMPK in turn amplifies Sirt1 activity by promoting induction of nicotinamide phosphoribosyltranferase, rate-limiting for generation of Sirt1"s obligate substrate NAD+.	NAD	311-315	protein kinase AMP-activated non-catalytic subunit beta 1	Homo sapiens	67-71
22546858-2	2012	Anti-aging sirtuin 1 (SIRT1), a             NAD+-dependent protein/histone deacetylase, is reduced in lungs of patients with COPD.	NAD	44-47	sirtuin 1	Homo sapiens	11-20
22546858-2	2012	Anti-aging sirtuin 1 (SIRT1), a             NAD+-dependent protein/histone deacetylase, is reduced in lungs of patients with COPD.	NAD	44-47	sirtuin 1	Homo sapiens	22-27
35301252-7	2022	Ferulic acid also enhances the activation of AMP-activated kinase (AMPK) by increasing expression and activity of its activating kinase LKB1-whereas AMPK in turn amplifies Sirt1 activity by promoting induction of nicotinamide phosphoribosyltranferase, rate-limiting for generation of Sirt1"s obligate substrate NAD+.	NAD	311-315	protein kinase AMP-activated non-catalytic subunit beta 1	Homo sapiens	149-153
35216453-9	2022	This allowed identification of relative amounts of neutrophils and CD4+ T cells in mixed cell suspensions, by using NADH signals as a differentiation marker.	NAD	116-120	CD4 antigen	Mus musculus	67-70
22561310-9	2012	Meanwhile, the effects of NAD or resveratrol on high glucose-inducing MCs senescence were also completely blocked by SiRNA-SIRT1.	NAD	26-29	sirtuin 1	Homo sapiens	123-128
35115484-7	2022	In addition to inducing increased NAD+ levels, NDUFV1 interacts with Src to attenuate LDHA phosphorylation at tyrosine 10 and reduce lactate production.	NAD	34-38	NADH:ubiquinone oxidoreductase core subunit V1	Homo sapiens	47-53
35108535-4	2022	We show that in hypoxic conditions, mitochondrial pyrroline 5-carboxylate reductase 1 (PYCR1) activity is increased, oxidizing NADH with the synthesis of proline as a by-product.	NAD	127-131	pyrroline-5-carboxylate reductase 1	Homo sapiens	50-85
35108535-4	2022	We show that in hypoxic conditions, mitochondrial pyrroline 5-carboxylate reductase 1 (PYCR1) activity is increased, oxidizing NADH with the synthesis of proline as a by-product.	NAD	127-131	pyrroline-5-carboxylate reductase 1	Homo sapiens	87-92
35001440-3	2022	In the nucleus accumbens (NAc), a region important for reward, both SIRT1 and the circadian transcription factor neuronal PAS domain protein 2 (NPAS2) are highly enriched, and both are regulated by the metabolic cofactor NAD+.	NAD	221-225	neuronal PAS domain protein 2	Mus musculus	113-142
35001440-3	2022	In the nucleus accumbens (NAc), a region important for reward, both SIRT1 and the circadian transcription factor neuronal PAS domain protein 2 (NPAS2) are highly enriched, and both are regulated by the metabolic cofactor NAD+.	NAD	221-225	neuronal PAS domain protein 2	Mus musculus	144-149
35013907-17	2022	TREM2 overexpression enhanced NAD+ and SIRT3 protein expression following LPS challenge in BV2 cells (p < 0.01 and p < 0.05, respectively).	NAD	30-34	triggering receptor expressed on myeloid cells 2	Mus musculus	0-5
35013907-23	2022	TREM2 overexpression ameliorates LPS-induced oxidative stress and neuroinflammation through enhancing SIRT3 function via NAD+.	NAD	121-125	triggering receptor expressed on myeloid cells 2	Mus musculus	0-5
35090502-10	2022	Our results revealed that NQO1 overexpression could significantly increase the ratio of NAD+/NADH and silencing information regulator 1 (Sirt1) expression and block tubular oxidative stress and apoptosis in diabetic kidneys.	NAD	88-92	NAD(P)H dehydrogenase, quinone 1	Mus musculus	26-30
35090502-10	2022	Our results revealed that NQO1 overexpression could significantly increase the ratio of NAD+/NADH and silencing information regulator 1 (Sirt1) expression and block tubular oxidative stress and apoptosis in diabetic kidneys.	NAD	93-97	NAD(P)H dehydrogenase, quinone 1	Mus musculus	26-30
35090502-11	2022	In vitro, NQO1 overexpression reduced the generation of ROS, NADPH oxidase 1 (Nox1) and Nox4, the Bax/Bcl-2 ratio and the expression of Cleaved Caspase-3 and increased NAD+/NADH levels and Sirt1 expression in HK-2 cells under HG conditions.	NAD	168-172	NAD(P)H dehydrogenase, quinone 1	Mus musculus	10-14
35090502-11	2022	In vitro, NQO1 overexpression reduced the generation of ROS, NADPH oxidase 1 (Nox1) and Nox4, the Bax/Bcl-2 ratio and the expression of Cleaved Caspase-3 and increased NAD+/NADH levels and Sirt1 expression in HK-2 cells under HG conditions.	NAD	173-177	NAD(P)H dehydrogenase, quinone 1	Mus musculus	10-14
35090502-13	2022	CONCLUSIONS: All these data suggest that NQO1 has a protective effect against oxidative stress and apoptosis in DN, which may be mediated by the regulation of Sirt1 through increasing intracellular NAD+/NADH levels.	NAD	198-202	NAD(P)H dehydrogenase, quinone 1	Mus musculus	41-45
35090502-13	2022	CONCLUSIONS: All these data suggest that NQO1 has a protective effect against oxidative stress and apoptosis in DN, which may be mediated by the regulation of Sirt1 through increasing intracellular NAD+/NADH levels.	NAD	203-207	NAD(P)H dehydrogenase, quinone 1	Mus musculus	41-45
2556968-14	1989	Since the cytosol normally maintains a highly oxidized NAD+/NADH redox ratio, it is interesting to speculate that increased availability of NADH from the oxidation of ethanol may support microsomal reduction of iron complexes, with the subsequent generation of reactive oxygen intermediates.	NAD	55-59	2,4-dienoyl-CoA reductase 1	Homo sapiens	140-144
2610514-2	1989	This note compares the substrate specificity of D-lactate dehydrogenase (D-LDH, EC 1.1.1.28) to that of L-lactate dehydrogenase (L-LDH, EC 1.1.1.27), illustrates three procedures that use D-LDH in synthesis and two methods for recycling NADH, and provides experimental details illustrating the use of D-LDH in organic synthesis.	NAD	237-241	lactate dehydrogenase D	Homo sapiens	48-71
2610514-2	1989	This note compares the substrate specificity of D-lactate dehydrogenase (D-LDH, EC 1.1.1.28) to that of L-lactate dehydrogenase (L-LDH, EC 1.1.1.27), illustrates three procedures that use D-LDH in synthesis and two methods for recycling NADH, and provides experimental details illustrating the use of D-LDH in organic synthesis.	NAD	237-241	lactate dehydrogenase D	Homo sapiens	73-78
2559189-5	1989	Reduced nicotinamideadenine dinucleotide was produced on the immobilized 3 alpha-HSD column and then determined fluorometrically.	NAD	8-40	aldo-keto reductase family 1 member C4	Homo sapiens	73-84
2819035-15	1989	In horse alcohol dehydrogenase and beta 1 beta 1, the guanidino group of Arg-369 is thought to stabilize the NAD(H)-enzyme complex by bonding to one of the pyrophosphate oxygens.	NAD	109-115	aldo-keto reductase family 1 member A1	Homo sapiens	9-30
2775561-4	1989	In other experiments the rate of methemoglobin reduction was measured in the above mixture with the addition of various other compounds such as NADH, cytochrome b5, and pure methemoglobin reductase.	NAD	144-148	hemoglobin subunit gamma 2	Homo sapiens	33-46
2499359-0	1989	The pathway of electron transfer in NADH:Q oxidoreductase.	NAD	36-40	thioredoxin reductase 1	Homo sapiens	43-57
2499359-1	1989	The pre-steady-state reduction by NADPH of NADH:Q oxidoreductase, as present in submitochondrial particles, has been further investigated with the rapid-mixing, rapid-freezing technique.	NAD	43-47	thioredoxin reductase 1	Homo sapiens	50-64
2499359-16	1989	This provides an explanation why NADH:Q oxidoreductase was not able to oxidise NADPH at pH 8.0, while part of the Fe-S clusters were still rapidly reduced.	NAD	33-37	thioredoxin reductase 1	Homo sapiens	40-54
2499359-17	1989	As a working hypothesis a dimeric structure for NADH:Q oxidoreductase is proposed.	NAD	48-52	thioredoxin reductase 1	Homo sapiens	55-69
2743579-3	1989	Thus, in lysates containing methemoglobin, NADH oxidation can be due firstly to methemoglobin reductase activity or secondly to the monooxygenase activity of methemoglobin, for which the substrate can be ribose 5-phosphate, a substrate also of transketolase.	NAD	43-47	hemoglobin subunit gamma 2	Homo sapiens	28-41
2743579-3	1989	Thus, in lysates containing methemoglobin, NADH oxidation can be due firstly to methemoglobin reductase activity or secondly to the monooxygenase activity of methemoglobin, for which the substrate can be ribose 5-phosphate, a substrate also of transketolase.	NAD	43-47	hemoglobin subunit gamma 2	Homo sapiens	80-93
2743579-3	1989	Thus, in lysates containing methemoglobin, NADH oxidation can be due firstly to methemoglobin reductase activity or secondly to the monooxygenase activity of methemoglobin, for which the substrate can be ribose 5-phosphate, a substrate also of transketolase.	NAD	43-47	hemoglobin subunit gamma 2	Homo sapiens	80-93
2464338-3	1989	The reduction of resorufin by NADPH-cytochrome P450 reductase was supported by NADPH but not NADH, and was not inhibited by dicumarol, which established that the reaction was not catalyzed by contaminating DT-diaphorase (NAD[P]H-quinone oxidoreductase).	NAD	93-97	cytochrome p450 oxidoreductase	Rattus norvegicus	30-61
2502049-3	1989	This method measures, with a standard luminometer, the reduced NAD produced and accumulated by the reaction of two dehydrogenase enzymes: the estradiol dehydrogenase for direct assay of estrogens (estrone + estradiol), the glucose-6-phosphate dehydrogenase for gonadotrophin determination.	NAD	63-66	glucose-6-phosphate dehydrogenase	Homo sapiens	223-256
3390470-1	1988	On changing stepwise the polypyrrole (PP) electrode potential a reverse change in the equilibrium concentration of a reduced coenzyme is observed in 0.1 M KNO3 solution containing nicotinamide adenine dinucleotide (NAD+), ethyl alcohol, alcohol dehydrogenase and electrode system based on PP-modified platinum.	NAD	215-219	aldo-keto reductase family 1 member A1	Homo sapiens	237-258
3338988-5	1988	This single protein, which forms GDP-L-fucose from GDP-4-keto-6-deoxy-D-mannose and NADH, appears to possess both epimerase and reductase capabilities and may be termed GDP-4-keto-6-deoxy-D-mannose-3,5-epimerase-4-reductase.	NAD	84-88	GDP-L-fucose synthase	Homo sapiens	169-223
3052244-1	1988	We have recently shown that cytoplasmic malate dehydrogenase (MDH-s) from several non-human species catalyses the reduction of aromatic alpha-keto acids in the presence of NADH (Friedrich et al.	NAD	172-176	malic enzyme 1	Homo sapiens	40-60
3052244-1	1988	We have recently shown that cytoplasmic malate dehydrogenase (MDH-s) from several non-human species catalyses the reduction of aromatic alpha-keto acids in the presence of NADH (Friedrich et al.	NAD	172-176	malic enzyme 1	Homo sapiens	62-67
3620453-4	1987	These observations indicated that ETF-QO reacts with the pool of ubiquinone that is reduced by NADH and succinic dehydrogenases.	NAD	95-99	electron transfer flavoprotein dehydrogenase	Homo sapiens	34-40
3115624-3	1987	The immobilized malate dehydrogenase catalyzed the reaction between oxaloacetate and NADH to form NAD in the coupled reaction originally proposed by Karmen.	NAD	85-89	malic enzyme 1	Homo sapiens	16-36
22399070-4	2012	We predict that Escherichia coli YbiA and related families of domains from diverse bacteria, eukaryotes, large DNA viruses and single strand RNA viruses are previously unrecognized components of NAD-utilizing pathways that probably operate on ADP-ribose derivatives.	NAD	195-198	hypothetical protein YbiA	Escherichia coli	33-37
3115624-3	1987	The immobilized malate dehydrogenase catalyzed the reaction between oxaloacetate and NADH to form NAD in the coupled reaction originally proposed by Karmen.	NAD	85-88	malic enzyme 1	Homo sapiens	16-36
22399070-6	2012	Likewise, we predict that another family of YbiA-related enzymes is likely to comprise a novel NAD-dependent ADP-ribosylation system for proteins, in conjunction with a previously unrecognized ADP-ribosyltransferase.	NAD	95-98	hypothetical protein YbiA	Escherichia coli	44-48
2954847-4	1987	The inhibition of oxygen consumption by NAD- and FAD-linked substrates was 40% for state 4 and 70% for ADP- or FCCP-stimulated respiration.	NAD	40-43	MAM domain containing glycosylphosphatidylinositol anchor 2	Mus musculus	103-107
22327552-5	2012	In addition, resveratrol strongly stimulates SIRT1 deacetylase activity in a dose-dependent manner by increasing its binding affinity to both the acetylated substrate and NAD(+).	NAD	171-177	sirtuin 1	Homo sapiens	45-50
22362590-3	2012	Furthermore we provide evidence that the cytosol of these cells contains factors (presumably enzymes) capable of employing either glutathione or NADH as re-reductants of ferric neuroglobin.	NAD	145-149	neuroglobin	Homo sapiens	177-188
3569292-1	1987	A simple point charge model has been used to estimate the effect of electrostatic interactions of bound NADH and NAD+ on ionizing groups in liver alcohol dehydrogenase.	NAD	104-108	aldo-keto reductase family 1 member A1	Homo sapiens	146-167
3569292-1	1987	A simple point charge model has been used to estimate the effect of electrostatic interactions of bound NADH and NAD+ on ionizing groups in liver alcohol dehydrogenase.	NAD	113-117	aldo-keto reductase family 1 member A1	Homo sapiens	146-167
3571184-6	1986	OM cytochrome b-mediated NADH-SDA reductase and rotenone-insensitive NADH-cytochrome c reductase activities were mainly present in the parenchymal cells of rat liver.	NAD	25-29	cytochrome b, mitochondrial	Rattus norvegicus	3-15
3727032-2	1986	NADH and nicotinic acid in high concentrations are shown to produce an inhibiting effect on the reverse malate dehydrogenase reaction which is determined by the nonspecific action either of the vitamin or its metabolites.	NAD	0-4	malic enzyme 1	Homo sapiens	104-124
2937805-7	1986	Poly-ADP-ribose polymerase, a nuclear enzyme associated with DNA damage and repair, which catalyzes conversion of NAD to nicotinamide and protein-bound poly-ADP-ribose, was activated by exposure of the cells to concentrations of 40 microM H2O2 or higher.	NAD	114-117	poly (ADP-ribose) polymerase family, member 1	Mus musculus	0-26
4074386-1	1985	Acrolein, a highly reactive aldehyde found in cigarette smoke, was shown to induce time-dependent inactivation of NAD+-linked 15-hydroxyprostaglandin dehydrogenase from porcine lung.	NAD	114-118	carbonyl reductase 1	Homo sapiens	126-163
22178470-2	2012	Sirtuin1 (SIRT1), a nicotinamide adenine dinucleotide (NAD(+))-dependent protein/histone deacetylase, regulates inflammation, senescence/aging, stress resistance, and deoxyribonucleic acid (DNA) damage repair via deacetylating intracellular signaling molecules and chromatin histones.	NAD	20-53	sirtuin 1	Homo sapiens	0-8
4074386-6	1985	Inactivation of pulmonary NAD+-linked 15-hydroxyprostaglandin dehydrogenase by acrolein may alter cellular and circulating thromboxane/prostacyclin ratios and subsequently disturb vascular homeostasis and augment inflammatory and anaphylactic responses in smokers.	NAD	26-29	carbonyl reductase 1	Homo sapiens	38-75
22178470-2	2012	Sirtuin1 (SIRT1), a nicotinamide adenine dinucleotide (NAD(+))-dependent protein/histone deacetylase, regulates inflammation, senescence/aging, stress resistance, and deoxyribonucleic acid (DNA) damage repair via deacetylating intracellular signaling molecules and chromatin histones.	NAD	20-53	sirtuin 1	Homo sapiens	10-15
22178470-2	2012	Sirtuin1 (SIRT1), a nicotinamide adenine dinucleotide (NAD(+))-dependent protein/histone deacetylase, regulates inflammation, senescence/aging, stress resistance, and deoxyribonucleic acid (DNA) damage repair via deacetylating intracellular signaling molecules and chromatin histones.	NAD	55-62	sirtuin 1	Homo sapiens	0-8
2995584-2	1985	Mercuric chloride and p-chloromercuriphenylsulfonate, inhibitors on NADH-cytochrome b5 reductase, at 32 microM inhibited NADH-supported palmitoyl-CoA elongation to 30 and 60% of control activity, respectively, whereas NADPH-supported palmitoyl-CoA elongation was unaffected by these mercurials.	NAD	68-72	cytochrome b5 type A	Rattus norvegicus	73-86
22178470-2	2012	Sirtuin1 (SIRT1), a nicotinamide adenine dinucleotide (NAD(+))-dependent protein/histone deacetylase, regulates inflammation, senescence/aging, stress resistance, and deoxyribonucleic acid (DNA) damage repair via deacetylating intracellular signaling molecules and chromatin histones.	NAD	55-62	sirtuin 1	Homo sapiens	10-15
2995584-3	1985	An antibody to rat liver NADH-cytochrome b5 reductase inhibited brain microsomal NADH-cytochrome b5 reductase activity and NADH-dependent palmitoyl-CoA elongation.	NAD	25-29	cytochrome b5 type A	Rattus norvegicus	30-43
2995584-3	1985	An antibody to rat liver NADH-cytochrome b5 reductase inhibited brain microsomal NADH-cytochrome b5 reductase activity and NADH-dependent palmitoyl-CoA elongation.	NAD	25-29	cytochrome b5 type A	Rattus norvegicus	86-99
22382036-3	2012	Recent findings indicate that a nicotinamide adenine dinucleotide (NAD(+))-dependent protein deacetylase (namely SIRT1) expressed by hypothalamic neurons is crucial for mounting responses against diet-induced obesity and type 2 diabetes mellitus (T2DM).	NAD	32-65	sirtuin 1	Homo sapiens	113-118
22382036-3	2012	Recent findings indicate that a nicotinamide adenine dinucleotide (NAD(+))-dependent protein deacetylase (namely SIRT1) expressed by hypothalamic neurons is crucial for mounting responses against diet-induced obesity and type 2 diabetes mellitus (T2DM).	NAD	67-74	sirtuin 1	Homo sapiens	113-118
2995584-6	1985	These results indicate the presence of an electron transport system, NADH-NADH-cytochrome b5 reductase-cytochrome b5-fatty acid elongation, in brain microsomes.	NAD	69-73	cytochrome b5 type A	Rattus norvegicus	79-92
2995584-6	1985	These results indicate the presence of an electron transport system, NADH-NADH-cytochrome b5 reductase-cytochrome b5-fatty acid elongation, in brain microsomes.	NAD	69-73	cytochrome b5 type A	Rattus norvegicus	103-116
3919063-3	1985	The present study was conducted to determine whether these nucleoside analogs and their dinucleotide derivatives interfere with NAD metabolism and in particular with the NAD-dependent enzyme, poly(ADP-ribose) polymerase.	NAD	170-173	poly (ADP-ribose) polymerase family, member 1	Mus musculus	192-219
22457647-2	2012	From this perspective, we interpret recent evidence to mean that lactate transmission serves the maintenance of network metabolism by two different mechanisms, one by regulating the formation of cAMP via the lactate receptor GPR81, the other by adjusting the NADH/NAD(+) redox ratios, both linked to the maintenance of brain energy turnover and possibly cerebral blood flow.	NAD	259-263	hydroxycarboxylic acid receptor 1	Homo sapiens	225-230
22457647-2	2012	From this perspective, we interpret recent evidence to mean that lactate transmission serves the maintenance of network metabolism by two different mechanisms, one by regulating the formation of cAMP via the lactate receptor GPR81, the other by adjusting the NADH/NAD(+) redox ratios, both linked to the maintenance of brain energy turnover and possibly cerebral blood flow.	NAD	264-270	hydroxycarboxylic acid receptor 1	Homo sapiens	225-230
22008468-1	2012	Yeast NAD(+)-specific isocitrate dehydrogenase (IDH) is an octameric enzyme composed of four each of regulatory IDH1 and catalytic IDH2 subunits that share 42% sequence identity.	NAD	6-12	isocitrate dehydrogenase (NAD(+)) IDH2	Saccharomyces cerevisiae S288C	131-135
22008468-2	2012	IDH2 contains catalytic isocitrate/Mg2+ and NAD+ binding sites whereas IDH1 contains homologous binding sites, respectively, for cooperative binding of isocitrate and for allosteric binding of AMP.	NAD	44-48	isocitrate dehydrogenase (NAD(+)) IDH2	Saccharomyces cerevisiae S288C	0-4
3919063-6	1985	The analogs also serve as weak inhibitors of poly(ADP-ribose) polymerase, which is an NAD-utilizing, chromatin-bound enzyme, whose function is required for normal DNA repair processes.	NAD	86-89	poly (ADP-ribose) polymerase family, member 1	Mus musculus	45-72
6386467-1	1984	Heterotropic cooperativity effects in the binding of alcohols and NAD+ or NADH to liver alcohol dehydrogenase have been examined by equilibrium measurements and stopped-flow kinetic studies.	NAD	66-70	aldo-keto reductase family 1 member A1	Homo sapiens	88-109
6386467-1	1984	Heterotropic cooperativity effects in the binding of alcohols and NAD+ or NADH to liver alcohol dehydrogenase have been examined by equilibrium measurements and stopped-flow kinetic studies.	NAD	74-78	aldo-keto reductase family 1 member A1	Homo sapiens	88-109
6496965-4	1984	GA3PDH was inhibited by ATP (Ki = 2.27 mM), ADP (Ki = 1.21 mM) and AMP (Ki = 0.73 mM) competitively with NAD (Km = 0.24 mM).	NAD	105-108	glyceraldehyde-3-phosphate dehydrogenase	Rattus norvegicus	0-6
6589599-6	1984	The binding sites have the relative affinities NADPH greater than NADH greater than NADP+ greater than NAD+.	NAD	66-70	2,4-dienoyl-CoA reductase 1	Homo sapiens	47-52
6376489-3	1984	This microsomal reductase converts acetoacetyl-CoA to beta-hydroxybutyryl-CoA at a rate of 70 nmol/min/mg of protein; the enzyme has a specific requirement for NADH and appears to obtain electrons directly from the reduced pyridine nucleotide without the intervention of cytochrome b5 and its flavoprotein reductase.	NAD	160-164	cytochrome b5 type A	Rattus norvegicus	271-284
16663575-4	1984	Total NAD was not influenced by growth conditions and was mainly present in oxidized form.These results indicate that NADPH is the electron donor for the high Fe(III) reduction activity found in iron-deficient roots, a process that is part of the Fe-uptake mechanism.	NAD	6-9	2,4-dienoyl-CoA reductase 1	Homo sapiens	118-123
6365555-1	1984	The interaction of liver alcohol dehydrogenase with NADH and aldehyde substrates has been characterized with respect to ternary-complex formation by the apparently non-preferred pathway which involves intermediate formation of binary enzyme X aldehyde complexes.	NAD	52-56	aldo-keto reductase family 1 member A1	Homo sapiens	25-46
6365555-3	1984	The rate of NADH (or NAD+) association to liver alcohol dehydrogenase is not detectably affected by DACA binding to the enzyme, but the NADH dissociation rate decreases approximately by a factor of 6.	NAD	12-16	aldo-keto reductase family 1 member A1	Homo sapiens	48-69
6365555-3	1984	The rate of NADH (or NAD+) association to liver alcohol dehydrogenase is not detectably affected by DACA binding to the enzyme, but the NADH dissociation rate decreases approximately by a factor of 6.	NAD	21-25	aldo-keto reductase family 1 member A1	Homo sapiens	48-69
6365555-8	1984	A flow analysis is presented which indicates that coenzyme and substrate are actually bound in random order to liver alcohol dehydrogenase during the enzymic reduction of aldehydes by NADH.	NAD	184-188	aldo-keto reductase family 1 member A1	Homo sapiens	117-138
6537216-10	1984	Both ethanol and phenobarbital elevated cytochrome P-450; ethanol also elevated cytochrome b5 measured as NADH-reducible cytochrome.	NAD	106-110	cytochrome b5 type A	Rattus norvegicus	80-93
6654894-3	1983	The rate of reoxidation of NADH-reduced microsomal cytochrome b5 was markedly stimulated (up to 3-fold) by the addition of increasing concentrations of beta-ketohexadecanoyl-CoA (1-8 microM).	NAD	27-31	cytochrome b5 type A	Rattus norvegicus	51-64
6654894-8	1983	Although trans-2-hexadecenoyl-CoA significantly stimulated the NADH-reduced cytochrome b5 reoxidation rate under aerobic conditions, it did not have any stimulatory effect under anaerobic conditions.	NAD	63-67	cytochrome b5 type A	Rattus norvegicus	76-89
6415289-0	1983	Comparison of AMP and NADH binding to glycogen phosphorylase b.	NAD	22-26	glycogen phosphorylase B	Homo sapiens	38-62
6415289-3	1983	Kinetic studies demonstrate that NADH inhibits the AMP activation of glycogen phosphorylase b.	NAD	33-37	glycogen phosphorylase B	Homo sapiens	69-93
6885813-1	1983	UDP-glucose 4-epimerase from Saccharomyces fragilis has 1 mol of NAD firmly bound per mol of the dimeric apoenzyme.	NAD	65-68	ATP-dependent RNA helicase HAS1	Saccharomyces cerevisiae S288C	52-57
6444203-6	1983	Thus the reduction of cytochrome b5 by NADH and NADPH is the diffusion-dependent reaction in the redox-chains of microsomes only.	NAD	39-43	cytochrome b5 type A	Rattus norvegicus	22-35
6404246-4	1983	It has been shown that larval LDH incubated with beta-nicotinamide adenine dinucleotide exhibits two additional minor bands with an electrophoretic mobility similar to that of the minor bands of both pupae and adults.	NAD	49-87	Lactate dehydrogenase	Drosophila melanogaster	30-33
6641701-3	1983	This relaxation phenomenon is also shown to be NAD dependent and to be correlated with the formation of hyper(ADP-ribosyl)ated forms of histone H1.	NAD	47-50	H1.0 linker histone	Homo sapiens	136-146
6356161-4	1983	At ethanol concentrations above 10 mM, substrate inhibition, consistent with the formation a dead-end ADH-NADH-ethanol complex, also becomes a rate-limiting factor.	NAD	106-110	aldo-keto reductase family 1 member A1	Homo sapiens	102-105
6659341-0	1983	[Activity and molecular forms of nicotinamide adenine dinucleotide- and nicotinamide adenine dinucleotide phosphate-dependent malate dehydrogenase in bull spermatozoa].	NAD	33-66	malic enzyme 1	Homo sapiens	126-146
6293814-6	1982	HMG 1 and HMG 2 were found to be ADP-ribosylated, the reaction being dependent on NAD concentration and time.	NAD	82-85	high mobility group protein B2	Bos taurus	10-15
6806275-6	1982	Thus, microsomal cytochrome P-450 appears to be reduced via two independent pathways of electron transport from NADH; the biphasic reduction occurs via cytochrome P-450 reductase while the slower monophasic reduction occurs via cytochrome b5.	NAD	112-116	cytochrome p450 oxidoreductase	Rattus norvegicus	152-178
6749494-2	1982	Complex formation at the general anion-binding site of the liver alcohol dehydrogenase subunit has been characterized by transient-state kinetic methods, using NADH as a reporter ligand.	NAD	160-164	aldo-keto reductase family 1 member A1	Homo sapiens	65-86
7079734-5	1982	In addition, the unusual capacity of S-adenosylhomocysteine hydrolase to form stable complexes with adenosine and its cofactor, nicotinamide adenine dinucleotide, suggest that evolution of its gene may have involved recombination of a portion of the adenosine deaminase gene with an adenine nucleotide domain-coding sequence of another preexisting gene.	NAD	128-161	adenosine deaminase	Homo sapiens	250-269
7048723-5	1981	Activity of LDH (lactate dehydrogenase) of mixed rumen microorganisms is regulated by the NADH/NAD(H) balance and the ATP concentration.	NAD	90-94	LDH	Bos taurus	12-15
7048723-5	1981	Activity of LDH (lactate dehydrogenase) of mixed rumen microorganisms is regulated by the NADH/NAD(H) balance and the ATP concentration.	NAD	90-94	LDH	Bos taurus	17-38
7048723-5	1981	Activity of LDH (lactate dehydrogenase) of mixed rumen microorganisms is regulated by the NADH/NAD(H) balance and the ATP concentration.	NAD	95-101	LDH	Bos taurus	12-15
7048723-5	1981	Activity of LDH (lactate dehydrogenase) of mixed rumen microorganisms is regulated by the NADH/NAD(H) balance and the ATP concentration.	NAD	95-101	LDH	Bos taurus	17-38
7306493-1	1981	The binding of NAD+ and of its fluorescent analogue, nicotinamide 1,N6-ethenoadenine dinucleotide, to glyceraldehyde-3-phosphate dehydrogenase purified from the muscles of young and old rats was studied in detail.	NAD	15-19	glyceraldehyde-3-phosphate dehydrogenase	Rattus norvegicus	102-142
7248931-0	1981	Nicotinamide adenine dinucleotide-dependent 15-hydroxyprostaglandin dehydrogenase activity in hydatidiform mole tissue and choriocarcinoma cells.	NAD	0-33	carbonyl reductase 1	Homo sapiens	44-81
7248931-2	1981	To evaluate the possible role of prostaglandin catabolism in neoplastic cells, we measured nicotinamide adenine dinucleotide-dependent 15-hydroxyprostaglandin dehydrogenase activity in hydatidiform mole tissue and in choriocarcinoma cells maintained in monolayer culture.	NAD	91-124	carbonyl reductase 1	Homo sapiens	135-172
7248931-3	1981	The specific activity of nicotinamide adenine dinucleotide-dependent 15-hydroxyprostaglandin dehydrogenase in hydatidiform mole tissue (0 to 1.2 nmol 15-ketoprostaglandin E2 formed x min-1 x mg-1 cytosolic protein) and in choriocarcinoma cells (1.0 nmol 15-ketoprostaglandin E2 x min-1 x mg-1 protein) was strikingly less than that found in normal placental tissue [11.4 +/- 2.3 (S.E.)	NAD	25-58	carbonyl reductase 1	Homo sapiens	69-106
24233801-1	1981	myo-Inositol-1-phosphate synthase (EC 5.5.1.4) from rat testes, an NAD(+)-containing enzyme, which convertsD-glucose 6-phosphate to 1L-myo-inositol 1-phosphate, could be immobilized together with its cofactor and bovine serum albumin by crosslinking with glutaraldehyde at pH 4.5.	NAD	67-73	albumin	Rattus norvegicus	220-233
22125309-1	2012	Sirtuin 1 also known as NAD-dependent deacetylase sirtuin 1, is a protein that in humans is encoded by the Sirt1 gene.	NAD	24-27	sirtuin 1	Homo sapiens	0-9
22125309-1	2012	Sirtuin 1 also known as NAD-dependent deacetylase sirtuin 1, is a protein that in humans is encoded by the Sirt1 gene.	NAD	24-27	sirtuin 1	Homo sapiens	50-59
22125309-1	2012	Sirtuin 1 also known as NAD-dependent deacetylase sirtuin 1, is a protein that in humans is encoded by the Sirt1 gene.	NAD	24-27	sirtuin 1	Homo sapiens	107-112
7260196-5	1981	Hence only the reactions of cytochrome b5 reduction by NADH- and NADPH-specific flavoproteins are diffusion-dependent processes in the microsomal oxidation chain.	NAD	55-59	cytochrome b5 type A	Rattus norvegicus	28-41
22118797-6	2012	We found that both ATP and NAD induce a dose-dependent decrease on the Treg CD4+ CD25+ population.	NAD	27-30	CD4 antigen	Mus musculus	76-79
7016531-21	1981	The particular mode of binding and properties of the active-site zinc ion in liver alcohol dehydrogenase suggest that the catalytic function of the metal ion can be related primarily to facilitation of the process of alcohol oxidation through facilitation of the alcoholate ion formation step now established to precede hydride transfer to NAD+.	NAD	340-344	aldo-keto reductase family 1 member A1	Homo sapiens	83-104
22118797-6	2012	We found that both ATP and NAD induce a dose-dependent decrease on the Treg CD4+ CD25+ population.	NAD	27-30	interleukin 2 receptor, alpha chain	Mus musculus	81-85
22432057-8	2012	XRCC1tp cells showed increased toxicity to MMS, enhanced MMS-induced depletion of NADH suggesting increased PARP activity, and normal functional repair of MMS-induced DNA damage.	NAD	82-86	X-ray repair complementing defective repair in Chinese hamster cells 1	Mus musculus	0-5
7213760-1	1981	Salicylate hydroxylase (salicylate, NADH: oxygen oxidoreductase (1-hydroxylating, decarboxylating), EC 1.14.13.1) in Pseudomonas putida catalyzed hydroxylation of the substrate analogue, salicylaldehyde, to form catechol and formate with stoichiometric consumption of NADH and O2.	NAD	36-40	salicylate hydroxylase	Pseudomonas putida	0-22
21883939-5	2012	A critical source of endothelial ROS is a family of non-phagocytic nicotinamide adenine dinucleotide phosphate (NADPH) oxidases, including the prototypic Nox2-based NADPH oxidases, Nox1, Nox4 and Nox5.	NAD	67-100	cytochrome b-245 beta chain	Homo sapiens	154-158
7011796-0	1981	Effect of NADH on the pKa of zinc-bound water in liver alcohol dehydrogenase.	NAD	10-14	aldo-keto reductase family 1 member A1	Homo sapiens	55-76
7011796-8	1981	NADH complex appears to be typical for an aquo ligand in the inner-sphere ligand field provided by the zinc-binding amino acid residues in liver alcohol dehydrogenase.	NAD	0-4	aldo-keto reductase family 1 member A1	Homo sapiens	145-166
7005209-4	1980	On the basis of the data obtained, the following scheme is proposed as the mechanism of this enzyme reaction: [Formula: see text], where E and E" are the enzyme unit (one subunit of alcohol dehydrogenase) and an intermediate form of the enzyme unit-substrate compound which appears by two-electron reduction of the enzyme unit-substrate compound, respectively, S is p-nitrosophenol (p-NSP), N is NADH, and P1 and P2 are NAD+ and p-aminophenol (p-AmP), respectively.	NAD	396-400	aldo-keto reductase family 1 member A1	Homo sapiens	182-203
23071729-1	2012	NADH-quinone oxidoreductase 1 (NQO1) modulates cellular NAD(+)/NADH ratio which has been associated with the aging and anti-aging mechanisms of calorie restriction (CR).	NAD	56-62	NAD(P)H dehydrogenase, quinone 1	Mus musculus	0-29
23071729-1	2012	NADH-quinone oxidoreductase 1 (NQO1) modulates cellular NAD(+)/NADH ratio which has been associated with the aging and anti-aging mechanisms of calorie restriction (CR).	NAD	56-62	NAD(P)H dehydrogenase, quinone 1	Mus musculus	31-35
23071729-1	2012	NADH-quinone oxidoreductase 1 (NQO1) modulates cellular NAD(+)/NADH ratio which has been associated with the aging and anti-aging mechanisms of calorie restriction (CR).	NAD	0-4	NAD(P)H dehydrogenase, quinone 1	Mus musculus	31-35
7005209-4	1980	On the basis of the data obtained, the following scheme is proposed as the mechanism of this enzyme reaction: [Formula: see text], where E and E" are the enzyme unit (one subunit of alcohol dehydrogenase) and an intermediate form of the enzyme unit-substrate compound which appears by two-electron reduction of the enzyme unit-substrate compound, respectively, S is p-nitrosophenol (p-NSP), N is NADH, and P1 and P2 are NAD+ and p-aminophenol (p-AmP), respectively.	NAD	420-424	aldo-keto reductase family 1 member A1	Homo sapiens	182-203
7005210-6	1980	In the reaction catalyzed by this enzyme, 2 mol of NADH were consumed per mol p-nitrosophenol (p-NSP) reduced to p-aminophenol (p-AmP).	NAD	51-55	sperm antigen with calponin homology and coiled-coil domains 1	Homo sapiens	97-100
20697895-5	2012	Resveratrol upregulated the expression of the NAD-dependent deacetylase sirtuin 1 mRNA and downregulated the expression of the Bcl-X(L) mRNA, and resveratrol-induced MH7A cell death, mitochondrial damage, and caspase-3/-9 activation were prevented by sirtinol, an inhibitor of sirtuin 1.	NAD	46-49	sirtuin 1	Homo sapiens	72-81
7005210-10	1980	NAD+ showed an inhibition competitive with NADH and one uncompetitive with p-NSP.	NAD	0-4	sperm antigen with calponin homology and coiled-coil domains 1	Homo sapiens	77-80
7402332-3	1980	Here we have studied the effect of vanadate on malate dehydrogenase (MDH, EC1.1.1.37) catalysed oxidation of NADH during the formation of malate from oxalacetate in vitro.	NAD	109-113	malic enzyme 1	Homo sapiens	47-67
22962634-0	2012	The NAD(+)-dependent protein deacetylase activity of SIRT1 is regulated by its oligomeric status.	NAD	4-10	sirtuin 1	Homo sapiens	53-58
7402332-3	1980	Here we have studied the effect of vanadate on malate dehydrogenase (MDH, EC1.1.1.37) catalysed oxidation of NADH during the formation of malate from oxalacetate in vitro.	NAD	109-113	malic enzyme 1	Homo sapiens	69-72
7391131-0	1980	Localization and biosynthesis of NADH-cytochrome b5 reductase, an integral membrane protein, in rat liver cells.	NAD	33-37	cytochrome b5 type A	Rattus norvegicus	38-51
7400118-5	1980	These results apparently suggest that the NADPH-flavin reductase system is able to reduce methemoglobin in erythrocytes at a moderate speed with about 1 microM flavin, and the reduction was estimated to vary from less than 1% to about 20% of that by the NADH-cytochrome b5 reductase system with 1 microM cytochrome b5, depending on the uptake of flavin by human erythrocytes.	NAD	254-258	hemoglobin subunit gamma 2	Homo sapiens	90-103
22052907-9	2011	Notably, the activity of TTHA0420-DeltaC5 was about 10 times higher than that of the wild-type enzyme at 20-40  C. Our findings suggest that the C-terminal region of TTHA0420 may regulate the alternative binding of NADH and substrate flavin to the enzyme.	NAD	215-219	flavin reductase family protein	Thermus thermophilus HB8	25-33
22052907-9	2011	Notably, the activity of TTHA0420-DeltaC5 was about 10 times higher than that of the wild-type enzyme at 20-40  C. Our findings suggest that the C-terminal region of TTHA0420 may regulate the alternative binding of NADH and substrate flavin to the enzyme.	NAD	215-219	flavin reductase family protein	Thermus thermophilus HB8	166-174
6778467-5	1980	The V values at different NADH concentrations appeared to correlate with the concentration of reduced cytochrome b5 that the added NADH could sustain during the incubation period.	NAD	26-30	cytochrome b5 type A	Rattus norvegicus	102-115
21950728-1	2011	SIRT1 belongs to the silent information regulator 2 (Sir2) protein family of enzymes and functions as a NAD(+) -dependent class III histone deacetylase.	NAD	104-110	sirtuin 1	Homo sapiens	0-5
6778467-5	1980	The V values at different NADH concentrations appeared to correlate with the concentration of reduced cytochrome b5 that the added NADH could sustain during the incubation period.	NAD	131-135	cytochrome b5 type A	Rattus norvegicus	102-115
6778467-6	1980	Tetrahydronicotinamide adenine dinucleotide (NADH3), a structural analogue of NADH, reduced demethylase activity without affecting NADPH-cytochrome P450 reductase activity or the concentration of reduced cytochrome b5.	NAD	45-49	cytochrome b5 type A	Rattus norvegicus	204-217
6987673-2	1980	These studies have identified human liver alcohol dehydrogenase as the unknown NAD(H)-dependent liver enzyme specific for the free hydroxyl group at C3 of the cardiac genins; this hydroxyl is the critical site of the genins" enzymatic oxidation and concomitant pharmacological inactivation in humans.	NAD	79-85	aldo-keto reductase family 1 member A1	Homo sapiens	42-63
466784-4	1979	Modification of a commercially available hexokinase/glucose-6-phosphate dehydrogenase reagent system for glucose provides that the rate of production of NADH be first-order in total glucose concentration within about 30 s after sample and reagent are mixed.	NAD	153-157	glucose-6-phosphate dehydrogenase	Homo sapiens	52-85
223843-1	1979	The tetrameric glyceraldehyde-3-phosphate dehydrogenase from rabbit muscle binds NAD+ and some of its analogues in a negatively cooperative manner, whereas other NAD+ analogues bind non-cooperatively to this enzyme.	NAD	81-85	glyceraldehyde-3-phosphate dehydrogenase	Oryctolagus cuniculus	15-55
223843-1	1979	The tetrameric glyceraldehyde-3-phosphate dehydrogenase from rabbit muscle binds NAD+ and some of its analogues in a negatively cooperative manner, whereas other NAD+ analogues bind non-cooperatively to this enzyme.	NAD	162-166	glyceraldehyde-3-phosphate dehydrogenase	Oryctolagus cuniculus	15-55
223843-7	1979	These results in conjunction with other data support the view that the negative cooperativity in NAD+ binding to glyceraldehyde-3-phosphate dehydrogenase results from ligand-induced conformational changes.	NAD	97-101	glyceraldehyde-3-phosphate dehydrogenase	Oryctolagus cuniculus	113-153
218945-3	1979	253, 8593-8597) as the mechanism for the observed decrease in protein fluorescence of liver alcohol dehydrogenase seen with alkaline pH, or with the formation of a ternary complex with NAD+ and trifluoroethanol.	NAD	185-189	aldo-keto reductase family 1 member A1	Homo sapiens	92-113
43909-1	1979	These studies have shown that addition of p-nitroanisole to a reaction mixture containing rat liver microsomes resulted in an increase the reoxidation rate of NADH-reduced cytochrome b5.	NAD	159-163	cytochrome b5 type A	Rattus norvegicus	172-185
43909-2	1979	Fortification of rat liver microsomes with partially purified cytochrome b5 produces an increase in both NADPH-dependent and NADH-dependent p-nitroanisole O-demethylation activity.	NAD	125-129	cytochrome b5 type A	Rattus norvegicus	62-75
43909-4	1979	Addition of either purified cytochrome P-450 or cytochrome P-448 to an incubation mixture containing phenobarbital-treated rat liver microsomes enhanced the NADH-dependent p-nitroanisole O-demethylation activity.	NAD	157-161	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	48-64
43909-5	1979	These results suggest that NADH-dependent and, in part, NADPH-dependent O-demethylations are catalyzed by cytochrome P-448 and cytochrome P-450 receiving electrons from cytochrome b5.	NAD	27-31	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	106-122
43909-5	1979	These results suggest that NADH-dependent and, in part, NADPH-dependent O-demethylations are catalyzed by cytochrome P-448 and cytochrome P-450 receiving electrons from cytochrome b5.	NAD	27-31	cytochrome b5 type A	Rattus norvegicus	169-182
215122-7	1978	The reduction by NADH of the cytochrome b of mixtures of Complexes I and III is biphasic.	NAD	17-21	mitochondrially encoded cytochrome b	Homo sapiens	29-41
206461-0	1978	Biospecific interaction on solid phase between alcohol dehydrogenase and an immobilized NADH analogue studied by fluorometry.	NAD	88-92	aldo-keto reductase family 1 member A1	Homo sapiens	47-68
744000-5	1978	NADPH was five times as effective a hydrogen donor as NADH when the washed microsomal fraction was the source of the enzyme.	NAD	54-58	2,4-dienoyl-CoA reductase 1	Homo sapiens	0-5
25065-2	1978	NAD(+) (and not NADH) forms poly(ADP-ribose), an inhibitor of DNA synthesis, in a reaction catalysed by poly(ADP-ribose) polymerase.	NAD	0-6	poly(ADP-ribose) polymerase 1	Gallus gallus	104-131
624282-1	1978	Initial rate studies at pH 7.6 with three aldehydes, product inhibition patterns with NADH and dead-end inhibition with adenosine diphosphoribose show that the kinetic mechanism of glyceraldehyde-3-phosphate dehydrogenase from rabbit muscle cannot be ordered, and support an enzyme-substitution mechanism.	NAD	86-90	glyceraldehyde-3-phosphate dehydrogenase	Oryctolagus cuniculus	181-221
23176-5	1978	The rate of O-2 generation in the particulate fraction was higher in the presence of NADPH than in the presence of NADH.	NAD	115-119	immunoglobulin kappa variable 1D-39	Homo sapiens	12-15
270717-7	1977	Unlike cholera toxin, the serine protease stimulation is immediate (within the first 5 min) and requires no additional factors (e.g., NAD(+)).	NAD	134-140	cell division cycle 34, ubiqiutin conjugating enzyme	Rattus norvegicus	26-41
215394-3	1977	The reduced coenzyme binds in an open conformation similar to that of NAD bound to malate dehydrogenase.	NAD	70-73	malic enzyme 1	Homo sapiens	83-103
1012291-2	1976	Activity of SDH, MDH (NAD), CYO- and alfa-GPDH (NAD) in the pericaryon is low, of the LDH moderate and the activity of G6PDH, NADPH-diaphorese, acid phosphatase, TPP-ase and non-specific esterase expressed.	NAD	48-51	serine dehydratase	Rattus norvegicus	12-15
183744-0	1976	An investigation of the nicotinamide-adenine dinucleotide-induced "tightening" of the structure of glyceraldehyde 3-phosphate dehydrogenase.	NAD	24-57	glyceraldehyde-3-phosphate dehydrogenase	Oryctolagus cuniculus	99-139
183746-7	1976	Initial-velocity patterns of the overall pyruvate dehydrogenase reaction obtained with varying TPP, CoA and NAD+ concentrations at a fixed pyruvate concentration were consistent with a sequential three-site Ping Pong mechanism; in the presence of oxaloacetate and citrate synthase to remove acetyl-CoA (an inhibitor of the overall reaction) the values of Km for NAD+ and CoA were 53+/- 5 muM and 1.9+/-0.2 muM respectively.	NAD	108-112	citrate synthase	Sus scrofa	264-280
2319-1	1976	In a number of animal species soluble NADH-cytochrome b5 reductase of erythrocytes was compared with membrane-bound NADH-cytochrome b5 reductase of liver microsomes by using an antibody to purified NADH-cytochrome b5 reductase from rat liver microsomes.	NAD	38-42	cytochrome b5 type A	Rattus norvegicus	43-56
174813-4	1976	Copurified alpha-ketoglutarate dehydrogenase displayed apparent KM values for alpha-ketoglutarate, nicotinamide adenine dinucleotide, and CoA of 1.25 mM, 67 muM, and 50 muM, respectively.	NAD	99-132	oxoglutarate (alpha-ketoglutarate) dehydrogenase (lipoamide)	Mus musculus	11-44
21998399-1	2011	UNLABELLED: OBJECTIVE Wld(S) (Wallerian degeneration slow), a fusion protein from a spontaneous mutation containing full-length nicotinamide mononucleotide adenylyltransferase 1, has NAD biosynthesis activity and protects axon from degeneration robustly.	NAD	183-186	nicotinamide nucleotide adenylyltransferase 1	Mus musculus	128-177
173391-0	1975	Conformational changes of glyceraldehyde-3-phosphate dehydrogenase induced by the binding of NAD.	NAD	93-96	glyceraldehyde-3-phosphate dehydrogenase	Oryctolagus cuniculus	26-66
21395487-3	2011	Overactivation of poly(ADP-ribose) polymerase-1 (PARP-1) can rapidly reduce the levels of beta-nicotinamide adenine dinucleotide and adenosine triphosphate and ultimately promote necrosis.	NAD	90-128	poly (ADP-ribose) polymerase family, member 1	Mus musculus	18-47
173391-2	1975	The fluorescence of the natural coenzyme, NADH, is used to monitor the environment of the nicotinamide moiety at the active centre of rabbit muscle glyceraldehyde-3-phosphate dehydrogenase (EC 1.2.1.12).	NAD	42-46	glyceraldehyde-3-phosphate dehydrogenase	Oryctolagus cuniculus	148-188
21395487-3	2011	Overactivation of poly(ADP-ribose) polymerase-1 (PARP-1) can rapidly reduce the levels of beta-nicotinamide adenine dinucleotide and adenosine triphosphate and ultimately promote necrosis.	NAD	90-128	poly (ADP-ribose) polymerase family, member 1	Mus musculus	49-55
21807113-4	2011	Sirt1, a NAD-dependent class III histone deacetylase, has a paradoxical role in tumorigenesis by deacetylating several transcription factors, including p53, E2F1 and forkhead proteins.	NAD	9-12	sirtuin 1	Homo sapiens	0-5
1191670-2	1975	Incubation of rat homogeneous detergent-solubilized cytochrome b5 with rat liver microsomes resulted in specific binding of the hemoprotein which was rapidly reduced by NADH.	NAD	169-173	cytochrome b5 type A	Rattus norvegicus	52-65
1191670-4	1975	However, the extra-bound detergent-solubilized cytochrome b5 did inhibit NADPH-dependent N-demethylations, the NADH synergism and NADPH cytochrome P-450 reductase activity.	NAD	111-115	cytochrome b5 type A	Rattus norvegicus	47-60
1158861-4	1975	All 4 residues could be made inaccessible to modification when a malate dehydrogenase-NADH-hydroxymalonate ternary complex was formed.	NAD	86-90	malic enzyme 1	Homo sapiens	65-85
21826702-1	2011	The mammalian nicotinamide-adenine dinucleotide (NAD)-dependent deacetylase Sirt1 impacts different processes involved in the maintenance of brain integrity and in the pathogenic pathways associated with several neurodegenerative disorders, including Alzheimer"s disease.	NAD	14-47	sirtuin 1	Homo sapiens	76-81
21826702-1	2011	The mammalian nicotinamide-adenine dinucleotide (NAD)-dependent deacetylase Sirt1 impacts different processes involved in the maintenance of brain integrity and in the pathogenic pathways associated with several neurodegenerative disorders, including Alzheimer"s disease.	NAD	49-52	sirtuin 1	Homo sapiens	76-81
22017869-1	2011	In mammals, the Sirtuins are composed of seven Sir2 orthologs (Sirt1-7) with a conserved deacetylase core that utilizes NAD(+) as a cofactor.	NAD	120-126	sirtuin 1	Homo sapiens	47-51
1158861-14	1975	When fluorescence titrations were used to monitor the ability of cytoplasmic malate dehydrogenase to form a binary complex with NADH and to form a ternary complex with NADH and hydroxymalonate, only the formation of ternary complex seemed to be effected by arginine modification.	NAD	128-132	malic enzyme 1	Homo sapiens	77-97
22017869-1	2011	In mammals, the Sirtuins are composed of seven Sir2 orthologs (Sirt1-7) with a conserved deacetylase core that utilizes NAD(+) as a cofactor.	NAD	120-126	sirtuin 1	Homo sapiens	63-68
1158861-14	1975	When fluorescence titrations were used to monitor the ability of cytoplasmic malate dehydrogenase to form a binary complex with NADH and to form a ternary complex with NADH and hydroxymalonate, only the formation of ternary complex seemed to be effected by arginine modification.	NAD	168-172	malic enzyme 1	Homo sapiens	77-97
21982712-2	2011	One such pathway is mediated by nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme in mammalian NAD(+) biosynthesis, and the NAD(+)-dependent protein deacetylase SIRT1.	NAD	118-124	sirtuin 1	Homo sapiens	184-189
21982712-2	2011	One such pathway is mediated by nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme in mammalian NAD(+) biosynthesis, and the NAD(+)-dependent protein deacetylase SIRT1.	NAD	147-153	sirtuin 1	Homo sapiens	184-189
1216963-0	1975	[Proceedings: Influence of phospholipids and membrane structure on enzyme activity of NADH: mondehydroascorbate oxidoreductase].	NAD	86-90	thioredoxin reductase 1	Homo sapiens	112-127
172159-8	1975	It is also shown that the NAD radical which appears in the course of this reaction reduces the peroxidase; the rate constant of this process is (5 +/- 0,5) -10(4) M-1 sec-1.	NAD	26-29	secretory blood group 1, pseudogene	Homo sapiens	167-172
21836635-1	2011	The nicotinamide adenine dinucleotide (NAD(+))-dependent deacetylase SIRT1 is a major metabolic regulator activated by energy stresses such as fasting or calorie restriction.	NAD	4-37	sirtuin 1	Homo sapiens	69-74
21836635-1	2011	The nicotinamide adenine dinucleotide (NAD(+))-dependent deacetylase SIRT1 is a major metabolic regulator activated by energy stresses such as fasting or calorie restriction.	NAD	39-46	sirtuin 1	Homo sapiens	69-74
21836635-2	2011	SIRT1 activation during fasting not only relies on the increase in the NAD(+)/NADH ratio caused by energy deprivation but also involves an upregulation of SIRT1 mRNA and protein levels in various metabolic tissues.	NAD	71-77	sirtuin 1	Homo sapiens	0-5
21836635-2	2011	SIRT1 activation during fasting not only relies on the increase in the NAD(+)/NADH ratio caused by energy deprivation but also involves an upregulation of SIRT1 mRNA and protein levels in various metabolic tissues.	NAD	78-82	sirtuin 1	Homo sapiens	0-5
1058474-4	1975	Generation of MCAF depends on prior interaction of cholera toxin with either dithiothreitol, NADH, NAD, or a low-molecular-weight component (less than 700 daltons) present in cytoplasm.	NAD	93-97	chemokine (C-C motif) ligand 2	Mus musculus	14-18
21565994-2	2011	We hypothesized that lack of LDHC disrupts glycolysis by feedback inhibition, either by causing a defect in renewal of the NAD(+) cofactor essential for activity of glyceraldehyde 3-phosphate dehydrogenase, sperm (GAPDHS), or an accumulation of pyruvate.	NAD	123-129	lactate dehydrogenase C	Mus musculus	29-33
21565994-2	2011	We hypothesized that lack of LDHC disrupts glycolysis by feedback inhibition, either by causing a defect in renewal of the NAD(+) cofactor essential for activity of glyceraldehyde 3-phosphate dehydrogenase, sperm (GAPDHS), or an accumulation of pyruvate.	NAD	123-129	glyceraldehyde-3-phosphate dehydrogenase	Mus musculus	165-205
1058474-4	1975	Generation of MCAF depends on prior interaction of cholera toxin with either dithiothreitol, NADH, NAD, or a low-molecular-weight component (less than 700 daltons) present in cytoplasm.	NAD	93-96	chemokine (C-C motif) ligand 2	Mus musculus	14-18
21565994-4	2011	We found that in sperm lacking LDHC, glucose consumption was disrupted, but the NAD:NADH ratio and pyruvate levels were unchanged, and pyruvate was rapidly metabolized to lactate.	NAD	80-83	lactate dehydrogenase C	Mus musculus	31-35
1058474-5	1975	Subsequent exposure of this pretreated cholera toxin to cell membranes from a variety of mouse ascites cancer cells is followed rapidly by the appearance of MCAF, which no longer requires dithiothreitol, NADH, or NAD for the activation of adenylate cyclase.	NAD	204-208	chemokine (C-C motif) ligand 2	Mus musculus	157-161
21565994-4	2011	We found that in sperm lacking LDHC, glucose consumption was disrupted, but the NAD:NADH ratio and pyruvate levels were unchanged, and pyruvate was rapidly metabolized to lactate.	NAD	84-88	lactate dehydrogenase C	Mus musculus	31-35
1058474-5	1975	Subsequent exposure of this pretreated cholera toxin to cell membranes from a variety of mouse ascites cancer cells is followed rapidly by the appearance of MCAF, which no longer requires dithiothreitol, NADH, or NAD for the activation of adenylate cyclase.	NAD	204-207	chemokine (C-C motif) ligand 2	Mus musculus	157-161
167830-1	1975	The binding of NAD+, NADH and adenosine diphosphoribose (Ado-PP-Rib) to a stable, highly active and nucleotide-free preparation of rabbit muscle glyceraldehyde-3-phosphate dehydrogenase (D-glyceraldehyde-3-phosphate: NAD+ oxidoreductase (phosphorylating), EC 1.2.1.12) has been studied.	NAD	15-19	glyceraldehyde-3-phosphate dehydrogenase	Oryctolagus cuniculus	145-185
21677689-1	2011	The NAD(+)-dependent deacetylase, sirtuin 1 (SIRT1), has been recently been suspected to have a role in tumorigenesis.	NAD	4-10	sirtuin 1	Homo sapiens	34-43
21677689-1	2011	The NAD(+)-dependent deacetylase, sirtuin 1 (SIRT1), has been recently been suspected to have a role in tumorigenesis.	NAD	4-10	sirtuin 1	Homo sapiens	45-50
21188613-3	2011	Under fermentative conditions yeast reoxidizes excess NADH through glycerol production which involves NADH-dependent glycerol-3-phosphate dehydrogenases (Gpd1p and Gpd2p).	NAD	54-58	glycerol-3-phosphate dehydrogenase (NAD(+)) GPD1	Saccharomyces cerevisiae S288C	154-159
167830-1	1975	The binding of NAD+, NADH and adenosine diphosphoribose (Ado-PP-Rib) to a stable, highly active and nucleotide-free preparation of rabbit muscle glyceraldehyde-3-phosphate dehydrogenase (D-glyceraldehyde-3-phosphate: NAD+ oxidoreductase (phosphorylating), EC 1.2.1.12) has been studied.	NAD	21-25	glyceraldehyde-3-phosphate dehydrogenase	Oryctolagus cuniculus	145-185
235764-2	1975	Both NADPH and HADH were capable of acting as cofactors for the reduction of GSSG and the following kinetic values were obtained: Km, GSSG = 120 muM; Km, NADPH = 37 muM; Vmax = 23 mumoles NADPH/min/mg protein, Km, NADH = 420 muM; Vmax = 3 mumoles NADH/min/mg protein.	NAD	214-218	hydroxyacyl-coenzyme A dehydrogenase, mitochondrial	Oryctolagus cuniculus	15-19
21188613-3	2011	Under fermentative conditions yeast reoxidizes excess NADH through glycerol production which involves NADH-dependent glycerol-3-phosphate dehydrogenases (Gpd1p and Gpd2p).	NAD	102-106	glycerol-3-phosphate dehydrogenase (NAD(+)) GPD1	Saccharomyces cerevisiae S288C	154-159
21188613-5	2011	We investigated the possibility of converting this excess NADH to NAD(+) by transforming a double mutant (gpd1 gpd2 ) with alternative oxidoreductase genes that might restore the redox balance and produce either sorbitol or propane-1,2-diol.	NAD	58-62	glycerol-3-phosphate dehydrogenase (NAD(+)) GPD1	Saccharomyces cerevisiae S288C	106-110
235764-2	1975	Both NADPH and HADH were capable of acting as cofactors for the reduction of GSSG and the following kinetic values were obtained: Km, GSSG = 120 muM; Km, NADPH = 37 muM; Vmax = 23 mumoles NADPH/min/mg protein, Km, NADH = 420 muM; Vmax = 3 mumoles NADH/min/mg protein.	NAD	247-251	hydroxyacyl-coenzyme A dehydrogenase, mitochondrial	Oryctolagus cuniculus	15-19
21188613-5	2011	We investigated the possibility of converting this excess NADH to NAD(+) by transforming a double mutant (gpd1 gpd2 ) with alternative oxidoreductase genes that might restore the redox balance and produce either sorbitol or propane-1,2-diol.	NAD	66-72	glycerol-3-phosphate dehydrogenase (NAD(+)) GPD1	Saccharomyces cerevisiae S288C	106-110
4152749-0	1974	A nicotinamide-adenine dinucleotide assay utilizing liver alcohol dehydrogenase.	NAD	2-35	aldo-keto reductase family 1 member A1	Homo sapiens	58-79
21652783-2	2011	We previously showed that resveratrol (3,5,4"-trihydroxy-trans-stilbene), an antioxidant and activator of the NAD(+)-dependent protein deacetylase SIRT1, delays the progression of heart failure and prolongs the lifespan of delta-sarcoglycan-deficient hamsters.	NAD	110-116	sarcoglycan, delta (dystrophin-associated glycoprotein)	Mus musculus	223-240
21477609-9	2011	Decreased Cyclin D1 and increased CyclinD1/CDK inhibitors p21 and p27 levels in DPN/letrozole treated tumors were observed, suggesting that the combination treatment may inhibit tumor growth by blocking G1/S phase cell cycle progression.	NAD	80-83	cyclin D1	Mus musculus	34-42
21477609-9	2011	Decreased Cyclin D1 and increased CyclinD1/CDK inhibitors p21 and p27 levels in DPN/letrozole treated tumors were observed, suggesting that the combination treatment may inhibit tumor growth by blocking G1/S phase cell cycle progression.	NAD	80-83	cyclin-dependent kinase inhibitor 1A (P21)	Mus musculus	58-61
4366080-0	1973	Conformation of nicotinamide adenine dinucleotide bound to cytoplasmic malate dehydrogenase.	NAD	16-49	malic enzyme 1	Homo sapiens	71-91
21477609-9	2011	Decreased Cyclin D1 and increased CyclinD1/CDK inhibitors p21 and p27 levels in DPN/letrozole treated tumors were observed, suggesting that the combination treatment may inhibit tumor growth by blocking G1/S phase cell cycle progression.	NAD	80-83	cyclin-dependent kinase inhibitor 1B	Mus musculus	66-69
21715639-7	2011	The underlying mechanisms for this shift in differentiation direction involve the astrogenesis promoting Sirt1 via an increased NAD/NADH ratio in ogg1(-/-) cells.	NAD	128-131	8-oxoguanine DNA-glycosylase 1	Mus musculus	146-150
21715639-7	2011	The underlying mechanisms for this shift in differentiation direction involve the astrogenesis promoting Sirt1 via an increased NAD/NADH ratio in ogg1(-/-) cells.	NAD	132-136	8-oxoguanine DNA-glycosylase 1	Mus musculus	146-150
4345616-0	1972	Determination of serum guanase by means of a NADH-linked reaction.	NAD	45-49	guanine deaminase	Homo sapiens	23-30
21658598-2	2011	(2011) show here that the NAD(+)-dependent SIRT1 (H4K16; H1K26) deacetylase acts in concert with the LSD1 (H3K4) demethylase to repress Notch-induced transcription, thus coupling two distinct histone modifications at a key epigenetic switch for Notch target genes.	NAD	26-32	sirtuin 1	Homo sapiens	43-48
4337572-0	1972	[Semidehydro-D(-)-ascorbic acid as a substrate of microsomal NADH: semidehydroascorbate oxidoreductase (EC 1.6.5.4)].	NAD	61-65	thioredoxin reductase 1	Homo sapiens	88-102
21658598-2	2011	(2011) show here that the NAD(+)-dependent SIRT1 (H4K16; H1K26) deacetylase acts in concert with the LSD1 (H3K4) demethylase to repress Notch-induced transcription, thus coupling two distinct histone modifications at a key epigenetic switch for Notch target genes.	NAD	26-32	lysine demethylase 1A	Homo sapiens	101-105
4326162-0	1971	The binding of NAD+ to rabbit muscle glyceraldehyde-3-phosphate dehydrogenase studied by protein fluorescence quenching.	NAD	15-19	glyceraldehyde-3-phosphate dehydrogenase	Oryctolagus cuniculus	37-77
21328323-3	2011	A novel enzyme-coupled NADH-recycling system is proposed based on the concurrent oxidation of a sacrificial sec-alcohol catalyzed by an alcohol dehydrogenase (ADH-A).	NAD	23-27	aldo-keto reductase family 1 member A1	Homo sapiens	136-157
21328323-3	2011	A novel enzyme-coupled NADH-recycling system is proposed based on the concurrent oxidation of a sacrificial sec-alcohol catalyzed by an alcohol dehydrogenase (ADH-A).	NAD	23-27	aldo-keto reductase family 1 member A1	Homo sapiens	159-164
5543874-0	1971	Electrophoretic and functional variants of NADH-methemoglobin reductase in hereditary methemoglobinemia.	NAD	43-47	hemoglobin subunit gamma 2	Homo sapiens	48-61
5543874-4	1971	Precise correlations between levels of NADH-methemoglobin reductase activity, electrophoretic mobility, and clinical severity of methemoglobinemia, however, could not be drawn.	NAD	39-43	hemoglobin subunit gamma 2	Homo sapiens	44-57
21054562-1	2011	A longevity gene product, Sir2 (silent information regulator 2) is a NAD-dependent histone deacetylase involved in longevity in yeasts, worms and flies.	NAD	69-72	sirtuin 1	Homo sapiens	26-30
4318766-0	1970	A reduced nicotinamide adenine dinucleotide--linked kinetic assay for adenosine deaminase activity.	NAD	10-43	adenosine deaminase	Homo sapiens	70-89
4320046-1	1970	THE GLYCERIDE GLYCEROL ANALYSIS DEPENDS, AFTER SAPONIFICATION OF TRIGLYCERIDES, ON A LINKED ENZYMATIC PROCEDURE USING GLYCEROKINASE, PYRUVATE KINASE, AND LACTATE DEHYDROGENASE: the final conversion of NADH to NAD(+) is followed fluorimetrically.	NAD	201-205	glycerol kinase	Homo sapiens	118-131
21454709-1	2011	The NAD-dependent histone deacetylase Sirt1 is a negative regulator of T cell activation.	NAD	4-7	sirtuin 1	Homo sapiens	38-43
4320046-1	1970	THE GLYCERIDE GLYCEROL ANALYSIS DEPENDS, AFTER SAPONIFICATION OF TRIGLYCERIDES, ON A LINKED ENZYMATIC PROCEDURE USING GLYCEROKINASE, PYRUVATE KINASE, AND LACTATE DEHYDROGENASE: the final conversion of NADH to NAD(+) is followed fluorimetrically.	NAD	209-215	glycerol kinase	Homo sapiens	118-131
21589930-0	2011	Nrt1 and Tna1-independent export of NAD+ precursor vitamins promotes NAD+ homeostasis and allows engineering of vitamin production.	NAD	36-40	Tna1p	Saccharomyces cerevisiae S288C	9-13
21589930-0	2011	Nrt1 and Tna1-independent export of NAD+ precursor vitamins promotes NAD+ homeostasis and allows engineering of vitamin production.	NAD	69-73	Tna1p	Saccharomyces cerevisiae S288C	9-13
4308723-0	1969	The rates of binding of reduced nicotinamide-adenine dinucleotide analogs to liver alcohol dehydrogenase.	NAD	32-65	aldo-keto reductase family 1 member A1	Homo sapiens	83-104
4385432-3	1968	In the presence of microsomal fraction fortified with NAD(+), cholest-5-ene-3beta,7alpha-diol was converted into 7alpha-hydroxycholest-4-en-3-one, and when this fraction was fortified with NADPH small amounts of cholest-5-ene-3beta-7alpha,12alpha-triol were formed.	NAD	54-60	2,4-dienoyl-CoA reductase 1	Homo sapiens	189-194
4296126-0	1968	The relationship of NADH-dependent diaphorase activity and methemoglobin reduction in human erythrocytes.	NAD	20-24	hemoglobin subunit gamma 2	Homo sapiens	59-72
21409597-1	2011	Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) plays an essential role in glycolysis by catalyzing the conversion of D-glyceraldehyde 3-phosphate (D-G3P) to 1,3-diphosphoglycerate using NAD(+) as a cofactor.	NAD	188-194	phosphorylating glyceraldehyde-3-phosphate dehydrogenase	Thermococcus kodakarensis KOD1	0-40
21409597-1	2011	Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) plays an essential role in glycolysis by catalyzing the conversion of D-glyceraldehyde 3-phosphate (D-G3P) to 1,3-diphosphoglycerate using NAD(+) as a cofactor.	NAD	188-194	phosphorylating glyceraldehyde-3-phosphate dehydrogenase	Thermococcus kodakarensis KOD1	42-47
21409597-4	2011	GAPDH-tk is a thermostable protein with a half-life of 5 h at 80-90 C. The apparent K (m) values for NAD(+) and D-G3P were 77.8 +- 7.5 muM and 49.3 +- 3.0 muM, respectively, with V (max) values of 45.1 +- 0.8 U/mg and 59.6 +- 1.3 U/mg, respectively.	NAD	101-107	phosphorylating glyceraldehyde-3-phosphate dehydrogenase	Thermococcus kodakarensis KOD1	0-5
4291964-0	1967	The binding of NADH to liver alcohol dehydrogenase: a two step reaction.	NAD	15-19	aldo-keto reductase family 1 member A1	Homo sapiens	29-50
21401809-5	2011	Furthermore, we show that in the absence of other proteins Hst3 and Hst4 can deacetylate nucleosomal histone H3-K56 in a nicotinamide adenine dinucleotide(NAD)(+) -dependent manner.	NAD	121-154	NAD-dependent histone deacetylase HST4	Saccharomyces cerevisiae S288C	68-72
21401809-5	2011	Furthermore, we show that in the absence of other proteins Hst3 and Hst4 can deacetylate nucleosomal histone H3-K56 in a nicotinamide adenine dinucleotide(NAD)(+) -dependent manner.	NAD	155-158	NAD-dependent histone deacetylase HST4	Saccharomyces cerevisiae S288C	68-72
4291356-6	1966	Michaelis constants for NAD formation, measured in a coupled assay with NMN adenylyltransferase and alcohol dehydrogenase at pH8.0 and 25 degrees , in the presence of 3mm concentrations of the unvaried reactants, were 88+/-7mum-ATP, 42+/-4mum-NMN and 85+/-4mum-Mg(2+).	NAD	24-27	aldo-keto reductase family 1 member A1	Sus scrofa	100-121
14087322-0	1963	LIVER ALCOHOL DEHYDROGENASE-DPN-PYRAZOLE COMPLEX: A MODEL OF A TERNARY INTERMEDIATE IN THE ENZYME REACTION.	NAD	28-31	aldo-keto reductase family 1 member A1	Homo sapiens	6-27
20522127-7	2011	The mode of action of MXC and HPTE on 3beta-HSD activity was non-competitive with the substrate pregnenolone, but was competitive with the cofactor NAD(+) .	NAD	148-154	hydroxy-delta-5-steroid dehydrogenase, 3 beta- and steroid delta-isomerase 1	Homo sapiens	38-47
21245135-0	2011	NAD+-dependent SIRT1 deacetylase participates in epigenetic reprogramming during endotoxin tolerance.	NAD	0-4	sirtuin 1	Homo sapiens	15-20
21245135-3	2011	After TLR4 signaling, SIRT1 rapidly accumulated at the promoters of TNF-alpha and IL-1beta, but not IkappaBalpha; SIRT1 promoter binding was dependent on its co-factor, NAD(+).	NAD	169-175	sirtuin 1	Homo sapiens	22-27
21245135-3	2011	After TLR4 signaling, SIRT1 rapidly accumulated at the promoters of TNF-alpha and IL-1beta, but not IkappaBalpha; SIRT1 promoter binding was dependent on its co-factor, NAD(+).	NAD	169-175	sirtuin 1	Homo sapiens	114-119
21245135-10	2011	We conclude that TLR4 stimulation and human sepsis activate pathways that couple NAD(+) and its sensor SIRT1 with epigenetic reprogramming.	NAD	81-87	sirtuin 1	Homo sapiens	103-108
13719494-0	1961	An inhibitor of liver alcohol dehydrogenase in preparations of reduced diphosphopyridine nucleotide.	NAD	71-99	aldo-keto reductase family 1 member A1	Homo sapiens	22-43
21406402-8	2011	Importantly, we find that the combination of BER and NAD(+) biosynthesis inhibition significantly sensitizes glioma cells with elevated expression of MGMT and those deficient in MMR, two genotypes normally associated with TMZ resistance.	NAD	53-59	O-6-methylguanine-DNA methyltransferase	Homo sapiens	150-154
34059674-4	2021	The acetyltransferase MYST1 stimulated by Acetyl-CoA, and the deacetylase SIRT2 stimulated by NAD +, are identified as direct regulators of PAX7 acetylation and asymmetric division in muscle stem cells.	NAD	94-99	paired box 7	Mus musculus	140-144
33988989-4	2021	The HD-CNTf rod mu-ES has been evaluated by electrochemical determination of biologically important analytes, i.e., dopamine (DA), beta-nicotinamide adenine dinucleotide (NADH), a diuretic drug, i.e., furosemide, and a heavy metal, i.e., lead ions (Pb2+).	NAD	171-175	ciliary neurotrophic factor	Homo sapiens	7-11
20816746-1	2011	The P450cam monooxygenase system consists of three separate proteins: the FAD-containing, NADH-dependent oxidoreductase (putidaredoxin reductase or Pdr), cytochrome P450cam and the 2Fe2S ferredoxin (putidaredoxin or Pdx), which transfers electrons from Pdr to P450cam.	NAD	90-94	PDR	Homo sapiens	148-151
20816746-1	2011	The P450cam monooxygenase system consists of three separate proteins: the FAD-containing, NADH-dependent oxidoreductase (putidaredoxin reductase or Pdr), cytochrome P450cam and the 2Fe2S ferredoxin (putidaredoxin or Pdx), which transfers electrons from Pdr to P450cam.	NAD	90-94	PDR	Homo sapiens	253-256
33709773-13	2021	Restoring mitochondrial metabolism with the NAD precursor nicotinamide riboside (NR) rapidly reverses aortic aneurysm in Fbn1c1039g/+ mice.	NAD	44-47	fibrillin 1	Mus musculus	121-125
21390332-7	2011	GR resulted in an increased expression of SIRT1, a NAD-dependent histone deacetylase, which has positive correlation with CR-induced longevity.	NAD	51-54	sirtuin 1	Homo sapiens	42-47
34029951-15	2021	We demonstrated that R1 promotes post-stroke angiogenesis via activating NAMPT-NAD+-SIRT1 cascade.	NAD	79-83	sirtuin 1	Homo sapiens	84-89
21170645-3	2011	A major role of mammalian TDO is to supply nicotinamide adenine dinucleotide (NAD(+)).	NAD	43-76	tryptophan 2,3-dioxygenase	Homo sapiens	26-29
21170645-3	2011	A major role of mammalian TDO is to supply nicotinamide adenine dinucleotide (NAD(+)).	NAD	78-84	tryptophan 2,3-dioxygenase	Homo sapiens	26-29
21170645-4	2011	In fungi, the IDO homologue is thought to be expressed constitutively and supply NAD(+), as TDO is absent from their genomes.	NAD	81-87	tryptophan 2,3-dioxygenase	Homo sapiens	92-95
34040894-3	2021	A decreased level of Nicotinamide phosphoribosyltransferase (Nampt)-an important enzyme in the salvage pathway of NAD+ synthesis-has been found under certain pathological conditions, while the mechanisms underlying the Nampt decrease are unclear.	NAD	114-118	nicotinamide phosphoribosyltransferase	Rattus norvegicus	21-59
21245319-1	2011	Numerous studies indicate that Sirtuin 1 (SIRT1), a mammalian nicotinamide adenine dinucleotide (NAD(+))-dependent histone deacetylase (HDAC), plays a crucial role in p53-mediated stress responses by deacetylating p53.	NAD	62-95	sirtuin 1	Homo sapiens	31-40
21245319-1	2011	Numerous studies indicate that Sirtuin 1 (SIRT1), a mammalian nicotinamide adenine dinucleotide (NAD(+))-dependent histone deacetylase (HDAC), plays a crucial role in p53-mediated stress responses by deacetylating p53.	NAD	62-95	sirtuin 1	Homo sapiens	42-47
21245319-1	2011	Numerous studies indicate that Sirtuin 1 (SIRT1), a mammalian nicotinamide adenine dinucleotide (NAD(+))-dependent histone deacetylase (HDAC), plays a crucial role in p53-mediated stress responses by deacetylating p53.	NAD	62-95	histone deacetylase 9	Homo sapiens	115-134
21245319-1	2011	Numerous studies indicate that Sirtuin 1 (SIRT1), a mammalian nicotinamide adenine dinucleotide (NAD(+))-dependent histone deacetylase (HDAC), plays a crucial role in p53-mediated stress responses by deacetylating p53.	NAD	62-95	histone deacetylase 9	Homo sapiens	136-140
21245319-1	2011	Numerous studies indicate that Sirtuin 1 (SIRT1), a mammalian nicotinamide adenine dinucleotide (NAD(+))-dependent histone deacetylase (HDAC), plays a crucial role in p53-mediated stress responses by deacetylating p53.	NAD	97-103	sirtuin 1	Homo sapiens	31-40
21245319-1	2011	Numerous studies indicate that Sirtuin 1 (SIRT1), a mammalian nicotinamide adenine dinucleotide (NAD(+))-dependent histone deacetylase (HDAC), plays a crucial role in p53-mediated stress responses by deacetylating p53.	NAD	97-103	sirtuin 1	Homo sapiens	42-47
21245319-1	2011	Numerous studies indicate that Sirtuin 1 (SIRT1), a mammalian nicotinamide adenine dinucleotide (NAD(+))-dependent histone deacetylase (HDAC), plays a crucial role in p53-mediated stress responses by deacetylating p53.	NAD	97-103	histone deacetylase 9	Homo sapiens	115-134
34040894-3	2021	A decreased level of Nicotinamide phosphoribosyltransferase (Nampt)-an important enzyme in the salvage pathway of NAD+ synthesis-has been found under certain pathological conditions, while the mechanisms underlying the Nampt decrease are unclear.	NAD	114-118	nicotinamide phosphoribosyltransferase	Rattus norvegicus	61-66
34040894-3	2021	A decreased level of Nicotinamide phosphoribosyltransferase (Nampt)-an important enzyme in the salvage pathway of NAD+ synthesis-has been found under certain pathological conditions, while the mechanisms underlying the Nampt decrease are unclear.	NAD	114-118	nicotinamide phosphoribosyltransferase	Rattus norvegicus	219-224
34040894-4	2021	The purpose of this study is to test the hypothesis that oxidative stress can produce decreased Nampt, and to investigate the biological effects of Nampt on NAD+ synthesis and cell survival under both basal and oxidative stress conditions.	NAD	157-161	nicotinamide phosphoribosyltransferase	Rattus norvegicus	148-153
34040894-8	2021	Collectively, our study has indicated that oxidative stress is a pathological factor leading to decreased Nampt, which plays important roles in oxidative stress-produced decreases in NAD+ levels and cell survival.	NAD	183-187	nicotinamide phosphoribosyltransferase	Rattus norvegicus	106-111
21245319-1	2011	Numerous studies indicate that Sirtuin 1 (SIRT1), a mammalian nicotinamide adenine dinucleotide (NAD(+))-dependent histone deacetylase (HDAC), plays a crucial role in p53-mediated stress responses by deacetylating p53.	NAD	97-103	histone deacetylase 9	Homo sapiens	136-140
34040894-9	2021	Our findings have indicated major roles of Nampt in maintaining NAD+ levels and cell survival under both basal and oxidative stress conditions.	NAD	64-68	nicotinamide phosphoribosyltransferase	Rattus norvegicus	43-48
33957971-14	2021	CONCLUSION: This study identifies a significant role of miR-34a playing in MSC replicative senescence and natural senescence via targeting Nampt and further mediating by NAD+-Sirt1 pathway, carrying great implications for optimal strategies for MSC therapeutic applications.	NAD	170-174	sirtuin 1	Homo sapiens	175-180
21130087-1	2011	One of the functions mediated by sirtuin 1 (SIRT1), the NAD(+)-dependent protein deacetylase, has been suggested to be neuroprotective since resveratrol, a SIRT1 activator, inhibits 1-methyl-4-phenylpyridinium ion (MPP(+))-induced cytotoxicity.	NAD	56-62	sirtuin 1	Homo sapiens	33-42
33749979-5	2021	Moreover, SIRT7 interacts with KCC4 in a NAD+ -dependent manner and increases its stability and activity in HEK293 cells.	NAD	41-45	sirtuin 7	Homo sapiens	10-15
21130087-1	2011	One of the functions mediated by sirtuin 1 (SIRT1), the NAD(+)-dependent protein deacetylase, has been suggested to be neuroprotective since resveratrol, a SIRT1 activator, inhibits 1-methyl-4-phenylpyridinium ion (MPP(+))-induced cytotoxicity.	NAD	56-62	sirtuin 1	Homo sapiens	44-49
21130087-1	2011	One of the functions mediated by sirtuin 1 (SIRT1), the NAD(+)-dependent protein deacetylase, has been suggested to be neuroprotective since resveratrol, a SIRT1 activator, inhibits 1-methyl-4-phenylpyridinium ion (MPP(+))-induced cytotoxicity.	NAD	56-62	sirtuin 1	Homo sapiens	156-161
21691086-0	2011	NAD blocks high glucose induced mesangial hypertrophy via activation of the sirtuins-AMPK-mTOR pathway.	NAD	0-3	mechanistic target of rapamycin kinase	Rattus norvegicus	90-94
21691086-8	2011	Activating Sirtuins by NAD blocked the activation of pro-hypertrophic Akt signaling, and augmented the activity of the antihypertrophic AMPK signaling in MCs, which prevented the subsequent induction of mTOR-mediated protein synthesis.	NAD	23-26	mechanistic target of rapamycin kinase	Rattus norvegicus	203-207
33978360-6	2021	SIRT1 is an NAD-dependent deacetylase that has a role in regulation of metabolic activities.	NAD	12-15	sirtuin 1	Homo sapiens	0-5
22179986-6	2011	A search for the histone deacetylase (HDAC) that counterbalanced CLOCK activity revealed that SIRT1, a nicotinamide adenine dinucleotide (NAD(+))-dependent HDAC, functions in a circadian manner.	NAD	103-136	sirtuin 1	Homo sapiens	94-99
22179986-6	2011	A search for the histone deacetylase (HDAC) that counterbalanced CLOCK activity revealed that SIRT1, a nicotinamide adenine dinucleotide (NAD(+))-dependent HDAC, functions in a circadian manner.	NAD	138-145	sirtuin 1	Homo sapiens	94-99
21785227-6	2011	TRPM channels (TRPM2, TRPM4 and TRPM5) control insulin secretion levels by sensing intracellular Ca2+ increase, NAD metabolites, or hormone receptor activation.	NAD	112-115	transient receptor potential cation channel subfamily M member 2	Homo sapiens	15-20
20981034-6	2011	A major source for cardiovascular, renal and neural ROS is a family of non-phagocytic nicotinamide adenine dinucleotide phosphate (NADPH) oxidases (Nox), including the prototypic Nox2 homolog-based NADPH oxidase, as well as other Noxes, such as Nox1 and Nox4.	NAD	86-119	cytochrome b-245 beta chain	Homo sapiens	179-183
21031461-10	2011	These data suggest that high-glucose-induced PARP1 activation might play a role in glucose toxicity by down-regulating SIRT1 and AMPK activity through NAD depletion and resulting in insulin insensitivity.	NAD	151-154	sirtuin 1	Homo sapiens	119-124
22180829-1	2011	NAD-dependent Class III histone deacetylase SIRT1 is a multiple functional protein and has been demonstrated critically involved in stress response, cellular metabolism and aging through deacetylating variety of substrates including p53, forkhead transcription factors, PGC-1alpha, NF-kappaB, Ku70 and histones.	NAD	0-3	sirtuin 1	Homo sapiens	44-49
22180829-1	2011	NAD-dependent Class III histone deacetylase SIRT1 is a multiple functional protein and has been demonstrated critically involved in stress response, cellular metabolism and aging through deacetylating variety of substrates including p53, forkhead transcription factors, PGC-1alpha, NF-kappaB, Ku70 and histones.	NAD	0-3	X-ray repair cross complementing 6	Homo sapiens	293-297
21314614-0	2010	Novel inhibitors of glyceraldehyde-3-phosphate dehydrogenase: covalent modification of NAD-binding site by aromatic thiols.	NAD	87-90	glyceraldehyde-3-phosphate dehydrogenase	Oryctolagus cuniculus	20-60
21314614-3	2010	Potential GAPDH inhibitors were screened in silico, and three compounds with high affinity to the NAD-binding site and theoretically capable of forming a disulfide bond with amino acid residue Cys149 were found among cysteine and glutathione derivatives.	NAD	98-101	glyceraldehyde-3-phosphate dehydrogenase	Oryctolagus cuniculus	10-15
21428798-1	2010	BACKGROUND: SRT1720 and SRT2183 were described recently as activators of the NAD+-dependent deacetylase, SIRT1.	NAD	77-80	sirtuin 1	Homo sapiens	105-110
20935547-2	2010	To achieve this goal, we have been studying mechanisms of mammalian aging and longevity, focusing on the physiological importance of the mammalian nicotinamide adenine dinucleotide (NAD)--dependent protein deacetylase SIRT1 and systemic NAD biosynthesis mediated by nicotinamide phosphoribosyltransferase for the regulation of metabolism and aging.	NAD	147-180	sirtuin 1	Homo sapiens	218-223
20935547-2	2010	To achieve this goal, we have been studying mechanisms of mammalian aging and longevity, focusing on the physiological importance of the mammalian nicotinamide adenine dinucleotide (NAD)--dependent protein deacetylase SIRT1 and systemic NAD biosynthesis mediated by nicotinamide phosphoribosyltransferase for the regulation of metabolism and aging.	NAD	182-185	sirtuin 1	Homo sapiens	218-223
20012353-9	2010	Apoptosis-inducing factor (Aif) expression was increased in DPN-treated tumors, while active caspase 9 was up-regulated in PPT-treated mice, demonstrating the involvement of the intrinsic apoptotic pathway in estrogen-induced regression in this model.	NAD	60-63	apoptosis-inducing factor, mitochondrion-associated 1	Mus musculus	0-25
20012353-9	2010	Apoptosis-inducing factor (Aif) expression was increased in DPN-treated tumors, while active caspase 9 was up-regulated in PPT-treated mice, demonstrating the involvement of the intrinsic apoptotic pathway in estrogen-induced regression in this model.	NAD	60-63	apoptosis-inducing factor, mitochondrion-associated 1	Mus musculus	27-30
20595677-4	2010	Mammalian SIRT1, the most extensively studied family member, couples protein deacetylation with NAD(+) hydrolysis and links cellular energy and redox state to multiple signaling and survival pathways.	NAD	96-102	sirtuin 1	Homo sapiens	10-15
20813124-4	2010	NAD(+)-dependent histone deacetylase sirtuin1 (SIRT1) prolongs mammalian cellular lifespan.	NAD	0-6	sirtuin 1	Homo sapiens	37-45
20813124-4	2010	NAD(+)-dependent histone deacetylase sirtuin1 (SIRT1) prolongs mammalian cellular lifespan.	NAD	0-6	sirtuin 1	Homo sapiens	47-52
20813124-11	2010	Thus, NaDC3 promotes cellular senescence probably by inhibiting NAD(+)-dependent SIRT1.	NAD	64-70	sirtuin 1	Homo sapiens	81-86
20488443-6	2010	We then analyzed the gene expressions of HAECs, ESECs and iPSECs, and observed that the expression level of Sirt1, a nicotinamide adenine dinucleotide (NAD+)-dependent histone deacetylase, is higher in ESECs and iPSECs than in HAECs.	NAD	117-150	sirtuin 1	Homo sapiens	108-113
20488443-6	2010	We then analyzed the gene expressions of HAECs, ESECs and iPSECs, and observed that the expression level of Sirt1, a nicotinamide adenine dinucleotide (NAD+)-dependent histone deacetylase, is higher in ESECs and iPSECs than in HAECs.	NAD	152-155	sirtuin 1	Homo sapiens	108-113
20551293-3	2010	We first showed that morphine"s antinociceptive potency was increased by the intracerebroventricular injection of CD38 substrate beta-NAD(+) in mice.	NAD	129-140	CD38 antigen	Mus musculus	114-118
20638362-1	2010	CD38 is a multifunctional enzyme that has both ADP-ribosyl cyclase and cADPR hydrolase activities, being capable of cleaving NAD(+) to cyclic ADP ribose (cADPR) and hydrolyzing cADPR to ADPR.	NAD	125-131	CD38 antigen	Mus musculus	0-4
20638362-2	2010	It has been reported that there is markedly a reduction of cADPR and elevation of NAD in many tissues from CD38 knockout (CD38(-/-)) mice.	NAD	82-85	CD38 antigen	Mus musculus	107-111
20638362-2	2010	It has been reported that there is markedly a reduction of cADPR and elevation of NAD in many tissues from CD38 knockout (CD38(-/-)) mice.	NAD	82-85	CD38 antigen	Mus musculus	122-126
20638362-4	2010	We hypothesize that CD38 knockout may have a protective effect in oxidative stresses through elevating NAD and decreasing cADPR.	NAD	103-106	CD38 antigen	Mus musculus	20-24
20531298-6	2010	Recently, it became clear that the energy sensor, AMP-activated kinase (AMPK) translates the effects of energy stress into altered Sirt1 activity by regulating the intracellular level of its co-substrate nicotinamide adenine dinucleotide (NAD)(+).	NAD	204-237	sirtuin 1	Homo sapiens	131-136
20506278-2	2010	Tat transactivating activity is controlled by nicotinamide adenine nucleotide(+) (NAD(+))-dependent deacetylase sirtuin 1 (SIRT1).	NAD	82-89	sirtuin 1	Homo sapiens	123-128
20506278-3	2010	Nicotinamide phosphoribosyltransferase (Nampt) is a rate-limiting enzyme in the conversion of nicotinamide into NAD(+), which is crucial for SIRT1 activation.	NAD	112-118	sirtuin 1	Homo sapiens	141-146
20689156-1	2010	SIRT1 is a NAD+-dependent deacetylase implicated in longevity and diverse physiological processes.	NAD	11-14	sirtuin 1	Homo sapiens	0-5
20739737-7	2010	Additionally, stimulation of the AMP-activated Protein Kinase concomitantly inhibited mTOR signaling and cell death, while neither event was affected by overexpression of the NAD+ dependent deacetylase Sirt-1, another cellular sensor of nutrient scarcity.	NAD	175-179	sirtuin 1	Homo sapiens	202-208
19897060-5	2010	More strikingly, we and others have discovered a novel circadian clock feedback loop in which both the rate-limiting enzyme in mammalian NAD biosynthesis, nicotinamide phosphoribosyltransferase (NAMPT), and NAD levels display circadian oscillations and modulate CLOCK:BMAL1-mediated circadian transcriptional regulation through SIRT1, demonstrating a new function of NAD as a "metabolic oscillator."	NAD	137-140	aryl hydrocarbon receptor nuclear translocator like	Homo sapiens	268-273
19897060-5	2010	More strikingly, we and others have discovered a novel circadian clock feedback loop in which both the rate-limiting enzyme in mammalian NAD biosynthesis, nicotinamide phosphoribosyltransferase (NAMPT), and NAD levels display circadian oscillations and modulate CLOCK:BMAL1-mediated circadian transcriptional regulation through SIRT1, demonstrating a new function of NAD as a "metabolic oscillator."	NAD	137-140	sirtuin 1	Homo sapiens	328-333
19897060-5	2010	More strikingly, we and others have discovered a novel circadian clock feedback loop in which both the rate-limiting enzyme in mammalian NAD biosynthesis, nicotinamide phosphoribosyltransferase (NAMPT), and NAD levels display circadian oscillations and modulate CLOCK:BMAL1-mediated circadian transcriptional regulation through SIRT1, demonstrating a new function of NAD as a "metabolic oscillator."	NAD	207-210	aryl hydrocarbon receptor nuclear translocator like	Homo sapiens	268-273
19897060-5	2010	More strikingly, we and others have discovered a novel circadian clock feedback loop in which both the rate-limiting enzyme in mammalian NAD biosynthesis, nicotinamide phosphoribosyltransferase (NAMPT), and NAD levels display circadian oscillations and modulate CLOCK:BMAL1-mediated circadian transcriptional regulation through SIRT1, demonstrating a new function of NAD as a "metabolic oscillator."	NAD	207-210	sirtuin 1	Homo sapiens	328-333
19897060-5	2010	More strikingly, we and others have discovered a novel circadian clock feedback loop in which both the rate-limiting enzyme in mammalian NAD biosynthesis, nicotinamide phosphoribosyltransferase (NAMPT), and NAD levels display circadian oscillations and modulate CLOCK:BMAL1-mediated circadian transcriptional regulation through SIRT1, demonstrating a new function of NAD as a "metabolic oscillator."	NAD	207-210	aryl hydrocarbon receptor nuclear translocator like	Homo sapiens	268-273
19897060-5	2010	More strikingly, we and others have discovered a novel circadian clock feedback loop in which both the rate-limiting enzyme in mammalian NAD biosynthesis, nicotinamide phosphoribosyltransferase (NAMPT), and NAD levels display circadian oscillations and modulate CLOCK:BMAL1-mediated circadian transcriptional regulation through SIRT1, demonstrating a new function of NAD as a "metabolic oscillator."	NAD	207-210	sirtuin 1	Homo sapiens	328-333
19897060-6	2010	These findings reveal a novel system dynamics of a recently proposed systemic regulatory network regulated by NAMPT-mediated NAD biosynthesis and SIRT1, namely, the NAD World.	NAD	165-168	sirtuin 1	Homo sapiens	146-151
33879006-5	2021	We used a spectrophotometric method, based on enzymatic oxidation of d-lactate by d-lactate dehydrogenase (D-LDH) coupled to the reduction of nicotinamide-adenine dinucleotide (NAD+).	NAD	177-181	lactate dehydrogenase D	Homo sapiens	82-105
33879006-5	2021	We used a spectrophotometric method, based on enzymatic oxidation of d-lactate by d-lactate dehydrogenase (D-LDH) coupled to the reduction of nicotinamide-adenine dinucleotide (NAD+).	NAD	177-181	lactate dehydrogenase D	Homo sapiens	107-112
33528041-6	2021	The expression of genes encoding for nicotinamide adenine dinucleotide (NAD+ ) biosynthetic enzymes-Nmnat3 and Nampt-and NAD+ levels were decreased, suggesting that NAD+ is essential for maintaining lysosomal acidification.	NAD	37-70	nicotinamide nucleotide adenylyltransferase 3	Mus musculus	100-106
33528041-6	2021	The expression of genes encoding for nicotinamide adenine dinucleotide (NAD+ ) biosynthetic enzymes-Nmnat3 and Nampt-and NAD+ levels were decreased, suggesting that NAD+ is essential for maintaining lysosomal acidification.	NAD	72-76	nicotinamide nucleotide adenylyltransferase 3	Mus musculus	100-106
33857309-5	2021	SIRT1, another energy sensor activated by NAD+ in nutrient-deficient states, is reciprocally activated by AMPK, and can deacetylate and activate transcription factors such as PCG-1alpha, TFAM and NRF2 that regulate mitochondrial biogenesis.	NAD	42-46	sirtuin 1	Homo sapiens	0-5
33935952-4	2021	Silence information regulator 1 (SIRT1), a nicotinamide adenine dinucleotide (NAD)-dependent histone deacetylase, also plays a critical role in PD development and might be a potential target for PD therapy.	NAD	43-76	sirtuin 1	Homo sapiens	0-31
33935952-4	2021	Silence information regulator 1 (SIRT1), a nicotinamide adenine dinucleotide (NAD)-dependent histone deacetylase, also plays a critical role in PD development and might be a potential target for PD therapy.	NAD	43-76	sirtuin 1	Homo sapiens	33-38
33935952-4	2021	Silence information regulator 1 (SIRT1), a nicotinamide adenine dinucleotide (NAD)-dependent histone deacetylase, also plays a critical role in PD development and might be a potential target for PD therapy.	NAD	78-81	sirtuin 1	Homo sapiens	0-31
33935952-4	2021	Silence information regulator 1 (SIRT1), a nicotinamide adenine dinucleotide (NAD)-dependent histone deacetylase, also plays a critical role in PD development and might be a potential target for PD therapy.	NAD	78-81	sirtuin 1	Homo sapiens	33-38
33854178-1	2021	The NAD+-dependent deacetylase SIRT1 controls key metabolic functions by deacetylating target proteins and strategies that promote SIRT1 function such as SIRT1 overexpression or NAD+ boosters alleviate metabolic complications.	NAD	4-8	sirtuin 1	Homo sapiens	31-36
33854178-1	2021	The NAD+-dependent deacetylase SIRT1 controls key metabolic functions by deacetylating target proteins and strategies that promote SIRT1 function such as SIRT1 overexpression or NAD+ boosters alleviate metabolic complications.	NAD	4-8	sirtuin 1	Homo sapiens	131-136
33854178-7	2021	Supplementing preadipocytes with the NAD+ booster nicotinamide mononucleotide (NMN) during differentiation increased expression levels of leptin, SIRT1, and PGC-1alpha and its transcriptional targets, and reduced levels of pro-fibrotic collagens (Col6A1 and Col6A3) in a SIRT1-dependent manner.	NAD	37-41	sirtuin 1	Homo sapiens	146-151
33854178-7	2021	Supplementing preadipocytes with the NAD+ booster nicotinamide mononucleotide (NMN) during differentiation increased expression levels of leptin, SIRT1, and PGC-1alpha and its transcriptional targets, and reduced levels of pro-fibrotic collagens (Col6A1 and Col6A3) in a SIRT1-dependent manner.	NAD	37-41	sirtuin 1	Homo sapiens	271-276
33920410-6	2021	We show here that overexpression of GCK inhibits the proliferation of HCC cells via induction of intracellular lactate accumulation and subsequently causes energy crisis due to NAD+ depletion.	NAD	177-181	glucokinase	Homo sapiens	36-39
33412125-7	2021	A survey of cAMP effectors revealed that only selective inhibition of exchange protein activated by cAMP 1 (Epac1), but not protein kinase A (PKA) or Epac2, suppressed complex I-dependent respiration and significantly increased the cytosolic NADH/NAD+ redox state.	NAD	242-246	Rap guanine nucleotide exchange factor 3	Homo sapiens	70-106
33412125-7	2021	A survey of cAMP effectors revealed that only selective inhibition of exchange protein activated by cAMP 1 (Epac1), but not protein kinase A (PKA) or Epac2, suppressed complex I-dependent respiration and significantly increased the cytosolic NADH/NAD+ redox state.	NAD	242-246	Rap guanine nucleotide exchange factor 3	Homo sapiens	108-113
33412125-7	2021	A survey of cAMP effectors revealed that only selective inhibition of exchange protein activated by cAMP 1 (Epac1), but not protein kinase A (PKA) or Epac2, suppressed complex I-dependent respiration and significantly increased the cytosolic NADH/NAD+ redox state.	NAD	247-251	Rap guanine nucleotide exchange factor 3	Homo sapiens	70-106
33412125-7	2021	A survey of cAMP effectors revealed that only selective inhibition of exchange protein activated by cAMP 1 (Epac1), but not protein kinase A (PKA) or Epac2, suppressed complex I-dependent respiration and significantly increased the cytosolic NADH/NAD+ redox state.	NAD	247-251	Rap guanine nucleotide exchange factor 3	Homo sapiens	108-113
33412125-9	2021	In conclusion, our study shows that, via the regulation of complex I-dependent mitochondrial respiration, sAC-Epac1 signaling regulates the cytosolic NADH/NAD+ redox state, and coordinates oxidative phosphorylation and glycolysis to maintain cellular energy homeostasis.	NAD	150-154	Rap guanine nucleotide exchange factor 3	Homo sapiens	110-115
33412125-9	2021	In conclusion, our study shows that, via the regulation of complex I-dependent mitochondrial respiration, sAC-Epac1 signaling regulates the cytosolic NADH/NAD+ redox state, and coordinates oxidative phosphorylation and glycolysis to maintain cellular energy homeostasis.	NAD	155-159	Rap guanine nucleotide exchange factor 3	Homo sapiens	110-115
33650791-3	2021	Previous reports suggest that ERalpha expression can be regulated by sirt1 (sirtuin 1), a nicotinamide adenine dinucleotide (NAD+)-dependent class III histone deacetylases that modulates activity of several substrates involved in cellular stress, metabolism, proliferation, senescence, protein degradation and apoptosis.	NAD	90-123	sirtuin 1	Homo sapiens	69-74
33650791-3	2021	Previous reports suggest that ERalpha expression can be regulated by sirt1 (sirtuin 1), a nicotinamide adenine dinucleotide (NAD+)-dependent class III histone deacetylases that modulates activity of several substrates involved in cellular stress, metabolism, proliferation, senescence, protein degradation and apoptosis.	NAD	90-123	sirtuin 1	Homo sapiens	76-85
33650791-3	2021	Previous reports suggest that ERalpha expression can be regulated by sirt1 (sirtuin 1), a nicotinamide adenine dinucleotide (NAD+)-dependent class III histone deacetylases that modulates activity of several substrates involved in cellular stress, metabolism, proliferation, senescence, protein degradation and apoptosis.	NAD	125-129	sirtuin 1	Homo sapiens	69-74
33650791-3	2021	Previous reports suggest that ERalpha expression can be regulated by sirt1 (sirtuin 1), a nicotinamide adenine dinucleotide (NAD+)-dependent class III histone deacetylases that modulates activity of several substrates involved in cellular stress, metabolism, proliferation, senescence, protein degradation and apoptosis.	NAD	125-129	sirtuin 1	Homo sapiens	76-85
33790300-6	2021	Mechanistically these "SLE-like" conditions increase CD8+ T cell NAD+ consumption resulting in impaired mitochondrial respiration and reduced cell viability, both of which can be rectified by NAD+ supplementation.	NAD	65-69	CD8a molecule	Homo sapiens	53-56
33790300-6	2021	Mechanistically these "SLE-like" conditions increase CD8+ T cell NAD+ consumption resulting in impaired mitochondrial respiration and reduced cell viability, both of which can be rectified by NAD+ supplementation.	NAD	192-196	CD8a molecule	Homo sapiens	53-56
33427354-6	2021	We successfully used NAD+ from the nanoreactors for the the continuous production of NAD+ to 1) sense glucose in an artificial glucose metabolism, and 2) to reduce the non-oxygen binding methemoglobin to oxygen-binding hemoglobin.	NAD	21-25	hemoglobin subunit gamma 2	Homo sapiens	187-200
33427354-6	2021	We successfully used NAD+ from the nanoreactors for the the continuous production of NAD+ to 1) sense glucose in an artificial glucose metabolism, and 2) to reduce the non-oxygen binding methemoglobin to oxygen-binding hemoglobin.	NAD	85-89	hemoglobin subunit gamma 2	Homo sapiens	187-200
33738675-4	2021	In mammals, sirtuin family comprises seven members (SIRT1-SIRT7), and they all possess a conserved NAD+ binding catalytic domain, termed the sirtuin core domain which is imperative for their activity.	NAD	99-103	sirtuin 1	Homo sapiens	52-57
20563732-1	2010	Screening in a database has revealed that Cryptosporidium hominis encodes a silent information regulator 2 (Sir2), a nicotinamide adenine dinucleotide (NAD)-dependent protein deacetylase.	NAD	117-150	sirtuin 1	Homo sapiens	108-112
20563732-1	2010	Screening in a database has revealed that Cryptosporidium hominis encodes a silent information regulator 2 (Sir2), a nicotinamide adenine dinucleotide (NAD)-dependent protein deacetylase.	NAD	152-155	sirtuin 1	Homo sapiens	108-112
20668205-3	2010	One factor that mediates the effects of diet restriction is the mammalian nicotinamide adenine dinucleotide (NAD)-dependent deacetylase SIRT1.	NAD	74-107	sirtuin 1	Homo sapiens	136-141
20668205-3	2010	One factor that mediates the effects of diet restriction is the mammalian nicotinamide adenine dinucleotide (NAD)-dependent deacetylase SIRT1.	NAD	109-112	sirtuin 1	Homo sapiens	136-141
20554659-1	2010	Pyridoxine-dependent epilepsy was recently shown to be due to mutations in the ALDH7A1 gene, which encodes antiquitin, an enzyme that catalyses the nicotinamide adenine dinucleotide-dependent dehydrogenation of l-alpha-aminoadipic semialdehyde/L-Delta1-piperideine 6-carboxylate.	NAD	148-181	aldehyde dehydrogenase 7 family member A1	Homo sapiens	79-86
20439498-6	2010	Importantly, lowering the NAD(+) concentration and inhibiting the Hst1/Sum1 HDAC complex elevated the intracellular thiamine concentration due to increased thiamine biosynthesis and transport, implicating NAD(+) in the control of thiamine homeostasis.	NAD	205-211	Sum1p	Saccharomyces cerevisiae S288C	71-75
20026274-3	2010	Sirtuin 1 (SIRT1), which functions as a nicotinamide adenine dinucleotide (NAD(+))-dependent protein deacetylase, deacetylates a wide variety of metabolic molecules in response to the cellular energy and redox status and as such causes significant changes in metabolic homeostasis.	NAD	40-73	sirtuin 1	Homo sapiens	0-9
20026274-3	2010	Sirtuin 1 (SIRT1), which functions as a nicotinamide adenine dinucleotide (NAD(+))-dependent protein deacetylase, deacetylates a wide variety of metabolic molecules in response to the cellular energy and redox status and as such causes significant changes in metabolic homeostasis.	NAD	40-73	sirtuin 1	Homo sapiens	11-16
20026274-3	2010	Sirtuin 1 (SIRT1), which functions as a nicotinamide adenine dinucleotide (NAD(+))-dependent protein deacetylase, deacetylates a wide variety of metabolic molecules in response to the cellular energy and redox status and as such causes significant changes in metabolic homeostasis.	NAD	75-81	sirtuin 1	Homo sapiens	0-9
20026274-3	2010	Sirtuin 1 (SIRT1), which functions as a nicotinamide adenine dinucleotide (NAD(+))-dependent protein deacetylase, deacetylates a wide variety of metabolic molecules in response to the cellular energy and redox status and as such causes significant changes in metabolic homeostasis.	NAD	75-81	sirtuin 1	Homo sapiens	11-16
20421294-7	2010	Activation of AMPK by CA-alpha1 increases the SIRT1 activator NAD(+) content and SIRT1 expression in macrophages.	NAD	62-68	sirtuin 1	Homo sapiens	46-51
20171913-3	2010	The 3D structure of NAD(+)-dependent LAD1 was developed based on the crystal structure of human sorbitol dehydrogenase as a template.	NAD	20-26	ladinin 1	Homo sapiens	37-41
20179323-1	2010	The replication terminator protein Fob1 of Saccharomyces cerevisiae is multifunctional, and it not only promotes polar replication fork arrest at the tandem Ter sites located in the intergenic spacer region of rDNA but also loads the NAD-dependent histone deacetylase Sir2 at Ter sites via a protein complex called RENT (regulator of nucleolar silencing and telophase exit).	NAD	234-237	replication fork barrier binding protein FOB1	Saccharomyces cerevisiae S288C	35-39
20081535-7	2010	MEASUREMENTS AND MAIN RESULTS: Acetylcholine-induced endothelium-dependent relaxation decreased, whereas nicotinamide adenine dinucleotide-stimulated superoxide radical production in the aorta and aortic p22phox, p47phox, gp91phox, NOX1, and NOX4 mRNA concentrations increased in trauma-hemorrhaged rats vs. sham rats.	NAD	105-138	cytochrome b-245 beta chain	Rattus norvegicus	222-230
20081535-7	2010	MEASUREMENTS AND MAIN RESULTS: Acetylcholine-induced endothelium-dependent relaxation decreased, whereas nicotinamide adenine dinucleotide-stimulated superoxide radical production in the aorta and aortic p22phox, p47phox, gp91phox, NOX1, and NOX4 mRNA concentrations increased in trauma-hemorrhaged rats vs. sham rats.	NAD	105-138	NADPH oxidase 1	Rattus norvegicus	232-236
20081535-7	2010	MEASUREMENTS AND MAIN RESULTS: Acetylcholine-induced endothelium-dependent relaxation decreased, whereas nicotinamide adenine dinucleotide-stimulated superoxide radical production in the aorta and aortic p22phox, p47phox, gp91phox, NOX1, and NOX4 mRNA concentrations increased in trauma-hemorrhaged rats vs. sham rats.	NAD	105-138	NADPH oxidase 4	Rattus norvegicus	242-246
20054824-0	2010	Extracellular beta-nicotinamide adenine dinucleotide (beta-NAD) promotes the endothelial cell barrier integrity via PKA- and EPAC1/Rac1-dependent actin cytoskeleton rearrangement.	NAD	14-52	Rap guanine nucleotide exchange factor 3	Homo sapiens	125-130
20054824-0	2010	Extracellular beta-nicotinamide adenine dinucleotide (beta-NAD) promotes the endothelial cell barrier integrity via PKA- and EPAC1/Rac1-dependent actin cytoskeleton rearrangement.	NAD	14-52	Rac family small GTPase 1	Homo sapiens	131-135
20054824-0	2010	Extracellular beta-nicotinamide adenine dinucleotide (beta-NAD) promotes the endothelial cell barrier integrity via PKA- and EPAC1/Rac1-dependent actin cytoskeleton rearrangement.	NAD	54-62	Rap guanine nucleotide exchange factor 3	Homo sapiens	125-130
20054824-0	2010	Extracellular beta-nicotinamide adenine dinucleotide (beta-NAD) promotes the endothelial cell barrier integrity via PKA- and EPAC1/Rac1-dependent actin cytoskeleton rearrangement.	NAD	54-62	Rac family small GTPase 1	Homo sapiens	131-135
20335654-1	2010	This issue of the JCI includes studies demonstrating that sirtuin 1 (Sirt1), a NAD+-dependent deacetylase, slows renal senescence and safeguards cells in the renal medulla.	NAD	79-82	sirtuin 1	Homo sapiens	58-67
20335654-1	2010	This issue of the JCI includes studies demonstrating that sirtuin 1 (Sirt1), a NAD+-dependent deacetylase, slows renal senescence and safeguards cells in the renal medulla.	NAD	79-82	sirtuin 1	Homo sapiens	69-74
20171739-1	2010	Poly(ADP-ribose) polymerase-1 (Parp-1) is a nuclear enzyme that uses NAD(+) as a substrate to catalyze the addition of ADP-ribose polymers on a variety of nuclear proteins, modifying transiently their biological functions.	NAD	69-75	poly (ADP-ribose) polymerase family, member 1	Mus musculus	0-29
20171739-1	2010	Poly(ADP-ribose) polymerase-1 (Parp-1) is a nuclear enzyme that uses NAD(+) as a substrate to catalyze the addition of ADP-ribose polymers on a variety of nuclear proteins, modifying transiently their biological functions.	NAD	69-75	poly (ADP-ribose) polymerase family, member 1	Mus musculus	31-37
20035840-1	2010	Activation of poly (ADP-ribose) polymerases (PARP) contributes to ischemic damage by causing neuronal nicotinamide adenine dinucleotide (NAD(+)) depletion, release of apoptosis-inducing factor and consequent caspase-independent cell death.	NAD	102-135	poly (ADP-ribose) polymerase family, member 1	Mus musculus	45-49
20035840-1	2010	Activation of poly (ADP-ribose) polymerases (PARP) contributes to ischemic damage by causing neuronal nicotinamide adenine dinucleotide (NAD(+)) depletion, release of apoptosis-inducing factor and consequent caspase-independent cell death.	NAD	137-144	poly (ADP-ribose) polymerase family, member 1	Mus musculus	45-49
20026255-9	2010	Furthermore, resveratrol may indirectly increase Sirt1 activity in recovering or spared cells via AMPK"s elevation of NAD levels, which then translates into an overall beneficial outcome.	NAD	118-121	sirtuin 1	Homo sapiens	49-54
20117162-4	2010	The mitochondrial Nmnat3 and cytoplasm-localized mutants of Wld(S) and Nmnat1 have similar or even stronger effect than Wld(S) to delay axon degeneration, which suggest that increased mitochondrial or local NAD synthesis might contribute to the protective function of Wld(S) and Nmnats.	NAD	207-210	nicotinamide nucleotide adenylyltransferase 1	Mus musculus	71-77
21203970-4	2010	At molecular level, although Wld(S) is a fusion protein, the nicotinamide mononucleotide adenylyl transferase 1 (Nmnat1) is required and sufficient for the protective effects of Wld(S), indicating a critical role of NAD biosynthesis and perhaps energy metabolism in axon degeneration.	NAD	216-219	nicotinamide nucleotide adenylyltransferase 1	Mus musculus	61-111
21203970-4	2010	At molecular level, although Wld(S) is a fusion protein, the nicotinamide mononucleotide adenylyl transferase 1 (Nmnat1) is required and sufficient for the protective effects of Wld(S), indicating a critical role of NAD biosynthesis and perhaps energy metabolism in axon degeneration.	NAD	216-219	nicotinamide nucleotide adenylyltransferase 1	Mus musculus	113-119
20036704-2	2010	Autofluorescence excited by ultraviolet light has been most extensively studied, and is due to reduced pyridine nucleotides (NADH and NADPH, collectively termed NAD(P)H).	NAD	125-129	2,4-dienoyl-CoA reductase 1	Homo sapiens	161-168
19887595-2	2010	NAD+ is an obligate cosubstrate for mammalian sirtuin-1 (SIRT1), a deacetylase that activates peroxisome proliferator-activated receptor-gamma coactivator-1alpha (PGC-1alpha), which in turn can activate mitochondrial biogenesis.	NAD	0-4	sirtuin 1	Homo sapiens	46-55
19887595-2	2010	NAD+ is an obligate cosubstrate for mammalian sirtuin-1 (SIRT1), a deacetylase that activates peroxisome proliferator-activated receptor-gamma coactivator-1alpha (PGC-1alpha), which in turn can activate mitochondrial biogenesis.	NAD	0-4	sirtuin 1	Homo sapiens	57-62
19915031-5	2010	Consistent with earlier studies, deletion of the two genes encoding NAD-dependent glycerol-3-phosphate dehydrogenase (GPD1 and GPD2) led to elimination of glycerol production and an inability to grow anaerobically.	NAD	68-71	glycerol-3-phosphate dehydrogenase (NAD(+)) GPD1	Saccharomyces cerevisiae S288C	118-122
20160399-13	2010	We assume that, in vivo, starvation increases lipolysis-derived free fatty acid and activates PPARdelta and the resultant increase in SIRT1 expression, in addition to the activation by NAD and AMPK, facilitates the deacetylation of a variety of proteins involved in mitochondrial beta-oxidation pathway and cell survival.	NAD	185-188	sirtuin 1	Homo sapiens	134-139
19913571-5	2010	Exercise training induced SIRT1 activity due to the positive effect of exercise on the activity of nicotinamide phosphoribosyltransferase (NAMPT) and thereby the production of sirtuin-fueling NAD(+).	NAD	192-198	nicotinamide phosphoribosyltransferase	Rattus norvegicus	99-137
19913571-5	2010	Exercise training induced SIRT1 activity due to the positive effect of exercise on the activity of nicotinamide phosphoribosyltransferase (NAMPT) and thereby the production of sirtuin-fueling NAD(+).	NAD	192-198	nicotinamide phosphoribosyltransferase	Rattus norvegicus	139-144
19913571-9	2010	Regular exercise decelerates the deleterious effects of the aging process via SIRT1-dependent pathways through the stimulation of NAD(+) biosynthesis by NAMPT.	NAD	130-136	nicotinamide phosphoribosyltransferase	Rattus norvegicus	153-158
19812894-8	2010	These results indicate that HPR can oxidise NADH at sufficient rate in the absence of PMDH to support beta-oxidation and hence seed germination.	NAD	44-48	hydroxypyruvate reductase	Arabidopsis thaliana	28-31
19843076-1	2009	Resveratrol is a plant polyphenol capable of exerting beneficial metabolic effects which are thought to be mediated in large by the activation of the NAD(+)-dependent protein deacetylase SIRT1.	NAD	150-156	sirtuin 1	Sus scrofa	187-192
19801601-8	2009	Moreover, in vitro assays demonstrated that histone acetyltransferase p300 can catalyze H3 Lys(23) propionylation, whereas histone deacetylase Sir2 can remove this modification in the presence of NAD(+).	NAD	196-202	sirtuin 1	Homo sapiens	143-147
19855187-2	2009	NAD(+) also serves as a substrate for cellular enzymes, including poly (ADPribose) polymerase (PARP)-1 and Sirt1.	NAD	0-6	sirtuin 1	Homo sapiens	107-112
19855187-4	2009	NAD(+) in the nucleus enhances the activity of Sirt1, thereby modulating transcription.	NAD	0-6	sirtuin 1	Homo sapiens	47-52
19819976-5	2009	Because ROS influence osteoblast RANKL expression, studies analyzed the effect of CSF-1 on reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activity and Nox1 and Nox4 proteins.	NAD	99-132	colony stimulating factor 1 (macrophage)	Mus musculus	82-87
33738675-4	2021	In mammals, sirtuin family comprises seven members (SIRT1-SIRT7), and they all possess a conserved NAD+ binding catalytic domain, termed the sirtuin core domain which is imperative for their activity.	NAD	99-103	sirtuin 7	Homo sapiens	58-63
33737560-2	2021	Sirtuin-1 (Silent information regulator family protein 1, SIRT1), an oxidized nicotinamide adenine dinucleotide (NAD+)-dependent protein deacetylase, plays an important role in protection against several neurodegenerative disorders.	NAD	78-111	sirtuin 1	Homo sapiens	0-9
19571038-4	2009	Both proteins share sequence similarities to the yeast 3-oxoacyl-(acyl carrier protein) reductase (Oar1p) and the bacterial FabG, although HsKAR is NADH dependent, whereas FabG and Oar1p are NADPH dependent.	NAD	148-152	3-oxoacyl-[acyl-carrier-protein] reductase (NADPH)	Saccharomyces cerevisiae S288C	99-104
19458327-9	2009	RDH10 can use both NAD(+) and NADP(+) as cofactors for 11-cis-RDH activity, although NAD(+) cofactor confers more robust activity.	NAD	19-25	retinol dehydrogenase 10	Homo sapiens	0-5
19458327-9	2009	RDH10 can use both NAD(+) and NADP(+) as cofactors for 11-cis-RDH activity, although NAD(+) cofactor confers more robust activity.	NAD	85-91	retinol dehydrogenase 10	Homo sapiens	0-5
33737560-2	2021	Sirtuin-1 (Silent information regulator family protein 1, SIRT1), an oxidized nicotinamide adenine dinucleotide (NAD+)-dependent protein deacetylase, plays an important role in protection against several neurodegenerative disorders.	NAD	78-111	sirtuin 1	Homo sapiens	11-56
33737560-2	2021	Sirtuin-1 (Silent information regulator family protein 1, SIRT1), an oxidized nicotinamide adenine dinucleotide (NAD+)-dependent protein deacetylase, plays an important role in protection against several neurodegenerative disorders.	NAD	78-111	sirtuin 1	Homo sapiens	58-63
33737560-2	2021	Sirtuin-1 (Silent information regulator family protein 1, SIRT1), an oxidized nicotinamide adenine dinucleotide (NAD+)-dependent protein deacetylase, plays an important role in protection against several neurodegenerative disorders.	NAD	113-117	sirtuin 1	Homo sapiens	0-9
33737560-2	2021	Sirtuin-1 (Silent information regulator family protein 1, SIRT1), an oxidized nicotinamide adenine dinucleotide (NAD+)-dependent protein deacetylase, plays an important role in protection against several neurodegenerative disorders.	NAD	113-117	sirtuin 1	Homo sapiens	11-56
33737560-2	2021	Sirtuin-1 (Silent information regulator family protein 1, SIRT1), an oxidized nicotinamide adenine dinucleotide (NAD+)-dependent protein deacetylase, plays an important role in protection against several neurodegenerative disorders.	NAD	113-117	sirtuin 1	Homo sapiens	58-63
33562281-0	2021	Exogenous NAD+ Postpones the D-Gal-Induced Senescence of Bone Marrow-Derived Mesenchymal Stem Cells via Sirt1 Signaling.	NAD	10-14	sirtuin 1	Homo sapiens	104-109
33562281-4	2021	Further investigation showed that exogenous NAD+ weakened BMSC senescence by increasing Sirtuin 1 (Sirt1) expression.	NAD	44-48	sirtuin 1	Homo sapiens	88-97
33562281-4	2021	Further investigation showed that exogenous NAD+ weakened BMSC senescence by increasing Sirtuin 1 (Sirt1) expression.	NAD	44-48	sirtuin 1	Homo sapiens	99-104
33562281-6	2021	In addition, the reduced expression of Sirt1 by small interfering RNA abolished the beneficial effects of exogenous NAD+ in terms of postponing BMSCs senescence induced by D-gal.	NAD	116-120	sirtuin 1	Homo sapiens	39-44
33562281-7	2021	Taken together, our results indicate that exogenous NAD+ could postpone D-gal-induced BMSC senescence through Sirt1 signaling, providing a potential method for obtaining high quality BMSCs to support their research and clinical application.	NAD	52-56	sirtuin 1	Homo sapiens	110-115
33478087-6	2021	The cellular redox state, together with the low mDeltaPsi, pushes to drive NNT reverse reaction, at the expense of its antioxidant potential, thus consuming NADPH to support NADH production.	NAD	174-178	2,4-dienoyl-CoA reductase 1	Homo sapiens	157-162
33440786-4	2021	In this review, we provide an overview of the current knowledge of NAD+ metabolism, highlighting the functional liaison with mono(ADP-ribosyl)ating enzymes, such as the well-known ARTD10 (also named PARP10), SIRT6, and SIRT7.	NAD	67-71	sirtuin 7	Homo sapiens	219-224
33420179-7	2021	Our results should motivate design of integrated electrolyzer platforms that deploy this heterogeneous catalyst for direct electrochemical regeneration of NADH/NADPH, which is central to design of next-generation biofuel fermentation strategies, biological solar converters, energy-storage devices, and artificial photosynthesis.	NAD	155-159	2,4-dienoyl-CoA reductase 1	Homo sapiens	160-165
33171124-3	2021	Here, we find nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme of the NAD+ biogenesis, drives interferon gamma (IFNgamma)-induced PD-L1 expression in multiple types of tumors and governs tumor immune evasion in a CD8+ T cell-dependent manner.	NAD	94-98	CD8a molecule	Homo sapiens	237-240
33751435-1	2021	Quantitative Analysis of the Interaction with NAD+ of the Apoptosis Inducing Factor (AIF) Harboring FAD in the Reduced State.	NAD	46-50	apoptosis inducing factor mitochondria associated 1	Homo sapiens	58-83
33751435-1	2021	Quantitative Analysis of the Interaction with NAD+ of the Apoptosis Inducing Factor (AIF) Harboring FAD in the Reduced State.	NAD	46-50	apoptosis inducing factor mitochondria associated 1	Homo sapiens	85-88
33751435-3	2021	As a case study, here we describe the quantitative analysis of the redox-dependent interaction of the mammalian apoptosis inducing factor (AIF) with its NAD+ ligand.	NAD	153-157	apoptosis inducing factor mitochondria associated 1	Homo sapiens	112-137
33751435-3	2021	As a case study, here we describe the quantitative analysis of the redox-dependent interaction of the mammalian apoptosis inducing factor (AIF) with its NAD+ ligand.	NAD	153-157	apoptosis inducing factor mitochondria associated 1	Homo sapiens	139-142
33751435-4	2021	In particular, we report a protocol for the spectrophotometric titration of AIF in its reduced state under anaerobic conditions with NAD+, in order to determine the dissociation constant of the resulting complex.	NAD	133-137	apoptosis inducing factor mitochondria associated 1	Homo sapiens	76-79
33046442-1	2020	NAD-dependent deacetylase sirtuin-1 (SIRT1) is a class III histone deacetylase that positively regulates cancer-related pathways such as proliferation and stress resistance.	NAD	0-3	sirtuin 1	Homo sapiens	37-42
19703561-8	2009	For SDR-O a weak conversion of retinal into retinol was detectable in the presence of the cofactor NADH.	NAD	99-103	short chain dehydrogenase/reductase family 9C member 7	Homo sapiens	4-9
19703994-6	2009	The cytotoxicity of GMX1778 can be bypassed with exogenous nicotinic acid (NA), which permits NAD(+) repletion via NA phosphoribosyltransferase 1 (NAPRT1).	NAD	94-100	nicotinate phosphoribosyltransferase	Homo sapiens	115-145
19703994-6	2009	The cytotoxicity of GMX1778 can be bypassed with exogenous nicotinic acid (NA), which permits NAD(+) repletion via NA phosphoribosyltransferase 1 (NAPRT1).	NAD	94-100	nicotinate phosphoribosyltransferase	Homo sapiens	147-153
19681075-2	2009	Highlights of the sequence are a diastereoselective construction of the C3a-bromo-hexahydropyrrolo[2,3-b]indole nucleus, its Co(I)-induced C3a-C3a" dimerization, and the twofold or sequential amide-bond formation before cyclization to the diketopiperazine of the homo- or heterodimeric alkaloids, respectively.	NAD	125-130	complement C3	Homo sapiens	72-75
19681075-2	2009	Highlights of the sequence are a diastereoselective construction of the C3a-bromo-hexahydropyrrolo[2,3-b]indole nucleus, its Co(I)-induced C3a-C3a" dimerization, and the twofold or sequential amide-bond formation before cyclization to the diketopiperazine of the homo- or heterodimeric alkaloids, respectively.	NAD	125-130	complement C3	Homo sapiens	139-142
19681075-2	2009	Highlights of the sequence are a diastereoselective construction of the C3a-bromo-hexahydropyrrolo[2,3-b]indole nucleus, its Co(I)-induced C3a-C3a" dimerization, and the twofold or sequential amide-bond formation before cyclization to the diketopiperazine of the homo- or heterodimeric alkaloids, respectively.	NAD	125-130	complement C3	Homo sapiens	139-142
19716821-0	2009	SIRT1 markedly extends replicative lifespan if the NAD+ salvage pathway is enhanced.	NAD	51-55	sirtuin 1	Homo sapiens	0-5
19716821-5	2009	Thus, SIRT1 can markedly postpone SMC senescence, but this requires overcoming an otherwise vulnerable nicotinamide adenine dinucleotide salvage reaction in aging SMCs.	NAD	103-136	sirtuin 1	Homo sapiens	6-11
19564482-4	2009	Gene expression and physiological data generated post hoc identified a retrograde response to mitochondrial deficiency, which was confirmed by showing Rtg1-dependent NADH accumulation in the engineered yeast strain.	NAD	166-170	Rtg1p	Saccharomyces cerevisiae S288C	151-155
19531481-4	2009	Here we identify PARP1, a DNA-binding protein with an NAD+-dependent enzymatic activity, as a cofactor of Oct4 and Sox2 to regulate expression of their target gene FGF4.	NAD	54-58	SRY-box transcription factor 2	Homo sapiens	115-119
19470756-1	2009	Poly(ADP-ribose) polymerase 1 (PARP1) and SIRT1 deacetylase are two NAD-dependent enzymes which play major roles in the decision of a cell to live or to die in a stress situation.	NAD	68-71	poly (ADP-ribose) polymerase family, member 1	Mus musculus	0-29
19470756-1	2009	Poly(ADP-ribose) polymerase 1 (PARP1) and SIRT1 deacetylase are two NAD-dependent enzymes which play major roles in the decision of a cell to live or to die in a stress situation.	NAD	68-71	poly (ADP-ribose) polymerase family, member 1	Mus musculus	31-36
19478080-0	2009	Enzymes in the NAD+ salvage pathway regulate SIRT1 activity at target gene promoters.	NAD	15-19	sirtuin 1	Homo sapiens	45-50
19478080-1	2009	In mammals, nicotinamide phosphoribosyltransferase (NAMPT) and nicotinamide mononucleotide adenylyltransferase 1 (NMNAT-1) constitute a nuclear NAD(+) salvage pathway which regulates the functions of NAD(+)-dependent enzymes such as the protein deacetylase SIRT1.	NAD	144-150	sirtuin 1	Homo sapiens	257-262
19478080-1	2009	In mammals, nicotinamide phosphoribosyltransferase (NAMPT) and nicotinamide mononucleotide adenylyltransferase 1 (NMNAT-1) constitute a nuclear NAD(+) salvage pathway which regulates the functions of NAD(+)-dependent enzymes such as the protein deacetylase SIRT1.	NAD	200-206	sirtuin 1	Homo sapiens	257-262
19478080-3	2009	However, little is known about the molecular mechanisms by which NAD(+) biosynthetic enzymes regulate SIRT1 activity to control gene transcription in the nucleus.	NAD	65-71	sirtuin 1	Homo sapiens	102-107
19433578-1	2009	The NAD-dependent deacetylase SirT1 regulates factors involved in stress response and cell survival and is a potential drug target of activators and inhibitors.	NAD	4-7	sirtuin 1	Homo sapiens	30-35
19411844-5	2009	Moreover, SIRT1, which is a mammalian member of sirtuin family of NAD(+)-dependent deacetylases, regulates the deacetylation of H3K56.	NAD	66-72	sirtuin 1	Homo sapiens	10-15
19410549-5	2009	During fasting, NAD in liver mitochondria increases, thereby triggering SIRT5 deacetylation of CPS1 and adaptation to the increase in amino acid catabolism.	NAD	16-19	carbamoyl-phosphate synthetase 1	Mus musculus	95-99
18931329-1	2009	The multifunctional surface protein CD38 acts as a receptor with ecto-enzymatic activity, hydrolyzing NAD to generate several products known to exhibit Ca2+-mobilizing properties.	NAD	102-105	CD38 antigen	Mus musculus	36-40
18926804-8	2009	RDH-E2 is a member of the short-chain dehydrogenase/reductase (SDR) superfamily of proteins, and is most closely related to the group of SDRs comprised of both NAD(+)- and NADP(+)-dependent enzymes with activities toward retinoid and steroid substrates.	NAD	160-166	short chain dehydrogenase/reductase family 16C member 5	Homo sapiens	0-6
33020065-0	2020	Cell type-specific roles of CD38 in the interactions of isoniazid with NAD+ in the liver.	NAD	71-75	CD38 antigen	Mus musculus	28-32
33020065-3	2020	Our previous work revealed the CD38-dependent interactions of isoniazid (INH), an anti-tuberculosis drug, with NAD+ to form INH-NAD adduct.	NAD	111-115	CD38 antigen	Mus musculus	31-35
18926804-11	2009	Furthermore, RDH-E2 expressed in Sf9 insect cells as a fusion to the C-terminal His(6)-tag and purified using Ni(2+)-affinity chromatography recognizes all-trans-retinol and all-trans-retinaldehyde as substrates and exhibits a strong preference for NAD(+)/NADH as cofactors.	NAD	249-255	short chain dehydrogenase/reductase family 16C member 5	Homo sapiens	13-19
18926804-11	2009	Furthermore, RDH-E2 expressed in Sf9 insect cells as a fusion to the C-terminal His(6)-tag and purified using Ni(2+)-affinity chromatography recognizes all-trans-retinol and all-trans-retinaldehyde as substrates and exhibits a strong preference for NAD(+)/NADH as cofactors.	NAD	256-260	short chain dehydrogenase/reductase family 16C member 5	Homo sapiens	13-19
33020065-3	2020	Our previous work revealed the CD38-dependent interactions of isoniazid (INH), an anti-tuberculosis drug, with NAD+ to form INH-NAD adduct.	NAD	111-114	CD38 antigen	Mus musculus	31-35
18926804-13	2009	The preference for NAD(+) suggests that RDH-E2 is likely to function in the oxidative direction in vivo, further supporting its potential role in the oxidation of retinol to retinaldehyde for retinoic acid biosynthesis in human keratinocytes.	NAD	19-25	short chain dehydrogenase/reductase family 16C member 5	Homo sapiens	40-46
33020065-8	2020	These data suggest that hepatic non-parenchymal cells, such as KC and HSC, are the major cell types responsible for the CD38-dependent interactions of INH with NAD+ in the liver.	NAD	160-164	CD38 antigen	Mus musculus	120-124
19013439-5	2009	We show that the ADHFe1 gene is related to bacterial GHB dehydrogenases and has a conserved NAD-binding site.	NAD	92-95	alcohol dehydrogenase iron containing 1	Homo sapiens	17-23
33020065-10	2020	Our work also revealed the essential roles of non-parenchymal cells including KC and HSC in the CD38-dependent interactions of NAD+ with INH, leading to the formation of both INH-NAD and AcINH-NAD in the liver.	NAD	127-131	CD38 antigen	Mus musculus	96-100
32366137-1	2020	The human sirtuin silent information regulator 1 (SIRT1) is a NAD+-dependent deacetylase enzyme.	NAD	62-65	sirtuin 1	Homo sapiens	50-55
18997065-1	2009	Sirtuin1 (Sirt1) is a NAD-dependent deacetylase that plays important roles in a variety of biological processes.	NAD	22-25	sirtuin 1	Sus scrofa	0-8
18997065-1	2009	Sirtuin1 (Sirt1) is a NAD-dependent deacetylase that plays important roles in a variety of biological processes.	NAD	22-25	sirtuin 1	Sus scrofa	10-15
32599075-15	2020	Treatment of tumour-bearing mice with a blocker of activin receptor ligands restores depleted muscle NAD+ and Nrk2 as well as decreased muscle protein synthesis.	NAD	101-105	activin A receptor, type 1	Mus musculus	51-67
19173742-1	2009	BACKGROUND: SIRT1 is a mammalian homologue of NAD+-dependent deacetylase sirtuin family.	NAD	46-49	sirtuin 1	Homo sapiens	12-17
19071085-1	2009	We examined in HepG2 cells whether glucose-induced changes in AMP-activated protein kinase (AMPK) activity could be mediated by SIRT1, an NAD(+)-dependent histone/protein deacetylase that has been linked to the increase in longevity caused by caloric restriction.	NAD	138-144	sirtuin 1	Homo sapiens	128-133
33120985-9	2020	Thus, NAD+ is a significant source of adenosine and UA in the airways in mouse models of allergic airway disease, and the capacity for their generation from NAD+ is augmented by CD38, a major NADase with high affinity for NAD+.	NAD	6-10	CD38 antigen	Mus musculus	178-182
33120985-9	2020	Thus, NAD+ is a significant source of adenosine and UA in the airways in mouse models of allergic airway disease, and the capacity for their generation from NAD+ is augmented by CD38, a major NADase with high affinity for NAD+.	NAD	157-161	CD38 antigen	Mus musculus	178-182
33120985-9	2020	Thus, NAD+ is a significant source of adenosine and UA in the airways in mouse models of allergic airway disease, and the capacity for their generation from NAD+ is augmented by CD38, a major NADase with high affinity for NAD+.	NAD	157-161	CD38 antigen	Mus musculus	178-182
33082370-3	2020	CD38 is an enzyme that catalyses the hydrolysis of nicotinamide adenine dinucleotide (NAD+) and is a candidate molecule for regulating neurodegeneration and neuroinflammation.	NAD	51-84	CD38 antigen	Mus musculus	0-4
33082370-3	2020	CD38 is an enzyme that catalyses the hydrolysis of nicotinamide adenine dinucleotide (NAD+) and is a candidate molecule for regulating neurodegeneration and neuroinflammation.	NAD	86-90	CD38 antigen	Mus musculus	0-4
32729989-1	2020	The NAD+ -dependent sirtuin deacetylase, Sirt1, regulates key transcription factors strongly implicated in ageing and lifespan.	NAD	4-7	sirtuin 1	Homo sapiens	41-46
32729989-8	2020	Our data suggest that defects emerge in aged females lacking oocyte-Sirt1 due to concurrent age-related changes such as reduced NAD+ and sirtuin expression levels, which compromise compensatory mechanisms that can cover for Sirt1 loss in younger oocytes.	NAD	128-132	sirtuin 1	Homo sapiens	68-73
33087267-4	2020	These signaling enzymes include nicotinamide adenine dinucleotide (NAD+) dependent poly(ADP-ribose) polymerases (PARP1, PARP2) and class III deacetylases (SIRT1, SIRT6) that comprise a key PARP-NAD-SIRT axis to facilitate the regulation and coordination of BER in the mammalian cell.	NAD	32-65	sirtuin 1	Homo sapiens	155-160
32796716-1	2020	Sirtuin1 (Sirt1) has a NAD (+) binding domain and modulates the acetylation status of peroxisome proliferator-activated receptor-gamma coactivator-1alpha (PGC1alpha) and Fork Head Box O1 transcription factor (Foxo1) according to the nutritional status.	NAD	23-30	sirtuin 1	Homo sapiens	0-8
32796716-1	2020	Sirtuin1 (Sirt1) has a NAD (+) binding domain and modulates the acetylation status of peroxisome proliferator-activated receptor-gamma coactivator-1alpha (PGC1alpha) and Fork Head Box O1 transcription factor (Foxo1) according to the nutritional status.	NAD	23-30	sirtuin 1	Homo sapiens	10-15
32748289-0	2020	Selective NADH communication from alpha-ketoglutarate dehydrogenase to mitochondrial transhydrogenase prevents reactive oxygen species formation under reducing conditions in the heart.	NAD	10-14	oxoglutarate (alpha-ketoglutarate) dehydrogenase (lipoamide)	Mus musculus	34-67
32748289-3	2020	At high NADH levels, alpha-ketoglutarate dehydrogenase (alpha-KGDH) is a major source of superoxide in skeletal muscle mitochondria with low NNT activity.	NAD	8-12	oxoglutarate (alpha-ketoglutarate) dehydrogenase (lipoamide)	Mus musculus	21-54
32388637-2	2020	Here, the nuclear NAD-dependent histone-deacetylase Sirtuin1 (SIRT1) seems to be important.	NAD	18-21	sirtuin 1	Homo sapiens	52-60
32388637-2	2020	Here, the nuclear NAD-dependent histone-deacetylase Sirtuin1 (SIRT1) seems to be important.	NAD	18-21	sirtuin 1	Homo sapiens	62-67
32086007-1	2020	Cellular energy demands are readily changed during physical exercise resulting in adaptive responses by signaling proteins of metabolic processes, including the NAD+ dependent lysine deacetylase SIRT1.	NAD	161-164	sirtuin 1	Homo sapiens	195-200
32572044-6	2020	NAD is the substrate for the CD157- and CD38-dependent production of cADPR.	NAD	0-3	CD38 antigen	Mus musculus	40-44
32278117-3	2020	This study aims to identify changes of specific components of NAD+/SIRTs system in white adipose tissue (WAT) and brown adipose tissue (BAT) of mice upon energy imbalance, focusing on key enzymes in NAD+ salvage (Nampt, Nmnat1, Nrk1), clearance (Nnmt, Aox1, Cyp2e1) and consumption pathways (Sirt1, Sirt2, Sirt3, Sirt6, Parp1).	NAD	62-66	nicotinamide nucleotide adenylyltransferase 1	Mus musculus	220-226
32278117-3	2020	This study aims to identify changes of specific components of NAD+/SIRTs system in white adipose tissue (WAT) and brown adipose tissue (BAT) of mice upon energy imbalance, focusing on key enzymes in NAD+ salvage (Nampt, Nmnat1, Nrk1), clearance (Nnmt, Aox1, Cyp2e1) and consumption pathways (Sirt1, Sirt2, Sirt3, Sirt6, Parp1).	NAD	62-66	nicotinamide N-methyltransferase	Mus musculus	246-250
32278117-3	2020	This study aims to identify changes of specific components of NAD+/SIRTs system in white adipose tissue (WAT) and brown adipose tissue (BAT) of mice upon energy imbalance, focusing on key enzymes in NAD+ salvage (Nampt, Nmnat1, Nrk1), clearance (Nnmt, Aox1, Cyp2e1) and consumption pathways (Sirt1, Sirt2, Sirt3, Sirt6, Parp1).	NAD	62-66	aldehyde oxidase 1	Mus musculus	252-256
32278117-3	2020	This study aims to identify changes of specific components of NAD+/SIRTs system in white adipose tissue (WAT) and brown adipose tissue (BAT) of mice upon energy imbalance, focusing on key enzymes in NAD+ salvage (Nampt, Nmnat1, Nrk1), clearance (Nnmt, Aox1, Cyp2e1) and consumption pathways (Sirt1, Sirt2, Sirt3, Sirt6, Parp1).	NAD	62-66	poly (ADP-ribose) polymerase family, member 1	Mus musculus	320-325
32278117-3	2020	This study aims to identify changes of specific components of NAD+/SIRTs system in white adipose tissue (WAT) and brown adipose tissue (BAT) of mice upon energy imbalance, focusing on key enzymes in NAD+ salvage (Nampt, Nmnat1, Nrk1), clearance (Nnmt, Aox1, Cyp2e1) and consumption pathways (Sirt1, Sirt2, Sirt3, Sirt6, Parp1).	NAD	199-203	nicotinamide nucleotide adenylyltransferase 1	Mus musculus	220-226
32278117-3	2020	This study aims to identify changes of specific components of NAD+/SIRTs system in white adipose tissue (WAT) and brown adipose tissue (BAT) of mice upon energy imbalance, focusing on key enzymes in NAD+ salvage (Nampt, Nmnat1, Nrk1), clearance (Nnmt, Aox1, Cyp2e1) and consumption pathways (Sirt1, Sirt2, Sirt3, Sirt6, Parp1).	NAD	199-203	nicotinamide N-methyltransferase	Mus musculus	246-250
32278117-3	2020	This study aims to identify changes of specific components of NAD+/SIRTs system in white adipose tissue (WAT) and brown adipose tissue (BAT) of mice upon energy imbalance, focusing on key enzymes in NAD+ salvage (Nampt, Nmnat1, Nrk1), clearance (Nnmt, Aox1, Cyp2e1) and consumption pathways (Sirt1, Sirt2, Sirt3, Sirt6, Parp1).	NAD	199-203	aldehyde oxidase 1	Mus musculus	252-256
32523953-4	2020	Here, we show that the decline of mitochondrial function generated by a lack of Ca2+ transfer induces a DRP-1 independent mitochondrial fragmentation that at an early time is mediated by an increase in the NAD+/NADH ratio and activation of SIRT1.	NAD	206-210	utrophin	Homo sapiens	104-109
32523953-4	2020	Here, we show that the decline of mitochondrial function generated by a lack of Ca2+ transfer induces a DRP-1 independent mitochondrial fragmentation that at an early time is mediated by an increase in the NAD+/NADH ratio and activation of SIRT1.	NAD	211-215	utrophin	Homo sapiens	104-109
32410431-0	2020	[Effects of nicotinamide mononucleotide adenylyl transferase 3 on mitochondrial function and anti-oxidative stress of rabbit bone marrow mesenchymal stem cells via regulating nicotinamide adenine dinucleotide levels].	NAD	175-208	nicotinamide/nicotinic acid mononucleotide adenylyltransferase 3	Oryctolagus cuniculus	12-62
32410431-1	2020	Objective: To investigate the effect of nicotinamide mononucleotide adenosyl transferase 3 (NMNAT3) on the mitochondrial function and anti-oxidative stress of rabbit bone marrow mesenchymal stem cells (BMSCs) under oxidative stress in vitro by regulating nicotinamide adenine dinucleotide (NAD +) levels.	NAD	255-288	nicotinamide/nicotinic acid mononucleotide adenylyltransferase 3	Oryctolagus cuniculus	40-90
32410431-1	2020	Objective: To investigate the effect of nicotinamide mononucleotide adenosyl transferase 3 (NMNAT3) on the mitochondrial function and anti-oxidative stress of rabbit bone marrow mesenchymal stem cells (BMSCs) under oxidative stress in vitro by regulating nicotinamide adenine dinucleotide (NAD +) levels.	NAD	255-288	nicotinamide/nicotinic acid mononucleotide adenylyltransferase 3	Oryctolagus cuniculus	92-98
32410431-1	2020	Objective: To investigate the effect of nicotinamide mononucleotide adenosyl transferase 3 (NMNAT3) on the mitochondrial function and anti-oxidative stress of rabbit bone marrow mesenchymal stem cells (BMSCs) under oxidative stress in vitro by regulating nicotinamide adenine dinucleotide (NAD +) levels.	NAD	290-295	nicotinamide/nicotinic acid mononucleotide adenylyltransferase 3	Oryctolagus cuniculus	40-90
32410431-1	2020	Objective: To investigate the effect of nicotinamide mononucleotide adenosyl transferase 3 (NMNAT3) on the mitochondrial function and anti-oxidative stress of rabbit bone marrow mesenchymal stem cells (BMSCs) under oxidative stress in vitro by regulating nicotinamide adenine dinucleotide (NAD +) levels.	NAD	290-295	nicotinamide/nicotinic acid mononucleotide adenylyltransferase 3	Oryctolagus cuniculus	92-98
32410431-16	2020	Conclusion: NMNAT3 can effectively improve the mitochondrial function of rabbit BMSCs via increasing the NAD + levels, and enhance its anti-oxidative stress and improve the survival of BMSCs under oxidative stress conditions.	NAD	105-110	nicotinamide/nicotinic acid mononucleotide adenylyltransferase 3	Oryctolagus cuniculus	12-18
32397145-9	2020	In addition, the recent advances of studies on NAD-dependent deacetylase sirtuin-1 (SIRT1) regulation of autophagy, the role of senescence-associated secretory phenotype (SASP) in cells senescence and their regulation by polyphenols have been highlighted as well.	NAD	47-50	sirtuin 1	Homo sapiens	84-89
31502386-1	2020	The NAD+ -dependent protein deacetylase silent information regulator 1 (SIRT1) targets multiple proteins for deacetylation, and it has been implicated in a variety of cellular pathways and human diseases.	NAD	4-7	sirtuin 1	Homo sapiens	40-70
31502386-1	2020	The NAD+ -dependent protein deacetylase silent information regulator 1 (SIRT1) targets multiple proteins for deacetylation, and it has been implicated in a variety of cellular pathways and human diseases.	NAD	4-7	sirtuin 1	Homo sapiens	72-77
32179648-2	2020	The prokaryotic NAD synthetase enzyme NadE catalyzes the last step of NAD+ biosynthesis, converting nicotinic acid adenine dinucleotide (NaAD) to NAD+ Some members of the NadE family use l-glutamine as a nitrogen donor and are named NadEGln Previous gene neighborhood analysis has indicated that the bacterial nadE gene is frequently clustered with the gene encoding the regulatory signal transduction protein PII, suggesting a functional relationship between these proteins in response to the nutritional status and the carbon/nitrogen ratio of the bacterial cell.	NAD	70-74	NAD synthetase 1	Homo sapiens	16-30
19448856-1	2009	Arabidopsis thaliana AtNUDT7, a homodimeric Nudix hydrolase active on ADP-ribose and NADH, exerts negative control on the major signaling complex involved in plant defense activation and programmed cell death.	NAD	85-89	MutT/nudix family protein	Arabidopsis thaliana	21-28
32179648-2	2020	The prokaryotic NAD synthetase enzyme NadE catalyzes the last step of NAD+ biosynthesis, converting nicotinic acid adenine dinucleotide (NaAD) to NAD+ Some members of the NadE family use l-glutamine as a nitrogen donor and are named NadEGln Previous gene neighborhood analysis has indicated that the bacterial nadE gene is frequently clustered with the gene encoding the regulatory signal transduction protein PII, suggesting a functional relationship between these proteins in response to the nutritional status and the carbon/nitrogen ratio of the bacterial cell.	NAD	70-74	brain expressed X-linked 3	Homo sapiens	38-42
19746271-1	2009	Apoptosis-inducing factor (AIF) is a mitochondrial flavoprotein that mediates both NADH-oxidizing and caspase-independent apoptosis.	NAD	83-87	apoptosis inducing factor mitochondria associated 1	Homo sapiens	0-25
19746271-1	2009	Apoptosis-inducing factor (AIF) is a mitochondrial flavoprotein that mediates both NADH-oxidizing and caspase-independent apoptosis.	NAD	83-87	apoptosis inducing factor mitochondria associated 1	Homo sapiens	27-30
32179648-2	2020	The prokaryotic NAD synthetase enzyme NadE catalyzes the last step of NAD+ biosynthesis, converting nicotinic acid adenine dinucleotide (NaAD) to NAD+ Some members of the NadE family use l-glutamine as a nitrogen donor and are named NadEGln Previous gene neighborhood analysis has indicated that the bacterial nadE gene is frequently clustered with the gene encoding the regulatory signal transduction protein PII, suggesting a functional relationship between these proteins in response to the nutritional status and the carbon/nitrogen ratio of the bacterial cell.	NAD	70-74	brain expressed X-linked 3	Homo sapiens	171-175
19130305-0	2009	The NAD World: a new systemic regulatory network for metabolism and aging--Sirt1, systemic NAD biosynthesis, and their importance.	NAD	4-7	sirtuin 1	Homo sapiens	75-80
32179648-2	2020	The prokaryotic NAD synthetase enzyme NadE catalyzes the last step of NAD+ biosynthesis, converting nicotinic acid adenine dinucleotide (NaAD) to NAD+ Some members of the NadE family use l-glutamine as a nitrogen donor and are named NadEGln Previous gene neighborhood analysis has indicated that the bacterial nadE gene is frequently clustered with the gene encoding the regulatory signal transduction protein PII, suggesting a functional relationship between these proteins in response to the nutritional status and the carbon/nitrogen ratio of the bacterial cell.	NAD	70-74	brain expressed X-linked 3	Homo sapiens	310-314
19130305-1	2009	For the past several years, it has been demonstrated that the NAD-dependent protein deacetylase Sirt1 and nicotinamide phosphoribosyltransferase (Nampt)-mediated systemic NAD biosynthesis together play a critical role in the regulation of metabolism and possibly aging in mammals.	NAD	62-65	sirtuin 1	Homo sapiens	96-101
32179648-2	2020	The prokaryotic NAD synthetase enzyme NadE catalyzes the last step of NAD+ biosynthesis, converting nicotinic acid adenine dinucleotide (NaAD) to NAD+ Some members of the NadE family use l-glutamine as a nitrogen donor and are named NadEGln Previous gene neighborhood analysis has indicated that the bacterial nadE gene is frequently clustered with the gene encoding the regulatory signal transduction protein PII, suggesting a functional relationship between these proteins in response to the nutritional status and the carbon/nitrogen ratio of the bacterial cell.	NAD	146-150	NAD synthetase 1	Homo sapiens	16-30
19130305-1	2009	For the past several years, it has been demonstrated that the NAD-dependent protein deacetylase Sirt1 and nicotinamide phosphoribosyltransferase (Nampt)-mediated systemic NAD biosynthesis together play a critical role in the regulation of metabolism and possibly aging in mammals.	NAD	171-174	sirtuin 1	Homo sapiens	96-101
19130305-3	2009	Conceptually, in the NAD World, systemic NAD biosynthesis mediated by intra- and extracellular Nampt functions as a driver that keeps up the pace of metabolism in multiple tissues/organs, and the NAD-dependent deacetylase Sirt1 serves as a universal mediator that executes metabolic effects in a tissue-dependent manner in response to changes in systemic NAD biosynthesis.	NAD	21-24	sirtuin 1	Homo sapiens	222-227
32179648-2	2020	The prokaryotic NAD synthetase enzyme NadE catalyzes the last step of NAD+ biosynthesis, converting nicotinic acid adenine dinucleotide (NaAD) to NAD+ Some members of the NadE family use l-glutamine as a nitrogen donor and are named NadEGln Previous gene neighborhood analysis has indicated that the bacterial nadE gene is frequently clustered with the gene encoding the regulatory signal transduction protein PII, suggesting a functional relationship between these proteins in response to the nutritional status and the carbon/nitrogen ratio of the bacterial cell.	NAD	146-150	brain expressed X-linked 3	Homo sapiens	38-42
19130305-3	2009	Conceptually, in the NAD World, systemic NAD biosynthesis mediated by intra- and extracellular Nampt functions as a driver that keeps up the pace of metabolism in multiple tissues/organs, and the NAD-dependent deacetylase Sirt1 serves as a universal mediator that executes metabolic effects in a tissue-dependent manner in response to changes in systemic NAD biosynthesis.	NAD	41-44	sirtuin 1	Homo sapiens	222-227
19130305-3	2009	Conceptually, in the NAD World, systemic NAD biosynthesis mediated by intra- and extracellular Nampt functions as a driver that keeps up the pace of metabolism in multiple tissues/organs, and the NAD-dependent deacetylase Sirt1 serves as a universal mediator that executes metabolic effects in a tissue-dependent manner in response to changes in systemic NAD biosynthesis.	NAD	41-44	sirtuin 1	Homo sapiens	222-227
19130305-3	2009	Conceptually, in the NAD World, systemic NAD biosynthesis mediated by intra- and extracellular Nampt functions as a driver that keeps up the pace of metabolism in multiple tissues/organs, and the NAD-dependent deacetylase Sirt1 serves as a universal mediator that executes metabolic effects in a tissue-dependent manner in response to changes in systemic NAD biosynthesis.	NAD	41-44	sirtuin 1	Homo sapiens	222-227
32179648-2	2020	The prokaryotic NAD synthetase enzyme NadE catalyzes the last step of NAD+ biosynthesis, converting nicotinic acid adenine dinucleotide (NaAD) to NAD+ Some members of the NadE family use l-glutamine as a nitrogen donor and are named NadEGln Previous gene neighborhood analysis has indicated that the bacterial nadE gene is frequently clustered with the gene encoding the regulatory signal transduction protein PII, suggesting a functional relationship between these proteins in response to the nutritional status and the carbon/nitrogen ratio of the bacterial cell.	NAD	146-150	brain expressed X-linked 3	Homo sapiens	171-175
32179648-2	2020	The prokaryotic NAD synthetase enzyme NadE catalyzes the last step of NAD+ biosynthesis, converting nicotinic acid adenine dinucleotide (NaAD) to NAD+ Some members of the NadE family use l-glutamine as a nitrogen donor and are named NadEGln Previous gene neighborhood analysis has indicated that the bacterial nadE gene is frequently clustered with the gene encoding the regulatory signal transduction protein PII, suggesting a functional relationship between these proteins in response to the nutritional status and the carbon/nitrogen ratio of the bacterial cell.	NAD	146-150	brain expressed X-linked 3	Homo sapiens	310-314
32278088-4	2020	While the buildup of NADPH in chloroplasts provides operation of the malate valve leading to establishment of NADH/NAD+ ratios in different cell compartments, the production of NADH by mitochondria drives citrate export by establishing conditions for the operation of the citrate valve.	NAD	110-114	2,4-dienoyl-CoA reductase 1	Homo sapiens	21-26
32278088-4	2020	While the buildup of NADPH in chloroplasts provides operation of the malate valve leading to establishment of NADH/NAD+ ratios in different cell compartments, the production of NADH by mitochondria drives citrate export by establishing conditions for the operation of the citrate valve.	NAD	115-119	2,4-dienoyl-CoA reductase 1	Homo sapiens	21-26
19029946-3	2009	Furthermore, reduction of the FMN cofactor by either NADH or light irradiation results in the binding of the b-Zip transcription factor Yap4 to the Lot6-proteasome complex, indicating that recruitment of the transcription factor depends on the redox state of the quinone reductase.	NAD	53-57	Cin5p	Saccharomyces cerevisiae S288C	136-140
32278088-4	2020	While the buildup of NADPH in chloroplasts provides operation of the malate valve leading to establishment of NADH/NAD+ ratios in different cell compartments, the production of NADH by mitochondria drives citrate export by establishing conditions for the operation of the citrate valve.	NAD	177-181	2,4-dienoyl-CoA reductase 1	Homo sapiens	21-26
32363189-3	2020	Mechanistic studies demonstrated that overexpression of CD38 specifically downregulated the expression of Rab7 and its adaptor protein pleckstrin homology domain-containing protein family member 1 (PLEKHM1) through nicotinamide adenine dinucleotide (NAD)-dependent and non-NAD-dependent pathways, respectively.	NAD	215-248	CD38 antigen	Mus musculus	56-60
32363189-3	2020	Mechanistic studies demonstrated that overexpression of CD38 specifically downregulated the expression of Rab7 and its adaptor protein pleckstrin homology domain-containing protein family member 1 (PLEKHM1) through nicotinamide adenine dinucleotide (NAD)-dependent and non-NAD-dependent pathways, respectively.	NAD	215-248	pleckstrin homology domain containing, family M (with RUN domain) member 1	Mus musculus	198-205
18798872-3	2009	It has been reported that the AtNUDX2 protein has pyrophosphatase activities towards both ADP-ribose and NADH (Ogawa et al., 2005).	NAD	105-109	nudix hydrolase homolog 2	Arabidopsis thaliana	30-37
32363189-3	2020	Mechanistic studies demonstrated that overexpression of CD38 specifically downregulated the expression of Rab7 and its adaptor protein pleckstrin homology domain-containing protein family member 1 (PLEKHM1) through nicotinamide adenine dinucleotide (NAD)-dependent and non-NAD-dependent pathways, respectively.	NAD	250-253	CD38 antigen	Mus musculus	56-60
18798872-8	2009	The results indicate that overexpression of AtNUDX2, encoding ADP-ribose pyrophosphatase, confers enhanced tolerance of oxidative stress on Arabidopsis plants, resulting from maintenance of NAD(+) and ATP levels by nucleotide recycling from free ADP-ribose molecules under stress conditions.	NAD	190-196	nudix hydrolase homolog 2	Arabidopsis thaliana	44-51
32363189-3	2020	Mechanistic studies demonstrated that overexpression of CD38 specifically downregulated the expression of Rab7 and its adaptor protein pleckstrin homology domain-containing protein family member 1 (PLEKHM1) through nicotinamide adenine dinucleotide (NAD)-dependent and non-NAD-dependent pathways, respectively.	NAD	250-253	pleckstrin homology domain containing, family M (with RUN domain) member 1	Mus musculus	198-205
19390693-9	2009	Dose dependent studies indicated that SVOP demonstrates the highest affinity for NAD, in contrast to SV2, which binds both NAD and ATP with equal affinity.	NAD	123-126	synaptic vesicle glycoprotein 2A	Homo sapiens	101-104
32250733-0	2020	Nicotinamide mononucleotide adenylyltransferase uses its NAD+ substrate-binding site to chaperone phosphorylated Tau.	NAD	57-61	tau	Drosophila melanogaster	113-116
19076449-6	2008	To examine whether NAD(+) mediates neuroprotective effects, nicotinamide, a precursor of NAD(+) and inhibitor of SIRT1 and poly (ADP-ribose) polymerase 1 (PARP1) (two NAD(+)-dependent enzymes), was employed.	NAD	19-25	poly (ADP-ribose) polymerase family, member 1	Mus musculus	155-160
19076449-7	2008	Nicotinamide attenuated excitotoxic death and preserved cellular NAD(+) levels to support SIRT1 and PARP 1 activities.	NAD	65-71	poly (ADP-ribose) polymerase family, member 1	Mus musculus	100-106
32250733-6	2020	Our work uncovers a dedicated chaperone of pTau and suggests NMNAT as a key node between NAD+ metabolism and Tau homeostasis in aging and neurodegeneration.	NAD	89-93	tau	Drosophila melanogaster	44-47
31713761-3	2020	Sirtuin 2 (SIRT2) is a member of nicotinamide adenine dinucleotide (NAD+)-dependent protein deacetylases involved in a wide range of pathophysiological processes.	NAD	33-66	sirtuin 2	Rattus norvegicus	0-9
18562191-1	2008	A simple and sensitive method for the electrocatalytic detection of NADH on a carbon paste electrode modified with a redox-active (NC)(2)C(6)H(3)-NO/(NC)(2)C(6)H(3)-NHOH (NOPH/NHOHPH) electrogenerated in situ from 4-nitrophthalonitrile (4-NPHN) is presented.	NAD	68-72	NPHS1 adhesion molecule, nephrin	Homo sapiens	239-243
18562191-2	2008	The electrode modified with 4-NPHN showed an efficient electrocatalytic activity towards the oxidation of NADH with activation overpotential of 0.12V vs. Ag/AgCl.	NAD	106-110	NPHS1 adhesion molecule, nephrin	Homo sapiens	30-34
18562191-3	2008	The formation of an intermediate charge transfer complex is proposed for the charge transfer reaction between NADH and the 4-NPHN-resulting system.	NAD	110-114	NPHS1 adhesion molecule, nephrin	Homo sapiens	125-129
31713761-3	2020	Sirtuin 2 (SIRT2) is a member of nicotinamide adenine dinucleotide (NAD+)-dependent protein deacetylases involved in a wide range of pathophysiological processes.	NAD	33-66	sirtuin 2	Rattus norvegicus	11-16
31713761-3	2020	Sirtuin 2 (SIRT2) is a member of nicotinamide adenine dinucleotide (NAD+)-dependent protein deacetylases involved in a wide range of pathophysiological processes.	NAD	68-72	sirtuin 2	Rattus norvegicus	0-9
31713761-3	2020	Sirtuin 2 (SIRT2) is a member of nicotinamide adenine dinucleotide (NAD+)-dependent protein deacetylases involved in a wide range of pathophysiological processes.	NAD	68-72	sirtuin 2	Rattus norvegicus	11-16
31697031-1	2020	BACKGROUND/OBJECTIVES: Sjogren - Larsson syndrome (SLS) is a rare autosomal recessive disease of the mutation ALDH3A2 that identifies a part of fatty acids for fatty aldehyde dehydrogenase: NAD-oxidoreductase enzyme complex.	NAD	190-193	aldehyde dehydrogenase 3 family member A2	Homo sapiens	110-117
18755687-3	2008	Using INS-1-derived 832/13 cells, it has recently been shown by other laboratories that NADP-dependent cytosolic malic enzyme (MEc), but not NAD-dependent mitochondrial malic enzyme (MEm), regulates GSIS.	NAD	88-91	chemokine (C-C motif) ligand 28	Mus musculus	127-130
31697031-1	2020	BACKGROUND/OBJECTIVES: Sjogren - Larsson syndrome (SLS) is a rare autosomal recessive disease of the mutation ALDH3A2 that identifies a part of fatty acids for fatty aldehyde dehydrogenase: NAD-oxidoreductase enzyme complex.	NAD	190-193	aldehyde dehydrogenase 3 family member A2	Homo sapiens	160-188
32209328-3	2020	Previous studies have shown that increased cellular NAD+ and NAD+/NADH ratio increase INa through suppression of mitochondrial reactive oxygen species and PKC-mediated NaV1.5 phosphorylation.	NAD	52-56	internexin neuronal intermediate filament protein alpha	Homo sapiens	86-89
32209328-3	2020	Previous studies have shown that increased cellular NAD+ and NAD+/NADH ratio increase INa through suppression of mitochondrial reactive oxygen species and PKC-mediated NaV1.5 phosphorylation.	NAD	61-65	internexin neuronal intermediate filament protein alpha	Homo sapiens	86-89
18828915-11	2008	BNA2, which is involved in NAD+ synthesis, plays previously unidentified roles in the cellular response to telomere uncapping.	NAD	27-31	dioxygenase BNA2	Saccharomyces cerevisiae S288C	0-4
32209328-3	2020	Previous studies have shown that increased cellular NAD+ and NAD+/NADH ratio increase INa through suppression of mitochondrial reactive oxygen species and PKC-mediated NaV1.5 phosphorylation.	NAD	66-70	internexin neuronal intermediate filament protein alpha	Homo sapiens	86-89
32209328-4	2020	In addition, NAD+-dependent deacetylation of NaV1.5 at K1479 by Sirtuin 1 increases NaV1.5 membrane trafficking and INa.	NAD	13-17	sirtuin 1	Homo sapiens	64-73
32209328-4	2020	In addition, NAD+-dependent deacetylation of NaV1.5 at K1479 by Sirtuin 1 increases NaV1.5 membrane trafficking and INa.	NAD	13-17	internexin neuronal intermediate filament protein alpha	Homo sapiens	116-119
18685043-2	2008	The reduction of hydroxypyruvate to glycerate catalyzed by hydroxypyruvate reductase (HPR) in the peroxisomes is thought to be facilitated by the production of NADH by peroxisomal malate dehydrogenase (PMDH).	NAD	160-164	hydroxypyruvate reductase	Arabidopsis thaliana	59-84
32266141-1	2020	Nicotinamide phosphoribosyltransferase (NAMPT) and nicotinate phosphoribosyltransferase (NAPRT) are two intracellular enzymes that catalyze the first step in the biosynthesis of NAD from nicotinamide and nicotinic acid, respectively.	NAD	178-181	nicotinate phosphoribosyltransferase	Homo sapiens	51-87
18685043-2	2008	The reduction of hydroxypyruvate to glycerate catalyzed by hydroxypyruvate reductase (HPR) in the peroxisomes is thought to be facilitated by the production of NADH by peroxisomal malate dehydrogenase (PMDH).	NAD	160-164	hydroxypyruvate reductase	Arabidopsis thaliana	86-89
32266141-1	2020	Nicotinamide phosphoribosyltransferase (NAMPT) and nicotinate phosphoribosyltransferase (NAPRT) are two intracellular enzymes that catalyze the first step in the biosynthesis of NAD from nicotinamide and nicotinic acid, respectively.	NAD	178-181	nicotinate phosphoribosyltransferase	Homo sapiens	89-94
31926163-4	2020	SIRT6, which is an ADP-ribosyltransferase and NAD+-dependent deacetylase of acetyl and long-chain fatty acyl groups, playing central roles in lipid and glucose metabolism, is closely related to the occurrence of diabetes and obesity caused by overnutrition and aging.	NAD	46-49	sirtuin 6	Bos taurus	0-5
18786399-3	2008	We report crystal structures of the bacterial sirtuin, Sir2Tm, in complex with an S-alkylamidate intermediate, analogous to the naturally occurring O-alkylamidate intermediate, and a Sir2Tm ternary complex containing a dissociated NAD(+) analog and acetylated peptide.	NAD	231-237	sirtuin 1	Homo sapiens	55-59
31025603-1	2020	The sirtuin family comprises seven NAD+-dependent histone deacetylases named SIRT1 to SIRT7.	NAD	35-39	sirtuin 1	Homo sapiens	77-82
18775325-5	2008	We show that a Sir3 chimera-bearing Hos3, an unrelated NAD(+)-independent histone deacetylase, substitutes for Sir2 in silencing.	NAD	55-61	chromatin-silencing protein SIR3	Saccharomyces cerevisiae S288C	15-19
18502750-2	2008	Here, we present evidence that RDH10 is, in fact, a strictly NAD(+)-dependent enzyme with multisubstrate specificity that recognizes cis-retinols as well as all-trans-retinol as substrates.	NAD	61-67	retinol dehydrogenase 10	Homo sapiens	31-36
31025603-1	2020	The sirtuin family comprises seven NAD+-dependent histone deacetylases named SIRT1 to SIRT7.	NAD	35-39	sirtuin 7	Homo sapiens	86-91
18502750-3	2008	RDH10 has a relatively high apparent K(m) value for NAD(+) (~100 microm) but the lowest apparent K(m) value for all-trans-retinol (~0.035 microm) among all NAD(+)-dependent retinoid oxidoreductases.	NAD	52-58	retinol dehydrogenase 10	Homo sapiens	0-5
31025603-9	2020	Preferred orientations of NAD+ and acetyl-lysine inside SIRT7 were found, with all components forming a stable complex.	NAD	26-30	sirtuin 7	Homo sapiens	56-61
18502750-3	2008	RDH10 has a relatively high apparent K(m) value for NAD(+) (~100 microm) but the lowest apparent K(m) value for all-trans-retinol (~0.035 microm) among all NAD(+)-dependent retinoid oxidoreductases.	NAD	156-162	retinol dehydrogenase 10	Homo sapiens	0-5
18502750-5	2008	Consistent with its preference for NAD(+), RDH10 functions exclusively in the oxidative direction in the cells, increasing the levels of retinaldehyde and retinoic acid.	NAD	35-41	retinol dehydrogenase 10	Homo sapiens	43-48
31859031-8	2020	Sirt1 thus achieves neuroprotection by promoting calcium regulation, and NAD+ dysregulation underlies Sirt1 dysfunction in SCA7, indicating that cerebellar ataxias exhibit altered calcium homeostasis because of metabolic dysregulation, suggesting shared therapy targets.	NAD	73-77	sirtuin 1	Homo sapiens	102-107
18174234-5	2008	15-Hydroxyprostaglandin dehydrogenase [NAD(+)] (15-PGDH), a key enzyme in prostaglandin degradation, was identified as an upregulated protein in SGC7901 cells transfected with the COX-2siRNA plasmid.	NAD	39-45	carbonyl reductase 1	Homo sapiens	0-37
31843644-7	2020	In this study, we also find that the SIRT7 enzyme can specifically transfer a single moiety of ADP ribose on other nuclear proteins, with a preference for NAD+.	NAD	155-158	sirtuin 7	Homo sapiens	37-42
18646549-5	2008	Later investigations indicated the possibility of the participation in electron transport for reticular CYP isoenzymes, alternative NADH-dependent reticular system composed of cytochrome b5 reductase (CBR) and cytochrome b5.	NAD	132-136	carbonyl reductase 1	Homo sapiens	176-199
18646549-5	2008	Later investigations indicated the possibility of the participation in electron transport for reticular CYP isoenzymes, alternative NADH-dependent reticular system composed of cytochrome b5 reductase (CBR) and cytochrome b5.	NAD	132-136	carbonyl reductase 1	Homo sapiens	201-204
32059481-16	2020	Consistently, the inhibition of both PARP-1 and SIRT-1 increased the NAD+/NADH-ratio in BAFs.	NAD	69-72	poly (ADP-ribose) polymerase family, member 1	Mus musculus	37-43
32059481-16	2020	Consistently, the inhibition of both PARP-1 and SIRT-1 increased the NAD+/NADH-ratio in BAFs.	NAD	74-78	poly (ADP-ribose) polymerase family, member 1	Mus musculus	37-43
32059481-17	2020	This suggests that cellular NAD+/NADH ratios control the complex interactions of PARP-1, H1 and SIRT-1 and regulate the interplay of parylation and acetylation/de-acetylation events with low NAD+/NADH ratios (reverse Warburg effect), promoting PARP-1 activation and estrogen synthesis in BAFs.	NAD	28-31	poly (ADP-ribose) polymerase family, member 1	Mus musculus	81-87
32059481-17	2020	This suggests that cellular NAD+/NADH ratios control the complex interactions of PARP-1, H1 and SIRT-1 and regulate the interplay of parylation and acetylation/de-acetylation events with low NAD+/NADH ratios (reverse Warburg effect), promoting PARP-1 activation and estrogen synthesis in BAFs.	NAD	28-31	poly (ADP-ribose) polymerase family, member 1	Mus musculus	244-250
17964195-4	2008	The methemoglobin level was 38.0% in the propositus with 70% reduction in NADH-b(5)R activity.	NAD	74-78	hemoglobin subunit gamma 2	Homo sapiens	4-17
32059481-17	2020	This suggests that cellular NAD+/NADH ratios control the complex interactions of PARP-1, H1 and SIRT-1 and regulate the interplay of parylation and acetylation/de-acetylation events with low NAD+/NADH ratios (reverse Warburg effect), promoting PARP-1 activation and estrogen synthesis in BAFs.	NAD	33-37	poly (ADP-ribose) polymerase family, member 1	Mus musculus	81-87
32059481-17	2020	This suggests that cellular NAD+/NADH ratios control the complex interactions of PARP-1, H1 and SIRT-1 and regulate the interplay of parylation and acetylation/de-acetylation events with low NAD+/NADH ratios (reverse Warburg effect), promoting PARP-1 activation and estrogen synthesis in BAFs.	NAD	33-37	poly (ADP-ribose) polymerase family, member 1	Mus musculus	244-250
32059481-17	2020	This suggests that cellular NAD+/NADH ratios control the complex interactions of PARP-1, H1 and SIRT-1 and regulate the interplay of parylation and acetylation/de-acetylation events with low NAD+/NADH ratios (reverse Warburg effect), promoting PARP-1 activation and estrogen synthesis in BAFs.	NAD	33-36	poly (ADP-ribose) polymerase family, member 1	Mus musculus	81-87
32059481-17	2020	This suggests that cellular NAD+/NADH ratios control the complex interactions of PARP-1, H1 and SIRT-1 and regulate the interplay of parylation and acetylation/de-acetylation events with low NAD+/NADH ratios (reverse Warburg effect), promoting PARP-1 activation and estrogen synthesis in BAFs.	NAD	33-36	poly (ADP-ribose) polymerase family, member 1	Mus musculus	244-250
18311572-1	2008	The NAD-dependent mitochondrial malate dehydrogenase (mMDH, EC1.1.1.37) plays pivotal roles in tricarboxylic acid and is crucial for the survival and pathogenecity of parasites.	NAD	4-7	malate dehydrogenase 2, NAD (mitochondrial)	Mus musculus	54-58
32059481-17	2020	This suggests that cellular NAD+/NADH ratios control the complex interactions of PARP-1, H1 and SIRT-1 and regulate the interplay of parylation and acetylation/de-acetylation events with low NAD+/NADH ratios (reverse Warburg effect), promoting PARP-1 activation and estrogen synthesis in BAFs.	NAD	196-200	poly (ADP-ribose) polymerase family, member 1	Mus musculus	81-87
32059481-17	2020	This suggests that cellular NAD+/NADH ratios control the complex interactions of PARP-1, H1 and SIRT-1 and regulate the interplay of parylation and acetylation/de-acetylation events with low NAD+/NADH ratios (reverse Warburg effect), promoting PARP-1 activation and estrogen synthesis in BAFs.	NAD	196-200	poly (ADP-ribose) polymerase family, member 1	Mus musculus	244-250
32046066-2	2020	TRPM2 channels are activated by beta-NAD+, ADP-ribose (ADPR), cyclic ADPR, and 2"-deoxyadenosine 5"-diphosphoribose.	NAD	32-40	transient receptor potential cation channel subfamily M member 2	Homo sapiens	0-5
32046066-3	2020	It has been shown that TRPM2 cation channels and CD38, a type II or type III transmembrane protein with ADP-ribosyl cyclase activity, simultaneously play a role in heat-sensitive and NAD+ metabolite-dependent intracellular free Ca2+ concentration increases in hypothalamic oxytocinergic neurons.	NAD	183-186	transient receptor potential cation channel subfamily M member 2	Homo sapiens	23-28
31241768-6	2020	Changes in AMPK phosphorylation that were caused by SCD1 down- and upregulation affected NAD+ levels following changes in NAD+ -dependent deacetylase sirtuin-1 (SIRT1) activity and histone 3 (H3K9) acetylation and methylation status.	NAD	89-93	stearoyl-Coenzyme A desaturase 1	Mus musculus	52-56
31241768-6	2020	Changes in AMPK phosphorylation that were caused by SCD1 down- and upregulation affected NAD+ levels following changes in NAD+ -dependent deacetylase sirtuin-1 (SIRT1) activity and histone 3 (H3K9) acetylation and methylation status.	NAD	122-126	stearoyl-Coenzyme A desaturase 1	Mus musculus	52-56
31241768-8	2020	These data show that SCD1 is involved in nucleotide (ATP and NAD+ ) metabolism and suggest that the SCD1-dependent regulation of muscle steatosis and insulin sensitivity are mediated by cooperation between AMPK- and SIRT1-regulated pathways.	NAD	61-65	stearoyl-Coenzyme A desaturase 1	Mus musculus	21-25
31995750-5	2020	The activation of TTP by Sirt1-dependent deacetylation, in response to increased NAD+ levels, suppresses the acute inflammatory response and decreases Rheb expression, inhibits mTORC1, and induces autophagolysosomes for bacterial clearance.	NAD	81-84	sirtuin 1	Homo sapiens	25-30
31959836-5	2020	Reduced intracellular NAD+ levels suppressed recruitment of the DNA repair protein XRCC1 to sites of genomic DNA damage and impacted the amount of accumulated DNA damage.	NAD	22-25	X-ray repair cross complementing 1	Homo sapiens	83-88
31542820-3	2020	The requirement of cofactor NADH/NADPH leads to high cost for the industrial application of carbonyl reductases.	NAD	28-32	2,4-dienoyl-CoA reductase 1	Homo sapiens	33-38
32445451-3	2020	The above actions of berberine may mainly depend on activating AMPK and its downstream targets such as mammalian target of rapamycin (mTOR), sirtuin1 (SIRT1) , nuclear factor erythroid-2 related factor-2 (Nrf2), nuclear factor-kappaB (NF-kappaB), phosphoinositide 3-kinase / protein kinase B (PI3K/Akt), nicotinamide adenine dinucleotide (NAD+ ), and p38 mitogen-activated protein kinase (p38 MAPK).	NAD	304-337	protein kinase AMP-activated non-catalytic subunit beta 1	Homo sapiens	63-67
32445451-3	2020	The above actions of berberine may mainly depend on activating AMPK and its downstream targets such as mammalian target of rapamycin (mTOR), sirtuin1 (SIRT1) , nuclear factor erythroid-2 related factor-2 (Nrf2), nuclear factor-kappaB (NF-kappaB), phosphoinositide 3-kinase / protein kinase B (PI3K/Akt), nicotinamide adenine dinucleotide (NAD+ ), and p38 mitogen-activated protein kinase (p38 MAPK).	NAD	339-343	protein kinase AMP-activated non-catalytic subunit beta 1	Homo sapiens	63-67
31735083-11	2020	Interestingly, we demonstrated that treatment with nicotinamide mononucleotide, a known key NAD+ intermediate, ameliorated agonist-induced cardiac hypertrophies in a Sirt7-dependent manner in vitro.	NAD	92-95	sirtuin 7	Mus musculus	166-171
31599159-3	2019	Here, we report that ARH1, ARH3 and macrodomain proteins i.e. MacroD1, MacroD2, C6orf130 (TARG1), Af1521, hydrolyzed alpha-NAD+ but not beta-NAD+.	NAD	117-126	mono-ADP ribosylhydrolase 2	Homo sapiens	71-78
31781169-7	2019	Functional studies revealed that ZFAS1 can promote cancer cell migration by elevating intracellular reactive oxygen species production by inhibiting nicotinamide adenine dinucleotide dehydrogenase expression, indicating that translated ZFAS1 may be an essential oncogene in the progression of HCC.	NAD	149-182	ZNFX1 antisense RNA 1	Homo sapiens	33-38
31781169-7	2019	Functional studies revealed that ZFAS1 can promote cancer cell migration by elevating intracellular reactive oxygen species production by inhibiting nicotinamide adenine dinucleotide dehydrogenase expression, indicating that translated ZFAS1 may be an essential oncogene in the progression of HCC.	NAD	149-182	ZNFX1 antisense RNA 1	Homo sapiens	236-241
31719572-2	2019	Sirtuin 1 (SIRT1), an NAD+ (nicotinamide adenine dinucleotide)-dependent deacetylase in the proximal tubule, may be involved in renal injury associated with ageing.	NAD	22-26	sirtuin 1	Homo sapiens	0-9
31719572-2	2019	Sirtuin 1 (SIRT1), an NAD+ (nicotinamide adenine dinucleotide)-dependent deacetylase in the proximal tubule, may be involved in renal injury associated with ageing.	NAD	22-26	sirtuin 1	Homo sapiens	11-16
31719572-2	2019	Sirtuin 1 (SIRT1), an NAD+ (nicotinamide adenine dinucleotide)-dependent deacetylase in the proximal tubule, may be involved in renal injury associated with ageing.	NAD	28-61	sirtuin 1	Homo sapiens	0-9
31719572-2	2019	Sirtuin 1 (SIRT1), an NAD+ (nicotinamide adenine dinucleotide)-dependent deacetylase in the proximal tubule, may be involved in renal injury associated with ageing.	NAD	28-61	sirtuin 1	Homo sapiens	11-16
31634899-10	2019	In conclusion, FSP1/CoQ10/NAD(P)H exists as a stand-alone parallel system, which co-operates with GPX4 and glutathione (GSH) to suppress phospholipid peroxidation (pLPO) and ferroptosis.	NAD	26-33	S100 calcium binding protein A4	Homo sapiens	15-19
31657440-6	2019	Remarkably, "pyridoxamine-phosphate oxidase-related proteins" (PNPO-RP) from Nostoc punctiforme, A. thaliana and the yeast S. cerevisiae (Ygr017w) were not detectably active on pyridox(am)ine-5"-P, but oxidized 6-NADH, 6-NADPH and 2-NADH suggesting that this may be their main catalytic function.	NAD	211-217	pyridoxamine 5'-phosphate oxidase	Homo sapiens	63-67
31657440-6	2019	Remarkably, "pyridoxamine-phosphate oxidase-related proteins" (PNPO-RP) from Nostoc punctiforme, A. thaliana and the yeast S. cerevisiae (Ygr017w) were not detectably active on pyridox(am)ine-5"-P, but oxidized 6-NADH, 6-NADPH and 2-NADH suggesting that this may be their main catalytic function.	NAD	231-237	pyridoxamine 5'-phosphate oxidase	Homo sapiens	63-67
31657440-8	2019	Inactivation of renalase and of PNPO in mammalian cells and of Ygr017w in yeasts led to the accumulation of a reduced form of 6-NADH, tentatively identified as 4,5,6-NADH3, which can also be produced in vitro by reduction of 6-NADH by glyceraldehyde-3-phosphate dehydrogenase or glucose-6-phosphate dehydrogenase.	NAD	126-132	pyridoxamine 5'-phosphate oxidase	Homo sapiens	32-36
31657440-8	2019	Inactivation of renalase and of PNPO in mammalian cells and of Ygr017w in yeasts led to the accumulation of a reduced form of 6-NADH, tentatively identified as 4,5,6-NADH3, which can also be produced in vitro by reduction of 6-NADH by glyceraldehyde-3-phosphate dehydrogenase or glucose-6-phosphate dehydrogenase.	NAD	160-171	pyridoxamine 5'-phosphate oxidase	Homo sapiens	32-36
31657440-8	2019	Inactivation of renalase and of PNPO in mammalian cells and of Ygr017w in yeasts led to the accumulation of a reduced form of 6-NADH, tentatively identified as 4,5,6-NADH3, which can also be produced in vitro by reduction of 6-NADH by glyceraldehyde-3-phosphate dehydrogenase or glucose-6-phosphate dehydrogenase.	NAD	164-170	pyridoxamine 5'-phosphate oxidase	Homo sapiens	32-36
31657440-10	2019	These findings indicate that two different classes of enzymes using either FAD (renalase) or FMN (PNPOs and PNPO-RPs) as a cofactor play an as yet unsuspected role in removing damaged forms of NAD(P).	NAD	193-196	pyridoxamine 5'-phosphate oxidase	Homo sapiens	98-102
31645480-0	2019	CD38-NAD+-Sirt1 axis In T cell immunotherapy.	NAD	5-8	sirtuin 1	Homo sapiens	10-15
30403147-2	2019	Recent Advances and Critical Issues: Aspects of vascular remodeling induction mechanisms described are associated with shifts in glucose metabolism through the pentose phosphate pathway and increased cytosolic NADPH generation by glucose-6-phosphate dehydrogenase, increased glycolysis generation of cytosolic NADH and lactate, mitochondrial dysfunction associated with superoxide dismutase-2 depletion, changes in reactive oxygen species and iron metabolism, and redox signaling.	NAD	310-314	glucose-6-phosphate dehydrogenase	Homo sapiens	230-263
31340416-1	2019	The reduction of halocarbons by NADH models and NADH under ambient conditions is reported as a new type of reactivity pointing towards a hitherto unknown disruptive pathway for NADH/NADPH-dependent processes.	NAD	32-36	2,4-dienoyl-CoA reductase 1	Homo sapiens	182-187
31340416-1	2019	The reduction of halocarbons by NADH models and NADH under ambient conditions is reported as a new type of reactivity pointing towards a hitherto unknown disruptive pathway for NADH/NADPH-dependent processes.	NAD	48-52	2,4-dienoyl-CoA reductase 1	Homo sapiens	182-187
31340416-1	2019	The reduction of halocarbons by NADH models and NADH under ambient conditions is reported as a new type of reactivity pointing towards a hitherto unknown disruptive pathway for NADH/NADPH-dependent processes.	NAD	48-52	2,4-dienoyl-CoA reductase 1	Homo sapiens	182-187
31679124-4	2019	The mechanisms underlying the age-related decline in [NAD+] in cells of the neurovascular unit are likely multifaceted and may include increased utilization of NAD+ by activated poly (ADP-ribose) polymerase (PARP-1).	NAD	54-58	poly (ADP-ribose) polymerase family, member 1	Mus musculus	208-214
31679124-4	2019	The mechanisms underlying the age-related decline in [NAD+] in cells of the neurovascular unit are likely multifaceted and may include increased utilization of NAD+ by activated poly (ADP-ribose) polymerase (PARP-1).	NAD	160-164	poly (ADP-ribose) polymerase family, member 1	Mus musculus	178-206
31679124-4	2019	The mechanisms underlying the age-related decline in [NAD+] in cells of the neurovascular unit are likely multifaceted and may include increased utilization of NAD+ by activated poly (ADP-ribose) polymerase (PARP-1).	NAD	160-164	poly (ADP-ribose) polymerase family, member 1	Mus musculus	208-214
31679124-11	2019	Thus, PARP-1 activation, likely by decreasing NAD+ availability, contributes to age-related endothelial dysfunction and neurovascular uncoupling, exacerbating cognitive decline.	NAD	46-50	poly (ADP-ribose) polymerase family, member 1	Mus musculus	6-12
31295065-3	2019	As quercetin activates PGC-1alpha through Sirtuin-1, an NAD+-dependent deacetylase, the depleted NAD+ in dystrophic skeletal muscle may limit quercetin efficacy, hence, supplementation with the NAD+ donor, nicotinamide riboside (NR), may facilitate quercetin efficacy.	NAD	56-59	sirtuin 1	Homo sapiens	42-51
31295065-3	2019	As quercetin activates PGC-1alpha through Sirtuin-1, an NAD+-dependent deacetylase, the depleted NAD+ in dystrophic skeletal muscle may limit quercetin efficacy, hence, supplementation with the NAD+ donor, nicotinamide riboside (NR), may facilitate quercetin efficacy.	NAD	56-60	sirtuin 1	Homo sapiens	42-51
31295065-3	2019	As quercetin activates PGC-1alpha through Sirtuin-1, an NAD+-dependent deacetylase, the depleted NAD+ in dystrophic skeletal muscle may limit quercetin efficacy, hence, supplementation with the NAD+ donor, nicotinamide riboside (NR), may facilitate quercetin efficacy.	NAD	97-101	sirtuin 1	Homo sapiens	42-51
31575956-7	2019	Antioxidant enzymes transcriptionally regulated by Nrf2 and involved in GSH, NADPH, and NADH generation were significantly lower including PRX1 and PRX3, GPX4, GSTP1, GCLC, and MTHFD2.	NAD	88-92	methylenetetrahydrofolate dehydrogenase (NADP+ dependent) 2, methenyltetrahydrofolate cyclohydrolase	Homo sapiens	177-183
31575956-10	2019	Cell viability, ROS, NADPH, NADH, and ATP levels were fully rescued by TRPM2 and partially by Nrf2.	NAD	28-32	transient receptor potential cation channel subfamily M member 2	Homo sapiens	71-76
31569682-1	2019	Poly(ADP-ribose) polymerase (Parp)-1 catalyzes polyADP-ribosylation using NAD+ and is involved in the DNA damage response, genome stability, and transcription.	NAD	74-78	poly (ADP-ribose) polymerase family, member 1	Mus musculus	0-36
31576091-13	2019	Parp1 and Sirt1 are two NAD+-dependent enzymes which play major roles in the decision of a cell to live or die in the context of stress .	NAD	24-27	poly (ADP-ribose) polymerase family, member 1	Mus musculus	0-5
31576091-14	2019	We showed that NAD+ depletion attributed to Parp1 activation after DNA damage was caused by oxidative stress in hepatocytes and resulted in Sirt1 activity inhibition.	NAD	15-18	poly (ADP-ribose) polymerase family, member 1	Mus musculus	44-49
31511522-5	2019	These NAPRT-induced effects are independent of NAD-biosynthetic activity, but rely on NAPRT binding to TLR4.	NAD	47-50	nicotinate phosphoribosyltransferase	Mus musculus	6-11
31463593-5	2019	Furthermore, our in vitro reconstitution experiments with Dph1-Dph2 mutants suggested that the Dph1 cluster serves a catalytic role, while the Dph2 cluster facilitates the reduction of the Dph1 cluster by the physiological reducing system Dph3/Cbr1/NADH.	NAD	249-253	diphthamide biosynthesis 1	Homo sapiens	58-62
17974626-10	2008	These studies support that cytoplasmic or nuclear NADH, uniquely produced by glucose metabolism, mediates effects of glucose on AgRP expression.	NAD	50-54	agouti related neuropeptide	Homo sapiens	128-132
31463593-5	2019	Furthermore, our in vitro reconstitution experiments with Dph1-Dph2 mutants suggested that the Dph1 cluster serves a catalytic role, while the Dph2 cluster facilitates the reduction of the Dph1 cluster by the physiological reducing system Dph3/Cbr1/NADH.	NAD	249-253	diphthamide biosynthesis 3	Homo sapiens	239-243
31430957-2	2019	Resistance to sorafenib develops frequently and could be mediated by the nicotinamide adenine dinucleotide (NAD)-dependent deacetylase sirtuin (SIRT)1.	NAD	73-106	sirtuin 1	Homo sapiens	144-150
18082271-1	2008	The influence of de novo synthesis of nicotinamide adenine dinucleotide (NAD) through the kynurenine (KYN) pathway of tryptophan (TRP) degradation on gene transcription of inducible nitric oxide synthase (iNOS) and nitric oxide (NO) production in chicken interferon gamma (ChIFN-gamma)-stimulated and non-stimulated chicken macrophage cell line HD11 was investigated.	NAD	38-71	lysosomal-associated protein transmembrane 4A	Mus musculus	130-133
18082271-1	2008	The influence of de novo synthesis of nicotinamide adenine dinucleotide (NAD) through the kynurenine (KYN) pathway of tryptophan (TRP) degradation on gene transcription of inducible nitric oxide synthase (iNOS) and nitric oxide (NO) production in chicken interferon gamma (ChIFN-gamma)-stimulated and non-stimulated chicken macrophage cell line HD11 was investigated.	NAD	38-71	interferon gamma	Gallus gallus	255-284
18082271-1	2008	The influence of de novo synthesis of nicotinamide adenine dinucleotide (NAD) through the kynurenine (KYN) pathway of tryptophan (TRP) degradation on gene transcription of inducible nitric oxide synthase (iNOS) and nitric oxide (NO) production in chicken interferon gamma (ChIFN-gamma)-stimulated and non-stimulated chicken macrophage cell line HD11 was investigated.	NAD	73-76	lysosomal-associated protein transmembrane 4A	Mus musculus	130-133
18082271-1	2008	The influence of de novo synthesis of nicotinamide adenine dinucleotide (NAD) through the kynurenine (KYN) pathway of tryptophan (TRP) degradation on gene transcription of inducible nitric oxide synthase (iNOS) and nitric oxide (NO) production in chicken interferon gamma (ChIFN-gamma)-stimulated and non-stimulated chicken macrophage cell line HD11 was investigated.	NAD	73-76	interferon gamma	Gallus gallus	255-284
18082271-5	2008	Inhibition of poly(ADP-ribose) polymerase (PARP), a nuclear enzyme involved in DNA repair, replication and transcription, which cleaves NAD into nicotinamide and ADP-ribose, down regulated iNOS gene transcription and NO production in ChIFN-gamma-stimulated HD11 cells.	NAD	136-139	poly(ADP-ribose) polymerase 1	Gallus gallus	14-41
18082271-5	2008	Inhibition of poly(ADP-ribose) polymerase (PARP), a nuclear enzyme involved in DNA repair, replication and transcription, which cleaves NAD into nicotinamide and ADP-ribose, down regulated iNOS gene transcription and NO production in ChIFN-gamma-stimulated HD11 cells.	NAD	136-139	poly(ADP-ribose) polymerase 1	Gallus gallus	43-47
18082271-7	2008	This effect is most likely a result of PARP1 automodification in the presence of NAD, known to facilitate transcription by changing chromatin structure and to allow NFkappaB binding to iNOS promoter which is hindered by direct protein-protein interaction between NFkappaB and unmodified PARP1.	NAD	81-84	poly(ADP-ribose) polymerase 1	Gallus gallus	39-44
18082271-7	2008	This effect is most likely a result of PARP1 automodification in the presence of NAD, known to facilitate transcription by changing chromatin structure and to allow NFkappaB binding to iNOS promoter which is hindered by direct protein-protein interaction between NFkappaB and unmodified PARP1.	NAD	81-84	poly(ADP-ribose) polymerase 1	Gallus gallus	287-292
31430957-2	2019	Resistance to sorafenib develops frequently and could be mediated by the nicotinamide adenine dinucleotide (NAD)-dependent deacetylase sirtuin (SIRT)1.	NAD	108-111	sirtuin 1	Homo sapiens	144-150
31430957-3	2019	We aimed to test whether sorafenib efficacy is influenced by cellular NAD levels and NAD-dependent SIRT1 function.	NAD	85-88	sirtuin 1	Homo sapiens	99-104
31386694-1	2019	Sirt1, a member of the sirtuin gene family, encodes the most conserved mammalian NAD+-dependent deacetylase enzyme responsible for removing acetyl groups from many proteins.	NAD	81-84	sirtuin 1	Homo sapiens	0-5
18086531-1	2008	Reduction of ferric methemoglobin (metHb) to its ferrous form is observed by short-time ultraviolet A (UVA) irradiation of metHb together with nicotinamide adenine dinucleotide (NADH).	NAD	143-176	hemoglobin subunit gamma 2	Homo sapiens	20-33
18086531-1	2008	Reduction of ferric methemoglobin (metHb) to its ferrous form is observed by short-time ultraviolet A (UVA) irradiation of metHb together with nicotinamide adenine dinucleotide (NADH).	NAD	143-176	hemoglobin subunit gamma 2	Homo sapiens	35-40
18086531-1	2008	Reduction of ferric methemoglobin (metHb) to its ferrous form is observed by short-time ultraviolet A (UVA) irradiation of metHb together with nicotinamide adenine dinucleotide (NADH).	NAD	178-182	hemoglobin subunit gamma 2	Homo sapiens	20-33
18086531-1	2008	Reduction of ferric methemoglobin (metHb) to its ferrous form is observed by short-time ultraviolet A (UVA) irradiation of metHb together with nicotinamide adenine dinucleotide (NADH).	NAD	178-182	hemoglobin subunit gamma 2	Homo sapiens	35-40
18086531-4	2008	Accordingly, the O2-binding ability of the protein increases by short-time UVA irradiation of metHb together with NADH, which corresponds with the reduction of metHb, while it decreases by long-time UVA irradiation, which corresponds with the structural destruction.	NAD	114-118	hemoglobin subunit gamma 2	Homo sapiens	94-99
18086531-4	2008	Accordingly, the O2-binding ability of the protein increases by short-time UVA irradiation of metHb together with NADH, which corresponds with the reduction of metHb, while it decreases by long-time UVA irradiation, which corresponds with the structural destruction.	NAD	114-118	hemoglobin subunit gamma 2	Homo sapiens	160-165
30605226-1	2019	Sirtuin-1 (Sirt1), a member of the NAD-dependent sirtuin family of histone/protein deacetylases (HDAC), is an important target for immunotherapy due to its role in deacetylating the transcription factors Foxp3 and thymic retinoid acid receptor related orphan receptor gamma (RORgammat).	NAD	35-38	sirtuin 1	Homo sapiens	0-9
30605226-1	2019	Sirtuin-1 (Sirt1), a member of the NAD-dependent sirtuin family of histone/protein deacetylases (HDAC), is an important target for immunotherapy due to its role in deacetylating the transcription factors Foxp3 and thymic retinoid acid receptor related orphan receptor gamma (RORgammat).	NAD	35-38	sirtuin 1	Homo sapiens	11-16
29723660-2	2019	SIRT1, a NAD+-dependent protein deacetylase, deacetylates the p65 of NF-kappaB and shows protective effects in kidney disorders.	NAD	9-12	sirtuin 1	Homo sapiens	0-5
18991691-4	2008	Niacin is a precursor of NAD+, the substrate for the activity of DNA repair enzyme PARP-1 and, consequently, may contribute to maintaining genomic stability.	NAD	25-29	poly (ADP-ribose) polymerase family, member 1	Mus musculus	83-89
31073968-0	2019	Palmitic Acid-Induced NAD+ Depletion is Associated with the Reduced Function of SIRT1 and Increased Expression of BACE1 in Hippocampal Neurons.	NAD	22-26	sirtuin 1	Homo sapiens	80-85
31073968-4	2019	A possible molecular mechanism involved in the effects of PA may be through dysfunction of the NAD+ sensor enzyme, SIRT1.	NAD	95-99	sirtuin 1	Homo sapiens	115-120
31073968-6	2019	PA reduced the total amount of NAD+ in neurons that caused an increase in p65 K310 acetylation due to inhibition of SIRT1 activity and low protein content.	NAD	31-35	sirtuin 1	Homo sapiens	116-121
30936458-3	2019	In this study, we report that lactate uptake alters the NAD+/NADH ratio in the cancer cells, which culminates with SIRT1-dependent PGC-1alpha activation and subsequent enhancement of mitochondrial mass and activity.	NAD	56-60	sirtuin 1	Homo sapiens	115-120
30936458-3	2019	In this study, we report that lactate uptake alters the NAD+/NADH ratio in the cancer cells, which culminates with SIRT1-dependent PGC-1alpha activation and subsequent enhancement of mitochondrial mass and activity.	NAD	61-65	sirtuin 1	Homo sapiens	115-120
31261609-1	2019	Sirtuin-1 (SIRT1) is a class-III histone deacetylase (HDAC), an NAD+-dependent enzyme deeply involved in gene regulation, genome stability maintenance, apoptosis, autophagy, senescence, proliferation, aging, and tumorigenesis.	NAD	64-68	sirtuin 1	Homo sapiens	0-9
31261609-1	2019	Sirtuin-1 (SIRT1) is a class-III histone deacetylase (HDAC), an NAD+-dependent enzyme deeply involved in gene regulation, genome stability maintenance, apoptosis, autophagy, senescence, proliferation, aging, and tumorigenesis.	NAD	64-68	sirtuin 1	Homo sapiens	11-16
31244614-1	2019	CD38 is an enzyme that catalyzes the synthesis of cyclic adenosine diphosphate-ribose from nicotinamide adenine dinucleotide (NAD+).	NAD	91-124	CD38 antigen	Mus musculus	0-4
31244614-1	2019	CD38 is an enzyme that catalyzes the synthesis of cyclic adenosine diphosphate-ribose from nicotinamide adenine dinucleotide (NAD+).	NAD	126-130	CD38 antigen	Mus musculus	0-4
31244614-7	2019	Further experiments revealed that these observations were associated with reduced levels of glial activation and inflammatory responses including phagocytosis, most likely through the enhanced level of NAD+ in CD38-deleted condition.	NAD	202-206	CD38 antigen	Mus musculus	210-214
31214115-0	2019	Hepatic DNA Damage Induced by Electronic Cigarette Exposure Is Associated With the Modulation of NAD+/PARP1/SIRT1 Axis.	NAD	97-101	poly (ADP-ribose) polymerase family, member 1	Mus musculus	102-107
18570652-6	2008	Both NAD-dependent and Pttg1-dependent pathways were responsible for mediating different subsets of these alterations, also incorporating changes in VCP/p97 localization and Ube1 expression.	NAD	5-8	valosin containing protein	Mus musculus	149-152
18379989-6	2008	In contrast to (or together with) the anaerobic NO-reductase activity, HMP has also been shown to be able to catalyze the oxidation of NO to NO(3) (-) (NO-dioxygenase activity) both in vivo and in vitro in the presence of O(2) and NADH.	NAD	231-235	inner membrane mitochondrial protein	Homo sapiens	71-74
18379989-7	2008	HMP has also been shown to be capable of catalyzing the reduction of several alkylhydroperoxide substrates into their corresponding alcohols using NADH as an electron donor.	NAD	147-151	inner membrane mitochondrial protein	Homo sapiens	0-3
17954559-5	2008	Expression of the group 2 genes is selectively repressed by the NAD-dependent deacetylase SIRT1 in mature 3T3-L1 adipocytes, since knockdown of SIRT1 through the constitutive expression of a corresponding RNA interference enhances their expression without affecting the expression of classic adipogenic genes, such as adiponectin and FABP4/aP2.	NAD	64-67	sirtuin 1	Homo sapiens	90-95
17954559-5	2008	Expression of the group 2 genes is selectively repressed by the NAD-dependent deacetylase SIRT1 in mature 3T3-L1 adipocytes, since knockdown of SIRT1 through the constitutive expression of a corresponding RNA interference enhances their expression without affecting the expression of classic adipogenic genes, such as adiponectin and FABP4/aP2.	NAD	64-67	sirtuin 1	Homo sapiens	144-149
31063745-1	2019	The NAD+-dependent deacetylase Sirtuin 1 (SIRT1) regulates cell metabolism, proliferation, and DNA repair and acts as a tumor suppressor in breast cancer.	NAD	4-8	sirtuin 1	Homo sapiens	42-47
17964805-2	2008	The hydroxylases obtain reducing equivalents from NAD(P)H via an electron transfer chain that is initiated by an oxidoreductase containing an N-terminal ferredoxin domain and C-terminal flavin- and NAD-binding domains.	NAD	50-53	oxidoreductase	Escherichia coli	113-127
18221243-6	2008	The protein implicated in this protective process is the silent information regulator 2 (SIR2, SIRT1 in mammals), an enzyme that belongs to a nicotinamide adenine dinucleotide (NAD)+-dependent protein deacetylases.	NAD	142-175	sirtuin 1	Homo sapiens	95-100
30753815-4	2019	We recently developed small molecule inhibitors of nicotinamide N-methyltransferase (NNMT), an enzyme overexpressed with aging in skeletal muscles and linked to impairment of the NAD+ salvage pathway, dysregulated sirtuin 1 activity, and increased muSC senescence.	NAD	179-183	nicotinamide N-methyltransferase	Mus musculus	51-83
18206804-3	2008	Reactive oxygen species formation by the nicotinamide adenine dinucleotide phosphate oxidases Nox1 and Nox2 in arteries is a consequence of an activation of the enzymes by different stimuli such as growth factors, cytokines, and cardiovascular risk factors (cigarette smoke, high blood pressure, oxidized lipids).	NAD	41-74	cytochrome b-245 beta chain	Homo sapiens	103-107
17853438-2	2007	It has been proposed that the mitochondrial permeability transition (MPT) is required for NAD(+) to be released from mitochondria and subsequently consumed by PARP-1.	NAD	90-96	poly (ADP-ribose) polymerase family, member 1	Mus musculus	159-165
17853438-6	2007	Inhibition of the mitochondrial permeability transition with cyclosporine-A (CsA) prevented PARP-1-induced NAD(+) depletion to a varying degree in the four cell types tested.	NAD	107-113	poly (ADP-ribose) polymerase family, member 1	Mus musculus	92-98
17853438-9	2007	These results confirm that it is the cytosolic NAD(+) pool that is consumed by PARP-1 and that the mitochondrial NAD(+) pool is consumed only after MPT permits mitochondrial NAD(+) to exit into the cytosol.	NAD	47-53	poly (ADP-ribose) polymerase family, member 1	Mus musculus	79-85
17888864-3	2007	The substrate specificity differs from that of rat NAD+-dependent 3alpha-HSD (AKR1C17) that shares 95% sequence identity with AKR1C16.	NAD	51-55	aldo-keto reductase family 1, member C14	Rattus norvegicus	66-76
17806102-1	2007	The NAD(+)-dependent protein deacetylase SIRT1 is linked to cellular survival pathways by virtue of keeping the tumor suppressor gene p53 and members of the forkhead transcription factor family deacetylated.	NAD	4-10	sirtuin 1	Homo sapiens	41-46
17983578-1	2007	The NAD-dependent deacetylase SIRT1 regulates lipid and carbohydrate metabolism and has been shown to extend life span in several species.	NAD	4-7	sirtuin 1	Homo sapiens	30-35
17964266-1	2007	Human SIRT1 is an NAD+-dependent deacetylase protein that plays a role in cell death/survival, senescence, and endocrine signaling.	NAD	18-21	sirtuin 1	Homo sapiens	6-11
17628866-7	2007	We tested a diverse set of suramin analogues to elucidate the inhibition of the NAD(+)-dependent histone deacetylases SIRT1 and SIRT2 and discovered selective inhibitors of human sirtuins with potency in the two-digit nanomolar range.	NAD	80-86	sirtuin 1	Homo sapiens	118-123
18035827-1	2007	Fatty aldehyde dehydrogenase (FALDH) is an NAD+-dependent oxidoreductase involved in the metabolism of fatty alcohols.	NAD	43-46	aldehyde dehydrogenase 3 family member A2	Homo sapiens	0-28
18035827-1	2007	Fatty aldehyde dehydrogenase (FALDH) is an NAD+-dependent oxidoreductase involved in the metabolism of fatty alcohols.	NAD	43-46	aldehyde dehydrogenase 3 family member A2	Homo sapiens	30-35
17624472-1	2007	Sirt1, a conserved nicotinamide adenine dinucleotide (NAD(+))-dependent deacetylase, has been implicated in modulating transcriptional silencing and cell survival, and seems to play a key role in carcinogenesis through deacetylation of important regulatory proteins.	NAD	19-52	sirtuin 1	Homo sapiens	0-5
17624472-1	2007	Sirt1, a conserved nicotinamide adenine dinucleotide (NAD(+))-dependent deacetylase, has been implicated in modulating transcriptional silencing and cell survival, and seems to play a key role in carcinogenesis through deacetylation of important regulatory proteins.	NAD	54-61	sirtuin 1	Homo sapiens	0-5
17449130-8	2007	The decrease in the supply of NADH and FADH(2) to the respiratory chain derives from impairments in glucose metabolism including glycolysis (e.g. MODY2 and exposure to NO) and the shuttles (e.g. diabetic state and exposure to ketone body).	NAD	30-34	glucokinase	Homo sapiens	146-151
17660350-6	2007	In vitro enzymatic assays revealed that ADP-ribose and NADH are preferred substrates of NUDT7, and the hydrolysis activity of NUDT7 is essential for its biological function and is sensitive to inhibition by Ca(2+).	NAD	55-59	MutT/nudix family protein	Arabidopsis thaliana	88-93
17660350-8	2007	However, the nudt7 mutation leads to perturbation of cellular redox homeostasis and a higher level of NADH in pathogen-challenged leaves.	NAD	102-106	MutT/nudix family protein	Arabidopsis thaliana	13-18
17475203-5	2007	Thus, AKR1C17 represents a novel NAD(+)-dependent type of cytosolic 3alpha-HSD with unique inhibitor sensitivity and tissue distribution.	NAD	33-39	aldo-keto reductase family 1, member C14	Rattus norvegicus	68-78
17846587-4	2007	The enzyme preferred FAD as a cofactor and NADH rather than NADPH as an electron donor.	NAD	43-47	BRCA2 DNA repair associated	Homo sapiens	21-24
17711401-1	2007	Poly(ADP-ribose) polymerase-1 (PARP-1) is an enzyme best known for its role in DNA repair and as a mediator of NAD+ depletion and energy failure-induced cell death.	NAD	111-115	poly (ADP-ribose) polymerase family, member 1	Mus musculus	0-29
17711401-1	2007	Poly(ADP-ribose) polymerase-1 (PARP-1) is an enzyme best known for its role in DNA repair and as a mediator of NAD+ depletion and energy failure-induced cell death.	NAD	111-115	poly (ADP-ribose) polymerase family, member 1	Mus musculus	31-37
17676954-3	2007	Hst1p is an NAD(+)-dependent histone deacetylase that acts with Sum1p to repress a subset of midsporulation genes.	NAD	12-18	Sum1p	Saccharomyces cerevisiae S288C	64-69
17429946-2	2007	Here we report two 1 A resolution crystal structures of liver alcohol dehydrogenase in complex with NADH and two inhibitors: dimethyl sulfoxide and isobutyramide.	NAD	100-104	aldo-keto reductase family 1 member A1	Homo sapiens	62-83
17360427-2	2007	It includes NAD(+)-dependent protein deacetylation by members of the Sir2 family and protein modification by poly(ADP-ribose) polymerase 1 (PARP-1).	NAD	12-18	sirtuin 1	Homo sapiens	69-73
17295611-4	2007	In particular, NAD+ serves as a substrate for ADP-ribosylation reactions and for the Sir2 family of NAD+-dependent protein deacetylases as well as a precursor of the calcium mobilizing molecule cADPr (cyclic ADP-ribose).	NAD	15-19	sirtuin 1	Homo sapiens	85-89
17253767-1	2007	Abeta binding alcohol dehydrogenase (ABAD) is an NAD-dependent mitochondrial dehydrogenase.	NAD	49-52	hydroxysteroid 17-beta dehydrogenase 10	Homo sapiens	0-35
17253767-1	2007	Abeta binding alcohol dehydrogenase (ABAD) is an NAD-dependent mitochondrial dehydrogenase.	NAD	49-52	hydroxysteroid 17-beta dehydrogenase 10	Homo sapiens	37-41
17253767-9	2007	Conversely, NAD inhibits the Abeta-ABAD interaction.	NAD	12-15	hydroxysteroid 17-beta dehydrogenase 10	Homo sapiens	35-39
17253767-10	2007	Binding of Abeta and binding of NAD to ABAD are likely mutually exclusive.	NAD	32-35	hydroxysteroid 17-beta dehydrogenase 10	Homo sapiens	39-43
17082363-4	2007	The AMP-activated protein kinase, hypoxia-inducible factor 1, peroxisome proliferator-activated receptors, and Sirt1 proteins all contribute to altering skeletal muscle gene expression by sensing changes in the concentrations of AMP, molecular oxygen, intracellular free fatty acids, and NAD+, respectively.	NAD	288-292	sirtuin 1	Homo sapiens	111-116
17701476-3	2007	Like their yeast homologs, the mammalian sirtuins (SIRT1-7) are class III HDACs and require NAD(+) as a cofactor to deacetylate substrates ranging from histones to transcriptional regulators.	NAD	92-98	sirtuin 1	Homo sapiens	51-58
17060362-5	2007	Moreover, in a simplified CFS using purified mutant cytochrome b558 and recombinant p67phox, p47phox, and Rac1proteins, we found that the Km for NADPH and for NADH was about three times higher than those of purified WT cytochrome b558, indicating that the Leu505Arg mutation induces a slight decrease of the affinity for NADPH and NADH.	NAD	159-163	mitochondrially encoded cytochrome b	Homo sapiens	52-64
17060362-5	2007	Moreover, in a simplified CFS using purified mutant cytochrome b558 and recombinant p67phox, p47phox, and Rac1proteins, we found that the Km for NADPH and for NADH was about three times higher than those of purified WT cytochrome b558, indicating that the Leu505Arg mutation induces a slight decrease of the affinity for NADPH and NADH.	NAD	159-163	neutrophil cytosolic factor 1	Homo sapiens	93-100
17060362-5	2007	Moreover, in a simplified CFS using purified mutant cytochrome b558 and recombinant p67phox, p47phox, and Rac1proteins, we found that the Km for NADPH and for NADH was about three times higher than those of purified WT cytochrome b558, indicating that the Leu505Arg mutation induces a slight decrease of the affinity for NADPH and NADH.	NAD	159-163	Rac family small GTPase 1	Homo sapiens	106-110
17060362-5	2007	Moreover, in a simplified CFS using purified mutant cytochrome b558 and recombinant p67phox, p47phox, and Rac1proteins, we found that the Km for NADPH and for NADH was about three times higher than those of purified WT cytochrome b558, indicating that the Leu505Arg mutation induces a slight decrease of the affinity for NADPH and NADH.	NAD	331-335	mitochondrially encoded cytochrome b	Homo sapiens	52-64
17060362-5	2007	Moreover, in a simplified CFS using purified mutant cytochrome b558 and recombinant p67phox, p47phox, and Rac1proteins, we found that the Km for NADPH and for NADH was about three times higher than those of purified WT cytochrome b558, indicating that the Leu505Arg mutation induces a slight decrease of the affinity for NADPH and NADH.	NAD	331-335	neutrophil cytosolic factor 1	Homo sapiens	93-100
17060362-5	2007	Moreover, in a simplified CFS using purified mutant cytochrome b558 and recombinant p67phox, p47phox, and Rac1proteins, we found that the Km for NADPH and for NADH was about three times higher than those of purified WT cytochrome b558, indicating that the Leu505Arg mutation induces a slight decrease of the affinity for NADPH and NADH.	NAD	331-335	Rac family small GTPase 1	Homo sapiens	106-110
17083911-4	2006	The product, oxidized nicotinamide adenine dinucleotide phosphate (NADP(+)), formed following the reaction of NADK with NAD(+) and adenosine 5"-triphosphate was detected with the aid of glucose-6-phosphate dehydrogenase or NADP(+)-isocitrate dehydrogenase, iodonitrotetrazolium chloride, and phenazine methosulfate.	NAD	120-126	glucose-6-phosphate dehydrogenase	Homo sapiens	186-219
16904242-4	2006	)-evoked systemic inflammation enhanced PARP-1 activity in the mouse brain, leading to the lowering of beta-NAD(+) concentration, to translocation of apoptosis inducing factor from mitochondria to the nucleus, and to enhanced lipid peroxidation.	NAD	103-114	poly (ADP-ribose) polymerase family, member 1	Mus musculus	40-46
16905546-6	2006	Further experiments showed accumulation of NADH and NRH, cofactors for NQO1 and NQO2, indicating altered intracellular redox status.	NAD	43-47	NAD(P)H dehydrogenase, quinone 1	Mus musculus	71-75
16935261-0	2006	Regulation of SIRT 1 mediated NAD dependent deacetylation: a novel role for the multifunctional enzyme CD38.	NAD	30-33	CD38 antigen	Mus musculus	103-107
16935261-1	2006	The SIRT 1 enzyme is a NAD dependent deacetylase implicated in ageing, cell protection, and energy metabolism in mammalian cells.	NAD	23-26	sirtuin 1	Homo sapiens	4-10
16935261-4	2006	However, the major enzymatic activity of CD38 is the hydrolysis of NAD.	NAD	67-70	CD38 antigen	Mus musculus	41-45
16935261-7	2006	We propose that by modulating availability of NAD to the SIRT1 enzyme, CD38 may regulate SIRT1 enzymatic activity.	NAD	46-49	CD38 antigen	Mus musculus	71-75
16935261-8	2006	We observed that in CD38 knockout mice, tissue levels of NAD are significantly increased.	NAD	57-60	CD38 antigen	Mus musculus	20-24
16935261-13	2006	Our data support the novel concept that nuclear CD38 is a major regulator of cellular/nuclear NAD level, and SIRT1 activity.	NAD	94-97	CD38 antigen	Mus musculus	48-52
16919249-1	2006	To investigate whether neural nitric oxide synthase (nNOS) in the parabrachial nucleus (PB) is involved in processing visceral noxious stimulation, we mapped the distribution of histochemical staining for nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d), a marker for nNOS, and immunohistochemical staining for Fos, a neuronal activity marker, in the subnuclei of the PB following 2% formalin injection into the stomach of rats.	NAD	205-238	nitric oxide synthase 1	Rattus norvegicus	53-57
16632544-9	2006	This type of cell death was blocked by repletion of cellular NAD levels as well as by activation of the longevity factor Sir2alpha deacetylase, indicating that PARP induction and subsequent depletion of NAD levels are the sequence of events causing angiotensin II-mediated cardiomyocyte cell death.	NAD	61-64	poly (ADP-ribose) polymerase family, member 1	Mus musculus	160-164
17042794-7	2006	Furthermore, neuronal cultures derived from the Wld(s) mouse, which overexpress the NAD(+) synthetic enzyme nicotinamide mononucleotide adenyl transferase (NMNAT-1), had reduced sensitivity to Zn(2+) neurotoxicity.	NAD	84-90	nicotinamide nucleotide adenylyltransferase 1	Rattus norvegicus	156-163
16807375-0	2006	Regulation of mouse hepatic alpha-amino-beta-carboxymuconate-epsilon-semialdehyde decarboxylase, a key enzyme in the tryptophan-nicotinamide adenine dinucleotide pathway, by hepatocyte nuclear factor 4alpha and peroxisome proliferator-activated receptor alpha.	NAD	128-161	amino carboxymuconate semialdehyde decarboxylase	Mus musculus	28-95
16807375-2	2006	alpha-Amino-beta-carboxymuconate-epsilon-semialdehyde decarboxylase (ACMSD) is the key enzyme regulating de novo synthesis of NAD from l-tryptophan (Trp), designated the Trp-NAD pathway.	NAD	126-129	amino carboxymuconate semialdehyde decarboxylase	Mus musculus	0-67
16807375-2	2006	alpha-Amino-beta-carboxymuconate-epsilon-semialdehyde decarboxylase (ACMSD) is the key enzyme regulating de novo synthesis of NAD from l-tryptophan (Trp), designated the Trp-NAD pathway.	NAD	126-129	amino carboxymuconate semialdehyde decarboxylase	Mus musculus	69-74
16807375-2	2006	alpha-Amino-beta-carboxymuconate-epsilon-semialdehyde decarboxylase (ACMSD) is the key enzyme regulating de novo synthesis of NAD from l-tryptophan (Trp), designated the Trp-NAD pathway.	NAD	174-177	amino carboxymuconate semialdehyde decarboxylase	Mus musculus	0-67
16807375-2	2006	alpha-Amino-beta-carboxymuconate-epsilon-semialdehyde decarboxylase (ACMSD) is the key enzyme regulating de novo synthesis of NAD from l-tryptophan (Trp), designated the Trp-NAD pathway.	NAD	174-177	amino carboxymuconate semialdehyde decarboxylase	Mus musculus	69-74
16965620-14	2006	The ERbeta agonist DPN caused a decrease of the PR mRNA levels, which was also found for PRAB and PRB immunostaining in the GE.	NAD	19-22	RB transcriptional corepressor 1	Rattus norvegicus	98-101
16965620-17	2006	The ERbeta agonist DPN decreased the mRNA levels of PRAB and PRB, as well as the PRAB protein level in GE.	NAD	19-22	RB transcriptional corepressor 1	Rattus norvegicus	61-64
16892051-1	2006	The nicotinamide adenine dinucleotide (NAD)-dependent deacetylase Sir2 (silent information regulator 2) regulates gene silencing in yeast and promotes lifespan extension during caloric restriction.	NAD	4-37	sirtuin 1	Homo sapiens	66-70
16892051-1	2006	The nicotinamide adenine dinucleotide (NAD)-dependent deacetylase Sir2 (silent information regulator 2) regulates gene silencing in yeast and promotes lifespan extension during caloric restriction.	NAD	39-42	sirtuin 1	Homo sapiens	66-70
16757471-4	2006	With NAD+ as a cofactor, recombinant 15-hydroxyprostaglandin dehydrogenase acted as an 18-hydroxyl dehydrogenase to form 18-oxo-RvE1.	NAD	5-9	carbonyl reductase 1	Homo sapiens	37-74
16582021-1	2006	Poly(ADP-ribose) polymerase-1 (PARP-1), the most abundant member of the PARP family, is a nuclear enzyme that catalyzes ADP-ribose transfer from NAD+ to specific acceptor proteins in response to DNA damage.	NAD	145-149	poly (ADP-ribose) polymerase family, member 1	Mus musculus	0-29
16582021-1	2006	Poly(ADP-ribose) polymerase-1 (PARP-1), the most abundant member of the PARP family, is a nuclear enzyme that catalyzes ADP-ribose transfer from NAD+ to specific acceptor proteins in response to DNA damage.	NAD	145-149	poly (ADP-ribose) polymerase family, member 1	Mus musculus	31-37
16582021-1	2006	Poly(ADP-ribose) polymerase-1 (PARP-1), the most abundant member of the PARP family, is a nuclear enzyme that catalyzes ADP-ribose transfer from NAD+ to specific acceptor proteins in response to DNA damage.	NAD	145-149	poly (ADP-ribose) polymerase family, member 1	Mus musculus	31-35
16814740-1	2006	Cytochrome b5 reductase (cb5r), a member of the flavoprotein transhydrogenase family of oxidoreductase enzymes, catalyzes the transfer of reducing equivalents from the physiological electron donor, NADH, to two molecules of cytochrome b5.	NAD	198-202	cytochrome b5	Canis lupus familiaris	0-13
16814740-7	2006	Initial-rate kinetic studies revealed the canine diaphorase domain retained a marked preference for NADH versus NADPH as reducing substrate and exhibited kcat"s of 767 and 600 s(-1) for NADH:ferricyanide reductase and NADH:cytochrome b5 reductase activities, respectively, with Km"s of 7, 8, and 12 microM for NADH, K3Fe(CN)6, and cytochrome b5, respectively.	NAD	100-104	cytochrome b5	Canis lupus familiaris	223-236
16814740-7	2006	Initial-rate kinetic studies revealed the canine diaphorase domain retained a marked preference for NADH versus NADPH as reducing substrate and exhibited kcat"s of 767 and 600 s(-1) for NADH:ferricyanide reductase and NADH:cytochrome b5 reductase activities, respectively, with Km"s of 7, 8, and 12 microM for NADH, K3Fe(CN)6, and cytochrome b5, respectively.	NAD	100-104	cytochrome b5	Canis lupus familiaris	331-344
16814740-7	2006	Initial-rate kinetic studies revealed the canine diaphorase domain retained a marked preference for NADH versus NADPH as reducing substrate and exhibited kcat"s of 767 and 600 s(-1) for NADH:ferricyanide reductase and NADH:cytochrome b5 reductase activities, respectively, with Km"s of 7, 8, and 12 microM for NADH, K3Fe(CN)6, and cytochrome b5, respectively.	NAD	186-190	cytochrome b5	Canis lupus familiaris	223-236
16814740-7	2006	Initial-rate kinetic studies revealed the canine diaphorase domain retained a marked preference for NADH versus NADPH as reducing substrate and exhibited kcat"s of 767 and 600 s(-1) for NADH:ferricyanide reductase and NADH:cytochrome b5 reductase activities, respectively, with Km"s of 7, 8, and 12 microM for NADH, K3Fe(CN)6, and cytochrome b5, respectively.	NAD	186-190	cytochrome b5	Canis lupus familiaris	331-344
16814740-7	2006	Initial-rate kinetic studies revealed the canine diaphorase domain retained a marked preference for NADH versus NADPH as reducing substrate and exhibited kcat"s of 767 and 600 s(-1) for NADH:ferricyanide reductase and NADH:cytochrome b5 reductase activities, respectively, with Km"s of 7, 8, and 12 microM for NADH, K3Fe(CN)6, and cytochrome b5, respectively.	NAD	186-190	cytochrome b5	Canis lupus familiaris	223-236
16814740-7	2006	Initial-rate kinetic studies revealed the canine diaphorase domain retained a marked preference for NADH versus NADPH as reducing substrate and exhibited kcat"s of 767 and 600 s(-1) for NADH:ferricyanide reductase and NADH:cytochrome b5 reductase activities, respectively, with Km"s of 7, 8, and 12 microM for NADH, K3Fe(CN)6, and cytochrome b5, respectively.	NAD	186-190	cytochrome b5	Canis lupus familiaris	331-344
16814740-7	2006	Initial-rate kinetic studies revealed the canine diaphorase domain retained a marked preference for NADH versus NADPH as reducing substrate and exhibited kcat"s of 767 and 600 s(-1) for NADH:ferricyanide reductase and NADH:cytochrome b5 reductase activities, respectively, with Km"s of 7, 8, and 12 microM for NADH, K3Fe(CN)6, and cytochrome b5, respectively.	NAD	186-190	cytochrome b5	Canis lupus familiaris	223-236
16814740-7	2006	Initial-rate kinetic studies revealed the canine diaphorase domain retained a marked preference for NADH versus NADPH as reducing substrate and exhibited kcat"s of 767 and 600 s(-1) for NADH:ferricyanide reductase and NADH:cytochrome b5 reductase activities, respectively, with Km"s of 7, 8, and 12 microM for NADH, K3Fe(CN)6, and cytochrome b5, respectively.	NAD	186-190	cytochrome b5	Canis lupus familiaris	331-344
16782877-10	2006	Finally, we show that mutation of the CtBP NADH binding site impairs the ability of the proteins to dimerize and to associate with BKLF.	NAD	43-47	Kruppel like factor 3	Homo sapiens	131-135
16783373-1	2006	Nicotinamide phosphoribosyltransferase (Nampt) synthesizes nicotinamide mononucleotide (NMN) from nicotinamide in a mammalian NAD+ biosynthetic pathway and is required for SirT1 activity in vivo.	NAD	126-130	sirtuin 1	Homo sapiens	172-177
16733230-10	2006	CONCLUSIONS: Insulin stimulates NAD(P)H oxidase activity and with Ang II synergistically stimulates it in cultured rat VSMC by increasing the NADH/NAD(+) redox potential, but not by phosphatidylinositol 3-kinase or heterotrimeric G(iota) protein-dependent pathways.	NAD	142-146	angiogenin	Rattus norvegicus	66-69
16733230-10	2006	CONCLUSIONS: Insulin stimulates NAD(P)H oxidase activity and with Ang II synergistically stimulates it in cultured rat VSMC by increasing the NADH/NAD(+) redox potential, but not by phosphatidylinositol 3-kinase or heterotrimeric G(iota) protein-dependent pathways.	NAD	147-153	angiogenin	Rattus norvegicus	66-69
16533815-2	2006	Previous x-ray structures of complexes of the nucleotide-binding components of transhydrogenase ("dI2dIII1" complexes) indicate that the dihydronicotinamide ring of NADH can move from a distal position relative to the nicotinamide ring of NADP+ to a proximal position.	NAD	165-169	Inhibitor-2	Drosophila melanogaster	98-106
16533815-8	2006	X-ray structures of dI2dIII1 complexes carrying the mutations showed that their effects were restricted to the locality of the bound NAD(H).	NAD	133-139	Inhibitor-2	Drosophila melanogaster	20-28
16601673-3	2006	beta-NAD(+)- or ADP-ribose-evoked TRPM2 activity is robustly potentiated at elevated temperatures.	NAD	0-11	transient receptor potential cation channel, subfamily M, member 2	Mus musculus	34-39
16481327-8	2006	In addition, using an in vivo NADH photobleaching technique, we demonstrate that mitochondrial NADH metabolism is reduced in p66(shc-/-) cells.	NAD	30-34	src homology 2 domain-containing transforming protein C1	Mus musculus	125-128
16481327-8	2006	In addition, using an in vivo NADH photobleaching technique, we demonstrate that mitochondrial NADH metabolism is reduced in p66(shc-/-) cells.	NAD	30-34	src homology 2 domain-containing transforming protein C1	Mus musculus	129-132
16481327-8	2006	In addition, using an in vivo NADH photobleaching technique, we demonstrate that mitochondrial NADH metabolism is reduced in p66(shc-/-) cells.	NAD	95-99	src homology 2 domain-containing transforming protein C1	Mus musculus	125-128
16481327-8	2006	In addition, using an in vivo NADH photobleaching technique, we demonstrate that mitochondrial NADH metabolism is reduced in p66(shc-/-) cells.	NAD	95-99	src homology 2 domain-containing transforming protein C1	Mus musculus	129-132
16628003-6	2006	Our findings establish a functional link between the two NAD+-dependent enzyme systems and provide a physiological interpretation for the mechanism of death in cells lacking SIRT1.	NAD	57-61	sirtuin 1	Homo sapiens	174-179
16477420-1	2006	Mevalonate kinase can be conveniently assayed by coupling to two other reactions and monitoring the consumption of NADH optically at 340 nm.	NAD	115-119	mevalonate kinase	Saccharomyces cerevisiae S288C	0-17
16041576-8	2006	In addition, genes involved in NAD metabolism, i.e. BNA2, BNA3, BNA4 and BNA6, or those involved in the TCA cycle and glutamate metabolism, i.e. MEU1, CIT1, CIT2, KDG1 and KDG2, displayed significant changes in expression.	NAD	31-34	dioxygenase BNA2	Saccharomyces cerevisiae S288C	52-56
16455971-2	2006	Here we show that micromolar concentrations of nicotinamide adenine dinucleotide (NAD) induce a rapid increase of annexin V staining in NKT cells in vitro, a response that requires expression of P2X(7)Rs.	NAD	47-80	annexin A5	Mus musculus	114-123
16502325-0	2006	A kinetic study on the phenothiazine dependent oxidation of NADH by bovine ceruloplasmin.	NAD	60-64	ceruloplasmin and hephaestin like 1	Bos taurus	75-88
16388603-3	2006	Sir2 proteins (sirtuins) catalyze the chemical conversion of NAD+ and acetylated lysine to nicotinamide, deacetylated lysine, and 2"-O-acetyl-ADP-ribose (OAADPr).	NAD	61-65	sirtuin 1	Homo sapiens	0-4
16207712-5	2005	The beneficial effect of NAD repletion was seen, however, only when Sir2alpha was intact.	NAD	25-28	sirtuin 1	Homo sapiens	68-77
16207712-6	2005	Knocking down Sir2alpha levels by small interfering RNA eliminated this benefit, indicating that Sir2alpha is a downstream target of NAD replenishment leading to cell protection.	NAD	133-136	sirtuin 1	Homo sapiens	14-23
16207712-6	2005	Knocking down Sir2alpha levels by small interfering RNA eliminated this benefit, indicating that Sir2alpha is a downstream target of NAD replenishment leading to cell protection.	NAD	133-136	sirtuin 1	Homo sapiens	97-106
16207712-7	2005	NAD repletion also prevented loss of the transcriptional regulatory activity of the Sir2alpha catalytic core domain resulting from PARP activation.	NAD	0-3	sirtuin 1	Homo sapiens	84-93
16207712-9	2005	These data demonstrate that, in stressed cardiac myocytes, depletion of cellular NAD levels forms a link between PARP activation and reduced Sir2alpha deacetylase activity, contributing to myocyte cell death during heart failure.	NAD	81-84	sirtuin 1	Homo sapiens	141-150
16100107-1	2005	The mitochondrial NAD-dependent methylenetetrahydrofolate dehydrogenase-cyclohydrolase (NMDMC) is believed to have evolved from a trifunctional NADP-dependent methylenetetrahydrofolate dehydrogenase-cyclohydrolase-synthetase.	NAD	18-21	methylenetetrahydrofolate dehydrogenase (NADP+ dependent) 2, methenyltetrahydrofolate cyclohydrolase	Homo sapiens	88-93
16100107-8	2005	NMDMC uses Pi and magnesium to adapt an NADP binding site for NAD binding.	NAD	40-43	methylenetetrahydrofolate dehydrogenase (NADP+ dependent) 2, methenyltetrahydrofolate cyclohydrolase	Homo sapiens	0-5
16305310-1	2005	NAD synthetase is responsible for the conversion of nicotinic acid adenine dinucleotide to nicotinamide adenine dinucleotide.	NAD	91-124	NAD synthetase 1	Homo sapiens	0-14
16157265-3	2005	The results indicated that apart from the two subunits of cellular RNA polymerase complex, BTF3 and ATF5, this nsp10 protein was also able to interact specifically with the NADH 4L subunit and cytochrome oxidase II.	NAD	173-177	activating transcription factor 5	Homo sapiens	100-104
16079181-1	2005	Sir2 is a NAD+-dependent protein deacetylase that extends lifespan in yeast and worms.	NAD	10-13	sirtuin 1	Homo sapiens	0-4
16166628-9	2005	Instead, the NAD+-dependent deacetylase SIRT1 can potently induce MEF2 deacetylation.	NAD	13-17	sirtuin 1	Homo sapiens	40-45
16116196-0	2005	High sensitivity of CD4+CD25+ regulatory T cells to extracellular metabolites nicotinamide adenine dinucleotide and ATP: a role for P2X7 receptors.	NAD	78-111	CD4 antigen	Mus musculus	20-23
16116196-2	2005	In this study we demonstrate that micromolar concentrations of the common cell metabolite NAD induce death in murine forkhead/winged helix transcription factor gene-expressing CD4+CD25+ regulatory T cells with high efficiency and within minutes.	NAD	90-93	CD4 antigen	Mus musculus	176-179
16116196-6	2005	Injection of NAD or benzoylbenzoyl-ATP causes preferential induction of a cell death signal in CD4+CD25+ cells.	NAD	13-16	CD4 antigen	Mus musculus	95-98
15967408-2	2005	Mitochondrial glycerophosphate dehydrogenase (mGPDH) participates in the reoxidation of cytosolic NADH by delivering reducing equivalents from this molecule into the electron transport chain, thus sustaining glycolysis.	NAD	98-102	glycerol phosphate dehydrogenase 2, mitochondrial	Mus musculus	46-51
15899856-2	2005	Their assembly into silent chromatin is believed to require the deacetylation of histones by the NAD-dependent deacetylase Sir2 and the subsequent interaction of Sir3 and Sir4 with these hypoacetylated regions of chromatin.	NAD	97-100	chromatin-silencing protein SIR4	Saccharomyces cerevisiae S288C	171-175
15716268-1	2005	In lower organisms, increased expression of the NAD-dependent deacetylase Sir2 augments lifespan.	NAD	48-51	sirtuin 1	Homo sapiens	74-78
15781114-2	2005	As an enzyme, CD38 catalyzes the conversion of NAD(+) and NADP to several metabolites including cADPR and NAADP, which mediate Ca(2+) release from separate intracellular stores, and ADPR, which activates the TRPM2 plasma membrane Ca(2+) channel.	NAD	47-53	CD38 antigen	Mus musculus	14-18
15781114-2	2005	As an enzyme, CD38 catalyzes the conversion of NAD(+) and NADP to several metabolites including cADPR and NAADP, which mediate Ca(2+) release from separate intracellular stores, and ADPR, which activates the TRPM2 plasma membrane Ca(2+) channel.	NAD	47-53	transient receptor potential cation channel, subfamily M, member 2	Mus musculus	208-213
15781611-4	2005	An analysis of untreated skin revealed an altered intracellular redox state due to accumulation of NADH and reduced levels of NAD/NADH in NQO1-null mice as compared with wild-type mice.	NAD	99-103	NAD(P)H dehydrogenase, quinone 1	Mus musculus	138-142
15565635-1	2005	Human cyotsolic malate dehydrogenase (MDH1) is important in transporting NADH equivalents across the mitochondrial membrane, controlling tricarboxylic acid (TCA) cycle pool size and providing contractile function.	NAD	73-77	malic enzyme 1	Homo sapiens	16-36
15557339-7	2005	Using single deletion mutants of Nde1p or Nde2p, we have shown that glycerol 3-phosphate oxidation via Gut2p is inhibited fully when NADH is oxidized via Nde1p, whereas only 50% of glycerol 3-phosphate oxidation is inhibited when Nde2p is functioning.	NAD	133-137	NADH-ubiquinone reductase (H(+)-translocating) NDE1	Saccharomyces cerevisiae S288C	33-38
15557339-7	2005	Using single deletion mutants of Nde1p or Nde2p, we have shown that glycerol 3-phosphate oxidation via Gut2p is inhibited fully when NADH is oxidized via Nde1p, whereas only 50% of glycerol 3-phosphate oxidation is inhibited when Nde2p is functioning.	NAD	133-137	NADH-ubiquinone reductase (H(+)-translocating) NDE2	Saccharomyces cerevisiae S288C	42-47
15557339-7	2005	Using single deletion mutants of Nde1p or Nde2p, we have shown that glycerol 3-phosphate oxidation via Gut2p is inhibited fully when NADH is oxidized via Nde1p, whereas only 50% of glycerol 3-phosphate oxidation is inhibited when Nde2p is functioning.	NAD	133-137	NADH-ubiquinone reductase (H(+)-translocating) NDE1	Saccharomyces cerevisiae S288C	154-159
15557339-7	2005	Using single deletion mutants of Nde1p or Nde2p, we have shown that glycerol 3-phosphate oxidation via Gut2p is inhibited fully when NADH is oxidized via Nde1p, whereas only 50% of glycerol 3-phosphate oxidation is inhibited when Nde2p is functioning.	NAD	133-137	NADH-ubiquinone reductase (H(+)-translocating) NDE2	Saccharomyces cerevisiae S288C	230-235
15720144-9	2005	The system with a relatively higher concentration of NADPH favored formation of anti-BPDE via P450 1A1/P450 1B1, while the system with the higher concentration of NAD+ favored formation of BP-7,8-dione via AKR1A1.	NAD	163-167	aldo-keto reductase family 1 member A1	Homo sapiens	206-212
15719057-2	2005	We report here that Tat is deacetylated by human sirtuin 1 (SIRT1), a nicotinamide adenine dinucleotide-dependent class III protein deacetylase in vitro and in vivo.	NAD	70-103	sirtuin 1	Homo sapiens	49-58
15719057-2	2005	We report here that Tat is deacetylated by human sirtuin 1 (SIRT1), a nicotinamide adenine dinucleotide-dependent class III protein deacetylase in vitro and in vivo.	NAD	70-103	sirtuin 1	Homo sapiens	60-65
15808017-3	2005	Alcohol dehydrogenase (ADH) oxidizes ethanol to acetaldehyde using the coenzyme nicotinamide adenine dinucleotide (NAD), which is concurrently reduced to form NADH.	NAD	80-113	aldo-keto reductase family 1 member A1	Homo sapiens	0-21
15808017-3	2005	Alcohol dehydrogenase (ADH) oxidizes ethanol to acetaldehyde using the coenzyme nicotinamide adenine dinucleotide (NAD), which is concurrently reduced to form NADH.	NAD	80-113	aldo-keto reductase family 1 member A1	Homo sapiens	23-26
15808017-3	2005	Alcohol dehydrogenase (ADH) oxidizes ethanol to acetaldehyde using the coenzyme nicotinamide adenine dinucleotide (NAD), which is concurrently reduced to form NADH.	NAD	115-118	aldo-keto reductase family 1 member A1	Homo sapiens	0-21
15808017-3	2005	Alcohol dehydrogenase (ADH) oxidizes ethanol to acetaldehyde using the coenzyme nicotinamide adenine dinucleotide (NAD), which is concurrently reduced to form NADH.	NAD	115-118	aldo-keto reductase family 1 member A1	Homo sapiens	23-26
15808017-3	2005	Alcohol dehydrogenase (ADH) oxidizes ethanol to acetaldehyde using the coenzyme nicotinamide adenine dinucleotide (NAD), which is concurrently reduced to form NADH.	NAD	159-163	aldo-keto reductase family 1 member A1	Homo sapiens	0-21
15808017-3	2005	Alcohol dehydrogenase (ADH) oxidizes ethanol to acetaldehyde using the coenzyme nicotinamide adenine dinucleotide (NAD), which is concurrently reduced to form NADH.	NAD	159-163	aldo-keto reductase family 1 member A1	Homo sapiens	23-26
15562437-3	2005	PARP-1 is an abundant nuclear enzyme that, when activated by DNA damage, consumes nicotinamide adenine dinucleotide (NAD)+ to form poly(ADP-ribose) on acceptor proteins.	NAD	82-115	poly (ADP-ribose) polymerase family, member 1	Mus musculus	0-6
15562437-3	2005	PARP-1 is an abundant nuclear enzyme that, when activated by DNA damage, consumes nicotinamide adenine dinucleotide (NAD)+ to form poly(ADP-ribose) on acceptor proteins.	NAD	117-122	poly (ADP-ribose) polymerase family, member 1	Mus musculus	0-6
15562437-5	2005	We used mouse astrocyte cultures to explore the bioenergetic effects of NAD+ depletion by PARP-1 and the role of NAD+ depletion in this cell death program.	NAD	72-76	poly (ADP-ribose) polymerase family, member 1	Mus musculus	90-96
15562437-7	2005	PARP-1 activation led to a rapid but incomplete depletion of astrocyte NAD+, a near-complete block in glycolysis, and eventual cell death.	NAD	71-75	poly (ADP-ribose) polymerase family, member 1	Mus musculus	0-6
15562437-10	2005	These studies suggest PARP-1 activation leads to rapid depletion of the cytosolic but not the mitochondrial NAD+ pool.	NAD	108-112	poly (ADP-ribose) polymerase family, member 1	Mus musculus	22-28
15465812-0	2004	Biochemical regulation of mammalian AMP-activated protein kinase activity by NAD and NADH.	NAD	77-80	protein kinase AMP-activated non-catalytic subunit beta 1	Homo sapiens	36-64
15465812-0	2004	Biochemical regulation of mammalian AMP-activated protein kinase activity by NAD and NADH.	NAD	85-89	protein kinase AMP-activated non-catalytic subunit beta 1	Homo sapiens	36-64
15465812-7	2004	The recombinant T172D-AMPK, which was mutated to mimic the phosphorylated state, was activated by beta-NAD in a dose-dependent manner, whereas NADH inhibited its activity.	NAD	98-106	protein kinase AMP-activated non-catalytic subunit beta 1	Homo sapiens	22-26
15465812-7	2004	The recombinant T172D-AMPK, which was mutated to mimic the phosphorylated state, was activated by beta-NAD in a dose-dependent manner, whereas NADH inhibited its activity.	NAD	143-147	protein kinase AMP-activated non-catalytic subunit beta 1	Homo sapiens	22-26
30753815-4	2019	We recently developed small molecule inhibitors of nicotinamide N-methyltransferase (NNMT), an enzyme overexpressed with aging in skeletal muscles and linked to impairment of the NAD+ salvage pathway, dysregulated sirtuin 1 activity, and increased muSC senescence.	NAD	179-183	nicotinamide N-methyltransferase	Mus musculus	85-89
31043584-2	2019	SIRT1 is a NAD dependent protein deacetylase and implicated in diverse cellular processes such as DNA damage repair, and cancer progression.	NAD	11-14	sirtuin 1	Homo sapiens	0-5
15465812-8	2004	We explored the effect of NADH on AMPK by systematically varying the concentrations of ATP, NADH, peptide substrate, and AMP.	NAD	26-30	protein kinase AMP-activated non-catalytic subunit beta 1	Homo sapiens	34-38
15465812-9	2004	Based on our findings and established activation of AMPK by AMP, we proposed a model for the regulation by NADH.	NAD	107-111	protein kinase AMP-activated non-catalytic subunit beta 1	Homo sapiens	52-56
31003681-7	2019	The changes of mean scores of TCSS, VPT, ABI and the plasma glucose levels in the Gua Sha group showed a significant change from baseline to week 12, indicating that Gua Sha therapy induced progressive improvement in the management of DPN symptoms, sensory function, peripheral artery disease and glucose levels.	NAD	235-238	DExD-box helicase 21	Homo sapiens	82-85
31003681-7	2019	The changes of mean scores of TCSS, VPT, ABI and the plasma glucose levels in the Gua Sha group showed a significant change from baseline to week 12, indicating that Gua Sha therapy induced progressive improvement in the management of DPN symptoms, sensory function, peripheral artery disease and glucose levels.	NAD	235-238	DExD-box helicase 21	Homo sapiens	166-169
31003681-10	2019	CONCLUSION: Gua Sha therapy appears to be effective at reducing the severity of DPN in a clinically relevant dimension, and at improving other health outcomes in patients with DPN.	NAD	80-83	DExD-box helicase 21	Homo sapiens	12-15
31003681-10	2019	CONCLUSION: Gua Sha therapy appears to be effective at reducing the severity of DPN in a clinically relevant dimension, and at improving other health outcomes in patients with DPN.	NAD	176-179	DExD-box helicase 21	Homo sapiens	12-15
31003681-11	2019	While this study found that Gua Sha therapy is a promising treatment in reducing the symptoms of patients with DPN, further, larger sample studies are required to confirm the effects of Gua Sha therapy in patients with DPN.	NAD	111-114	DExD-box helicase 21	Homo sapiens	28-31
31080405-0	2019	SIRT2, ERK and Nrf2 Mediate NAD+ Treatment-Induced Increase in the Antioxidant Capacity of PC12 Cells Under Basal Conditions.	NAD	28-32	sirtuin 2	Rattus norvegicus	0-5
31080405-6	2019	These NAD+-induced changes can be prevented by both SIRT2 siRNA and the SIRT2 inhibitor AGK2.	NAD	6-10	sirtuin 2	Rattus norvegicus	52-57
31080405-6	2019	These NAD+-induced changes can be prevented by both SIRT2 siRNA and the SIRT2 inhibitor AGK2.	NAD	6-10	sirtuin 2	Rattus norvegicus	72-77
31080405-8	2019	Moreover, the NAD+-induced ERK activation can be blocked by both SIRT2 siRNA and AGK2.	NAD	14-18	sirtuin 2	Rattus norvegicus	65-70
31080405-9	2019	Collectively, our study has provided the first evidence that NAD+ can enhance directly the antioxidant capacity of the cells under basal conditions, which is mediated by SIRT2, ERK, and Nrf2.	NAD	61-65	sirtuin 2	Rattus norvegicus	170-175
31118974-7	2019	Moreover, SAB increased HG- or PA-induced expression of Sirtuin 1 (Sirt1), a nicotinamide adenine dinucleotide- (NAD+-) dependent histone deacetylase.	NAD	77-110	sirtuin 1	Homo sapiens	56-65
31118974-7	2019	Moreover, SAB increased HG- or PA-induced expression of Sirtuin 1 (Sirt1), a nicotinamide adenine dinucleotide- (NAD+-) dependent histone deacetylase.	NAD	77-110	sirtuin 1	Homo sapiens	67-72
30782483-3	2019	NAD+-dependent deacylase Sirt1 deacetylates Bmal1 and Per2 to regulate circadian rhythms.	NAD	0-4	sirtuin 1	Homo sapiens	25-30
30782483-3	2019	NAD+-dependent deacylase Sirt1 deacetylates Bmal1 and Per2 to regulate circadian rhythms.	NAD	0-4	aryl hydrocarbon receptor nuclear translocator like	Homo sapiens	44-49
30782483-3	2019	NAD+-dependent deacylase Sirt1 deacetylates Bmal1 and Per2 to regulate circadian rhythms.	NAD	0-4	period circadian regulator 2	Homo sapiens	54-58
30805760-1	2019	SIRT1 is an NAD+-dependent deacetylase, whose activators have potential therapeutic applications in the age-related, metabolic, neurode-generative and cardiovascular diseases.	NAD	12-15	sirtuin 1	Homo sapiens	0-5
30996792-2	2019	PARP-1 employs NAD+ to modify substrate proteins via the attachment of poly(ADP-ribose) chains.	NAD	15-19	poly (ADP-ribose) polymerase family, member 1	Mus musculus	0-6
15347677-5	2004	The mitochondrial reduction-oxidation (red-ox) state, as indicated by the NADH/NAD+ ratio, is 5-fold higher, and hepatic TCA cycle intermediate concentrations are dramatically increased in the PEPCK null livers.	NAD	74-78	phosphoenolpyruvate carboxykinase 1, cytosolic	Mus musculus	193-198
15347677-5	2004	The mitochondrial reduction-oxidation (red-ox) state, as indicated by the NADH/NAD+ ratio, is 5-fold higher, and hepatic TCA cycle intermediate concentrations are dramatically increased in the PEPCK null livers.	NAD	79-83	phosphoenolpyruvate carboxykinase 1, cytosolic	Mus musculus	193-198
15347677-7	2004	Disruption of hepatic cataplerosis due to loss of PEPCK leads to the accumulation of TCA cycle intermediates and a nearly complete blockage of gluconeogenesis from amino acids and lactate (an energy demanding process) but intact gluconeogenesis from glycerol (which contributes to net NADH production).	NAD	285-289	phosphoenolpyruvate carboxykinase 1, cytosolic	Mus musculus	50-55
15578928-2	2004	SIR2 was discovered as a gene required for mating in S. cerevisiae 25 years ago, but it was only recently that Sir2"s activity as an NAD-dependent protein deacetylase was established.	NAD	133-136	sirtuin 1	Homo sapiens	0-4
15578928-2	2004	SIR2 was discovered as a gene required for mating in S. cerevisiae 25 years ago, but it was only recently that Sir2"s activity as an NAD-dependent protein deacetylase was established.	NAD	133-136	sirtuin 1	Homo sapiens	111-115
15578928-4	2004	In addition to Sir2, yeast have four additional NAD-dependent histone deacetylases Hst1-4 (for homologue of Sir2), with distinct cellular roles.	NAD	48-51	sirtuin 1	Homo sapiens	108-112
15302869-9	2004	On the other hand, enhancement of the automodification of PARP-1 by the addition of NAD+, its substrate, promoted the DNA binding of NF-kappaB.	NAD	84-88	poly (ADP-ribose) polymerase family, member 1	Mus musculus	58-64
15726813-1	2004	The effect of aluminum on hydrogen peroxide production and peroxidase-catalyzed NADH oxidation was studied in barley roots germinated and grown between two layers of moistened filter paper.	NAD	80-84	prx7	Hordeum vulgare	59-69
15726813-8	2004	The anionic peroxidase was activated in the Al-treated root tips and also oxidized NADH but was detectable only after a long incubation time.	NAD	83-87	prx7	Hordeum vulgare	12-22
15342248-3	2004	We have determined the crystal structure of human ABAD/HSD10 complexed with NAD(+) and an inhibitory small molecule.	NAD	76-82	hydroxysteroid 17-beta dehydrogenase 10	Homo sapiens	50-54
15313611-1	2004	The hyperthermophilic archaeon Archaeoglobus fulgidus contains an L-Ala dehydrogenase (AlaDH, EC 1.4.1.1) that is not homologous to known bacterial dehydrogenases and appears to represent a previously unrecognized archaeal group of NAD-dependent dehydrogenases.	NAD	232-235	aminolevulinate dehydratase	Homo sapiens	87-92
15313611-3	2004	We report the structure of the NAD-bound AF1665 AlaDH (AF-AlaDH) at 2.3 A in a C2 crystal form with the 70 kDa dimer in the asymmetric unit, as the first structural representative of this family.	NAD	31-34	aminolevulinate dehydratase	Homo sapiens	48-53
15313611-3	2004	We report the structure of the NAD-bound AF1665 AlaDH (AF-AlaDH) at 2.3 A in a C2 crystal form with the 70 kDa dimer in the asymmetric unit, as the first structural representative of this family.	NAD	31-34	aminolevulinate dehydratase	Homo sapiens	55-63
15313611-5	2004	Although both types of AlaDH enzyme include a Rossmann-type NAD-binding domain, the arrangement of strands in the C-terminal half of this domain is novel, and the other (catalytic) domain in the archaeal protein has a new fold.	NAD	60-63	aminolevulinate dehydratase	Homo sapiens	23-28
15301953-5	2004	Using this method, the kinetics of the reaction of the cosubstrate nicotinamide adenine dinucleotide and the competitive inhibitor nicotinamide with SIRT1 and SIRT2 has been analyzed.	NAD	67-100	sirtuin 1	Homo sapiens	149-154
15343021-1	2004	OBJECTIVES: 11beta-hydroxysteroid dehydrogenase type 2 (11beta-HSD2), which requires oxidized nicotinamide adenine dinucleotide as a cofactor, metabolizes endogenous glucocorticoids.	NAD	94-127	hydroxysteroid 11-beta dehydrogenase 2	Rattus norvegicus	56-67
15253727-10	2004	Kallikrein gene transfer significantly increased nitric oxide and cyclic guanosine monophosphate (cGMP) levels in conjunction with reduced salt-induced nicotinamide adenine dinucleotide/nicotinamide adenine dinucleotide phosphate (NADH/NADPH) oxidase activity, superoxide production, transforming growth factor-beta1 (TGF-beta1) mRNA and protein levels, and TGF-beta1 immunostaining.	NAD	152-185	kallikrein related peptidase 4	Homo sapiens	0-10
15275909-2	2004	Due to the longer half-life of F-18, compared to C-11, labeling DPN with F-18 allows for alternative experimental protocols and potentially the evaluation of endogenous opioid release.	NAD	64-67	mastermind like domain containing 1	Homo sapiens	31-35
15275909-2	2004	Due to the longer half-life of F-18, compared to C-11, labeling DPN with F-18 allows for alternative experimental protocols and potentially the evaluation of endogenous opioid release.	NAD	64-67	mastermind like domain containing 1	Homo sapiens	73-77
15148320-2	2004	Our previous studies on intact pancreatic islets used two-photon NAD(P)H imaging as a quantitative measure of the combined redox signal from NADH and NADPH (referred to as NAD(P)H).	NAD	141-145	2,4-dienoyl-CoA reductase 1	Homo sapiens	65-72
30930849-1	2019	Background: Silent information regulator 2 homolog 1 (SIRT1) is an evolutionarily conserved enzymes with nicotinamide adenine dinucleotide (NAD)+-dependent deacetylase activity.	NAD	105-138	sirtuin 1	Homo sapiens	54-59
30930849-1	2019	Background: Silent information regulator 2 homolog 1 (SIRT1) is an evolutionarily conserved enzymes with nicotinamide adenine dinucleotide (NAD)+-dependent deacetylase activity.	NAD	140-143	sirtuin 1	Homo sapiens	54-59
30871086-1	2019	Sirtuins (SIRT1-7) are NAD+-dependent protein deacetylases/ADP ribosyltransferases with important roles in chromatin silencing, cell cycle regulation, cellular differentiation, cellular stress response, metabolism and aging.	NAD	23-26	sirtuin 1	Homo sapiens	10-17
30304565-2	2019	Recently, the NAD+ -dependent deacetylase, sirtuin 1 (SIRT1), has been reported to play a key role in the development of malignant tumors.	NAD	14-17	sirtuin 1	Homo sapiens	43-52
30304565-2	2019	Recently, the NAD+ -dependent deacetylase, sirtuin 1 (SIRT1), has been reported to play a key role in the development of malignant tumors.	NAD	14-17	sirtuin 1	Homo sapiens	54-59
29486586-8	2019	High nicotinamide nucleotide transhydrogenase expression induced NADPH dehydrogenation to compensate for the NADH shortage resulting from the dysfunction of the Krebs cycle.	NAD	109-113	2,4-dienoyl-CoA reductase 1	Homo sapiens	65-70
30686754-3	2019	METHODS: We have proposed that the oxoglutarate carrier SLC25A11 is important for ATP production in cancer by NADH transportation from the cytosol to mitochondria as a malate.	NAD	110-114	solute carrier family 25 (mitochondrial carrier oxoglutarate carrier), member 11	Mus musculus	56-64
30686754-10	2019	INTERPRETATION: Cancer cells critically depended on the oxoglutarate carrier SLC25A11 for transporting NADH from cytosol to mitochondria as a malate form for the purpose of ATP production.	NAD	103-107	solute carrier family 25 (mitochondrial carrier oxoglutarate carrier), member 11	Mus musculus	77-85
31132911-1	2019	The NAD+-dependent histone deacetylase SIRT1 was shown to be associated with aging and longevity.	NAD	4-8	sirtuin 1	Homo sapiens	39-44
30626014-8	2019	We validated by WB the underexpression of NADH:ubiquinone oxidoreductase core subunit S1 (p = 0.01), as well as the overexpression of superoxide dismutase 1 (p = 0.03) and peroxiredoxin 4 (p = 0.04) in spermatozoa of ROS+ group.	NAD	42-46	peroxiredoxin 4	Homo sapiens	172-187
31657686-6	2019	RESULTS: Infusion of apelin into PVN of Wistar-Kyoto (WKY) rats induced chronic increases in systolic blood pressure (SBP), diastolic blood pressure (DBP), mean arterial pressure (MAP), plasma norepinephrine (NE) level, maximal depressor response to hexamethonium (Hex), NAD(P)H oxidase activity, superoxide anions levels, and Nox4 expression.	NAD	271-278	apelin	Rattus norvegicus	21-27
29958894-3	2019	Among the host responses to the release of ATP, NAD+ and related small molecules is their breakdown on behalf of a panel of leukocyte ectonucleotidases - CD38, CD39, CD73, CD157, CD203a and CD203c -, whose activities are concatenated to form two nucleotide-catabolizing channels defined as the canonical and non-canonical adenosinergic pathways.	NAD	48-52	ectonucleotide pyrophosphatase/phosphodiesterase 3	Homo sapiens	190-196
31208524-0	2019	Role of mitochondria in diabetic peripheral neuropathy: Influencing the NAD+-dependent SIRT1-PGC-1alpha-TFAM pathway.	NAD	72-75	sirtuin 1	Homo sapiens	87-92
31208524-5	2019	One of the key pathways that is impaired in diabetic peripheral neuropathy (DPN) is the energy sensing pathway comprising the nicotinamide-adenine dinucleotide (NAD+)-dependent Sirtuin 1 (SIRT1)/peroxisome proliferator-activated receptor-gamma coactivator alpha (PGC-1alpha)/Mt transcription factor A (TFAM or mtTFA) signaling pathway.	NAD	126-159	sirtuin 1	Homo sapiens	177-186
31208524-5	2019	One of the key pathways that is impaired in diabetic peripheral neuropathy (DPN) is the energy sensing pathway comprising the nicotinamide-adenine dinucleotide (NAD+)-dependent Sirtuin 1 (SIRT1)/peroxisome proliferator-activated receptor-gamma coactivator alpha (PGC-1alpha)/Mt transcription factor A (TFAM or mtTFA) signaling pathway.	NAD	126-159	sirtuin 1	Homo sapiens	188-193
30318462-4	2018	Reductive TCA requires malate dehydrogenase (MDH) and maintains the redox state of the NAD+/NADH pool.	NAD	87-91	malate dehydrogenase 2, NAD (mitochondrial)	Mus musculus	45-48
30318462-4	2018	Reductive TCA requires malate dehydrogenase (MDH) and maintains the redox state of the NAD+/NADH pool.	NAD	92-96	malate dehydrogenase 2, NAD (mitochondrial)	Mus musculus	45-48
30415949-1	2018	Current models of SIRT1 enzymatic regulation primarily consider the effects of fluctuating levels of its co-substrate NAD+, which binds to the stably folded catalytic domain.	NAD	118-122	sirtuin 1	Homo sapiens	18-23
30558548-4	2018	Additionally, titers of anti-NAD-dependent protein deacetylase sirtuin-1(SIRT1) antibodies were significantly higher in AS patients than in RA (P &lt; 0.05) and PsA (P &lt; 0.05) patients.	NAD	29-32	sirtuin 1	Homo sapiens	63-72
30558548-4	2018	Additionally, titers of anti-NAD-dependent protein deacetylase sirtuin-1(SIRT1) antibodies were significantly higher in AS patients than in RA (P &lt; 0.05) and PsA (P &lt; 0.05) patients.	NAD	29-32	sirtuin 1	Homo sapiens	73-78
30359575-3	2018	PARP-1 activation is NAD+ dependent and takes part in DNA repair and in chromatin remodelling and has a function in transcriptional regulation, intracellular trafficking and energy metabolism.	NAD	21-25	poly (ADP-ribose) polymerase family, member 1	Mus musculus	0-6
30574122-1	2018	The mammalian Sirtuins (SIRT1-7) are an evolutionarily conserved family of NAD+-dependent deacylase and mono-ADP-ribosyltransferase.	NAD	75-78	sirtuin 1	Homo sapiens	24-29
30246938-4	2018	Nicotinamide adenine dinucleotide (NAD)-dependent methanol dehydrogenase (Mdh), 3-hexulose-6-phosphate synthase (Hps) and 6-phospho-3-hexuloisomerase (Phi) from different sources were first screened for catalytic activity.	NAD	0-33	malate dehydrogenase 2	Homo sapiens	74-77
30246938-4	2018	Nicotinamide adenine dinucleotide (NAD)-dependent methanol dehydrogenase (Mdh), 3-hexulose-6-phosphate synthase (Hps) and 6-phospho-3-hexuloisomerase (Phi) from different sources were first screened for catalytic activity.	NAD	35-38	malate dehydrogenase 2	Homo sapiens	74-77
29869077-2	2018	As the members of the nicotinamide adenine dinucleotide-dependent family of histone deacetylases, class I sirtuin genes (including SIRT1, SIRT2 and SIRT3) play crucial roles in regulating lipid metabolism, cellular growth and metabolism, suggesting that they are potential candidate genes affecting body measurement traits in animals.	NAD	22-55	sirtuin 1	Bos taurus	131-136
29470999-4	2018	METHODS: Isolated dendritic cells and bone marrow-derived mast cells (MCs) were used to characterize the mechanisms of action of NAD+ on CD4+ T-cell fate in vitro.	NAD	129-133	CD4 antigen	Mus musculus	137-140
29470999-5	2018	Furthermore, NAD+-mediated CD4+ T-cell differentiation was investigated in vivo by using wild-type C57BL/6, MC-/-, MHC class II-/-, Wiskott-Aldrich syndrome protein (WASP)-/-, 5C.C7 recombination-activating gene 2 (Rag2)-/-, and CD11b-DTR transgenic mice.	NAD	13-17	CD4 antigen	Mus musculus	27-30
30546461-2	2018	Nicotinamide phosphoribosyltransferase (NAMPT), the key enzyme in the nicotinamide-adenine dinucleotide (NAD+)-mediated pathway for the activation of silent information regulator 1 (SIRT1), serves a key function in HCC cell invasion and metastasis.	NAD	70-103	sirtuin 1	Homo sapiens	150-180
30546461-2	2018	Nicotinamide phosphoribosyltransferase (NAMPT), the key enzyme in the nicotinamide-adenine dinucleotide (NAD+)-mediated pathway for the activation of silent information regulator 1 (SIRT1), serves a key function in HCC cell invasion and metastasis.	NAD	70-103	sirtuin 1	Homo sapiens	182-187
30546461-2	2018	Nicotinamide phosphoribosyltransferase (NAMPT), the key enzyme in the nicotinamide-adenine dinucleotide (NAD+)-mediated pathway for the activation of silent information regulator 1 (SIRT1), serves a key function in HCC cell invasion and metastasis.	NAD	105-109	sirtuin 1	Homo sapiens	150-180
30546461-2	2018	Nicotinamide phosphoribosyltransferase (NAMPT), the key enzyme in the nicotinamide-adenine dinucleotide (NAD+)-mediated pathway for the activation of silent information regulator 1 (SIRT1), serves a key function in HCC cell invasion and metastasis.	NAD	105-109	sirtuin 1	Homo sapiens	182-187
15165865-10	2004	Similarity also exists between liver alcohol dehydrogenase and cAMP-dependent protein kinase whereby groups on NAD and ATP, respectively, mimic the backbone of a single amino acid residue in a process where a three residue segment located at the terminus of a beta-sheet, moves to form hydrogen bonds with the mimic that resemble those found in a parallel beta-sheet.	NAD	111-114	aldo-keto reductase family 1 member A1	Homo sapiens	37-58
30546461-7	2018	Furthermore, FK866 inhibited the SIRT1-mediated EMT, invasion and migration of HCC cells by decreasing the expression of the NAMPT/NAD+ pathway.	NAD	131-135	sirtuin 1	Homo sapiens	33-38
30546461-8	2018	Taken together, the results of the present study suggest that FK866 may be an effective drug targeting HCC metastasis and invasion, and that the NAMPT/NAD+/SIRT1 pathway may be a potential therapeutic target for HCC.	NAD	151-155	sirtuin 1	Homo sapiens	156-161
30519156-1	2018	Silent mating type information regulation 2 homolog 1 (Sirt1), a nicotine adenine dinucleotide (NAD+)-dependent enzyme, is well-known in playing a part in longevity.	NAD	96-101	sirtuin 1	Homo sapiens	55-60
15150415-7	2004	Together, these studies provide insights into the chemistry of NAD(+) cleavage and acetylation by Sir2 proteins and have implications for the design of Sir2-specific regulatory molecules.	NAD	63-69	sirtuin 1	Homo sapiens	98-102
15150415-7	2004	Together, these studies provide insights into the chemistry of NAD(+) cleavage and acetylation by Sir2 proteins and have implications for the design of Sir2-specific regulatory molecules.	NAD	63-69	sirtuin 1	Homo sapiens	152-156
15173392-7	2004	Furthermore, hepatic HO-1 protein content was best described by a regression model that included mitochondrial NADH:cytochrome c reductase and succinate:cytochrome c reductase activities, but not cytochrome c oxidase activity (R(2) = 0.54, P &lt; 0.02).	NAD	111-115	heme oxygenase 1	Rattus norvegicus	21-25
30460421-1	2018	We have recently identified a positive feedback loop in which c-MYC increases silent information regulator 1 (SIRT1) protein level and activity through transcriptional activation of nicotinamide phosphoribosyltransferase (NAMPT) and NAD+ increase.	NAD	233-237	sirtuin 1	Homo sapiens	78-108
30460421-1	2018	We have recently identified a positive feedback loop in which c-MYC increases silent information regulator 1 (SIRT1) protein level and activity through transcriptional activation of nicotinamide phosphoribosyltransferase (NAMPT) and NAD+ increase.	NAD	233-237	sirtuin 1	Homo sapiens	110-115
30459716-1	2018	Metformin has been proposed to operate as an agonist of SIRT1, a nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase that mimics most of the metabolic responses to calorie restriction.	NAD	65-98	sirtuin 1	Homo sapiens	56-61
14985416-1	2004	The massive activation of poly(ADP-ribose) polymerase-1 (PARP-1) by DNA-damaging stimuli, such as exposure to reactive oxygen species (ROS), can lead to cell injury via severe, irreversible depletion of the NAD and ATP pool, and PARP-1 inhibitors have been expected to rescue neurons from degeneration in a number of disease models.	NAD	207-210	poly (ADP-ribose) polymerase family, member 1	Mus musculus	26-55
30459716-6	2018	Third, metformin was predicted to interact with the C-terminal regulatory segment of SIRT1 bound to the NAD+ hydrolysis product ADP-ribose, a "C-pocket"-related mechanism that appears to be essential for mechanism-based activation of SIRT1.	NAD	104-108	sirtuin 1	Homo sapiens	85-90
14985416-1	2004	The massive activation of poly(ADP-ribose) polymerase-1 (PARP-1) by DNA-damaging stimuli, such as exposure to reactive oxygen species (ROS), can lead to cell injury via severe, irreversible depletion of the NAD and ATP pool, and PARP-1 inhibitors have been expected to rescue neurons from degeneration in a number of disease models.	NAD	207-210	poly (ADP-ribose) polymerase family, member 1	Mus musculus	57-63
14985416-1	2004	The massive activation of poly(ADP-ribose) polymerase-1 (PARP-1) by DNA-damaging stimuli, such as exposure to reactive oxygen species (ROS), can lead to cell injury via severe, irreversible depletion of the NAD and ATP pool, and PARP-1 inhibitors have been expected to rescue neurons from degeneration in a number of disease models.	NAD	207-210	poly (ADP-ribose) polymerase family, member 1	Mus musculus	229-235
30459716-6	2018	Third, metformin was predicted to interact with the C-terminal regulatory segment of SIRT1 bound to the NAD+ hydrolysis product ADP-ribose, a "C-pocket"-related mechanism that appears to be essential for mechanism-based activation of SIRT1.	NAD	104-108	sirtuin 1	Homo sapiens	234-239
30459716-7	2018	Enzymatic assays confirmed that the net biochemical effect of metformin and other biguanides such as a phenformin was to improve the catalytic efficiency of SIRT1 operating in conditions of low NAD+ in vitro.	NAD	194-198	sirtuin 1	Homo sapiens	157-162
30459716-9	2018	These findings might have important implications for understanding how metformin might confer health benefits via maintenance of SIRT1 activity during the aging process when NAD+ levels decline.	NAD	174-178	sirtuin 1	Homo sapiens	129-134
14960594-0	2004	Poly(ADP-ribose) polymerase-1-mediated cell death in astrocytes requires NAD+ depletion and mitochondrial permeability transition.	NAD	73-77	poly (ADP-ribose) polymerase family, member 1	Mus musculus	0-29
28753256-7	2018	Correspondingly, NADH significantly inhibited TNF-alpha and enhanced IL-10 production with elevation of both M1/M2 macrophage markers.	NAD	17-21	interleukin 10	Homo sapiens	69-74
14960594-2	2004	Here we show that NAD(+) depletion and mitochondrial permeability transition (MPT) are sequential and necessary steps in PARP-1-mediated cell death.	NAD	18-24	poly (ADP-ribose) polymerase family, member 1	Mus musculus	121-127
14960594-9	2004	Furthermore, both cyclosporin A and NAD(+) blocked translocation of the apoptosis-inducing factor from mitochondria to nuclei, a step previously shown necessary for PARP-1-induced cell death.	NAD	36-42	poly (ADP-ribose) polymerase family, member 1	Mus musculus	165-171
30078073-4	2018	We present evidence for C4-specific paralogs of NAD-malic enzyme 2, MPC1 and MPC2 (mitochondrial pyruvate carriers) via increased transcript abundance and associated rates of evolution, implicating them as genes recruited to perform C4 photosynthesis within NAD-ME and PEPCK subtypes.	NAD	48-51	phosphoenolpyruvate carboxykinase 2, mitochondrial	Homo sapiens	269-274
14960594-10	2004	These results suggest that NAD(+) depletion and MPT are necessary intermediary steps linking PARP-1 activation to AIF translocation and cell death.	NAD	27-33	poly (ADP-ribose) polymerase family, member 1	Mus musculus	93-99
14680476-7	2004	Furthermore we find that GCY1, encoding a putative glycerol dehydrogenase, GPP2, encoding a NAD-dependent glycerol-3-phosphate phosphatase, and DCS2, a homologue to a decapping enzyme, have decreased mRNA levels in the yap4 -deleted strain.	NAD	92-95	glycerol-1-phosphatase HOR2	Saccharomyces cerevisiae S288C	75-79
30382125-4	2018	The assay achieves the quantification of extracellular NAD+ by means of a two-step enzymatic cycling reaction, based on alcohol dehydrogenase.	NAD	55-59	aldo-keto reductase family 1 member A1	Homo sapiens	120-141
15019043-2	2004	When excited at 340 nm, it results in fluorescence emission having maxima around 436 nm, which is fairly specific for nicotinamide adenine dinucleotide, reduced form (NADH) and nicotinamide adenine dinucleotide phosphate, reduced form (NADPH).	NAD	118-151	2,4-dienoyl-CoA reductase 1	Homo sapiens	236-241
30184433-2	2018	Conversely, overactivation of PARP can lead to NAD+ depletion, mitochondrial energy failure, and cell death.	NAD	47-51	poly (ADP-ribose) polymerase family, member 1	Mus musculus	30-34
15019043-2	2004	When excited at 340 nm, it results in fluorescence emission having maxima around 436 nm, which is fairly specific for nicotinamide adenine dinucleotide, reduced form (NADH) and nicotinamide adenine dinucleotide phosphate, reduced form (NADPH).	NAD	167-171	2,4-dienoyl-CoA reductase 1	Homo sapiens	236-241
15026177-10	2004	The D36A/K37R mutant shifted the cofactor preference of both 3 beta-HSD and isomerase from NAD(H) to NADP(H).	NAD	91-97	hydroxy-delta-5-steroid dehydrogenase, 3 beta- and steroid delta-isomerase 1	Homo sapiens	61-71
14980222-1	2004	The NAD-dependent deacetylase SIR2 and the forkhead transcription factor DAF-16 regulate lifespan in model organisms, such as yeast and C. elegans.	NAD	4-7	sirtuin 1	Homo sapiens	30-34
17564302-2	2004	Extensive cellular damage can overactivate PARP-1, which rapidly depletes the cellular stores of NAD+ and ATP, resulting in necrotic cell death.	NAD	97-101	poly (ADP-ribose) polymerase family, member 1	Mus musculus	43-49
30247868-1	2018	Poly(ADP-ribose) polymerase 14 (PARP14) is a member of the PARP family of enzymes that transfer ADP-ribose from NAD+ to nucleophilic amino acids on target proteins, a process known as mono-ADP-ribosylation (MARylation).	NAD	112-116	poly(ADP-ribose) polymerase family member 14	Homo sapiens	0-30
30247868-1	2018	Poly(ADP-ribose) polymerase 14 (PARP14) is a member of the PARP family of enzymes that transfer ADP-ribose from NAD+ to nucleophilic amino acids on target proteins, a process known as mono-ADP-ribosylation (MARylation).	NAD	112-116	poly(ADP-ribose) polymerase family member 14	Homo sapiens	32-38
30247868-4	2018	Herein we engineered a PARP14 variant that uses an NAD+ analog that is orthogonal to wild-type PARPs for identifying PARP14-specific MARylation targets.	NAD	51-55	poly(ADP-ribose) polymerase family member 14	Homo sapiens	23-29
30247868-4	2018	Herein we engineered a PARP14 variant that uses an NAD+ analog that is orthogonal to wild-type PARPs for identifying PARP14-specific MARylation targets.	NAD	51-55	poly(ADP-ribose) polymerase family member 14	Homo sapiens	117-123
30347698-1	2018	The combination of metal nanoparticles (Pd or Pt NPs) with NAD-dependent thermostable alcohol dehydrogenase (TADH) resulted in the one-flask catalytic double reduction of 3-methyl-2-cyclohexenone to 3-(1S,3S)-methylcyclohexanol.	NAD	59-62	aldo-keto reductase family 1 member A1	Homo sapiens	86-107
30195617-8	2018	KEY FINDINGS: Transcriptomic analysis revealed that genes involved in NAD+ synthesis (Nampt and Nmnat1) in the BAT were negatively correlated with body weight and fat mass.	NAD	70-74	nicotinamide nucleotide adenylyltransferase 1	Mus musculus	96-102
12909645-4	2003	To address this question, NAD+ metabolizing activities were accurately examined in developing and adult Cd38-/- mouse brain protein extracts and cells.	NAD	26-30	CD38 antigen	Mus musculus	104-108
29980616-9	2018	We further revealed that decreased NAD inactivated sirtuin 1, resulting in increased signal transducer and activator of transcription 3 (STAT3) acetylation and phosphorylation, and STAT3 activation.	NAD	35-38	sirtuin 1	Homo sapiens	51-60
29937372-4	2018	AOX substantially increases the rate of NADH oxidation by O2 without affecting the membrane integrity, the supercomplexes, or NADH-linked oxidative phosphorylation.	NAD	40-44	acyl-CoA oxidase 1	Homo sapiens	0-3
14517300-8	2003	Nevertheless, expression of Glut1 and HK1 promoted increased cytosolic NADH and NADPH levels relative to those of the control cells upon growth factor withdrawal, prevented activation of Bax, and promoted growth factor-independent survival.	NAD	71-75	solute carrier family 2 member 1	Homo sapiens	28-33
29527628-14	2018	Values of serum alanine aminotransferase (ALAT), aspartate aminotransferase (ASAT), urea, and creatinine increased significantly in the DPN and diabetic rats without peripheral neuropathy (PN) compared with control group.	NAD	136-139	glutamic--pyruvic transaminase	Rattus norvegicus	16-40
14503867-1	2003	Microsomal cytochrome b(5) reductase (EC 1.6.2.2) catalyzes the reduction of ferricytochrome b(5) using NADH as the physiological electron donor.	NAD	104-108	cytochrome b5 type A	Rattus norvegicus	11-26
14503867-5	2003	Wild-type (WT) cytochrome b(5) reductase showed a 3700-fold preference for NADH whereas the mutant with the highest NADPH efficiency, D239T, showed an 11-fold preference for NADPH, a 39200-fold increase.	NAD	75-79	cytochrome b5 type A	Rattus norvegicus	15-30
29527628-14	2018	Values of serum alanine aminotransferase (ALAT), aspartate aminotransferase (ASAT), urea, and creatinine increased significantly in the DPN and diabetic rats without peripheral neuropathy (PN) compared with control group.	NAD	136-139	glutamic--pyruvic transaminase	Rattus norvegicus	42-46
12832414-2	2003	Our earlier studies show that the two enzyme reactions are linked by the coenzyme product, NADH, of the 3 beta-HSD activity.	NAD	91-95	hydroxy-delta-5-steroid dehydrogenase, 3 beta- and steroid delta-isomerase 1	Homo sapiens	104-114
29746824-0	2018	Reduction of 2-methoxy-1,4-naphtoquinone by mitochondrially-localized Nqo1 yielding NAD+ supports substrate-level phosphorylation during respiratory inhibition.	NAD	84-88	NAD(P)H dehydrogenase, quinone 1	Mus musculus	70-74
12832414-5	2003	Homology modeling with UDP-galactose-4-epimerase predicts that Asp36 is responsible for the NAD(H) specificity of human 3 beta-HSD/isomerase and identifies the Rossmann-fold coenzyme domain at the amino terminus.	NAD	92-98	hydroxy-delta-5-steroid dehydrogenase, 3 beta- and steroid delta-isomerase 1	Homo sapiens	120-130
12832414-7	2003	The D36A/K37R mutant shifts the cofactor preference of both 3 beta-HSD and isomerase from NAD(H) to NADP(H), which shows that the two activities utilize a common coenzyme domain.	NAD	90-96	hydroxy-delta-5-steroid dehydrogenase, 3 beta- and steroid delta-isomerase 1	Homo sapiens	60-70
29663373-2	2018	NAMPT (nicotinamide phosphoribosyl transferase), which catalyzes the rate-limiting step in the NAD+ salvage pathway, increases during in vitro osteogenic differentiation and inhibits RANKL-induced osteoclast differentiation.	NAD	95-99	nicotinamide phosphoribosyltransferase	Rattus norvegicus	0-5
12962626-2	2003	Redox changes from overproduction of the coenzyme NADH by SDH may play a role in diabetes-induced dysfunction in sensitive tissues, making SDH a therapeutic target for diabetic complications.	NAD	50-54	succinate dehydrogenase complex iron sulfur subunit B	Homo sapiens	58-61
12962626-2	2003	Redox changes from overproduction of the coenzyme NADH by SDH may play a role in diabetes-induced dysfunction in sensitive tissues, making SDH a therapeutic target for diabetic complications.	NAD	50-54	succinate dehydrogenase complex iron sulfur subunit B	Homo sapiens	139-142
29663373-2	2018	NAMPT (nicotinamide phosphoribosyl transferase), which catalyzes the rate-limiting step in the NAD+ salvage pathway, increases during in vitro osteogenic differentiation and inhibits RANKL-induced osteoclast differentiation.	NAD	95-99	nicotinamide phosphoribosyltransferase	Rattus norvegicus	7-46
12962626-3	2003	We have purified and determined the crystal structures of human SDH alone, SDH with NAD(+), and SDH with NADH and an inhibitor that is competitive with fructose.	NAD	84-90	succinate dehydrogenase complex iron sulfur subunit B	Homo sapiens	75-78
30147698-2	2018	IBD-related inflammation is also marked by defective expression of Sirt1, a class III NAD+-dependent deacetylase, which promotes ubiquitination-mediated proteosomal degradation of various intracellular proteins and triggers anti-inflammatory signals.	NAD	86-89	sirtuin 1	Homo sapiens	67-72
12962626-3	2003	We have purified and determined the crystal structures of human SDH alone, SDH with NAD(+), and SDH with NADH and an inhibitor that is competitive with fructose.	NAD	84-90	succinate dehydrogenase complex iron sulfur subunit B	Homo sapiens	75-78
29706024-0	2018	Overexpression of CYB5R3 and NQO1, two NAD+ -producing enzymes, mimics aspects of caloric restriction.	NAD	39-43	cytochrome b5 reductase 3	Mus musculus	18-24
12700160-2	2003	The NAD+-dependent type 2 (11betaHSD2) enzyme is an oxidase that inactivates cortisol and corticosterone, conferring extrinsic specificity of the mineralocorticoid receptor for aldosterone.	NAD	4-8	hydroxysteroid 11-beta dehydrogenase 2	Rattus norvegicus	27-37
12700160-11	2003	NAD+-dependent enzymatic activity in the absence or presence of a reducing agent demonstrated that the increase in 11betaHSD2 protein was not associated with an increase in in vitro activity unless the dimers were reduced to monomers.	NAD	0-4	hydroxysteroid 11-beta dehydrogenase 2	Rattus norvegicus	115-125
12829633-1	2003	Poly (ADP-ribose) polymerase (PARP) is a nuclear enzyme that consumes NAD in response to DNA strand breaks.	NAD	70-73	poly (ADP-ribose) polymerase family, member 1	Mus musculus	0-28
12829633-1	2003	Poly (ADP-ribose) polymerase (PARP) is a nuclear enzyme that consumes NAD in response to DNA strand breaks.	NAD	70-73	poly (ADP-ribose) polymerase family, member 1	Mus musculus	30-34
12829633-2	2003	The PARP inhibitor nicotinamide prevents NAD consumption and protects islet beta-cells from chemically induced necrosis but not cytokine-induced apoptosis.	NAD	41-44	poly (ADP-ribose) polymerase family, member 1	Mus musculus	4-8
12818203-3	2003	The coenzyme and substrate specificity of ADH8, that has 50-65% sequence identity with vertebrate NAD(H)-dependent ADHs, suggest a role in aldehyde reduction probably as a retinal reductase.	NAD	98-104	alcohol dehydrogenase iron containing 1	Homo sapiens	42-46
12818203-6	2003	NADP(H) binds to ADH8 in an extended conformation that superimposes well with the NAD(H) molecules found in NAD(H)-dependent ADH complexes.	NAD	82-88	alcohol dehydrogenase iron containing 1	Homo sapiens	17-21
12818203-6	2003	NADP(H) binds to ADH8 in an extended conformation that superimposes well with the NAD(H) molecules found in NAD(H)-dependent ADH complexes.	NAD	82-88	alcohol dehydrogenase iron containing 1	Homo sapiens	17-20
12818203-6	2003	NADP(H) binds to ADH8 in an extended conformation that superimposes well with the NAD(H) molecules found in NAD(H)-dependent ADH complexes.	NAD	108-114	alcohol dehydrogenase iron containing 1	Homo sapiens	17-21
12818203-6	2003	NADP(H) binds to ADH8 in an extended conformation that superimposes well with the NAD(H) molecules found in NAD(H)-dependent ADH complexes.	NAD	108-114	alcohol dehydrogenase iron containing 1	Homo sapiens	17-20
12818203-7	2003	No additional reshaping of the dinucleotide-binding site is observed which explains why NAD(H) can also be used as a cofactor by ADH8.	NAD	88-94	alcohol dehydrogenase iron containing 1	Homo sapiens	129-133
12606624-1	2003	Excessive activation of poly(ADP-ribose) polymerase-1 (PARP-1), a nuclear enzyme catalyzing the transfer of ADP-ribose units from NAD to acceptor proteins, induces cellular energy failure by NAD and ATP depletion and has been proposed to play a causative role in a number of pathological conditions, including ischemia/reperfusion injury.	NAD	130-133	poly (ADP-ribose) polymerase family, member 1	Mus musculus	24-53
12606624-1	2003	Excessive activation of poly(ADP-ribose) polymerase-1 (PARP-1), a nuclear enzyme catalyzing the transfer of ADP-ribose units from NAD to acceptor proteins, induces cellular energy failure by NAD and ATP depletion and has been proposed to play a causative role in a number of pathological conditions, including ischemia/reperfusion injury.	NAD	130-133	poly (ADP-ribose) polymerase family, member 1	Mus musculus	55-61
12606624-1	2003	Excessive activation of poly(ADP-ribose) polymerase-1 (PARP-1), a nuclear enzyme catalyzing the transfer of ADP-ribose units from NAD to acceptor proteins, induces cellular energy failure by NAD and ATP depletion and has been proposed to play a causative role in a number of pathological conditions, including ischemia/reperfusion injury.	NAD	191-194	poly (ADP-ribose) polymerase family, member 1	Mus musculus	24-53
12606624-1	2003	Excessive activation of poly(ADP-ribose) polymerase-1 (PARP-1), a nuclear enzyme catalyzing the transfer of ADP-ribose units from NAD to acceptor proteins, induces cellular energy failure by NAD and ATP depletion and has been proposed to play a causative role in a number of pathological conditions, including ischemia/reperfusion injury.	NAD	191-194	poly (ADP-ribose) polymerase family, member 1	Mus musculus	55-61
12736687-3	2003	In Saccharomyces cerevisiae, lifespan extension by calorie restriction requires the NAD+-dependent histone deacetylase, Sir2 (ref.	NAD	84-87	sirtuin 1	Homo sapiens	120-124
12765698-3	2003	As cells transfected with TRPM2, neutrophil granulocytes display non-selective cation currents and typical channel activity evoked by intracellular ADP-ribose and NAD.	NAD	163-166	transient receptor potential cation channel subfamily M member 2	Homo sapiens	26-31
12765698-4	2003	Thus, stimulation of TRPM2 is likely to occur after activation of CD38 (producing ADP-ribose) and during the oxidative burst (enhancing the NAD concentration).	NAD	140-143	transient receptor potential cation channel subfamily M member 2	Homo sapiens	21-26
12562755-1	2003	Yeast NAD(+)-specific isocitrate dehydrogenase (IDH) is an allosterically regulated octameric enzyme composed of two types of homologous subunits designated IDH1 and IDH2.	NAD	6-12	isocitrate dehydrogenase (NAD(+)) IDH2	Saccharomyces cerevisiae S288C	166-170
12562755-5	2003	The primary kinetic effects of D286A/I287A and of H281A replacements in IDH2 were found to be a dramatic reduction in apparent affinity of the holoenzyme for NAD(+) and a concomitant reduction in V(max).	NAD	158-164	isocitrate dehydrogenase (NAD(+)) IDH2	Saccharomyces cerevisiae S288C	72-76
12562755-10	2003	In this study, we also demonstrate that a prerequisite for holoenzyme binding of NAD(+) is binding of isocitrate/Mg(2+) at the IDH2 catalytic site.	NAD	81-87	isocitrate dehydrogenase (NAD(+)) IDH2	Saccharomyces cerevisiae S288C	127-131
12628750-1	2003	Poly(ADP-ribose) polymerases (PARPs) are a group of protein-modifying and nucleotide-polymerizing enzymes able to catalyze the transfer of multiple ADP-ribose units from NAD to substrate proteins.	NAD	170-173	poly (ADP-ribose) polymerase family, member 1	Mus musculus	30-35
12702242-1	2003	Under anaerobic conditions, Saccharomyces cerevisiae uses NADH-dependent glycerol-3-phosphate dehydrogenase (Gpd1p and Gpd2p) to re-oxidize excess NADH, yielding substantial amounts of glycerol.	NAD	58-62	glycerol-3-phosphate dehydrogenase (NAD(+)) GPD1	Saccharomyces cerevisiae S288C	109-114
12702242-1	2003	Under anaerobic conditions, Saccharomyces cerevisiae uses NADH-dependent glycerol-3-phosphate dehydrogenase (Gpd1p and Gpd2p) to re-oxidize excess NADH, yielding substantial amounts of glycerol.	NAD	147-151	glycerol-3-phosphate dehydrogenase (NAD(+)) GPD1	Saccharomyces cerevisiae S288C	109-114
12605868-3	2003	A relatively rapid continuous spectrophotometric assay which uses 15-hydroxyprostaglandin dehydrogenase (PGDH) to couple the oxidation of the 15-hydroxy group of PGE(2) to the formation of NADH was developed.	NAD	189-193	carbonyl reductase 1	Homo sapiens	66-103
12604209-0	2003	Tetrameric NAD-dependent alcohol dehydrogenase.	NAD	11-14	aldo-keto reductase family 1 member A1	Homo sapiens	25-46
12604209-1	2003	Three-dimensional structures of the ethanol-induced, tetrameric alcohol dehydrogenase from Escherichia coli have recently been determined in the absence and presence of NAD.	NAD	169-172	aldo-keto reductase family 1 member A1	Homo sapiens	64-85
12600773-7	2003	The binding constant of ADH with nicotinamide adenine dinucleotide (NAD) was also determined as 1.87 x 10(4) M(-1).	NAD	33-66	aldo-keto reductase family 1 member A1	Homo sapiens	24-27
12600773-7	2003	The binding constant of ADH with nicotinamide adenine dinucleotide (NAD) was also determined as 1.87 x 10(4) M(-1).	NAD	68-71	aldo-keto reductase family 1 member A1	Homo sapiens	24-27
12399474-6	2002	0, the recombinant AtNUDT1 catalyzed the hydrolysis of NADH with a K(m) value of 0.	NAD	55-59	nudix hydrolase 1	Arabidopsis thaliana	19-26
12600270-0	2002	Kinetic mechanism of mitochondrial NADH:ubiquinone oxidoreductase interaction with nucleotide substrates of the transhydrogenase reaction.	NAD	35-39	thioredoxin reductase 1	Homo sapiens	51-65
12416991-7	2002	Two-substrate kinetic analysis and dead-end inhibition studies for 5alpha-DHP reduction and allopregnanolone oxidation indicated that 3alpha-HSD type III utilized a ternary complex (sequential) kinetic mechanism, with nicotinamide adenine dinucleotide cofactor binding before steroid substrate and leaving after steroid product.	NAD	218-251	aldo-keto reductase family 1 member C4	Homo sapiens	134-144
12411473-9	2002	NADH-generated O2- and mRNA expression of p22(phox), gp91(phox), and nox-1 were comparable between the 2 strains of rat.	NAD	0-4	NADPH oxidase 1	Rattus norvegicus	69-74
12597242-1	2002	Using the mice that lack mitochondrial glycerol-3-phosphate dehydrogenase (mGPDH), a rate limiting enzyme of the glycerol-phosphate NADH shuttle, we investigated the role of the NADH shuttle system in amylase secretion in response to acetylcholine (ACh) in pancreatic acinar cells.	NAD	132-136	glycerol phosphate dehydrogenase 2, mitochondrial	Mus musculus	75-80
29706024-0	2018	Overexpression of CYB5R3 and NQO1, two NAD+ -producing enzymes, mimics aspects of caloric restriction.	NAD	39-43	NAD(P)H dehydrogenase, quinone 1	Mus musculus	29-33
29636359-3	2018	Alteration in mitochondrial function resulted in strengthened NAD+ metabolism, here considered as a key mechanism of chemoresistance, particularly, of succinate dehydrogenase subunit B (SDHB)-mutated cluster I PCPGs via the PARP1/BER DNA repair pathway.	NAD	62-66	poly (ADP-ribose) polymerase family, member 1	Mus musculus	224-229
29679894-11	2018	Both in vivo and in vitro experiments showed that NR activated SirT1 through increasing NAD+ levels, decreased oxidative stress, increased deacetylation of PGC-1alpha and mitochondrial function.	NAD	88-92	sirtuin 1	Homo sapiens	63-68
30018712-9	2018	Western blot data indicated that NADH promoted the microtubule associated protein 1A/1B-light chain 3(LC3)-I to LC3II and the expression of IL-1beta and TNFalpha decreased in a dose dependent manner.	NAD	33-37	microtubule-associated protein 1A	Rattus norvegicus	51-87
29879377-1	2018	SIRT7, a member of the sirtuin family, with coenzyme NAD catalyzes protein deacetylation and has been implicated in multiple biologic processes; however, its function in mammalian oocytes remains to be explored.	NAD	53-56	sirtuin 7	Homo sapiens	0-5
29872122-0	2018	NNMT activation can contribute to the development of fatty liver disease by modulating the NAD + metabolism.	NAD	91-96	nicotinamide N-methyltransferase	Mus musculus	0-4
29872122-4	2018	When fed a high fat diet containing NAM, a precursor for nicotinamide adenine dinucleotide (NAD)+, these NNMT-overexpressing mice exhibit fatty liver deterioration following increased expression of the genes mediating fatty acid uptake and decreased very low-density lipoprotein secretion.	NAD	57-90	nicotinamide N-methyltransferase	Mus musculus	105-109
29872122-4	2018	When fed a high fat diet containing NAM, a precursor for nicotinamide adenine dinucleotide (NAD)+, these NNMT-overexpressing mice exhibit fatty liver deterioration following increased expression of the genes mediating fatty acid uptake and decreased very low-density lipoprotein secretion.	NAD	92-97	nicotinamide N-methyltransferase	Mus musculus	105-109
29872122-5	2018	NNMT overactivation decreased the NAD+ content in the liver and also decreased gene activity related to fatty acid oxidation by inhibiting NAD+-dependent deacetylase Sirt3 function.	NAD	34-38	nicotinamide N-methyltransferase	Mus musculus	0-4
29872122-5	2018	NNMT overactivation decreased the NAD+ content in the liver and also decreased gene activity related to fatty acid oxidation by inhibiting NAD+-dependent deacetylase Sirt3 function.	NAD	139-143	nicotinamide N-methyltransferase	Mus musculus	0-4
29627626-1	2018	Poly (ADP-ribose) polymerase 1 (PARP1) is a DNA damage sensor that catalyzes the poly (ADP-ribose) (PAR) onto a variety of target proteins, such as histones, DSB repair factors and PARP1 itself under consumption of NAD+.	NAD	215-219	jumping translocation breakpoint	Homo sapiens	32-35
29740774-4	2018	SIRT1 is a NAD+-dependent deacetylase that can deacetylate and activate peroxisome proliferator-activated receptor-gamma coactivator 1alpha (PGC-1alpha), a master regulator of mitochondrial integrity, biogenesis, and function.	NAD	11-14	sirtuin 1	Homo sapiens	0-5
29896286-1	2018	The silent information regulation factor 1 (sirtuin Type 1, SIRT1), as a kind of NAD+ dependent class III histone deacetylation enzyme, has been found to be involved in tumor proliferation, invasion, and metastasis.	NAD	81-85	sirtuin 1	Homo sapiens	44-58
29896286-1	2018	The silent information regulation factor 1 (sirtuin Type 1, SIRT1), as a kind of NAD+ dependent class III histone deacetylation enzyme, has been found to be involved in tumor proliferation, invasion, and metastasis.	NAD	81-85	sirtuin 1	Homo sapiens	60-65
29642888-3	2018	RESULTS: A new metabolic module was established here, in which, permease Gap1p for L-phenylalanine transportation, catalytic enzymes Aro8p, Aro10p and Adh2p in Ehrlich pathway respectively responsible for transamination, decarboxylation and reduction were assembled, besides, glutamate dehydrogenase Gdh2p was harbored for re-supplying another substrate 2-oxoglutarate, relieving product glutamate repression and regenerating cofactor NADH.	NAD	435-439	bifunctional 2-aminoadipate transaminase/aromatic-amino-acid:2-oxoglutarate transaminase	Saccharomyces cerevisiae S288C	133-138
29594560-7	2018	Compared with an obviously enhanced yield of ergosterol in the wild-type strain, decreases of both the ergosta-5,7-dienol levels and the total sterol yield were found in Deltaerg5-upc2-1, probably due to the unbalanced NADH/NAD+ ratio observed in the erg5 knockouts, suggesting the whole-cell redox homeostasis was also vital for end-product biosynthesis.	NAD	219-223	C-22 sterol desaturase	Saccharomyces cerevisiae S288C	175-179
29594560-7	2018	Compared with an obviously enhanced yield of ergosterol in the wild-type strain, decreases of both the ergosta-5,7-dienol levels and the total sterol yield were found in Deltaerg5-upc2-1, probably due to the unbalanced NADH/NAD+ ratio observed in the erg5 knockouts, suggesting the whole-cell redox homeostasis was also vital for end-product biosynthesis.	NAD	224-228	C-22 sterol desaturase	Saccharomyces cerevisiae S288C	175-179
29307841-0	2018	ROS-Mediated 15-Hydroxyprostaglandin Dehydrogenase Degradation via Cysteine Oxidation Promotes NAD+-Mediated Epithelial-Mesenchymal Transition.	NAD	95-99	carbonyl reductase 1	Homo sapiens	13-50
29307841-3	2018	We revealed that decreased NAD triggered reactive oxygen species (ROS)-mediated degradation of 15-hydroxyprostaglandin dehydrogenase (15-PGDH), which drove cells to undergo epithelial-mesenchymal transition (EMT).	NAD	27-30	carbonyl reductase 1	Homo sapiens	95-132
29307841-3	2018	We revealed that decreased NAD triggered reactive oxygen species (ROS)-mediated degradation of 15-hydroxyprostaglandin dehydrogenase (15-PGDH), which drove cells to undergo epithelial-mesenchymal transition (EMT).	NAD	27-30	carbonyl reductase 1	Homo sapiens	134-141
29307841-6	2018	We demonstrated that 15-PGDH silencing promoted EMT, whereas supplementation with NAD precursors increased NAD and 15-PGDH stability, and reversed the EMT process.	NAD	82-85	carbonyl reductase 1	Homo sapiens	115-122
29307841-7	2018	Taken together, these results suggest that declining NAD levels contribute to age-dependent increases in cancer incidence, and repletion of NAD precursors is beneficial for increasing 15-PGDH expression.	NAD	140-143	carbonyl reductase 1	Homo sapiens	184-191
29341930-7	2018	In PC-3 cells, ERbeta-selective agonist DPN decreased the expression of N-cadherin.	NAD	40-43	cadherin 2	Homo sapiens	72-82
29341930-8	2018	DPN-induced downregulation of N-cadherin was blocked by pretreatment with the ERbeta-selective antagonist (PHTPP), indicating that ERbeta1 is the upstream receptor regulating the expression of N-cadherin.	NAD	0-3	cadherin 2	Homo sapiens	30-40
29341930-8	2018	DPN-induced downregulation of N-cadherin was blocked by pretreatment with the ERbeta-selective antagonist (PHTPP), indicating that ERbeta1 is the upstream receptor regulating the expression of N-cadherin.	NAD	0-3	cadherin 2	Homo sapiens	193-203
29359564-4	2018	A reverse reaction of ADH was employed for detection of gaseous AcH where a relationship between fluorescence intensity from nicotinamide adenine dinucleotide and the concentration of AcH was inversely proportional; thus, the concentration distribution of AcH was measured by detecting the fluorescence decrease.	NAD	125-158	aldo-keto reductase family 1 member A1	Homo sapiens	22-25
29432159-3	2018	Here we report that 3xTgAD/Polbeta+/- mice have a reduced cerebral NAD+/NADH ratio indicating impaired cerebral energy metabolism, which is normalized by nicotinamide riboside (NR) treatment.	NAD	67-71	polymerase (DNA directed), alpha 1	Mus musculus	27-34
29432159-3	2018	Here we report that 3xTgAD/Polbeta+/- mice have a reduced cerebral NAD+/NADH ratio indicating impaired cerebral energy metabolism, which is normalized by nicotinamide riboside (NR) treatment.	NAD	72-76	polymerase (DNA directed), alpha 1	Mus musculus	27-34
12597242-5	2002	In also mGPDH-deficient cells treated with AOA, thus in this situation all mitochondrial NADH shuttles being dysfunctioning, ACh induced amylase release in a similar amount to that in AOA-untreated cells.	NAD	89-93	glycerol phosphate dehydrogenase 2, mitochondrial	Mus musculus	8-13
28976891-0	2018	The inhibition of the mitochondrial F1FO-ATPase activity when activated by Ca2+ opens new regulatory roles for NAD.	NAD	111-114	carbonic anhydrase 2	Homo sapiens	75-78
28976891-1	2018	The mitochondrial F1FO-ATPase is uncompetitively inhibited by NAD+ only when the natural cofactor Mg2+ is replaced by Ca2+, a mode putatively involved in cell death.	NAD	62-66	carbonic anhydrase 2	Homo sapiens	118-121
28976891-2	2018	The Ca2+-dependent F1FO-ATPase is also inhibited when NAD+ concentration in mitochondria is raised by acetoacetate.	NAD	54-58	carbonic anhydrase 2	Homo sapiens	4-7
28976891-5	2018	Consistently, NAD+ may play a new role, not associated with redox and non-redox enzymatic reactions, in the Ca2+-dependent regulation of the F1FO-ATPase activity.	NAD	14-18	carbonic anhydrase 2	Homo sapiens	108-111
12374852-0	2002	SIRT3, a human SIR2 homologue, is an NAD-dependent deacetylase localized to mitochondria.	NAD	37-40	sirtuin 1	Homo sapiens	15-19
29320709-3	2018	(2018) demonstrate that intratumoral CD4+ T cell functions and memory can be improved by targeting a CD38-NAD+-Sirt1-Foxo1 metabolic circuit.	NAD	106-110	sirtuin 1	Homo sapiens	111-116
12392591-6	2002	In addition, hydroxycelecoxib oxidation by different variants of recombinant human alcohol dehydrogenase (ADH1-3) was analysed by spectrophotometric monitoring of NADH generation from NAD+.	NAD	163-167	aldo-keto reductase family 1 member A1	Homo sapiens	83-104
12392591-6	2002	In addition, hydroxycelecoxib oxidation by different variants of recombinant human alcohol dehydrogenase (ADH1-3) was analysed by spectrophotometric monitoring of NADH generation from NAD+.	NAD	184-188	aldo-keto reductase family 1 member A1	Homo sapiens	83-104
29320743-5	2018	SIRT1 is activated in times of energy demand by high levels of nicotinamide adenine dinucleotide (NAD+) and controls mitochondrial biogenesis and function.	NAD	63-96	sirtuin 1	Homo sapiens	0-5
29320743-5	2018	SIRT1 is activated in times of energy demand by high levels of nicotinamide adenine dinucleotide (NAD+) and controls mitochondrial biogenesis and function.	NAD	98-102	sirtuin 1	Homo sapiens	0-5
29074724-3	2018	We demonstrate here that glucose deprivation or hypoxia results in the AMPK-mediated phosphorylation of phosphoribosyl pyrophosphate synthetase 1 (PRPS1) S180 and PRPS2 S183, leading to conversion of PRPS hexamers to monomers and thereby inhibiting PRPS1/2 activity, nucleotide synthesis, and nicotinamide adenine dinucleotide (NAD) production.	NAD	293-326	phosphoribosyl pyrophosphate synthetase 2	Homo sapiens	163-168
29074724-3	2018	We demonstrate here that glucose deprivation or hypoxia results in the AMPK-mediated phosphorylation of phosphoribosyl pyrophosphate synthetase 1 (PRPS1) S180 and PRPS2 S183, leading to conversion of PRPS hexamers to monomers and thereby inhibiting PRPS1/2 activity, nucleotide synthesis, and nicotinamide adenine dinucleotide (NAD) production.	NAD	293-326	microseminoprotein beta	Homo sapiens	147-151
29074724-3	2018	We demonstrate here that glucose deprivation or hypoxia results in the AMPK-mediated phosphorylation of phosphoribosyl pyrophosphate synthetase 1 (PRPS1) S180 and PRPS2 S183, leading to conversion of PRPS hexamers to monomers and thereby inhibiting PRPS1/2 activity, nucleotide synthesis, and nicotinamide adenine dinucleotide (NAD) production.	NAD	328-331	phosphoribosyl pyrophosphate synthetase 2	Homo sapiens	163-168
29074724-3	2018	We demonstrate here that glucose deprivation or hypoxia results in the AMPK-mediated phosphorylation of phosphoribosyl pyrophosphate synthetase 1 (PRPS1) S180 and PRPS2 S183, leading to conversion of PRPS hexamers to monomers and thereby inhibiting PRPS1/2 activity, nucleotide synthesis, and nicotinamide adenine dinucleotide (NAD) production.	NAD	328-331	microseminoprotein beta	Homo sapiens	147-151
28923496-1	2018	BACKGROUND &amp; AIMS: The mitochondrial nicotinamide adenine dinucleotide (NAD) kinase (NADK2, also called MNADK) catalyzes phosphorylation of NAD to yield NADP.	NAD	76-79	NAD kinase 2, mitochondrial	Mus musculus	89-94
28923496-1	2018	BACKGROUND &amp; AIMS: The mitochondrial nicotinamide adenine dinucleotide (NAD) kinase (NADK2, also called MNADK) catalyzes phosphorylation of NAD to yield NADP.	NAD	76-79	NAD kinase 2, mitochondrial	Mus musculus	108-113
29159687-2	2018	We hypothesized that this may arise from the downregulation of the NAD+-dependent deacetylase SIRT1.	NAD	67-70	sirtuin 1	Homo sapiens	94-99
30112992-2	2018	PARP14 transfers a negatively charged ADP-ribose unit from a donor NAD+ molecule onto a target protein, post-translationally.	NAD	67-71	poly(ADP-ribose) polymerase family member 14	Homo sapiens	0-6
29225823-3	2017	The mitochondrial enzyme MTHFD2 has been reported to use NAD+ as a cofactor while the isozyme MTHFD2L utilizes NAD+ or NADP+ at physiologically relevant conditions.	NAD	57-61	methylenetetrahydrofolate dehydrogenase (NADP+ dependent) 2, methenyltetrahydrofolate cyclohydrolase	Homo sapiens	25-31
29225823-3	2017	The mitochondrial enzyme MTHFD2 has been reported to use NAD+ as a cofactor while the isozyme MTHFD2L utilizes NAD+ or NADP+ at physiologically relevant conditions.	NAD	57-61	methylenetetrahydrofolate dehydrogenase (NADP+ dependent) 2 like	Homo sapiens	94-101
29225823-3	2017	The mitochondrial enzyme MTHFD2 has been reported to use NAD+ as a cofactor while the isozyme MTHFD2L utilizes NAD+ or NADP+ at physiologically relevant conditions.	NAD	111-115	methylenetetrahydrofolate dehydrogenase (NADP+ dependent) 2, methenyltetrahydrofolate cyclohydrolase	Homo sapiens	25-31
29225823-3	2017	The mitochondrial enzyme MTHFD2 has been reported to use NAD+ as a cofactor while the isozyme MTHFD2L utilizes NAD+ or NADP+ at physiologically relevant conditions.	NAD	111-115	methylenetetrahydrofolate dehydrogenase (NADP+ dependent) 2 like	Homo sapiens	94-101
29225823-5	2017	Results: Kinetic analysis shows that purified human MTHFD2 exhibits dual redox cofactor specificity, utilizing either NADP+ or NAD+ with the more physiologically relevant pentaglutamate folate substrate.	NAD	127-131	methylenetetrahydrofolate dehydrogenase (NADP+ dependent) 2, methenyltetrahydrofolate cyclohydrolase	Homo sapiens	52-58
29225823-7	2017	Our kinetic analysis clearly supports a role for MTHFD2 in mitochondrial NADPH production, indicating that this enzyme is likely responsible for mitochondrial production of both NADH and NADPH in rapidly proliferating cells.	NAD	178-182	methylenetetrahydrofolate dehydrogenase (NADP+ dependent) 2, methenyltetrahydrofolate cyclohydrolase	Homo sapiens	49-55
28772201-3	2017	The ADH entrapped within the MADQUAT that was present on the carbon nanoscaffolds exhibited a high electron exchange capability with the electrode through its cofactor beta-nicotinamide adenine dinucleotide hydrate and beta-nicotinamide adenine dinucleotide reduced disodium salt hydrate (NAD+/NADH) redox reaction.	NAD	168-206	aldo-keto reductase family 1 member A1	Homo sapiens	4-7
28772201-3	2017	The ADH entrapped within the MADQUAT that was present on the carbon nanoscaffolds exhibited a high electron exchange capability with the electrode through its cofactor beta-nicotinamide adenine dinucleotide hydrate and beta-nicotinamide adenine dinucleotide reduced disodium salt hydrate (NAD+/NADH) redox reaction.	NAD	289-293	aldo-keto reductase family 1 member A1	Homo sapiens	4-7
28772201-3	2017	The ADH entrapped within the MADQUAT that was present on the carbon nanoscaffolds exhibited a high electron exchange capability with the electrode through its cofactor beta-nicotinamide adenine dinucleotide hydrate and beta-nicotinamide adenine dinucleotide reduced disodium salt hydrate (NAD+/NADH) redox reaction.	NAD	294-298	aldo-keto reductase family 1 member A1	Homo sapiens	4-7
28860121-1	2017	Nicotinamide phosphoribosyltransferase (NAMPT) and nicotinic acid phosphoribosyltransferase (NAPRT) are rate-limiting enzymes in the NAD+ synthesis pathway.	NAD	133-137	nicotinate phosphoribosyltransferase	Homo sapiens	51-91
28860121-1	2017	Nicotinamide phosphoribosyltransferase (NAMPT) and nicotinic acid phosphoribosyltransferase (NAPRT) are rate-limiting enzymes in the NAD+ synthesis pathway.	NAD	133-137	nicotinate phosphoribosyltransferase	Homo sapiens	93-98
28860121-13	2017	In conclusion, this study identified NAMPT as a potential target for treatment of chondrosarcoma.Implications: Chondrosarcoma patients, especially those of high histologic grade with lower expression and hypermethylation of NAPRT, may benefit from inhibition of the NAD synthesis pathway.	NAD	266-269	nicotinate phosphoribosyltransferase	Homo sapiens	224-229
29150439-5	2017	Tumor-derived lactate translationally inhibits FIP200 expression by down-regulating the nicotinamide adenine dinucleotide level while potentially up-regulating the inhibitory effect of adenylate-uridylate-rich elements within the 3" untranslated region of Fip200 mRNA.	NAD	88-121	RB1 inducible coiled-coil 1	Homo sapiens	47-53
28826100-4	2017	Moreover, silent information regulator of transcription 1 (SIRT1), a NAD+-dependent class III histone deacetylase, was up-regulated after pretreatment with resveratrol.	NAD	69-73	sirtuin 1	Homo sapiens	59-64
29104634-1	2017	Nicotinamide phosphoribosyltransferase (Nampt) is a key enzyme in the nicotinamide adenine dinucleotide (NAD+) biosynthetic pathway.	NAD	70-103	nicotinamide phosphoribosyltransferase	Rattus norvegicus	40-45
12351438-3	2002	The activity and concentration of the two key enzymes of the NADH shuttles, mitochondrial glycerol phosphate dehydrogenase (mGPDH) and mitochondrial malate dehydrogenase (mMDH), were eight- and threefold lower, respectively, in fetal compared with adult rat islets.	NAD	61-65	glycerol phosphate dehydrogenase 2, mitochondrial	Mus musculus	124-129
12200115-2	2002	The present study describes biotransformation of RDX via route 3 by a diaphorase (EC 1.8.1.4) from Clostridium kluyveri using NADH as electron donor.	NAD	126-130	radixin	Homo sapiens	49-52
12200115-8	2002	A comparative study between native- and apo-enzymes showed the possible involvement of flavin mononucleotide (FMN) in catalyzing the transfer of a redox equivalent (e/H(+)) from NADH to RDX to produce RDX(.-) responsible for secondary decomposition.	NAD	178-182	radixin	Homo sapiens	186-189
12200115-8	2002	A comparative study between native- and apo-enzymes showed the possible involvement of flavin mononucleotide (FMN) in catalyzing the transfer of a redox equivalent (e/H(+)) from NADH to RDX to produce RDX(.-) responsible for secondary decomposition.	NAD	178-182	radixin	Homo sapiens	201-204
12032156-1	2002	In the yeast Saccharomyces cerevisiae, the two most important systems for conveying excess cytosolic NADH to the mitochondrial respiratory chain are external NADH dehydrogenase (Nde1p/Nde2p) and the glycerol-3-phosphate dehydrogenase shuttle.	NAD	101-105	NADH-ubiquinone reductase (H(+)-translocating) NDE1	Saccharomyces cerevisiae S288C	178-183
12032156-1	2002	In the yeast Saccharomyces cerevisiae, the two most important systems for conveying excess cytosolic NADH to the mitochondrial respiratory chain are external NADH dehydrogenase (Nde1p/Nde2p) and the glycerol-3-phosphate dehydrogenase shuttle.	NAD	101-105	NADH-ubiquinone reductase (H(+)-translocating) NDE2	Saccharomyces cerevisiae S288C	184-189
12145146-4	2002	Benfluorex inhibited gluconeogenesis at the level of pyruvate carboxylase (45% fall in acetyl-CoA concentration) and of glyceraldehyde-3-phosphate dehydrogenase (decrease in ATP/ADP and NAD(+)/NADH ratios).	NAD	186-192	glyceraldehyde-3-phosphate dehydrogenase	Rattus norvegicus	120-160
11960981-2	2002	LTRPC2 is a cation channel recently reported to be activated by adenosine diphosphate-ribose (ADP-ribose) and NAD.	NAD	110-113	transient receptor potential cation channel subfamily M member 2	Homo sapiens	0-6
11960981-3	2002	Since ADP-ribose can be formed from NAD and NAD is elevated during oxidative stress, we studied whole cell currents and increases in the intercellular free calcium concentration ([Ca(2+)](i)) in long transient receptor potential channel 2 (LTRPC2)-transfected HEK 293 cells after stimulation with hydrogen peroxide (H(2)O(2)).	NAD	36-39	transient receptor potential cation channel subfamily M member 2	Homo sapiens	195-238
11960981-3	2002	Since ADP-ribose can be formed from NAD and NAD is elevated during oxidative stress, we studied whole cell currents and increases in the intercellular free calcium concentration ([Ca(2+)](i)) in long transient receptor potential channel 2 (LTRPC2)-transfected HEK 293 cells after stimulation with hydrogen peroxide (H(2)O(2)).	NAD	44-47	transient receptor potential cation channel subfamily M member 2	Homo sapiens	195-238
11985605-6	2002	Scatchard analysis and kinetic studies of xCTBP/xALDH1 indicate that NAD+ and T3 are noncompetitive inhibitors of thyroid-hormone-binding and ALDH activities, respectively.	NAD	69-73	C-terminal binding protein 2 like S homeolog	Xenopus laevis	42-47
11985605-8	2002	Although the in vitro studies indicate that NAD+ and NADH markedly decrease T3-binding to xCTBP/xALDH1 at approximately 10-4 m, a concentration equal to the NAD content in various Xenopus tissues, photoaffinity-labeling of [125I]T3 using cultured Xenopus cells demonstrates xCTBP/xALDH1 bound T3 within living cells.	NAD	44-48	C-terminal binding protein 2 like S homeolog	Xenopus laevis	90-95
11985605-8	2002	Although the in vitro studies indicate that NAD+ and NADH markedly decrease T3-binding to xCTBP/xALDH1 at approximately 10-4 m, a concentration equal to the NAD content in various Xenopus tissues, photoaffinity-labeling of [125I]T3 using cultured Xenopus cells demonstrates xCTBP/xALDH1 bound T3 within living cells.	NAD	44-48	C-terminal binding protein 2 like S homeolog	Xenopus laevis	274-279
11985605-8	2002	Although the in vitro studies indicate that NAD+ and NADH markedly decrease T3-binding to xCTBP/xALDH1 at approximately 10-4 m, a concentration equal to the NAD content in various Xenopus tissues, photoaffinity-labeling of [125I]T3 using cultured Xenopus cells demonstrates xCTBP/xALDH1 bound T3 within living cells.	NAD	53-57	C-terminal binding protein 2 like S homeolog	Xenopus laevis	90-95
11985605-8	2002	Although the in vitro studies indicate that NAD+ and NADH markedly decrease T3-binding to xCTBP/xALDH1 at approximately 10-4 m, a concentration equal to the NAD content in various Xenopus tissues, photoaffinity-labeling of [125I]T3 using cultured Xenopus cells demonstrates xCTBP/xALDH1 bound T3 within living cells.	NAD	53-57	C-terminal binding protein 2 like S homeolog	Xenopus laevis	274-279
11985605-8	2002	Although the in vitro studies indicate that NAD+ and NADH markedly decrease T3-binding to xCTBP/xALDH1 at approximately 10-4 m, a concentration equal to the NAD content in various Xenopus tissues, photoaffinity-labeling of [125I]T3 using cultured Xenopus cells demonstrates xCTBP/xALDH1 bound T3 within living cells.	NAD	44-47	C-terminal binding protein 2 like S homeolog	Xenopus laevis	90-95
11985605-8	2002	Although the in vitro studies indicate that NAD+ and NADH markedly decrease T3-binding to xCTBP/xALDH1 at approximately 10-4 m, a concentration equal to the NAD content in various Xenopus tissues, photoaffinity-labeling of [125I]T3 using cultured Xenopus cells demonstrates xCTBP/xALDH1 bound T3 within living cells.	NAD	44-47	C-terminal binding protein 2 like S homeolog	Xenopus laevis	274-279
11985605-9	2002	These results raise the possibility that an unknown factor(s) besides NAD+ and NADH may modulate the thyroid-hormone-binding activity of xCTBP/xALDH1.	NAD	70-74	C-terminal binding protein 2 like S homeolog	Xenopus laevis	137-142
11985605-9	2002	These results raise the possibility that an unknown factor(s) besides NAD+ and NADH may modulate the thyroid-hormone-binding activity of xCTBP/xALDH1.	NAD	79-83	C-terminal binding protein 2 like S homeolog	Xenopus laevis	137-142
11850500-5	2002	Stimulation of cells with physiological doses of cholecystokinin (CCK) triggered slow oscillations of NADH autofluorescence.	NAD	102-106	cholecystokinin	Mus musculus	49-64
11850500-5	2002	Stimulation of cells with physiological doses of cholecystokinin (CCK) triggered slow oscillations of NADH autofluorescence.	NAD	102-106	cholecystokinin	Mus musculus	66-69
11850500-13	2002	Supramaximal doses of ACh and CCK produced single large NADH transients.	NAD	56-60	cholecystokinin	Mus musculus	30-33
11795879-4	2002	Finally, NADH/NADPH inhibitors prevent the p66(Shc) Ser-phosphorylation induced by serum and by phorbol 12-myristate-13-acetate, which suggests that the direct target(s) of reactive oxygen species is(are) located upstream from the machinery connecting growth factor receptors to Ras.	NAD	9-13	SHC adaptor protein 1	Homo sapiens	47-50
11995411-8	2002	Nicotinamide positively regulates glyceraldehyde-3-phosphate dehydrogenase when NADH is added.	NAD	80-84	glyceraldehyde-3-phosphate dehydrogenase	Rattus norvegicus	34-74
11796116-3	2002	The NAD+ binding pocket of the bacterial XDH resembles that of the dehydrogenase form of the bovine enzyme rather than that of the oxidase form, which reduces O(2) instead of NAD+.	NAD	175-179	xanthine dehydrogenase	Bos taurus	41-44
11696188-4	2001	As leaves develop from young to mature, the nda1 transcript level increases, accompanied by an elevation in immunodetected NDA protein and internal rotenone-insensitive NADH oxidation.	NAD	169-173	internal alternative NAD(P)H-ubiquinone oxidoreductase A1, mitochondrial	Solanum tuberosum	44-48
11602898-10	2001	Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase components p47phox and cytochrome b558 were mobilized to the plasma membrane, whereas p67phox showed minimal change.	NAD	0-33	neutrophil cytosolic factor 1	Homo sapiens	71-78
11602898-10	2001	Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase components p47phox and cytochrome b558 were mobilized to the plasma membrane, whereas p67phox showed minimal change.	NAD	0-33	mitochondrially encoded cytochrome b	Homo sapiens	83-95
12005031-3	2001	Using NAD or NADP as the cofactor, 17beta-hydroxysteroid dehydrogenase (substrate: 5-androstene-3beta,17beta-diol) peaks were observed on pnd 16 for fetal Leydig cells and on pnd 19 and 37 for adult Leydig cells.	NAD	6-9	aldo-keto reductase family 1, member C12	Rattus norvegicus	35-70
12005031-7	2001	To conclude: (1) Generally, a stronger reaction for 17beta-hydroxysteroid dehydrogenase is shown with NAD as cofactor than with NADP; using NADP, fetal Leydig cells show a stronger staining than adult Leydig cells.	NAD	102-105	aldo-keto reductase family 1, member C12	Rattus norvegicus	52-87
11509734-2	2001	Intracellular pyrimidine nucleotides, adenosine 5"-diphosphoribose (ADPR), and nicotinamide adenine dinucleotide (NAD), directly activated LTRPC2, which functioned as a Ca2+-permeable nonselective cation channel and enabled Ca2+ influx into cells.	NAD	79-112	transient receptor potential cation channel subfamily M member 2	Homo sapiens	139-145
11509734-2	2001	Intracellular pyrimidine nucleotides, adenosine 5"-diphosphoribose (ADPR), and nicotinamide adenine dinucleotide (NAD), directly activated LTRPC2, which functioned as a Ca2+-permeable nonselective cation channel and enabled Ca2+ influx into cells.	NAD	114-117	transient receptor potential cation channel subfamily M member 2	Homo sapiens	139-145
11509734-4	2001	These results reveal that ADPR and NAD act as intracellular messengers and may have an important role in Ca2+ influx by activating LTRPC2 in immunocytes.	NAD	35-38	transient receptor potential cation channel subfamily M member 2	Homo sapiens	131-137
11441146-3	2001	Here we show that the DNA-binding activity of the Clock:BMAL1 and NPAS2:BMAL1 heterodimers is regulated by the redox state of nicotinamide adenine dinucleotide (NAD) cofactors in a purified system.	NAD	126-159	aryl hydrocarbon receptor nuclear translocator like	Homo sapiens	56-61
11441146-3	2001	Here we show that the DNA-binding activity of the Clock:BMAL1 and NPAS2:BMAL1 heterodimers is regulated by the redox state of nicotinamide adenine dinucleotide (NAD) cofactors in a purified system.	NAD	126-159	aryl hydrocarbon receptor nuclear translocator like	Homo sapiens	72-77
11441146-3	2001	Here we show that the DNA-binding activity of the Clock:BMAL1 and NPAS2:BMAL1 heterodimers is regulated by the redox state of nicotinamide adenine dinucleotide (NAD) cofactors in a purified system.	NAD	161-164	aryl hydrocarbon receptor nuclear translocator like	Homo sapiens	56-61
11441146-3	2001	Here we show that the DNA-binding activity of the Clock:BMAL1 and NPAS2:BMAL1 heterodimers is regulated by the redox state of nicotinamide adenine dinucleotide (NAD) cofactors in a purified system.	NAD	161-164	aryl hydrocarbon receptor nuclear translocator like	Homo sapiens	72-77
11418649-3	2001	Annexin V staining of cells was observed already 10 min after treatment with NAD in the absence of any additional signal.	NAD	77-80	annexin A5	Mus musculus	0-9
11294878-9	2001	Thus, the new short chain dehydrogenase represents a novel type of microsomal NAD(+)-dependent 3alpha-hydroxysteroid dehydrogenase with unique catalytic properties and tissue distribution.	NAD	78-84	dehydrogenase/reductase 9	Homo sapiens	95-130
11274199-1	2001	CD38 is a bifunctional ectoenzyme synthesizing from NAD(+) (ADP-ribosyl cyclase) and degrading (hydrolase) cyclic ADP-ribose (cADPR), a powerful universal calcium mobilizer from intracellular stores.	NAD	52-58	CD38 antigen	Mus musculus	0-4
11401531-4	2001	NAD-dependent inactivation and ADP-ribosylation of CD38, intracellular concentrations of cADPR and Ca(2+), and insulin secretion were measured following incubation of mouse pancreatic islet cells with NAD.	NAD	0-3	CD38 antigen	Mus musculus	51-55
11181553-1	2001	The NAD-dependent enzyme, 11beta-hydroxysteroid dehydrogenase type II (11 beta HSD2), catalyzes the unidirectional conversion of biologically active glucocorticoids to inactive metabolites.	NAD	4-7	hydroxysteroid 11-beta dehydrogenase 2	Rattus norvegicus	71-83
11311853-8	2001	Deamino-NADP, but not NAD, was a coenzyme for placental glucose-6-phosphate dehydrogenase.	NAD	8-11	glucose-6-phosphate dehydrogenase	Homo sapiens	56-89
11306060-1	2001	Liver alcohol dehydrogenase (E.C.1.1.1.1) is an NAD(+)/NADH dependent enzyme with a broad substrate specificity being active on an assortment of primary and secondary alcohols.	NAD	48-54	aldo-keto reductase family 1 member A1	Homo sapiens	6-27
11306060-1	2001	Liver alcohol dehydrogenase (E.C.1.1.1.1) is an NAD(+)/NADH dependent enzyme with a broad substrate specificity being active on an assortment of primary and secondary alcohols.	NAD	55-59	aldo-keto reductase family 1 member A1	Homo sapiens	6-27
11136248-4	2001	Kinetic analysis measuring cytochrome c activity revealed that the NADH-dependent k(cat) of W676A is equivalent (90%) to the NADPH-dependent k(cat) of the wild-type enzyme, with W676A having an approximately 1,000-fold higher specificity for NADH.	NAD	67-71	2,4-dienoyl-CoA reductase 1	Homo sapiens	125-130
11136248-4	2001	Kinetic analysis measuring cytochrome c activity revealed that the NADH-dependent k(cat) of W676A is equivalent (90%) to the NADPH-dependent k(cat) of the wild-type enzyme, with W676A having an approximately 1,000-fold higher specificity for NADH.	NAD	242-246	2,4-dienoyl-CoA reductase 1	Homo sapiens	125-130
11042259-3	2000	The rescued mutants display a partially re-established transcriptional control of the osmostress-induced expression of GPD1, a target gene of the HOG pathway encoding NAD(+)-dependent glycerol 3-phosphate dehydrogenase, and a partially recovered hyperosmolarity-induced production of glycerol.	NAD	167-173	glycerol-3-phosphate dehydrogenase (NAD(+)) GPD1	Saccharomyces cerevisiae S288C	119-123
10842169-2	2000	The GPD1 gene encodes NAD(+)-dependent glycerol-3-phosphate dehydrogenase, a key enzyme in the production of the compatible solute glycerol.	NAD	22-28	glycerol-3-phosphate dehydrogenase (NAD(+)) GPD1	Saccharomyces cerevisiae S288C	4-8
11006085-0	2000	Induction of NAD(+)-linked 15-hydroxyprostaglandin dehydrogenase expression by androgens in human prostate cancer cells.	NAD	13-19	carbonyl reductase 1	Homo sapiens	27-64
10920265-0	2000	Overexpression of salicylate hydroxylase and the crucial role of lys(163) as its NADH binding site.	NAD	81-85	salicylate hydroxylase	Pseudomonas putida	18-40
10920265-6	2000	Based on chemical modification of the salicylate hydroxylase from P. putida, Lys163 was previously proposed to be the NADH binding site.	NAD	118-122	salicylate hydroxylase	Pseudomonas putida	38-60
10891341-7	2000	We finally confirmed the ADP-ribosyl cyclase activity of the expressed CD38 by measuring its ability to catalyze the cyclization of the nicotinamide adenine dinucleotide (NAD(+)) surrogate, NGD(+), to its fluorescent nonhydrolyzable derivative, cGDPr.	NAD	136-169	CD38 antigen	Mus musculus	71-75
10891341-7	2000	We finally confirmed the ADP-ribosyl cyclase activity of the expressed CD38 by measuring its ability to catalyze the cyclization of the nicotinamide adenine dinucleotide (NAD(+)) surrogate, NGD(+), to its fluorescent nonhydrolyzable derivative, cGDPr.	NAD	171-178	CD38 antigen	Mus musculus	71-75
10861229-8	2000	For the Aplysia enzyme"s catalysed transformation of NAD(+) we favour a mechanism where the formation of cADP-ribose precedes that of ADP-ribose; i.e. macroscopically the invertebrate ADP-ribosyl cyclase conforms to a sequential reaction pathway as a limiting form of the partitioning mechanism.	NAD	53-59	ADP-ribosyl cyclase/cyclic ADP-ribose hydrolase	Aplysia californica	184-203
11005571-8	2000	The mechanisms of these unexpected effects were delineated by CLSM, using NAD(P)H fluorescence measurements, which showed that HGF/SF increased the oxidation of the mitochondrial NAD system.	NAD	74-77	hepatocyte growth factor	Mus musculus	127-133
10843183-7	2000	This Ala is highly conserved in the vertebrate 3betaHSD gene family and is located in the putative NAD-binding domain of the enzyme.	NAD	99-102	hydroxy-delta-5-steroid dehydrogenase, 3 beta- and steroid delta-isomerase 1	Homo sapiens	47-55
10781794-4	2000	Obtained data suggest that cytochrome b(5) is normally oriented towards the cytosol in the outer membrane, and can be accessible for endogenous cytochrome c reduction only through the outer membrane rupture or permeabilization, to activate external NADH oxidation.	NAD	249-253	cytochrome b, mitochondrial	Rattus norvegicus	27-39
10767627-5	2000	On the other hand, resistance of Parp(-/-) mice to DNA damage induced by reactive oxygen species implicates the contribution of Parp to cell death through NAD depletion.	NAD	155-158	poly (ADP-ribose) polymerase family, member 1	Mus musculus	128-132
10804881-3	2000	The ADH reaction produces reducing equivalents as NADH which results in various metabolic disorders such as hyperproteinemia IV and V, hypoglycaemia, lactacidosis, hyperuricaemia, and certain forms of porphyria.	NAD	50-54	aldo-keto reductase family 1 member A1	Homo sapiens	4-7
10700391-13	2000	The kinetic analysis of redox changes in lysosomes revealed that electron carriers operate in the sequence NADH &gt; FAD &gt; cytochrome b &gt; ubiquinone &gt; oxygen.	NAD	107-111	cytochrome b, mitochondrial	Rattus norvegicus	126-138
10713448-1	2000	The evolutionary history of the malate dehydrogenase (MDH) gene family [NAD-dependent MDH; EC 1.1.1.37 and NAD(P)-dependent MDH; EC 1.1.1.82] has received much attention.	NAD	72-75	malate dehydrogenase 2, NAD (mitochondrial)	Mus musculus	54-57
10713448-1	2000	The evolutionary history of the malate dehydrogenase (MDH) gene family [NAD-dependent MDH; EC 1.1.1.37 and NAD(P)-dependent MDH; EC 1.1.1.82] has received much attention.	NAD	72-75	malate dehydrogenase 2, NAD (mitochondrial)	Mus musculus	86-89
10713448-1	2000	The evolutionary history of the malate dehydrogenase (MDH) gene family [NAD-dependent MDH; EC 1.1.1.37 and NAD(P)-dependent MDH; EC 1.1.1.82] has received much attention.	NAD	72-75	malate dehydrogenase 2, NAD (mitochondrial)	Mus musculus	86-89
10683258-1	2000	Inosine 5"-monophosphate dehydrogenase (IMPDH) catalyzes the oxidation of inosine 5"-monophosphate (IMP) to xanthosine 5"-monophosphate with the concomitant reduction of NAD to NADH.	NAD	170-173	inosine-5'-monophosphate dehydrogenase 2	Cricetulus griseus	40-45
10683258-1	2000	Inosine 5"-monophosphate dehydrogenase (IMPDH) catalyzes the oxidation of inosine 5"-monophosphate (IMP) to xanthosine 5"-monophosphate with the concomitant reduction of NAD to NADH.	NAD	177-181	inosine-5'-monophosphate dehydrogenase 2	Cricetulus griseus	40-45
29104634-1	2017	Nicotinamide phosphoribosyltransferase (Nampt) is a key enzyme in the nicotinamide adenine dinucleotide (NAD+) biosynthetic pathway.	NAD	105-109	nicotinamide phosphoribosyltransferase	Rattus norvegicus	40-45
28842348-4	2017	The NADH-dependent generation of extracellular superoxide was prevented by knockdown of NDUFV-1, the first subunit of OXPHOS I receiving electrons from NADH and the NADH-improved insulin signaling was abolished by extracellular catalase.	NAD	4-8	NADH:ubiquinone oxidoreductase core subunit V1	Homo sapiens	88-95
28842348-4	2017	The NADH-dependent generation of extracellular superoxide was prevented by knockdown of NDUFV-1, the first subunit of OXPHOS I receiving electrons from NADH and the NADH-improved insulin signaling was abolished by extracellular catalase.	NAD	152-156	NADH:ubiquinone oxidoreductase core subunit V1	Homo sapiens	88-95
28842348-4	2017	The NADH-dependent generation of extracellular superoxide was prevented by knockdown of NDUFV-1, the first subunit of OXPHOS I receiving electrons from NADH and the NADH-improved insulin signaling was abolished by extracellular catalase.	NAD	152-156	NADH:ubiquinone oxidoreductase core subunit V1	Homo sapiens	88-95
28603221-1	2017	Resveratrol is a potent activator of NAD-dependent deacetyltransferase sirtuin-1 (SIRT1) and affects lipid metabolism and ATP generation in somatic cells.	NAD	37-40	sirtuin 1	Bos taurus	71-80
28603221-1	2017	Resveratrol is a potent activator of NAD-dependent deacetyltransferase sirtuin-1 (SIRT1) and affects lipid metabolism and ATP generation in somatic cells.	NAD	37-40	sirtuin 1	Bos taurus	82-87
29033913-3	2017	In the anaerobe Desulfovibrio vulgaris Hildenborough (DvH), there is an intriguing redundancy of the Trx system which includes a classical system using NADPH as electron source, a non-canonical system using NADH and an isolated TR (DvTRi).	NAD	207-211	trx	Desulfovibrio vulgaris str. Hildenborough	101-104
10746800-3	2000	Glycolysis and the oxidative pentose phosphate pathway generate NADH and NADPH to reduce methemoglobin, which is being continuously produced, and the antioxidant glutathione, which is present in high concentrations.	NAD	64-68	hemoglobin subunit gamma 2	Homo sapiens	89-102
10671998-11	2000	Thus, mutation of H230 of sheep liver serine hydroxymethyltransferase to Tyr leads to induction of an NADH oxidation activity implying that tyrosyl radicals may be mediating the reaction.	NAD	102-106	serine hydroxymethyltransferase, cytosolic	Ovis aries	38-69
10821426-2	2000	The DNase I sensitive and resistant chromatin contain 35% and 40%, respectively, of the total pADPR synthesized in intact nuclei incubated with [32P]NAD.	NAD	149-152	deoxyribonuclease 1	Rattus norvegicus	4-11
10636849-4	2000	Among these dehydrogenases, mitochondrial glycerol-3-phosphate dehydrogenase (mGPDH), the key enzyme of the glycerol phosphate NADH shuttle, is activated by cytosolic [Ca(2+)](i).	NAD	127-131	glycerol phosphate dehydrogenase 2, mitochondrial	Mus musculus	78-83
10636849-11	2000	Inhibition of the malate-aspartate NADH shuttle with aminooxyacetate only had minor effects in control islets but abolished the electrical, [Ca(2+)](i) and secretory responses in mGPDH(-/-) islets.	NAD	35-39	glycerol phosphate dehydrogenase 2, mitochondrial	Mus musculus	179-184
12760043-0	2000	Sir2: an NAD-dependent histone deacetylase that connects chromatin silencing, metabolism, and aging.	NAD	9-12	sirtuin 1	Homo sapiens	0-4
10644882-2	2000	The NAD(+)-dependent isoform, 11betaHSD2, is present in the distal nephron where it confers aldosterone specificity on mineralocorticoid receptors.	NAD	4-10	hydroxysteroid 11-beta dehydrogenase 2	Rattus norvegicus	30-40
10617673-5	2000	In vitro, the compounds enhanced the conversion of NAD(+) to NADH by GAPDH in the presence of AUUUA-rich RNA and converted GAPDH from its usual tetrameric form to a dimeric form.	NAD	51-57	glyceraldehyde-3-phosphate dehydrogenase	Rattus norvegicus	69-74
10617673-5	2000	In vitro, the compounds enhanced the conversion of NAD(+) to NADH by GAPDH in the presence of AUUUA-rich RNA and converted GAPDH from its usual tetrameric form to a dimeric form.	NAD	51-57	glyceraldehyde-3-phosphate dehydrogenase	Rattus norvegicus	123-128
10617673-5	2000	In vitro, the compounds enhanced the conversion of NAD(+) to NADH by GAPDH in the presence of AUUUA-rich RNA and converted GAPDH from its usual tetrameric form to a dimeric form.	NAD	61-65	glyceraldehyde-3-phosphate dehydrogenase	Rattus norvegicus	69-74
10617673-5	2000	In vitro, the compounds enhanced the conversion of NAD(+) to NADH by GAPDH in the presence of AUUUA-rich RNA and converted GAPDH from its usual tetrameric form to a dimeric form.	NAD	61-65	glyceraldehyde-3-phosphate dehydrogenase	Rattus norvegicus	123-128
10593891-8	1999	Unlike mammalian MTHFR, the plant enzymes strongly prefer NADH to NADPH, and are not inhibited by S-adenosylmethionine.	NAD	58-62	methylenetetrahydrofolate reductase	Homo sapiens	17-22
10593891-9	1999	An NADH-dependent MTHFR reaction could be reversible in plant cytosol, where the NADH/NAD ratio is 10(-3).	NAD	3-7	methylenetetrahydrofolate reductase	Homo sapiens	18-23
10593891-9	1999	An NADH-dependent MTHFR reaction could be reversible in plant cytosol, where the NADH/NAD ratio is 10(-3).	NAD	81-85	methylenetetrahydrofolate reductase	Homo sapiens	18-23
10593891-9	1999	An NADH-dependent MTHFR reaction could be reversible in plant cytosol, where the NADH/NAD ratio is 10(-3).	NAD	3-6	methylenetetrahydrofolate reductase	Homo sapiens	18-23
10574992-3	1999	Here we show that in the same cells E1A binding to members of the retinoblastoma protein family induces transcriptional down-regulation of the poly(ADP-ribose) polymerase (PARP) gene, coding for a NAD-dependent enzyme stimulated by DNA breaks.	NAD	197-200	poly (ADP-ribose) polymerase family, member 1	Mus musculus	143-170
10574992-3	1999	Here we show that in the same cells E1A binding to members of the retinoblastoma protein family induces transcriptional down-regulation of the poly(ADP-ribose) polymerase (PARP) gene, coding for a NAD-dependent enzyme stimulated by DNA breaks.	NAD	197-200	poly (ADP-ribose) polymerase family, member 1	Mus musculus	172-176
10562410-9	1999	This increase in NAD biosynthesis may provide an improved supply of substrate to the nuclear repair enzyme poly(ADP-ribose) polymerase assisting in DNA repair and hence cell viability.	NAD	17-20	poly (ADP-ribose) polymerase family, member 1	Mus musculus	107-134
10517700-4	1999	The permanent ektopic expression of hDAT in HEK-293 cells confers time and dose-dependent cytotoxicity at nanomolar concentrations of MPP+ with an IC50 value of 740 nM after 48 h. MPP+ initially induces a fast increase of cellular NADH content within the first 6 h, followed by a slow reduction of intracellular ATP (IC50 value of 690 nM after 48 h) as well as reduction of intracellular ATP/ADP ratio.	NAD	231-235	solute carrier family 6 member 3	Homo sapiens	36-40
10497258-1	1999	We report that the NAD-dependent Escherichia coli DNA ligase can support the growth of Saccharomyces cerevisiae strains deleted singly for CDC9 or doubly for CDC9 plus LIG4.	NAD	19-22	DNA ligase (ATP) CDC9	Saccharomyces cerevisiae S288C	139-143
10497258-1	1999	We report that the NAD-dependent Escherichia coli DNA ligase can support the growth of Saccharomyces cerevisiae strains deleted singly for CDC9 or doubly for CDC9 plus LIG4.	NAD	19-22	DNA ligase (ATP) CDC9	Saccharomyces cerevisiae S288C	158-162
10446379-1	1999	Thermal unfolding parameters were determined for a two-domain tetrameric enzyme, phosphorylating D-glyceraldehyde-3-phosphate dehydrogenase (GAPDH), and for its isolated NAD(+)-binding domain.	NAD	170-176	glyceraldehyde-3-phosphate dehydrogenase	Oryctolagus cuniculus	141-146
10446379-9	1999	Replacement of Cys149 by Ser or by Ala in the B. stearothermophilus GAPDH produced some stabilization, the effect of added NAD(+) being basically similar to that observed with the wild-type enzyme.	NAD	123-129	glyceraldehyde-3-phosphate dehydrogenase	Oryctolagus cuniculus	68-73
10381404-2	1999	The coupling protein B (MMOB) both activates the carboxylate-bridged diiron center in the hydroxylase (MMOH) for substrate oxidation and couples the reaction to electron transfer from NADH through the sMMO reductase.	NAD	184-188	prolyl 3-hydroxylase 3	Homo sapiens	13-22
29090276-4	2017	METHODS: A variety of experimental approaches, including NMR and NAD-linked assay systems were used to conduct a biochemical investigation of polyphosphate dependent glucokinase activity in mammalian tissues.	NAD	65-68	glucokinase	Homo sapiens	166-177
27578018-2	2017	It has been revealed that the impact of ROS can be suppressed by sirtuin 1 (SIRT1), a member of the highly conserved nicotinamide adenine dinucleotide-dependent class III histone deacetylases through protecting endothelial cells from oxidative injury.	NAD	117-150	sirtuin 1	Homo sapiens	65-74
27578018-2	2017	It has been revealed that the impact of ROS can be suppressed by sirtuin 1 (SIRT1), a member of the highly conserved nicotinamide adenine dinucleotide-dependent class III histone deacetylases through protecting endothelial cells from oxidative injury.	NAD	117-150	sirtuin 1	Homo sapiens	76-81
28621879-4	2017	PGRP-induced killing depended on the production of hydrogen peroxide, which required increased supply of NADH for respiratory chain oxidoreductases from central carbon catabolism (glycolysis and TCA cycle), and was controlled by cAMP-Crp.	NAD	105-109	catabolite gene activator protein	Escherichia coli	234-237
28714002-13	2017	Stochastic perturbation analysis revealed that NADH:ubiquinone oxidoreductase subunit B2 (NDUFB2), NDUFB8 and ubiquinol-cytochrome c reductase hinge protein (UQCRH) were associated with cellular respiration in Gram-negative samples, whereas large tumor suppressor kinase 2 (LATS2) was associated with G1/S transition of the mitotic cell cycle in Gram-positive samples.	NAD	47-51	large tumor suppressor kinase 2	Homo sapiens	241-272
28714002-13	2017	Stochastic perturbation analysis revealed that NADH:ubiquinone oxidoreductase subunit B2 (NDUFB2), NDUFB8 and ubiquinol-cytochrome c reductase hinge protein (UQCRH) were associated with cellular respiration in Gram-negative samples, whereas large tumor suppressor kinase 2 (LATS2) was associated with G1/S transition of the mitotic cell cycle in Gram-positive samples.	NAD	47-51	large tumor suppressor kinase 2	Homo sapiens	274-279
28714019-9	2017	As a result, the expression level of nicotinamide phosphoribosyltransferase (NAMPT) decreased, the synthesis of nicotinamide adenine dinucleotide (NAD+; an energy metabolism-associated coenzyme) became insufficient, and the NAD+/nicotinamide adenine dinucleotide hydride ratio was reduced.	NAD	112-145	nicotinamide phosphoribosyltransferase	Rattus norvegicus	77-82
28714019-9	2017	As a result, the expression level of nicotinamide phosphoribosyltransferase (NAMPT) decreased, the synthesis of nicotinamide adenine dinucleotide (NAD+; an energy metabolism-associated coenzyme) became insufficient, and the NAD+/nicotinamide adenine dinucleotide hydride ratio was reduced.	NAD	147-151	nicotinamide phosphoribosyltransferase	Rattus norvegicus	37-75
28714019-9	2017	As a result, the expression level of nicotinamide phosphoribosyltransferase (NAMPT) decreased, the synthesis of nicotinamide adenine dinucleotide (NAD+; an energy metabolism-associated coenzyme) became insufficient, and the NAD+/nicotinamide adenine dinucleotide hydride ratio was reduced.	NAD	147-151	nicotinamide phosphoribosyltransferase	Rattus norvegicus	77-82
28714019-9	2017	As a result, the expression level of nicotinamide phosphoribosyltransferase (NAMPT) decreased, the synthesis of nicotinamide adenine dinucleotide (NAD+; an energy metabolism-associated coenzyme) became insufficient, and the NAD+/nicotinamide adenine dinucleotide hydride ratio was reduced.	NAD	224-228	nicotinamide phosphoribosyltransferase	Rattus norvegicus	37-75
28714019-9	2017	As a result, the expression level of nicotinamide phosphoribosyltransferase (NAMPT) decreased, the synthesis of nicotinamide adenine dinucleotide (NAD+; an energy metabolism-associated coenzyme) became insufficient, and the NAD+/nicotinamide adenine dinucleotide hydride ratio was reduced.	NAD	224-228	nicotinamide phosphoribosyltransferase	Rattus norvegicus	77-82
28543772-0	2017	PARP inhibitor rucaparib induces changes in NAD levels in cells and liver tissues as assessed by MRS. Poly(adenosine diphosphate ribose) polymerases (PARPs) are multifunctional proteins which play a role in many cellular processes.	NAD	44-47	poly (ADP-ribose) polymerase family, member 1	Mus musculus	0-4
28543772-0	2017	PARP inhibitor rucaparib induces changes in NAD levels in cells and liver tissues as assessed by MRS. Poly(adenosine diphosphate ribose) polymerases (PARPs) are multifunctional proteins which play a role in many cellular processes.	NAD	44-47	poly (ADP-ribose) polymerase family, member 1	Mus musculus	150-155
29046881-1	2017	OBJECTIVE: To determine whether the NAD+ biosynthetic protein, nicotinamide mononucleotide adenylyltransferase-3 (NMNAT3), is a neuroprotective inducible enzyme capable of decreasing cerebral injury after neonatal hypoxia-ischemia (H-I) and reducing glutamate receptor-mediated excitotoxic neurodegeneration of immature neurons.	NAD	36-40	nicotinamide nucleotide adenylyltransferase 3	Mus musculus	63-112
29046881-1	2017	OBJECTIVE: To determine whether the NAD+ biosynthetic protein, nicotinamide mononucleotide adenylyltransferase-3 (NMNAT3), is a neuroprotective inducible enzyme capable of decreasing cerebral injury after neonatal hypoxia-ischemia (H-I) and reducing glutamate receptor-mediated excitotoxic neurodegeneration of immature neurons.	NAD	36-40	nicotinamide nucleotide adenylyltransferase 3	Mus musculus	114-120
28666871-5	2017	Recently, we demonstrated that the G307E replacement in murine AIF (equivalent to the pathogenic G308E in the human protein) dramatically decreases the rate of CT complex formation through the destabilization of the flavoprotein interaction with NAD(H).	NAD	246-252	apoptosis-inducing factor, mitochondrion-associated 1	Mus musculus	63-66
10329704-3	1999	Mitochondria have been demonstrated to be the proper location of this NAD+-dependent dehydrogenase in cells, although its primary structure is identical to an amyloid beta-peptide binding protein reportedly associated with the endoplasmic reticulum (ERAB).	NAD	70-73	hydroxysteroid 17-beta dehydrogenase 10	Homo sapiens	250-254
28666871-6	2017	To provide further insights into the structural bases of its altered functional properties, here we report the first crystal structure of an AIF pathogenic mutant variant in complex with NAD+ (murine AIF-G307ECT) in comparison with its oxidized form.	NAD	187-191	apoptosis-inducing factor, mitochondrion-associated 1	Mus musculus	141-144
28666871-6	2017	To provide further insights into the structural bases of its altered functional properties, here we report the first crystal structure of an AIF pathogenic mutant variant in complex with NAD+ (murine AIF-G307ECT) in comparison with its oxidized form.	NAD	187-191	apoptosis-inducing factor, mitochondrion-associated 1	Mus musculus	200-203
28666871-7	2017	With respect to wild type AIF, the mutation leads to an altered positioning of NAD+ adenylate moiety, which slows down CT complex formation.	NAD	79-83	apoptosis inducing factor mitochondria associated 1	Homo sapiens	26-29
28666871-8	2017	Moreover, the altered balance between the binding of the adenine/nicotinamide portions of the coenzyme determines a large drop in AIF-G307E ability to discriminate between NADH and NADPH.	NAD	172-176	apoptosis inducing factor mitochondria associated 1	Homo sapiens	130-133
28436948-8	2017	Mechanistically, energy stress-induced mitochondrial elongation facilitated cristae formation and assembly of respiratory complexes to enhance oxidative phosphorylation, which in turn exhibited a feedback inhibitory effect on glycolysis through NAD+-dependent SIRT1 activation.	NAD	245-249	sirtuin 1	Homo sapiens	260-265
28655758-1	2017	Sirtuin 7 (SIRT7), a member of the NAD+-dependent class III histone deacetylases, is involved in the regulation of various cellular processes and in resisting various stresses, such as hypoxia, low glucose levels, and DNA damage.	NAD	35-39	sirtuin 7	Homo sapiens	0-9
28655758-1	2017	Sirtuin 7 (SIRT7), a member of the NAD+-dependent class III histone deacetylases, is involved in the regulation of various cellular processes and in resisting various stresses, such as hypoxia, low glucose levels, and DNA damage.	NAD	35-39	sirtuin 7	Homo sapiens	11-16
28722654-5	2017	The extracellular lectin domain of LecRK-I.8 binds NAD+ with a dissociation constant of 436.5 +- 104.8 nM, although much higher concentrations are needed to trigger in vivo responses.	NAD	51-55	Concanavalin A-like lectin protein kinase family protein	Arabidopsis thaliana	35-44
28722654-6	2017	Mutations in LecRK-I.8 inhibit NAD+-induced immune responses, whereas overexpression of LecRK-I.8 enhances the Arabidopsis response to NAD+.	NAD	31-35	Concanavalin A-like lectin protein kinase family protein	Arabidopsis thaliana	13-22
28722654-6	2017	Mutations in LecRK-I.8 inhibit NAD+-induced immune responses, whereas overexpression of LecRK-I.8 enhances the Arabidopsis response to NAD+.	NAD	135-139	Concanavalin A-like lectin protein kinase family protein	Arabidopsis thaliana	88-97
28708087-4	2017	In this context, resveratrol activates SIRT1 (1) by directly binding to SIRT1; and (2) by increasing NAD+ levels by upregulating the salvage pathway through Nampt activation, an effect mediated by AMPK.	NAD	101-105	sirtuin 1	Homo sapiens	39-44
28400476-5	2017	In a system to dynamically visualize cellular metabolic responses mediated by GAD1, we monitored the cytosolic NADH:NAD+ equilibrium in tumor cells.	NAD	111-115	glutamate decarboxylase 1	Homo sapiens	78-82
28400476-5	2017	In a system to dynamically visualize cellular metabolic responses mediated by GAD1, we monitored the cytosolic NADH:NAD+ equilibrium in tumor cells.	NAD	116-120	glutamate decarboxylase 1	Homo sapiens	78-82
28400476-6	2017	Reducing GAD1 in metastatic cells by primary glia cell coculture abolished the capacity of metastatic cells to utilize extracellular glutamine, leading to cytosolic accumulation of NADH and increased oxidative status.	NAD	181-185	glutamate decarboxylase 1	Homo sapiens	9-13
28364022-1	2017	SIRT1, the most conserved mammalian NAD+-dependent protein deacetylase, is an important metabolic regulator.	NAD	36-39	sirtuin 1	Homo sapiens	0-5
28232491-4	2017	We show that ROC is composed of at least two subunits of NAD+-dependent retinol dehydrogenase 10 (RDH10), which catalyzes the oxidation of retinol to retinaldehyde, and two subunits of NADPH-dependent dehydrogenase reductase 3 (DHRS3), which catalyzes the reduction of retinaldehyde back to retinol.	NAD	57-60	retinol dehydrogenase 10	Homo sapiens	72-96
28232491-4	2017	We show that ROC is composed of at least two subunits of NAD+-dependent retinol dehydrogenase 10 (RDH10), which catalyzes the oxidation of retinol to retinaldehyde, and two subunits of NADPH-dependent dehydrogenase reductase 3 (DHRS3), which catalyzes the reduction of retinaldehyde back to retinol.	NAD	57-60	retinol dehydrogenase 10	Homo sapiens	98-103
28413646-2	2017	Malate dehydrogenase (MDH), as an important enzyme in cancer metabolism, is a source of NAD+ additional to lactate dehydrogenase (LDH).	NAD	88-92	malic enzyme 1	Homo sapiens	0-20
28413646-2	2017	Malate dehydrogenase (MDH), as an important enzyme in cancer metabolism, is a source of NAD+ additional to lactate dehydrogenase (LDH).	NAD	88-92	malic enzyme 1	Homo sapiens	22-25
28413646-8	2017	The higher tendency of C-MDH for NAD+ and malate generation in cancer cells is an effective approach for supporting glycolysis.	NAD	33-37	malic enzyme 1	Homo sapiens	25-28
27939939-1	2017	CD38 is an ectoenzyme that catalyzes the conversion of beta-nicotinamide adenine dinucleotide (beta-NAD) to cyclic adenosine diphosphoribose (cADPR) and adenosine diphosphoribose (ADPR) and NADP to nicotinic acid adenine dinucleotide phosphate (NAADP) and adenosine diphosphoribose-2"-phosphate (ADPR-P).	NAD	55-93	CD38 antigen	Mus musculus	0-4
27939939-1	2017	CD38 is an ectoenzyme that catalyzes the conversion of beta-nicotinamide adenine dinucleotide (beta-NAD) to cyclic adenosine diphosphoribose (cADPR) and adenosine diphosphoribose (ADPR) and NADP to nicotinic acid adenine dinucleotide phosphate (NAADP) and adenosine diphosphoribose-2"-phosphate (ADPR-P).	NAD	95-103	CD38 antigen	Mus musculus	0-4
10075087-4	1999	In contrast, catalysis of the oxidation of t-RAL to t-RA appeared to be solely NAD+ dependent.	NAD	79-83	RAS like proto-oncogene A	Homo sapiens	45-48
28336669-4	2017	The binding of NAD+ to the NHD domain of DBC1 (deleted in breast cancer 1) prevents it from inhibiting PARP1 [poly(adenosine diphosphate-ribose) polymerase], a critical DNA repair protein.	NAD	15-19	poly (ADP-ribose) polymerase family, member 1	Mus musculus	103-108
27882448-1	2017	Sirtuins (SIRT1-SIRT7) are unique histone deacetylases (HDACs) whose activity depends on NAD+ levels and thus on the cellular metabolic status.	NAD	89-93	sirtuin 1	Homo sapiens	10-15
10051636-2	1999	Because Parp uses NAD as a substrate, extensive DNA damage will result in reduction of cellular NAD level.	NAD	18-21	poly (ADP-ribose) polymerase family, member 1	Mus musculus	8-12
10051636-2	1999	Because Parp uses NAD as a substrate, extensive DNA damage will result in reduction of cellular NAD level.	NAD	96-99	poly (ADP-ribose) polymerase family, member 1	Mus musculus	8-12
27882448-1	2017	Sirtuins (SIRT1-SIRT7) are unique histone deacetylases (HDACs) whose activity depends on NAD+ levels and thus on the cellular metabolic status.	NAD	89-93	sirtuin 7	Homo sapiens	16-21
28228259-2	2017	Here, we show that the nicotinamide adenine dinucleotide (NAD)-dependent deacetylase, Sirt1, selectively prevents abnormal DNA methylation of some developmental genes in murine ESCs by antagonizing Dnmt3l.	NAD	23-56	DNA (cytosine-5-)-methyltransferase 3-like	Mus musculus	198-204
9988690-0	1999	Role of the flavin midpoint potential and NAD binding in determining NAD versus oxygen reactivity of xanthine oxidoreductase.	NAD	42-45	xanthine dehydrogenase	Bos taurus	101-124
28228259-2	2017	Here, we show that the nicotinamide adenine dinucleotide (NAD)-dependent deacetylase, Sirt1, selectively prevents abnormal DNA methylation of some developmental genes in murine ESCs by antagonizing Dnmt3l.	NAD	58-61	DNA (cytosine-5-)-methyltransferase 3-like	Mus musculus	198-204
9988690-0	1999	Role of the flavin midpoint potential and NAD binding in determining NAD versus oxygen reactivity of xanthine oxidoreductase.	NAD	69-72	xanthine dehydrogenase	Bos taurus	101-124
28162896-1	2017	SIRT1, the most conserved mammalian NAD+-dependent protein deacetylase, plays a vital role in the regulation of metabolism, stress responses, and genome stability.	NAD	36-39	sirtuin 1	Homo sapiens	0-5
9988690-2	1999	Enzyme forms differ in respect to their oxidizing substrates; XDH prefers NAD to molecular oxygen, whereas XO only reacts significantly with oxygen.	NAD	74-77	xanthine dehydrogenase	Bos taurus	62-65
9988690-10	1999	However, 1-deaza-XDH does exhibit xanthine/NAD activity, and 8-CN-XO has normal xanthine/oxygen activity.	NAD	43-46	xanthine dehydrogenase	Bos taurus	17-20
9988690-11	1999	The binding of NAD to oxidized XO and XDH was investigated by ultrafiltration and isothermal titration calorimetry.	NAD	15-18	xanthine dehydrogenase	Bos taurus	38-41
9988690-12	1999	The Kd for the binding of NAD to XDH was determined to be 280 +/- 145 microM by ultrafiltration and 160 +/- 40 microM by isothermal titration calorimetry.	NAD	26-29	xanthine dehydrogenase	Bos taurus	33-36
28209901-5	2017	Oral administration of the NAD+ precursor nicotinamide (vitamin B3), and/or gene therapy (driving expression of Nmnat1, a key NAD+-producing enzyme), was protective both prophylactically and as an intervention.	NAD	126-130	nicotinamide nucleotide adenylyltransferase 1	Mus musculus	112-118
10082668-0	1999	The NAD+ precursors, nicotinic acid and nicotinamide upregulate glyceraldehyde-3-phosphate dehydrogenase and glucose-6-phosphate dehydrogenase mRNA in Jurkat cells.	NAD	4-8	glucose-6-phosphate dehydrogenase	Homo sapiens	109-142
10082668-4	1999	Our findings suggest that the NAD+ precursors may protect against oxidative stress and DNA damage by up-regulating the stress response genes GAPDH and G6PD.	NAD	30-34	glucose-6-phosphate dehydrogenase	Homo sapiens	151-155
27929731-4	2017	In this report, using both human and murine models of CSCs, we demonstrate that basal levels of autophagy are required to maintain the pluripotency of CSCs, and that this process is differentially regulated by the rate-limiting enzyme in the NAD+ synthesis pathway NAMPT (nicotinamide phosphoribosyltransferase) and the transcription factor POU5F1/OCT4 (POU class 5 homeobox 1).	NAD	242-246	POU domain, class 5, transcription factor 1	Mus musculus	341-347
9890977-2	1999	Purified recombinant ERAB/HADH II catalyzed the NADH-dependent reduction of S-acetoacetyl-CoA with a Km of approximately 68 microM and a Vmax of approximately 430 micromol/min/mg.	NAD	48-52	hydroxysteroid 17-beta dehydrogenase 10	Homo sapiens	21-25
9890977-5	1999	We thus asked whether the enzyme might recognize alcohol substrates of which the aldehyde products could be cytotoxic; ERAB/HADH II catalyzed oxidation of a variety of simple alcohols (C2-C10) to their respective aldehydes in the presence of NAD+ and NAD-dependent oxidation of 17beta-estradiol.	NAD	242-246	hydroxysteroid 17-beta dehydrogenase 10	Homo sapiens	119-123
9890977-5	1999	We thus asked whether the enzyme might recognize alcohol substrates of which the aldehyde products could be cytotoxic; ERAB/HADH II catalyzed oxidation of a variety of simple alcohols (C2-C10) to their respective aldehydes in the presence of NAD+ and NAD-dependent oxidation of 17beta-estradiol.	NAD	242-245	hydroxysteroid 17-beta dehydrogenase 10	Homo sapiens	119-123
27929731-4	2017	In this report, using both human and murine models of CSCs, we demonstrate that basal levels of autophagy are required to maintain the pluripotency of CSCs, and that this process is differentially regulated by the rate-limiting enzyme in the NAD+ synthesis pathway NAMPT (nicotinamide phosphoribosyltransferase) and the transcription factor POU5F1/OCT4 (POU class 5 homeobox 1).	NAD	242-246	POU domain, class 5, transcription factor 1	Mus musculus	348-352
28147277-0	2017	Regulation of Serine-Threonine Kinase Akt Activation by NAD+-Dependent Deacetylase SIRT7.	NAD	56-59	sirtuin 7	Mus musculus	83-88
27345396-5	2017	Here, we show that the regulation of cancer invasion by OGT is dependent on the NAD+-dependent deacetylase SIRT1.	NAD	80-83	sirtuin 1	Homo sapiens	107-112
27535993-3	2017	This work presents a general stoichiometric model for C3, C2, C2+C4, and C4 assimilation (SMA) in which energetics, metabolite traffic, and the different decarboxylating enzymes (NAD-dependent malic enzyme, NADP-dependent malic enzyme, or phosphoenolpyruvate carboxykinase) are explicitly included.	NAD	179-182	malic enzyme 1	Homo sapiens	207-272
10668429-3	1999	Evidence from in vitro studies on nonneuronal cells in culture have shown that when fully activated by free radical-induced DNA damage, PARP depletes cellular NAD+ and consequently adenosine triphosphate (ATP) levels within a matter of minutes, and that this depletion is associated with a cell death that can be prevented by PARP inhibitors.	NAD	159-163	poly (ADP-ribose) polymerase family, member 1	Mus musculus	136-140
10668429-3	1999	Evidence from in vitro studies on nonneuronal cells in culture have shown that when fully activated by free radical-induced DNA damage, PARP depletes cellular NAD+ and consequently adenosine triphosphate (ATP) levels within a matter of minutes, and that this depletion is associated with a cell death that can be prevented by PARP inhibitors.	NAD	159-163	poly (ADP-ribose) polymerase family, member 1	Mus musculus	326-330
28058510-3	2017	Mammalian isocitrate dehydrogenase (IDH) 3 is a heterotetramer of 2alfa, 1beta, and 1gamma subunits, and IDH3A encodes the alfa subunit of the mitochondrial NAD+-dependent IDH.	NAD	157-161	isocitrate dehydrogenase (NAD(+)) 3 catalytic subunit alpha	Homo sapiens	105-110
16232608-0	1999	Effect of NAD+-dependent isocitrate dehydrogenase gene (IDH1, IDH2) disruption of sake yeast on organic acid composition in sake mash.	NAD	10-14	isocitrate dehydrogenase (NAD(+)) IDH2	Saccharomyces cerevisiae S288C	62-66
28058510-5	2017	We therefore propose that homozygosity for the p.Pro304His mutation is deleterious for mitochondrial NAD+-specific IDH3A activity in human.	NAD	101-105	isocitrate dehydrogenase (NAD(+)) 3 catalytic subunit alpha	Homo sapiens	115-120
10453439-9	1999	Niacin supplementation elevated skin NAD content, which is known to modulate the function of DNA strand scission surveillance proteins p53 and poly(ADP-ribose) polymerase, two proteins critical in cellular responses to UV-induced DNA damage.	NAD	37-40	poly (ADP-ribose) polymerase family, member 1	Mus musculus	143-170
27924925-5	2016	However, sirtuin 1 was downregulated and so the accumulation of NMN and NR was best explained by reduced flux through the amidated arm of the NAD+ salvage pathway due to reduced sirtuin activity.	NAD	142-146	sirtuin 1	Homo sapiens	9-18
9880405-6	1999	For example, 4 hours after ischemia, brain pHi in the severe hyperglycemia/normoxia group measured 6.46, compared with 6.84 in the hypoglycemia/normoxia group (P&lt;0.01), and NADH fluorescence measured 173% compared with 114%.	NAD	176-180	glucose-6-phosphate isomerase	Oryctolagus cuniculus	43-46
27756843-5	2016	Steady-state kinetic analyses and binding assays were consistent with Sirt1 S-nitrosation inhibiting binding of both the NAD+ and acetyl-lysine substrates.	NAD	121-125	sirtuin 1	Homo sapiens	70-75
9804757-1	1998	Poly(ADP-ribose) polymerase (PARP) (EC 2.4.2.30), the only enzyme known to synthesize ADP-ribose polymers from NAD+, is activated in response to DNA strand breaks and functions in the maintenance of genomic integrity.	NAD	111-115	poly (ADP-ribose) polymerase family, member 1	Mus musculus	0-27
9804757-1	1998	Poly(ADP-ribose) polymerase (PARP) (EC 2.4.2.30), the only enzyme known to synthesize ADP-ribose polymers from NAD+, is activated in response to DNA strand breaks and functions in the maintenance of genomic integrity.	NAD	111-115	poly (ADP-ribose) polymerase family, member 1	Mus musculus	29-33
27756843-7	2016	Molecular dynamics simulations suggested that Zn2+ loss due to Sirt1 S-nitrosation results in repositioning of the tetrathiolate subdomain away from the rest of the catalytic domain, thereby disrupting the NAD+ and acetyl-lysine-binding sites.	NAD	206-210	sirtuin 1	Homo sapiens	63-68
27372904-8	2016	These results suggest that VILIP-3, hippocalcin, and neurocalcin-delta provide a Ca2+-dependent modulation to the NADH-dependent microsomal electron transport.	NAD	114-118	hippocalcin	Homo sapiens	36-47
27613156-3	2016	Sirt1, an NAD+-dependent enzyme, is known to play an important protective role through deacetylation of many substrates involved in oxidative phosphorylation and reactive oxygen species generation.	NAD	10-14	sirtuin 1	Homo sapiens	0-5
9832086-3	1998	Following the activation of nonesterified fatty acids (NEFA) by acylCoA synthetase, the current assay utilizes UDP-glucose pyrophosphorylase to link inorganic pyrophosphate to the production of NADH through the reactions catalyzed by phosphoglucomutase and glucose-6-phosphate 1-dehydrogenase.	NAD	194-198	glucose-6-phosphate dehydrogenase	Homo sapiens	257-292
9633603-1	1998	The NAD(+)-dependent isocitrate dehydrogenase of Saccharomyces cerevisiae is an octamer composed of four Idh1p subunits and four Idh2p subunits.	NAD	4-8	isocitrate dehydrogenase (NAD(+)) IDH2	Saccharomyces cerevisiae S288C	129-134
27591175-2	2016	Sirtuins (SIRT1-7) are a family of nicotine adenine dinucleotide (NAD+)-dependent enzymes that catalyze post-translational modifications of proteins.	NAD	66-70	sirtuin 1	Homo sapiens	10-17
27694803-2	2016	Here, using a proteomic approach, we identified Saccharomyces cerevisiae cytochrome b5 reductase (Cbr1) as a NADH-dependent reductase for Dph3.	NAD	109-113	diphthamide biosynthesis 3	Homo sapiens	138-142
9576845-2	1998	The dominant-negative mutant hRac1(T17N) inhibits the NADH-stimulated production of ROS in HepG2 cells, whereas the constitutively activated hRac1(G12V) leads to an increase in intracellular ROS concentration.	NAD	54-58	Rac family small GTPase 1	Homo sapiens	29-34
27694803-3	2016	The NADH- and Cbr1-dependent reduction of Dph3 may provide a regulatory linkage between cellular metabolic state and protein translation.	NAD	4-8	diphthamide biosynthesis 3	Homo sapiens	42-46
27655688-5	2016	Here, we show that both classical histone deacetylase HDAC1 and NAD+-dependent deacetylase SIRT1 regulate acetylation level of APE1 and acetylation of APE1 enhances its AP-endonuclease activity both in vitro and in cells.	NAD	64-67	sirtuin 1	Homo sapiens	91-96
10375745-3	1998	The activities of GAPDH, PGK, and PK of the worms were determined by measuring the formation of NADH or consumption of NAD.	NAD	96-100	glyceraldehyde-3-phosphate dehydrogenase	Mus musculus	18-23
10375745-3	1998	The activities of GAPDH, PGK, and PK of the worms were determined by measuring the formation of NADH or consumption of NAD.	NAD	96-99	glyceraldehyde-3-phosphate dehydrogenase	Mus musculus	18-23
27846305-7	2016	We unexpectedly uncover intermediate "partial" yet stable states lying between the tip and stalk cell fates, and identify that internal cellular factors, such as NAD-dependent deacetylase sirtuin-1 (Sirt1) and Lunatic fringe 1 (Lfng1), can specifically determine the length of time a cell spends in these newly identified partial tip/stalk states.	NAD	162-165	sirtuin 1	Homo sapiens	188-197
27846305-7	2016	We unexpectedly uncover intermediate "partial" yet stable states lying between the tip and stalk cell fates, and identify that internal cellular factors, such as NAD-dependent deacetylase sirtuin-1 (Sirt1) and Lunatic fringe 1 (Lfng1), can specifically determine the length of time a cell spends in these newly identified partial tip/stalk states.	NAD	162-165	sirtuin 1	Homo sapiens	199-204
27592202-6	2016	Regulation of the SIRT/NAD system was associated with early (SIRT4, SIRT7, NAPRT1 and NMNAT2) and late phases (NMNAT3, NMRK2, ABCA1 and CD38) of glucose intolerance.	NAD	23-26	sirtuin 7	Mus musculus	68-73
27592202-6	2016	Regulation of the SIRT/NAD system was associated with early (SIRT4, SIRT7, NAPRT1 and NMNAT2) and late phases (NMNAT3, NMRK2, ABCA1 and CD38) of glucose intolerance.	NAD	23-26	nicotinate phosphoribosyltransferase	Mus musculus	75-81
27592202-6	2016	Regulation of the SIRT/NAD system was associated with early (SIRT4, SIRT7, NAPRT1 and NMNAT2) and late phases (NMNAT3, NMRK2, ABCA1 and CD38) of glucose intolerance.	NAD	23-26	nicotinamide nucleotide adenylyltransferase 3	Mus musculus	111-117
27592202-6	2016	Regulation of the SIRT/NAD system was associated with early (SIRT4, SIRT7, NAPRT1 and NMNAT2) and late phases (NMNAT3, NMRK2, ABCA1 and CD38) of glucose intolerance.	NAD	23-26	ATP-binding cassette, sub-family A (ABC1), member 1	Mus musculus	126-131
9531510-4	1998	The isolated enzyme has, as well, several characteristics that are unique to alcohol dehydrogenase (ADH) class III isoenzyme: it is capable of catalysing the NAD+-dependent oxidations of octanol (insensitive to inhibition by 4-methylpyrazole), methylcrotyl alcohol (stimulated by added pentanoate) and 12-hydroxydodecanoic acid, and also the NADH/NADPH-dependent reduction of octanal.	NAD	158-162	alcohol dehydrogenase 5 (class III), chi polypeptide	Rattus norvegicus	100-103
27592202-6	2016	Regulation of the SIRT/NAD system was associated with early (SIRT4, SIRT7, NAPRT1 and NMNAT2) and late phases (NMNAT3, NMRK2, ABCA1 and CD38) of glucose intolerance.	NAD	23-26	CD38 antigen	Mus musculus	136-140
9531510-4	1998	The isolated enzyme has, as well, several characteristics that are unique to alcohol dehydrogenase (ADH) class III isoenzyme: it is capable of catalysing the NAD+-dependent oxidations of octanol (insensitive to inhibition by 4-methylpyrazole), methylcrotyl alcohol (stimulated by added pentanoate) and 12-hydroxydodecanoic acid, and also the NADH/NADPH-dependent reduction of octanal.	NAD	342-346	alcohol dehydrogenase 5 (class III), chi polypeptide	Rattus norvegicus	100-103
27783719-2	2016	The nicotinamide/nicotinate mononucleotide adenylyltransferase (NMNAT, EC 2.7.7.1/18) enzyme catalyses the key step in the biosynthesis of NAD+.	NAD	139-143	nicotinamide nucleotide adenylyltransferase 1	Mus musculus	64-69
9525901-4	1998	Here we demonstrate that ectocellular expression of human CD38 in CD38(-) HeLa and 3T3 cells results in intracellular CD38 substrate (NAD+ + NADH) consumption and product (cADPR) accumulation.	NAD	134-138	CD38 antigen	Mus musculus	66-70
9525901-4	1998	Here we demonstrate that ectocellular expression of human CD38 in CD38(-) HeLa and 3T3 cells results in intracellular CD38 substrate (NAD+ + NADH) consumption and product (cADPR) accumulation.	NAD	141-145	CD38 antigen	Mus musculus	66-70
27425894-3	2016	Nicotinamide mononucleotide (NMN) is utilized by the NAD(+) salvage pathway enzyme, nicotinamide adenylyltransferase (Nmnat) to generate NAD(+).	NAD	53-59	nicotinamide nucleotide adenylyltransferase 1	Mus musculus	118-123
9511473-3	1998	The enzymes salicylate hydroxylase and tyrosinase were coimmobilized first in a carbon paste electrode for the sensitive detection of NADH.	NAD	134-138	tyrosinase	Homo sapiens	39-49
9511473-7	1998	Prior to adding PADH, the salicylate hydroxylase-tyrosinase carbon paste electrode was characterized in terms of its sensitivity to NADH, pH dependence, buffer composition, interferences, and stability.	NAD	132-136	tyrosinase	Homo sapiens	49-59
27425894-3	2016	Nicotinamide mononucleotide (NMN) is utilized by the NAD(+) salvage pathway enzyme, nicotinamide adenylyltransferase (Nmnat) to generate NAD(+).	NAD	137-143	nicotinamide nucleotide adenylyltransferase 1	Mus musculus	118-123
27783615-3	2016	Furthermore, the role of NAD, which is affected by hydrogen partial pressure (PH2), has often not been considered.	NAD	25-28	polyhomeotic homolog 2	Homo sapiens	78-81
27783615-4	2016	The aim of this study was to quantify the control of PH2 on reaction rates of specific fermentation pathways, methanogenesis and NADH oxidation in rumen microbes.	NAD	129-133	polyhomeotic homolog 2	Homo sapiens	53-56
27783615-7	2016	For NADH oxidation without ferredoxin oxidation, increasing PH2 within the rumen physiological range decreased FT from unity to zero for different NAD+ to NADH ratios and pH of 6.2 and 7.0, which indicates thermodynamic control of PH2.	NAD	4-8	polyhomeotic homolog 2	Homo sapiens	60-63
9453543-9	1998	Therefore, we suggest that PARP contributes to neuronal injury as an early event, probably by lethal NAD depletion, without any requirement for proteolytic cleavage.	NAD	101-104	poly (ADP-ribose) polymerase family, member 1	Mus musculus	27-31
27783615-7	2016	For NADH oxidation without ferredoxin oxidation, increasing PH2 within the rumen physiological range decreased FT from unity to zero for different NAD+ to NADH ratios and pH of 6.2 and 7.0, which indicates thermodynamic control of PH2.	NAD	147-151	polyhomeotic homolog 2	Homo sapiens	60-63
27732856-4	2016	Maintenance of the naive state requires the NAD-dependent deacetylase, SirT1, which deacetylates Oct4.	NAD	44-47	sirtuin 1	Homo sapiens	71-76
27423420-7	2016	Mechanistically, we identified NMNAT3 (nicotinamide mononucleotide adenylyltransferase 3), the rate-limiting enzyme for mitochondrial NAD biosynthesis, as a new target and binding partner of SIRT3.	NAD	134-137	nicotinamide nucleotide adenylyltransferase 3	Mus musculus	31-37
27423420-7	2016	Mechanistically, we identified NMNAT3 (nicotinamide mononucleotide adenylyltransferase 3), the rate-limiting enzyme for mitochondrial NAD biosynthesis, as a new target and binding partner of SIRT3.	NAD	134-137	nicotinamide nucleotide adenylyltransferase 3	Mus musculus	39-88
9516661-5	1998	Alcohol dehydrogenase catalyses the oxidation of ethanol with formation of NADH, which is monitored using NADH:FMN oxidoreductase and bacterial luciferase.	NAD	75-79	aldo-keto reductase family 1 member A1	Homo sapiens	0-21
27747304-0	2016	Superoxide anion scavenging activity of alk(en)yl phenol compounds by using PMS-NADH system.	NAD	80-84	ALK receptor tyrosine kinase	Homo sapiens	40-43
9516661-5	1998	Alcohol dehydrogenase catalyses the oxidation of ethanol with formation of NADH, which is monitored using NADH:FMN oxidoreductase and bacterial luciferase.	NAD	106-110	aldo-keto reductase family 1 member A1	Homo sapiens	0-21
9407098-3	1997	Recombinant CRAD uses NAD+ as its preferred cofactor and exhibits cooperative kinetics for cis-retinoids, but Michaelis-Menten kinetics for 3alpha-hydroxysterols.	NAD	22-26	retinol dehydrogenase 16	Mus musculus	12-16
9353290-0	1997	The oxidative half-reaction of xanthine dehydrogenase with NAD; reaction kinetics and steady-state mechanism.	NAD	59-62	xanthine dehydrogenase	Bos taurus	31-53
9353290-1	1997	The reaction between reduced xanthine dehydrogenase (XDH) from bovine milk and NAD has been studied in detail.	NAD	79-82	xanthine dehydrogenase	Bos taurus	29-51
9353290-1	1997	The reaction between reduced xanthine dehydrogenase (XDH) from bovine milk and NAD has been studied in detail.	NAD	79-82	xanthine dehydrogenase	Bos taurus	53-56
9353290-2	1997	An understanding of this reaction is necessary for a complete description of XDH turnover with its presumed natural electron acceptor and to address the preference of XDH for NAD over oxygen as a substrate.	NAD	175-178	xanthine dehydrogenase	Bos taurus	77-80
9353290-2	1997	An understanding of this reaction is necessary for a complete description of XDH turnover with its presumed natural electron acceptor and to address the preference of XDH for NAD over oxygen as a substrate.	NAD	175-178	xanthine dehydrogenase	Bos taurus	167-170
9353290-3	1997	The reaction between pre-reduced XDH and NAD was studied by stopped-flow spectrophotometry.	NAD	41-44	xanthine dehydrogenase	Bos taurus	33-36
9378973-0	1997	Human CD38, a leukocyte receptor and ectoenzyme, is a member of a novel eukaryotic gene family of nicotinamide adenine dinucleotide+-converting enzymes: extensive structural homology with the genes for murine bone marrow stromal cell antigen 1 and aplysian ADP-ribosyl cyclase.	NAD	98-131	CD38 antigen	Mus musculus	6-10
9321518-5	1997	The involvement of cytochrome b5 in the formation of N-acetyl-p-benzoquinone imine (NAPQI) was implicated through a synergistic effect of NADH on the NADPH-supported reaction.	NAD	138-142	cytochrome b5 type A	Rattus norvegicus	19-32
9334719-3	1997	Excessive activation of PARP can deplete NAD and ATP, which is consumed in regeneration of NAD, leading to cell death by energy depletion.	NAD	41-44	poly (ADP-ribose) polymerase family, member 1	Mus musculus	24-28
9334719-3	1997	Excessive activation of PARP can deplete NAD and ATP, which is consumed in regeneration of NAD, leading to cell death by energy depletion.	NAD	91-94	poly (ADP-ribose) polymerase family, member 1	Mus musculus	24-28
9268311-5	1997	In contrast, alanine replacement of the homologous Asp-286 and Ile-287 residues in IDH2 does not alter the allosteric response to AMP, but produces a 160-fold reduction in Vmax due to a 70-fold increase in the S0.5 value for NAD+.	NAD	225-229	isocitrate dehydrogenase (NAD(+)) IDH2	Saccharomyces cerevisiae S288C	83-87
9244391-0	1997	Mutations in the IDH2 gene encoding the catalytic subunit of the yeast NAD+-dependent isocitrate dehydrogenase can be suppressed by mutations in the CIT1 gene encoding citrate synthase and other genes of oxidative metabolism.	NAD	71-74	isocitrate dehydrogenase (NAD(+)) IDH2	Saccharomyces cerevisiae S288C	17-21
9202003-6	1997	(ii) When NADH or succinate was added to SMP inhibited at complex III by antimycin and energized by ATP, the bis-heme cytochrome b was reduced only partially.	NAD	10-14	cytochrome b	Bos taurus	118-130
9154936-14	1997	With the cytochrome b-containing liposomes, the Km values (O2- formation) for NADPH and NADH are 27.2 microM and 810 microM, and for INT reductase the Km values are 27.5 microM and 1017 microM, respectively.	NAD	88-92	cytochrome b	Bos taurus	9-21
26725653-3	2016	In this study, we hypothesize that it is not NAD+ as a cofactor in redox reactions and coenzyme in metabolic processes that has the ultimate role in aging, but rather the role of NAD+ in cellular signaling when used as substrate for sirtuins (SIRT1-7 in mammals) and PARPs [Poly(ADP-ribose) polymerases].	NAD	179-183	sirtuin 1	Homo sapiens	243-248
27790277-0	2016	Increased Cellular NAD+ Level through NQO1 Enzymatic Action Has Protective Effects on Bleomycin-Induced Lung Fibrosis in Mice.	NAD	19-23	NAD(P)H dehydrogenase, quinone 1	Mus musculus	38-42
27790277-4	2016	NADH:quinone oxidoreductase 1 (NQO1) is a homodimeric enzyme that catalyzes the oxidation of NADH to NAD+ by various quinones and thereby elevates the intracellular NAD+ levels.	NAD	0-4	NAD(P)H dehydrogenase, quinone 1	Mus musculus	31-35
27790277-4	2016	NADH:quinone oxidoreductase 1 (NQO1) is a homodimeric enzyme that catalyzes the oxidation of NADH to NAD+ by various quinones and thereby elevates the intracellular NAD+ levels.	NAD	101-105	NAD(P)H dehydrogenase, quinone 1	Mus musculus	0-29
27790277-4	2016	NADH:quinone oxidoreductase 1 (NQO1) is a homodimeric enzyme that catalyzes the oxidation of NADH to NAD+ by various quinones and thereby elevates the intracellular NAD+ levels.	NAD	101-105	NAD(P)H dehydrogenase, quinone 1	Mus musculus	31-35
27790277-4	2016	NADH:quinone oxidoreductase 1 (NQO1) is a homodimeric enzyme that catalyzes the oxidation of NADH to NAD+ by various quinones and thereby elevates the intracellular NAD+ levels.	NAD	165-169	NAD(P)H dehydrogenase, quinone 1	Mus musculus	0-29
27790277-4	2016	NADH:quinone oxidoreductase 1 (NQO1) is a homodimeric enzyme that catalyzes the oxidation of NADH to NAD+ by various quinones and thereby elevates the intracellular NAD+ levels.	NAD	165-169	NAD(P)H dehydrogenase, quinone 1	Mus musculus	31-35
27790277-12	2016	CONCLUSION: Our results suggest that beta-lapachone can protect against bleomycin-induced lung inflammation and fibrosis in mice and TGF-beta1-induced EMT in vitro, by elevating the NAD+/NADH ratio through NQO1 activation.	NAD	182-186	NAD(P)H dehydrogenase, quinone 1	Mus musculus	206-210
27477207-2	2016	In this study we used crystal structure of the MTB l-AlaDH bound with cofactor NAD(+) as a structural framework for virtual screening of our in-house database to identified new classes of l-AlaDH inhibitor.	NAD	79-85	aminolevulinate dehydratase	Homo sapiens	53-58
27477207-2	2016	In this study we used crystal structure of the MTB l-AlaDH bound with cofactor NAD(+) as a structural framework for virtual screening of our in-house database to identified new classes of l-AlaDH inhibitor.	NAD	79-85	aminolevulinate dehydratase	Homo sapiens	190-195
27611801-3	2016	Similar to LW6, compound 7 inhibited MDH2 activity in a competitive fashion, thereby reducing NADH level.	NAD	94-98	malate dehydrogenase 2	Homo sapiens	37-41
27337995-3	2016	We have observed that p49/STRAP alters the intracellular NAD/NADH ratio and induces protein deacetylation.	NAD	57-60	serum response factor binding protein 1	Homo sapiens	22-25
27337995-3	2016	We have observed that p49/STRAP alters the intracellular NAD/NADH ratio and induces protein deacetylation.	NAD	61-65	serum response factor binding protein 1	Homo sapiens	22-25
27498548-1	2016	BACKGROUND: SIRT7 is one of the histone deacetylases and is NAD-dependent.	NAD	60-63	sirtuin 7	Homo sapiens	12-17
27390344-6	2016	Furthermore, NAPRT1 downregulation, which we show occurs in all RCC cell lines tested, makes this tumor highly dependent on NAMPT for its NAD requirements, such that inhibition of NAMPT by KPT-9274 leads to decreased survival of these rapidly proliferating cells.	NAD	138-141	nicotinate phosphoribosyltransferase	Homo sapiens	13-19
27648125-7	2016	NAD(+) administration can also significantly attenuate I/R-induced decreases in SOD activity and SOD-2 protein levels in the hearts.	NAD	0-6	superoxide dismutase 2	Rattus norvegicus	80-83
27648125-7	2016	NAD(+) administration can also significantly attenuate I/R-induced decreases in SOD activity and SOD-2 protein levels in the hearts.	NAD	0-6	superoxide dismutase 2	Rattus norvegicus	97-102
27060251-3	2016	In response to physiological glutamate signals, cytosolic Ca(2+) activates respiration by stimulation of the NADH malate-aspartate shuttle through Ca(2+)-binding to the mitochondrial aspartate/glutamate carrier (Aralar/AGC1/Slc25a12), and by stimulation of adenine nucleotide uptake through Ca(2+) binding to the mitochondrial ATP-Mg/Pi carrier (SCaMC-3/Slc25a23).	NAD	109-113	solute carrier family 25 (mitochondrial carrier, Aralar), member 12	Mus musculus	224-232
27253997-4	2016	In OA cartilage, the levels of both Bmal1 and NAD(+) decreased significantly, which resulted in the inhibition of nicotinamide phosphoribosyltransferase activity and Sirt1 expression.	NAD	46-52	sirtuin 1	Homo sapiens	166-171
27253997-5	2016	Furthermore, the knockdown of Bmal1 was sufficient to decrease the level of NAD(+) and aggravate OA-like gene expression changes under the stimulation of IL-1beta.	NAD	76-82	aryl hydrocarbon receptor nuclear translocator like	Homo sapiens	30-35
26568303-7	2016	Finally, we showed that NAMPT increased the pool of NAD+ that could be converted to NADPH through the pentose phosphate pathway and inhibited the depletion of reduced glutathione under glucose deprivation.	NAD	52-56	2,4-dienoyl-CoA reductase 1	Homo sapiens	84-89
27207593-1	2016	The nicotinamide nucleotide adenylyltransferase 1 (NMNAT1) enzyme is essential for regenerating the nuclear pool of NAD(+) in all nucleated cells in the body, and mounting evidence also suggests that it has a separate role in neuroprotection.	NAD	116-122	nicotinamide nucleotide adenylyltransferase 1	Mus musculus	4-49
27207593-1	2016	The nicotinamide nucleotide adenylyltransferase 1 (NMNAT1) enzyme is essential for regenerating the nuclear pool of NAD(+) in all nucleated cells in the body, and mounting evidence also suggests that it has a separate role in neuroprotection.	NAD	116-122	nicotinamide nucleotide adenylyltransferase 1	Mus musculus	51-57
29512967-0	2016	[Physicochemical and catalytic properties of NAD+- dependent malate dehydrogenase isoforms from maize mesophyll0.	NAD	45-48	LOC100856934	Zea mays	61-81
27367673-0	2016	The NAD-Dependent Deacetylase Sirtuin-1 Regulates the Expression of Osteogenic Transcriptional Activator Runt-Related Transcription Factor 2 (Runx2) and Production of Matrix Metalloproteinase (MMP)-13 in Chondrocytes in Osteoarthritis.	NAD	4-7	sirtuin 1	Homo sapiens	30-39
27124741-1	2016	Silent information regulator type-1 (SIRT1) is the best-studied member of the Sirtuin (Sir2) family of nicotinamide dinucleotide (NAD)-dependent class III histone deacetylases (HDACs).	NAD	103-128	sirtuin 1	Homo sapiens	0-35
27124741-1	2016	Silent information regulator type-1 (SIRT1) is the best-studied member of the Sirtuin (Sir2) family of nicotinamide dinucleotide (NAD)-dependent class III histone deacetylases (HDACs).	NAD	103-128	sirtuin 1	Homo sapiens	37-42
27124741-1	2016	Silent information regulator type-1 (SIRT1) is the best-studied member of the Sirtuin (Sir2) family of nicotinamide dinucleotide (NAD)-dependent class III histone deacetylases (HDACs).	NAD	103-128	sirtuin 1	Homo sapiens	87-91
27124741-1	2016	Silent information regulator type-1 (SIRT1) is the best-studied member of the Sirtuin (Sir2) family of nicotinamide dinucleotide (NAD)-dependent class III histone deacetylases (HDACs).	NAD	130-133	sirtuin 1	Homo sapiens	0-35
27124741-1	2016	Silent information regulator type-1 (SIRT1) is the best-studied member of the Sirtuin (Sir2) family of nicotinamide dinucleotide (NAD)-dependent class III histone deacetylases (HDACs).	NAD	130-133	sirtuin 1	Homo sapiens	37-42
27124741-1	2016	Silent information regulator type-1 (SIRT1) is the best-studied member of the Sirtuin (Sir2) family of nicotinamide dinucleotide (NAD)-dependent class III histone deacetylases (HDACs).	NAD	130-133	sirtuin 1	Homo sapiens	87-91
26657715-5	2016	Sirtuin 1 (SIRT1), the mammalian ortholog of yeast longevity regulator Sir2, is a nicotinamide adenine dinucleotide (NAD)-dependent protein deacetylase that elicits a variety of vasoprotective functions.	NAD	82-115	sirtuin 1	Homo sapiens	0-9
26657715-5	2016	Sirtuin 1 (SIRT1), the mammalian ortholog of yeast longevity regulator Sir2, is a nicotinamide adenine dinucleotide (NAD)-dependent protein deacetylase that elicits a variety of vasoprotective functions.	NAD	82-115	sirtuin 1	Homo sapiens	11-16
26657715-5	2016	Sirtuin 1 (SIRT1), the mammalian ortholog of yeast longevity regulator Sir2, is a nicotinamide adenine dinucleotide (NAD)-dependent protein deacetylase that elicits a variety of vasoprotective functions.	NAD	117-120	sirtuin 1	Homo sapiens	0-9
26657715-5	2016	Sirtuin 1 (SIRT1), the mammalian ortholog of yeast longevity regulator Sir2, is a nicotinamide adenine dinucleotide (NAD)-dependent protein deacetylase that elicits a variety of vasoprotective functions.	NAD	117-120	sirtuin 1	Homo sapiens	11-16
27173464-12	2016	In addition, enhancing NAD pool significantly inhibited PARP and caspase-3 activates in db/db mice BM.	NAD	23-26	poly (ADP-ribose) polymerase family, member 1	Mus musculus	56-60
27173464-12	2016	In addition, enhancing NAD pool significantly inhibited PARP and caspase-3 activates in db/db mice BM.	NAD	23-26	caspase 3	Mus musculus	65-74
27002158-4	2016	Three distinct families of enzymes consume NAD(+) as substrate: poly(ADP-ribose) polymerases, ADP-ribosyl cyclases (CD38 and CD157), and sirtuins (SIRT1-7).	NAD	43-49	sirtuin 1	Homo sapiens	147-154
26704979-3	2016	Here we showed that the human Dicer protein interacts with SIRT7, an NAD(+)-dependent H3K18Ac (acetylated lysine 18 of histone H3) deacetylase, and holds a proportion of SIRT7 in the cytoplasm.	NAD	69-75	sirtuin 7	Homo sapiens	59-64
26704979-3	2016	Here we showed that the human Dicer protein interacts with SIRT7, an NAD(+)-dependent H3K18Ac (acetylated lysine 18 of histone H3) deacetylase, and holds a proportion of SIRT7 in the cytoplasm.	NAD	69-75	sirtuin 7	Homo sapiens	170-175
26926998-6	2016	maculicola ES4326, and transgenic expression of the coding region of ELO3/AtELP3 in elo3/Atelp3 restores NAD(+) responsiveness to the mutant plants, demonstrating that ELO3/AtELP3 is required for exogenous NAD(+)-induced defense responses.	NAD	206-212	radical SAM domain-containing protein / GCN5-related N-acetyltransferase (GNAT) family protein	Arabidopsis thaliana	89-95
26926998-7	2016	Furthermore, mutations in genes encoding the other five Arabidopsis Elongator subunits (ELO2/AtELP1, AtELP2, ELO1/AtELP4, AtELP5, and AtELP6) also compromise exogenous NAD(+)-induced PR gene expression and resistance to P. syringae pv.	NAD	168-174	Paxneb protein-like protein	Arabidopsis thaliana	109-113
27043630-1	2016	Clostridium botulinum exoenzyme C3 is the prototype of C3-like ADP-ribosyltransferases that modify the GTPases RhoA, B, and C. C3 catalyzes the transfer of an ADP-ribose moiety from the co-substrate nicotinamide adenine dinucleotide (NAD) to asparagine-41 of Rho-GTPases.	NAD	199-232	transforming protein RhoA	Cricetulus griseus	111-115
27043630-1	2016	Clostridium botulinum exoenzyme C3 is the prototype of C3-like ADP-ribosyltransferases that modify the GTPases RhoA, B, and C. C3 catalyzes the transfer of an ADP-ribose moiety from the co-substrate nicotinamide adenine dinucleotide (NAD) to asparagine-41 of Rho-GTPases.	NAD	234-237	transforming protein RhoA	Cricetulus griseus	111-115
30088710-1	2016	Silent information regulator 1(SIRT1),an NAD+dependent class-III histone deacetylase,is implicated in diverse cellular processes.	NAD	41-44	sirtuin 1	Homo sapiens	31-36
26582960-6	2016	Stx2a predominantly altered the nicotinamide adenine dinucleotide (NAD) cofactor pathway and the inflammation-modulating eicosanoid pathway, which are associated with lipid metabolism.	NAD	32-65	syntaxin 2	Homo sapiens	0-5
26582960-6	2016	Stx2a predominantly altered the nicotinamide adenine dinucleotide (NAD) cofactor pathway and the inflammation-modulating eicosanoid pathway, which are associated with lipid metabolism.	NAD	67-70	syntaxin 2	Homo sapiens	0-5
26582960-7	2016	In HRGEC, Stx2a strongly diminished NAD derivatives, leading to depletion of the energy substrate acetyl coenzyme A and the antioxidant glutathione.	NAD	36-39	syntaxin 2	Homo sapiens	10-15
26959057-1	2016	Sirt1 is a NAD+-dependent protein-modifying enzyme involved in regulating gene expression, DNA damage repair, metabolism and survival, as well as acts as an important subcellular target of resveratrol.	NAD	11-15	sirtuin 1	Homo sapiens	0-5
26681113-4	2016	The origin of NF-kappaB activation was related to the age-dependent Bmal1/Clock/RORalpha/Rev-Erbalpha loop disruption, which lowers NAD(+) levels, reducing the SIRT1 deacetylase ability to inactivate NF-kappaB.	NAD	132-138	nuclear receptor subfamily 1, group D, member 1	Mus musculus	89-101
26928119-0	2016	NAD(+) regulates Treg cell fate and promotes allograft survival via a systemic IL-10 production that is CD4(+) CD25(+) Foxp3(+) T cells independent.	NAD	0-6	interleukin 10	Homo sapiens	79-84
26928119-6	2016	Despite the reduced number of Tregs, known to promote homeostasis, and an increased number of pro-inflammatory Th17 cells, NAD(+) was able to promote an impressive allograft survival through a robust systemic IL-10 production that was CD4(+) CD25(+) Foxp3(+) independent.	NAD	123-129	interleukin 10	Homo sapiens	209-214
26879378-6	2016	RESULTS: A series of active whole-cell biocatalysts were constructed by over-expressing the (S)-selective omega-transaminase (VAMT) from Capsicum chinense together with the NADH-dependent (S)-selective alcohol dehydrogenase (SADH) originating from Rhodococcus erythropolis in strains with or without deletion of glycerol-3-phosphate dehydrogenases 1 and 2 (GPD1 and GPD2).	NAD	173-177	glycerol-3-phosphate dehydrogenase (NAD(+)) GPD1	Saccharomyces cerevisiae S288C	357-361
26756334-0	2016	Nmnat3 Is Dispensable in Mitochondrial NAD Level Maintenance In Vivo.	NAD	39-42	nicotinamide nucleotide adenylyltransferase 3	Mus musculus	0-6
26756334-4	2016	It has been proposed that NAD synthesis enzyme, Nmnat3, was localized in mitochondria, but its physiological relevance to the metabolism in mitochondria was not fully elucidated.	NAD	26-29	nicotinamide nucleotide adenylyltransferase 3	Mus musculus	48-54
26756334-5	2016	Previously, we have reported that murine Nmnat3 protein was strongly expressed in the cytoplasm of mature erythrocytes, in which mitochondria were absent, and Nmnat3-deficient mice (Nmnat3-KO mice) exhibited splenomegaly and hemolytic anemia due to reduced NAD levels in mature erythrocytes.	NAD	257-260	nicotinamide nucleotide adenylyltransferase 3	Mus musculus	41-47
26756334-6	2016	These results challenged the role of Nmnat3 in mitochondrial NAD synthesis.	NAD	61-64	nicotinamide nucleotide adenylyltransferase 3	Mus musculus	37-43
27110038-7	2016	In the presence of either of the reductase cofactors tested, NADPH or NADH, cytochrome b5 stimulated CYP1A1-mediated formation of both BaP-DNA adducts.	NAD	70-74	cytochrome b5 type A	Rattus norvegicus	76-89
27110038-8	2016	The results demonstrate that NADH can act as a sole electron donor for both the first and the second reduction of CYP1A1 during its reaction cycle catalyzing oxidation of BaP, and suggest that the NADH:cytochrome b5 reductase as the NADH-dependent reductase might substitute POR in this enzymatic system.	NAD	29-33	cytochrome b5 type A	Rattus norvegicus	202-215
27110038-8	2016	The results demonstrate that NADH can act as a sole electron donor for both the first and the second reduction of CYP1A1 during its reaction cycle catalyzing oxidation of BaP, and suggest that the NADH:cytochrome b5 reductase as the NADH-dependent reductase might substitute POR in this enzymatic system.	NAD	197-201	cytochrome b5 type A	Rattus norvegicus	202-215
26678339-4	2015	Mutant IDH1 lowered NAD+ levels by downregulating the NAD+ salvage pathway enzyme nicotinate phosphoribosyltransferase (Naprt1), sensitizing to NAD+ depletion via concomitant nicotinamide phosphoribosyltransferase (NAMPT) inhibition.	NAD	20-24	nicotinate phosphoribosyltransferase	Homo sapiens	82-118
26678339-4	2015	Mutant IDH1 lowered NAD+ levels by downregulating the NAD+ salvage pathway enzyme nicotinate phosphoribosyltransferase (Naprt1), sensitizing to NAD+ depletion via concomitant nicotinamide phosphoribosyltransferase (NAMPT) inhibition.	NAD	20-24	nicotinate phosphoribosyltransferase	Homo sapiens	120-126
26678339-4	2015	Mutant IDH1 lowered NAD+ levels by downregulating the NAD+ salvage pathway enzyme nicotinate phosphoribosyltransferase (Naprt1), sensitizing to NAD+ depletion via concomitant nicotinamide phosphoribosyltransferase (NAMPT) inhibition.	NAD	54-58	nicotinate phosphoribosyltransferase	Homo sapiens	82-118
26678339-4	2015	Mutant IDH1 lowered NAD+ levels by downregulating the NAD+ salvage pathway enzyme nicotinate phosphoribosyltransferase (Naprt1), sensitizing to NAD+ depletion via concomitant nicotinamide phosphoribosyltransferase (NAMPT) inhibition.	NAD	54-58	nicotinate phosphoribosyltransferase	Homo sapiens	120-126
26678339-4	2015	Mutant IDH1 lowered NAD+ levels by downregulating the NAD+ salvage pathway enzyme nicotinate phosphoribosyltransferase (Naprt1), sensitizing to NAD+ depletion via concomitant nicotinamide phosphoribosyltransferase (NAMPT) inhibition.	NAD	54-58	nicotinate phosphoribosyltransferase	Homo sapiens	82-118
26678339-4	2015	Mutant IDH1 lowered NAD+ levels by downregulating the NAD+ salvage pathway enzyme nicotinate phosphoribosyltransferase (Naprt1), sensitizing to NAD+ depletion via concomitant nicotinamide phosphoribosyltransferase (NAMPT) inhibition.	NAD	54-58	nicotinate phosphoribosyltransferase	Homo sapiens	120-126
26265307-2	2015	D-Lactate dehydrogenase (D-LDH) was utilized to catalyze D-lactate and NAD(+) to pyruvate and NADH, respectively.	NAD	94-98	lactate dehydrogenase D	Homo sapiens	0-23
26265307-2	2015	D-Lactate dehydrogenase (D-LDH) was utilized to catalyze D-lactate and NAD(+) to pyruvate and NADH, respectively.	NAD	94-98	lactate dehydrogenase D	Homo sapiens	25-30
26498527-4	2015	In the present study, we demonstrated that the hyper-activation of poly(ADP-ribose) polymerase-1 (PARP-1) is closely associated with the depletion of NAD(+) in the small intestine after cisplatin treatment, which results in downregulation of sirtuin1 (SIRT1) activity.	NAD	150-156	sirtuin 1	Homo sapiens	242-250
26498527-4	2015	In the present study, we demonstrated that the hyper-activation of poly(ADP-ribose) polymerase-1 (PARP-1) is closely associated with the depletion of NAD(+) in the small intestine after cisplatin treatment, which results in downregulation of sirtuin1 (SIRT1) activity.	NAD	150-156	sirtuin 1	Homo sapiens	252-257
26282612-7	2015	Also, the ERbeta activation by its agonist DPN changed the subcellular localization of p21, inducing an increase in the p21 nuclear expression, where it acts as a tumoral suppressor.	NAD	43-46	KRAS proto-oncogene, GTPase	Rattus norvegicus	87-90
26282612-7	2015	Also, the ERbeta activation by its agonist DPN changed the subcellular localization of p21, inducing an increase in the p21 nuclear expression, where it acts as a tumoral suppressor.	NAD	43-46	KRAS proto-oncogene, GTPase	Rattus norvegicus	120-123
26297909-1	2015	AIM: FK866 is an inhibitor of the NAD(+) synthesis rate-limiting enzyme nicotinamide phosphoribosyltransferase (NAMPT).	NAD	34-40	nicotinamide phosphoribosyltransferase	Rattus norvegicus	72-110
26297909-1	2015	AIM: FK866 is an inhibitor of the NAD(+) synthesis rate-limiting enzyme nicotinamide phosphoribosyltransferase (NAMPT).	NAD	34-40	nicotinamide phosphoribosyltransferase	Rattus norvegicus	112-117
26466337-11	2015	The higher NADH-dependent cytochrome c reductase activity together with the higher transcript levels of CBR.1 and CYB5 in the crtR- mutant as well as the lower NADH-dependent activity in CBS-cbr.1- strongly suggest that CBR.1-CYB5 via participates as an alternative electron donor pathway for P450 enzymes involved in ergosterol biosynthesis in X. dendrorhous.	NAD	11-15	solute carrier family 6 member 8	Homo sapiens	126-130
26466337-11	2015	The higher NADH-dependent cytochrome c reductase activity together with the higher transcript levels of CBR.1 and CYB5 in the crtR- mutant as well as the lower NADH-dependent activity in CBS-cbr.1- strongly suggest that CBR.1-CYB5 via participates as an alternative electron donor pathway for P450 enzymes involved in ergosterol biosynthesis in X. dendrorhous.	NAD	11-15	carbonyl reductase 1	Homo sapiens	191-194
26466337-11	2015	The higher NADH-dependent cytochrome c reductase activity together with the higher transcript levels of CBR.1 and CYB5 in the crtR- mutant as well as the lower NADH-dependent activity in CBS-cbr.1- strongly suggest that CBR.1-CYB5 via participates as an alternative electron donor pathway for P450 enzymes involved in ergosterol biosynthesis in X. dendrorhous.	NAD	11-15	carbonyl reductase 1	Homo sapiens	220-225
26466337-11	2015	The higher NADH-dependent cytochrome c reductase activity together with the higher transcript levels of CBR.1 and CYB5 in the crtR- mutant as well as the lower NADH-dependent activity in CBS-cbr.1- strongly suggest that CBR.1-CYB5 via participates as an alternative electron donor pathway for P450 enzymes involved in ergosterol biosynthesis in X. dendrorhous.	NAD	160-164	carbonyl reductase 1	Homo sapiens	191-194
26260980-1	2015	Aldehyde dehydrogenase 7A1 (ALDH7A1) is part of lysine catabolism and catalyzes the NAD(+)-dependent oxidation of alpha-aminoadipate semialdehyde to alpha-aminoadipate.	NAD	84-90	aldehyde dehydrogenase 7 family member A1	Homo sapiens	0-26
26260980-1	2015	Aldehyde dehydrogenase 7A1 (ALDH7A1) is part of lysine catabolism and catalyzes the NAD(+)-dependent oxidation of alpha-aminoadipate semialdehyde to alpha-aminoadipate.	NAD	84-90	aldehyde dehydrogenase 7 family member A1	Homo sapiens	28-35
26068950-3	2015	We identify the hydroxyprostaglandin dehydrogenase 15-(nicotinamide adenine dinucleotide) (HPGD/15-PGDH) tumor suppressor gene as a direct miR-620 target, which results in increased prostaglandin E2 (PGE2) levels.	NAD	55-88	carbonyl reductase 1	Homo sapiens	91-95
26224005-6	2015	In Dnd1 heterozygotes, lower oxygen availability was associated with metabolic differences, including lower levels of ATP and NADH in the left testis.	NAD	126-130	DND microRNA-mediated repression inhibitor 1	Mus musculus	3-7
26332964-5	2015	Specifically, the nicotinamide adenine dinucleotide (NAD)(+) -dependent deacetylases SIRT1 and SIRT6 have been linked to circadian control of gene expression.	NAD	18-51	sirtuin 1	Homo sapiens	85-90
26332964-5	2015	Specifically, the nicotinamide adenine dinucleotide (NAD)(+) -dependent deacetylases SIRT1 and SIRT6 have been linked to circadian control of gene expression.	NAD	53-56	sirtuin 1	Homo sapiens	85-90
26080614-3	2015	Conversely, overexpression of a nuclear poly (ADP-ribose) polymerase enzyme (PARP) after oxidative insult extremely brings about cellular injury due to excessive consumption of NAD and ATP.	NAD	177-180	poly (ADP-ribose) polymerase family, member 1	Mus musculus	77-81
26299580-1	2015	SIRT1 is one of seven mammalian homologs of Sir2 that catalyzes NAD(+)-dependent protein deacetylation.	NAD	64-70	sirtuin 1	Homo sapiens	0-5
26299580-1	2015	SIRT1 is one of seven mammalian homologs of Sir2 that catalyzes NAD(+)-dependent protein deacetylation.	NAD	64-70	sirtuin 1	Homo sapiens	44-48
26287487-6	2015	CD38, a multi-functional membrane receptor and enzyme, consumes NAD+ to generate products such as cyclic-ADP-ribose.	NAD	64-68	CD38 antigen	Mus musculus	0-4
26287487-7	2015	CD38 knockout mice show elevated tissue and blood NAD+ level.	NAD	50-54	CD38 antigen	Mus musculus	0-4
26287487-10	2015	These animal model results suggest that elevation of tissue NAD+ through genetic ablation of CD38 can profoundly alter energy homeostasis in animals that are maintained on a calorically-excessive Western diet.	NAD	60-64	CD38 antigen	Mus musculus	93-97
26009926-6	2015	With both immune fluorescence labeling and immunogold localization on electron microscopic thin sections aldolase and enolase were found apart from the cytoplasmic area particularly in the cross wall and at the septal cleft of dividing cells, whereas the non-excreted Ndh2, a soluble NADH:quinone oxidoreductase, is only seen attached to the inner side of the cytoplasmic membrane.	NAD	284-288	AT695_RS13760	Staphylococcus aureus	118-125
26219988-3	2015	The NAD(+)-dependent deacetylase Sirt1 has been reported to play positive roles in the regulation of cellular homeostasis in response to various stresses.	NAD	4-10	sirtuin 1	Homo sapiens	33-38
25893674-2	2015	The nicotinamide adenine dinucleotide (NAD) glycohydrolase CD38, which is expressed by neurons, astrocytes, and microglial cells, regulates inflammatory and repair processes in the brain and other tissues by degrading NAD and repressing the activity of other NAD-consuming enzymes and by producing NAD-derived metabolites that regulate calcium signaling and migration of inflammatory cells.	NAD	4-37	CD38 antigen	Mus musculus	59-63
25893674-2	2015	The nicotinamide adenine dinucleotide (NAD) glycohydrolase CD38, which is expressed by neurons, astrocytes, and microglial cells, regulates inflammatory and repair processes in the brain and other tissues by degrading NAD and repressing the activity of other NAD-consuming enzymes and by producing NAD-derived metabolites that regulate calcium signaling and migration of inflammatory cells.	NAD	39-42	CD38 antigen	Mus musculus	59-63
25893674-2	2015	The nicotinamide adenine dinucleotide (NAD) glycohydrolase CD38, which is expressed by neurons, astrocytes, and microglial cells, regulates inflammatory and repair processes in the brain and other tissues by degrading NAD and repressing the activity of other NAD-consuming enzymes and by producing NAD-derived metabolites that regulate calcium signaling and migration of inflammatory cells.	NAD	218-221	CD38 antigen	Mus musculus	59-63
25893674-2	2015	The nicotinamide adenine dinucleotide (NAD) glycohydrolase CD38, which is expressed by neurons, astrocytes, and microglial cells, regulates inflammatory and repair processes in the brain and other tissues by degrading NAD and repressing the activity of other NAD-consuming enzymes and by producing NAD-derived metabolites that regulate calcium signaling and migration of inflammatory cells.	NAD	218-221	CD38 antigen	Mus musculus	59-63
25893674-2	2015	The nicotinamide adenine dinucleotide (NAD) glycohydrolase CD38, which is expressed by neurons, astrocytes, and microglial cells, regulates inflammatory and repair processes in the brain and other tissues by degrading NAD and repressing the activity of other NAD-consuming enzymes and by producing NAD-derived metabolites that regulate calcium signaling and migration of inflammatory cells.	NAD	218-221	CD38 antigen	Mus musculus	59-63
25536389-6	2015	Interestingly, when cells were treated with the SIRT1 inhibitor EX527, the protective effects of PJ34 and NAD treatment were diminished.	NAD	106-109	sirtuin 1	Homo sapiens	48-53
25840449-8	2015	The protein expression levels of two nicotinamide adenine dinucleotide (NAD+)-dependent deacetylases, sirtuin 1 and sirtuin 3, were significantly but transiently upregulated 4 but not 24 h after irradiation.	NAD	37-70	sirtuin 1	Homo sapiens	102-111
25840449-8	2015	The protein expression levels of two nicotinamide adenine dinucleotide (NAD+)-dependent deacetylases, sirtuin 1 and sirtuin 3, were significantly but transiently upregulated 4 but not 24 h after irradiation.	NAD	72-75	sirtuin 1	Homo sapiens	102-111
26091232-3	2015	SIRT1, a nicotinamide adenine dinucleotide(+) -dependent histone/protein deacetylase, plays crucial roles in various physiological processes, including aging and apoptosis.	NAD	9-42	sirtuin 1	Homo sapiens	0-5
26109052-1	2015	Sirtuins with an extended N-terminal domain (NTD), represented by yeast Sir2 and human SIRT1, harbor intrinsic mechanisms for regulation of their NAD-dependent deacetylase activities.	NAD	146-149	sirtuin 1	Homo sapiens	87-92
25970806-1	2015	SIRT7 with coenzyme NAD catalyzes protein de-acetylation.	NAD	20-23	sirtuin 7	Homo sapiens	0-5
25716654-4	2015	Analysis of downstream targets of the mutations in these two genes showed that the HNRNPA0 mutation affected expression patterns in the PI3 kinase and ERK/MAPK signaling pathways, while the WIF1 variant influenced expression of genes that play a role in NAD biosynthesis.	NAD	254-257	WNT inhibitory factor 1	Homo sapiens	190-194
25788480-2	2015	Recent studies report that increased availability of intracellular NAD obtained by inhibition of the NAD-consuming enzyme poly(ADP-ribose) polymerase (PARP)-1 or supplementation with the NAD-precursor nicotinamide riboside (NR) ameliorates energetic derangement and symptoms in mouse models of mitochondrial disorders.	NAD	67-70	poly (ADP-ribose) polymerase family, member 1	Mus musculus	122-158
25788480-2	2015	Recent studies report that increased availability of intracellular NAD obtained by inhibition of the NAD-consuming enzyme poly(ADP-ribose) polymerase (PARP)-1 or supplementation with the NAD-precursor nicotinamide riboside (NR) ameliorates energetic derangement and symptoms in mouse models of mitochondrial disorders.	NAD	101-104	poly (ADP-ribose) polymerase family, member 1	Mus musculus	122-158
25788480-2	2015	Recent studies report that increased availability of intracellular NAD obtained by inhibition of the NAD-consuming enzyme poly(ADP-ribose) polymerase (PARP)-1 or supplementation with the NAD-precursor nicotinamide riboside (NR) ameliorates energetic derangement and symptoms in mouse models of mitochondrial disorders.	NAD	101-104	poly (ADP-ribose) polymerase family, member 1	Mus musculus	122-158
25788480-5	2015	Here, we show that human fibroblasts mutant for the NADH dehydrogenase (ubiquinone) Fe-S protein 1 (NDUFS1) subunit of respiratory complex I have similar ATP, NAD, and mitochondrial content compared with control cells, but show reduced mitochondrial membrane potential.	NAD	52-55	NADH:ubiquinone oxidoreductase core subunit S1	Homo sapiens	100-106
26054687-1	2015	BACKGROUND: Several members of the SIRT family (SIRT1-7), which are a highly conserved family of NAD(+)-dependent enzymes, play an important role in tumor formation.	NAD	97-103	sirtuin 1	Homo sapiens	48-53
25461268-4	2015	Sirtuin-1 (SIRT1) is a highly conserved nicotinamide adenine dinucleotide (NAD)-dependent histone deacetylase that plays a critical role in promoting cell survival under oxidative stress.	NAD	40-73	sirtuin 1	Homo sapiens	0-9
25461268-4	2015	Sirtuin-1 (SIRT1) is a highly conserved nicotinamide adenine dinucleotide (NAD)-dependent histone deacetylase that plays a critical role in promoting cell survival under oxidative stress.	NAD	40-73	sirtuin 1	Homo sapiens	11-16
25461268-4	2015	Sirtuin-1 (SIRT1) is a highly conserved nicotinamide adenine dinucleotide (NAD)-dependent histone deacetylase that plays a critical role in promoting cell survival under oxidative stress.	NAD	75-78	sirtuin 1	Homo sapiens	0-9
25461268-4	2015	Sirtuin-1 (SIRT1) is a highly conserved nicotinamide adenine dinucleotide (NAD)-dependent histone deacetylase that plays a critical role in promoting cell survival under oxidative stress.	NAD	75-78	sirtuin 1	Homo sapiens	11-16
25828863-5	2015	The inhibitors should allow for a more detailed assessment of how NAD elevation via CD38 inhibition affects physiology in NAD deficient states.	NAD	66-69	CD38 antigen	Mus musculus	84-88
25828863-5	2015	The inhibitors should allow for a more detailed assessment of how NAD elevation via CD38 inhibition affects physiology in NAD deficient states.	NAD	122-125	CD38 antigen	Mus musculus	84-88
25712525-4	2015	Subsequently, the PARP-1 over-activation-induced depletion of nicotinamide adenine dinucleotide (NAD(+))/adenosine triphosphate (ATP) after exposures to lethal doses of zinc or N-methyl-D-aspartate is significantly attenuated in cortical neuronal cultures.	NAD	62-95	poly (ADP-ribose) polymerase family, member 1	Mus musculus	18-24
25712525-4	2015	Subsequently, the PARP-1 over-activation-induced depletion of nicotinamide adenine dinucleotide (NAD(+))/adenosine triphosphate (ATP) after exposures to lethal doses of zinc or N-methyl-D-aspartate is significantly attenuated in cortical neuronal cultures.	NAD	97-103	poly (ADP-ribose) polymerase family, member 1	Mus musculus	18-24
25751424-0	2015	NAD(+)-SIRT1 control of H3K4 trimethylation through circadian deacetylation of MLL1.	NAD	0-6	sirtuin 1	Homo sapiens	7-12
25631045-3	2015	Sirtuin 1 (SIRT1), an NAD-dependent deacetylase, participates in a variety of human diseases.	NAD	22-25	sirtuin 1	Homo sapiens	0-9
25631045-3	2015	Sirtuin 1 (SIRT1), an NAD-dependent deacetylase, participates in a variety of human diseases.	NAD	22-25	sirtuin 1	Homo sapiens	11-16
25517228-3	2015	The role of poly(ADP-ribosyl)ation in HMGB1 release has been explored previously; however, PARP1 is a versatile enzyme and performs several other functions including cross-talk with another nicotinamide adenine dinucleotide- (NAD(+)) dependent member of the Class III histone deacetylases (HDACs), sirtuin-1 (SIRT1).	NAD	190-223	poly (ADP-ribose) polymerase family, member 1	Mus musculus	91-96
25517228-3	2015	The role of poly(ADP-ribosyl)ation in HMGB1 release has been explored previously; however, PARP1 is a versatile enzyme and performs several other functions including cross-talk with another nicotinamide adenine dinucleotide- (NAD(+)) dependent member of the Class III histone deacetylases (HDACs), sirtuin-1 (SIRT1).	NAD	226-233	poly (ADP-ribose) polymerase family, member 1	Mus musculus	91-96
25517228-8	2015	By utilizing an NAD(+)-based mechanism, PARP1 inhibition increases the activity of SIRT1.	NAD	16-22	poly (ADP-ribose) polymerase family, member 1	Mus musculus	40-45
25890336-6	2015	Following initial validation, pathways that include NAD synthetase 1 (NADSYN1) and protein kinase B (AKT2) were hypothesized and experimentally tested to provide a mechanistic basis for AMPK regulation of cell migration and maintenance of cellular NAD(+) concentrations during catabolic processes.	NAD	248-254	NAD synthetase 1	Homo sapiens	52-68
25890336-6	2015	Following initial validation, pathways that include NAD synthetase 1 (NADSYN1) and protein kinase B (AKT2) were hypothesized and experimentally tested to provide a mechanistic basis for AMPK regulation of cell migration and maintenance of cellular NAD(+) concentrations during catabolic processes.	NAD	248-254	NAD synthetase 1	Homo sapiens	70-77
25281273-2	2015	SIRT1 is a member of the histone deacetylase class III family of proteins and is an NAD(+)-dependent histone and protein deacetylase.	NAD	84-88	sirtuin 1	Homo sapiens	0-5
25755662-2	2015	Nicotinamide adenine dinucleotide(+)-dependent SORBITOL DEHYDROGENASE (SDH, E. C. 1.1.1.14) from Arabidopsis thaliana L. sorbitol dehydrogenase (AtSDH) is capable of oxidizing several polyols including sorbitol, ribitol, and xylitol.	NAD	0-33	lysine-ketoglutarate reductase/saccharopine dehydrogenase bifunctional enzyme	Arabidopsis thaliana	71-74
25755662-2	2015	Nicotinamide adenine dinucleotide(+)-dependent SORBITOL DEHYDROGENASE (SDH, E. C. 1.1.1.14) from Arabidopsis thaliana L. sorbitol dehydrogenase (AtSDH) is capable of oxidizing several polyols including sorbitol, ribitol, and xylitol.	NAD	0-33	lysine-ketoglutarate reductase/saccharopine dehydrogenase bifunctional enzyme	Arabidopsis thaliana	145-150
26045998-0	2015	Nicotinamide adenine dinucleotide (NAD) may affect DNA methyltransferase 1 through regulation of BRCA1 in ovarian cancer.	NAD	0-33	DNA methyltransferase 1	Homo sapiens	51-74
26045998-0	2015	Nicotinamide adenine dinucleotide (NAD) may affect DNA methyltransferase 1 through regulation of BRCA1 in ovarian cancer.	NAD	0-33	BRCA1 DNA repair associated	Homo sapiens	97-102
26045998-0	2015	Nicotinamide adenine dinucleotide (NAD) may affect DNA methyltransferase 1 through regulation of BRCA1 in ovarian cancer.	NAD	35-38	DNA methyltransferase 1	Homo sapiens	51-74
26045998-0	2015	Nicotinamide adenine dinucleotide (NAD) may affect DNA methyltransferase 1 through regulation of BRCA1 in ovarian cancer.	NAD	35-38	BRCA1 DNA repair associated	Homo sapiens	97-102
25633578-1	2015	In laboratory yeast strains with Sir2 and Fob1 function, wild-type NAD+ salvage is required for calorie restriction (CR) to extend replicative lifespan.	NAD	67-71	replication fork barrier binding protein FOB1	Saccharomyces cerevisiae S288C	42-46
25529796-2	2015	Herein, deletion of the NAD(+)-dependent histone deacetylase Sirt1 induced histological features of prostatic intraepithelial neoplasia at 7 months of age; these features were associated with increased cell proliferation and enhanced mitophagy.	NAD	24-30	sirtuin 1	Homo sapiens	61-66
25903518-1	2015	SIRT1 is an important protein that catalyzes the nicotinamide adenine dinucleotide (NAD)(+)-dependent deacetylation reaction, which is regarded as a novel target to treat metabolic disorders and aging-related diseases.	NAD	49-82	sirtuin 1	Homo sapiens	0-5
25903518-1	2015	SIRT1 is an important protein that catalyzes the nicotinamide adenine dinucleotide (NAD)(+)-dependent deacetylation reaction, which is regarded as a novel target to treat metabolic disorders and aging-related diseases.	NAD	84-91	sirtuin 1	Homo sapiens	0-5
25746104-1	2015	SIRT1 is a highly conserved NAD+-dependent protein deacetylase that is involved in diverse cellular processes.	NAD	28-31	sirtuin 1	Homo sapiens	0-5
25469273-2	2015	Sirtuin1 (SIRT1) is a nicotinamide adenine dinucleotide (NAD+)-dependent histone deacetylase that deacetylates a number of proteins and is overexpressed in several human malignancies.	NAD	22-55	sirtuin 1	Homo sapiens	0-8
25469273-2	2015	Sirtuin1 (SIRT1) is a nicotinamide adenine dinucleotide (NAD+)-dependent histone deacetylase that deacetylates a number of proteins and is overexpressed in several human malignancies.	NAD	22-55	sirtuin 1	Homo sapiens	10-15
25469273-2	2015	Sirtuin1 (SIRT1) is a nicotinamide adenine dinucleotide (NAD+)-dependent histone deacetylase that deacetylates a number of proteins and is overexpressed in several human malignancies.	NAD	57-60	sirtuin 1	Homo sapiens	0-8
25469273-2	2015	Sirtuin1 (SIRT1) is a nicotinamide adenine dinucleotide (NAD+)-dependent histone deacetylase that deacetylates a number of proteins and is overexpressed in several human malignancies.	NAD	57-60	sirtuin 1	Homo sapiens	10-15
25441760-4	2014	PARP inhibitors that compete with NAD(+) at the enzyme"s activity site can be used in BRCA-deficient cells as single agent therapies acting through the principle of synthetic lethality exploiting these cells deficient DNA double-strand break repair.	NAD	34-40	BRCA1 DNA repair associated	Homo sapiens	86-90
25199460-6	2014	SIRT1, a NAD(+)-dependent histone/non-histone protein deacetylase, has been reported to inhibit intracellular signaling mediated by SREBP-1 through deacetylation of this transcription factor.	NAD	9-15	sirtuin 1	Homo sapiens	0-5
25277684-2	2014	Nicotinamide phosphoribosyltransferase (Nampt), a rate-limiting enzyme in the NAD+ salvage pathway, plays an important role in controlling the level of NAD+ and the activity of Sirt1 in the heart and the cardiomyocytes therein.	NAD	78-82	sirtuin 1	Homo sapiens	177-182
25277684-2	2014	Nicotinamide phosphoribosyltransferase (Nampt), a rate-limiting enzyme in the NAD+ salvage pathway, plays an important role in controlling the level of NAD+ and the activity of Sirt1 in the heart and the cardiomyocytes therein.	NAD	152-156	sirtuin 1	Homo sapiens	177-182
25333616-5	2014	We found that leucine, tyrosine, arginine, homoarginine or glucose treatment of the GA1 model cells reduced the gene expression of caspase-3, caspase-8, caspase-9, bax, fos, and jun and restored the intracellular NADH and ATP levels.	NAD	213-217	caspase 3	Mus musculus	131-140
25171301-7	2014	In the same suspensions (i.e., containing C-SWCNT, NADH, and O2), pBR322 DNA plasmid was cleaved, although  OH was not detected when using  OH scavenging molecular probes.	NAD	51-55	translocator protein	Homo sapiens	66-69
25290058-0	2014	NAD+ protects against EAE by regulating CD4+ T-cell differentiation.	NAD	0-4	CD4 antigen	Mus musculus	40-43
25290058-2	2014	Here we show that nicotinamide adenine dinucleotide (NAD(+)) blocks experimental autoimmune encephalomyelitis (EAE), a mouse model of MS, by inducing immune homeostasis through CD4(+)IFNgamma(+)IL-10(+) T cells and reverses disease progression by restoring tissue integrity via remyelination and neuroregeneration.	NAD	18-51	CD4 antigen	Mus musculus	177-180
25290058-2	2014	Here we show that nicotinamide adenine dinucleotide (NAD(+)) blocks experimental autoimmune encephalomyelitis (EAE), a mouse model of MS, by inducing immune homeostasis through CD4(+)IFNgamma(+)IL-10(+) T cells and reverses disease progression by restoring tissue integrity via remyelination and neuroregeneration.	NAD	53-59	CD4 antigen	Mus musculus	177-180
25290058-3	2014	We show that NAD(+) regulates CD4(+) T-cell differentiation through tryptophan hydroxylase-1 (Tph1), independently of well-established transcription factors.	NAD	13-19	CD4 antigen	Mus musculus	30-33
25290058-4	2014	In the presence of NAD(+), the frequency of T-bet(-/-) CD4(+)IFNgamma(+) T cells was twofold higher than wild-type CD4(+) T cells cultured in conventional T helper 1 polarizing conditions.	NAD	19-25	CD4 antigen	Mus musculus	55-58
25290058-4	2014	In the presence of NAD(+), the frequency of T-bet(-/-) CD4(+)IFNgamma(+) T cells was twofold higher than wild-type CD4(+) T cells cultured in conventional T helper 1 polarizing conditions.	NAD	19-25	CD4 antigen	Mus musculus	115-118
25290058-5	2014	Our findings unravel a new pathway orchestrating CD4(+) T-cell differentiation and demonstrate that NAD(+) may serve as a powerful therapeutic agent for the treatment of autoimmune and other diseases.	NAD	100-106	CD4 antigen	Mus musculus	49-52
25085245-4	2014	This switch is triggered by the need to reduce the production of protons from glycolysis and further maintained by the NAD(+)-dependent increase in SIRT1 deacetylase activity to ensure intracellular pH homeostasis.	NAD	119-125	sirtuin 1	Homo sapiens	148-153
24835770-5	2014	RNA interference analysis and activity inhibition assay indicate that life-span extension was mediated by the upregulation of Sir-2.1, a NAD-dependent histone deacetylase ortholog of mammalian SIRT1.	NAD	137-140	sirtuin 1	Homo sapiens	193-198
24862934-2	2014	The NAD-dependent deacetylase sirtuin-1 (SIRT1), one member of the sirtuin family of proteins and an NAD-dependent deacetylase has been implicated in the regulation of multiple cellular processes, including inflammation, longevity, and metabolism.	NAD	4-7	sirtuin 1	Homo sapiens	41-46
24862934-2	2014	The NAD-dependent deacetylase sirtuin-1 (SIRT1), one member of the sirtuin family of proteins and an NAD-dependent deacetylase has been implicated in the regulation of multiple cellular processes, including inflammation, longevity, and metabolism.	NAD	101-104	sirtuin 1	Homo sapiens	41-46
24880091-6	2014	We show here that extracellular-signal-regulated kinase-5 regulates the transcription of the NADH(+)-dependent histone deacetylase silent mating type information regulation 2 homolog 1 (Sirtuin 1) in leukemic Jurkat T cells.	NAD	93-97	sirtuin 1	Homo sapiens	186-195
24865966-6	2014	In endothelial cells, the mitochondrion-driven reduction in both the cytosolic and mitochondrial NAD(+)/NADH ratio stimulated a compensatory increase in SIRT1 protein levels that had an anti-inflammatory effect.	NAD	97-103	sirtuin 1	Homo sapiens	153-158
24865966-6	2014	In endothelial cells, the mitochondrion-driven reduction in both the cytosolic and mitochondrial NAD(+)/NADH ratio stimulated a compensatory increase in SIRT1 protein levels that had an anti-inflammatory effect.	NAD	104-108	sirtuin 1	Homo sapiens	153-158
25101006-1	2014	BACKGROUND AND AIMS: AIF (apoptosis inducing factor) is a flavin and NADH containing protein located within mitochondria required for optimal function of the respiratory chain.	NAD	69-73	apoptosis-inducing factor, mitochondrion-associated 1	Mus musculus	21-24
24895128-1	2014	To address whether mitochondrial biogenesis is essential for skeletal myogenesis, C2C12 myogenesis was investigated after knockdown of NADH dehydrogenase (ubiquintone) flavoprotein 1 (NDUFV1), which is an oxidative phosphorylation complex I subunit that is the first subunit to accept electrons from NADH.	NAD	135-139	NADH:ubiquinone oxidoreductase core subunit V1	Homo sapiens	184-190
25033286-1	2014	Up-regulated sirtuin 1 (SIRT1), an NAD+-dependent class III histone deacetylase, deacetylates p53 and inhibits its transcriptional activity, leading to cell survival.	NAD	35-39	sirtuin 1	Homo sapiens	13-22
25033286-1	2014	Up-regulated sirtuin 1 (SIRT1), an NAD+-dependent class III histone deacetylase, deacetylates p53 and inhibits its transcriptional activity, leading to cell survival.	NAD	35-39	sirtuin 1	Homo sapiens	24-29
25051362-6	2014	Furthermore, adiponectin can increase AMP-activated protein kinase (AMPK) phosphorylation and NAD-dependent deacetylase sirtuin-1 (Sirt1) of PC cells.	NAD	94-97	sirtuin 1	Homo sapiens	131-136
24914854-2	2014	In mitochondria, AIF is present in a monomer-dimer equilibrium that after reduction by NADH gets displaced toward the dimer.	NAD	87-91	apoptosis inducing factor mitochondria associated 1	Homo sapiens	17-20
25000096-2	2014	Sirtuin 1(SIRT1), a NAD(+) dependent class III histone deacetylase is involved in a variety of human disorders such as obesity, type II diabetes, cancer and aging.	NAD	20-26	sirtuin 1	Homo sapiens	0-9
25000096-2	2014	Sirtuin 1(SIRT1), a NAD(+) dependent class III histone deacetylase is involved in a variety of human disorders such as obesity, type II diabetes, cancer and aging.	NAD	20-26	sirtuin 1	Homo sapiens	10-15
24959282-1	2014	Sirtuin 1 (Sirt1) is a nicotinamide adenine dinucleotide-dependent class III histone deacetylase.	NAD	23-56	sirtuin 1	Homo sapiens	0-9
24959282-1	2014	Sirtuin 1 (Sirt1) is a nicotinamide adenine dinucleotide-dependent class III histone deacetylase.	NAD	23-56	sirtuin 1	Homo sapiens	11-16
24578339-2	2014	CD38 is an ectoenzyme that consumes NAD(+) to produce cyclic ADP-ribose (cADPR), a potent agonist of ryanodine receptors.	NAD	36-42	CD38 antigen	Mus musculus	0-4
24699315-6	2014	The NAD(+)-linked 15-hydroxyprostaglandin dehydrogenase (15-PGDH/HPGD), a key enzyme that converts the protumorigenic prostaglandin E2 (PGE2) to its biologically inactive metabolite, was identified as a direct target of miR-21 in cholangiocarcinoma cells.	NAD	4-10	carbonyl reductase 1	Homo sapiens	18-55
24712520-3	2014	In cultured myocytes, coumestrol activated the silent information regulator two ortholog 1 (Sirt1) through the elevation of the intracellular NAD(+)/NADH ratio.	NAD	142-148	sirtuin 1	Homo sapiens	47-90
24712520-3	2014	In cultured myocytes, coumestrol activated the silent information regulator two ortholog 1 (Sirt1) through the elevation of the intracellular NAD(+)/NADH ratio.	NAD	142-148	sirtuin 1	Homo sapiens	92-97
24712520-3	2014	In cultured myocytes, coumestrol activated the silent information regulator two ortholog 1 (Sirt1) through the elevation of the intracellular NAD(+)/NADH ratio.	NAD	149-153	sirtuin 1	Homo sapiens	47-90
24712520-3	2014	In cultured myocytes, coumestrol activated the silent information regulator two ortholog 1 (Sirt1) through the elevation of the intracellular NAD(+)/NADH ratio.	NAD	149-153	sirtuin 1	Homo sapiens	92-97
24467670-6	2014	P5CR was able to use either NADPH or NADH as the electron donor, with contrasting affinities and maximum reaction rates.	NAD	37-41	pyrroline-5-carboxylate reductase 1	Homo sapiens	0-4
24449278-1	2014	SIRT1, an NAD-dependent deacetylase, plays a role in regulation of autophagy.	NAD	10-13	sirtuin 1	Homo sapiens	0-5
24717514-10	2014	NNMT inhibition increases adipose SAM and NAD(+) levels and upregulates ODC and SSAT activity as well as expression, owing to the effects of NNMT on histone H3 lysine 4 methylation in adipose tissue.	NAD	42-48	nicotinamide N-methyltransferase	Mus musculus	0-4
24717514-13	2014	Thus, NNMT is a novel regulator of histone methylation, polyamine flux and NAD(+)-dependent SIRT1 signalling, and is a unique and attractive target for treating obesity and type 2 diabetes.	NAD	75-81	nicotinamide N-methyltransferase	Mus musculus	6-10
24397908-1	2014	SIRT1 is a member of the histone deacetylase (HDAC) class III family of proteins and is an NAD-dependent histone and protein deacetylase.	NAD	91-94	sirtuin 1	Homo sapiens	0-5
24321770-1	2014	Parthanatos is a programmed necrotic demise characteristic of ATP (adenosine triphosphate) consumption due to NAD+ (nicotinamide adenine dinucleotide) depletion by poly(ADP-ribose) polymerase 1 (PARP1)-dependent poly(ADP-ribosyl)ation on target proteins.	NAD	110-114	poly (ADP-ribose) polymerase family, member 1	Mus musculus	164-193
24321770-1	2014	Parthanatos is a programmed necrotic demise characteristic of ATP (adenosine triphosphate) consumption due to NAD+ (nicotinamide adenine dinucleotide) depletion by poly(ADP-ribose) polymerase 1 (PARP1)-dependent poly(ADP-ribosyl)ation on target proteins.	NAD	110-114	poly (ADP-ribose) polymerase family, member 1	Mus musculus	195-200
24321770-1	2014	Parthanatos is a programmed necrotic demise characteristic of ATP (adenosine triphosphate) consumption due to NAD+ (nicotinamide adenine dinucleotide) depletion by poly(ADP-ribose) polymerase 1 (PARP1)-dependent poly(ADP-ribosyl)ation on target proteins.	NAD	116-149	poly (ADP-ribose) polymerase family, member 1	Mus musculus	164-193
24321770-1	2014	Parthanatos is a programmed necrotic demise characteristic of ATP (adenosine triphosphate) consumption due to NAD+ (nicotinamide adenine dinucleotide) depletion by poly(ADP-ribose) polymerase 1 (PARP1)-dependent poly(ADP-ribosyl)ation on target proteins.	NAD	116-149	poly (ADP-ribose) polymerase family, member 1	Mus musculus	195-200
24425865-5	2014	We show that acetylation of AceCS1 is cyclic and that its rhythmicity requires a functional circadian clock and the NAD(+)-dependent deacetylase SIRT1.	NAD	116-122	sirtuin 1	Homo sapiens	145-150
24587137-1	2014	Mitochondrial sn-glycerol 3-phosphate dehydrogenase (mGPDH) is a ubiquinone-linked enzyme in the mitochondrial inner membrane best characterized as part of the glycerol phosphate shuttle that transfers reducing equivalents from cytosolic NADH into the mitochondrial electron transport chain.	NAD	238-242	glycerol phosphate dehydrogenase 2, mitochondrial	Mus musculus	53-58
24551237-3	2014	Here we show that leucine exerts a direct effect on Sirt1 kinetics, reducing its Km for NAD(+) by &gt;50% and enabling low doses of resveratrol to further activate the enzyme (p = 0.012).	NAD	88-94	sirtuin 1	Homo sapiens	52-57
24506863-2	2014	A new study (Gomes et al., 2013) shows that reduced levels of nicotinamide adenine dinucleotide (NAD(+)) contribute to the mitochondrial decay associated with skeletal muscle aging and that sirtuin 1 (SIRT1) modulates this process.	NAD	62-95	sirtuin 1	Homo sapiens	190-199
24506863-2	2014	A new study (Gomes et al., 2013) shows that reduced levels of nicotinamide adenine dinucleotide (NAD(+)) contribute to the mitochondrial decay associated with skeletal muscle aging and that sirtuin 1 (SIRT1) modulates this process.	NAD	62-95	sirtuin 1	Homo sapiens	201-206
24275857-9	2014	Poly(ADP-ribose) polymerase-1-null lymphocytes also undergo lower NAD depletion and reduced cell death when exposed to the drug.	NAD	66-69	poly (ADP-ribose) polymerase family, member 1	Mus musculus	0-29
24498153-14	2014	Homology modelling of buffalo XOR showed several variations occurring in clusters, especially close to FAD binding pocket which could affect NAD(+) entry in the FAD centre.	NAD	141-147	xanthine dehydrogenase	Bos taurus	30-33
24416313-1	2014	Sirtuin 1 (SIRT1) is a nicotinamide adenine dinucleotide (NAD)-dependent deacetylase that is implicated in plethora of biological processes, including metabolism, aging, stress response, and tumorigenesis.	NAD	23-56	sirtuin 1	Homo sapiens	0-9
24416313-1	2014	Sirtuin 1 (SIRT1) is a nicotinamide adenine dinucleotide (NAD)-dependent deacetylase that is implicated in plethora of biological processes, including metabolism, aging, stress response, and tumorigenesis.	NAD	23-56	sirtuin 1	Homo sapiens	11-16
24416313-1	2014	Sirtuin 1 (SIRT1) is a nicotinamide adenine dinucleotide (NAD)-dependent deacetylase that is implicated in plethora of biological processes, including metabolism, aging, stress response, and tumorigenesis.	NAD	58-61	sirtuin 1	Homo sapiens	0-9
24416313-1	2014	Sirtuin 1 (SIRT1) is a nicotinamide adenine dinucleotide (NAD)-dependent deacetylase that is implicated in plethora of biological processes, including metabolism, aging, stress response, and tumorigenesis.	NAD	58-61	sirtuin 1	Homo sapiens	11-16
25486197-3	2014	Here, we showed that: (i) BRCA1 inactivation events (mutation and promoter methylation) were accompanied by elevated levels of NAD; (ii) the knockdown or overexpression of BRCA1 was an effective way to induce an increase or decrease of nicotinamide phosphoribosyltransferase (Nampt)-related NAD synthesis, respectively; and (iii) BRCA1 expression patterns were inversely correlated with NAD levels in human ovarian cancer specimens.	NAD	291-294	BRCA1 DNA repair associated	Homo sapiens	172-177
25486197-3	2014	Here, we showed that: (i) BRCA1 inactivation events (mutation and promoter methylation) were accompanied by elevated levels of NAD; (ii) the knockdown or overexpression of BRCA1 was an effective way to induce an increase or decrease of nicotinamide phosphoribosyltransferase (Nampt)-related NAD synthesis, respectively; and (iii) BRCA1 expression patterns were inversely correlated with NAD levels in human ovarian cancer specimens.	NAD	291-294	BRCA1 DNA repair associated	Homo sapiens	26-31
25486197-3	2014	Here, we showed that: (i) BRCA1 inactivation events (mutation and promoter methylation) were accompanied by elevated levels of NAD; (ii) the knockdown or overexpression of BRCA1 was an effective way to induce an increase or decrease of nicotinamide phosphoribosyltransferase (Nampt)-related NAD synthesis, respectively; and (iii) BRCA1 expression patterns were inversely correlated with NAD levels in human ovarian cancer specimens.	NAD	291-294	BRCA1 DNA repair associated	Homo sapiens	172-177
25486197-3	2014	Here, we showed that: (i) BRCA1 inactivation events (mutation and promoter methylation) were accompanied by elevated levels of NAD; (ii) the knockdown or overexpression of BRCA1 was an effective way to induce an increase or decrease of nicotinamide phosphoribosyltransferase (Nampt)-related NAD synthesis, respectively; and (iii) BRCA1 expression patterns were inversely correlated with NAD levels in human ovarian cancer specimens.	NAD	291-294	BRCA1 DNA repair associated	Homo sapiens	172-177
25486197-4	2014	In addition, it is worth noting that: (i) NAD incubation induced increased levels of BRCA1 in a concentration-dependent manner; (ii) Nampt knockdown-mediated reduction in NAD levels was effective at inhibiting BRCA1 expression; and (iii) the overexpression of Nampt led to higher NAD levels and a subsequent increase in BRCA1 levels in primary ovarian cancer cells and A2780, HO-8910 and ES2 ovarian cancer cell lines.	NAD	42-45	BRCA1 DNA repair associated	Homo sapiens	85-90
25486197-4	2014	In addition, it is worth noting that: (i) NAD incubation induced increased levels of BRCA1 in a concentration-dependent manner; (ii) Nampt knockdown-mediated reduction in NAD levels was effective at inhibiting BRCA1 expression; and (iii) the overexpression of Nampt led to higher NAD levels and a subsequent increase in BRCA1 levels in primary ovarian cancer cells and A2780, HO-8910 and ES2 ovarian cancer cell lines.	NAD	42-45	BRCA1 DNA repair associated	Homo sapiens	210-215
25486197-4	2014	In addition, it is worth noting that: (i) NAD incubation induced increased levels of BRCA1 in a concentration-dependent manner; (ii) Nampt knockdown-mediated reduction in NAD levels was effective at inhibiting BRCA1 expression; and (iii) the overexpression of Nampt led to higher NAD levels and a subsequent increase in BRCA1 levels in primary ovarian cancer cells and A2780, HO-8910 and ES2 ovarian cancer cell lines.	NAD	42-45	BRCA1 DNA repair associated	Homo sapiens	210-215
25486197-4	2014	In addition, it is worth noting that: (i) NAD incubation induced increased levels of BRCA1 in a concentration-dependent manner; (ii) Nampt knockdown-mediated reduction in NAD levels was effective at inhibiting BRCA1 expression; and (iii) the overexpression of Nampt led to higher NAD levels and a subsequent increase in BRCA1 levels in primary ovarian cancer cells and A2780, HO-8910 and ES2 ovarian cancer cell lines.	NAD	171-174	BRCA1 DNA repair associated	Homo sapiens	85-90
25486197-4	2014	In addition, it is worth noting that: (i) NAD incubation induced increased levels of BRCA1 in a concentration-dependent manner; (ii) Nampt knockdown-mediated reduction in NAD levels was effective at inhibiting BRCA1 expression; and (iii) the overexpression of Nampt led to higher NAD levels and a subsequent increase in BRCA1 levels in primary ovarian cancer cells and A2780, HO-8910 and ES2 ovarian cancer cell lines.	NAD	171-174	BRCA1 DNA repair associated	Homo sapiens	210-215
25486197-4	2014	In addition, it is worth noting that: (i) NAD incubation induced increased levels of BRCA1 in a concentration-dependent manner; (ii) Nampt knockdown-mediated reduction in NAD levels was effective at inhibiting BRCA1 expression; and (iii) the overexpression of Nampt led to higher NAD levels and a subsequent increase in BRCA1 levels in primary ovarian cancer cells and A2780, HO-8910 and ES2 ovarian cancer cell lines.	NAD	171-174	BRCA1 DNA repair associated	Homo sapiens	210-215
25486197-4	2014	In addition, it is worth noting that: (i) NAD incubation induced increased levels of BRCA1 in a concentration-dependent manner; (ii) Nampt knockdown-mediated reduction in NAD levels was effective at inhibiting BRCA1 expression; and (iii) the overexpression of Nampt led to higher NAD levels and a subsequent increase in BRCA1 levels in primary ovarian cancer cells and A2780, HO-8910 and ES2 ovarian cancer cell lines.	NAD	171-174	BRCA1 DNA repair associated	Homo sapiens	85-90
25486197-4	2014	In addition, it is worth noting that: (i) NAD incubation induced increased levels of BRCA1 in a concentration-dependent manner; (ii) Nampt knockdown-mediated reduction in NAD levels was effective at inhibiting BRCA1 expression; and (iii) the overexpression of Nampt led to higher NAD levels and a subsequent increase in BRCA1 levels in primary ovarian cancer cells and A2780, HO-8910 and ES2 ovarian cancer cell lines.	NAD	171-174	BRCA1 DNA repair associated	Homo sapiens	210-215
25486197-4	2014	In addition, it is worth noting that: (i) NAD incubation induced increased levels of BRCA1 in a concentration-dependent manner; (ii) Nampt knockdown-mediated reduction in NAD levels was effective at inhibiting BRCA1 expression; and (iii) the overexpression of Nampt led to higher NAD levels and a subsequent increase in BRCA1 levels in primary ovarian cancer cells and A2780, HO-8910 and ES2 ovarian cancer cell lines.	NAD	171-174	BRCA1 DNA repair associated	Homo sapiens	210-215
23761196-5	2014	Whereas SHR VSMCs exposure to angiotensin II overexpressed AT1R and Nox4 nicotinamide-adenine dinucleotide phosphate (NADPH) oxidase and slightly downregulated caveolin-1 expression, losartan decreased AT1R protein levels and increased caveolin-1 and Hsp70 expression in SHR VSMC membranes.	NAD	73-106	NADPH oxidase 4	Rattus norvegicus	68-72
25022271-3	2014	Resveratrol can activate the NAD-dependent deacetylase sirtuin 1 (SIRT1), leading to deacetylation of SIRT1 target molecules such as NF-kB and forkhead box O (FOXO) transcription factors.	NAD	29-32	sirtuin 1	Homo sapiens	66-71
25022271-3	2014	Resveratrol can activate the NAD-dependent deacetylase sirtuin 1 (SIRT1), leading to deacetylation of SIRT1 target molecules such as NF-kB and forkhead box O (FOXO) transcription factors.	NAD	29-32	sirtuin 1	Homo sapiens	102-107
24727683-10	2014	Taken together, these results indicate that IS impairs the iNampt-NAD(+)-Sirt1 system via AhR activation, which in turn promotes endothelial senescence.	NAD	66-72	sirtuin 1	Homo sapiens	73-78
25386563-3	2014	SIRT1 deacetylates target proteins using the coenzyme NAD(+) and is therefore linked to cellular energy metabolism and the redox state through multiple signalling and survival pathways.	NAD	54-60	sirtuin 1	Homo sapiens	0-5
24277839-6	2013	We were able to show that formation of a functional vascular system requires glutaredoxin 2-dependent reversible S-glutathionylation of the NAD(+)-dependent protein deacetylase sirtuin 1.	NAD	140-146	sirtuin 1	Danio rerio	177-186
23892229-10	2013	NMNAT catalyzes the reversible reaction that produces nicotinamide adenine dinucleotide (NAD) from nicotinamide mononucleotide (NMN).	NAD	54-87	nicotinamide nucleotide adenylyltransferase 1	Mus musculus	0-5
23892229-10	2013	NMNAT catalyzes the reversible reaction that produces nicotinamide adenine dinucleotide (NAD) from nicotinamide mononucleotide (NMN).	NAD	89-92	nicotinamide nucleotide adenylyltransferase 1	Mus musculus	0-5
24204194-0	2013	Dependence of tumor cell lines and patient-derived tumors on the NAD salvage pathway renders them sensitive to NAMPT inhibition with GNE-618.	NAD	65-68	glucosamine (UDP-N-acetyl)-2-epimerase/N-acetylmannosamine kinase	Homo sapiens	133-136
24204194-2	2013	A key enzyme in the NAD salvage pathway is nicotinamide phosphoribosyl transferase (NAMPT), and here, we describe GNE-618, an NAMPT inhibitor that depletes NAD and induces cell death in vitro and in vivo.	NAD	20-23	glucosamine (UDP-N-acetyl)-2-epimerase/N-acetylmannosamine kinase	Homo sapiens	114-117
24204194-2	2013	A key enzyme in the NAD salvage pathway is nicotinamide phosphoribosyl transferase (NAMPT), and here, we describe GNE-618, an NAMPT inhibitor that depletes NAD and induces cell death in vitro and in vivo.	NAD	156-159	glucosamine (UDP-N-acetyl)-2-epimerase/N-acetylmannosamine kinase	Homo sapiens	114-117
24204194-3	2013	While cells proficient for nicotinic acid phosphoribosyl transferase (NAPRT1) can be protected from NAMPT inhibition as they convert nicotinic acid (NA) to NAD independent of the salvage pathway, this protection only occurs if NA is added before NAD depletion.	NAD	156-159	nicotinate phosphoribosyltransferase	Homo sapiens	27-68
24204194-3	2013	While cells proficient for nicotinic acid phosphoribosyl transferase (NAPRT1) can be protected from NAMPT inhibition as they convert nicotinic acid (NA) to NAD independent of the salvage pathway, this protection only occurs if NA is added before NAD depletion.	NAD	156-159	nicotinate phosphoribosyltransferase	Homo sapiens	70-76
24204194-3	2013	While cells proficient for nicotinic acid phosphoribosyl transferase (NAPRT1) can be protected from NAMPT inhibition as they convert nicotinic acid (NA) to NAD independent of the salvage pathway, this protection only occurs if NA is added before NAD depletion.	NAD	246-249	nicotinate phosphoribosyltransferase	Homo sapiens	27-68
24204194-3	2013	While cells proficient for nicotinic acid phosphoribosyl transferase (NAPRT1) can be protected from NAMPT inhibition as they convert nicotinic acid (NA) to NAD independent of the salvage pathway, this protection only occurs if NA is added before NAD depletion.	NAD	246-249	nicotinate phosphoribosyltransferase	Homo sapiens	70-76
24204194-7	2013	Thus, we show that dependence of tumor cells on the NAD salvage pathway renders them sensitive to GNE-618 in vitro and in vivo, and our data support further evaluation of the use of NAMPT mRNA and protein levels as predictors of overall sensitivity.	NAD	52-55	glucosamine (UDP-N-acetyl)-2-epimerase/N-acetylmannosamine kinase	Homo sapiens	98-101
23499302-4	2013	Silent mating type information regulator 2 homolog 1 (SIRT1), a nicotinamide adenine dinucleotide (NAD+)-dependent class III histone deacetylase (HDAC), has also been implicated in protection against vascular aging and age-related vascular diseases.	NAD	64-97	sirtuin 1	Homo sapiens	54-59
23499302-4	2013	Silent mating type information regulator 2 homolog 1 (SIRT1), a nicotinamide adenine dinucleotide (NAD+)-dependent class III histone deacetylase (HDAC), has also been implicated in protection against vascular aging and age-related vascular diseases.	NAD	99-103	sirtuin 1	Homo sapiens	54-59
23943620-3	2013	Consistent with the dependence on NAD(+) in Sir2p-regulated silencing, we found that inositol depletion induces the expression of BNA2, which is required for the de novo synthesis of NAD(+).	NAD	34-40	dioxygenase BNA2	Saccharomyces cerevisiae S288C	130-134
23943620-3	2013	Consistent with the dependence on NAD(+) in Sir2p-regulated silencing, we found that inositol depletion induces the expression of BNA2, which is required for the de novo synthesis of NAD(+).	NAD	183-189	dioxygenase BNA2	Saccharomyces cerevisiae S288C	130-134
23747282-2	2013	The first assay is based on the reduction of Delta(1)-pyrroline-5-carboxylate (P5C), generated from ornithine by OAT, using human pyrroline 5-carboxylate reductase 1 (PYCR1), which results in the concomitant oxidation of NADH (nicotinamide adenine dinucleotide, reduced form) to NAD+ (nicotinamide adenine dinucleotide, oxidized form).	NAD	227-260	pyrroline-5-carboxylate reductase 1	Homo sapiens	130-165
23747282-2	2013	The first assay is based on the reduction of Delta(1)-pyrroline-5-carboxylate (P5C), generated from ornithine by OAT, using human pyrroline 5-carboxylate reductase 1 (PYCR1), which results in the concomitant oxidation of NADH (nicotinamide adenine dinucleotide, reduced form) to NAD+ (nicotinamide adenine dinucleotide, oxidized form).	NAD	227-260	pyrroline-5-carboxylate reductase 1	Homo sapiens	167-172
23747282-2	2013	The first assay is based on the reduction of Delta(1)-pyrroline-5-carboxylate (P5C), generated from ornithine by OAT, using human pyrroline 5-carboxylate reductase 1 (PYCR1), which results in the concomitant oxidation of NADH (nicotinamide adenine dinucleotide, reduced form) to NAD+ (nicotinamide adenine dinucleotide, oxidized form).	NAD	279-283	pyrroline-5-carboxylate reductase 1	Homo sapiens	45-77
23747282-2	2013	The first assay is based on the reduction of Delta(1)-pyrroline-5-carboxylate (P5C), generated from ornithine by OAT, using human pyrroline 5-carboxylate reductase 1 (PYCR1), which results in the concomitant oxidation of NADH (nicotinamide adenine dinucleotide, reduced form) to NAD+ (nicotinamide adenine dinucleotide, oxidized form).	NAD	279-283	pyrroline-5-carboxylate reductase 1	Homo sapiens	79-82
23747282-2	2013	The first assay is based on the reduction of Delta(1)-pyrroline-5-carboxylate (P5C), generated from ornithine by OAT, using human pyrroline 5-carboxylate reductase 1 (PYCR1), which results in the concomitant oxidation of NADH (nicotinamide adenine dinucleotide, reduced form) to NAD+ (nicotinamide adenine dinucleotide, oxidized form).	NAD	279-283	pyrroline-5-carboxylate reductase 1	Homo sapiens	130-165
23747282-2	2013	The first assay is based on the reduction of Delta(1)-pyrroline-5-carboxylate (P5C), generated from ornithine by OAT, using human pyrroline 5-carboxylate reductase 1 (PYCR1), which results in the concomitant oxidation of NADH (nicotinamide adenine dinucleotide, reduced form) to NAD+ (nicotinamide adenine dinucleotide, oxidized form).	NAD	279-283	pyrroline-5-carboxylate reductase 1	Homo sapiens	167-172
23747282-2	2013	The first assay is based on the reduction of Delta(1)-pyrroline-5-carboxylate (P5C), generated from ornithine by OAT, using human pyrroline 5-carboxylate reductase 1 (PYCR1), which results in the concomitant oxidation of NADH (nicotinamide adenine dinucleotide, reduced form) to NAD+ (nicotinamide adenine dinucleotide, oxidized form).	NAD	285-318	pyrroline-5-carboxylate reductase 1	Homo sapiens	45-77
23747282-2	2013	The first assay is based on the reduction of Delta(1)-pyrroline-5-carboxylate (P5C), generated from ornithine by OAT, using human pyrroline 5-carboxylate reductase 1 (PYCR1), which results in the concomitant oxidation of NADH (nicotinamide adenine dinucleotide, reduced form) to NAD+ (nicotinamide adenine dinucleotide, oxidized form).	NAD	285-318	pyrroline-5-carboxylate reductase 1	Homo sapiens	79-82
23747282-2	2013	The first assay is based on the reduction of Delta(1)-pyrroline-5-carboxylate (P5C), generated from ornithine by OAT, using human pyrroline 5-carboxylate reductase 1 (PYCR1), which results in the concomitant oxidation of NADH (nicotinamide adenine dinucleotide, reduced form) to NAD+ (nicotinamide adenine dinucleotide, oxidized form).	NAD	285-318	pyrroline-5-carboxylate reductase 1	Homo sapiens	130-165
23747282-2	2013	The first assay is based on the reduction of Delta(1)-pyrroline-5-carboxylate (P5C), generated from ornithine by OAT, using human pyrroline 5-carboxylate reductase 1 (PYCR1), which results in the concomitant oxidation of NADH (nicotinamide adenine dinucleotide, reduced form) to NAD+ (nicotinamide adenine dinucleotide, oxidized form).	NAD	285-318	pyrroline-5-carboxylate reductase 1	Homo sapiens	167-172
23797802-0	2013	Galloflavin suppresses lactate dehydrogenase activity and causes MYC downregulation in Burkitt lymphoma cells through NAD/NADH-dependent inhibition of sirtuin-1.	NAD	118-121	sirtuin 1	Homo sapiens	151-160
23797802-0	2013	Galloflavin suppresses lactate dehydrogenase activity and causes MYC downregulation in Burkitt lymphoma cells through NAD/NADH-dependent inhibition of sirtuin-1.	NAD	122-126	sirtuin 1	Homo sapiens	151-160
23891603-7	2013	However, NAMPT and NMNAT-mediated NAD(+) biosynthesis and ATP levels were severely compromised in liver of CD fed irradiated mice.	NAD	34-40	nicotinamide nucleotide adenylyltransferase 1	Mus musculus	19-24
23798679-5	2013	There is also evidence that metabolites such as NAD(+) (acting via deacetylases such as SIRT1 and SIRT2) and succinate (which regulates hypoxia-inducible factor 1alpha) are signals that regulate innate immunity.	NAD	48-54	sirtuin 1	Homo sapiens	88-93
23597856-3	2013	De-acetylation at this site is performed by sirtuin 1(SIRT1) and possibly other sirtuins in an NAD(+) dependent manner, such that SIRT1 inhibition promotes NF-kappaB transcriptional activity.	NAD	95-101	sirtuin 1	Homo sapiens	130-135
24009628-1	2013	BACKGROUND: Silent mating type information regulation 2 homolog 1 (SIRT1), an NAD+-dependent deacetylase, might act as a tumor promoter by inhibiting p53, but may also as a tumor suppressor by inhibiting several oncogenes such as beta-catenin and survivin.	NAD	78-81	sirtuin 1	Homo sapiens	67-72
23583951-6	2013	Knockdown of the NAD(+)-dependent protein deacetylase sirtuin 1 (SIRT1) by siRNA prevented the upregulation of eNOS mRNA and protein by resveratrol.	NAD	17-23	sirtuin 1	Homo sapiens	54-63
23583951-6	2013	Knockdown of the NAD(+)-dependent protein deacetylase sirtuin 1 (SIRT1) by siRNA prevented the upregulation of eNOS mRNA and protein by resveratrol.	NAD	17-23	sirtuin 1	Homo sapiens	65-70
23770670-4	2013	We recently identified a pathway by which the AHR target gene TiPARP (TCDD-inducible poly(ADP-ribose) polymerase) contributes to TCDD suppression of transcription of phosphoenolpyruvate carboxykinase (PEPCK), a key regulator of gluconeogenesis, by consuming NAD(+) and decreasing Sirtuin 1 activation of the peroxisome proliferator-activated receptor gamma coactivator 1alpha (PGC1alpha), a transcriptional activator of PEPCK.	NAD	258-264	phosphoenolpyruvate carboxykinase 2, mitochondrial	Homo sapiens	166-199
23770670-4	2013	We recently identified a pathway by which the AHR target gene TiPARP (TCDD-inducible poly(ADP-ribose) polymerase) contributes to TCDD suppression of transcription of phosphoenolpyruvate carboxykinase (PEPCK), a key regulator of gluconeogenesis, by consuming NAD(+) and decreasing Sirtuin 1 activation of the peroxisome proliferator-activated receptor gamma coactivator 1alpha (PGC1alpha), a transcriptional activator of PEPCK.	NAD	258-264	phosphoenolpyruvate carboxykinase 2, mitochondrial	Homo sapiens	201-206
23770670-4	2013	We recently identified a pathway by which the AHR target gene TiPARP (TCDD-inducible poly(ADP-ribose) polymerase) contributes to TCDD suppression of transcription of phosphoenolpyruvate carboxykinase (PEPCK), a key regulator of gluconeogenesis, by consuming NAD(+) and decreasing Sirtuin 1 activation of the peroxisome proliferator-activated receptor gamma coactivator 1alpha (PGC1alpha), a transcriptional activator of PEPCK.	NAD	258-264	sirtuin 1	Homo sapiens	280-289
23770670-4	2013	We recently identified a pathway by which the AHR target gene TiPARP (TCDD-inducible poly(ADP-ribose) polymerase) contributes to TCDD suppression of transcription of phosphoenolpyruvate carboxykinase (PEPCK), a key regulator of gluconeogenesis, by consuming NAD(+) and decreasing Sirtuin 1 activation of the peroxisome proliferator-activated receptor gamma coactivator 1alpha (PGC1alpha), a transcriptional activator of PEPCK.	NAD	258-264	phosphoenolpyruvate carboxykinase 2, mitochondrial	Homo sapiens	420-425
23880858-2	2013	Sirt1, an NAD+-dependent class III protein deacetylase, plays an important role in the regulation of the proinflammatory cytokines involved in inflammation-associated diseases.	NAD	10-14	sirtuin 1	Homo sapiens	0-5
23766555-0	2013	Electron Paramagnetic Resonance and Electron Spin Echo Studies of Co2+ Coordination by Nicotinamide Adenine Dinucleotide (NAD+) in Water Solution.	NAD	122-126	spindlin 1	Homo sapiens	45-49
23766555-1	2013	Co2+ binding to the nicotinamide adenine dinucleotide (NAD+) molecule in water solution was studied by electron paramagnetic resonance (EPR) and electron spin echo at low temperatures.	NAD	20-53	spindlin 1	Homo sapiens	154-158
23766555-1	2013	Co2+ binding to the nicotinamide adenine dinucleotide (NAD+) molecule in water solution was studied by electron paramagnetic resonance (EPR) and electron spin echo at low temperatures.	NAD	55-59	spindlin 1	Homo sapiens	154-158
23766555-3	2013	EPR spin-Hamiltonian parameters of the Co/NAD+ complex at 6 K are gz  = 2.01, gx  = 2.38, gy  = 3.06, Az  = 94 x 10-4 cm-1, Ax  = 33 x 10-4 cm-1 and Ay  = 71 x 10-4 cm-1.	NAD	42-46	spindlin 1	Homo sapiens	4-8
23742622-2	2013	However, the identification of the longevity protein silent regulator 2 (Sir2), the founding member of the sirtuin protein family, as being NAD+-dependent reignited interest in this metabolite.	NAD	140-144	sirtuin 1	Homo sapiens	53-71
23742622-2	2013	However, the identification of the longevity protein silent regulator 2 (Sir2), the founding member of the sirtuin protein family, as being NAD+-dependent reignited interest in this metabolite.	NAD	140-144	sirtuin 1	Homo sapiens	73-77
23742622-3	2013	The sirtuins (SIRT1-7 in mammals) utilize NAD+ to deacetylate proteins in different subcellular compartments with a variety of functions, but with a strong convergence on optimizing mitochondrial function.	NAD	42-46	sirtuin 1	Homo sapiens	14-19
23800187-1	2013	BACKGROUND: Sirtuins (SIRT1-7) are a family of NAD-dependent deacetylases, which play an important role in regulating cancer tumorigenesis; however, their role in oral cancer has been controversial.	NAD	47-50	sirtuin 1	Homo sapiens	22-29
23641059-4	2013	Superoxide production by a model bacterium within the ubiquitous Roseobacter clade involves an extracellular oxidoreductase that is stimulated by the reduced form of nicotinamide adenine dinucleotide (NADH), suggesting a surprising homology with eukaryotic organisms.	NAD	166-199	thioredoxin reductase 1	Homo sapiens	109-123
23529657-2	2013	Here, we report the steady-state kinetics for ADH, using a homogeneous enzyme preparation with formaldehyde as the substrate and nicotinamide adenine dinucleotide (NADH) as the cofactor.	NAD	129-162	aldo-keto reductase family 1 member A1	Homo sapiens	46-49
23529657-2	2013	Here, we report the steady-state kinetics for ADH, using a homogeneous enzyme preparation with formaldehyde as the substrate and nicotinamide adenine dinucleotide (NADH) as the cofactor.	NAD	164-168	aldo-keto reductase family 1 member A1	Homo sapiens	46-49
23335597-4	2013	Unexpectedly, overexpression of other genes in the salvage pathway for NAD(+) biosynthesis, including QNS1, NPT1 and PNC1 also protected against proteotoxicity.	NAD	71-77	glutamine-dependent NAD(+) synthetase	Saccharomyces cerevisiae S288C	102-106
23498864-6	2013	In the presence of NAD+, recombinant SDH exhibited greatest oxidative activity with sorbitol, ribitol and xylitol as substrates; other sugar alcohols were oxidized to a lesser extent.	NAD	19-23	lysine-ketoglutarate reductase/saccharopine dehydrogenase bifunctional enzyme	Arabidopsis thaliana	37-40
23370328-2	2013	The NAD(+)-dependent protein deacetylase Sirtuin-1 (Sirt1) has been implicated in carcinogenesis with dual roles depending on its subcellular localization.	NAD	4-8	sirtuin 1	Homo sapiens	41-50
23370328-2	2013	The NAD(+)-dependent protein deacetylase Sirtuin-1 (Sirt1) has been implicated in carcinogenesis with dual roles depending on its subcellular localization.	NAD	4-8	sirtuin 1	Homo sapiens	52-57
23478437-1	2013	The NAD+-dependent deacetylases Sirt1 and Sirt2 mediate cellular stress responses and are highly expressed in vascular endothelial cells.	NAD	4-7	sirtuin 1	Homo sapiens	32-37
23239498-2	2013	Previous studies implicated the nicotinamide adenine dinucleotide phosphate-reduced oxidase dual oxidase-1 (DUOX1) in redox signaling pathways involved in in vitro epithelial wound responses to infection and injury.	NAD	32-65	dual oxidase 1	Mus musculus	92-106
23239498-2	2013	Previous studies implicated the nicotinamide adenine dinucleotide phosphate-reduced oxidase dual oxidase-1 (DUOX1) in redox signaling pathways involved in in vitro epithelial wound responses to infection and injury.	NAD	32-65	dual oxidase 1	Mus musculus	108-113
23331011-7	2013	Mechanistically, MBD1 is associated with Twist and NAD-dependent deacetylase sirtuin-1 (SIRT1), thereby forming the Twist-MBD1-SIRT1 complex on the CDH1 promoter, which resulted in reduced E-cadherin transcription activity and increased cell EMT ability.	NAD	51-54	sirtuin 1	Homo sapiens	88-93
23331011-7	2013	Mechanistically, MBD1 is associated with Twist and NAD-dependent deacetylase sirtuin-1 (SIRT1), thereby forming the Twist-MBD1-SIRT1 complex on the CDH1 promoter, which resulted in reduced E-cadherin transcription activity and increased cell EMT ability.	NAD	51-54	sirtuin 1	Homo sapiens	127-132
23311358-0	2013	The 2.5 A crystal structure of the SIRT1 catalytic domain bound to nicotinamide adenine dinucleotide (NAD+) and an indole (EX527 analogue) reveals a novel mechanism of histone deacetylase inhibition.	NAD	67-100	sirtuin 1	Homo sapiens	35-40
23311358-0	2013	The 2.5 A crystal structure of the SIRT1 catalytic domain bound to nicotinamide adenine dinucleotide (NAD+) and an indole (EX527 analogue) reveals a novel mechanism of histone deacetylase inhibition.	NAD	102-106	sirtuin 1	Homo sapiens	35-40
23311358-5	2013	To elucidate the mechanism of SIRT inhibition by 27, we determined the 2.5 A crystal structure of the SIRT1 catalytic domain (residues 241-516) bound to NAD(+) and the 27 analogue compound 35.	NAD	153-159	sirtuin 1	Homo sapiens	102-107
23311358-8	2013	The SIRT1/NAD(+)/35 crystal structure defines a novel mechanism of histone deacetylase inhibition and provides a basis for understanding, and rationally improving, inhibition of this therapeutically important target by drug-like molecules.	NAD	10-16	sirtuin 1	Homo sapiens	4-9
22052036-2	2013	There is evidence that such changes relate to nitric oxide (NO) bioavailability, an endothelial compound produced by the action of endothelial NO synthase (eNOS), and is regulated by sirtuin-1 (Sirt1), a NAD(+)-dependent protein deacetylase.	NAD	204-210	sirtuin 1	Homo sapiens	183-192
23116202-1	2013	Saccharomyces cerevisiae has three distinct inner mitochondrial membrane NADH dehydrogenases mediating the transfer of electrons from NADH to CoQ (coenzyme Q): Nde1p, Nde2p and Ndi1p.	NAD	73-77	NADH-ubiquinone reductase (H(+)-translocating) NDE1	Saccharomyces cerevisiae S288C	160-165
23116202-1	2013	Saccharomyces cerevisiae has three distinct inner mitochondrial membrane NADH dehydrogenases mediating the transfer of electrons from NADH to CoQ (coenzyme Q): Nde1p, Nde2p and Ndi1p.	NAD	73-77	NADH-ubiquinone reductase (H(+)-translocating) NDE2	Saccharomyces cerevisiae S288C	167-172
23116202-2	2013	The active site of Ndi1p faces the matrix side, whereas the enzymatic activities of Nde1p and Nde2p are restricted to the intermembrane space side, where they are responsible for cytosolic NADH oxidation.	NAD	189-193	NADH-ubiquinone reductase (H(+)-translocating) NDE1	Saccharomyces cerevisiae S288C	84-89
23116202-2	2013	The active site of Ndi1p faces the matrix side, whereas the enzymatic activities of Nde1p and Nde2p are restricted to the intermembrane space side, where they are responsible for cytosolic NADH oxidation.	NAD	189-193	NADH-ubiquinone reductase (H(+)-translocating) NDE2	Saccharomyces cerevisiae S288C	94-99
23116202-8	2013	Altogether, our results indicate that impairment in the oxidation of cytosolic NADH by Nde1p is deleterious towards mitochondrial biogenesis due to an increase in reactive oxygen species release.	NAD	79-83	NADH-ubiquinone reductase (H(+)-translocating) NDE1	Saccharomyces cerevisiae S288C	87-92
23631196-3	2013	FoxO1 is a downstream effector of insulin signaling and Sirt1 is an NAD(+)-dependent deacetylase, both of which work as energy sensors at the cellular level.	NAD	68-72	sirtuin 1	Homo sapiens	56-61
23085506-10	2013	PARP-1 inhibition increased Sirt1 activity through an increased intracellular nicotinamide adenine dinucleotide (NAD(+)) level.	NAD	78-111	sirtuin 1	Homo sapiens	28-33
23085506-10	2013	PARP-1 inhibition increased Sirt1 activity through an increased intracellular nicotinamide adenine dinucleotide (NAD(+)) level.	NAD	113-119	sirtuin 1	Homo sapiens	28-33
23085506-13	2013	PARP-1 inhibition restored Sirt1 activity by increasing NAD(+) level and decreased iNOS and ICAM-1 expression by inhibiting NF-kappaB nuclear translocation and activity as well as NF-kappaB phosphorylation.	NAD	56-62	sirtuin 1	Homo sapiens	27-32
23116400-5	2013	AIF folds in three modules: a FAD-binding, a nicotine adenine dinucleotide (NADH)-binding and a C-terminal modules.	NAD	76-80	apoptosis inducing factor mitochondria associated 1	Homo sapiens	0-3
23116400-6	2013	Upon reduction of the flavin cofactor by NADH, conformational changes leading to AIF dimerization are proposed as a key early event in the mitochondrial sensing/signaling functions of AIF.	NAD	41-45	apoptosis inducing factor mitochondria associated 1	Homo sapiens	81-84
23116400-6	2013	Upon reduction of the flavin cofactor by NADH, conformational changes leading to AIF dimerization are proposed as a key early event in the mitochondrial sensing/signaling functions of AIF.	NAD	41-45	apoptosis inducing factor mitochondria associated 1	Homo sapiens	184-187
23123323-13	2013	CD38 was found to transduce the extracellular NAD(+) signal.	NAD	46-52	CD38 antigen	Mus musculus	0-4
23186252-1	2013	BACKGROUND: Equine neuroaxonal dystrophy/equine degenerative myeloencephalopathy (NAD/EDM) is a neurodegenerative disorder affecting young horses of various breeds that resembles ataxia with vitamin E deficiency in humans, an inherited disorder caused by mutations in the alpha-tocopherol transfer protein gene (TTPA).	NAD	82-85	alpha tocopherol transfer protein	Homo sapiens	312-316
24512730-1	2013	It has been reported that upregulated SIRT1 (NAD(+)-dependent class III histone deacetylase) deacetylates the p53 protein, represses its function, and allows for tumor cell growth in various cancers.	NAD	45-51	sirtuin 1	Homo sapiens	38-43
22909099-9	2012	This study suggests that NAD metabolism and intracellular NAM concentrations are important in Fob1-mediated rDNA recombination.	NAD	25-28	replication fork barrier binding protein FOB1	Saccharomyces cerevisiae S288C	94-98
23053940-2	2012	In addition to its pivotal role in energy metabolism, NAD(+) is also the indispensable substrate of poly (ADP-ribose) polymerase-1 (PARP-1) and sirtuin 1 (SIRT1).	NAD	54-60	sirtuin 1	Homo sapiens	144-153
23053940-2	2012	In addition to its pivotal role in energy metabolism, NAD(+) is also the indispensable substrate of poly (ADP-ribose) polymerase-1 (PARP-1) and sirtuin 1 (SIRT1).	NAD	54-60	sirtuin 1	Homo sapiens	155-160
23053940-4	2012	The NAD(+)-dependent modifications catalyzed by PARP-1 and SIRT1 liberate NAM, and NAM acts as feedback inhibitor of PARP-1 and SIRT1 through interacting with the enzymes at the binding site for NAD(+).	NAD	4-10	sirtuin 1	Homo sapiens	59-64
23053940-4	2012	The NAD(+)-dependent modifications catalyzed by PARP-1 and SIRT1 liberate NAM, and NAM acts as feedback inhibitor of PARP-1 and SIRT1 through interacting with the enzymes at the binding site for NAD(+).	NAD	4-10	sirtuin 1	Homo sapiens	128-133
23053940-4	2012	The NAD(+)-dependent modifications catalyzed by PARP-1 and SIRT1 liberate NAM, and NAM acts as feedback inhibitor of PARP-1 and SIRT1 through interacting with the enzymes at the binding site for NAD(+).	NAD	195-201	sirtuin 1	Homo sapiens	59-64
22249256-2	2012	Here, we propose a novel mechanism through which the nicotinamide adenine dinucleotide-dependent histone deacetylase SIRT1 regulates EMT in prostate cancer cells through cooperation with the EMT inducing transcription factor ZEB1.	NAD	53-86	sirtuin 1	Homo sapiens	117-122
22249256-2	2012	Here, we propose a novel mechanism through which the nicotinamide adenine dinucleotide-dependent histone deacetylase SIRT1 regulates EMT in prostate cancer cells through cooperation with the EMT inducing transcription factor ZEB1.	NAD	53-86	zinc finger E-box binding homeobox 1	Homo sapiens	225-229
22971926-9	2012	These results indicate that the decrease in MDH1 and subsequent reduction in NAD/NADH ratio, which causes SIRT1 inhibition, is a likely carbohydrate metabolism-controlled cellular senescence mechanism.	NAD	77-80	sirtuin 1	Homo sapiens	106-111
22971926-9	2012	These results indicate that the decrease in MDH1 and subsequent reduction in NAD/NADH ratio, which causes SIRT1 inhibition, is a likely carbohydrate metabolism-controlled cellular senescence mechanism.	NAD	81-85	sirtuin 1	Homo sapiens	106-111
22828134-2	2012	Silent information regulator family protein 1 (SIRT1), as the founding member of nicotinamide adenine dinucleotide (NAD)-dependent deacetylases, has recently been demonstrated to have neuroprotective effect in several models of neurodegenerative diseases.	NAD	81-114	sirtuin 1	Homo sapiens	0-45
22828134-2	2012	Silent information regulator family protein 1 (SIRT1), as the founding member of nicotinamide adenine dinucleotide (NAD)-dependent deacetylases, has recently been demonstrated to have neuroprotective effect in several models of neurodegenerative diseases.	NAD	81-114	sirtuin 1	Homo sapiens	47-52
22735644-1	2012	Human DBC1 (deleted in breast cancer-1; KIAA1967) is a nuclear protein that, in response to DNA damage, competitively inhibits the NAD(+)-dependent deacetylase SIRT1, a regulator of p53 apoptotic functions in response to genotoxic stress.	NAD	131-137	sirtuin 1	Homo sapiens	160-165
22935421-4	2012	SIRT1, one of highly conserved NAD-dependent class III deacetylases, has been involved in several cellular processes and implicated in human diseases.	NAD	31-34	sirtuin 1	Homo sapiens	0-5
22822071-3	2012	Here, we show that several coenzyme A (CoA) derivatives, such as acetyl-CoA, butyryl-CoA, HMG-CoA, and malonyl-CoA, as well as NADPH but not NADP(+), NADH, or NAD(+), act as allosteric activators of recombinant HDAC1 and HDAC2 in vitro following a mixed activation kinetic.	NAD	150-154	2,4-dienoyl-CoA reductase 1	Homo sapiens	127-132
22822071-3	2012	Here, we show that several coenzyme A (CoA) derivatives, such as acetyl-CoA, butyryl-CoA, HMG-CoA, and malonyl-CoA, as well as NADPH but not NADP(+), NADH, or NAD(+), act as allosteric activators of recombinant HDAC1 and HDAC2 in vitro following a mixed activation kinetic.	NAD	159-165	2,4-dienoyl-CoA reductase 1	Homo sapiens	127-132
22822071-7	2012	The similarity in structures of the identified metabolites and the exquisite selectivity of NADPH over NADP(+), NADH, and NAD(+) as an HDAC activator reveal a previously unrecognized biochemical feature of the HDAC proteins with important consequences for regulation of histone acetylation as well as the development of more specific and potent HDAC inhibitors.	NAD	112-116	2,4-dienoyl-CoA reductase 1	Homo sapiens	92-97
22822071-7	2012	The similarity in structures of the identified metabolites and the exquisite selectivity of NADPH over NADP(+), NADH, and NAD(+) as an HDAC activator reveal a previously unrecognized biochemical feature of the HDAC proteins with important consequences for regulation of histone acetylation as well as the development of more specific and potent HDAC inhibitors.	NAD	122-128	2,4-dienoyl-CoA reductase 1	Homo sapiens	92-97
22730114-1	2012	Sirtuins 1-7 (SIRT1-7) belong to the third class of deacetylase enzymes, which are dependent on NAD(+)  for activity.	NAD	96-102	sirtuin 1	Homo sapiens	0-12
22730114-1	2012	Sirtuins 1-7 (SIRT1-7) belong to the third class of deacetylase enzymes, which are dependent on NAD(+)  for activity.	NAD	96-102	sirtuin 1	Homo sapiens	14-21
23431834-3	2012	PMCA activity of washed red cell membrane was measured by coupling with pyruvate kinase, using phosphoenolpyruvate as substrate, and lactate dehydrogenase to convert pyruvate to lactate employing beta-NADH as co-factor.	NAD	196-205	ATPase plasma membrane Ca2+ transporting 2	Homo sapiens	0-4
23193674-1	2012	Silent information regulator factor 2-related enzyme 1 (Sirtuins 1, SIRT1) is a nicotinamide adenine dinucleotide (NAD)-dependent deacetylase, which can deacetylate histone and non-histone proteins and other transcription factors, and is involved in the regulation of many physiological functions, including gene transcription, energy metabolism, cell senescence and oxidative stress.	NAD	80-113	sirtuin 1	Homo sapiens	68-73
23193674-1	2012	Silent information regulator factor 2-related enzyme 1 (Sirtuins 1, SIRT1) is a nicotinamide adenine dinucleotide (NAD)-dependent deacetylase, which can deacetylate histone and non-histone proteins and other transcription factors, and is involved in the regulation of many physiological functions, including gene transcription, energy metabolism, cell senescence and oxidative stress.	NAD	115-118	sirtuin 1	Homo sapiens	68-73
22585221-1	2012	We report the use of a known pyridochromanone inhibitor with antibacterial activity to assess the validity of NAD(+)-dependent DNA ligase (LigA) as an antibacterial target in Staphylococcus aureus.	NAD	110-116	AT695_RS03215	Staphylococcus aureus	131-137
22585221-1	2012	We report the use of a known pyridochromanone inhibitor with antibacterial activity to assess the validity of NAD(+)-dependent DNA ligase (LigA) as an antibacterial target in Staphylococcus aureus.	NAD	110-116	AT695_RS03215	Staphylococcus aureus	139-143
22465780-2	2012	SIRT1, a class III histone deacetylase, and PARP-1, a poly(ADP-ribose) polymerase, are two NAD(+)-dependent enzymes that have been shown to be involved in the regulation of the clock.	NAD	91-97	sirtuin 1	Homo sapiens	0-5
22682224-2	2012	In line with this premise, decreased activity of PARP-1 or CD38-both NAD(+) consumers-increases NAD(+) bioavailability, resulting in SIRT1 activation and protection against metabolic disease.	NAD	69-75	sirtuin 1	Homo sapiens	133-138
22343344-4	2012	METHODS: We used the nicotinamide adenine dinucleotide phosphate (NADPH)-diaphorase (NADPH-d) reaction as a qualitative marker of nNOS enzyme activity.	NAD	21-54	nitric oxide synthase 1	Rattus norvegicus	130-134
22358185-1	2012	Glycerol-3-phosphate dehydrogenase (GPDH) catalyzes the conversion of dihydroxyacetone phosphate (DHAP) and NADH to glycerol-3-phosphate (G3P) and NAD(+).	NAD	108-112	uncharacterized protein	Chlamydomonas reinhardtii	0-34
22358185-1	2012	Glycerol-3-phosphate dehydrogenase (GPDH) catalyzes the conversion of dihydroxyacetone phosphate (DHAP) and NADH to glycerol-3-phosphate (G3P) and NAD(+).	NAD	108-112	uncharacterized protein	Chlamydomonas reinhardtii	36-40
22358185-1	2012	Glycerol-3-phosphate dehydrogenase (GPDH) catalyzes the conversion of dihydroxyacetone phosphate (DHAP) and NADH to glycerol-3-phosphate (G3P) and NAD(+).	NAD	147-153	uncharacterized protein	Chlamydomonas reinhardtii	0-34
22358185-1	2012	Glycerol-3-phosphate dehydrogenase (GPDH) catalyzes the conversion of dihydroxyacetone phosphate (DHAP) and NADH to glycerol-3-phosphate (G3P) and NAD(+).	NAD	147-153	uncharacterized protein	Chlamydomonas reinhardtii	36-40
22351627-7	2012	Degradation of beta-NAD(+) to ADPR and other metabolites appears to be mediated by pathways besides CD38, the main NAD-glycohydrolase in mammals.	NAD	15-26	CD38 antigen	Mus musculus	100-104
22619752-1	2012	Leishmania infantum nicotinamidase, encoded by the Lipnc1 gene, converts nicotinamide into nicotinicacid to ensure Nicotinamide-Adenine-Dinucleotide (NAD+) biosynthesis.	NAD	115-148	Nicotinamide amidase	Drosophila melanogaster	20-34
22619752-1	2012	Leishmania infantum nicotinamidase, encoded by the Lipnc1 gene, converts nicotinamide into nicotinicacid to ensure Nicotinamide-Adenine-Dinucleotide (NAD+) biosynthesis.	NAD	150-154	Nicotinamide amidase	Drosophila melanogaster	20-34
22799020-1	2012	Sirtuin1 (Sirt1) is a NAD-dependent class III histone deacetylase (HDAC), and regulates pulmonary immune/inflammatory system and the aging process mainly through post-translational modification.	NAD	22-25	sirtuin 1	Homo sapiens	0-8
22799020-1	2012	Sirtuin1 (Sirt1) is a NAD-dependent class III histone deacetylase (HDAC), and regulates pulmonary immune/inflammatory system and the aging process mainly through post-translational modification.	NAD	22-25	sirtuin 1	Homo sapiens	10-15
22479251-1	2012	SIRT1 is an NAD-dependent deacetylase that regulates stress response pathways.	NAD	12-15	sirtuin 1	Homo sapiens	0-5
22449973-4	2012	In neonatal rat cardiomyocytes, overexpression of Nmnat2 but not its catalytically inactive mutant blocked angiotensin II (Ang II)-induced cardiac hypertrophy, which was dependent on activation of SIRT6 through maintaining the intracellular NAD level.	NAD	241-244	nicotinamide nucleotide adenylyltransferase 2	Rattus norvegicus	50-56
22330808-3	2012	SIRT1, nicotinamide adenine dinucleotide (NAD(+))-dependent protein deacetylase, has been implicated in a variety of cellular processes such as inflammatory injury and the control of multidrug resistance in cancer.	NAD	7-40	sirtuin 1	Homo sapiens	0-5
22340598-3	2012	We show that the NAD(+)-dependent deacetylase SIRT1 is overexpressed in human CML LSC.	NAD	17-23	sirtuin 1	Homo sapiens	46-51
22315973-2	2012	The mechanisms underlying WldS -mediated axonal protection are unclear, although many studies have attributed WldS neuroprotection to the NAD+-synthesizing Nmnat1 portion of the fusion protein.	NAD	138-142	nicotinamide nucleotide adenylyltransferase 1	Mus musculus	156-162
22214983-6	2012	The mode of action of DCHP on 3beta-HSD activity was competitive with the substrate pregnenolone but noncompetitive with the cofactor NAD+.	NAD	134-138	hydroxy-delta-5-steroid dehydrogenase, 3 beta- and steroid delta-isomerase 1	Homo sapiens	30-39
21742010-1	2012	Nicotinate phosphoribosyltransferase (NaPRT, EC 2.4.2.11) catalyzes the conversion of nicotinate (Na) to nicotinate mononucleotide, the first reaction of the Preiss-Handler pathway for the biosynthesis of NAD(+).	NAD	205-211	nicotinate phosphoribosyltransferase	Homo sapiens	0-36
21742010-1	2012	Nicotinate phosphoribosyltransferase (NaPRT, EC 2.4.2.11) catalyzes the conversion of nicotinate (Na) to nicotinate mononucleotide, the first reaction of the Preiss-Handler pathway for the biosynthesis of NAD(+).	NAD	205-211	nicotinate phosphoribosyltransferase	Homo sapiens	38-43
21742010-2	2012	Even though NaPRT activity has been described to be responsible for the ability of Na to increase NAD(+) levels in human cells more effectively than nicotinamide (Nam), so far a limited number of studies on the human NaPRT have appeared.	NAD	98-104	nicotinate phosphoribosyltransferase	Homo sapiens	12-17
22204321-5	2012	For examples, the key NAD(+)-dependent enzymes SIRT1 and SIRT2 have been indicated to strongly affect the pathological changes of PD and AD; PARP-1 inhibition can profoundly reduce the brain injury in the animal models of multiple neurological diseases; and administration of either NAD(+) or nicotinamide can also decrease ischemic brain damage.	NAD	22-28	sirtuin 1	Homo sapiens	47-52
22124156-1	2012	SIRT1 is an NAD-dependent deacetylase and epigenetic regulator essential for normal mammalian development and homeostasis.	NAD	12-15	sirtuin 1	Homo sapiens	0-5
22157016-1	2012	SIRT1 is one of seven mammalian sirtuin (silent information regulator 2-related) proteins that harbor NAD(+)-dependent protein deacetylase activity and is implicated in multiple metabolic and age-associated pathways and disorders.	NAD	102-108	sirtuin 1	Homo sapiens	0-5
22157016-3	2012	Here we show that the conserved catalytic core domain of SIRT1 has very low catalytic activity toward several known protein substrates, but that regions N- and C-terminal to the catalytic core potentiate catalytic efficiency by between 12- and 45-fold, with the N-terminal domain contributing predominantly to catalytic rate, relatively independent of the nature of the acetyl-lysine protein substrate, and the C-terminal domain contributing significantly to the K(m) for NAD(+).	NAD	472-478	sirtuin 1	Homo sapiens	57-62
22100343-3	2012	Recently, CD38-associated ADP-ribosylcyclase has been reported to use an NAD(P)H oxidase product, NAD(+) or NADP(+), to produce cyclic ADP-ribose (cADPR) or nicotinic acid adenine dinucleotide phosphate, which mediates intracellular Ca(2+) signaling.	NAD	98-104	CD38 antigen	Mus musculus	10-14
23226010-9	2012	Of particular interest was a two-gene transcriptional unit that consisted of genes for a universal stress protein and a sirtuin Sir2 (deacetylase enzyme for NAD+-dependent acetate utilization).	NAD	157-161	sirtuin 1	Homo sapiens	128-132
22106091-0	2012	Targeting sirtuin 1 to improve metabolism: all you need is NAD(+)?	NAD	59-65	sirtuin 1	Homo sapiens	10-19
22106091-2	2012	SIRT1 senses changes in intracellular NAD(+) levels, which reflect energy level, and uses this information to adapt the cellular energy output such that it matches cellular energy requirements.	NAD	38-44	sirtuin 1	Homo sapiens	0-5
22720044-2	2012	The last step of NAD synthesis is the ATP-dependent amidation of deamido-NAD by NAD synthetase (NADS).	NAD	17-20	NAD synthetase 1	Homo sapiens	80-94
22720044-2	2012	The last step of NAD synthesis is the ATP-dependent amidation of deamido-NAD by NAD synthetase (NADS).	NAD	17-20	NAD synthetase 1	Homo sapiens	96-100
22295107-5	2012	The treatment with estradiol (E2), anti-estrogenic agents 4-hydroxytamoxifen and ICI 182780, ERbeta specific ligand DPN and GPR30 agonist G1 led to a rapid activation of p-ERK1/2, suggesting the involvement of ERalpha36, ERbeta and GPR30 in the non-genomic signaling pathway in these cells.	NAD	116-119	G protein-coupled estrogen receptor 1	Homo sapiens	232-237
21917911-9	2011	Of importance, pharmacological inhibition or silencing of the NAD-dependent enzyme SIRT1 abrogated the ability of eNAD to provide protection from staurosporine, having no effect on eNAD-dependent protection from C2-ceramide or N-methyl-N"-nitro-N-nitrosoguanidine.	NAD	62-65	sirtuin 1	Homo sapiens	83-88
21890893-7	2011	Nicotinamide phosphoribosyltransferase (NAMPT) that synthesizes NAD(+) required for SIRT1 activation exerts similar effects on CIITA activity.	NAD	64-70	sirtuin 1	Homo sapiens	84-89
24822350-1	2011	Silence information regulator 2 (Sir2) family is a group of conserved deacetylases, widely existed in organisms from archaea to mammals, and characterized by NAD(+)-dependent deacetylase and ADP-ribosyltransferase activities.	NAD	158-164	sirtuin 1	Homo sapiens	0-31
24822350-1	2011	Silence information regulator 2 (Sir2) family is a group of conserved deacetylases, widely existed in organisms from archaea to mammals, and characterized by NAD(+)-dependent deacetylase and ADP-ribosyltransferase activities.	NAD	158-164	sirtuin 1	Homo sapiens	33-37
21920899-1	2011	The NAD-dependent histone deacetylase silent information regulator 1 (SIRT1) is overexpressed and catalytically activated in a number of human cancers, but recent studies have actually suggested that it may function as a tumor suppressor and metastasis inhibitor in vivo.	NAD	4-7	sirtuin 1	Homo sapiens	38-68
21920899-1	2011	The NAD-dependent histone deacetylase silent information regulator 1 (SIRT1) is overexpressed and catalytically activated in a number of human cancers, but recent studies have actually suggested that it may function as a tumor suppressor and metastasis inhibitor in vivo.	NAD	4-7	sirtuin 1	Homo sapiens	70-75
21913670-4	2011	The Co(II) complex derived from (Bz)NP2 displays dual coordination modes: one in the tetrahedral complex [((Bz)NP2)Co(I)(2)]; and the other in a square pyramidal variant, [((Bz)NP2)Co(I)(2)].	NAD	115-120	neuronal pentraxin 2	Homo sapiens	36-39
21913670-4	2011	The Co(II) complex derived from (Bz)NP2 displays dual coordination modes: one in the tetrahedral complex [((Bz)NP2)Co(I)(2)]; and the other in a square pyramidal variant, [((Bz)NP2)Co(I)(2)].	NAD	115-120	neuronal pentraxin 2	Homo sapiens	111-114
21913670-4	2011	The Co(II) complex derived from (Bz)NP2 displays dual coordination modes: one in the tetrahedral complex [((Bz)NP2)Co(I)(2)]; and the other in a square pyramidal variant, [((Bz)NP2)Co(I)(2)].	NAD	115-120	neuronal pentraxin 2	Homo sapiens	111-114
21913670-4	2011	The Co(II) complex derived from (Bz)NP2 displays dual coordination modes: one in the tetrahedral complex [((Bz)NP2)Co(I)(2)]; and the other in a square pyramidal variant, [((Bz)NP2)Co(I)(2)].	NAD	181-186	neuronal pentraxin 2	Homo sapiens	36-39
21689736-2	2011	In mammals, TDO is mainly expressed in the liver and primarily supplies nicotinamide adenine dinucleotide (NAD(+)).	NAD	72-105	tryptophan 2,3-dioxygenase	Homo sapiens	12-15
21689736-2	2011	In mammals, TDO is mainly expressed in the liver and primarily supplies nicotinamide adenine dinucleotide (NAD(+)).	NAD	107-113	tryptophan 2,3-dioxygenase	Homo sapiens	12-15
21873234-5	2011	BATF, together with c-Jun, transcriptionally inhibited expression of the nicotinamide adenine dinucleotide (NAD(+))-dependent deacetylase Sirt1, resulting in increased histone acetylation of the T-bet locus and increased cellular NAD(+), which increased ATP production.	NAD	73-106	basic leucine zipper ATF-like transcription factor	Homo sapiens	0-4
21873234-5	2011	BATF, together with c-Jun, transcriptionally inhibited expression of the nicotinamide adenine dinucleotide (NAD(+))-dependent deacetylase Sirt1, resulting in increased histone acetylation of the T-bet locus and increased cellular NAD(+), which increased ATP production.	NAD	73-106	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	20-25
21873234-5	2011	BATF, together with c-Jun, transcriptionally inhibited expression of the nicotinamide adenine dinucleotide (NAD(+))-dependent deacetylase Sirt1, resulting in increased histone acetylation of the T-bet locus and increased cellular NAD(+), which increased ATP production.	NAD	73-106	sirtuin 1	Homo sapiens	138-143
21873234-5	2011	BATF, together with c-Jun, transcriptionally inhibited expression of the nicotinamide adenine dinucleotide (NAD(+))-dependent deacetylase Sirt1, resulting in increased histone acetylation of the T-bet locus and increased cellular NAD(+), which increased ATP production.	NAD	108-114	basic leucine zipper ATF-like transcription factor	Homo sapiens	0-4
21873234-5	2011	BATF, together with c-Jun, transcriptionally inhibited expression of the nicotinamide adenine dinucleotide (NAD(+))-dependent deacetylase Sirt1, resulting in increased histone acetylation of the T-bet locus and increased cellular NAD(+), which increased ATP production.	NAD	108-114	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	20-25
21873234-5	2011	BATF, together with c-Jun, transcriptionally inhibited expression of the nicotinamide adenine dinucleotide (NAD(+))-dependent deacetylase Sirt1, resulting in increased histone acetylation of the T-bet locus and increased cellular NAD(+), which increased ATP production.	NAD	108-114	sirtuin 1	Homo sapiens	138-143
21873234-5	2011	BATF, together with c-Jun, transcriptionally inhibited expression of the nicotinamide adenine dinucleotide (NAD(+))-dependent deacetylase Sirt1, resulting in increased histone acetylation of the T-bet locus and increased cellular NAD(+), which increased ATP production.	NAD	230-236	basic leucine zipper ATF-like transcription factor	Homo sapiens	0-4
21873234-5	2011	BATF, together with c-Jun, transcriptionally inhibited expression of the nicotinamide adenine dinucleotide (NAD(+))-dependent deacetylase Sirt1, resulting in increased histone acetylation of the T-bet locus and increased cellular NAD(+), which increased ATP production.	NAD	230-236	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	20-25
21873234-5	2011	BATF, together with c-Jun, transcriptionally inhibited expression of the nicotinamide adenine dinucleotide (NAD(+))-dependent deacetylase Sirt1, resulting in increased histone acetylation of the T-bet locus and increased cellular NAD(+), which increased ATP production.	NAD	230-236	sirtuin 1	Homo sapiens	138-143
21937766-4	2011	We found that rhythmicity of NAD(+) was altered in the CD38-deficient mice.	NAD	29-35	CD38 antigen	Mus musculus	55-59
21937766-8	2011	Metabolomic analysis identified alterations in the circadian levels of several amino acids, specifically tryptophan levels were reduced in the CD38-null mice at a circadian time paralleling with elevated NAD(+) levels.	NAD	204-210	CD38 antigen	Mus musculus	143-147
21615689-0	2011	Reducing expression of NAD+ synthesizing enzyme NMNAT1 does not affect the rate of Wallerian degeneration.	NAD	23-27	nicotinamide nucleotide adenylyltransferase 1	Mus musculus	48-54
21615689-1	2011	NAD(+) synthesizing enzyme NMNAT1 constitutes most of the sequence of neuroprotective protein Wld(S), which delays axon degeneration by 10-fold.	NAD	0-6	nicotinamide nucleotide adenylyltransferase 1	Mus musculus	27-33
21527346-7	2011	One of the motifs contained Arg-229, which participates in interactions with the phosphate group of NADPH and appears be a determinant of the preferential binding of bFMO to NADPH rather than NADH.	NAD	192-196	2,4-dienoyl-CoA reductase 1	Homo sapiens	100-105
20868295-7	2011	This review discusses accumulated data with respect to the AIF structure and outlines evidence that supports the prevalent mechanistic view on the apoptogenic actions of the flavoprotein, as well as the emerging concept of AIF as a redox sensor capable of linking NAD(H)-dependent metabolic pathways to apoptosis.	NAD	264-270	apoptosis inducing factor mitochondria associated 1	Homo sapiens	223-226
21416482-3	2011	Similar transcriptional regulation by Npas2/Bmal1 heterodimer formation operates in the brain, which is dependent on the redox state (i.e., NAD/NADH).	NAD	140-143	neuronal PAS domain protein 2	Rattus norvegicus	38-43
21416482-3	2011	Similar transcriptional regulation by Npas2/Bmal1 heterodimer formation operates in the brain, which is dependent on the redox state (i.e., NAD/NADH).	NAD	140-143	aryl hydrocarbon receptor nuclear translocator-like	Rattus norvegicus	44-49
21416482-3	2011	Similar transcriptional regulation by Npas2/Bmal1 heterodimer formation operates in the brain, which is dependent on the redox state (i.e., NAD/NADH).	NAD	144-148	neuronal PAS domain protein 2	Rattus norvegicus	38-43
21416482-3	2011	Similar transcriptional regulation by Npas2/Bmal1 heterodimer formation operates in the brain, which is dependent on the redox state (i.e., NAD/NADH).	NAD	144-148	aryl hydrocarbon receptor nuclear translocator-like	Rattus norvegicus	44-49
21416483-3	2011	Similar transcriptional regulation by NPAS2/BMAL1 heterodimer formation operates in the brain, which depends on the redox state (i.e., NAD/NADH).	NAD	135-138	neuronal PAS domain protein 2	Rattus norvegicus	38-43
21416483-3	2011	Similar transcriptional regulation by NPAS2/BMAL1 heterodimer formation operates in the brain, which depends on the redox state (i.e., NAD/NADH).	NAD	135-138	aryl hydrocarbon receptor nuclear translocator-like	Rattus norvegicus	44-49
21416483-3	2011	Similar transcriptional regulation by NPAS2/BMAL1 heterodimer formation operates in the brain, which depends on the redox state (i.e., NAD/NADH).	NAD	139-143	neuronal PAS domain protein 2	Rattus norvegicus	38-43
21416483-3	2011	Similar transcriptional regulation by NPAS2/BMAL1 heterodimer formation operates in the brain, which depends on the redox state (i.e., NAD/NADH).	NAD	139-143	aryl hydrocarbon receptor nuclear translocator-like	Rattus norvegicus	44-49
21296058-8	2011	Mass spectrometry analysis of hydrogen peroxide inactivated BADH revealed oxidation of M278, M243, M241 and H335 in the absence and oxidation of M94, M327 and M278 in the presence of NAD(+).	NAD	183-189	aldehyde dehydrogenase 7 family member A1	Homo sapiens	60-64
21296058-9	2011	Molecular modeling of BADH revealed that the oxidized methionine and histidine residues are near the NAD(+) binding site.	NAD	101-107	aldehyde dehydrogenase 7 family member A1	Homo sapiens	22-26
21288303-2	2011	Sirt1 is an NAD-dependent protein deacetylase and a critical factor in the modulation of cellular responses to altered metabolic flux.	NAD	12-15	sirtuin 1	Homo sapiens	0-5
21329659-5	2011	SIRT1 (Sirtuin 1), a NAD-dependent class III histone deacetylase and a member of the sirtuin family of proteins, partially mediates deacetylation of PXR.	NAD	21-24	sirtuin 1	Homo sapiens	0-5
21329659-5	2011	SIRT1 (Sirtuin 1), a NAD-dependent class III histone deacetylase and a member of the sirtuin family of proteins, partially mediates deacetylation of PXR.	NAD	21-24	sirtuin 1	Homo sapiens	7-16
21149440-1	2011	Forkhead transcription factor FoxO1 and the NAD(+)-dependent histone deacetylase SIRT1 are evolutionarily conserved regulators of the development of aging, oxidative stress resistance, insulin resistance, and metabolism in species ranging from invertebrates to mammals.	NAD	44-50	sirtuin 1	Homo sapiens	81-86
21204775-2	2011	Resveratrol (Rsv), a polyphenol that extends the lifespan of diverse species is an activator of SIRT1, a NAD(+) dependent deacetylating enzyme in mammalian cells.	NAD	105-111	sirtuin 1	Homo sapiens	96-101
22068106-1	2011	Arabidopsis thaliana AtNUDT7 Nudix pyrophosphatase hydrolyzes NADH and ADP-ribose in vitro and is an important factor in the cellular response to diverse biotic and abiotic stresses.	NAD	62-66	MutT/nudix family protein	Arabidopsis thaliana	21-28
21586363-4	2011	The CD38/CD157 family of extracellular NADases degrades NAD(+) and generates Ca(2+)-active metabolites, including cyclic ADP ribose and ADP ribose.	NAD	56-62	CD38 antigen	Mus musculus	4-8
20431281-8	2011	Silent mating type information regulation 2 homolog 1 Saccharomyces cerevisiae (SIRT1) is a nicotinamide adenine dinucleotide (NAD+)-dependent histone deacetylase that may also be involved in aging and diseases.	NAD	92-125	sirtuin 1	Homo sapiens	80-85
20431281-8	2011	Silent mating type information regulation 2 homolog 1 Saccharomyces cerevisiae (SIRT1) is a nicotinamide adenine dinucleotide (NAD+)-dependent histone deacetylase that may also be involved in aging and diseases.	NAD	127-131	sirtuin 1	Homo sapiens	80-85
22084601-7	2011	Inhibition of KP metabolism under these conditions can compromise cell viability, NAD-dependent SIRT1 activity and CNS function, unless alternative precursors for NAD(+) synthesis are made available.	NAD	82-85	sirtuin 1	Homo sapiens	96-101
21870251-2	2011	Since PARP-1 gene is expressed constitutively, its activation cannot be surmised from increased expression of its mRNA or protein, but by demonstrating the consequences of its catalytic -reaction which results in consumption of the substrate nicotinamide adenine dinucleotide (NAD(+)) and formation of three products, namely, polymer of ADP-ribose (pADPr or PAR), nicotinamide, and protons.	NAD	242-275	jumping translocation breakpoint	Homo sapiens	6-9
21870251-2	2011	Since PARP-1 gene is expressed constitutively, its activation cannot be surmised from increased expression of its mRNA or protein, but by demonstrating the consequences of its catalytic -reaction which results in consumption of the substrate nicotinamide adenine dinucleotide (NAD(+)) and formation of three products, namely, polymer of ADP-ribose (pADPr or PAR), nicotinamide, and protons.	NAD	277-283	jumping translocation breakpoint	Homo sapiens	6-9
22355666-1	2011	SIRT1 is a NAD+ dependent protein deacetylase known to increase longevity in model organisms.	NAD	11-14	sirtuin 1	Homo sapiens	0-5
21048160-6	2010	A search for the histone deacetylase (HDAC) that counterbalances CLOCK activity revealed that SIRT1, a nicotinamide adenin dinucleotide (NAD(+))-dependent HDAC, functions in a circadian manner.	NAD	137-144	sirtuin 1	Homo sapiens	94-99
20876337-5	2010	The slow-growing mmdh1mmdh2 mutant has elevated leaf respiration rate in the dark and light, without loss of photosynthetic capacity, suggesting that mMDH normally uses NADH to reduce oxaloacetate to malate, which is then exported to the cytosol, rather than to drive mitochondrial respiration.	NAD	169-173	malate dehydrogenase 2, NAD (mitochondrial)	Mus musculus	150-154
20813094-1	2010	Overexpression of SIRT1, a NAD+-dependent class III histone deacetylases (HDACs), is implicated in many cancers and therefore could become a promising antitumor target.	NAD	27-31	sirtuin 1	Homo sapiens	18-23
20685355-4	2010	Ethylenediamine, an o-quinone trap, prevented the formation of o-quinone and oxidations of AA and NADH mediated by tyrosinase bioactivation of CAPE.	NAD	98-102	tyrosinase	Homo sapiens	115-125
20426787-1	2010	BACKGROUND: SIRT1, an NAD(+) -dependent histone/protein deacetylase, controls a broad range of cellular functions.	NAD	22-28	sirtuin 1	Homo sapiens	12-17
20626250-3	2010	We hypothesized that resveratrol (RSV), a polyphenolic molecule that enhances mammalian NAD(+)-dependent SIRT1 deacetylases and may increase life span, would improve motor function and survival in the SOD1 mouse model via modulation of p53 acetylation.	NAD	88-94	sirtuin 1	Homo sapiens	105-110
20638297-5	2010	These studies suggest that insulin signaling underpins mitochondrial electron transport chain integrity and activity by suppressing FOXO1/HMOX1 and maintaining the NAD(+)/NADH ratio, the mediator of the SIRT1/PGC1alpha pathway for mitochondrial biogenesis and function.	NAD	164-170	sirtuin 1	Homo sapiens	203-208
20638297-5	2010	These studies suggest that insulin signaling underpins mitochondrial electron transport chain integrity and activity by suppressing FOXO1/HMOX1 and maintaining the NAD(+)/NADH ratio, the mediator of the SIRT1/PGC1alpha pathway for mitochondrial biogenesis and function.	NAD	171-175	sirtuin 1	Homo sapiens	203-208
20832105-3	2010	Here we show that in liver the activity of PARP-1, an NAD(+)-dependent ADP-ribosyltransferase, oscillates in a daily manner and is regulated by feeding.	NAD	54-60	poly (ADP-ribose) polymerase family, member 1	Mus musculus	43-49
20651248-5	2010	Resveratrol, an activator of the Nicotinamide adenine dinucleotide (NAD) dependent protein deacetylase SIRT1, reversed acetylation but not phosphorylation of Smad3 and inhibited TGF-beta1-induced up-regulation of collagen IV and fibronectin mRNA levels.	NAD	33-66	sirtuin 1	Homo sapiens	103-108
20651248-5	2010	Resveratrol, an activator of the Nicotinamide adenine dinucleotide (NAD) dependent protein deacetylase SIRT1, reversed acetylation but not phosphorylation of Smad3 and inhibited TGF-beta1-induced up-regulation of collagen IV and fibronectin mRNA levels.	NAD	68-71	sirtuin 1	Homo sapiens	103-108
20531298-6	2010	Recently, it became clear that the energy sensor, AMP-activated kinase (AMPK) translates the effects of energy stress into altered Sirt1 activity by regulating the intracellular level of its co-substrate nicotinamide adenine dinucleotide (NAD)(+).	NAD	239-242	sirtuin 1	Homo sapiens	131-136
20704736-2	2010	Several independent studies have demonstrated that Arabidopsis nudix hydrolase 7 (AtNUDT7) hydrolyzes NADH and ADP-ribose.	NAD	102-106	MutT/nudix family protein	Arabidopsis thaliana	82-89
20704736-6	2010	Secondly, we evaluate the biochemical and molecular consequences of increased NADH levels due to loss of function of AtNUDT7 in Arabidopsis.	NAD	78-82	MutT/nudix family protein	Arabidopsis thaliana	117-124
20704736-10	2010	Compared with WT plants, levels of glutathione, NAD+, NADH, and in turn NADH:NAD+ ratio were higher in Atnudt7-1 plants growing in 12:3:1 potting mix.	NAD	48-52	MutT/nudix family protein	Arabidopsis thaliana	103-110
20704736-10	2010	Compared with WT plants, levels of glutathione, NAD+, NADH, and in turn NADH:NAD+ ratio were higher in Atnudt7-1 plants growing in 12:3:1 potting mix.	NAD	54-58	MutT/nudix family protein	Arabidopsis thaliana	103-110
20704736-10	2010	Compared with WT plants, levels of glutathione, NAD+, NADH, and in turn NADH:NAD+ ratio were higher in Atnudt7-1 plants growing in 12:3:1 potting mix.	NAD	72-76	MutT/nudix family protein	Arabidopsis thaliana	103-110
20704736-10	2010	Compared with WT plants, levels of glutathione, NAD+, NADH, and in turn NADH:NAD+ ratio were higher in Atnudt7-1 plants growing in 12:3:1 potting mix.	NAD	77-81	MutT/nudix family protein	Arabidopsis thaliana	103-110
20704736-11	2010	Infiltrating NADH and ADP-ribose into WT leaves was sufficient to induce AtNUDT7 protein.	NAD	13-17	MutT/nudix family protein	Arabidopsis thaliana	73-80
20704736-16	2010	Our data suggests AtNUDT7 plays an important role in maintaining redox homeostasis, particularly for maintaining NADH:NAD+ balance for normal growth and development.	NAD	113-117	MutT/nudix family protein	Arabidopsis thaliana	18-25
20704736-16	2010	Our data suggests AtNUDT7 plays an important role in maintaining redox homeostasis, particularly for maintaining NADH:NAD+ balance for normal growth and development.	NAD	118-122	MutT/nudix family protein	Arabidopsis thaliana	18-25
19879981-0	2010	SIRT1-dependent regulation of chromatin and transcription: linking NAD(+) metabolism and signaling to the control of cellular functions.	NAD	67-73	sirtuin 1	Homo sapiens	0-5
19879981-3	2010	As an NAD(+)-dependent enzyme, SIRT1 regulates gene expression programs in response to cellular metabolic status, thereby coordinating metabolic adaptation of the whole organism.	NAD	6-12	sirtuin 1	Homo sapiens	31-36
19879981-8	2010	Cellular energy state, specifically NAD(+) metabolism, plays a major role in the regulation of SIRT1 activity.	NAD	36-42	sirtuin 1	Homo sapiens	95-100
19879981-9	2010	Recent studies on the NAD(+) biosynthetic enzymes in the salvage pathway, nicotinamide phosphoribosyltransferase (NAMPT) and nicotinamide mononucleotide adenylyltransferase 1 (NMNAT-1), have revealed important functions for these enzymes in SIRT1-dependent transcription regulation.	NAD	22-28	sirtuin 1	Homo sapiens	241-246
20471503-1	2010	NAD(+)-dependent Class III histone deacetylase SIRT1 is a multiple function protein critically involved in stress responses, cellular metabolism and aging through deacetylating a variety of substrates including p53, forkhead-box transcription factors, PGC-1alpha, NF-kappaB, Ku70 and histones.	NAD	0-6	sirtuin 1	Homo sapiens	47-52
20471503-1	2010	NAD(+)-dependent Class III histone deacetylase SIRT1 is a multiple function protein critically involved in stress responses, cellular metabolism and aging through deacetylating a variety of substrates including p53, forkhead-box transcription factors, PGC-1alpha, NF-kappaB, Ku70 and histones.	NAD	0-6	X-ray repair cross complementing 6	Homo sapiens	275-279
20413424-2	2010	Furthermore, because sirtuins require NAD for their deacetylase activity, nicotinamide phosphoribosyltransferase (Nampt), which is a rate-limiting enzyme in the intracellular NAD biosynthetic pathway, influences their activity.	NAD	175-178	nicotinamide phosphoribosyltransferase	Rattus norvegicus	74-112
20413424-2	2010	Furthermore, because sirtuins require NAD for their deacetylase activity, nicotinamide phosphoribosyltransferase (Nampt), which is a rate-limiting enzyme in the intracellular NAD biosynthetic pathway, influences their activity.	NAD	175-178	nicotinamide phosphoribosyltransferase	Rattus norvegicus	114-119
20448046-1	2010	The transcriptional co-activator PGC-1alpha and the NAD(+)-dependent deacetylase SIRT1 are considered important inducers of mitochondrial biogenesis because in the nucleus they regulate transcription of nucleus-encoded mitochondrial genes.	NAD	52-58	sirtuin 1	Homo sapiens	81-86
20465256-1	2010	This study reports the reduction of metmyoglobin (MMb) via oxidation of malate to oxaloacetate and the regeneration of reduced nicotinamide adenine dinucleotide (NADH) via malate dehydrogenase (MDH).	NAD	127-160	malic enzyme 1	Homo sapiens	172-192
20465256-1	2010	This study reports the reduction of metmyoglobin (MMb) via oxidation of malate to oxaloacetate and the regeneration of reduced nicotinamide adenine dinucleotide (NADH) via malate dehydrogenase (MDH).	NAD	162-166	malic enzyme 1	Homo sapiens	172-192
20561897-1	2010	Poly(ADP-ribose) polymerase-1 (PARP-1) is a sensor for DNA strand breaks and some unusual DNA structures and catalyzes poly(ADP-ribosyl)ation of nuclear proteins with NAD(+) serving as substrate.	NAD	167-173	poly (ADP-ribose) polymerase family, member 1	Mus musculus	0-29
20561897-1	2010	Poly(ADP-ribose) polymerase-1 (PARP-1) is a sensor for DNA strand breaks and some unusual DNA structures and catalyzes poly(ADP-ribosyl)ation of nuclear proteins with NAD(+) serving as substrate.	NAD	167-173	poly (ADP-ribose) polymerase family, member 1	Mus musculus	31-37
20188745-1	2010	AIM: Poly(ADP-ribose) polymerase-1 (PARP-1) is a DNA repair enzyme, and its excessive activation, following ischemia, trauma, etc., depletes cellular nicotinamide adenine dinucleotide (NAD(+)) as a substrate and eventually leads to brain cell death.	NAD	150-183	poly (ADP-ribose) polymerase family, member 1	Mus musculus	5-34
20188745-1	2010	AIM: Poly(ADP-ribose) polymerase-1 (PARP-1) is a DNA repair enzyme, and its excessive activation, following ischemia, trauma, etc., depletes cellular nicotinamide adenine dinucleotide (NAD(+)) as a substrate and eventually leads to brain cell death.	NAD	150-183	poly (ADP-ribose) polymerase family, member 1	Mus musculus	36-42
20188745-1	2010	AIM: Poly(ADP-ribose) polymerase-1 (PARP-1) is a DNA repair enzyme, and its excessive activation, following ischemia, trauma, etc., depletes cellular nicotinamide adenine dinucleotide (NAD(+)) as a substrate and eventually leads to brain cell death.	NAD	185-191	poly (ADP-ribose) polymerase family, member 1	Mus musculus	5-34
20188745-1	2010	AIM: Poly(ADP-ribose) polymerase-1 (PARP-1) is a DNA repair enzyme, and its excessive activation, following ischemia, trauma, etc., depletes cellular nicotinamide adenine dinucleotide (NAD(+)) as a substrate and eventually leads to brain cell death.	NAD	185-191	poly (ADP-ribose) polymerase family, member 1	Mus musculus	36-42
20188745-2	2010	Nicotinamide, an NAD(+) precursor and a PARP-1 inhibitor, is known to prevent PARP-1-triggered cell death, but there is no available information on the mechanisms involved in its transport.	NAD	17-23	poly (ADP-ribose) polymerase family, member 1	Mus musculus	78-84
20127344-7	2010	NADP+-dependent IDH activity was determined in comparison with activity of NAD+-dependent IDH and all other NADPH-producing dehydrogenases, glucose-6-phosphate dehydrogenase, 6-phosphogluconate dehydrogenase, malate dehydrogenase, and hexose-6-phosphate dehydrogenase.	NAD	0-3	malic enzyme 1	Homo sapiens	209-229
20149740-4	2010	The NAD(+)-dependent deacetylase SIRT1 mediates adaptation to environmental stresses by adjusting cellular responses to the energetic state of the cell and recent studies highlight important functions of SIRT1 in regulating vascular growth, shape, and function.	NAD	4-10	sirtuin 1	Homo sapiens	33-38
20149740-4	2010	The NAD(+)-dependent deacetylase SIRT1 mediates adaptation to environmental stresses by adjusting cellular responses to the energetic state of the cell and recent studies highlight important functions of SIRT1 in regulating vascular growth, shape, and function.	NAD	4-10	sirtuin 1	Homo sapiens	204-209
20054824-10	2010	Our studies also show the involvement of cAMP-dependent protein kinase A and EPAC1 pathways as well as small GTPase Rac1 in beta-NAD-induced EC barrier enhancement.	NAD	124-132	Rac family small GTPase 1	Homo sapiens	116-120
20054824-11	2010	With these results, we conclude that beta-NAD regulates the pulmonary EC barrier integrity via small GTPase Rac1- and MLCP- dependent signaling pathways.	NAD	37-45	Rac family small GTPase 1	Homo sapiens	108-112
20181750-10	2010	These results indicated that AtNUDX6 is a modulator of NADH rather than ADP-Rib metabolism and that, through induction of TRX-h5 expression, AtNUDX6 significantly impacts the plant immune response as a positive regulator of NPR1-dependent SA signaling pathways.	NAD	55-59	regulatory protein (NPR1)	Arabidopsis thaliana	224-228
19796917-3	2010	Diminished activity of the CD38 ectoenzyme that normally represents a counter-regulatory competitor for the NAD substrate represents one mechanism enhancing ART2.2 activity.	NAD	108-111	CD38 antigen	Mus musculus	27-31
20026609-1	2010	Gpd1p is a cytosolic NAD(+)-dependent glycerol 3-phosphate dehydrogenase that also localizes to peroxisomes and plays an essential role in the cellular response to osmotic stress and a role in redox balance.	NAD	21-27	glycerol-3-phosphate dehydrogenase (NAD(+)) GPD1	Saccharomyces cerevisiae S288C	0-5
20169165-2	2010	SIRT1 is a NAD+ dependent deacetylase that is known to regulate caloric restriction mediated longevity in model organisms, and has also been linked to the insulin/IGF signaling pathway.	NAD	11-14	sirtuin 1	Homo sapiens	0-5
20060806-1	2010	Sirtuin1 (SIRT1) deacetylase and poly(ADP-ribose)-polymerase-1 (PARP-1) respond to environmental cues, and both require NAD(+) cofactor for their enzymatic activities.	NAD	120-126	poly (ADP-ribose) polymerase family, member 1	Mus musculus	33-62
20060806-1	2010	Sirtuin1 (SIRT1) deacetylase and poly(ADP-ribose)-polymerase-1 (PARP-1) respond to environmental cues, and both require NAD(+) cofactor for their enzymatic activities.	NAD	120-126	poly (ADP-ribose) polymerase family, member 1	Mus musculus	64-70
20060806-2	2010	However, the functional link between environmental/oxidative stress-mediated activation of PARP-1 and SIRT1 through NAD(+) cofactor availability is not known.	NAD	116-122	poly (ADP-ribose) polymerase family, member 1	Mus musculus	91-97
20060806-3	2010	We investigated whether NAD(+) depletion by PARP-1 activation plays a role in environmental stimuli/oxidant-induced reduction in SIRT1 activity.	NAD	24-30	poly (ADP-ribose) polymerase family, member 1	Mus musculus	44-50
20060806-5	2010	Pharmacological PARP-1 inhibition prevented oxidant-induced NAD(+) loss and attenuated loss of SIRT1 activity.	NAD	60-66	poly (ADP-ribose) polymerase family, member 1	Mus musculus	16-22
20060806-6	2010	Oxidants decreased SIRT1 activity in lung epithelial cells; however increasing cellular NAD(+) cofactor levels by PARP-1 inhibition or NAD(+) precursors was unable to restore SIRT1 activity.	NAD	88-94	poly (ADP-ribose) polymerase family, member 1	Mus musculus	114-120
20047315-1	2010	Tryptophan 2,3-dioxygenase (TDO) is an essential enzyme in the pathway of NAD biosynthesis and important for all living organisms.	NAD	74-77	tryptophan 2,3-dioxygenase	Homo sapiens	0-26
20047315-1	2010	Tryptophan 2,3-dioxygenase (TDO) is an essential enzyme in the pathway of NAD biosynthesis and important for all living organisms.	NAD	74-77	tryptophan 2,3-dioxygenase	Homo sapiens	28-31
19711072-2	2010	Overexpression of the genes coding for NAD(+)-specific glutamate dehydrogenase (GDH2) of S. cerevisiae or NADPH-utilising glyceraldehyde-3-phosphate dehydrogenase (gapB) of Bacillus subtilis enabled growth of the pgi1 mutant strains on D-glucose.	NAD	39-45	glucose-6-phosphate isomerase	Saccharomyces cerevisiae S288C	213-217
21335947-6	2010	The E2-induced Ngb increase requires estrogen receptor (ER) beta, but not ERalpha, as evaluated by the mimetic effect of ERbeta-specific agonist DPN and by the blockage of E2 effect in ERbeta-silenced SK-N-BE cells.	NAD	145-148	neuroglobin	Homo sapiens	15-18
21208528-6	2010	Initial velocity assays of betaine aldehyde dehydrogenase in the presence of hydrogen peroxide (0-200 muM) showed noncompetitive inhibition with respect to NAD(+) or to betaine aldehyde at saturating concentrations of the other substrate at pH 7.0 or 8.0.	NAD	156-162	aldehyde dehydrogenase 7 family member A1	Homo sapiens	27-57
22219708-3	2010	Silencing information regulator (SirT1), a member of the sirtuin family, is a NAD-dependent histone deacetylase and an essential mediator for longevity in normal cells by calorie restriction.	NAD	78-81	sirtuin 1	Homo sapiens	33-38
20027304-1	2009	SIRT1 is a NAD-dependent deacetylase that regulates a variety of pathways including the stress protection pathway.	NAD	11-14	sirtuin 1	Homo sapiens	0-5
19682970-0	2009	A fluorometric assay of SIRT1 deacetylation activity through quantification of nicotinamide adenine dinucleotide.	NAD	79-112	sirtuin 1	Homo sapiens	24-29
19782043-5	2009	Since NADH:flavorubredoxin oxidoreductase from E. coli, that was shown to reduce ferric Ngb, shares sequence similarity with the human apoptosis-inducing factor (AIF), AIF has been proposed by us as a candidate Ngb reductase.	NAD	6-10	oxidoreductase	Escherichia coli	27-41
19782043-5	2009	Since NADH:flavorubredoxin oxidoreductase from E. coli, that was shown to reduce ferric Ngb, shares sequence similarity with the human apoptosis-inducing factor (AIF), AIF has been proposed by us as a candidate Ngb reductase.	NAD	6-10	neuroglobin	Homo sapiens	88-91
19782043-5	2009	Since NADH:flavorubredoxin oxidoreductase from E. coli, that was shown to reduce ferric Ngb, shares sequence similarity with the human apoptosis-inducing factor (AIF), AIF has been proposed by us as a candidate Ngb reductase.	NAD	6-10	neuroglobin	Homo sapiens	211-214
19462229-1	2009	The nicotinamide adenine dinucleotide (NAD)-activated protein deacetylase Sir2p/Sirt1 has been strongly implicated in the modulation of replicative lifespan and promotion of longevity.	NAD	4-37	sirtuin 1	Homo sapiens	74-79
19462229-1	2009	The nicotinamide adenine dinucleotide (NAD)-activated protein deacetylase Sir2p/Sirt1 has been strongly implicated in the modulation of replicative lifespan and promotion of longevity.	NAD	4-37	sirtuin 1	Homo sapiens	80-85
19462229-1	2009	The nicotinamide adenine dinucleotide (NAD)-activated protein deacetylase Sir2p/Sirt1 has been strongly implicated in the modulation of replicative lifespan and promotion of longevity.	NAD	39-42	sirtuin 1	Homo sapiens	74-79
19462229-1	2009	The nicotinamide adenine dinucleotide (NAD)-activated protein deacetylase Sir2p/Sirt1 has been strongly implicated in the modulation of replicative lifespan and promotion of longevity.	NAD	39-42	sirtuin 1	Homo sapiens	80-85
19948032-9	2009	DPN increased Ckb and s100g only in C1 and P1 rats, respectively.	NAD	0-3	creatine kinase B	Rattus norvegicus	14-17
19887544-0	2009	Experimental cancer therapy using restoration of NAD+ -linked 15-hydroxyprostaglandin dehydrogenase expression.	NAD	49-53	carbonyl reductase 1	Homo sapiens	62-99
19887544-2	2009	It has been shown that expression of NAD(+)-linked 15-hydroxyprostaglandin dehydrogenase (15-PGDH), a key enzyme responsible for PGE(2) inactivation, is suppressed in the majority of cancers, including breast and colon carcinoma.	NAD	37-43	carbonyl reductase 1	Homo sapiens	51-88
19887544-2	2009	It has been shown that expression of NAD(+)-linked 15-hydroxyprostaglandin dehydrogenase (15-PGDH), a key enzyme responsible for PGE(2) inactivation, is suppressed in the majority of cancers, including breast and colon carcinoma.	NAD	37-43	carbonyl reductase 1	Homo sapiens	90-97
19289152-0	2009	From heterochromatin islands to the NAD World: a hierarchical view of aging through the functions of mammalian Sirt1 and systemic NAD biosynthesis.	NAD	36-39	sirtuin 1	Homo sapiens	111-116
19289152-4	2009	Since a surprising discovery of their NAD-dependent deacetylase activity, Sir2 proteins, now called "sirtuins," have been emerging as a critical epigenetic regulator for aging.	NAD	38-41	sirtuin 1	Homo sapiens	74-78
19289152-5	2009	In this review, I will follow the process of conceptual development from the heterochromatin island hypothesis to a novel, comprehensive concept of a systemic regulatory network for mammalian aging, named "NAD World," summarizing recent studies on the mammalian NAD-dependent deacetylase Sirt1 and nicotinamide phosphoribosyltransferase (Nampt)-mediated systemic NAD biosynthesis.	NAD	206-209	sirtuin 1	Homo sapiens	288-293
19289152-5	2009	In this review, I will follow the process of conceptual development from the heterochromatin island hypothesis to a novel, comprehensive concept of a systemic regulatory network for mammalian aging, named "NAD World," summarizing recent studies on the mammalian NAD-dependent deacetylase Sirt1 and nicotinamide phosphoribosyltransferase (Nampt)-mediated systemic NAD biosynthesis.	NAD	262-265	sirtuin 1	Homo sapiens	288-293
19672559-1	2009	Poly(ADP-ribose) polymerase-1 (Parp-1) and the protein deacetylase SirT1 are two of the most effective NAD(+)-consuming enzymes in the cell with key functions in genome integrity and chromatin-based pathways.	NAD	103-109	poly (ADP-ribose) polymerase family, member 1	Mus musculus	0-29
19672559-1	2009	Poly(ADP-ribose) polymerase-1 (Parp-1) and the protein deacetylase SirT1 are two of the most effective NAD(+)-consuming enzymes in the cell with key functions in genome integrity and chromatin-based pathways.	NAD	103-109	poly (ADP-ribose) polymerase family, member 1	Mus musculus	31-37
19716516-0	2009	Structural and mechanistic roles of three consecutive Pro residues of porcine NADH-cytochrome b(5) reductase for the binding of beta-NADH.	NAD	128-137	mitochondrially encoded cytochrome b	Homo sapiens	83-95
19716516-1	2009	Well-conserved three consecutive Pro residues (Pro247-249) in the NADH-binding subdomain of NADH-cytochrome b(5) reductase were proposed to form a basal part of the NADH-binding site.	NAD	66-70	mitochondrially encoded cytochrome b	Homo sapiens	97-109
19716516-1	2009	Well-conserved three consecutive Pro residues (Pro247-249) in the NADH-binding subdomain of NADH-cytochrome b(5) reductase were proposed to form a basal part of the NADH-binding site.	NAD	92-96	mitochondrially encoded cytochrome b	Homo sapiens	97-109
19267881-1	2009	SIRT1, a nicotinamide adenine dinucleotide (NAD(+))-dependent histone/protein deacetylase, has been extensively studied recently for its critical role in the regulation of physiology, calorie restriction and aging.	NAD	9-42	sirtuin 1	Homo sapiens	0-5
19267881-1	2009	SIRT1, a nicotinamide adenine dinucleotide (NAD(+))-dependent histone/protein deacetylase, has been extensively studied recently for its critical role in the regulation of physiology, calorie restriction and aging.	NAD	44-51	sirtuin 1	Homo sapiens	0-5
19645416-1	2009	The tricarboxylic acid cycle NAD+-specific isocitrate dehydrogenase (IDH) of Saccharomyces cerevisiae is an octameric enzyme composed of four heterodimers of regulatory IDH1 and catalytic IDH2 subunits.	NAD	29-33	isocitrate dehydrogenase (NAD(+)) IDH2	Saccharomyces cerevisiae S288C	188-192
19555662-0	2009	Transcriptional activation of NAD+-dependent protein deacetylase SIRT1 by nuclear receptor TLX.	NAD	30-34	sirtuin 1	Homo sapiens	65-70
19519662-5	2009	Our results demonstrate that receptor-internalizing agonists (like DAMGO, beta-endorphin, methadone, piritramide, fentanyl, sufentanil, and etonitazene) strongly induce NADH/NADPH-mediated ROS synthesis via PLD-dependent signaling pathways, whereas agonists that do not induce MOPr endocytosis and PLD2 activation (like morphine, buprenorphine, hydromorphone, and oxycodone) failed to activate ROS synthesis in transfected human embryonic kidney 293 cells.	NAD	169-173	phospholipase D2	Homo sapiens	298-302
19519662-6	2009	These findings indicate that the agonist-selective PLD2 activation plays a key role in the regulation of NADH/NADPH-mediated ROS formation by opioids.	NAD	105-109	phospholipase D2	Homo sapiens	51-55
19621365-2	2009	To illustrate this concept, we examined the factors and levels required for optimization of reaction conditions for the conversion of nicotinamide adenine dinucleotide to nicotinamide adenine dinucleotide, reduced form by glucose-6-phosphate dehydrogenase in the conversion of glucose-6-phosphate to 6-phosphogluconate.	NAD	134-167	glucose-6-phosphate dehydrogenase	Homo sapiens	222-255
19621365-2	2009	To illustrate this concept, we examined the factors and levels required for optimization of reaction conditions for the conversion of nicotinamide adenine dinucleotide to nicotinamide adenine dinucleotide, reduced form by glucose-6-phosphate dehydrogenase in the conversion of glucose-6-phosphate to 6-phosphogluconate.	NAD	171-204	glucose-6-phosphate dehydrogenase	Homo sapiens	222-255
19533035-1	2009	Visfatin (Nampt/PBEF) plays a pivotal role in the salvage pathway for NAD(+) biosynthesis.	NAD	70-76	nicotinamide phosphoribosyltransferase	Rattus norvegicus	0-8
19533035-1	2009	Visfatin (Nampt/PBEF) plays a pivotal role in the salvage pathway for NAD(+) biosynthesis.	NAD	70-76	nicotinamide phosphoribosyltransferase	Rattus norvegicus	10-15
19533035-1	2009	Visfatin (Nampt/PBEF) plays a pivotal role in the salvage pathway for NAD(+) biosynthesis.	NAD	70-76	nicotinamide phosphoribosyltransferase	Rattus norvegicus	16-20
19454650-6	2009	Additionally, extracellular ADPR production by the ectoenzyme CD38 from its substrates NAD+ (nicotinamide adenine dinucleotide) or cADPR causes IP3-dependent Ca2+ release via P2Y and adenosine receptors.	NAD	87-91	CD38 antigen	Mus musculus	62-66
19454650-6	2009	Additionally, extracellular ADPR production by the ectoenzyme CD38 from its substrates NAD+ (nicotinamide adenine dinucleotide) or cADPR causes IP3-dependent Ca2+ release via P2Y and adenosine receptors.	NAD	93-126	CD38 antigen	Mus musculus	62-66
19458223-3	2009	The Wld(s) protein is normally localized to the nucleus, and contains the N terminus of ubiquitination factor Ube4b fused to full-length Nmnat1, an NAD biosynthetic enzyme.	NAD	148-151	nicotinamide nucleotide adenylyltransferase 1	Mus musculus	137-143
19439605-2	2009	We previously showed that increased nicotinamide adenine dinucleotide (NAD)-synthesizing activity by overexpression of nicotinamide mononucleotide adenylyltransferase (NMNAT) is the essential component of the Wld(s) protein, the expression of which is responsible for the delayed Wallerian degeneration phenotype in wld(s) mice.	NAD	36-69	nicotinamide nucleotide adenylyltransferase 1	Mus musculus	168-173
19439605-2	2009	We previously showed that increased nicotinamide adenine dinucleotide (NAD)-synthesizing activity by overexpression of nicotinamide mononucleotide adenylyltransferase (NMNAT) is the essential component of the Wld(s) protein, the expression of which is responsible for the delayed Wallerian degeneration phenotype in wld(s) mice.	NAD	71-74	nicotinamide nucleotide adenylyltransferase 1	Mus musculus	168-173
19262508-6	2009	AMPK enhances SIRT1 activity by increasing cellular NAD+ levels, resulting in the deacetylation and modulation of the activity of downstream SIRT1 targets that include the peroxisome proliferator-activated receptor-gamma coactivator 1alpha and the forkhead box O1 (FOXO1) and O3 (FOXO3a) transcription factors.	NAD	52-56	forkhead box O3	Mus musculus	280-286
19302375-3	2009	Nicotinamide phosphoribosyltransferase (Nampt), also known as PBEF and visfatin, is rate-limiting for NAD+ salvage from nicotinamide and confers resistance to oxidative stress via SIRT1.	NAD	102-106	sirtuin 1	Homo sapiens	180-185
19136651-4	2009	RESEARCH DESIGN AND METHODS: We used beta-lapachone (betaL), a natural substrate of NADH:quinone oxidoreductase 1 (NQO1), to stimulate NADH oxidation.	NAD	84-88	NAD(P)H dehydrogenase, quinone 1	Mus musculus	115-119
19136651-7	2009	RESULTS: NQO1-dependent NADH oxidation by betaL strongly provoked mitochondrial fatty acid oxidation in vitro and in vivo.	NAD	24-28	NAD(P)H dehydrogenase, quinone 1	Mus musculus	9-13
19136651-11	2009	CONCLUSIONS: Pharmacological activation of NADH oxidation by NQO1 resolves obesity and related phenotypes in mice, opening the possibility that it may provide the basis for a new therapy for the treatment of metabolic syndrome.	NAD	43-47	NAD(P)H dehydrogenase, quinone 1	Mus musculus	61-65
19071213-1	2009	Resveratrol increases longevity through SirT1, which is activated with NAD(+) supplied by an anti-aging enzyme PBEF.	NAD	71-77	nicotinamide phosphoribosyltransferase	Rattus norvegicus	111-115
19237596-2	2009	This unusual chimeric protein fuses a 70-amino acid N-terminal sequence from the Ube4b multiubiquitination factor with the nicotinamide adenine dinucleotide-synthesizing enzyme nicotinamide mononucleotide adenylyl transferase 1.	NAD	123-156	nicotinamide nucleotide adenylyltransferase 1	Mus musculus	177-227
19056727-4	2009	As many type II NAD(P)H dehydrogenases, Nda2 uses NADH as a preferential substrate, but in contrast to the eukaryotic enzymes described so far, contains non-covalently bound FMN as a cofactor.	NAD	50-54	uncharacterized protein	Chlamydomonas reinhardtii	40-44
19056727-7	2009	Chlorophyll fluorescence measurements performed on thylakoid membranes show that Nda2 is able to interact with thylakoid membranes of C. reinhardtii by reducing PQs from exogenous NADH or NADPH.	NAD	180-184	uncharacterized protein	Chlamydomonas reinhardtii	81-85
19178345-2	2009	The detection limit can reach down to 0.2 amol of NAD(+) and 1 amol of NADH with a homemade capillary electrophoresis laser-induced fluorescence (CE-LIF) setup.	NAD	50-56	LIF, interleukin 6 family cytokine	Rattus norvegicus	149-152
19178345-2	2009	The detection limit can reach down to 0.2 amol of NAD(+) and 1 amol of NADH with a homemade capillary electrophoresis laser-induced fluorescence (CE-LIF) setup.	NAD	71-75	LIF, interleukin 6 family cytokine	Rattus norvegicus	149-152
19124283-3	2009	METHODS: FALDH activity was determined by incubating fibroblast homogenates with omega-hydroxy-C22:0 in the presence of NAD(+).	NAD	120-126	aldehyde dehydrogenase 3 family member A2	Homo sapiens	9-14
19372760-6	2009	The phenotype is attributed to the overexpression of a chimeric protein Wlds which contains a short fragment of the ubiquitin assembly protein UFD2 and the full-length nicotinamide adenine dinucleotide (NAD) synthetic enzyme Nicotinamide mononucleotide adenylyl-transferase-1 (Nmnat-1).	NAD	168-201	nicotinamide nucleotide adenylyltransferase 1	Mus musculus	225-275
19149601-3	2009	SIRT1 is an NAD-dependent deacetylase with critical functions in the maintenance of homeostasis and cell survival.	NAD	12-15	sirtuin 1	Homo sapiens	0-5
18922599-2	2009	Over-expression of the NAD+-dependent histone deacetylase Sirt1 increased MPC proliferation and cell cycle progression as evidenced by increased 5-bromo-2"-deoxyuridine (BrdU) incorporation, an increase in cell number, proliferating cell nuclear antigen expression, and the phosphorylation of retinoblastoma protein.	NAD	23-27	sirtuin 1	Homo sapiens	58-63
18817890-9	2009	In addition, the HDAC activity of the NAD(+)-dependent SIRT1 enzyme is regulated in a circadian manner.	NAD	38-44	sirtuin 1	Homo sapiens	55-60
18563176-3	2009	SIRT1, the human ortholog of the yeast Sir2 by closest sequence similarity, is a nicotinamide adenine dinucleotide (NAD(+))-dependent deacetylase with enzymatic properties indistinguishable from the yeast enzyme.	NAD	81-114	sirtuin 1	Homo sapiens	0-5
18563176-3	2009	SIRT1, the human ortholog of the yeast Sir2 by closest sequence similarity, is a nicotinamide adenine dinucleotide (NAD(+))-dependent deacetylase with enzymatic properties indistinguishable from the yeast enzyme.	NAD	81-114	sirtuin 1	Homo sapiens	39-43
18563176-3	2009	SIRT1, the human ortholog of the yeast Sir2 by closest sequence similarity, is a nicotinamide adenine dinucleotide (NAD(+))-dependent deacetylase with enzymatic properties indistinguishable from the yeast enzyme.	NAD	116-122	sirtuin 1	Homo sapiens	0-5
18563176-3	2009	SIRT1, the human ortholog of the yeast Sir2 by closest sequence similarity, is a nicotinamide adenine dinucleotide (NAD(+))-dependent deacetylase with enzymatic properties indistinguishable from the yeast enzyme.	NAD	116-122	sirtuin 1	Homo sapiens	39-43
19352492-8	2009	CONCLUSIONS/SIGNIFICANCE: Pxmp2 is the first peroxisomal channel identified, and its existence leads to prediction that the mammalian peroxisomal membrane is permeable to small solutes while transfer of "bulky" metabolites, e.g., cofactors (NAD/H, NADP/H, and CoA) and ATP, requires specific transporters.	NAD	241-244	peroxisomal membrane protein 2	Homo sapiens	26-31
19390637-5	2009	We found that Saccharomyces cerevisiae cells null for all GAPDH paralogues (Tdh1, Tdh2, and Tdh3) survived the counter-selection of a GAPDH-encoding plasmid when the NAD(+) metabolizing deacetylase Sir2 was overexpressed.	NAD	166-172	glyceraldehyde-3-phosphate dehydrogenase (phosphorylating) TDH1	Saccharomyces cerevisiae S288C	76-80
18957417-1	2008	SirT1 is an NAD-dependent histone deacetylase that regulates gene expression, differentiation, development, and organism life span.	NAD	12-15	sirtuin 1	Homo sapiens	0-5
19020091-2	2008	Cotransforming rho degrees cells with the NADH dehydrogenase of Saccharomyces cerevisiae, Ndi1 and Aox recovered the NADH DH/CoQ reductase and the CoQ oxidase activities.	NAD	42-46	acyl-CoA oxidase 1	Homo sapiens	99-102
19020091-4	2008	Coexpression of AOX and NDI1 further improves the recycling of NAD(+).	NAD	63-69	acyl-CoA oxidase 1	Homo sapiens	16-19
19029811-3	2008	At least two proteins are activated in response to reduced nutrient availability: AMP-activated protein kinase (AMPK) and NAD(+)-dependent deacetylase SIRT1.	NAD	122-128	sirtuin 1	Homo sapiens	151-156
19261981-3	2008	Sir2 encodes a NAD(+)-dependent histone deacetylase and its overexpression extends the lifespan through silencing of specific chromatin regions.	NAD	15-21	sirtuin 1	Homo sapiens	0-4
18799617-4	2008	H3 K56 is acetylated by Rtt109p before its incorporation into chromatin during S phase, and this modification is then removed by the NAD(+)-dependent deacetylases Hst3p and Hst4p during G2/M phase.	NAD	133-139	NAD-dependent histone deacetylase HST4	Saccharomyces cerevisiae S288C	173-178
18588503-7	2008	One, the glycerol-phosphate shuttle plays as major a role in NADH oxidation in ASE cell mitochondria as it does in insect muscle mitochondria.	NAD	61-65	arylsulfatase L	Homo sapiens	79-82
18838864-1	2008	Mammalian SIRT1 is an NAD-dependent deacetylase with critical roles in the maintenance of homeostasis and cell survival.	NAD	22-25	sirtuin 1	Homo sapiens	10-15
18588919-5	2008	This recombinant cattle tick protein has potent NAD(+)-dependent SSADH activity, but possesses also marked enzymatic activity on other aliphatic and aromatic aldehyde substrates.	NAD	48-54	aldehyde dehydrogenase 5 family member A1	Homo sapiens	65-70
18605724-4	2008	However, while cofactor depletion by clip 1 was in part restored by subsequent NAD(+) addition, the tweezer (2) inhibition requires the competitive action of lysine derivatives.	NAD	79-85	CAP-Gly domain containing linker protein 1	Homo sapiens	37-43
18358225-2	2008	In this paper, two distinct assays to measure SIRT1 activity are described: a microfluidic mobility shift assay utilizing a fluorophore-labeled peptide substrate and a bioluminescence assay based upon quantitation of remaining NAD(+).	NAD	227-233	sirtuin 1	Homo sapiens	46-51
18445470-6	2008	In the final step, the ammonia is then converted to NAD by NAD synthetase (EC 6.3.1.5).	NAD	52-55	NAD synthetase 1	Homo sapiens	59-73
18295330-1	2008	NADH:ubiquinone oxidoreductase or complex I is a large multisubunit assembly of the mitochondrial inner membrane that channels high-energy electrons from metabolic NADH into the electron transport chain (ETC).	NAD	0-4	thioredoxin reductase 1	Homo sapiens	16-30
19080518-8	2008	However, HSP, JAK2 and NADH genes had significantly higher copy numbers in group 1 than in group 2 (5766, 7653, 3200 in group 1 and 3341, 3094, 1522 in group 2, respectively; all P &lt; 0.05).	NAD	23-27	heat shock protein 90 beta family member 2, pseudogene	Homo sapiens	9-12
18585217-0	2008	Electrocatalytic oxidation of NADH at gold nanoparticles loaded poly(3,4-ethylenedioxythiophene)-poly(styrene sulfonic acid) film modified electrode and integration of alcohol dehydrogenase for alcohol sensing.	NAD	30-34	aldo-keto reductase family 1 member A1	Homo sapiens	168-189
18182499-7	2008	The first is mediated by an as yet unidentified, microsomal NAD(+)-dependent alcohol dehydrogenase and fatty aldehyde dehydrogenase, which is encoded by the ALDH3A2 gene and is deficient in patients with Sjogren-Larsson syndrome.	NAD	60-66	aldehyde dehydrogenase 3 family member A2	Homo sapiens	103-131
18182499-7	2008	The first is mediated by an as yet unidentified, microsomal NAD(+)-dependent alcohol dehydrogenase and fatty aldehyde dehydrogenase, which is encoded by the ALDH3A2 gene and is deficient in patients with Sjogren-Larsson syndrome.	NAD	60-66	aldehyde dehydrogenase 3 family member A2	Homo sapiens	157-164
18418069-5	2008	Hence, we propose that DBC1 and its homologs are likely to regulate the activity of SIRT1 or related deacetylases by sensing the soluble products or substrates of the NAD-dependent deacetylation reaction.	NAD	167-170	sirtuin 1	Homo sapiens	84-89
18041763-0	2008	Polyubiquitylation of PARP-1 through ubiquitin K48 is modulated by activated DNA, NAD+, and dipeptides.	NAD	82-86	poly (ADP-ribose) polymerase family, member 1	Mus musculus	22-28
18041763-1	2008	Poly(ADP-ribose) polymerase-1 (PARP-1) is the most abundant and the best-studied isoform of a family of enzymes that catalyze the polymerization of ADP-ribose from NAD(+) onto target proteins.	NAD	164-170	poly (ADP-ribose) polymerase family, member 1	Mus musculus	0-29
18041763-1	2008	Poly(ADP-ribose) polymerase-1 (PARP-1) is the most abundant and the best-studied isoform of a family of enzymes that catalyze the polymerization of ADP-ribose from NAD(+) onto target proteins.	NAD	164-170	poly (ADP-ribose) polymerase family, member 1	Mus musculus	31-37
18041763-7	2008	NAD(+) inhibited ubiquitylation of PARP-1, while dipeptides ArgAla and LeuAla enhanced ubiquitylation of PARP-1.	NAD	0-6	poly (ADP-ribose) polymerase family, member 1	Mus musculus	35-41
18310337-5	2008	Proteomic, enzymatic, and Western blot analyses identified the approximately 50-kDa protein as an NAD(+)- and metal ion-dependent phospho-alpha-glucosidase.	NAD	98-104	LSEI_2686	Lactobacillus paracasei ATCC 334	138-155
18174544-2	2008	Human sirtuin (SIRT1), an antiaging and antiinflammatory protein, is a metabolic NAD(+)-dependent protein/histone deacetylase that regulates proinflammatory mediators by deacetylating histone and nonhistone proteins.	NAD	81-87	sirtuin 1	Homo sapiens	15-20
18239056-3	2008	The present study tests the hypothesis that activation of SREBP-1 by ethanol may be mediated by mammalian sirtuin 1 (SIRT1), a NAD(+)-dependent class III protein deacetylase.	NAD	127-133	sirtuin 1	Homo sapiens	106-115
18239056-3	2008	The present study tests the hypothesis that activation of SREBP-1 by ethanol may be mediated by mammalian sirtuin 1 (SIRT1), a NAD(+)-dependent class III protein deacetylase.	NAD	127-133	sirtuin 1	Homo sapiens	117-122
17989923-6	2008	The metabolic model predicted the involvement of a transhydrogenase that generates additional NADH from NADPH, thereby increasing ATP regeneration in the respiratory chain.	NAD	94-98	2,4-dienoyl-CoA reductase 1	Homo sapiens	104-109
18198128-4	2008	In addition, we introduced a novel reduction protocol for metNgb based on NADH:flavorubredoxin oxidoreductase (FlRd-red) from Escherichia coli, a candidate for the Ngb reducing activity recently identified in E. coli extracts.	NAD	74-78	neuroglobin	Homo sapiens	61-64
18329615-2	2008	We find that the viral transactivator Tat promotes hyperactivation of T cells by blocking the nicotinamide adenine dinucleotide (NAD(+))-dependent deacetylase SIRT1.	NAD	94-127	sirtuin 1	Homo sapiens	159-164
18329615-2	2008	We find that the viral transactivator Tat promotes hyperactivation of T cells by blocking the nicotinamide adenine dinucleotide (NAD(+))-dependent deacetylase SIRT1.	NAD	129-136	sirtuin 1	Homo sapiens	159-164
18320031-1	2008	Sir2, a NAD-dependent deacetylase, modulates lifespan in yeasts, worms and flies.	NAD	8-11	sirtuin 1	Homo sapiens	0-4
18250367-2	2008	Studies suggest that c-src activates the reduced nicotinamide-adenine dinucleotide phosphate (NADPH) oxidase/superoxide system, and reactive oxygen species stimulate the RhoA/Rho kinase pathway.	NAD	49-82	SRC proto-oncogene, non-receptor tyrosine kinase	Rattus norvegicus	21-26
18166151-3	2008	Here we show that extracellular NAD enhances Fcgamma receptor (FcgammaR)-mediated phagocytosis in J774A.1 macrophages via the conversion into cyclic ADP-ribose (cADPR), a potent calcium mobilizer, by CD38, an ADP-ribosyl cyclase.	NAD	32-35	CD38 antigen	Mus musculus	200-204
18166151-4	2008	Extracellular NAD increased the phagocytosis of IgG-coated sheep red blood cells (IgG-SRBC) in J774A.1 macrophages, which was completely abolished by pretreatment of 8-bromo-cADPR, an antagonist of cADPR, or CD38 knockdown.	NAD	14-17	CD38 antigen	Mus musculus	208-212
18166151-5	2008	Extracellular NAD increased basal intracellular Ca(2+) concentration, which also was abolished by pretreatment of 8-bromo-cADPR or CD38 knockdown.	NAD	14-17	CD38 antigen	Mus musculus	131-135
18204789-1	2008	The sirtuin 1 protein (SIRT1) is a member of the class III NAD+-dependent histone deacetylases, which are also referred to as the "sirtuins".	NAD	59-62	sirtuin 1	Homo sapiens	4-13
18204789-1	2008	The sirtuin 1 protein (SIRT1) is a member of the class III NAD+-dependent histone deacetylases, which are also referred to as the "sirtuins".	NAD	59-62	sirtuin 1	Homo sapiens	23-28
18235502-1	2008	SIRT1 is an NAD-dependent deacetylase critically involved in stress responses, cellular metabolism and, possibly, ageing.	NAD	12-15	sirtuin 1	Homo sapiens	0-5
19734127-8	2008	The prevailing hypothesis is that products of Akt activation, c-FLIP and XIAP, which exhibit anticaspase activities to block FAS signaling when sphingosine-1-phospate is elevated, are down regulated to permit apoptosis when sphingosine-1-phosphate is decreased by inhibition of sphingosine kinase under conditions of elevated cytosolic NADH associated with anticancer drug inhibition of ENOX2.	NAD	336-340	X-linked inhibitor of apoptosis	Homo sapiens	73-77
18336298-2	2008	Thus far, eighteen HDAC family members have been identified and they can be divided into two categories, i.e., zinc-dependent enzymes (HDAC1-11) and NAD(+)-dependent enzymes (SIRT1-7).	NAD	149-155	sirtuin 1	Homo sapiens	175-180
19107194-1	2008	BACKGROUND: SIR2 is an NAD(+)-dependent deacetylase [1]-[3] implicated in the regulation of lifespan in species as diverse as yeast [4], worms [5], and flies [6].	NAD	23-29	sirtuin 1	Homo sapiens	12-16
18804703-5	2008	The MTHFD2 protein is a bifunctional protein with dehydrogenase and cyclohydrolase activities that arose from a trifunctional precursor through the loss of the synthetase domain and a novel adaptation to NAD rather than NADP specificity for the dehydrogenase.	NAD	204-207	methylenetetrahydrofolate dehydrogenase (NADP+ dependent) 2, methenyltetrahydrofolate cyclohydrolase	Homo sapiens	4-10
18371655-6	2007	The CNF film promotes better the electron transfer of NADH minimizing the oxidation potential at +0.352 V. Moreover higher currents for the NADH oxidation peak have been observed for these electrodes.	NAD	54-58	NPHS1 adhesion molecule, nephrin	Homo sapiens	4-7
18371655-6	2007	The CNF film promotes better the electron transfer of NADH minimizing the oxidation potential at +0.352 V. Moreover higher currents for the NADH oxidation peak have been observed for these electrodes.	NAD	140-144	NPHS1 adhesion molecule, nephrin	Homo sapiens	4-7
18025229-1	2007	The ectoenzyme CD38 catalyzes the production of cyclic ADP-ribose (cADPR) and ADP-ribose (ADPR) from its substrate, NAD(+).	NAD	116-122	CD38 antigen	Mus musculus	15-19
18047806-7	2007	Incubation of hGDH2 was uncompetitive with respect of NADH and non-competitive with respect of 2-oxoglutarate.	NAD	54-58	glutamate dehydrogenase 2	Homo sapiens	14-19
17901049-1	2007	NAD+ -dependent Sir2 family deacetylases and insulin signaling pathway are both conserved across species to regulate aging process.	NAD	0-4	sirtuin 1	Homo sapiens	16-20
18004385-5	2007	SIRT1 is an NAD+-dependent deacetylase that targets histone H4 at lysine 16 (refs 3 and 4), and through an unknown mechanism facilitates increased levels of H3K9me3 (ref.	NAD	12-15	sirtuin 1	Homo sapiens	0-5
17961220-2	2007	The main function of PARP-1 is to catalyze the transfer of ADP-ribose units from nicotinamide adenine dinucleotide (NAD+) to a large array of acceptor proteins, which comprises histones, transcription factors, as well as PARP-1 itself.	NAD	81-114	poly (ADP-ribose) polymerase family, member 1	Mus musculus	21-27
17961220-2	2007	The main function of PARP-1 is to catalyze the transfer of ADP-ribose units from nicotinamide adenine dinucleotide (NAD+) to a large array of acceptor proteins, which comprises histones, transcription factors, as well as PARP-1 itself.	NAD	81-114	poly (ADP-ribose) polymerase family, member 1	Mus musculus	221-227
17961220-2	2007	The main function of PARP-1 is to catalyze the transfer of ADP-ribose units from nicotinamide adenine dinucleotide (NAD+) to a large array of acceptor proteins, which comprises histones, transcription factors, as well as PARP-1 itself.	NAD	116-120	poly (ADP-ribose) polymerase family, member 1	Mus musculus	21-27
17961220-2	2007	The main function of PARP-1 is to catalyze the transfer of ADP-ribose units from nicotinamide adenine dinucleotide (NAD+) to a large array of acceptor proteins, which comprises histones, transcription factors, as well as PARP-1 itself.	NAD	116-120	poly (ADP-ribose) polymerase family, member 1	Mus musculus	221-227
17938244-1	2007	The nicotinamide adenine dinucleotide (NAD(+))-dependent histone deacetylase Sir2 regulates life-span in various species.	NAD	4-37	sirtuin 1	Homo sapiens	77-81
17938244-1	2007	The nicotinamide adenine dinucleotide (NAD(+))-dependent histone deacetylase Sir2 regulates life-span in various species.	NAD	39-46	sirtuin 1	Homo sapiens	77-81
17919258-3	2007	PARP overactivation, on the one hand, depletes its substrate, NAD+, slowing the rate of glycolysis, electron transport, and ATP formation, eventually leading to the functional impairment or death of the endothelial cells and cardiomyocytes.	NAD	62-66	poly (ADP-ribose) polymerase family, member 1	Mus musculus	0-4
17603759-6	2007	Mitochondrial fractions also contained an NADH-linked, "alpha-ketoglutarate reductase", which similarly co-purified with mitochondrial L-malate dehydrogenase (mMDH).	NAD	42-46	malate dehydrogenase 2, NAD (mitochondrial)	Mus musculus	159-163
17555954-2	2007	Enzyme ADH (alcohol dehydrogenase) and its coenzyme NAD+ have been used to improve the selectivity of the sensor.	NAD	52-56	aldo-keto reductase family 1 member A1	Homo sapiens	7-10
17555954-2	2007	Enzyme ADH (alcohol dehydrogenase) and its coenzyme NAD+ have been used to improve the selectivity of the sensor.	NAD	52-56	aldo-keto reductase family 1 member A1	Homo sapiens	12-33
17761430-5	2007	Most probably, plants use both enzymes (B5R and CPR) and their respective electron donors (NADH and NADPH) to reduce cytochrome b(5), which can donate reducing equivalents to a series of lipid-modification reactions such as desaturation and hydroxylation.	NAD	91-95	NADPH--cytochrome P450 reductase-like	Gossypium hirsutum	48-51
17692540-4	2007	The ability of TCR-dependent Ca(2+) signals to stimulate mitochondrial NADH production in excess of that utilized for ATP synthesis was dependent on Bax and Bak.	NAD	71-75	BCL2 antagonist/killer 1	Homo sapiens	157-160
17289849-6	2007	Here, we present the first evidence that microsomal nicotinamide adenine dinucleotide-dependent 3alpha-hydroxysteroid dehydrogenase/epimerase activities are widely distributed in human tissues with the highest activity levels found in liver and testis and lower levels in lung, spleen, brain, kidney, and ovary.	NAD	52-85	dehydrogenase/reductase 9	Homo sapiens	96-131
17481556-1	2007	15-hydroxyprostaglandin dehydrogenase (15-PGDH) catalyzes NAD(+)-linked oxidation of 15 (S)-hydroxyl group of prostaglandins and lipoxins and is the key enzyme responsible for the biological inactivation of these eicosanoids.	NAD	58-64	carbonyl reductase 1	Homo sapiens	0-37
17481556-1	2007	15-hydroxyprostaglandin dehydrogenase (15-PGDH) catalyzes NAD(+)-linked oxidation of 15 (S)-hydroxyl group of prostaglandins and lipoxins and is the key enzyme responsible for the biological inactivation of these eicosanoids.	NAD	58-64	carbonyl reductase 1	Homo sapiens	39-46
17307730-6	2007	Nampt-mediated SMC lifespan extension was associated with increased activity of the NAD+-dependent longevity enzyme SIRT1 and was abrogated in Nampt-overexpressing cells transduced with a dominant-negative form of SIRT1 (H363Y).	NAD	84-88	sirtuin 1	Homo sapiens	116-121
17307730-6	2007	Nampt-mediated SMC lifespan extension was associated with increased activity of the NAD+-dependent longevity enzyme SIRT1 and was abrogated in Nampt-overexpressing cells transduced with a dominant-negative form of SIRT1 (H363Y).	NAD	84-88	sirtuin 1	Homo sapiens	214-219
17207661-2	2007	Here, we describe the evidence that the silent information regulator 2 (SIR2) gene, which encodes a nicotinamide adenine dinucleotide (NAD)-dependent deacetylase, regulates lifespan and mediates CR in lower species such as Saccharomyces cerevisiae and Caenorhabditis elegans.	NAD	100-133	sirtuin 1	Homo sapiens	72-76
17207661-2	2007	Here, we describe the evidence that the silent information regulator 2 (SIR2) gene, which encodes a nicotinamide adenine dinucleotide (NAD)-dependent deacetylase, regulates lifespan and mediates CR in lower species such as Saccharomyces cerevisiae and Caenorhabditis elegans.	NAD	135-138	sirtuin 1	Homo sapiens	72-76
17173333-1	2007	The enzyme glyoxylate reductase reversibly reduces glyoxylate to glycolate, or alternatively hydroxypyruvate to D-glycerate, using either NADPH or NADH as a co-factor.	NAD	147-151	glyoxylate reductase	Saccharomyces cerevisiae S288C	11-31
17595514-0	2007	H2O2 accelerates cellular senescence by accumulation of acetylated p53 via decrease in the function of SIRT1 by NAD+ depletion.	NAD	112-116	sirtuin 1	Homo sapiens	103-108
17595514-1	2007	It has been reported that p53 acetylation, which promotes cellular senescence, can be regulated by the NAD(+)-dependent deacetylase SIRT1, the human homolog of yeast Sir2, a protein that modulates lifespan.	NAD	103-109	sirtuin 1	Homo sapiens	132-137
17099246-1	2006	The nicotinamide adenine dinucleotide (NAD(+))-dependent protein deacetylase SIRT1 has been linked to fatty acid metabolism via suppression of peroxysome proliferator-activated receptor gamma (PPAR-gamma) and to inflammatory processes by deacetylating the transcription factor NF-kappaB.	NAD	4-37	sirtuin 1	Homo sapiens	77-82
17119153-2	2006	The mammalian sirtuin SIRT1 has been shown to deacetylate several proteins in an NAD(+)-dependent manner.	NAD	81-87	sirtuin 1	Homo sapiens	22-27
17125375-1	2006	A highly efficient photocatalytic system for hydrogen evolution with dihydronicotinamide coenzyme (NADH) as a sacrificial agent in an aqueous solution has been constructed by using water-soluble platinum clusters functionalized with methyl viologen-alkanethiol (MVA2+) and a simple electron-donor dyad, 9-mesityl-10-methylacridinium ion (Acr+-Mes), which is capable of fast photoinduced electron transfer but extremely slow back electron transfer.	NAD	99-103	centrosomal protein 57	Homo sapiens	262-266
17125375-6	2006	This indicates electron transfer from NAD* to Acr+-Mes to give Acr*-Mes, which undergoes the electron-transfer reduction of MVA2+-PtC, leading to the efficient hydrogen evolution.	NAD	38-42	centrosomal protein 57	Homo sapiens	124-128
17172838-5	2006	Removal of K56 acetylation takes place in the G2/M phase of the cell cycle and is dependent upon Hst3 and Hst4, two proteins that are related to the NAD+-dependent histone deacetylase Sir2.	NAD	149-153	NAD-dependent histone deacetylase HST4	Saccharomyces cerevisiae S288C	106-110
16923962-5	2006	Human SIRT1 (hSIRT1) repression of DHT-induced AR signaling requires the NAD-dependent catalytic function of hSIRT1 and the AR lysine residues deacetylated by SIRT1.	NAD	73-76	sirtuin 1	Homo sapiens	6-11
16923962-5	2006	Human SIRT1 (hSIRT1) repression of DHT-induced AR signaling requires the NAD-dependent catalytic function of hSIRT1 and the AR lysine residues deacetylated by SIRT1.	NAD	73-76	sirtuin 1	Homo sapiens	13-19
16923962-5	2006	Human SIRT1 (hSIRT1) repression of DHT-induced AR signaling requires the NAD-dependent catalytic function of hSIRT1 and the AR lysine residues deacetylated by SIRT1.	NAD	73-76	sirtuin 1	Homo sapiens	109-115
16923962-5	2006	Human SIRT1 (hSIRT1) repression of DHT-induced AR signaling requires the NAD-dependent catalytic function of hSIRT1 and the AR lysine residues deacetylated by SIRT1.	NAD	73-76	sirtuin 1	Homo sapiens	14-19
17098719-1	2006	Sirt1 (Sirtuin type 1), a member of the conserved sirtuin family, is a NAD+ -dependent histone deacetylase.	NAD	71-75	sirtuin 1	Homo sapiens	0-5
17098719-1	2006	Sirt1 (Sirtuin type 1), a member of the conserved sirtuin family, is a NAD+ -dependent histone deacetylase.	NAD	71-75	sirtuin 1	Homo sapiens	7-21
16956582-7	2006	As CD38 is the major NAD+ -degrading enzyme present in the bone marrow, these results suggest that CD38-mediated inhibition of osteoclastogenesis is related to its NADase activity, not its ADPribosyl cyclase activity.	NAD	21-25	CD38 antigen	Mus musculus	3-7
16956582-7	2006	As CD38 is the major NAD+ -degrading enzyme present in the bone marrow, these results suggest that CD38-mediated inhibition of osteoclastogenesis is related to its NADase activity, not its ADPribosyl cyclase activity.	NAD	21-25	CD38 antigen	Mus musculus	99-103
16828555-3	2006	A three-dimensional (3D) structure of 15-PGDH based on the crystal structures of the levodione reductase and tropinone reductase-II was generated and used for docking study with NAD+ coenzyme and PGE2 substrate.	NAD	178-182	carbonyl reductase 1	Homo sapiens	38-45
16998474-7	2006	These results provide a crucial link between neddylation and transcriptional regulation by SIRT1, a NAD-dependent histone deacetylase that prolongs life span in yeast and worms.	NAD	100-103	sirtuin 1	Homo sapiens	91-96
16884682-1	2006	Yeast NAD+-specific isocitrate dehydrogenase (IDH) is an octamer of four IDH1 and four IDH2 subunits, and the basic structural unit of the enzyme is an IDH1/IDH2 heterodimer.	NAD	6-10	isocitrate dehydrogenase (NAD(+)) IDH2	Saccharomyces cerevisiae S288C	87-91
16884682-1	2006	Yeast NAD+-specific isocitrate dehydrogenase (IDH) is an octamer of four IDH1 and four IDH2 subunits, and the basic structural unit of the enzyme is an IDH1/IDH2 heterodimer.	NAD	6-10	isocitrate dehydrogenase (NAD(+)) IDH2	Saccharomyces cerevisiae S288C	157-161
16751189-2	2006	In this study we report for the first time that promotion of the NAD+-dependent sirtuin, SIRT1-mediated deacetylase activity, may be a mechanism by which CR influences Alzheimer disease (AD)-type amyloid neuropathology.	NAD	65-69	sirtuin 1	Homo sapiens	89-94
16750163-0	2006	Decreased cADPR and increased NAD+ in the Cd38-/- mouse.	NAD	30-34	CD38 antigen	Mus musculus	42-46
16750163-1	2006	CD38 is a type II glycoprotein that catalyzes the formation of cyclic ADP-ribose (cADPR), an intracellular calcium signalling molecule, from nicotinamide adenine dinucleotide (NAD(+)).	NAD	141-174	CD38 antigen	Mus musculus	0-4
16750163-1	2006	CD38 is a type II glycoprotein that catalyzes the formation of cyclic ADP-ribose (cADPR), an intracellular calcium signalling molecule, from nicotinamide adenine dinucleotide (NAD(+)).	NAD	176-182	CD38 antigen	Mus musculus	0-4
16750163-4	2006	We also report significant increases in brain, lung, and kidney NAD(+) in the Cd38(-/-) mouse, and provide the first experimental demonstration of the proximate relationship between CD38 and NAD(+).	NAD	64-70	CD38 antigen	Mus musculus	78-82
16750163-4	2006	We also report significant increases in brain, lung, and kidney NAD(+) in the Cd38(-/-) mouse, and provide the first experimental demonstration of the proximate relationship between CD38 and NAD(+).	NAD	191-197	CD38 antigen	Mus musculus	182-186
16571104-12	2006	The findings of the present study indicate that the hydroxylation requires complex formation between Des2 and mb5 via their membrane-spanning domains and electron transfer from NADH to the substrate via the reduction of mb5 by b5R.	NAD	177-181	cytochrome b5 reductase 3	Mus musculus	227-230
16618762-1	2006	SIRT1 and other NAD-dependent deacetylases have been implicated in control of cellular responses to stress and in tumorigenesis through deacetylation of important regulatory proteins, including p53 and the BCL6 oncoprotein.	NAD	16-19	sirtuin 1	Homo sapiens	0-5
16618762-1	2006	SIRT1 and other NAD-dependent deacetylases have been implicated in control of cellular responses to stress and in tumorigenesis through deacetylation of important regulatory proteins, including p53 and the BCL6 oncoprotein.	NAD	16-19	BCL6 transcription repressor	Homo sapiens	206-210
16618762-2	2006	Hereby, we describe the identification of a compound we named cambinol that inhibits NAD-dependent deacetylase activity of human SIRT1 and SIRT2.	NAD	85-88	sirtuin 1	Homo sapiens	129-134
16585549-14	2006	Both ART2-deficient and CD38/ART2 combined deficient T cells were resistant to NAD-induced killing in vitro, whereas CD38-deficient but ART2-intact T cells showed increased sensitivity, particularly the CD4+ CD25+ subset.	NAD	79-82	CD38 antigen	Mus musculus	24-28
16442077-12	2006	Physiologically, therefore, modulation of the expression of the NAD(+)-sensing enzyme, CD38, by Ca(2+), cAMP, and cytokines, such as TNF-alpha may contribute to coupling the intense metabolic activity of osteoclasts and osteoblasts to their respective bone-resorbing and bone-forming functions.	NAD	64-70	CD38 antigen	Mus musculus	87-91
16603817-6	2006	Kinetic studies of ALDH1A1 dehydrogenase activity in the presence or absence of each cation revealed that the inhibition mode by cations was uncompetitive against acetaldehyde, retinal, and NAD+, and that their inhibitory potencies were greater against acetaldehyde than retinal.	NAD	190-194	aldehyde dehydrogenase 1 family member A1 L homeolog	Xenopus laevis	19-26
16455971-2	2006	Here we show that micromolar concentrations of nicotinamide adenine dinucleotide (NAD) induce a rapid increase of annexin V staining in NKT cells in vitro, a response that requires expression of P2X(7)Rs.	NAD	82-85	annexin A5	Mus musculus	114-123
16325850-1	2006	Tetrameric rabbit muscle glyceraldehyde 3-phosphate dehydrogenase (GAPDH; EC 1.2.1.12) binds successively four molecules of its cofactor (NAD+) with affinities of ca 10(11) M(-1), 10(9) M(-1), 10(7) M(-1), and 10(5) M(-1).	NAD	138-142	glyceraldehyde-3-phosphate dehydrogenase	Oryctolagus cuniculus	67-72
16325850-4	2006	Reduction of the GAPDH dynamics, with consequent improvements in its internal bonding, can account for the increase in NAD+ binding affinity from 10(5) M(-1) to 10(11) M(-1).	NAD	119-123	glyceraldehyde-3-phosphate dehydrogenase	Oryctolagus cuniculus	17-22
16388584-3	2006	The library was screened using the human NAD+-dependent deacetylase SIRT1 for the most efficiently deacetylated peptide sequences.	NAD	41-45	sirtuin 1	Homo sapiens	68-73
16328012-0	2006	Cloning, chromosomal characterization and mapping of the NAD-dependent histone deacetylases gene sirtuin 1.	NAD	57-60	sirtuin 1	Homo sapiens	97-106
16288037-1	2005	SIRT1 is a conserved NAD-dependent deacetylase that regulates life span in accord with nutritional provision.	NAD	21-24	sirtuin 1	Homo sapiens	0-5
16007178-7	2005	PPT upregulated while DPN downregulated cyclin D1 and proliferating cell nuclear antigen (PCNA).	NAD	22-25	cyclin D1	Mus musculus	40-49
16007178-7	2005	PPT upregulated while DPN downregulated cyclin D1 and proliferating cell nuclear antigen (PCNA).	NAD	22-25	proliferating cell nuclear antigen	Mus musculus	54-88
16007178-7	2005	PPT upregulated while DPN downregulated cyclin D1 and proliferating cell nuclear antigen (PCNA).	NAD	22-25	proliferating cell nuclear antigen	Mus musculus	90-94
16000154-9	2005	We propose that the NADH glycerol phosphate shuttle participates in generating a pool of ATP that serves either as a co-factor or a modulator of the kinases involved in the phosphorylation of p300/CBP during hypoxia.	NAD	20-24	CREB binding protein	Rattus norvegicus	197-200
16023112-1	2005	When the influence of ADP-ribosylation on the activities of the purified human glutamate dehydrogenase isozymes (hGDH1 and hGDH2) was measured in the presence of 100 microM NAD+ for 60 min, hGDH isozymes were inhibited by up to 75%.	NAD	173-177	glutamate dehydrogenase 2	Homo sapiens	123-128
15908215-0	2005	Understanding human 15-hydroxyprostaglandin dehydrogenase binding with NAD+ and PGE2 by homology modeling, docking and molecular dynamics simulation.	NAD	71-75	carbonyl reductase 1	Homo sapiens	20-57
15908215-1	2005	Homology modeling, molecular docking, and molecular dynamics simulation have been performed to determine human 15-hydroxyprostaglandin dehydrogenase (15-PGDH) binding with its NAD+ cofactor and prostaglandin E2 (PGE2) substrate.	NAD	176-180	carbonyl reductase 1	Homo sapiens	111-148
15908215-1	2005	Homology modeling, molecular docking, and molecular dynamics simulation have been performed to determine human 15-hydroxyprostaglandin dehydrogenase (15-PGDH) binding with its NAD+ cofactor and prostaglandin E2 (PGE2) substrate.	NAD	176-180	carbonyl reductase 1	Homo sapiens	150-157
15883020-7	2005	Recombinant Gor enzyme was purified and characterized, and was found to have a novel ability to use both, NADPH and NADH, as electron donor.	NAD	116-120	REXO1 like 1, pseudogene	Homo sapiens	12-15
15834613-2	2005	Sjogren-Larsson Syndrome (SLS) is caused by an autosomal recessive defect in the gene coding for fatty aldehyde dehydrogenase (FALDH), an enzyme necessary for the oxidation of long-chain aliphatic aldehydes to fatty acid as one enzyme of the fatty alcohol:nicotinamide-adenine dinucleotide (NAD+)-oxidoreductase complex (FAO).	NAD	256-289	aldehyde dehydrogenase 3 family member A2	Homo sapiens	97-125
15834613-2	2005	Sjogren-Larsson Syndrome (SLS) is caused by an autosomal recessive defect in the gene coding for fatty aldehyde dehydrogenase (FALDH), an enzyme necessary for the oxidation of long-chain aliphatic aldehydes to fatty acid as one enzyme of the fatty alcohol:nicotinamide-adenine dinucleotide (NAD+)-oxidoreductase complex (FAO).	NAD	256-289	aldehyde dehydrogenase 3 family member A2	Homo sapiens	127-132
15834613-2	2005	Sjogren-Larsson Syndrome (SLS) is caused by an autosomal recessive defect in the gene coding for fatty aldehyde dehydrogenase (FALDH), an enzyme necessary for the oxidation of long-chain aliphatic aldehydes to fatty acid as one enzyme of the fatty alcohol:nicotinamide-adenine dinucleotide (NAD+)-oxidoreductase complex (FAO).	NAD	291-294	aldehyde dehydrogenase 3 family member A2	Homo sapiens	97-125
15834613-2	2005	Sjogren-Larsson Syndrome (SLS) is caused by an autosomal recessive defect in the gene coding for fatty aldehyde dehydrogenase (FALDH), an enzyme necessary for the oxidation of long-chain aliphatic aldehydes to fatty acid as one enzyme of the fatty alcohol:nicotinamide-adenine dinucleotide (NAD+)-oxidoreductase complex (FAO).	NAD	291-294	aldehyde dehydrogenase 3 family member A2	Homo sapiens	127-132
15870898-4	2005	Sequence analysis showed that LDHL harbors all the domains (one lactate/malate dehydrogenase, NAD binding domain and one lactate/malate dehydrogenase, alpha/beta C-terminal domain) in lactate dehydrogenase gene family.	NAD	94-97	lactate dehydrogenase A like 6B	Homo sapiens	30-34
15863098-2	2005	These genes encode for proteins with high homology to the mitochondrial internal (Ndi1p) and external (Nde1p) alternative NADH:ubiquinone oxidoreductases from Saccharomyces cerevisiae and complement the respective mutations.	NAD	122-126	NADH-ubiquinone reductase (H(+)-translocating) NDE1	Saccharomyces cerevisiae S288C	103-108
15744310-5	2005	We find that once SIRT1 is induced, it interacts with and deacetylates PGC-1alpha at specific lysine residues in an NAD(+)-dependent manner.	NAD	116-122	sirtuin 1	Homo sapiens	18-23
15734680-2	2005	Recent studies identified a gene, SIR2, which encodes an NAD-dependent deacetylase and may mediate the effects of calorie restriction.	NAD	57-60	sirtuin 1	Homo sapiens	34-38
15684044-5	2005	Overexpression of Ezh2 in tissue culture promotes formation of a previously undescribed PRC complex, PRC4, that contains the NAD+-dependent histone deacetylase SirT1 and isoform 2 of the PRC component Eed.	NAD	125-129	sirtuin 1	Homo sapiens	160-165
23045123-1	2005	NADH cytochrome b(5) reductase (b(5)R; EC 1.6.2.2; Diaphorase I; NADH: ferricytochrome b(5) oxidoreductase) is an FAD-containing protein, which, along with the hemoprotein cytochrome b(5) (cyt b(5)), mediates electron transfer from NADH to fatty acid desaturases, P450 oxidases, methemoglobin, and ascorbyl free radical.	NAD	0-4	hemoglobin subunit gamma 2	Homo sapiens	279-292
16435189-4	2005	FALDH activity was assessed by incubating fibroblast homogenates with phytol in the presence of NAD+, followed by hexane extraction of the samples and quantification of phytenic acid production by gas chromatography-mass spectrometry (GC-MS).	NAD	96-100	aldehyde dehydrogenase 3 family member A2	Homo sapiens	0-5
15381699-0	2004	The NAD biosynthesis pathway mediated by nicotinamide phosphoribosyltransferase regulates Sir2 activity in mammalian cells.	NAD	4-7	sirtuin 1	Homo sapiens	90-94
15381699-2	2004	The evolutionarily conserved Sir2 protein family requires NAD for its deacetylase activity and regulates a variety of biological processes, such as stress response, differentiation, metabolism, and aging.	NAD	58-61	sirtuin 1	Homo sapiens	29-33
15381699-3	2004	Despite its absolute requirement for NAD, the regulation of Sir2 function by NAD biosynthesis pathways is poorly understood in mammals.	NAD	37-40	sirtuin 1	Homo sapiens	60-64
15381699-3	2004	Despite its absolute requirement for NAD, the regulation of Sir2 function by NAD biosynthesis pathways is poorly understood in mammals.	NAD	77-80	sirtuin 1	Homo sapiens	60-64
15381699-8	2004	These findings suggest that NAD biosynthesis mediated by Nampt regulates the function of Sir2alpha and thereby plays an important role in controlling various biological events in mammals.	NAD	28-31	sirtuin 1	Homo sapiens	89-98
15456267-2	2004	Rat liver, human HeLa, and human recombinant class I and II histone deacetylases (HDACs) as well as human recombinant NAD(+)-dependent SIRT1 (class III enzyme) were used in these studies.	NAD	118-124	sirtuin 1	Homo sapiens	135-140
15469825-1	2004	We characterized human SirT1, one of the human homologs of the budding yeast Sir2p, an NAD+-dependent histone deacetylase involved in establishing repressive chromatin and increased life span.	NAD	87-90	sirtuin 1	Homo sapiens	23-28
15449954-0	2004	Effects of deletion and site-directed mutations on ligation steps of NAD+-dependent DNA ligase: a biochemical analysis of BRCA1 C-terminal domain.	NAD	69-73	BRCA1 DNA repair associated	Homo sapiens	122-127
15449954-2	2004	In this study, we investigate the effects on ligation steps by deletion and site-directed mutagenesis of the BRCA1 C-terminal (BRCT) domain using NAD(+)-dependent DNA ligase from Thermus species AK16D.	NAD	146-152	BRCA1 DNA repair associated	Homo sapiens	109-114
15291757-8	2004	S123A utilizes NAD as a cofactor for 3beta-HSD and NADH as the activator for isomerase with K(m) values that are similar to wild-type.	NAD	15-18	hydroxy-delta-5-steroid dehydrogenase, 3 beta- and steroid delta-isomerase 1	Homo sapiens	37-46
15308206-1	2004	When overexpressed, the NAD-dependent protein deacetylase Sir2 extends the lifespan of both budding yeast and the nematode worm Caenorhabditis elegans.	NAD	24-27	sirtuin 1	Homo sapiens	58-62
15126506-7	2004	Deacetylation of FOXOs involves binding of the NAD-dependent deacetylase hSir2(SIRT1).	NAD	47-50	sirtuin 1	Homo sapiens	73-78
15126506-7	2004	Deacetylation of FOXOs involves binding of the NAD-dependent deacetylase hSir2(SIRT1).	NAD	47-50	sirtuin 1	Homo sapiens	79-84
33873776-5	2004	A second group of proteins unrelated to those above, the sirtuins (Sir2) and poly ADP-ribose polymerases (PARPs), cleave NAD and transfer the ADP-ribose group to acetyl groups and proteins, respectively.	NAD	121-124	sirtuin 1	Homo sapiens	67-71
33873776-13	2004	Sir2 is an NAD dependant histone deacetylase 37 VIII.	NAD	11-14	sirtuin 1	Homo sapiens	0-4
15175298-2	2004	ArgR also induces the operon that encodes a catabolic NAD(+)-dependent glutamate dehydrogenase (GDH), which converts l-glutamate, the product of the AST pathway, in alpha-ketoglutarate.	NAD	54-60	transcriptional regulator ArgR	Pseudomonas aeruginosa PAO1	0-4
14734561-10	2004	In the presence of DNA and NAD(+), PARP-1 poly(ADP-ribosyl)ates itself and Ku70/80 but not WRN, and gel-shift assays showed that poly-(ADP-ribosyl)ation of Ku70/80 decreases the DNA-binding affinity of this factor.	NAD	27-33	X-ray repair cross complementing 6	Homo sapiens	75-79
14734561-10	2004	In the presence of DNA and NAD(+), PARP-1 poly(ADP-ribosyl)ates itself and Ku70/80 but not WRN, and gel-shift assays showed that poly-(ADP-ribosyl)ation of Ku70/80 decreases the DNA-binding affinity of this factor.	NAD	27-33	X-ray repair cross complementing 6	Homo sapiens	156-160
14756569-1	2004	ADH2 is a member of one of the six classes of mammalian alcohol dehydrogenases, which catalyze the reversible oxidation of alcohols using NAD(+) as a cofactor.	NAD	138-144	alcohol dehydrogenase 1B (class I), beta polypeptide	Homo sapiens	0-4
14652693-0	2004	NADH-reductive stress in Saccharomyces cerevisiae induces the expression of the minor isoform of glyceraldehyde-3-phosphate dehydrogenase (TDH1).	NAD	0-4	glyceraldehyde-3-phosphate dehydrogenase (phosphorylating) TDH1	Saccharomyces cerevisiae S288C	139-143
14652693-6	2004	We therefore propose that TDH1 has properties not displayed by the other TDH isogenes and that its expression is regulated by reductive stress caused by an excess of cytoplasmic NADH.	NAD	178-182	glyceraldehyde-3-phosphate dehydrogenase (phosphorylating) TDH1	Saccharomyces cerevisiae S288C	26-30
15047725-7	2004	The recombinant soluble cytochrome b(5) showed an asymmetrical absorption spectrum at 560 nm as is shown by mammalian cytochromes b(5) upon reduction with NADH and NADH-cytochrome b(5) reductase.	NAD	155-159	mitochondrially encoded cytochrome b	Homo sapiens	24-36
14727515-1	2003	The yeast silent information regulator 2 (Sir2) is an NAD-dependent histone deacetylase and silences transcription at the mating type loci, telomeres and the ribosomal DNA.	NAD	54-57	sirtuin 1	Homo sapiens	42-46
12927790-0	2003	NAD+ repletion prevents PARP-1-induced glycolytic blockade and cell death in cultured mouse astrocytes.	NAD	0-4	poly (ADP-ribose) polymerase family, member 1	Mus musculus	24-30
12927790-2	2003	When activated, PARP-1 consumes NAD(+) to form ADP-ribose polymers on acceptor proteins.	NAD	32-38	poly (ADP-ribose) polymerase family, member 1	Mus musculus	16-22
12927790-6	2003	Activation of PARP-1 with the DNA alkylating agent N-methyl-N"-nitro-N-nitrosoguanidine (MNNG) produced NAD(+) depletion, glycolytic blockade, and cell death.	NAD	104-110	poly (ADP-ribose) polymerase family, member 1	Mus musculus	14-20
12927790-9	2003	These results suggest that NAD(+) depletion is the cause of glycolytic failure after PARP-1 activation.	NAD	27-33	poly (ADP-ribose) polymerase family, member 1	Mus musculus	85-91
14511320-3	2003	PARP was activated in cultured mouse cortical astrocytes after a toxic acute Zn2+ exposure (350 microm Zn2+ for 15 min), but not in cortical neurons or glia after exposure to a toxic chronic Zn2+ exposure (40 microm Zn2+ for 1-4 h), an exposure sufficient to deplete NAD+ and ATP levels.	NAD	267-271	poly (ADP-ribose) polymerase family, member 1	Mus musculus	0-4
12867035-7	2003	CtBP proteins can undergo an NADH-induced conformational change, which we show here results in a loss of their Hdm2 binding ability.	NAD	29-33	MDM2 proto-oncogene	Homo sapiens	111-115
12817083-2	2003	The crystal structures of bovine milk XDH and XO demonstrated that atoms in the highly charged active-site loop (Gln-423-Lys-433) around the FAD cofactor underwent large dislocations during the conversion, blocking the approach of the NAD+ substrate to FAD in the XO form as well as changing the electrostatic environment around FAD.	NAD	235-239	xanthine dehydrogenase	Bos taurus	38-41
12855651-8	2003	Whole cell PARP-1 inhibition by BZ3, BZ5, BZ6, TI1, and TI4 was confirmed by attenuation of DNA damage-induced NAD(+) depletion.	NAD	111-117	poly (ADP-ribose) polymerase family, member 1	Mus musculus	11-17
15639914-4	2003	It is clear that SIR2 has two coupled enzymatic activities, histone deacetylation and NAD breakdown activities, and produces a novel compound, O-acetyl-ADP-ribose in the enzymatic reactions.	NAD	86-89	sirtuin 1	Homo sapiens	17-21
15639914-6	2003	Moreover, the relationship between the NAD cleavage and the deacetylase activity of SIR2 shows that the histone deacetylase activity is not its only crucial function.	NAD	39-42	sirtuin 1	Homo sapiens	84-88
12620835-3	2003	Both UFAs are formed in S. cerevisiae by the oxygen- and NADH-dependent desaturation of palmitic acid (C(16:0)) and stearic acid (C(18:0)), respectively, catalyzed by a single integral membrane desaturase encoded by the OLE1 gene.	NAD	57-61	stearoyl-CoA 9-desaturase	Saccharomyces cerevisiae S288C	220-224
12631576-2	2003	CD38 catalyzes the cyclization of its substrate, NAD+, to the Ca2+-releasing second messenger, cyclic ADP-ribose (cADPr).	NAD	49-53	CD38 antigen	Mus musculus	0-4
12631576-13	2003	We speculate that CD38 functions as a cellular NAD+ "sensor," particularly during periods of active motility and secretion.	NAD	47-51	CD38 antigen	Mus musculus	18-22
12403647-2	2003	In addition to its major NAD+-glycohydrolase activity, CD38 is also able to synthesize cyclic ADP-ribose, an endogenous calcium-regulating molecule, from NAD+.	NAD	25-29	CD38 antigen	Mus musculus	55-59
12505999-2	2003	We have measured mitochondrial oxygen consumption and the mitochondrial NADH concentration on single ascidian eggs and found that they increase in phase with each series of meiotic Ca(2+) waves emitted by two pacemakers (PM1 and PM2).	NAD	72-76	transmembrane protein 11	Homo sapiens	221-224
12435734-5	2003	TrxR1 reduced ubiquinone maximally at a physiological pH of 7.5 at similar rates using either NADPH or NADH as cofactors.	NAD	103-107	thioredoxin reductase 1	Homo sapiens	0-5
12504087-3	2003	Up-regulation of GRP78 in V79 Chinese hamster cell lines was achieved by treating the cells with NAD antagonist 6-aminonicotinamide (6AN), inhibitor of glucose metabolism such as 2-deoxyglucose (2dG).	NAD	97-100	endoplasmic reticulum chaperone BiP	Cricetulus griseus	17-22
12673357-7	2003	We also established that in extracts from PARP-1 deficient mouse cells, repair of both regular and reduced abasic sites was increased with respect to normal extracts and was NAD(+)-independent, suggesting that in both short- and long-patch BER PARP-1 slows down, rather than stimulates, the repair reaction.	NAD	174-180	poly (ADP-ribose) polymerase family, member 1	Mus musculus	42-48
15206766-8	2003	In contrast to the high activity of 3-hydroxyanthranilate 3,4-dioxygenase, aminocarboxymuconate-semialdehyde decarboxylase is 30-35 times less active, showing the efficiency of conversion of tryptophan to NAD.	NAD	205-208	3-hydroxyanthranilate 3,4-dioxygenase	Rattus norvegicus	36-73
12766354-2	2003	Nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d) reactivity was markedly reduced in the hippocampal CA1, CA2 and CA3 sectors as well as in the dentate gyrus, suggesting a suppression of NO production in these areas.	NAD	0-33	carbonic anhydrase 3	Rattus norvegicus	129-132
14965345-8	2003	In addition, UDE domain was shown to have both sequence and structure analogous to a segment of NAD-reducing hydrogenase HOXS a subunit which is believed to interact with thioredoxin.	NAD	96-99	thioredoxin 1	Mus musculus	171-182
15686116-1	2003	Overactivation of poly(ADP-ribose) polymerase-1 (PARP-1) in response to oxidative stress has been shown to contribute to necrotic cell death by consuming NAD+ and ATP.	NAD	154-158	poly (ADP-ribose) polymerase family, member 1	Mus musculus	18-47
15686116-1	2003	Overactivation of poly(ADP-ribose) polymerase-1 (PARP-1) in response to oxidative stress has been shown to contribute to necrotic cell death by consuming NAD+ and ATP.	NAD	154-158	poly (ADP-ribose) polymerase family, member 1	Mus musculus	49-55
12368285-1	2002	In mammals cyclic ADP-ribose (cADPR), a universal calcium mobilizer from intracellular stores, is generated from NAD(+) at the outer cell surface by the multifunctional ectoenzyme CD38 and by related ADP-ribosyl cyclases.	NAD	113-119	CD38 antigen	Mus musculus	180-184
12468268-1	2002	15-Hydroxyprostaglandin dehydrogenase (15-PGDH) catalyzes NAD(+)-dependent oxidation of 15(S)-hydroxyl group of prostaglandins and has been considered a key enzyme involved in biological inactivation of prostaglandins.	NAD	58-64	carbonyl reductase 1	Homo sapiens	0-37
12468268-1	2002	15-Hydroxyprostaglandin dehydrogenase (15-PGDH) catalyzes NAD(+)-dependent oxidation of 15(S)-hydroxyl group of prostaglandins and has been considered a key enzyme involved in biological inactivation of prostaglandins.	NAD	58-64	carbonyl reductase 1	Homo sapiens	39-46
12351438-3	2002	The activity and concentration of the two key enzymes of the NADH shuttles, mitochondrial glycerol phosphate dehydrogenase (mGPDH) and mitochondrial malate dehydrogenase (mMDH), were eight- and threefold lower, respectively, in fetal compared with adult rat islets.	NAD	61-65	malate dehydrogenase 2, NAD (mitochondrial)	Mus musculus	171-175
12351438-6	2002	Increasing NADH shuttle activity by transduction of fetal rat islets with mGPDH cDNA enabled the fetal islets to secrete insulin when stimulated with glucose.	NAD	11-15	glycerol phosphate dehydrogenase 2, mitochondrial	Mus musculus	74-79
12135624-5	2002	The EtOH loss was significantly higher (than the loss observed during metabolism of EtOH alone) only in EtOH-Hex and EtOH-Hep systems, which may be explained by the fact that reoxidation of NADH to NAD+ is quicker in these systems than dissociation of the alcohol dehydrogenase (ADH)-NADH complex.	NAD	190-194	heparanase	Rattus norvegicus	122-125
12135624-5	2002	The EtOH loss was significantly higher (than the loss observed during metabolism of EtOH alone) only in EtOH-Hex and EtOH-Hep systems, which may be explained by the fact that reoxidation of NADH to NAD+ is quicker in these systems than dissociation of the alcohol dehydrogenase (ADH)-NADH complex.	NAD	198-202	heparanase	Rattus norvegicus	122-125
12102657-5	2002	Overactivation of PARP depletes the cellular stores of NAD+, the substrate of PARP, and the ensuing "cellular energetic catastrophy" results in necrotic cell death.	NAD	55-59	poly (ADP-ribose) polymerase family, member 1	Mus musculus	18-22
12102657-5	2002	Overactivation of PARP depletes the cellular stores of NAD+, the substrate of PARP, and the ensuing "cellular energetic catastrophy" results in necrotic cell death.	NAD	55-59	poly (ADP-ribose) polymerase family, member 1	Mus musculus	78-82
11884393-4	2002	We show that Npt1 and a previously uncharacterized salvage pathway enzyme, Nma2, are both concentrated in the nucleus, indicating that a significant amount of NAD(+) is regenerated in this organelle.	NAD	159-165	nicotinamide-nucleotide adenylyltransferase NMA2	Saccharomyces cerevisiae S288C	75-79
11854472-2	2002	Excessive activation of PARP-1 by cellular insults depletes its substrate beta-nicotinamide adenine dinucleotide and ATP, leading to cell death.	NAD	74-112	poly (ADP-ribose) polymerase family, member 1	Mus musculus	24-30
11939620-0	2002	Insulin increases NADH/NAD+ redox state, which stimulates guanylate cyclase in vascular smooth muscle.	NAD	18-22	insulin	Canis lupus familiaris	0-7
11939620-0	2002	Insulin increases NADH/NAD+ redox state, which stimulates guanylate cyclase in vascular smooth muscle.	NAD	23-27	insulin	Canis lupus familiaris	0-7
11939620-5	2002	RESULTS: Insulin (1 nmol/L) increased cGMP production fivefold in VSMC with iNOS while raising the lactate-to-pyruvate ratio (LPR) from 3.1 +/- 0.5 to 10.0 +/- 1.6 (P &lt; .05), indicating a rise in the ratio of reduced/oxidized nicotinamide adenine dinucleotide (NADH/NAD+) redox state of the cell.	NAD	229-262	insulin	Canis lupus familiaris	9-16
11939620-5	2002	RESULTS: Insulin (1 nmol/L) increased cGMP production fivefold in VSMC with iNOS while raising the lactate-to-pyruvate ratio (LPR) from 3.1 +/- 0.5 to 10.0 +/- 1.6 (P &lt; .05), indicating a rise in the ratio of reduced/oxidized nicotinamide adenine dinucleotide (NADH/NAD+) redox state of the cell.	NAD	264-268	insulin	Canis lupus familiaris	9-16
11939620-5	2002	RESULTS: Insulin (1 nmol/L) increased cGMP production fivefold in VSMC with iNOS while raising the lactate-to-pyruvate ratio (LPR) from 3.1 +/- 0.5 to 10.0 +/- 1.6 (P &lt; .05), indicating a rise in the ratio of reduced/oxidized nicotinamide adenine dinucleotide (NADH/NAD+) redox state of the cell.	NAD	269-273	insulin	Canis lupus familiaris	9-16
11939620-11	2002	CONCLUSION: We conclude that insulin increases cGMP production in VSMC with iNOS by raising the cell NADH/NAD+ redox state, which may increase the availability of iNOS-derived NO.	NAD	101-105	insulin	Canis lupus familiaris	29-36
11959023-2	2002	The NAD(+)-dependent cytosolic glyceraldehyde-3-phosphate dehydrogenase (GAPDH, EC 1.2.1.12) has been purified to homogeneity from skeletal muscle of the newt Pleurodeles waltl (Amphibia, Urodela).	NAD	4-10	glyceraldehyde-3-phosphate dehydrogenase	Oryctolagus cuniculus	73-78
11804595-3	2002	This sensitivity of LTRPC2 to redox state modifiers was attributable to an agonistic binding of nicotinamide adenine dinucleotide (beta-NAD+) to the MutT motif.	NAD	96-129	transient receptor potential cation channel subfamily M member 2	Homo sapiens	20-26
11804595-3	2002	This sensitivity of LTRPC2 to redox state modifiers was attributable to an agonistic binding of nicotinamide adenine dinucleotide (beta-NAD+) to the MutT motif.	NAD	131-140	transient receptor potential cation channel subfamily M member 2	Homo sapiens	20-26
11796116-1	2002	Xanthine dehydrogenase (XDH), a complex molybdo/iron-sulfur/flavoprotein, catalyzes the oxidation of hypoxanthine to xanthine followed by oxidation of xanthine to uric acid with concomitant reduction of NAD+.	NAD	203-207	xanthine dehydrogenase	Bos taurus	24-27
11796116-3	2002	The NAD+ binding pocket of the bacterial XDH resembles that of the dehydrogenase form of the bovine enzyme rather than that of the oxidase form, which reduces O(2) instead of NAD+.	NAD	4-8	xanthine dehydrogenase	Bos taurus	41-44
11602597-7	2001	This mechanism may avoid: (i) leakage of NAD(+) from cells; (ii) depletion of intracellular NAD(+) by CD38; (iii) overproduction of intracellular cADPR resulting in potentially cytotoxic [Ca(2+)](i).	NAD	41-47	CD38 antigen	Mus musculus	102-106
11602597-7	2001	This mechanism may avoid: (i) leakage of NAD(+) from cells; (ii) depletion of intracellular NAD(+) by CD38; (iii) overproduction of intracellular cADPR resulting in potentially cytotoxic [Ca(2+)](i).	NAD	92-98	CD38 antigen	Mus musculus	102-106
11747420-1	2001	The Sir2 enzyme family is responsible for a newly classified chemical reaction, NAD(+)-dependent protein deacetylation.	NAD	80-86	sirtuin 1	Homo sapiens	4-8
11747420-2	2001	New peptide substrates, the reaction mechanism, and the products of the acetyl transfer to NAD(+) are described for SIR2.	NAD	91-97	sirtuin 1	Homo sapiens	116-120
11747420-5	2001	The mechanism of acetyl transfer to NAD(+) includes (1) ADP ribosylation of the peptide acyl oxygen to form a high-energy O-alkyl amidate intermediate, (2) attack of the 2"-OH group on the amidate to form a 1",2"-acyloxonium species, (3) hydrolysis to 2"-AADPR by the attack of water on the carbonyl carbon, and (4) an SIR2-independent transesterification equilibrating the 2"- and 3"-AADPRs.	NAD	36-42	sirtuin 1	Homo sapiens	319-323
11713283-4	2001	In contrast, deletion of the external NADH dehydrogenases NDE1 and NDE2, which feed electrons from NADH into the electron transport chain, abrogated the levels of heat-induced intracellular fluorescence and nuclear mutation frequency.	NAD	38-42	NADH-ubiquinone reductase (H(+)-translocating) NDE1	Saccharomyces cerevisiae S288C	58-62
11713283-4	2001	In contrast, deletion of the external NADH dehydrogenases NDE1 and NDE2, which feed electrons from NADH into the electron transport chain, abrogated the levels of heat-induced intracellular fluorescence and nuclear mutation frequency.	NAD	38-42	NADH-ubiquinone reductase (H(+)-translocating) NDE2	Saccharomyces cerevisiae S288C	67-71
11714283-1	2001	Yeast NAD(+)-specific isocitrate dehydrogenase is an allosterically regulated octameric enzyme composed of four each of two homologous but nonidentical subunits designated IDH1 and IDH2.	NAD	6-12	isocitrate dehydrogenase (NAD(+)) IDH2	Saccharomyces cerevisiae S288C	181-185
11576624-2	2001	The NAD(+)-dependent 11-HSD 2 in the kidney inactivates corticosterone and cortisol, allowing aldosterone, which is not metabolized, access to the receptor.	NAD	4-10	hydroxysteroid 11-beta dehydrogenase 2	Rattus norvegicus	24-29
11593040-1	2001	Excessive activation of poly(ADP-ribose) polymerase 1 (PARP1) leads to NAD(+) depletion and cell death during ischemia and other conditions that generate extensive DNA damage.	NAD	71-77	poly (ADP-ribose) polymerase family, member 1	Mus musculus	24-53
11593040-1	2001	Excessive activation of poly(ADP-ribose) polymerase 1 (PARP1) leads to NAD(+) depletion and cell death during ischemia and other conditions that generate extensive DNA damage.	NAD	71-77	poly (ADP-ribose) polymerase family, member 1	Mus musculus	55-60
11593040-2	2001	When activated by DNA strand breaks, PARP1 uses NAD(+) as substrate to form ADP-ribose polymers on specific acceptor proteins.	NAD	48-54	poly (ADP-ribose) polymerase family, member 1	Mus musculus	37-42
11593040-7	2001	The PARP1 inhibitor benzamide and the PARG inhibitor gallotannin both prevented the NAD(+) depletion that otherwise results from PARP1 activation by MNNG or H(2)O(2).	NAD	84-90	poly (ADP-ribose) polymerase family, member 1	Mus musculus	4-9
11593040-7	2001	The PARP1 inhibitor benzamide and the PARG inhibitor gallotannin both prevented the NAD(+) depletion that otherwise results from PARP1 activation by MNNG or H(2)O(2).	NAD	84-90	poly (ADP-ribose) glycohydrolase	Mus musculus	38-42
11593040-7	2001	The PARP1 inhibitor benzamide and the PARG inhibitor gallotannin both prevented the NAD(+) depletion that otherwise results from PARP1 activation by MNNG or H(2)O(2).	NAD	84-90	poly (ADP-ribose) polymerase family, member 1	Mus musculus	129-134
11593040-10	2001	These results suggest that PARG inhibitors do not inhibit PARP1 directly, but instead prevent PARP1-mediated cell death by slowing the turnover of poly(ADP-ribose) and thus slowing NAD(+) consumption.	NAD	181-187	poly (ADP-ribose) glycohydrolase	Mus musculus	27-31
11593040-10	2001	These results suggest that PARG inhibitors do not inhibit PARP1 directly, but instead prevent PARP1-mediated cell death by slowing the turnover of poly(ADP-ribose) and thus slowing NAD(+) consumption.	NAD	181-187	poly (ADP-ribose) polymerase family, member 1	Mus musculus	94-99
11736628-3	2001	Experimental evidence is presented supporting the idea that negative cooperativity of NAD+ binding and half-of-the-sites reactivity exhibited by GAPDH are generated by different mechanisms.	NAD	86-90	glyceraldehyde-3-phosphate dehydrogenase	Oryctolagus cuniculus	145-150
11478886-8	2001	The pH dependence of k(cat), the steady-state NADH level, and the fraction of NADH formed with saturating dTDP-xylose show shifts in the pK(a) assigned to Tyr160 to more basic values by mutation of Lys164 and Thr134.	NAD	46-50	TAR DNA-binding protein-43 homolog	Drosophila melanogaster	106-110
11478886-8	2001	The pH dependence of k(cat), the steady-state NADH level, and the fraction of NADH formed with saturating dTDP-xylose show shifts in the pK(a) assigned to Tyr160 to more basic values by mutation of Lys164 and Thr134.	NAD	78-82	TAR DNA-binding protein-43 homolog	Drosophila melanogaster	106-110
11478886-9	2001	The pK(a) of Tyr160, as determined by the pH dependence of NADH formation by dTDP-xylose, is 6.41.	NAD	59-63	TAR DNA-binding protein-43 homolog	Drosophila melanogaster	77-81
11746662-2	2001	Overexpression of LSP1 in NAD 47/89 patient"s neutrophils created hair-like projections on the patient"s neutrophil cell surfaces and inhibited neutrophil cell motility and transfection of LSP1 in serial cell lines recreate the NAD 47/89 phenotype and produce branching hair-like surface projections.	NAD	26-29	lymphocyte specific protein 1	Homo sapiens	18-22
11746662-2	2001	Overexpression of LSP1 in NAD 47/89 patient"s neutrophils created hair-like projections on the patient"s neutrophil cell surfaces and inhibited neutrophil cell motility and transfection of LSP1 in serial cell lines recreate the NAD 47/89 phenotype and produce branching hair-like surface projections.	NAD	228-231	lymphocyte specific protein 1	Homo sapiens	18-22
11746662-2	2001	Overexpression of LSP1 in NAD 47/89 patient"s neutrophils created hair-like projections on the patient"s neutrophil cell surfaces and inhibited neutrophil cell motility and transfection of LSP1 in serial cell lines recreate the NAD 47/89 phenotype and produce branching hair-like surface projections.	NAD	228-231	lymphocyte specific protein 1	Homo sapiens	189-193
11444838-2	2001	However, we have found that NAD, as a coenzyme of d-glyceraldehyde-3-phosphate dehydrogenase (GAPDH), also stimulates the discharge of GAPDH folding intermediate from its stable complex with GroEL formed in the absence of ATP and assists refolding with the same yield as ATP/Mg(2+) does.	NAD	28-31	heat shock protein family D (Hsp60) member 1	Homo sapiens	191-196
11444838-5	2001	Different from ATP, NAD triggers the release of GAPDH intermediates bound by GroEL via binding with GAPDH itself but not with GroEL, and the released intermediates all folded to native molecules without the formation of aggregation.	NAD	20-23	heat shock protein family D (Hsp60) member 1	Homo sapiens	77-82
11313477-7	2001	We have investigated the novel mechanism whereby Sum1-1 causes Sir-independent silencing at HMR and present the following findings: Sum1-1 requires the Sir2 homolog, Hst1, for silencing and most probably requires the NAD(+)-dependent deacetylase activity of this protein.	NAD	217-223	Sum1p	Saccharomyces cerevisiae S288C	49-55
11313477-7	2001	We have investigated the novel mechanism whereby Sum1-1 causes Sir-independent silencing at HMR and present the following findings: Sum1-1 requires the Sir2 homolog, Hst1, for silencing and most probably requires the NAD(+)-dependent deacetylase activity of this protein.	NAD	217-223	Sum1p	Saccharomyces cerevisiae S288C	132-138
11290854-8	2001	ADH activity of the strains that produced more than 100 nmol of acetaldehyde/10(9) colony-forming units/hr (n = 23) varied from 3.9 to 1253 nmol of nicotinamide adenine dinucleotide per minute per milligram of protein, and Km values for ethanol ranged from 0.65 to 116 mM and from 0.5 to 3.1 M (high Km).	NAD	148-181	aldo-keto reductase family 1 member A1	Homo sapiens	0-3
11042198-1	2001	Yeast mitochondrial NAD(+)-specific isocitrate dehydrogenase is an octamer composed of four each of two nonidentical but related subunits designated IDH1 and IDH2.	NAD	20-26	isocitrate dehydrogenase (NAD(+)) IDH2	Saccharomyces cerevisiae S288C	158-162
11136248-7	2001	Furthermore, NADPH was a potent inhibitor of the W676A NADH-dependent cytochrome c reduction and CYP1A2 activity.	NAD	55-59	2,4-dienoyl-CoA reductase 1	Homo sapiens	13-18
11113971-2	2000	NAD(+)-dependent glycerol-3-phosphate dehydrogenase in S. cerevisiae is present in two isoforms, coded for by two different genes, GPD1 and GPD2.	NAD	0-6	glycerol-3-phosphate dehydrogenase (NAD(+)) GPD1	Saccharomyces cerevisiae S288C	131-135
11113971-7	2000	At low demand for NADH reoxidation via glycerol formation, the GPD1, GPD2, GPP1, and GPP2 genes were all expressed at basal levels.	NAD	18-22	glycerol-3-phosphate dehydrogenase (NAD(+)) GPD1	Saccharomyces cerevisiae S288C	63-67
11113971-7	2000	At low demand for NADH reoxidation via glycerol formation, the GPD1, GPD2, GPP1, and GPP2 genes were all expressed at basal levels.	NAD	18-22	glycerol-1-phosphatase HOR2	Saccharomyces cerevisiae S288C	85-89
11113971-8	2000	The dynamics of the gene induction and the glycerol formation at low demand for NADH reoxidation point to an important role of the Gpd1p; deletion of the GPD1 gene strongly altered the expression patterns of the GPD2 and GPP1 genes under such conditions.	NAD	80-84	glycerol-3-phosphate dehydrogenase (NAD(+)) GPD1	Saccharomyces cerevisiae S288C	154-158
11076501-3	2000	The results were compatible with the postulated reaction mechanism, in which NAD(+) initially oxidizes glucosyl C4 of dTDP-glucose to NADH and dTDP-4-ketoglucose.	NAD	77-83	TAR DNA-binding protein-43 homolog	Drosophila melanogaster	118-122
11076501-3	2000	The results were compatible with the postulated reaction mechanism, in which NAD(+) initially oxidizes glucosyl C4 of dTDP-glucose to NADH and dTDP-4-ketoglucose.	NAD	77-83	TAR DNA-binding protein-43 homolog	Drosophila melanogaster	143-147
11076501-3	2000	The results were compatible with the postulated reaction mechanism, in which NAD(+) initially oxidizes glucosyl C4 of dTDP-glucose to NADH and dTDP-4-ketoglucose.	NAD	134-138	TAR DNA-binding protein-43 homolog	Drosophila melanogaster	118-122
11076501-5	2000	Hydride transfer from NADH to C6 of dTDP-4-ketoglucose-5,6-ene regenerates NAD(+) and produces the product dTDP-4-keto-6-deoxyglucose.	NAD	22-26	TAR DNA-binding protein-43 homolog	Drosophila melanogaster	36-40
11076501-5	2000	Hydride transfer from NADH to C6 of dTDP-4-ketoglucose-5,6-ene regenerates NAD(+) and produces the product dTDP-4-keto-6-deoxyglucose.	NAD	22-26	TAR DNA-binding protein-43 homolog	Drosophila melanogaster	107-111
11076501-5	2000	Hydride transfer from NADH to C6 of dTDP-4-ketoglucose-5,6-ene regenerates NAD(+) and produces the product dTDP-4-keto-6-deoxyglucose.	NAD	75-81	TAR DNA-binding protein-43 homolog	Drosophila melanogaster	36-40
11076501-5	2000	Hydride transfer from NADH to C6 of dTDP-4-ketoglucose-5,6-ene regenerates NAD(+) and produces the product dTDP-4-keto-6-deoxyglucose.	NAD	75-81	TAR DNA-binding protein-43 homolog	Drosophila melanogaster	107-111
11023795-3	2000	We report the crystal structure of rat HADH II/ABAD as a binary complex with its NADH cofactor to 2.0 A resolution, as a ternary complex with NAD(+) and 3-ketobutyrate (acetoacetate) to 1.4 A resolution, and as a ternary complex with NADH and 17 beta-estradiol to 1.7 A resolution.	NAD	81-85	hydroxysteroid 17-beta dehydrogenase 10	Homo sapiens	47-51
11023795-3	2000	We report the crystal structure of rat HADH II/ABAD as a binary complex with its NADH cofactor to 2.0 A resolution, as a ternary complex with NAD(+) and 3-ketobutyrate (acetoacetate) to 1.4 A resolution, and as a ternary complex with NADH and 17 beta-estradiol to 1.7 A resolution.	NAD	142-148	hydroxysteroid 17-beta dehydrogenase 10	Homo sapiens	47-51
11023795-3	2000	We report the crystal structure of rat HADH II/ABAD as a binary complex with its NADH cofactor to 2.0 A resolution, as a ternary complex with NAD(+) and 3-ketobutyrate (acetoacetate) to 1.4 A resolution, and as a ternary complex with NADH and 17 beta-estradiol to 1.7 A resolution.	NAD	234-238	hydroxysteroid 17-beta dehydrogenase 10	Homo sapiens	47-51
10987849-1	2000	It has been proposed that NAD depletion resulting from excessive activation of poly(ADP-ribose) polymerase is responsible for secondary energy failure after transient cerebral ischemia.	NAD	26-29	poly (ADP-ribose) polymerase family, member 1	Mus musculus	79-106
10958667-1	2000	Poly(ADP-ribose) polymerase (PARP) is a DNA binding zinc finger protein that catalyzes the transfer of ADP-ribose residues from NAD(+) to itself and different chromatin constituents, forming branched ADP-ribose polymers.	NAD	128-134	poly (ADP-ribose) polymerase family, member 1	Mus musculus	0-27
10958667-1	2000	Poly(ADP-ribose) polymerase (PARP) is a DNA binding zinc finger protein that catalyzes the transfer of ADP-ribose residues from NAD(+) to itself and different chromatin constituents, forming branched ADP-ribose polymers.	NAD	128-134	poly (ADP-ribose) polymerase family, member 1	Mus musculus	29-33
11115148-10	2000	We propose that redox changes associated with the alteration of cellular nicotinamide adenine dinucleotide and polyadenosine diphosphoribose are involved in lactate-mediated VEGF expression.	NAD	73-106	vascular endothelial growth factor A	Oryctolagus cuniculus	174-178
10933785-5	2000	The HH-Histag-BDH-PC complex (and HH-BDH derived therefrom by enterokinase cleavage) has apparent Michaelis constants (K(m) values) for NAD(+), NADH, (R)-3-hydroxybutyrate (HOB), and acetoacetate (AcAc) similar to those for bovine heart or rat liver BDH.	NAD	136-142	3-hydroxybutyrate dehydrogenase 1	Rattus norvegicus	37-40
10933785-5	2000	The HH-Histag-BDH-PC complex (and HH-BDH derived therefrom by enterokinase cleavage) has apparent Michaelis constants (K(m) values) for NAD(+), NADH, (R)-3-hydroxybutyrate (HOB), and acetoacetate (AcAc) similar to those for bovine heart or rat liver BDH.	NAD	144-148	3-hydroxybutyrate dehydrogenase 1	Rattus norvegicus	37-40
11037109-10	2000	Except for AKR1C4, the enzymes had a strong preference for NADPH over NADH, and the highest activities were measured with an NADPH-regenerating system.	NAD	70-74	aldo-keto reductase family 1 member C4	Homo sapiens	11-17
10809783-2	2000	Poly(ADP-ribose) polymerase-1 (PARP-1) is an abundant nuclear enzyme that catalyzes the synthesis of poly(ADP-ribose) (pADPr) from its substrate NAD(+) upon binding to DNA strand breaks.	NAD	145-151	poly (ADP-ribose) polymerase family, member 1	Mus musculus	0-29
10809783-2	2000	Poly(ADP-ribose) polymerase-1 (PARP-1) is an abundant nuclear enzyme that catalyzes the synthesis of poly(ADP-ribose) (pADPr) from its substrate NAD(+) upon binding to DNA strand breaks.	NAD	145-151	poly (ADP-ribose) polymerase family, member 1	Mus musculus	31-37
10809783-12	2000	Like PARP-1, sPARP-1 is localized in the cell nucleus, uses NAD(+) as a substrate and is inhibited by nicotinamide analogues.	NAD	60-66	poly (ADP-ribose) polymerase family, member 1	Mus musculus	5-11
10809783-12	2000	Like PARP-1, sPARP-1 is localized in the cell nucleus, uses NAD(+) as a substrate and is inhibited by nicotinamide analogues.	NAD	60-66	poly (ADP-ribose) polymerase family, member 1	Mus musculus	13-20
10803568-3	2000	While the type I 3alpha-HSD enzyme (3alpha-HSD1 or AKR1C9) is an oxidoreductase in vitro and could theoretically be responsible for factors 2 and 3, we have shown previously that rat Leydig cells have two 3alpha-HSD activities: a cytosolic NADP(H)- dependent activity, characteristic of 3alpha-HSD1, and a microsomal NAD(H)-dependent activity.	NAD	317-323	aldo-keto reductase family 1, member C14	Rattus norvegicus	17-27
10803568-3	2000	While the type I 3alpha-HSD enzyme (3alpha-HSD1 or AKR1C9) is an oxidoreductase in vitro and could theoretically be responsible for factors 2 and 3, we have shown previously that rat Leydig cells have two 3alpha-HSD activities: a cytosolic NADP(H)- dependent activity, characteristic of 3alpha-HSD1, and a microsomal NAD(H)-dependent activity.	NAD	317-323	aldo-keto reductase family 1, member C14	Rattus norvegicus	51-57
10803568-3	2000	While the type I 3alpha-HSD enzyme (3alpha-HSD1 or AKR1C9) is an oxidoreductase in vitro and could theoretically be responsible for factors 2 and 3, we have shown previously that rat Leydig cells have two 3alpha-HSD activities: a cytosolic NADP(H)- dependent activity, characteristic of 3alpha-HSD1, and a microsomal NAD(H)-dependent activity.	NAD	317-323	aldo-keto reductase family 1, member C14	Rattus norvegicus	36-46
10803568-5	2000	To identify the microsomal NAD(H)-dependent 3alpha-HSD in rat Leydig cells, degenerate primers were used to amplify a number of short-chain alcohol dehydrogenases.	NAD	27-33	aldo-keto reductase family 1, member C14	Rattus norvegicus	44-54
10803568-12	2000	In cell homogenates and subcellular fractions, RoDH2 catalyzed both 3alpha-HSD oxidation and reduction reactions that were NAD(H) dependent, and the enzyme activities were located in the microsomes.	NAD	123-129	aldo-keto reductase family 1, member C14	Rattus norvegicus	68-78
10777777-4	2000	However, an alternative to direct Zn(2+) inhibition of GAPDH was raised by the observation that Zn(2+) exposure also induced an early decrease in nicotinamide-adenine dinucleotide (NAD(+)) levels, an event itself capable of inhibiting GAPDH.	NAD	146-179	glyceraldehyde-3-phosphate dehydrogenase	Mus musculus	55-60
10758003-2	2000	Inosine 5"- monophosphate dehydrogenase (IMPDH) is the enzyme that catalyzes the oxidation of IMP to XMP with the concomitant reduction of nicotinamide adenine dinucleotide (from NAD(+) to NADH).	NAD	139-172	inosine-5'-monophosphate dehydrogenase 2	Cricetulus griseus	41-46
10758003-2	2000	Inosine 5"- monophosphate dehydrogenase (IMPDH) is the enzyme that catalyzes the oxidation of IMP to XMP with the concomitant reduction of nicotinamide adenine dinucleotide (from NAD(+) to NADH).	NAD	179-185	inosine-5'-monophosphate dehydrogenase 2	Cricetulus griseus	41-46
10758003-2	2000	Inosine 5"- monophosphate dehydrogenase (IMPDH) is the enzyme that catalyzes the oxidation of IMP to XMP with the concomitant reduction of nicotinamide adenine dinucleotide (from NAD(+) to NADH).	NAD	189-193	inosine-5'-monophosphate dehydrogenase 2	Cricetulus griseus	41-46
10705374-9	2000	Also, strain TN23 (gpd1-Delta1 gpd2-Delta1 YEp24-PGKp-cth-PGKt) was unable to grow anaerobically, leading to the conclusion that the NAD(+) pool became limiting in biomass synthesis before the nucleotide levels favoured a transhydrogenase reaction that could convert NADH and NADP(+) to NADPH and NAD(+).	NAD	133-139	glycerol-3-phosphate dehydrogenase (NAD(+)) GPD1	Saccharomyces cerevisiae S288C	19-23
10705374-9	2000	Also, strain TN23 (gpd1-Delta1 gpd2-Delta1 YEp24-PGKp-cth-PGKt) was unable to grow anaerobically, leading to the conclusion that the NAD(+) pool became limiting in biomass synthesis before the nucleotide levels favoured a transhydrogenase reaction that could convert NADH and NADP(+) to NADPH and NAD(+).	NAD	267-271	glycerol-3-phosphate dehydrogenase (NAD(+)) GPD1	Saccharomyces cerevisiae S288C	19-23
10705374-9	2000	Also, strain TN23 (gpd1-Delta1 gpd2-Delta1 YEp24-PGKp-cth-PGKt) was unable to grow anaerobically, leading to the conclusion that the NAD(+) pool became limiting in biomass synthesis before the nucleotide levels favoured a transhydrogenase reaction that could convert NADH and NADP(+) to NADPH and NAD(+).	NAD	297-303	glycerol-3-phosphate dehydrogenase (NAD(+)) GPD1	Saccharomyces cerevisiae S288C	19-23
10677544-1	2000	Poly(ADP-ribose) polymerase (PARP) transfers ADP ribose groups from NAD(+) to nuclear proteins after activation by DNA strand breaks.	NAD	68-74	poly (ADP-ribose) polymerase family, member 1	Mus musculus	0-27
10677544-1	2000	Poly(ADP-ribose) polymerase (PARP) transfers ADP ribose groups from NAD(+) to nuclear proteins after activation by DNA strand breaks.	NAD	68-74	poly (ADP-ribose) polymerase family, member 1	Mus musculus	29-33
10677544-2	2000	PARP overactivation by massive DNA damage causes cell death via NAD(+) and ATP depletion.	NAD	64-70	poly (ADP-ribose) polymerase family, member 1	Mus musculus	0-4
10677544-7	2000	An increase in NAD(+) levels after treatment with NMDA antagonists or NOS inhibitors, as well as in nNOS(-/-) mice, indicates that basal glutamate-PARP activity regulates neuronal energy dynamics.	NAD	15-21	poly (ADP-ribose) polymerase family, member 1	Mus musculus	147-151
10570184-3	1999	Overactivation of PARP after cellular insults can lead to cell death caused by depletion of the enzyme"s substrate beta-nicotinamide adenine dinucleotide and of ATP.	NAD	115-153	poly (ADP-ribose) polymerase family, member 1	Mus musculus	18-22
10557279-2	1999	We have determined the structure of the complex of SQD1 from Arabidopsis thaliana with NAD(+) and the putative substrate UDP-glucose at 1.6-A resolution.	NAD	87-93	sulfoquinovosyldiacylglycerol 1	Arabidopsis thaliana	51-55
10510460-4	1999	E-2 displaced [3H]-DPN binding in CHOmu and SH-SY5Y cells with pKi values of 7.82+/-0.11 and 8.43+/-0.13 respectively.	NAD	19-22	cystatin 12, pseudogene	Homo sapiens	0-3
10458590-1	1999	Poly(ADP-ribose) polymerase (PARP), or poly-(ADP-ribose) synthetase, is a nuclear enzyme that consumes NAD when activated by DNA damage.	NAD	103-106	poly (ADP-ribose) polymerase family, member 1	Mus musculus	0-27
10458590-1	1999	Poly(ADP-ribose) polymerase (PARP), or poly-(ADP-ribose) synthetase, is a nuclear enzyme that consumes NAD when activated by DNA damage.	NAD	103-106	poly (ADP-ribose) polymerase family, member 1	Mus musculus	29-33
10084958-9	1999	There was a clear partitioning of NADP(H)-dependent activity into the cytosolic fraction of Leydig cells, whereas on Days 35 and 90, Leydig cells also contained a microsomal NAD(H)-activated 3alpha-HSD.	NAD	174-180	aldo-keto reductase family 1, member C14	Rattus norvegicus	191-201
10084958-10	1999	We conclude that 1) the cytosolic 3alpha-HSD in Leydig cells on Day 21 behaves as a unidirectional NADPH-dependent reductase; 2) by Day 35, a microsomal NAD(H)-dependent enzyme activity is present and may account for predominance of 3alpha-HSD oxidation over reduction and the resultant high capacity of Leydig cells on Day 90 to synthesize DHT from 3alpha-DIOL.	NAD	153-159	aldo-keto reductase family 1, member C14	Rattus norvegicus	34-44
10084958-10	1999	We conclude that 1) the cytosolic 3alpha-HSD in Leydig cells on Day 21 behaves as a unidirectional NADPH-dependent reductase; 2) by Day 35, a microsomal NAD(H)-dependent enzyme activity is present and may account for predominance of 3alpha-HSD oxidation over reduction and the resultant high capacity of Leydig cells on Day 90 to synthesize DHT from 3alpha-DIOL.	NAD	153-159	aldo-keto reductase family 1, member C14	Rattus norvegicus	233-243
10085078-5	1999	By photoaffinity labeling with [125I]T3, a T3-binding site in the xCTBP was estimated to reside in amino acid residues 93-114, which is distinct from the active site of the enzyme but present in the NAD+ binding domain.	NAD	199-203	C-terminal binding protein 2 like S homeolog	Xenopus laevis	66-71
9895226-7	1999	The data obtained suggests that: (1) expression of ADH and XOR or AOX in breast tissue provides the enzymes that generate ROS; (2) metabolism of alcohol produces acetaldehyde and NADH that can both be substrates for XOR or AOX and thereby result in ROS formation; and (3) ROS generated by XOR or AOX can induce the carcinogenic mutations and DNA damage found in breast cancer.	NAD	179-183	aldo-keto reductase family 1 member A1	Homo sapiens	51-54
10193578-1	1999	Dihydrolipoamide dehydrogenase (LADH) lipoamide reductase activity decreased whereas enzyme diaphorase activity increased after LADH treatment with myeloperoxidase (MPO) dependent systems (MPO/H2O2/halide, MPO/NADH/halide and MPO/H2O2/nitrite systems.	NAD	210-214	myeloperoxidase	Equus caballus	148-163
10193578-1	1999	Dihydrolipoamide dehydrogenase (LADH) lipoamide reductase activity decreased whereas enzyme diaphorase activity increased after LADH treatment with myeloperoxidase (MPO) dependent systems (MPO/H2O2/halide, MPO/NADH/halide and MPO/H2O2/nitrite systems.	NAD	210-214	myeloperoxidase	Equus caballus	165-168
10193578-1	1999	Dihydrolipoamide dehydrogenase (LADH) lipoamide reductase activity decreased whereas enzyme diaphorase activity increased after LADH treatment with myeloperoxidase (MPO) dependent systems (MPO/H2O2/halide, MPO/NADH/halide and MPO/H2O2/nitrite systems.	NAD	210-214	myeloperoxidase	Equus caballus	189-192
10193578-1	1999	Dihydrolipoamide dehydrogenase (LADH) lipoamide reductase activity decreased whereas enzyme diaphorase activity increased after LADH treatment with myeloperoxidase (MPO) dependent systems (MPO/H2O2/halide, MPO/NADH/halide and MPO/H2O2/nitrite systems.	NAD	210-214	myeloperoxidase	Equus caballus	189-192
10193578-1	1999	Dihydrolipoamide dehydrogenase (LADH) lipoamide reductase activity decreased whereas enzyme diaphorase activity increased after LADH treatment with myeloperoxidase (MPO) dependent systems (MPO/H2O2/halide, MPO/NADH/halide and MPO/H2O2/nitrite systems.	NAD	210-214	myeloperoxidase	Equus caballus	189-192
10193578-6	1999	LADH inactivation by the MPO/NADH/halide systems was prevented by catalase and enhanced by superoxide dismutase, in close agreement with H2O2 production by the LADH/NADH system.	NAD	29-33	myeloperoxidase	Equus caballus	25-28
10193578-6	1999	LADH inactivation by the MPO/NADH/halide systems was prevented by catalase and enhanced by superoxide dismutase, in close agreement with H2O2 production by the LADH/NADH system.	NAD	165-169	myeloperoxidase	Equus caballus	25-28
10048020-2	1999	Here we report the isolation of a new yeast mutant, gan1-1, exhibiting dramatically decreased NAD-linked glutamate dehydrogenase (NAD-GDH) and glutamine synthetase (GS) activities.	NAD	94-97	Hfi1p	Saccharomyces cerevisiae S288C	52-58
9882448-6	1999	TBE-R1 utilized NADH or NADPH equally as cofactor, and the Km values of NADH and NADPH for TBE with TBE-R1 were estimated to be 15 and 29 microM, respectively.	NAD	16-20	aldo-keto reductase family 1, member C12	Rattus norvegicus	0-6
9882448-6	1999	TBE-R1 utilized NADH or NADPH equally as cofactor, and the Km values of NADH and NADPH for TBE with TBE-R1 were estimated to be 15 and 29 microM, respectively.	NAD	72-76	aldo-keto reductase family 1, member C12	Rattus norvegicus	100-106
10668429-1	1999	Decreases in mouse brain NAD+ and ATP caused by MPTP are prevented by the PARP inhibitor benzamide.	NAD	25-29	poly (ADP-ribose) polymerase family, member 1	Mus musculus	74-78
10668429-2	1999	Poly(ADP-ribose) polymerase (PARP) is a DNA binding protein that uses nicotinamide adenine dinucleotide (NAD+) as a substrate.	NAD	70-103	poly (ADP-ribose) polymerase family, member 1	Mus musculus	0-27
10668429-2	1999	Poly(ADP-ribose) polymerase (PARP) is a DNA binding protein that uses nicotinamide adenine dinucleotide (NAD+) as a substrate.	NAD	70-103	poly (ADP-ribose) polymerase family, member 1	Mus musculus	29-33
10668429-2	1999	Poly(ADP-ribose) polymerase (PARP) is a DNA binding protein that uses nicotinamide adenine dinucleotide (NAD+) as a substrate.	NAD	105-109	poly (ADP-ribose) polymerase family, member 1	Mus musculus	0-27
10668429-2	1999	Poly(ADP-ribose) polymerase (PARP) is a DNA binding protein that uses nicotinamide adenine dinucleotide (NAD+) as a substrate.	NAD	105-109	poly (ADP-ribose) polymerase family, member 1	Mus musculus	29-33
10092955-5	1999	TQ was tested as a substrate for mice hepatic DT-diaphorase in the presence of NADH.	NAD	79-83	NAD(P)H dehydrogenase, quinone 1	Mus musculus	46-59
9890650-3	1999	Spin-trapping studies of incubations containing DCF, 5,5-dimethyl-1-pyrroline N-oxide (DMPO) and either reduced glutathione (GSH) or reduced NADH demonstrate, under irradiation with visible light, the production of the superoxide dismutase-sensitive DMPO/*OOH adduct.	NAD	141-145	spindlin 1	Homo sapiens	0-4
10403507-3	1999	Raised activities of two enzymes catalysing NAD synthesis from nicotinic acid (nicotinic acid phosphoribosyltransferase: NAPRT, and NAD synthetase: NADs) was found in erythrocyte lysates from all patients.	NAD	44-47	nicotinate phosphoribosyltransferase	Homo sapiens	121-126
10403507-3	1999	Raised activities of two enzymes catalysing NAD synthesis from nicotinic acid (nicotinic acid phosphoribosyltransferase: NAPRT, and NAD synthetase: NADs) was found in erythrocyte lysates from all patients.	NAD	44-47	NAD synthetase 1	Homo sapiens	132-146
9851831-1	1998	At pH 7.05 NADH-X prepared by incubating NADH with glyceraldehyde-3-phosphate dehydrogenase (E.C.	NAD	11-15	glyceraldehyde-3-phosphate dehydrogenase	Oryctolagus cuniculus	51-91
9851831-1	1998	At pH 7.05 NADH-X prepared by incubating NADH with glyceraldehyde-3-phosphate dehydrogenase (E.C.	NAD	41-45	glyceraldehyde-3-phosphate dehydrogenase	Oryctolagus cuniculus	51-91
9795136-0	1998	Decreases in mouse brain NAD+ and ATP induced by 1-methyl-4-phenyl-1, 2,3,6-tetrahydropyridine (MPTP): prevention by the poly(ADP-ribose) polymerase inhibitor, benzamide.	NAD	25-29	poly (ADP-ribose) polymerase family, member 1	Mus musculus	121-148
9795136-3	1998	In vitro, the activation of PARP by free radical damaged DNA has been shown to be correlated with rapid decreases in the cellular levels of its substrate nicotinamide adenine dinucleotide (NAD+), and ATP.	NAD	154-187	poly (ADP-ribose) polymerase family, member 1	Mus musculus	28-32
9795136-3	1998	In vitro, the activation of PARP by free radical damaged DNA has been shown to be correlated with rapid decreases in the cellular levels of its substrate nicotinamide adenine dinucleotide (NAD+), and ATP.	NAD	189-193	poly (ADP-ribose) polymerase family, member 1	Mus musculus	28-32
9795136-14	1998	]; (2) show that MPTP causes a regionally-dependent (striatal and midbrain) loss of NAD+; (3) indicate that the PARP inhibitor benzamide can prevent these losses without interfering with MPTP-induced striatal dopamine release; and (4) provide further evidence to suggest an involvement of PARP in MPTP-induced neurotoxicity in vivo.	NAD	84-88	poly (ADP-ribose) polymerase family, member 1	Mus musculus	112-116
9749838-8	1998	The 3beta-HSD activities of the Y253F, Y253,254F and wild-type enzymes reduced NAD+ with similar kinetic values.	NAD	79-83	hydroxy-delta-5-steroid dehydrogenase, 3 beta- and steroid delta-isomerase 1	Homo sapiens	4-13
9689052-11	1998	These results indicated that the S. cerevisiae Ndi1 was expressed functionally in CCL16-B2 cells and catalyzed electron transfer from NADH in the matrix to ubiquinone-10 in the inner mitochondrial membranes.	NAD	134-138	LOW QUALITY PROTEIN: C-C motif chemokine 16	Cricetulus griseus	82-87
9580328-8	1998	We suggest that ROS generation by inhibition of the NADH-dependent plasma membrane electron transport system resulted in the oxidation of mitochondrial megachannel pores that allows for the disruption of deltapsi(m) and apoptosis, and that AP-1 activation is not required for vanilloid-induced apoptosis.	NAD	52-56	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	240-244
9553766-3	1998	The structural homology between CD38 and the cyclase family members extends to functional homology, as the extracellular domain of CD38 can mediate the catalysis of beta-NAD+ into nicotinamide, ADP-ribose (ADPR) and, to a lesser extent, into cyclic ADPR-ribose (cADPR).	NAD	165-174	CD38 antigen	Mus musculus	32-36
9553766-3	1998	The structural homology between CD38 and the cyclase family members extends to functional homology, as the extracellular domain of CD38 can mediate the catalysis of beta-NAD+ into nicotinamide, ADP-ribose (ADPR) and, to a lesser extent, into cyclic ADPR-ribose (cADPR).	NAD	165-174	CD38 antigen	Mus musculus	131-135
9405293-10	1998	NADH alone stimulated the activities of PDK1 and PDK2 by 20 and 30% respectively.	NAD	0-4	pyruvate dehydrogenase kinase 1	Homo sapiens	40-44
12075544-4	1998	It was hypothesized that increased serum lactate dehydrogenase (LDH) activity and pyruvate concentration overwhelmed the oxamate LDH inhibitor in the enzymatic HCO3- assay, resulting in consumption of NADH and falsely elevated spectrophotometric reading.	NAD	201-205	LDH	Bos taurus	41-62
12075544-4	1998	It was hypothesized that increased serum lactate dehydrogenase (LDH) activity and pyruvate concentration overwhelmed the oxamate LDH inhibitor in the enzymatic HCO3- assay, resulting in consumption of NADH and falsely elevated spectrophotometric reading.	NAD	201-205	LDH	Bos taurus	64-67
12075544-4	1998	It was hypothesized that increased serum lactate dehydrogenase (LDH) activity and pyruvate concentration overwhelmed the oxamate LDH inhibitor in the enzymatic HCO3- assay, resulting in consumption of NADH and falsely elevated spectrophotometric reading.	NAD	201-205	LDH	Bos taurus	129-132
9409558-11	1997	However, when TRX reductase and nicotinamide adenine dinucleotide (NADPH) were added to the extracellular medium with TRX, more than 80% of E. coli TRX was found to be in a fully reduced state in human adenocarcinoma (A549) cells.	NAD	32-65	2,4-dienoyl-CoA reductase 1	Homo sapiens	67-72
9432004-0	1997	Mechanism of NADH transfer between alcohol dehydrogenase and glyceraldehyde-3-phosphate dehydrogenase.	NAD	13-17	aldo-keto reductase family 1 member A1	Homo sapiens	35-56
9432004-1	1997	Steady-state and transient-state kinetic experiments have been performed to test the proposal that there is a direct (channelled) transfer of NADH from glyceraldehyde-3-phosphate dehydrogenase to alcohol dehydrogenase.	NAD	142-146	aldo-keto reductase family 1 member A1	Homo sapiens	196-217
9390645-1	1997	Poly(ADP-ribose)polymerase (PARP, EC 2.4.2.30), an abundant nuclear protein activated by DNA nicks, mediates cell death in vitro by nicotinamide adenine dinucleotide (NAD) depletion after exposure to nitric oxide.	NAD	132-165	poly (ADP-ribose) polymerase family, member 1	Mus musculus	0-26
9390645-1	1997	Poly(ADP-ribose)polymerase (PARP, EC 2.4.2.30), an abundant nuclear protein activated by DNA nicks, mediates cell death in vitro by nicotinamide adenine dinucleotide (NAD) depletion after exposure to nitric oxide.	NAD	132-165	poly (ADP-ribose) polymerase family, member 1	Mus musculus	28-32
9390645-1	1997	Poly(ADP-ribose)polymerase (PARP, EC 2.4.2.30), an abundant nuclear protein activated by DNA nicks, mediates cell death in vitro by nicotinamide adenine dinucleotide (NAD) depletion after exposure to nitric oxide.	NAD	167-170	poly (ADP-ribose) polymerase family, member 1	Mus musculus	0-26
9390645-1	1997	Poly(ADP-ribose)polymerase (PARP, EC 2.4.2.30), an abundant nuclear protein activated by DNA nicks, mediates cell death in vitro by nicotinamide adenine dinucleotide (NAD) depletion after exposure to nitric oxide.	NAD	167-170	poly (ADP-ribose) polymerase family, member 1	Mus musculus	28-32
9390645-6	1997	Levels of NAD--the substrate of PARP--were reduced 2 hours after reperfusion and were 35% of contralateral levels at 24 hours.	NAD	10-14	poly (ADP-ribose) polymerase family, member 1	Mus musculus	32-36
9336832-0	1997	Unusual conformation of nicotinamide adenine dinucleotide (NAD) bound to diphtheria toxin: a comparison with NAD bound to the oxidoreductase enzymes.	NAD	24-57	thioredoxin reductase 1	Homo sapiens	126-140
9336832-0	1997	Unusual conformation of nicotinamide adenine dinucleotide (NAD) bound to diphtheria toxin: a comparison with NAD bound to the oxidoreductase enzymes.	NAD	109-112	thioredoxin reductase 1	Homo sapiens	126-140
9336832-2	1997	For the oxidoreductase enzymes, NAD(P) functions as a cofactor in electron transfer, whereas for DT, NAD is a labile substrate in which the N-glycosidic bond between the nicotinamide ring and the N-ribose is cleaved.	NAD	32-35	thioredoxin reductase 1	Homo sapiens	8-22
9336832-4	1997	Whereas the majority of oxidoreductase-bound NAD(P) conformations are found to be similar, the conformation of NAD bound to DT is found to be unusual.	NAD	45-48	thioredoxin reductase 1	Homo sapiens	24-38
9323038-0	1997	NADH:Fe(III)-chelate reductase of maize roots is an active cytochrome b5 reductase.	NAD	0-4	ferric-chelate reductase (NADH)2	Zea mays	59-82
9278404-3	1997	Most differences between XO and XDH are localized to the FAD center, the site at which the oxidizing substrates NAD and molecular oxygen react.	NAD	112-115	xanthine dehydrogenase	Bos taurus	32-35
9286695-1	1997	In this paper we present the entire genomic sequence as well as the cDNA sequence of two new human genes encoding the gamma subunit of the NAD(+)-dependent isocitrate dehydrogenase (H-IDH gamma) and the translocon-associated protein delta subunit (TRAP delta).	NAD	139-145	signal sequence receptor subunit 4	Homo sapiens	203-246
9286695-1	1997	In this paper we present the entire genomic sequence as well as the cDNA sequence of two new human genes encoding the gamma subunit of the NAD(+)-dependent isocitrate dehydrogenase (H-IDH gamma) and the translocon-associated protein delta subunit (TRAP delta).	NAD	139-145	signal sequence receptor subunit 4	Homo sapiens	248-258
9135568-3	1997	We have developed a gas chromatographic mass spectrometric assay for dexamethasone and 11-dehydrodexamethasone and have confirmed in vitro that dexamethasone is a substrate for 11 beta-HSD2 but not 11 beta-HSD1 (conversion to 11-dehydrodexamethasone 0.6 +/- 0.3% in homogenates of rat liver with NADP+ for 11 beta-HSD1, and 29.4 +/- 10.3% and 40.0 +/- 2.0% in homogenates of rat and human kidney respectively with NAD+ for 11 beta-HSD2).	NAD	414-418	hydroxysteroid 11-beta dehydrogenase 2	Rattus norvegicus	177-189
9079661-8	1997	Steady-state kinetics of xanthine/oxygen and NADH/oxygen turnover of XDH were determined to have kcat values of 2.1 +/- 0.1 and 2.5 +/- 0.9 s-1, respectively, at 25 degrees C, pH 7.5.	NAD	45-49	xanthine dehydrogenase	Bos taurus	69-72
9079661-9	1997	XDH is therefore capable of catalyzing the formation of reduced oxygen species at one-third the rate of xanthine/NAD turnover, 6.3 s-1 (Hunt, J., and Massey, V. (1992) J. Biol.	NAD	113-116	xanthine dehydrogenase	Bos taurus	0-3
28487632-6	2017	Here, we demonstrate that WldS increases retinal NAD levels.	NAD	49-52	wallerian degeneration	Mus musculus	26-30
28487632-7	2017	Coupled with nicotinamide administration (an NAD precursor), it robustly protects from glaucomatous neurodegeneration in a mouse model of glaucoma (94% of eyes having no glaucoma, more than WldS or nicotinamide alone).	NAD	45-48	wallerian degeneration	Mus musculus	190-194
28160567-2	2017	EwS development is driven by a specific chromosomal translocation resulting in the generation of a chimeric EWS-ETS transcription factor, most frequently EWS-FLI1.Nicotinamide adenine dinucleotide (NAD) is a key metabolite of energy metabolism involved in cellular redox reactions, DNA repair, and in the maintenance of genomic stability.	NAD	163-196	EWS RNA binding protein 1	Homo sapiens	0-3
28160567-2	2017	EwS development is driven by a specific chromosomal translocation resulting in the generation of a chimeric EWS-ETS transcription factor, most frequently EWS-FLI1.Nicotinamide adenine dinucleotide (NAD) is a key metabolite of energy metabolism involved in cellular redox reactions, DNA repair, and in the maintenance of genomic stability.	NAD	163-196	EWS RNA binding protein 1	Homo sapiens	108-111
28088384-4	2017	RTC-1-induced inhibition of NADH:ubiquinone oxidoreductase was found to promote glucose uptake in C2C12 myotubes in vitro, through the activation of the Akt substrate of 160kDa (AS160), in response to the increased activity of Akt and AMP-activated protein kinase (AMPK).	NAD	28-32	TBC1 domain family, member 4	Mus musculus	153-176
27821631-6	2017	Analysis of global gene expression profiles in nondiseased primary proximal tubule cells from black patients revealed that the nicotinate phosphoribosyltransferase gene, responsible for NAD biosynthesis, was among the top downregulated transcripts in cells with two APOL1 renal-risk variants compared with those without renal-risk variants; nicotinate phosphoribosyltransferase also displayed gene expression patterns linked to mitochondrial dysfunction in HEK293 Tet-on APOL1 cell pathway analyses.	NAD	186-189	apolipoprotein L1	Homo sapiens	266-271
27821631-6	2017	Analysis of global gene expression profiles in nondiseased primary proximal tubule cells from black patients revealed that the nicotinate phosphoribosyltransferase gene, responsible for NAD biosynthesis, was among the top downregulated transcripts in cells with two APOL1 renal-risk variants compared with those without renal-risk variants; nicotinate phosphoribosyltransferase also displayed gene expression patterns linked to mitochondrial dysfunction in HEK293 Tet-on APOL1 cell pathway analyses.	NAD	186-189	apolipoprotein L1	Homo sapiens	471-476
28183718-6	2017	https://doi.org/10.1083/jcb.201607091) demonstrate how heat shock factor 1 (HSF1) uncouples metabolic control from proteostatic regulation and unveils HSF1 as a critical transcriptional regulator of NAD+ metabolism.	NAD	199-203	heat shock transcription factor 1	Homo sapiens	55-74
28183718-6	2017	https://doi.org/10.1083/jcb.201607091) demonstrate how heat shock factor 1 (HSF1) uncouples metabolic control from proteostatic regulation and unveils HSF1 as a critical transcriptional regulator of NAD+ metabolism.	NAD	199-203	heat shock transcription factor 1	Homo sapiens	76-80
28183718-6	2017	https://doi.org/10.1083/jcb.201607091) demonstrate how heat shock factor 1 (HSF1) uncouples metabolic control from proteostatic regulation and unveils HSF1 as a critical transcriptional regulator of NAD+ metabolism.	NAD	199-203	heat shock transcription factor 1	Homo sapiens	151-155
27986658-1	2017	The present study investigates the physiological role of Kvbeta1 subunit for sensing pyridine nucleotide (NADH/NAD+) changes in the heart.	NAD	106-110	potassium voltage-gated channel, shaker-related subfamily, beta member 1	Mus musculus	57-64
27986658-1	2017	The present study investigates the physiological role of Kvbeta1 subunit for sensing pyridine nucleotide (NADH/NAD+) changes in the heart.	NAD	111-115	potassium voltage-gated channel, shaker-related subfamily, beta member 1	Mus musculus	57-64
27986658-6	2017	These data reveal that Kvbeta1.1 is required in the mediated inactivation of Kv4.2 currents, when NADH (lactate) levels are increased.	NAD	98-102	potassium voltage-gated channel, shaker-related subfamily, beta member 1	Mus musculus	23-32
27986658-7	2017	In vivo, isoproterenol infusion led to increased NADH in the heart along with QTc prolongation in wild-type mice; regardless of the approach, our data show that Kvbeta1.1 recognizes NADH changes and modulates Kv4.2 currents affecting AP and QTc durations.	NAD	49-53	potassium voltage-gated channel, shaker-related subfamily, beta member 1	Mus musculus	161-170
27986658-7	2017	In vivo, isoproterenol infusion led to increased NADH in the heart along with QTc prolongation in wild-type mice; regardless of the approach, our data show that Kvbeta1.1 recognizes NADH changes and modulates Kv4.2 currents affecting AP and QTc durations.	NAD	182-186	potassium voltage-gated channel, shaker-related subfamily, beta member 1	Mus musculus	161-170
27986658-8	2017	Overall, this study uses multiple levels of investigation, including the heterologous overexpression system, cardiomyocyte, ex vivo, and ECG, and clearly depicts that Kvbeta1.1 is an obligatory sensor of NADH/NAD changes in vivo, with a physiological role in the heart.NEW &amp; NOTEWORTHY Cardiac electrical activity is mediated by ion channels, and Kv4.2 plays a significant role, along with its binding partner, the Kvbeta1.1 subunit.	NAD	204-208	potassium voltage-gated channel, shaker-related subfamily, beta member 1	Mus musculus	167-176
27986658-8	2017	Overall, this study uses multiple levels of investigation, including the heterologous overexpression system, cardiomyocyte, ex vivo, and ECG, and clearly depicts that Kvbeta1.1 is an obligatory sensor of NADH/NAD changes in vivo, with a physiological role in the heart.NEW &amp; NOTEWORTHY Cardiac electrical activity is mediated by ion channels, and Kv4.2 plays a significant role, along with its binding partner, the Kvbeta1.1 subunit.	NAD	204-207	potassium voltage-gated channel, shaker-related subfamily, beta member 1	Mus musculus	167-176
27989687-1	2017	BACKGROUND: The reduced form of nicotinamide adenine dinucleotide (NADH) increases in cardiomyopathy, activates protein kinase C (PKC), up-regulates mitochondrial reactive oxygen species (mitoROS), and down-regulates the cardiac Na+ channel (NaV1.5).	NAD	32-65	protein kinase C delta	Homo sapiens	130-133
27989687-1	2017	BACKGROUND: The reduced form of nicotinamide adenine dinucleotide (NADH) increases in cardiomyopathy, activates protein kinase C (PKC), up-regulates mitochondrial reactive oxygen species (mitoROS), and down-regulates the cardiac Na+ channel (NaV1.5).	NAD	67-71	protein kinase C delta	Homo sapiens	130-133
28134365-1	2017	Ndi1 is a special type-II complex I nicotinamide-adenine-dinucleotide (NADH):ubiquinone (UQ) oxidoreductase in the yeast respiratory chain, with two bound UQs (UQI and UQII) mediating electron transfer from flavin cofactors to ubiquinone, in the absence of Fe-S chains.	NAD	36-69	NADH-ubiquinone reductase (H(+)-translocating) NDI1	Saccharomyces cerevisiae S288C	0-4
28134365-1	2017	Ndi1 is a special type-II complex I nicotinamide-adenine-dinucleotide (NADH):ubiquinone (UQ) oxidoreductase in the yeast respiratory chain, with two bound UQs (UQI and UQII) mediating electron transfer from flavin cofactors to ubiquinone, in the absence of Fe-S chains.	NAD	71-75	NADH-ubiquinone reductase (H(+)-translocating) NDI1	Saccharomyces cerevisiae S288C	0-4
28035412-1	2017	The adipokine nicotinamide phosphoribosyltransferase (Nampt), also known as pre-B-cell colony-enhancing factor or the insulin-mimetic hormone visfatin, has a crucial role in the conversion of nicotinamide to nicotinamide mononucleotide during biosynthesis of the coenzyme nicotinamide adenine dinucleotide.	NAD	272-305	nicotinamide phosphoribosyltransferase	Homo sapiens	14-52
28035412-1	2017	The adipokine nicotinamide phosphoribosyltransferase (Nampt), also known as pre-B-cell colony-enhancing factor or the insulin-mimetic hormone visfatin, has a crucial role in the conversion of nicotinamide to nicotinamide mononucleotide during biosynthesis of the coenzyme nicotinamide adenine dinucleotide.	NAD	272-305	nicotinamide phosphoribosyltransferase	Homo sapiens	54-59
28052027-5	2017	On these bases, we investigated whether the ligation of ERbeta by a selective agonist, the 2,3-bis(4-hydroxyphenyl)-propionitrile (DPN), could impact HL tumor growth.	NAD	131-134	estrogen receptor 2	Homo sapiens	56-62
28052027-7	2017	In nonobese diabetic/severe combined immunodeficient (NOD/SCID) mice engrafted with HL cells, ERbeta activation by DPN was able to reduce lymphoma growth up to 60% and this associated with the induction of tumor cell autophagy.	NAD	115-118	estrogen receptor 2 (beta)	Mus musculus	94-100
28042046-3	2017	With a small substrate and a weak binding cofactor, (NAD+), inhibitor development for PHGDH remains challenging.	NAD	53-57	phosphoglycerate dehydrogenase	Homo sapiens	86-91
27665518-5	2017	Glucose dehydrogenase was successfully immobilized at the surface of DTNB-based electrodes and, in the presence of NAD+, the resulting bioelectrode achieved efficient glucose oxidation with high current densities of 2.03mAcm-2.	NAD	115-119	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	0-21
27634671-12	2017	Knockdown of NOX4 caused an increased mitochondrial membrane potential, decreased mitochondrial superoxide levels, reduced number of apoptotic cells, decreased lipid accumulation, and improved ATP levels and NAD+/NADH ratio after ethanol treatment.	NAD	208-212	NADPH oxidase 4	Mus musculus	13-17
27634671-12	2017	Knockdown of NOX4 caused an increased mitochondrial membrane potential, decreased mitochondrial superoxide levels, reduced number of apoptotic cells, decreased lipid accumulation, and improved ATP levels and NAD+/NADH ratio after ethanol treatment.	NAD	213-217	NADPH oxidase 4	Mus musculus	13-17
27577743-1	2017	As a nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase, demalonylase, and desuccinylase, sirtuin 5 (SIRT5) in host cells has been reportedly observed in the mitochondria, in the cytosol/cytoplasm or in the nucleus.	NAD	5-38	sirtuin 5	Homo sapiens	102-111
27577743-1	2017	As a nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase, demalonylase, and desuccinylase, sirtuin 5 (SIRT5) in host cells has been reportedly observed in the mitochondria, in the cytosol/cytoplasm or in the nucleus.	NAD	5-38	sirtuin 5	Homo sapiens	113-118
27577743-1	2017	As a nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase, demalonylase, and desuccinylase, sirtuin 5 (SIRT5) in host cells has been reportedly observed in the mitochondria, in the cytosol/cytoplasm or in the nucleus.	NAD	40-43	sirtuin 5	Homo sapiens	102-111
27577743-1	2017	As a nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase, demalonylase, and desuccinylase, sirtuin 5 (SIRT5) in host cells has been reportedly observed in the mitochondria, in the cytosol/cytoplasm or in the nucleus.	NAD	40-43	sirtuin 5	Homo sapiens	113-118
27287071-9	2016	CONCLUSIONS: Our results show intracellular NAD+ level as crucial for proliferation and survival of Waldenstrom macroglobulinemia cells, and provides the mechanistic preclinical rationale for targeting Nampt, either alone or with Ibrutinib, to overcome drug resistance and improve patient outcome in Waldenstrom macroglobulinemia.	NAD	44-48	nicotinamide phosphoribosyltransferase	Homo sapiens	202-207
27353858-2	2016	NADH kinase (Pos5) from Saccharomyces cerevisiae catalyzes the phosphorylation of NADH to generate NADPH.	NAD	0-4	NADH kinase	Saccharomyces cerevisiae S288C	13-17
27353858-6	2016	Intracellular cofactor concentration analysis revealed that the ratio of NADP/NAD in pos5 overexpression strain was two times more compared with that of the control without pos5.	NAD	73-76	NADH kinase	Saccharomyces cerevisiae S288C	85-89
26903444-3	2016	RESULTS: Among AFA components, PCB presented the strongest inhibitory effect on UGDH activity, acting as a competitive inhibitor with respect to UDP-glucose and a non-competitive inhibitor with respect to NAD(+).	NAD	205-211	UDP-glucose 6-dehydrogenase	Homo sapiens	80-84
27733626-7	2016	Altogether our results identify Alc1 as an important player in the fast kinetics of the NAD+- and ATP-dependent chromatin relaxation upon DNA damage in vivo.	NAD	88-92	chromodomain helicase DNA binding protein 1 like	Homo sapiens	32-36
27428041-4	2016	Enzymes, such as nicotinamide nucleotide transhydrogenase (NNT) and nicotinamide mononucleotide adenylyltransferase 3 (NMNAT3), that control mitochondrial NAD+ levels appear to be susceptible to aging.	NAD	155-159	nicotinamide nucleotide adenylyltransferase 3	Homo sapiens	68-117
27428041-4	2016	Enzymes, such as nicotinamide nucleotide transhydrogenase (NNT) and nicotinamide mononucleotide adenylyltransferase 3 (NMNAT3), that control mitochondrial NAD+ levels appear to be susceptible to aging.	NAD	155-159	nicotinamide nucleotide adenylyltransferase 3	Homo sapiens	119-125
27428041-7	2016	Importantly, restoring mitochondrial NAD+ levels by overexpressing NNT and NMNAT3 enhanced reprogramming efficiency of aged somatic cells and extended the lifespan of human mesenchymal stem cells by delaying replicative senescence.	NAD	37-41	nicotinamide nucleotide adenylyltransferase 3	Homo sapiens	75-81
27671644-8	2016	Dimerization of the TIR domain from the Caenorhabditis elegans SARM1 ortholog TIR-1 leads to NAD+ loss and neuronal death, indicating these activities are an evolutionarily conserved feature of SARM1 function.	NAD	93-97	ADP-ribosyl cyclase/cyclic ADP-ribose hydrolase;NAD(+) hydrolase tir-1	Caenorhabditis elegans	78-83
27681422-7	2016	We further demonstrate that the NAD(+)-dependent mitochondrial deacylases SIRT3 and SIRT5 play important roles in retinal homeostasis and that NAD(+) deficiency causes SIRT3 dysfunction.	NAD	32-38	sirtuin 5	Mus musculus	84-89
27474736-1	2016	The forward reaction of nicotinamide nucleotide transhydrogenase (NNT) reduces NADP(+) at the expense of NADH oxidation and H(+) movement down the electrochemical potential across the inner mitochondrial membrane, establishing an NADPH/NADP(+) ratio severalfold higher than the NADH/NAD(+) ratio in the matrix.	NAD	105-109	2,4-dienoyl CoA reductase 1, mitochondrial	Mus musculus	230-235
27474736-1	2016	The forward reaction of nicotinamide nucleotide transhydrogenase (NNT) reduces NADP(+) at the expense of NADH oxidation and H(+) movement down the electrochemical potential across the inner mitochondrial membrane, establishing an NADPH/NADP(+) ratio severalfold higher than the NADH/NAD(+) ratio in the matrix.	NAD	278-282	2,4-dienoyl CoA reductase 1, mitochondrial	Mus musculus	230-235
27474736-1	2016	The forward reaction of nicotinamide nucleotide transhydrogenase (NNT) reduces NADP(+) at the expense of NADH oxidation and H(+) movement down the electrochemical potential across the inner mitochondrial membrane, establishing an NADPH/NADP(+) ratio severalfold higher than the NADH/NAD(+) ratio in the matrix.	NAD	283-289	2,4-dienoyl CoA reductase 1, mitochondrial	Mus musculus	230-235
26898756-1	2016	Sirt6 is a histone deacetylase with NAD(+)-dependent activity.	NAD	36-42	sirtuin 6	Homo sapiens	0-5
27576732-1	2016	We previously demonstrated that Pre-B-cell colony-enhancing factor (PBEF), also known as nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme in mammalian NAD(+) biosynthesis pathway, plays a brain and neuronal protective role in ischemic stroke.	NAD	175-181	nicotinamide phosphoribosyltransferase	Homo sapiens	32-66
27576732-1	2016	We previously demonstrated that Pre-B-cell colony-enhancing factor (PBEF), also known as nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme in mammalian NAD(+) biosynthesis pathway, plays a brain and neuronal protective role in ischemic stroke.	NAD	175-181	nicotinamide phosphoribosyltransferase	Homo sapiens	68-72
27576732-1	2016	We previously demonstrated that Pre-B-cell colony-enhancing factor (PBEF), also known as nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme in mammalian NAD(+) biosynthesis pathway, plays a brain and neuronal protective role in ischemic stroke.	NAD	175-181	nicotinamide phosphoribosyltransferase	Homo sapiens	89-127
27576732-1	2016	We previously demonstrated that Pre-B-cell colony-enhancing factor (PBEF), also known as nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme in mammalian NAD(+) biosynthesis pathway, plays a brain and neuronal protective role in ischemic stroke.	NAD	175-181	nicotinamide phosphoribosyltransferase	Homo sapiens	129-134
27576732-5	2016	Furthermore, these beneficial effects by PBEF are dependent on its enzymatic activity of NAD(+) synthesis.	NAD	89-95	nicotinamide phosphoribosyltransferase	Homo sapiens	41-45
27509854-1	2016	Complex I (NADH:ubiquinone oxidoreductase), one of the largest membrane-bound enzymes in the cell, powers ATP synthesis in mammalian mitochondria by using the reducing potential of NADH to drive protons across the inner mitochondrial membrane.	NAD	11-15	apurinic/apyrimidinic endodeoxyribonuclease 1	Homo sapiens	0-10
28725474-6	2016	The mammalian NAD+-dependent protein deacetylase SIRT1 and the key NAD+ biosynthetic enzyme NAMPT mediate these inter-tissue communications.	NAD	14-18	nicotinamide phosphoribosyltransferase	Homo sapiens	92-97
28725474-6	2016	The mammalian NAD+-dependent protein deacetylase SIRT1 and the key NAD+ biosynthetic enzyme NAMPT mediate these inter-tissue communications.	NAD	67-71	nicotinamide phosphoribosyltransferase	Homo sapiens	92-97
27462772-4	2016	Nicotinamide phosphoribosyl transferase (NAMPT) is the main enzyme responsible for recycling cytosolic NAD+ in hypoxic conditions.	NAD	103-107	nicotinamide phosphoribosyltransferase	Homo sapiens	0-39
27462772-4	2016	Nicotinamide phosphoribosyl transferase (NAMPT) is the main enzyme responsible for recycling cytosolic NAD+ in hypoxic conditions.	NAD	103-107	nicotinamide phosphoribosyltransferase	Homo sapiens	41-46
27608947-1	2016	Nicotinamide phosphoribosyltransferase (NAMPT) catalyzes the first rate-limiting step in converting nicotinamide to NAD(+), essential for a number of enzymes and regulatory proteins involved in a variety of cellular processes, including deacetylation enzyme SIRT1 which modulates several tumor suppressors such as p53 and FOXO.	NAD	116-122	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
27062141-3	2016	Nicotinamide mononucleotide adenylyltransferase 2 and sterile alpha and armadillo motif-containing protein 1 play essential roles in the maintenance of axon integrity by regulating the level of nicotinamide adenine dinucleotide, which seems to be the key molecule involved in the maintenance of axonal health.	NAD	194-227	nicotinamide nucleotide adenylyltransferase 2	Mus musculus	0-49
27404390-5	2016	During ethanol metabolism, a low NAD(+)/NADH ratio repressed NAD-dependent deacetylase sirtuin 1 (SIRT1) activity, concomitantly resulting in increased acetylated PPARgamma with high transcriptional activity.	NAD	33-39	peroxisome proliferator activated receptor gamma	Mus musculus	163-172
26095832-3	2016	One class MDH, the plastid-localized NAD-dependent MDH (plNAD-MDH) is known to be important for plant survival in a dark environment, but its biochemical and enzymatic properties have not been well characterized.	NAD	37-40	malate dehydrogenase	Arabidopsis thaliana	10-13
26095832-3	2016	One class MDH, the plastid-localized NAD-dependent MDH (plNAD-MDH) is known to be important for plant survival in a dark environment, but its biochemical and enzymatic properties have not been well characterized.	NAD	37-40	malate dehydrogenase	Arabidopsis thaliana	51-54
26095832-3	2016	One class MDH, the plastid-localized NAD-dependent MDH (plNAD-MDH) is known to be important for plant survival in a dark environment, but its biochemical and enzymatic properties have not been well characterized.	NAD	37-40	malate dehydrogenase	Arabidopsis thaliana	51-54
27181414-1	2016	Recent research in nutritional control of aging suggests that cytosolic increases in the reduced form of nicotinamide adenine dinucleotide and decreasing nicotinamide adenine dinucleotide metabolism plays a central role in controlling the longevity gene products sirtuin 1 (SIRT1), adenosine monophosphate-activated protein kinase (AMPK) and forkhead box O3 (FOXO3).	NAD	105-138	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	282-330
27181414-1	2016	Recent research in nutritional control of aging suggests that cytosolic increases in the reduced form of nicotinamide adenine dinucleotide and decreasing nicotinamide adenine dinucleotide metabolism plays a central role in controlling the longevity gene products sirtuin 1 (SIRT1), adenosine monophosphate-activated protein kinase (AMPK) and forkhead box O3 (FOXO3).	NAD	105-138	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	332-336
27181414-1	2016	Recent research in nutritional control of aging suggests that cytosolic increases in the reduced form of nicotinamide adenine dinucleotide and decreasing nicotinamide adenine dinucleotide metabolism plays a central role in controlling the longevity gene products sirtuin 1 (SIRT1), adenosine monophosphate-activated protein kinase (AMPK) and forkhead box O3 (FOXO3).	NAD	154-187	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	282-330
27181414-1	2016	Recent research in nutritional control of aging suggests that cytosolic increases in the reduced form of nicotinamide adenine dinucleotide and decreasing nicotinamide adenine dinucleotide metabolism plays a central role in controlling the longevity gene products sirtuin 1 (SIRT1), adenosine monophosphate-activated protein kinase (AMPK) and forkhead box O3 (FOXO3).	NAD	154-187	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	332-336
27180906-2	2016	Here, we uncover an epigenetic program mediated by the NAD(+)-dependent histone deacetylase Sirtuin 6 (SIRT6) that is critical for suppression of pancreatic ductal adenocarcinoma (PDAC), one of the most lethal malignancies.	NAD	55-61	sirtuin 6	Homo sapiens	92-101
27180906-2	2016	Here, we uncover an epigenetic program mediated by the NAD(+)-dependent histone deacetylase Sirtuin 6 (SIRT6) that is critical for suppression of pancreatic ductal adenocarcinoma (PDAC), one of the most lethal malignancies.	NAD	55-61	sirtuin 6	Homo sapiens	103-108
27018006-2	2016	Nicotinamide phosphoribosyltransferase (NAMPT), also an adipokine known as visfatin, is the rate-limiting enzyme for mammalian nicotinamide adenine dinucleotide (NAD) salvage synthesis by generating nicotinamide mononucleotide (NMN) from nicotinamide.	NAD	127-160	nicotinamide phosphoribosyltransferase	Homo sapiens	0-38
27018006-2	2016	Nicotinamide phosphoribosyltransferase (NAMPT), also an adipokine known as visfatin, is the rate-limiting enzyme for mammalian nicotinamide adenine dinucleotide (NAD) salvage synthesis by generating nicotinamide mononucleotide (NMN) from nicotinamide.	NAD	127-160	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
27018006-2	2016	Nicotinamide phosphoribosyltransferase (NAMPT), also an adipokine known as visfatin, is the rate-limiting enzyme for mammalian nicotinamide adenine dinucleotide (NAD) salvage synthesis by generating nicotinamide mononucleotide (NMN) from nicotinamide.	NAD	127-160	nicotinamide phosphoribosyltransferase	Homo sapiens	75-83
27018006-2	2016	Nicotinamide phosphoribosyltransferase (NAMPT), also an adipokine known as visfatin, is the rate-limiting enzyme for mammalian nicotinamide adenine dinucleotide (NAD) salvage synthesis by generating nicotinamide mononucleotide (NMN) from nicotinamide.	NAD	162-165	nicotinamide phosphoribosyltransferase	Homo sapiens	0-38
27018006-2	2016	Nicotinamide phosphoribosyltransferase (NAMPT), also an adipokine known as visfatin, is the rate-limiting enzyme for mammalian nicotinamide adenine dinucleotide (NAD) salvage synthesis by generating nicotinamide mononucleotide (NMN) from nicotinamide.	NAD	162-165	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
27018006-2	2016	Nicotinamide phosphoribosyltransferase (NAMPT), also an adipokine known as visfatin, is the rate-limiting enzyme for mammalian nicotinamide adenine dinucleotide (NAD) salvage synthesis by generating nicotinamide mononucleotide (NMN) from nicotinamide.	NAD	162-165	nicotinamide phosphoribosyltransferase	Homo sapiens	75-83
27018006-4	2016	NAMPT-mediated NAD biosynthesis in neural stem/progenitor cells is important for their proliferation, self-renewal, and formation of oligodendrocytes in vivo and in vitro.	NAD	15-18	nicotinamide phosphoribosyltransferase	Homo sapiens	0-5
27155879-4	2016	These mitochondrial changes appear to be IP3R3-dependent and resulted in decreased NAD/NADH ratios and higher electron transport chain oxidase activity.	NAD	83-86	inositol 1,4,5-trisphosphate receptor type 3	Homo sapiens	41-46
27155879-4	2016	These mitochondrial changes appear to be IP3R3-dependent and resulted in decreased NAD/NADH ratios and higher electron transport chain oxidase activity.	NAD	87-91	inositol 1,4,5-trisphosphate receptor type 3	Homo sapiens	41-46
26485210-0	2016	NAMPT and NAMPT-controlled NAD Metabolism in Vascular Repair.	NAD	27-30	nicotinamide phosphoribosyltransferase	Homo sapiens	10-15
26485210-3	2016	Nicotinamide phosphoribosyltransferase (NAMPT) is the rate-limiting enzyme for NAD biosynthesis in mammals.	NAD	79-82	nicotinamide phosphoribosyltransferase	Homo sapiens	0-38
26485210-3	2016	Nicotinamide phosphoribosyltransferase (NAMPT) is the rate-limiting enzyme for NAD biosynthesis in mammals.	NAD	79-82	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
26485210-5	2016	Rapidly accumulating data in the past decade show that NAMPT and NAMPT-controlled NAD metabolism regulate fundamental biological functions in endothelial cells, vascular smooth muscle cells, and endothelial progenitor cells.	NAD	82-85	nicotinamide phosphoribosyltransferase	Homo sapiens	65-70
26485210-6	2016	The NAD-consuming proteins, including sirtuins, poly-ADP-ribose polymerases (PARPs), and CD38, may contribute to the regulatory effects of NAMPT-NAD axis in these cells and vascular repair.	NAD	4-7	nicotinamide phosphoribosyltransferase	Homo sapiens	139-144
26485210-6	2016	The NAD-consuming proteins, including sirtuins, poly-ADP-ribose polymerases (PARPs), and CD38, may contribute to the regulatory effects of NAMPT-NAD axis in these cells and vascular repair.	NAD	145-148	nicotinamide phosphoribosyltransferase	Homo sapiens	139-144
26485210-7	2016	This review discusses the current data regarding NAMPT and NAMPT-controlled NAD metabolism in vascular repair and the clinical potential translational application of NAMPT-related products in treatment of cardiovascular and cerebrovascular disease.	NAD	76-79	nicotinamide phosphoribosyltransferase	Homo sapiens	59-64
26485210-7	2016	This review discusses the current data regarding NAMPT and NAMPT-controlled NAD metabolism in vascular repair and the clinical potential translational application of NAMPT-related products in treatment of cardiovascular and cerebrovascular disease.	NAD	76-79	nicotinamide phosphoribosyltransferase	Homo sapiens	59-64
27159677-4	2016	Cellular glycolysis, including cellular glucose uptake, lactate, ATP/ADP and NAD+/NADH ratios, are also inhibited by miR-186.	NAD	77-81	microRNA 186	Homo sapiens	117-124
27159677-4	2016	Cellular glycolysis, including cellular glucose uptake, lactate, ATP/ADP and NAD+/NADH ratios, are also inhibited by miR-186.	NAD	82-86	microRNA 186	Homo sapiens	117-124
26886147-4	2016	SIRT6, one of the highly conserved NAD-dependent class III deacetylases, has been implicated in cardiovascular diseases.	NAD	35-38	sirtuin 6	Homo sapiens	0-5
26516686-2	2016	For instance, the use of GDh NAD(+)-dependent for glucose oxidation is of great interest in biofuel cell technology because the enzyme are unaffected by the presence of molecular oxygen commonly present in electrolyte.	NAD	29-35	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	25-28
26675349-3	2016	Here, we show that the NAD(+)-dependent deacetylase SIRT6 is highly expressed in MM cells, as an adaptive response to genomic stability, and that high SIRT6 levels are associated with adverse prognosis.	NAD	23-29	sirtuin 6	Homo sapiens	52-57
26675349-3	2016	Here, we show that the NAD(+)-dependent deacetylase SIRT6 is highly expressed in MM cells, as an adaptive response to genomic stability, and that high SIRT6 levels are associated with adverse prognosis.	NAD	23-29	sirtuin 6	Homo sapiens	151-156
26687331-1	2016	Human xanthine oxidoreductase (XOR) catalyzes the last two steps of purine catabolism and is present in two interconvertible forms, which may utilize O2 or NAD(+) as electron acceptors.	NAD	156-162	xanthine dehydrogenase	Homo sapiens	6-29
26687331-1	2016	Human xanthine oxidoreductase (XOR) catalyzes the last two steps of purine catabolism and is present in two interconvertible forms, which may utilize O2 or NAD(+) as electron acceptors.	NAD	156-162	xanthine dehydrogenase	Homo sapiens	31-34
26717993-1	2016	SIRT6, a member of the mammalian sirtuins family, functions as a mono-ADP-ribosyl transferase and NAD(+)-dependent deacylase of both acetyl groups and long-chain fatty acyl groups.	NAD	98-104	sirtuin 6	Homo sapiens	0-5
26675378-2	2016	As cancer cells have increased NAD requirements, the main NAD salvage enzymes in humans, nicotinamide phosphoribosyltransferase (NAMPT) and nicotinate phosphoribosyltransferase (NAPRT), are involved in the development of novel anti-cancer therapies.	NAD	31-34	nicotinamide phosphoribosyltransferase	Homo sapiens	89-127
26675378-2	2016	As cancer cells have increased NAD requirements, the main NAD salvage enzymes in humans, nicotinamide phosphoribosyltransferase (NAMPT) and nicotinate phosphoribosyltransferase (NAPRT), are involved in the development of novel anti-cancer therapies.	NAD	31-34	nicotinamide phosphoribosyltransferase	Homo sapiens	129-134
26675378-2	2016	As cancer cells have increased NAD requirements, the main NAD salvage enzymes in humans, nicotinamide phosphoribosyltransferase (NAMPT) and nicotinate phosphoribosyltransferase (NAPRT), are involved in the development of novel anti-cancer therapies.	NAD	58-61	nicotinamide phosphoribosyltransferase	Homo sapiens	89-127
26675378-2	2016	As cancer cells have increased NAD requirements, the main NAD salvage enzymes in humans, nicotinamide phosphoribosyltransferase (NAMPT) and nicotinate phosphoribosyltransferase (NAPRT), are involved in the development of novel anti-cancer therapies.	NAD	58-61	nicotinamide phosphoribosyltransferase	Homo sapiens	129-134
26001219-7	2016	Use of a pan-sirtuin inhibitor and shRNA-mediated protein knockdown led us to uncover a role for the NAD(+)-dependent family of sirtuins, and in particular for SIRT2 and SIRT5, in the regulation of the necroptotic cell death program.	NAD	101-107	sirtuin 5	Mus musculus	170-175
25384549-6	2016	High expression of NaDC3 caused a prominent increase in intracellular levels of Krebs cycle intermediates and NADH.	NAD	110-114	solute carrier family 13 member 3	Homo sapiens	19-24
25384549-7	2016	Exogenous NADH and NAD(+) may aggravate and attenuate the aging phenotypes induced by NaDC3, respectively.	NAD	10-14	solute carrier family 13 member 3	Homo sapiens	86-91
25384549-7	2016	Exogenous NADH and NAD(+) may aggravate and attenuate the aging phenotypes induced by NaDC3, respectively.	NAD	19-25	solute carrier family 13 member 3	Homo sapiens	86-91
25384549-8	2016	These results suggest that NaDC3 can induce premature cellular senescence by promoting the transport of Krebs cycle intermediates, increasing generation of NADH and reactive oxygen species and leading to oxidative damage.	NAD	156-160	solute carrier family 13 member 3	Homo sapiens	27-32
26819426-7	2016	:  RESULTS: Serum Cys-c levels were significantly higher in the DPN group than that in the NDPN group [(1.04+-0.43) vs (0.80+-0.25) mg/L, P&lt;0.01].	NAD	64-67	cystatin C	Homo sapiens	18-23
26819426-12	2016	Binary logistic regression analysis found that age, Cys-c and HbA1C were independent risk factors for predicting DPN in T2DM patients (all P&lt;0.01).	NAD	113-116	cystatin C	Homo sapiens	52-57
26819426-13	2016	ROC curve analysis revealed that the optimal cutoff of Cys-c to predict DPN in T2DM patients was 0.996 mg/L, the sensitivity was 43.9%, the specificity was 83.7%, and the area under curve was 0.663. :  CONCLUSION: Serum Cys-c levels are well correlated with VPT in patients with T2DM.	NAD	72-75	cystatin C	Homo sapiens	55-60
26819426-13	2016	ROC curve analysis revealed that the optimal cutoff of Cys-c to predict DPN in T2DM patients was 0.996 mg/L, the sensitivity was 43.9%, the specificity was 83.7%, and the area under curve was 0.663. :  CONCLUSION: Serum Cys-c levels are well correlated with VPT in patients with T2DM.	NAD	72-75	cystatin C	Homo sapiens	220-225
26330291-0	2015	A Nampt inhibitor FK866 mimics vitamin B3 deficiency by causing senescence of human fibroblastic Hs68 cells via attenuation of NAD(+)-SIRT1 signaling.	NAD	127-133	nicotinamide phosphoribosyltransferase	Homo sapiens	2-7
26330291-3	2015	FK866 (a Nampt inhibitor) can reduce intracellular NAD(+) level and induce senescence of human Hs68 cells.	NAD	51-57	nicotinamide phosphoribosyltransferase	Homo sapiens	9-14
26492815-2	2015	Here we determined three crystal structures of mTDH: wild-type (WT) in the apo form; in complex with NAD(+) and a substrate analog, glycerol, or with only NAD(+); as well as the R180K variant with NAD(+).	NAD	101-107	L-threonine dehydrogenase	Mus musculus	47-51
26538317-1	2015	Nicotinamide phosphoribosyltransferase (NAMPT), also an adipokine known as visfatin, acts via enzymatic activity to synthesize nicotinamide mononucleotide (NMN) and then to maintain homeostasis of nicotinamide adenine dinucleotide (NAD), which plays a dual role in energy metabolism and biological signaling.	NAD	197-230	nicotinamide phosphoribosyltransferase	Homo sapiens	0-38
26538317-1	2015	Nicotinamide phosphoribosyltransferase (NAMPT), also an adipokine known as visfatin, acts via enzymatic activity to synthesize nicotinamide mononucleotide (NMN) and then to maintain homeostasis of nicotinamide adenine dinucleotide (NAD), which plays a dual role in energy metabolism and biological signaling.	NAD	197-230	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
26538317-1	2015	Nicotinamide phosphoribosyltransferase (NAMPT), also an adipokine known as visfatin, acts via enzymatic activity to synthesize nicotinamide mononucleotide (NMN) and then to maintain homeostasis of nicotinamide adenine dinucleotide (NAD), which plays a dual role in energy metabolism and biological signaling.	NAD	197-230	nicotinamide phosphoribosyltransferase	Homo sapiens	75-83
26538317-1	2015	Nicotinamide phosphoribosyltransferase (NAMPT), also an adipokine known as visfatin, acts via enzymatic activity to synthesize nicotinamide mononucleotide (NMN) and then to maintain homeostasis of nicotinamide adenine dinucleotide (NAD), which plays a dual role in energy metabolism and biological signaling.	NAD	232-235	nicotinamide phosphoribosyltransferase	Homo sapiens	0-38
26538317-1	2015	Nicotinamide phosphoribosyltransferase (NAMPT), also an adipokine known as visfatin, acts via enzymatic activity to synthesize nicotinamide mononucleotide (NMN) and then to maintain homeostasis of nicotinamide adenine dinucleotide (NAD), which plays a dual role in energy metabolism and biological signaling.	NAD	232-235	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
26538317-1	2015	Nicotinamide phosphoribosyltransferase (NAMPT), also an adipokine known as visfatin, acts via enzymatic activity to synthesize nicotinamide mononucleotide (NMN) and then to maintain homeostasis of nicotinamide adenine dinucleotide (NAD), which plays a dual role in energy metabolism and biological signaling.	NAD	232-235	nicotinamide phosphoribosyltransferase	Homo sapiens	75-83
26538317-2	2015	Of note, the NAMPT metabolic pathway connects NAD-dependent sirtuin (SIRT) signaling, constituting a strong intrinsic defense system against various stresses.	NAD	46-49	nicotinamide phosphoribosyltransferase	Homo sapiens	13-18
26432643-4	2015	In contrast, human recombinant NMNAT3 localizes to the mitochondrial matrix and is able to catalyze NAD(+) biosynthesis in vitro.	NAD	100-106	nicotinamide nucleotide adenylyltransferase 3	Homo sapiens	31-37
26432643-5	2015	However, whether the endogenous NMNAT3 protein is functionally effective at generating NAD(+) in mitochondria of intact human cells still remains to be demonstrated.	NAD	87-93	nicotinamide nucleotide adenylyltransferase 3	Homo sapiens	32-38
26432643-10	2015	We provide further support for the alternative possibility, namely intramitochondrial NAD(+) synthesis, by demonstrating the presence of endogenous NMNAT3 in the mitochondria of human cells.	NAD	86-92	nicotinamide nucleotide adenylyltransferase 3	Homo sapiens	148-154
26058697-8	2015	We further showed that ketones" effects were achieved by upregulating NAD(+)-dependent SIRT3 and its downstream substrates forkhead box O3a (FoxO3a) and superoxide dismutase 2 (SOD2) in the penumbra region since knocking down SIRT3 in vitro diminished ketones" beneficial effects.	NAD	70-76	superoxide dismutase 2	Homo sapiens	153-175
26058697-8	2015	We further showed that ketones" effects were achieved by upregulating NAD(+)-dependent SIRT3 and its downstream substrates forkhead box O3a (FoxO3a) and superoxide dismutase 2 (SOD2) in the penumbra region since knocking down SIRT3 in vitro diminished ketones" beneficial effects.	NAD	70-76	superoxide dismutase 2	Homo sapiens	177-181
26206299-8	2015	In contrast, 2,3-bis-4-hydroxyphenyl (DPN), a specific agonist for ERbeta, had no effect on neurite outgrowth.	NAD	38-41	estrogen receptor 2 (beta)	Mus musculus	67-73
28649542-3	2015	The diagnosis of NADH-CYB5R3 deficiency was made by the demonstration of significantly reduced NADH-CYB5R3 activity in the patient and intermediate enzyme activity in both the parents.	NAD	17-21	cytochrome b5 reductase 3	Homo sapiens	22-28
26481044-2	2015	The rate-limiting step in the major pathway of mammalian NAD(+) biosynthesis is mediated by nicotinamide phosphoribosyltransferase (Nampt).	NAD	57-63	nicotinamide phosphoribosyltransferase	Homo sapiens	92-130
26481044-2	2015	The rate-limiting step in the major pathway of mammalian NAD(+) biosynthesis is mediated by nicotinamide phosphoribosyltransferase (Nampt).	NAD	57-63	nicotinamide phosphoribosyltransferase	Homo sapiens	132-137
26089537-4	2015	The contribution of the ADO-generating ectoenzymes in the regulatory response was shown by: 1) selective inhibition of the enzymatic activities of CD39, CD73, and CD38; 2) the ability of suppressor T cells to convert exogenously added ATP and NAD(+) to ADO; and 3) a positive correlation between ectoenzyme expression, ADO levels, and suppression abilities.	NAD	243-249	2-aminoethanethiol (cysteamine) dioxygenase	Mus musculus	24-27
26162744-4	2015	GalE and related enzymes display unusual enzymologic, chemical, and stereochemical properties; including irreversible binding of the cofactor NAD and uridine nucleotide-induced activation of this cofactor.	NAD	142-145	UDP-galactose-4-epimerase	Homo sapiens	0-4
26215259-1	2015	Nicotinamide phosphoribosyltransferase (NAMPT) is a regulator of the intracellular nicotinamide adenine dinucleotide (NAD) pool.	NAD	83-116	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
26215259-1	2015	Nicotinamide phosphoribosyltransferase (NAMPT) is a regulator of the intracellular nicotinamide adenine dinucleotide (NAD) pool.	NAD	118-121	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
26215259-4	2015	Through its NAD-biosynthetic activity, NAMPT influences the activity of NAD-dependent enzymes, thereby regulating cellular metabolism.	NAD	12-15	nicotinamide phosphoribosyltransferase	Homo sapiens	39-44
26215259-4	2015	Through its NAD-biosynthetic activity, NAMPT influences the activity of NAD-dependent enzymes, thereby regulating cellular metabolism.	NAD	72-75	nicotinamide phosphoribosyltransferase	Homo sapiens	39-44
25819580-1	2015	OBJECTIVE: SIRT6, a member of the sirtuin family of nicotinamide adenine dinucleotide (NAD(+))-dependent protein deacetylases, has been implicated as a key factor in aging-related diseases.	NAD	52-85	sirtuin 6	Homo sapiens	11-16
26185373-10	2015	This was concomitant with increased levels of NAD(+) (0.87 +- 0.22 vs 1.195 +- 0.144, P &lt; 0.05) the co-factor necessary for SIRT1 activity, as well as with decreases in ac-FoxO1 expression.	NAD	46-52	forkhead box O1	Rattus norvegicus	175-180
26018082-1	2015	Leber congenital amaurosis 9 (LCA9) is an autosomal recessive retinal degeneration condition caused by mutations in the NAD(+) biosynthetic enzyme NMNAT1.	NAD	120-126	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	147-153
26024774-0	2015	Apoptosis induced by NAD depletion is inhibited by KN-93 in a CaMKII-independent manner.	NAD	21-24	calcium/calmodulin dependent protein kinase II gamma	Homo sapiens	62-68
26024774-1	2015	Nicotinamide phosphoribosyltransferase (NAMPT) is a key enzyme that catalyzes the synthesis of nicotinamide mononucleotide from nicotinamide (Nam) in the salvage pathway of mammalian NAD biosynthesis.	NAD	183-186	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
26024774-2	2015	Several potent NAMPT inhibitors have been identified and used to investigate the role of intracellular NAD and to develop therapeutics.	NAD	103-106	nicotinamide phosphoribosyltransferase	Homo sapiens	15-20
26024774-3	2015	NAD depletion induced by NAMPT inhibitors depolarizes mitochondrial membrane potential and causes apoptosis in a range of cell types.	NAD	0-3	nicotinamide phosphoribosyltransferase	Homo sapiens	25-30
25446886-3	2015	Cyt-b5 can augment the 17,20-lyase activity of CYP17A1 by promoting the interaction of CYP17A1 and POR; enhance the 16-ene-synthase activity of CYP17A1 by acting as an electron donor; and enhance the activity of 3betaHSD by increasing the affinity of 3betaHSD for its cofactor NAD(+).	NAD	277-283	cytochrome P450 family 17 subfamily A member 1	Homo sapiens	47-54
25709099-2	2015	NAD is generated de novo from tryptophan or recycled from NAM through the NAMPT-dependent salvage pathway.	NAD	0-3	nicotinamide phosphoribosyltransferase	Homo sapiens	74-79
25709099-5	2015	Hence, they are more reliant on the NAMPT salvage pathway for NAD regeneration making this enzyme an attractive therapeutic target for cancer.	NAD	62-65	nicotinamide phosphoribosyltransferase	Homo sapiens	36-41
25864423-6	2015	Frm2 primarily utilizes NADH to reduce 4-NQO.	NAD	24-28	type II nitroreductase	Saccharomyces cerevisiae S288C	0-4
25863291-6	2015	IR increased cardiomyocyte apoptosis; the cleavage of caspase 3, induced a transient upregulation of SIRT1 and downregulation of SIRT6 expression, but decreased SIRT1 activity and reduced NAD(+) content.	NAD	188-194	caspase 3	Rattus norvegicus	54-63
25944913-0	2015	Inhibition of Nicotinamide Phosphoribosyltransferase (NAMPT), an Enzyme Essential for NAD+ Biosynthesis, Leads to Altered Carbohydrate Metabolism in Cancer Cells.	NAD	86-90	nicotinamide phosphoribosyltransferase	Homo sapiens	14-52
25944913-0	2015	Inhibition of Nicotinamide Phosphoribosyltransferase (NAMPT), an Enzyme Essential for NAD+ Biosynthesis, Leads to Altered Carbohydrate Metabolism in Cancer Cells.	NAD	86-90	nicotinamide phosphoribosyltransferase	Homo sapiens	54-59
25944913-1	2015	Nicotinamide phosphoribosyltransferase (NAMPT) has been extensively studied due to its essential role in NAD(+) biosynthesis in cancer cells and the prospect of developing novel therapeutics.	NAD	105-111	nicotinamide phosphoribosyltransferase	Homo sapiens	0-38
25944913-1	2015	Nicotinamide phosphoribosyltransferase (NAMPT) has been extensively studied due to its essential role in NAD(+) biosynthesis in cancer cells and the prospect of developing novel therapeutics.	NAD	105-111	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
26124772-0	2015	Caenorhabditis elegans expressing the Saccharomyces cerevisiae NADH alternative dehydrogenase Ndi1p, as a tool to identify new genes involved in complex I related diseases.	NAD	63-67	NADH-ubiquinone reductase (H(+)-translocating) NDI1	Saccharomyces cerevisiae S288C	94-99
27308565-1	2016	Nicotinamide phosphoribosyltransferase (NAMPT) is crucial for nicotinamide adenine dinucleotide (NAD(+)) biosynthesis in mammalian cells.	NAD	62-95	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
27308565-1	2016	Nicotinamide phosphoribosyltransferase (NAMPT) is crucial for nicotinamide adenine dinucleotide (NAD(+)) biosynthesis in mammalian cells.	NAD	97-104	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
27308565-2	2016	NAMPT inhibitors represent multifunctional anticancer agents that act on NAD(+) metabolism to shut down glycolysis, nucleotide biosynthesis, and ATP generation and act indirectly as PARP and sirtuin inhibitors.	NAD	73-79	nicotinamide phosphoribosyltransferase	Homo sapiens	0-5
27308565-3	2016	The selectivity of NAMPT inhibitors preys on the increased metabolic requirements to replenish NAD(+) in cancer cells.	NAD	95-101	nicotinamide phosphoribosyltransferase	Homo sapiens	19-24
25878356-3	2015	There is also a concomitant increase in NADH-dependent glutamate dehydrogenase (GDH) activity during the ripening transition.	NAD	40-44	glutamate dehydrogenase	Solanum lycopersicum	80-83
25839883-1	2015	Class I sirtuin genes including SIRT1, SIRT2 and SIRT3, are members of the nicotinamide adenine dinucleotide (NAD)-dependent family of histone deacetylases, and play essential roles in senescence, metabolism, and apoptosis.	NAD	75-108	sirtuin 2	Bos taurus	39-44
25839883-1	2015	Class I sirtuin genes including SIRT1, SIRT2 and SIRT3, are members of the nicotinamide adenine dinucleotide (NAD)-dependent family of histone deacetylases, and play essential roles in senescence, metabolism, and apoptosis.	NAD	110-113	sirtuin 2	Bos taurus	39-44
25945581-4	2015	Here, it is shown that the putative betaine aldehyde dehydrogenase SACOL2628 from the early MRSA isolate COL (SaBADH) utilizes betaine aldehyde as the primary substrate and nicotinamide adenine dinucleotide (NAD(+)) as the cofactor.	NAD	173-206	AT695_RS04200	Staphylococcus aureus	36-66
25945581-4	2015	Here, it is shown that the putative betaine aldehyde dehydrogenase SACOL2628 from the early MRSA isolate COL (SaBADH) utilizes betaine aldehyde as the primary substrate and nicotinamide adenine dinucleotide (NAD(+)) as the cofactor.	NAD	208-214	AT695_RS04200	Staphylococcus aureus	36-66
25765152-0	2015	A structural model for FOXRED1, an FAD-dependent oxidoreductase necessary for NADH: Ubiquinone oxidoreductase (complex I) assembly.	NAD	78-82	FAD dependent oxidoreductase domain containing 1	Homo sapiens	23-30
25413692-11	2015	Modeling indicated that the lack of activity in ALDH1B1*2 is likely due to poor NAD(+) binding.	NAD	80-86	aldehyde dehydrogenase 1 family member B1	Homo sapiens	48-55
25413692-12	2015	Modeling also suggests that ALDH1B1*3 may be less able to metabolize all-trans retinaldehyde and that ALDH1B1*5 may bind NAD(+) poorly.	NAD	121-127	aldehyde dehydrogenase 1 family member B1	Homo sapiens	102-109
25413692-14	2015	One of the three human polymorphisms, ALDH1B1*2, is catalytically inactive, likely due to poor NAD(+) binding.	NAD	95-101	aldehyde dehydrogenase 1 family member B1	Homo sapiens	38-45
25870284-6	2015	Biochemical assays using mutant forms of GAPDH with either reduced activity or reduced affinity to SRR revealed that GAPDH suppresses SRR activity by direct binding to GAPDH and through NADH, a product of GAPDH.	NAD	186-190	serine racemase	Homo sapiens	99-102
25870284-6	2015	Biochemical assays using mutant forms of GAPDH with either reduced activity or reduced affinity to SRR revealed that GAPDH suppresses SRR activity by direct binding to GAPDH and through NADH, a product of GAPDH.	NAD	186-190	serine racemase	Homo sapiens	134-137
25870284-7	2015	NADH allosterically inhibits the activity of SRR by promoting the disassociation of ATP from SRR.	NAD	0-4	serine racemase	Homo sapiens	45-48
25870284-7	2015	NADH allosterically inhibits the activity of SRR by promoting the disassociation of ATP from SRR.	NAD	0-4	serine racemase	Homo sapiens	93-96
25876076-5	2015	Because the NAD+ biosynthetic enzyme nicotinamide phosphoribosyltransferase (NAMPT) in vitro is robustly potentiated by ATP, we hypothesized that nutritional energy might stimulate cellular NAMPT to produce NAD+ and thereby augment TNKS catalysis.	NAD	12-16	nicotinamide phosphoribosyltransferase	Homo sapiens	37-75
25876076-5	2015	Because the NAD+ biosynthetic enzyme nicotinamide phosphoribosyltransferase (NAMPT) in vitro is robustly potentiated by ATP, we hypothesized that nutritional energy might stimulate cellular NAMPT to produce NAD+ and thereby augment TNKS catalysis.	NAD	12-16	nicotinamide phosphoribosyltransferase	Homo sapiens	77-82
25876076-5	2015	Because the NAD+ biosynthetic enzyme nicotinamide phosphoribosyltransferase (NAMPT) in vitro is robustly potentiated by ATP, we hypothesized that nutritional energy might stimulate cellular NAMPT to produce NAD+ and thereby augment TNKS catalysis.	NAD	12-16	nicotinamide phosphoribosyltransferase	Homo sapiens	190-195
25876076-5	2015	Because the NAD+ biosynthetic enzyme nicotinamide phosphoribosyltransferase (NAMPT) in vitro is robustly potentiated by ATP, we hypothesized that nutritional energy might stimulate cellular NAMPT to produce NAD+ and thereby augment TNKS catalysis.	NAD	207-211	nicotinamide phosphoribosyltransferase	Homo sapiens	37-75
25876076-5	2015	Because the NAD+ biosynthetic enzyme nicotinamide phosphoribosyltransferase (NAMPT) in vitro is robustly potentiated by ATP, we hypothesized that nutritional energy might stimulate cellular NAMPT to produce NAD+ and thereby augment TNKS catalysis.	NAD	207-211	nicotinamide phosphoribosyltransferase	Homo sapiens	77-82
25876076-5	2015	Because the NAD+ biosynthetic enzyme nicotinamide phosphoribosyltransferase (NAMPT) in vitro is robustly potentiated by ATP, we hypothesized that nutritional energy might stimulate cellular NAMPT to produce NAD+ and thereby augment TNKS catalysis.	NAD	207-211	nicotinamide phosphoribosyltransferase	Homo sapiens	190-195
25541039-5	2015	SIRT5, which localizes in the mitochondrial matrix, is nicotinamide adenine dinucleotide (NAD(+))-dependent histone deacetylase.	NAD	90-96	sirtuin 5	Mus musculus	0-5
25580531-17	2015	NADH staining revealed that type I fibres were decreased and type IIb fibres increased in mice treated with Ang II at 1 week.	NAD	0-4	angiogenin, ribonuclease, RNase A family, 5	Mus musculus	108-111
25505128-2	2015	NAMPT is of interest for oncology, because it catalyzes the rate-limiting step in the salvage pathway to generate nicotinamide adenine dinucleotide (NAD), which is considered a universal energy- and signal-carrying molecule involved in cellular energy metabolism and many homeostatic functions.	NAD	114-147	nicotinamide phosphoribosyltransferase	Homo sapiens	0-5
25505128-2	2015	NAMPT is of interest for oncology, because it catalyzes the rate-limiting step in the salvage pathway to generate nicotinamide adenine dinucleotide (NAD), which is considered a universal energy- and signal-carrying molecule involved in cellular energy metabolism and many homeostatic functions.	NAD	149-152	nicotinamide phosphoribosyltransferase	Homo sapiens	0-5
25505128-6	2015	We demonstrate that this toxicity is not mitigated by coadministration of nicotinic acid (NA), which can enable NAD production through the NAMPT-independent pathway.	NAD	112-115	nicotinamide phosphoribosyltransferase	Homo sapiens	139-144
25894564-2	2015	Nicotinamide phosphoribosyltransferase (NAMPT) catalyzes the rate-limiting step of an important salvage pathway in which nicotinamide is recycled into NAD.	NAD	151-154	nicotinamide phosphoribosyltransferase	Homo sapiens	0-38
25894564-2	2015	Nicotinamide phosphoribosyltransferase (NAMPT) catalyzes the rate-limiting step of an important salvage pathway in which nicotinamide is recycled into NAD.	NAD	151-154	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
25894564-8	2015	We further demonstrate that the MK toxicity is on-target based on the evidence that nicotinic acid (NA), which is converted to NAD via a NAMPT-independent pathway, can mitigate NAMPTi toxicity to human CFU-MK in vitro and was also protective for the hematotoxicity in rats in vivo.	NAD	127-130	nicotinamide phosphoribosyltransferase	Homo sapiens	137-142
25406093-3	2015	Here we show that, in addition to catalyzing oxidation of 3-phosphoglycerate, PHGDH catalyzes NADH-dependent reduction of alpha-ketoglutarate (AKG) to the oncometabolite d-2-hydroxyglutarate (d-2HG).	NAD	94-98	phosphoglycerate dehydrogenase	Homo sapiens	78-83
25447145-4	2015	Here we describe three Arabidopsis ADH conformations obtained from two crystals, the apo crystal that was free of ligand, and the complex crystal that was with NAD.	NAD	160-163	alcohol dehydrogenase 1	Arabidopsis thaliana	35-38
25278485-5	2015	The molecular events triggered by Nampt include elevated production of NAD(+) and up-regulation of H2S producing enzymes, cystathionine beta synthase (CBS) and cystathionase (CTH) with 3-mercaptopyruvate sulfurtransferase (MST) being detectable only in 3D spheroids.	NAD	71-77	nicotinamide phosphoribosyltransferase	Homo sapiens	34-39
26075037-2	2015	Sirtuins (silent information regulator 2 (Sir2) proteins), NAD(+) dependent enzymes with deacetylase and/or mono-ADP-ribosyltransferase activity, are emerging as key antiaging molecules and regulators in many diseases.	NAD	59-65	ADP-ribosyltransferase 3 (inactive)	Homo sapiens	108-135
25433599-4	2014	A key enzyme in the PCB catabolic pathway is NAD-dependent cis-2,3-dihydrobiphenyl-2,3-diol dehydrogenase (BphB), for which the crystal structure from Pp has been crystallized in apo-, NAD-bound and biphenyldiol-/NAD-bound forms.	NAD	45-48	choline dehydrogenase	Pandoraea pnomenusa	92-105
25433599-4	2014	A key enzyme in the PCB catabolic pathway is NAD-dependent cis-2,3-dihydrobiphenyl-2,3-diol dehydrogenase (BphB), for which the crystal structure from Pp has been crystallized in apo-, NAD-bound and biphenyldiol-/NAD-bound forms.	NAD	185-188	choline dehydrogenase	Pandoraea pnomenusa	92-105
25433599-4	2014	A key enzyme in the PCB catabolic pathway is NAD-dependent cis-2,3-dihydrobiphenyl-2,3-diol dehydrogenase (BphB), for which the crystal structure from Pp has been crystallized in apo-, NAD-bound and biphenyldiol-/NAD-bound forms.	NAD	185-188	choline dehydrogenase	Pandoraea pnomenusa	92-105
26190959-4	2014	The nicotinamide adenine dinucleotide (NAD+) required in the hUGDH reaction is continuously regenerated in a three-step chemo-enzymatic cascade.	NAD	4-37	UDP-glucose 6-dehydrogenase	Homo sapiens	61-66
26190959-4	2014	The nicotinamide adenine dinucleotide (NAD+) required in the hUGDH reaction is continuously regenerated in a three-step chemo-enzymatic cascade.	NAD	39-43	UDP-glucose 6-dehydrogenase	Homo sapiens	61-66
26190959-7	2014	A comprehensive analysis of the coupled chemo-enzymatic reactions revealed pronounced inhibition of hUGDH by NADH and UDP-xylose as well as an adequate oxygen supply for PQ re-oxidation as major bottlenecks of effective performance of the overall multi-step reaction system.	NAD	109-113	UDP-glucose 6-dehydrogenase	Homo sapiens	100-105
25150110-5	2014	The natural ligands, NAD(+) and UDP-glucose, stabilize GALE.	NAD	21-27	UDP-galactose-4-epimerase	Homo sapiens	55-59
24444663-3	2014	We discuss here possible mechanisms of high photorespiratory flux maintenance in mitochondria and suggest that it is fulfilled under conditions where the concentrations of glycine decarboxylase reaction products NADH and CO2 achieve an equilibrium provided by malate dehydrogenase and carbonic anhydrase, respectively.	NAD	212-216	glycine decarboxylase	Homo sapiens	172-193
25239532-9	2014	Results suggested that hypothalamic glycolysis (inhibited by ALA and promoted by 2-deoxy-d-glucose) and SIRT1 (inhibited by NADH and promoted by NAD(+)), not PPARalpha, were probably involved in feed intake regulation in chickens.	NAD	124-128	sirtuin 1	Gallus gallus	104-109
25239532-9	2014	Results suggested that hypothalamic glycolysis (inhibited by ALA and promoted by 2-deoxy-d-glucose) and SIRT1 (inhibited by NADH and promoted by NAD(+)), not PPARalpha, were probably involved in feed intake regulation in chickens.	NAD	145-152	sirtuin 1	Gallus gallus	104-109
25070488-5	2014	Here we show that the mitochondrial class III NAD(+)-dependent deacetylase SIRT5 is overexpressed in human NSCLC and high expression of SIRT5 predicts poor survival.	NAD	46-52	sirtuin 5	Homo sapiens	75-80
25070488-5	2014	Here we show that the mitochondrial class III NAD(+)-dependent deacetylase SIRT5 is overexpressed in human NSCLC and high expression of SIRT5 predicts poor survival.	NAD	46-52	sirtuin 5	Homo sapiens	136-141
25243829-7	2014	NAD+ and NADH inhibited the generation of  O2- from XDH in a dose-dependent manner, with NAD+ exhibiting stronger inhibition than NADH at low physiological concentrations.	NAD	0-4	xanthine dehydrogenase	Gallus gallus	52-55
25243829-7	2014	NAD+ and NADH inhibited the generation of  O2- from XDH in a dose-dependent manner, with NAD+ exhibiting stronger inhibition than NADH at low physiological concentrations.	NAD	9-13	xanthine dehydrogenase	Gallus gallus	52-55
25243829-7	2014	NAD+ and NADH inhibited the generation of  O2- from XDH in a dose-dependent manner, with NAD+ exhibiting stronger inhibition than NADH at low physiological concentrations.	NAD	89-93	xanthine dehydrogenase	Gallus gallus	52-55
25243829-7	2014	NAD+ and NADH inhibited the generation of  O2- from XDH in a dose-dependent manner, with NAD+ exhibiting stronger inhibition than NADH at low physiological concentrations.	NAD	130-134	xanthine dehydrogenase	Gallus gallus	52-55
25243829-8	2014	Decreased amounts of NAD+ and NADH, which occur during and following tissue ischemia, enhanced the generation of  O2- from XDH in the presence of xanthine.	NAD	21-25	xanthine dehydrogenase	Gallus gallus	123-126
25243829-8	2014	Decreased amounts of NAD+ and NADH, which occur during and following tissue ischemia, enhanced the generation of  O2- from XDH in the presence of xanthine.	NAD	30-34	xanthine dehydrogenase	Gallus gallus	123-126
25243829-9	2014	It was observed that XDH-mediated oxygen radical generation markedly depressed Ca2+-ATPase activity of isolated sarcoplasmic reticulum vesicles from cardiac muscle, and this was modulated by NAD+ and NADH.	NAD	191-195	xanthine dehydrogenase	Gallus gallus	21-24
25243829-9	2014	It was observed that XDH-mediated oxygen radical generation markedly depressed Ca2+-ATPase activity of isolated sarcoplasmic reticulum vesicles from cardiac muscle, and this was modulated by NAD+ and NADH.	NAD	200-204	xanthine dehydrogenase	Gallus gallus	21-24
25052469-4	2014	Site directed mutagenesis of three residues from this group in the enzyme UDP-Galactose 4-epimerase belonging to SDR1E shows that the mutants promote the formation of NADH containing abortive complexes.	NAD	167-171	UDP-galactose-4-epimerase	Homo sapiens	74-99
25201160-1	2014	Nicotinamide phosphoribosyltransferase (NAMPT) and nicotinate phosphoribosyltransferase domain containing 1 (NAPRT1) are the main human NAD salvage enzymes.	NAD	136-139	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
25203508-3	2014	Here we provide a structural explanation for the stability of the heterotetramer from the crystal structure with NAD(+) and NADP(+) bound to the HSD17B8 and CBR4 subunits, respectively, and show that the catalytic activity of the NADPH- and ACP-dependent CBR4 subunit is crucial for a functional HsKAR.	NAD	113-119	hydroxysteroid 17-beta dehydrogenase 8	Homo sapiens	145-152
25203508-6	2014	The intrinsic NAD(+)- and CoA-dependent activity of the HSD17B8 subunit on the 3R-hydroxyacyl-CoA intermediates may indicate a role for this subunit in routing 3R-hydroxyacyl-CoA esters, potentially arising from the metabolism of unsaturated fatty acids, into the mitochondrial beta-oxidation pathway.	NAD	14-20	hydroxysteroid 17-beta dehydrogenase 8	Homo sapiens	56-63
24913741-5	2014	Subsequently, NADH is used in the conversion of resazurin to fluorescent resorufin by DI.	NAD	14-18	dihydrolipoamide dehydrogenase	Homo sapiens	86-88
25078575-4	2014	The three-gene unit hp0137-0139 in H. pylori 26695 encodes L-lactate dehydrogenase (LDH) that catalyzes the conversion of lactate to pyruvate in an NAD-dependent manner.	NAD	148-151	lactate utilization protein C	Helicobacter pylori 26695	20-26
25023514-2	2014	We show that ATP synthase beta is deacetylated by a human nicotinamide adenine dinucleotide (NAD(+))-dependent protein deacetylase, sirtuin 3, and its Drosophila melanogaster homologue, dSirt2.	NAD	93-99	Sirtuin 2	Drosophila melanogaster	186-192
24848608-1	2014	A succinylation-specific photo-cross-linking peptide probe has been developed for the NAD(+)-dependent hydrolase Sirtuin 5.	NAD	86-92	sirtuin 5	Homo sapiens	113-122
24859209-4	2014	The midpoint potential of the modified graphite was about -0.248 V (vs. normal hydrogen electrode, NHE), indicating that electrons could be easily transferred from NADH in bacteria to the electrode.	NAD	164-168	solute carrier family 9 member C1	Homo sapiens	99-102
24811750-3	2014	Here, we show that levels of NAD(+) and nicotinamide phosphoribosyltransferase (Nampt), the rate-limiting enzyme in mammalian NAD(+) biosynthesis, decrease with age in the hippocampus.	NAD	29-35	nicotinamide phosphoribosyltransferase	Homo sapiens	80-85
24811750-3	2014	Here, we show that levels of NAD(+) and nicotinamide phosphoribosyltransferase (Nampt), the rate-limiting enzyme in mammalian NAD(+) biosynthesis, decrease with age in the hippocampus.	NAD	126-132	nicotinamide phosphoribosyltransferase	Homo sapiens	40-78
24811750-3	2014	Here, we show that levels of NAD(+) and nicotinamide phosphoribosyltransferase (Nampt), the rate-limiting enzyme in mammalian NAD(+) biosynthesis, decrease with age in the hippocampus.	NAD	126-132	nicotinamide phosphoribosyltransferase	Homo sapiens	80-85
24811750-6	2014	Nampt is the main source of NSPC NAD(+) levels and required for G1/S progression of the NSPC cell cycle.	NAD	33-39	nicotinamide phosphoribosyltransferase	Homo sapiens	0-5
24811750-9	2014	These phenotypes recapitulate defects in NSPCs during aging, giving rise to the possibility that Nampt-mediated NAD(+) biosynthesis is a mediator of age-associated functional declines in NSPCs.	NAD	112-118	nicotinamide phosphoribosyltransferase	Homo sapiens	97-102
24657895-4	2014	One is the systemic, Nampt-controlled NAD+ (nicotinamide phosphoribosyltransferase) biosynthesis, where Nampt (nicotinamide phosphoribosyltransferase) acts as "propulsion" for metabolism and the other is NAD+ dependent deacetylase (SIRT1) - a regulator responsible for various biological effects, depending on its localisation in organism.	NAD	38-42	nicotinamide phosphoribosyltransferase	Homo sapiens	44-82
24657895-4	2014	One is the systemic, Nampt-controlled NAD+ (nicotinamide phosphoribosyltransferase) biosynthesis, where Nampt (nicotinamide phosphoribosyltransferase) acts as "propulsion" for metabolism and the other is NAD+ dependent deacetylase (SIRT1) - a regulator responsible for various biological effects, depending on its localisation in organism.	NAD	38-42	nicotinamide phosphoribosyltransferase	Homo sapiens	111-149
24657895-4	2014	One is the systemic, Nampt-controlled NAD+ (nicotinamide phosphoribosyltransferase) biosynthesis, where Nampt (nicotinamide phosphoribosyltransferase) acts as "propulsion" for metabolism and the other is NAD+ dependent deacetylase (SIRT1) - a regulator responsible for various biological effects, depending on its localisation in organism.	NAD	38-41	nicotinamide phosphoribosyltransferase	Homo sapiens	44-82
24657895-4	2014	One is the systemic, Nampt-controlled NAD+ (nicotinamide phosphoribosyltransferase) biosynthesis, where Nampt (nicotinamide phosphoribosyltransferase) acts as "propulsion" for metabolism and the other is NAD+ dependent deacetylase (SIRT1) - a regulator responsible for various biological effects, depending on its localisation in organism.	NAD	38-41	nicotinamide phosphoribosyltransferase	Homo sapiens	111-149
24598800-10	2014	We provide experimental evidence demonstrating that the Wld(S) gene is expressed in kidney cells and protects against the early stage of diabetes-induced renal dysfunction and extracellular matrix accumulation through delaying the reduction of the NAD(+)/NADH ratio, inhibiting the activation of p38 and ERK signaling, and suppressing oxidative stress as evidenced by the decreased NADPH oxidase activity and lower expression of TNF-alpha, IL-1, and IL-6.	NAD	248-254	wallerian degeneration	Mus musculus	56-59
24598800-10	2014	We provide experimental evidence demonstrating that the Wld(S) gene is expressed in kidney cells and protects against the early stage of diabetes-induced renal dysfunction and extracellular matrix accumulation through delaying the reduction of the NAD(+)/NADH ratio, inhibiting the activation of p38 and ERK signaling, and suppressing oxidative stress as evidenced by the decreased NADPH oxidase activity and lower expression of TNF-alpha, IL-1, and IL-6.	NAD	255-259	wallerian degeneration	Mus musculus	56-59
24759102-4	2014	Yeast cells lacking the ORF YCL047C/POF1 release considerably more NR compared with wild type, suggesting that POF1 plays an important role in NR/NAD(+) metabolism.	NAD	146-152	nicotinamide-nucleotide adenylyltransferase	Saccharomyces cerevisiae S288C	36-40
24759102-4	2014	Yeast cells lacking the ORF YCL047C/POF1 release considerably more NR compared with wild type, suggesting that POF1 plays an important role in NR/NAD(+) metabolism.	NAD	146-152	nicotinamide-nucleotide adenylyltransferase	Saccharomyces cerevisiae S288C	111-115
24759102-7	2014	Deletion of POF1 significantly lowers NAD(+) levels and decreases the efficiency of NR utilization, resistance to oxidative stress, and NR-induced life span extension.	NAD	38-44	nicotinamide-nucleotide adenylyltransferase	Saccharomyces cerevisiae S288C	12-16
24824795-0	2014	NAMPT-mediated salvage synthesis of NAD+ controls morphofunctional changes of macrophages.	NAD	36-40	nicotinamide phosphoribosyltransferase	Homo sapiens	0-5
24824795-3	2014	Here, we focus on the role of nicotinamide phosphoribosyltransferase (NAMPT), found in extracellular form as a cytokine and growth factor, and in intracellular form as one of the key enzymes for the production of NAD+ in macrophages.	NAD	213-217	nicotinamide phosphoribosyltransferase	Homo sapiens	30-68
24824795-3	2014	Here, we focus on the role of nicotinamide phosphoribosyltransferase (NAMPT), found in extracellular form as a cytokine and growth factor, and in intracellular form as one of the key enzymes for the production of NAD+ in macrophages.	NAD	213-217	nicotinamide phosphoribosyltransferase	Homo sapiens	70-75
24824795-4	2014	Inhibition of NAD+ salvage synthesis by the NAMPT-specific drug FK866 caused a decrease in cytosolic NAD+ levels in RAW 264.7 and Maf-DKO macrophages and led to significant downregulation of the glycolytic flux without directly affecting cell viability, proliferation, ATP production capacity or mitochondrial respiratory activity.	NAD	14-18	nicotinamide phosphoribosyltransferase	Homo sapiens	44-49
24824795-4	2014	Inhibition of NAD+ salvage synthesis by the NAMPT-specific drug FK866 caused a decrease in cytosolic NAD+ levels in RAW 264.7 and Maf-DKO macrophages and led to significant downregulation of the glycolytic flux without directly affecting cell viability, proliferation, ATP production capacity or mitochondrial respiratory activity.	NAD	101-105	nicotinamide phosphoribosyltransferase	Homo sapiens	44-49
24657618-3	2014	Crystal structures of human CtBP1 and CtBP2 in complex with MTOB and NAD(+) revealed two key features: a conserved tryptophan that likely contributes to substrate specificity and a hydrophilic cavity that links MTOB with an NAD(+) phosphate.	NAD	69-75	C-terminal binding protein 1	Homo sapiens	28-33
24504254-4	2014	Structure modeling of the human Edc3 Yjef_N along with other Yjef_N-containing proteins suggests that this molecule is related to NAD(H).	NAD	130-136	enhancer of mRNA decapping 3	Homo sapiens	32-36
24504254-5	2014	We now show human Edc3 directly binds NADH.	NAD	38-42	enhancer of mRNA decapping 3	Homo sapiens	18-22
24504254-7	2014	Mutations that are predicted to disrupt the binding and/or hydrolysis of an NAD-related molecule by yeast and human Edc3 affect the control of mRNA degradation and/or P-body composition in vivo.	NAD	76-79	enhancer of mRNA decapping 3	Homo sapiens	116-120
24504254-8	2014	This suggests that the interaction of Edc3 with an NAD-related molecule affects its function in the regulation of mRNA translation and degradation and provides a possible mechanism to couple the energetics of the cell to posttranscriptional control.	NAD	51-54	enhancer of mRNA decapping 3	Homo sapiens	38-42
24292505-8	2014	Finally, we found that extracellular NAD(+) inhibited spontaneous activation of caspase-9, but not caspase-8, and the pro-survival effect of extracellular NAD(+) was abrogated by the inhibitor of caspase-9, but not by the inhibitor of caspase-8.	NAD	37-43	caspase 8	Homo sapiens	235-244
24292505-8	2014	Finally, we found that extracellular NAD(+) inhibited spontaneous activation of caspase-9, but not caspase-8, and the pro-survival effect of extracellular NAD(+) was abrogated by the inhibitor of caspase-9, but not by the inhibitor of caspase-8.	NAD	155-161	caspase 8	Homo sapiens	235-244
24627100-3	2014	Visfatin, also known as nicotinamide phosphoribosyltransferase (NAMPT), modulates sirtuin1 (SIRT1) through the regulation of nicotinamide adenine dinucleotide (NAD).	NAD	125-158	nicotinamide phosphoribosyltransferase	Homo sapiens	0-8
24627100-3	2014	Visfatin, also known as nicotinamide phosphoribosyltransferase (NAMPT), modulates sirtuin1 (SIRT1) through the regulation of nicotinamide adenine dinucleotide (NAD).	NAD	125-158	nicotinamide phosphoribosyltransferase	Homo sapiens	24-62
24627100-3	2014	Visfatin, also known as nicotinamide phosphoribosyltransferase (NAMPT), modulates sirtuin1 (SIRT1) through the regulation of nicotinamide adenine dinucleotide (NAD).	NAD	125-158	nicotinamide phosphoribosyltransferase	Homo sapiens	64-69
24627100-3	2014	Visfatin, also known as nicotinamide phosphoribosyltransferase (NAMPT), modulates sirtuin1 (SIRT1) through the regulation of nicotinamide adenine dinucleotide (NAD).	NAD	160-163	nicotinamide phosphoribosyltransferase	Homo sapiens	0-8
24627100-3	2014	Visfatin, also known as nicotinamide phosphoribosyltransferase (NAMPT), modulates sirtuin1 (SIRT1) through the regulation of nicotinamide adenine dinucleotide (NAD).	NAD	160-163	nicotinamide phosphoribosyltransferase	Homo sapiens	24-62
24627100-3	2014	Visfatin, also known as nicotinamide phosphoribosyltransferase (NAMPT), modulates sirtuin1 (SIRT1) through the regulation of nicotinamide adenine dinucleotide (NAD).	NAD	160-163	nicotinamide phosphoribosyltransferase	Homo sapiens	64-69
24607900-5	2014	We find that SIRT6, one of the NAD(+)-dependent class III deacetylase SIRTUINs, is down-regulated in human glioma tissues and that the level of SIRT6 is negatively correlated with PCBP2 level while H3K9ac enrichment on the promoter of PCBP2 is positively correlated with PCBP2 expression.	NAD	31-37	sirtuin 6	Homo sapiens	13-18
24607900-5	2014	We find that SIRT6, one of the NAD(+)-dependent class III deacetylase SIRTUINs, is down-regulated in human glioma tissues and that the level of SIRT6 is negatively correlated with PCBP2 level while H3K9ac enrichment on the promoter of PCBP2 is positively correlated with PCBP2 expression.	NAD	31-37	sirtuin 6	Homo sapiens	144-149
24438340-8	2014	RNA profiling was used to examine the effects of SRC-1 perturbation on gene expression in the absence or presence of glucose, revealing that SRC-1 affects the expression of complex I of the mitochondrial electron transport chain, a set of enzymes responsible for the conversion of NADH to NAD(+).	NAD	281-285	nuclear receptor coactivator 1	Homo sapiens	141-146
24438340-8	2014	RNA profiling was used to examine the effects of SRC-1 perturbation on gene expression in the absence or presence of glucose, revealing that SRC-1 affects the expression of complex I of the mitochondrial electron transport chain, a set of enzymes responsible for the conversion of NADH to NAD(+).	NAD	289-295	nuclear receptor coactivator 1	Homo sapiens	141-146
24438340-9	2014	NAD(+) and NADH were subsequently identified as metabolites that underlie SRC-1"s response to glucose deprivation.	NAD	0-6	nuclear receptor coactivator 1	Homo sapiens	74-79
24438340-9	2014	NAD(+) and NADH were subsequently identified as metabolites that underlie SRC-1"s response to glucose deprivation.	NAD	11-15	nuclear receptor coactivator 1	Homo sapiens	74-79
24444429-6	2014	Comparison of bacterial NDH-2 with the yeast NADH dehydrogenase (Ndi1) structure revealed non-overlapping binding sites for quinone and NADH in the bacterial enzyme.	NAD	45-49	NADH-ubiquinone reductase (H(+)-translocating) NDI1	Saccharomyces cerevisiae S288C	65-69
24468396-4	2014	The reactions for the detection of glucose proceed as follows: glucose dehydrogenase oxidizes glucose to gluconolactone with NAD(+) as the electron acceptor to yield NADH, and NADH can be utilized by DTD to further react with the probe releasing resorufin.	NAD	125-131	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	63-84
24468396-4	2014	The reactions for the detection of glucose proceed as follows: glucose dehydrogenase oxidizes glucose to gluconolactone with NAD(+) as the electron acceptor to yield NADH, and NADH can be utilized by DTD to further react with the probe releasing resorufin.	NAD	166-170	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	63-84
24468396-4	2014	The reactions for the detection of glucose proceed as follows: glucose dehydrogenase oxidizes glucose to gluconolactone with NAD(+) as the electron acceptor to yield NADH, and NADH can be utilized by DTD to further react with the probe releasing resorufin.	NAD	176-180	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	63-84
24782383-2	2014	The functions of Nampt have been reported as a cytokine, an adipokine and the rate-limiting enzyme in nicotinamide adenine dinucleotide biosynthesis.	NAD	102-135	nicotinamide phosphoribosyltransferase	Homo sapiens	17-22
24611062-11	2014	Consistently, both PPT and DPN stimulated PAK and cofilin phosphorylation as well as actin polymerization.	NAD	27-30	cofilin 1	Homo sapiens	50-57
24586202-6	2014	Since two-pore domain K(+) channels regulate the resting membrane potentials of numerous cell types, we suggest that the SUP-18 IYD regulates the activity of the SUP-9 channel using NADH as a coenzyme and thus couples the metabolic state of muscle cells to muscle membrane excitability.	NAD	182-186	iodotyrosine deiodinase	Homo sapiens	128-131
24586202-6	2014	Since two-pore domain K(+) channels regulate the resting membrane potentials of numerous cell types, we suggest that the SUP-18 IYD regulates the activity of the SUP-9 channel using NADH as a coenzyme and thus couples the metabolic state of muscle cells to muscle membrane excitability.	NAD	182-186	Two pore potassium channel protein sup-9	Caenorhabditis elegans	162-167
24479481-2	2014	With a homodimeric conformation, it exerts nicotinamide phosphoribosyltransferase (Nampt) enzymatic activity, essential for nicotinamide adenine dinucleotide biosynthesis.	NAD	124-157	nicotinamide phosphoribosyltransferase	Homo sapiens	43-81
24479481-2	2014	With a homodimeric conformation, it exerts nicotinamide phosphoribosyltransferase (Nampt) enzymatic activity, essential for nicotinamide adenine dinucleotide biosynthesis.	NAD	124-157	nicotinamide phosphoribosyltransferase	Homo sapiens	83-88
24402199-3	2014	We have found that STD NMR, together with the use of selected mutations on FNR and of the non-FNR reacting coenzyme analogue NAD+, are appropriate tools to provide further information about the the interaction epitope.	NAD	125-129	ferredoxin reductase	Homo sapiens	94-97
25932355-6	2014	The activation of PGC-1alpha by FGF21 occurred via the NAD(+)-dependent deacetylase Sirtuin-1 (SIRT1) subsequent to an increase in the enzyme, nicotinamide phosphoribosyltransferase (Nampt).	NAD	55-61	nicotinamide phosphoribosyltransferase	Homo sapiens	143-181
24473773-3	2014	MacroH2A1.1 binds with high affinity O-acetyl ADP ribose, a small metabolite produced by the reaction catalysed by NAD+-dependent deacetylase SIRT1, whereas macroH2A1.2 is unable to do so.	NAD	115-119	macroH2A.1 histone	Mus musculus	0-9
24389478-1	2014	Nicotinamide phosphoribosyl transferase (NAMPT) is a key enzyme in the salvage pathway of mammalian nicotinamide adenine dinucleotide (NAD) biosynthesis, catalyzing the synthesis of nicotinamide mononucleotide from nicotinamide (Nam).	NAD	100-133	nicotinamide phosphoribosyltransferase	Homo sapiens	0-39
24389478-1	2014	Nicotinamide phosphoribosyl transferase (NAMPT) is a key enzyme in the salvage pathway of mammalian nicotinamide adenine dinucleotide (NAD) biosynthesis, catalyzing the synthesis of nicotinamide mononucleotide from nicotinamide (Nam).	NAD	100-133	nicotinamide phosphoribosyltransferase	Homo sapiens	41-46
24389478-1	2014	Nicotinamide phosphoribosyl transferase (NAMPT) is a key enzyme in the salvage pathway of mammalian nicotinamide adenine dinucleotide (NAD) biosynthesis, catalyzing the synthesis of nicotinamide mononucleotide from nicotinamide (Nam).	NAD	135-138	nicotinamide phosphoribosyltransferase	Homo sapiens	0-39
24389478-1	2014	Nicotinamide phosphoribosyl transferase (NAMPT) is a key enzyme in the salvage pathway of mammalian nicotinamide adenine dinucleotide (NAD) biosynthesis, catalyzing the synthesis of nicotinamide mononucleotide from nicotinamide (Nam).	NAD	135-138	nicotinamide phosphoribosyltransferase	Homo sapiens	41-46
24389478-2	2014	The diverse functions of NAD suggest that NAMPT inhibitors are potential drug candidates as anticancer agents, immunomodulators, or other agents.	NAD	25-28	nicotinamide phosphoribosyltransferase	Homo sapiens	42-47
24389478-6	2014	The mode of action was found to reduce intracellular NAD following apoptosis, suggesting that these compounds inhibit NAMPT in cell-based assay.	NAD	53-56	nicotinamide phosphoribosyltransferase	Homo sapiens	118-123
24247717-1	2014	ENOX1 is a highly conserved NADH oxidase that helps to regulate intracellular nicotinamide adenine dinucleotide levels in many cell types, including endothelial cells.	NAD	78-111	ecto-NOX disulfide-thiol exchanger 1	Danio rerio	0-5
24247717-7	2014	Using in vivo multiphoton microscopy, we show that morpholino-mediated knockdown of enox1 increases NADH levels, consistent with loss of enzyme.	NAD	100-104	ecto-NOX disulfide-thiol exchanger 1	Danio rerio	84-89
24247717-8	2014	VJ115 is a small-molecule inhibitor of Enox1"s oxidase activity shown to increase intracellular NADH in endothelial cells; we used VJ115 to determine if the oxidase activity was crucial for vascular development.	NAD	96-100	ecto-NOX disulfide-thiol exchanger 1	Danio rerio	39-44
24025713-3	2014	RESULTS: We demonstrated that pharmacologic and genetic targeting of Nampt, the key enzyme in the NAD salvage synthesis pathway, inhibits cell growth and survival of pancreatic cancer cells.	NAD	98-101	nicotinamide phosphoribosyltransferase	Homo sapiens	69-74
24025713-7	2014	However, we identified a role for the NAD degradation pathway mediated by the NADase CD38 on the sensitivity to Nampt inhibition.	NAD	38-41	nicotinamide phosphoribosyltransferase	Homo sapiens	112-117
24025713-10	2014	CONCLUSIONS: Our study demonstrates that NAD metabolism is essential for pancreatic cancer cell survival and proliferation and that targeting NAD synthesis via the Nampt pathway could lead to novel therapeutic treatments for pancreatic cancer.	NAD	142-145	nicotinamide phosphoribosyltransferase	Homo sapiens	164-169
25413783-1	2014	Nicotinamide phosphoribosyltransferase (NAMPT), an enzyme taking part in main NAD biosynthetic pathway, is an attractive target for anticancer therapy.	NAD	78-81	nicotinamide phosphoribosyltransferase	Homo sapiens	0-38
25413783-1	2014	Nicotinamide phosphoribosyltransferase (NAMPT), an enzyme taking part in main NAD biosynthetic pathway, is an attractive target for anticancer therapy.	NAD	78-81	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
24515575-7	2014	SLC25A12 encodes the neuronal aspartate-glutamate carrier 1 (AGC1) protein, an essential component of the neuronal malate/aspartate shuttle that transfers NADH and H(+) reducing equivalents from the cytosol to mitochondria.	NAD	155-159	solute carrier family 25 member 12	Homo sapiens	0-8
24515575-7	2014	SLC25A12 encodes the neuronal aspartate-glutamate carrier 1 (AGC1) protein, an essential component of the neuronal malate/aspartate shuttle that transfers NADH and H(+) reducing equivalents from the cytosol to mitochondria.	NAD	155-159	solute carrier family 25 member 12	Homo sapiens	61-65
24445236-3	2014	Cx43 possesses some unique properties [the ability to form either intercellular channels permeable for regulatory molecules and ions or hemichannels open to the extracellular space to provide release of cell metabolites; functional coupling with nicotinamide adenine dinucleotide (NAD+)-consuming and NAD+-dependent enzymatic processes] which may be of great importance for the fate of the stem cells.	NAD	246-279	gap junction protein alpha 1	Homo sapiens	0-4
24445236-3	2014	Cx43 possesses some unique properties [the ability to form either intercellular channels permeable for regulatory molecules and ions or hemichannels open to the extracellular space to provide release of cell metabolites; functional coupling with nicotinamide adenine dinucleotide (NAD+)-consuming and NAD+-dependent enzymatic processes] which may be of great importance for the fate of the stem cells.	NAD	281-285	gap junction protein alpha 1	Homo sapiens	0-4
24445236-3	2014	Cx43 possesses some unique properties [the ability to form either intercellular channels permeable for regulatory molecules and ions or hemichannels open to the extracellular space to provide release of cell metabolites; functional coupling with nicotinamide adenine dinucleotide (NAD+)-consuming and NAD+-dependent enzymatic processes] which may be of great importance for the fate of the stem cells.	NAD	301-305	gap junction protein alpha 1	Homo sapiens	0-4
24097869-9	2013	CONCLUSIONS: Tumor-specific promoter hypermethylation of NAPRT1 inactivates one of two NAD salvage pathways, resulting in synthetic lethality with the coadministration of a NAMPT inhibitor.	NAD	87-90	nicotinamide phosphoribosyltransferase	Homo sapiens	173-178
24010612-4	2013	We observed that osmotic stress determined the production and accumulation of intracellular glycerol, and the expression of NADH-dependent glycerol-3-phosphate dehydrogenase (GPD) activity was elevated.	NAD	124-128	glycerol-3-phosphate dehydrogenase	Saccharomyces cerevisiae S288C	139-173
24010612-4	2013	We observed that osmotic stress determined the production and accumulation of intracellular glycerol, and the expression of NADH-dependent glycerol-3-phosphate dehydrogenase (GPD) activity was elevated.	NAD	124-128	glycerol-3-phosphate dehydrogenase	Saccharomyces cerevisiae S288C	175-178
24403854-1	2013	Nicotinamide adenine dinucleotide (NAD) is a metabolite essential for cell survival and generated de novo from tryptophan or recycled from nicotinamide (NAM) through the nicotinamide phosphoribosyltransferase (NAMPT)-dependent salvage pathway.	NAD	0-33	nicotinamide phosphoribosyltransferase	Homo sapiens	210-215
24403854-1	2013	Nicotinamide adenine dinucleotide (NAD) is a metabolite essential for cell survival and generated de novo from tryptophan or recycled from nicotinamide (NAM) through the nicotinamide phosphoribosyltransferase (NAMPT)-dependent salvage pathway.	NAD	35-38	nicotinamide phosphoribosyltransferase	Homo sapiens	170-208
24403854-1	2013	Nicotinamide adenine dinucleotide (NAD) is a metabolite essential for cell survival and generated de novo from tryptophan or recycled from nicotinamide (NAM) through the nicotinamide phosphoribosyltransferase (NAMPT)-dependent salvage pathway.	NAD	35-38	nicotinamide phosphoribosyltransferase	Homo sapiens	210-215
24403854-4	2013	Moreover, the therapeutic index of NAMPT inhibitors may be increased by in NAPRT-deficient tumors by NA supplementation as normal tissues may regenerate NAD through NAPRT1.	NAD	153-156	nicotinamide phosphoribosyltransferase	Homo sapiens	35-40
24437277-0	2013	[Importance of NAMPT-mediated NAD-biosynthesis and NAD-dependent deacetylase SIRT1 in the crosstalk between circadian rhythm and metabolism].	NAD	30-33	nicotinamide phosphoribosyltransferase	Homo sapiens	15-20
24437277-3	2013	We recently found that the key NAD biosynthetic enzyme, nicotinamide phosphoribosyltransferase (NAMPT), and NAD-dependent deacetylase SIRT1 play a critical role in such crosstalk, by creating a novel feedback loop in which NAD functions as a "metabolic oscillator".	NAD	31-34	nicotinamide phosphoribosyltransferase	Homo sapiens	56-94
24437277-3	2013	We recently found that the key NAD biosynthetic enzyme, nicotinamide phosphoribosyltransferase (NAMPT), and NAD-dependent deacetylase SIRT1 play a critical role in such crosstalk, by creating a novel feedback loop in which NAD functions as a "metabolic oscillator".	NAD	31-34	nicotinamide phosphoribosyltransferase	Homo sapiens	96-101
24437277-3	2013	We recently found that the key NAD biosynthetic enzyme, nicotinamide phosphoribosyltransferase (NAMPT), and NAD-dependent deacetylase SIRT1 play a critical role in such crosstalk, by creating a novel feedback loop in which NAD functions as a "metabolic oscillator".	NAD	108-111	nicotinamide phosphoribosyltransferase	Homo sapiens	56-94
24437277-3	2013	We recently found that the key NAD biosynthetic enzyme, nicotinamide phosphoribosyltransferase (NAMPT), and NAD-dependent deacetylase SIRT1 play a critical role in such crosstalk, by creating a novel feedback loop in which NAD functions as a "metabolic oscillator".	NAD	108-111	nicotinamide phosphoribosyltransferase	Homo sapiens	96-101
24437277-3	2013	We recently found that the key NAD biosynthetic enzyme, nicotinamide phosphoribosyltransferase (NAMPT), and NAD-dependent deacetylase SIRT1 play a critical role in such crosstalk, by creating a novel feedback loop in which NAD functions as a "metabolic oscillator".	NAD	108-111	nicotinamide phosphoribosyltransferase	Homo sapiens	56-94
24437277-3	2013	We recently found that the key NAD biosynthetic enzyme, nicotinamide phosphoribosyltransferase (NAMPT), and NAD-dependent deacetylase SIRT1 play a critical role in such crosstalk, by creating a novel feedback loop in which NAD functions as a "metabolic oscillator".	NAD	108-111	nicotinamide phosphoribosyltransferase	Homo sapiens	96-101
24183972-2	2013	We report the application of sequential unbiased high-throughput chemical and ultracomplex small hairpin RNA (shRNA) screens to identify a distinctive class of inhibitors that target nicotinamide phosphoribosyl transferase (NAMPT), a rate-limiting enzyme in the biosynthesis of nicotinamide adenine dinucleotide, a crucial cofactor in many biochemical processes.	NAD	278-311	nicotinamide phosphoribosyltransferase	Homo sapiens	183-222
24183972-2	2013	We report the application of sequential unbiased high-throughput chemical and ultracomplex small hairpin RNA (shRNA) screens to identify a distinctive class of inhibitors that target nicotinamide phosphoribosyl transferase (NAMPT), a rate-limiting enzyme in the biosynthesis of nicotinamide adenine dinucleotide, a crucial cofactor in many biochemical processes.	NAD	278-311	nicotinamide phosphoribosyltransferase	Homo sapiens	224-229
24034216-4	2013	The main aim of the work is to fabricate NADH/LDH/Nano-CeO2/GCE bio-electrode for sensing lactate in human blood samples.	NAD	41-45	glycine decarboxylase	Homo sapiens	60-63
24034216-9	2013	The working electrode was fabricated by immobilizing nicotinamide adenine dinucleotide (NADH) and lactate dehydrogenase (LDH) on GCE surface with CeO2 nanoparticles as an interface.	NAD	53-86	glycine decarboxylase	Homo sapiens	129-132
24386506-1	2013	Nicotinamide phosphoribosyltransferase (Nampt) catalyzes the rate-limiting step of nicotinamide adenine dinucleotide (NAD) synthesis.	NAD	83-116	nicotinamide phosphoribosyltransferase	Homo sapiens	0-38
24386506-1	2013	Nicotinamide phosphoribosyltransferase (Nampt) catalyzes the rate-limiting step of nicotinamide adenine dinucleotide (NAD) synthesis.	NAD	83-116	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
24386506-1	2013	Nicotinamide phosphoribosyltransferase (Nampt) catalyzes the rate-limiting step of nicotinamide adenine dinucleotide (NAD) synthesis.	NAD	118-121	nicotinamide phosphoribosyltransferase	Homo sapiens	0-38
24386506-1	2013	Nicotinamide phosphoribosyltransferase (Nampt) catalyzes the rate-limiting step of nicotinamide adenine dinucleotide (NAD) synthesis.	NAD	118-121	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
24071366-6	2013	Through activity of mitochondrial transhydrogenase, NADH.H+ replenishes NADPH.H+, coenzyme of glutathione reductase which replenishes reduced form of glutathione (potent antioxidant).	NAD	52-56	glutathione-disulfide reductase	Homo sapiens	94-115
24055790-5	2013	Redox rebalancing was achieved by anaerobically activating the pyruvate dehydrogenase (PDH) complex and additionally tuning the expression level of NAD(+)-dependent formate dehydrogenase (fdh1 from Saccharomyces cerevisiae) through rational UTR engineering.	NAD	148-154	formate dehydrogenase (NAD+)	Saccharomyces cerevisiae S288C	188-192
24056782-6	2013	NAD(+) metabolism was observed to be affected both by the deletion of CCC2 and the level of bio-available extracellular copper.	NAD	0-6	Cu(2+)-transporting P-type ATPase CCC2	Saccharomyces cerevisiae S288C	70-74
23995837-4	2013	Here, we report that TR-mediated transcriptional activation of PCK1 and G6PC in human hepatic cells and mouse liver was FoxO1-dependent and furthermore required FoxO1 deacetylation by the NAD(+)-dependent deacetylase, SirT1.	NAD	188-194	glucose-6-phosphatase catalytic subunit 1	Homo sapiens	72-76
23940047-0	2013	Nicotinamide adenine dinucleotide-induced multimerization of the co-repressor CtBP1 relies on a switching tryptophan.	NAD	0-33	C-terminal binding protein 1	Homo sapiens	78-83
23940047-3	2013	In the current study we demonstrate that CtBP1 assembles into a tetramer in a NAD(H)-dependent manner, proceeding through a dimeric intermediate.	NAD	78-84	C-terminal binding protein 1	Homo sapiens	41-46
23803896-3	2013	First, the bile acids react with nicotinamide adenine dinucleotide (NAD(+)) under catalysis of 3alpha-hydroxysteroid dehydrogenase (3alpha-HSD), which is converted to 3-ketosteroid and concomitantly NAD(+) turns into reduced nicotinamide adenine dinucleotide (NADH).	NAD	33-66	aldo-keto reductase family 1 member C3	Homo sapiens	95-130
23803896-3	2013	First, the bile acids react with nicotinamide adenine dinucleotide (NAD(+)) under catalysis of 3alpha-hydroxysteroid dehydrogenase (3alpha-HSD), which is converted to 3-ketosteroid and concomitantly NAD(+) turns into reduced nicotinamide adenine dinucleotide (NADH).	NAD	33-66	aldo-keto reductase family 1 member C3	Homo sapiens	132-142
23803896-3	2013	First, the bile acids react with nicotinamide adenine dinucleotide (NAD(+)) under catalysis of 3alpha-hydroxysteroid dehydrogenase (3alpha-HSD), which is converted to 3-ketosteroid and concomitantly NAD(+) turns into reduced nicotinamide adenine dinucleotide (NADH).	NAD	68-74	aldo-keto reductase family 1 member C3	Homo sapiens	95-130
23803896-3	2013	First, the bile acids react with nicotinamide adenine dinucleotide (NAD(+)) under catalysis of 3alpha-hydroxysteroid dehydrogenase (3alpha-HSD), which is converted to 3-ketosteroid and concomitantly NAD(+) turns into reduced nicotinamide adenine dinucleotide (NADH).	NAD	68-74	aldo-keto reductase family 1 member C3	Homo sapiens	132-142
23803896-3	2013	First, the bile acids react with nicotinamide adenine dinucleotide (NAD(+)) under catalysis of 3alpha-hydroxysteroid dehydrogenase (3alpha-HSD), which is converted to 3-ketosteroid and concomitantly NAD(+) turns into reduced nicotinamide adenine dinucleotide (NADH).	NAD	199-205	aldo-keto reductase family 1 member C3	Homo sapiens	95-130
23803896-3	2013	First, the bile acids react with nicotinamide adenine dinucleotide (NAD(+)) under catalysis of 3alpha-hydroxysteroid dehydrogenase (3alpha-HSD), which is converted to 3-ketosteroid and concomitantly NAD(+) turns into reduced nicotinamide adenine dinucleotide (NADH).	NAD	199-205	aldo-keto reductase family 1 member C3	Homo sapiens	132-142
23803896-3	2013	First, the bile acids react with nicotinamide adenine dinucleotide (NAD(+)) under catalysis of 3alpha-hydroxysteroid dehydrogenase (3alpha-HSD), which is converted to 3-ketosteroid and concomitantly NAD(+) turns into reduced nicotinamide adenine dinucleotide (NADH).	NAD	225-258	aldo-keto reductase family 1 member C3	Homo sapiens	95-130
23803896-3	2013	First, the bile acids react with nicotinamide adenine dinucleotide (NAD(+)) under catalysis of 3alpha-hydroxysteroid dehydrogenase (3alpha-HSD), which is converted to 3-ketosteroid and concomitantly NAD(+) turns into reduced nicotinamide adenine dinucleotide (NADH).	NAD	225-258	aldo-keto reductase family 1 member C3	Homo sapiens	132-142
23803896-3	2013	First, the bile acids react with nicotinamide adenine dinucleotide (NAD(+)) under catalysis of 3alpha-hydroxysteroid dehydrogenase (3alpha-HSD), which is converted to 3-ketosteroid and concomitantly NAD(+) turns into reduced nicotinamide adenine dinucleotide (NADH).	NAD	260-264	aldo-keto reductase family 1 member C3	Homo sapiens	95-130
23803896-3	2013	First, the bile acids react with nicotinamide adenine dinucleotide (NAD(+)) under catalysis of 3alpha-hydroxysteroid dehydrogenase (3alpha-HSD), which is converted to 3-ketosteroid and concomitantly NAD(+) turns into reduced nicotinamide adenine dinucleotide (NADH).	NAD	260-264	aldo-keto reductase family 1 member C3	Homo sapiens	132-142
23880765-0	2013	CD73 protein as a source of extracellular precursors for sustained NAD+ biosynthesis in FK866-treated tumor cells.	NAD	67-71	5'-nucleotidase ecto	Homo sapiens	0-4
23880765-4	2013	Here we demonstrate that low micromolar concentrations of extracellular NAD(+) or NAD(+) precursors, nicotinamide mononucleotide (NMN) and NR, can reverse the FK866-induced cell death, this representing a plausible explanation for the failure of NAMPT inhibition as an anti-cancer therapy.	NAD	72-78	nicotinamide phosphoribosyltransferase	Homo sapiens	246-251
23880765-4	2013	Here we demonstrate that low micromolar concentrations of extracellular NAD(+) or NAD(+) precursors, nicotinamide mononucleotide (NMN) and NR, can reverse the FK866-induced cell death, this representing a plausible explanation for the failure of NAMPT inhibition as an anti-cancer therapy.	NAD	82-88	nicotinamide phosphoribosyltransferase	Homo sapiens	246-251
23756706-2	2013	SUMMARY ANSWER: Studies conducted in vitro demonstrate that the ERbeta agonist 2,3-bis(4-hydroxy-phenyl)-propionitrile (DPN) has EC type-specific effects on patterns of gene expression and network formation.	NAD	120-123	estrogen receptor 2	Homo sapiens	64-70
23756706-9	2013	PARTICIPANT/MATERIALS, SETTING, METHODS: Analysis of DPN-treated ECs using Taqman gene array cards focused on genes involved in angiogenesis and inflammation identified cell type-specific ERbeta-dependent changes in gene expression, with validation using qPCR and immunohistochemistry.	NAD	53-56	estrogen receptor 2	Homo sapiens	188-194
23968400-1	2013	BACKGROUND: Nicotinamide phosphoribosyltransferase (NAMPT) is the limiting enzyme in one of pathways of synthesis of Nicotinamide Adenine Dinucleotide, a redox coenzyme.	NAD	117-150	nicotinamide phosphoribosyltransferase	Homo sapiens	52-57
23823317-1	2013	We recently demonstrated that Nicotinamide phosphoribosyltransferase (Nampt) inhibition depletes intracellular NAD+ content leading, to autophagic multiple myeloma (MM) cell death.	NAD	111-115	nicotinamide phosphoribosyltransferase	Homo sapiens	30-68
23823317-1	2013	We recently demonstrated that Nicotinamide phosphoribosyltransferase (Nampt) inhibition depletes intracellular NAD+ content leading, to autophagic multiple myeloma (MM) cell death.	NAD	111-115	nicotinamide phosphoribosyltransferase	Homo sapiens	70-75
23838793-2	2013	Overexpression of both the 6-phosphofructokinase (pfkA) and pyruvate kinase (pykA) genes increased intracellular concentrations of ATP and NADH and also resistance to butanol toxicity.	NAD	139-143	pfkA	Clostridium acetobutylicum ATCC 824	27-48
23838793-2	2013	Overexpression of both the 6-phosphofructokinase (pfkA) and pyruvate kinase (pykA) genes increased intracellular concentrations of ATP and NADH and also resistance to butanol toxicity.	NAD	139-143	pfkA	Clostridium acetobutylicum ATCC 824	50-54
23794606-6	2013	Moreover, we show that the oral administration of pioglitazone, an agonist of PPARgamma, restored mitochondrial content and expression of master regulators of biogenesis, neutralized oxidative damage to proteins and DNA, and reversed bioenergetic failure in terms of ATP levels, NAD+/NADH ratios, pyruvate kinase and glutathione reductase activities.	NAD	279-283	peroxisome proliferator activated receptor gamma	Mus musculus	78-87
23794606-6	2013	Moreover, we show that the oral administration of pioglitazone, an agonist of PPARgamma, restored mitochondrial content and expression of master regulators of biogenesis, neutralized oxidative damage to proteins and DNA, and reversed bioenergetic failure in terms of ATP levels, NAD+/NADH ratios, pyruvate kinase and glutathione reductase activities.	NAD	284-288	peroxisome proliferator activated receptor gamma	Mus musculus	78-87
23707506-1	2013	Alcohol dehydrogenases (ADH) catalyze the interconversion between alcohols and aldehydes with the reduction of nicotinamide adenine dinucleotide (NAD(+)) to NADH.	NAD	111-144	alcohol dehydrogenase 1	Arabidopsis thaliana	24-27
23707506-1	2013	Alcohol dehydrogenases (ADH) catalyze the interconversion between alcohols and aldehydes with the reduction of nicotinamide adenine dinucleotide (NAD(+)) to NADH.	NAD	146-153	alcohol dehydrogenase 1	Arabidopsis thaliana	24-27
23707506-1	2013	Alcohol dehydrogenases (ADH) catalyze the interconversion between alcohols and aldehydes with the reduction of nicotinamide adenine dinucleotide (NAD(+)) to NADH.	NAD	157-161	alcohol dehydrogenase 1	Arabidopsis thaliana	24-27
23922874-3	2013	In our study, we found that the Nampt-specific chemical inhibitor FK866 significantly inhibited cell survival and reduced nicotinamide adenine dinucleotide (NAD) levels in LoVo and SW480 cell lines.	NAD	122-155	nicotinamide phosphoribosyltransferase	Homo sapiens	32-37
23922874-3	2013	In our study, we found that the Nampt-specific chemical inhibitor FK866 significantly inhibited cell survival and reduced nicotinamide adenine dinucleotide (NAD) levels in LoVo and SW480 cell lines.	NAD	157-160	nicotinamide phosphoribosyltransferase	Homo sapiens	32-37
23922874-9	2013	In conclusion, this study demonstrated that the NAD-salvaging biosynthesis pathway involving Nampt might play a role in colorectal cancer cell survival.	NAD	48-51	nicotinamide phosphoribosyltransferase	Homo sapiens	93-98
23737528-0	2013	The NAD+ synthesis enzyme nicotinamide mononucleotide adenylyltransferase (NMNAT1) regulates ribosomal RNA transcription.	NAD	4-8	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	75-81
23737528-1	2013	The chromosomal region encoding the nuclear NAD(+) synthesis enzyme nicotinamide mononucleotide adenylyltransferase (NMNAT1) is frequently deleted in human cancer.	NAD	44-50	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	117-123
23737528-3	2013	NMNAT1 binds to nucleomethylin and is recruited into a ternary complex containing the NAD(+)-dependent deacetylase SirT1.	NAD	86-92	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	0-6
23339688-4	2013	Fully active GalE is dimeric and contains one tightly bound nicotinamide adenine dinucleotide (NAD) per subunit.	NAD	60-93	UDP-galactose-4-epimerase	Homo sapiens	13-17
23339688-4	2013	Fully active GalE is dimeric and contains one tightly bound nicotinamide adenine dinucleotide (NAD) per subunit.	NAD	95-98	UDP-galactose-4-epimerase	Homo sapiens	13-17
23339688-7	2013	These include practically irreversible binding of NAD, nonstereospecific hydride transfer, uridine nucleotide-induced activation of NAD, Tyr149 as a base catalyst, and [GalE-NADH]-oxidation in one-electron steps by one-electron acceptors.	NAD	174-178	UDP-galactose-4-epimerase	Homo sapiens	169-173
23339688-10	2013	In crystal structures of GalE, NAD bound within a Rossmann-type fold and uridine nucleotides within a substrate domain.	NAD	31-34	UDP-galactose-4-epimerase	Homo sapiens	25-29
23339688-11	2013	Structures of [GalE-NADH] in complex with UDP-glc show Lys153, Tyr149, and Ser124 in contact with NAD or glucosyl-C4(OH).	NAD	20-24	UDP-galactose-4-epimerase	Homo sapiens	15-19
23339688-11	2013	Structures of [GalE-NADH] in complex with UDP-glc show Lys153, Tyr149, and Ser124 in contact with NAD or glucosyl-C4(OH).	NAD	20-23	UDP-galactose-4-epimerase	Homo sapiens	15-19
23339688-20	2013	The binding of uridine(5")-diphosphate (UDP) to GalE-[nicotinamide-1-15N]NAD shifts the 15N-signal upfield 3 ppm, whereas UDP-binding to GalE-[nicotinamide-4-13C]NAD shifts the 13C-signal downfield by 3.4 ppm.	NAD	73-76	UDP-galactose-4-epimerase	Homo sapiens	48-52
23339688-20	2013	The binding of uridine(5")-diphosphate (UDP) to GalE-[nicotinamide-1-15N]NAD shifts the 15N-signal upfield 3 ppm, whereas UDP-binding to GalE-[nicotinamide-4-13C]NAD shifts the 13C-signal downfield by 3.4 ppm.	NAD	73-76	UDP-galactose-4-epimerase	Homo sapiens	137-141
23339688-20	2013	The binding of uridine(5")-diphosphate (UDP) to GalE-[nicotinamide-1-15N]NAD shifts the 15N-signal upfield 3 ppm, whereas UDP-binding to GalE-[nicotinamide-4-13C]NAD shifts the 13C-signal downfield by 3.4 ppm.	NAD	162-165	UDP-galactose-4-epimerase	Homo sapiens	48-52
23339688-20	2013	The binding of uridine(5")-diphosphate (UDP) to GalE-[nicotinamide-1-15N]NAD shifts the 15N-signal upfield 3 ppm, whereas UDP-binding to GalE-[nicotinamide-4-13C]NAD shifts the 13C-signal downfield by 3.4 ppm.	NAD	162-165	UDP-galactose-4-epimerase	Homo sapiens	137-141
23786618-3	2013	In one of the adult fibroblast strains evaluated, these changes in procollagen-1 and NAD(+)/NADH in response to the complex of bioactives were in parallel with increased expression of mRNA biomarkers related primarily to dermal matrix and basement membrane structure, including COL1A1, COL3A1, COL5A1, COL14A1, ELN and LOXL2, in addition to SOD2, NAMPT and TGFBR3; MMP1 was decreased in expression.	NAD	85-91	superoxide dismutase 2	Homo sapiens	341-345
23786618-3	2013	In one of the adult fibroblast strains evaluated, these changes in procollagen-1 and NAD(+)/NADH in response to the complex of bioactives were in parallel with increased expression of mRNA biomarkers related primarily to dermal matrix and basement membrane structure, including COL1A1, COL3A1, COL5A1, COL14A1, ELN and LOXL2, in addition to SOD2, NAMPT and TGFBR3; MMP1 was decreased in expression.	NAD	85-91	nicotinamide phosphoribosyltransferase	Homo sapiens	347-352
23786618-3	2013	In one of the adult fibroblast strains evaluated, these changes in procollagen-1 and NAD(+)/NADH in response to the complex of bioactives were in parallel with increased expression of mRNA biomarkers related primarily to dermal matrix and basement membrane structure, including COL1A1, COL3A1, COL5A1, COL14A1, ELN and LOXL2, in addition to SOD2, NAMPT and TGFBR3; MMP1 was decreased in expression.	NAD	92-96	superoxide dismutase 2	Homo sapiens	341-345
23786618-3	2013	In one of the adult fibroblast strains evaluated, these changes in procollagen-1 and NAD(+)/NADH in response to the complex of bioactives were in parallel with increased expression of mRNA biomarkers related primarily to dermal matrix and basement membrane structure, including COL1A1, COL3A1, COL5A1, COL14A1, ELN and LOXL2, in addition to SOD2, NAMPT and TGFBR3; MMP1 was decreased in expression.	NAD	92-96	nicotinamide phosphoribosyltransferase	Homo sapiens	347-352
23510538-10	2013	CONCLUSIONS: HCV core protein induces alterations in cellular redox state (decrease in the NAD(+)/NADH ratio), which could influence the activity of SIRT1 and secondarily AMPK, then change the expression profile of glucose and lipid metabolism-related genes, thereby causing metabolism disorders of hepatocytes.	NAD	91-97	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	171-175
23510538-10	2013	CONCLUSIONS: HCV core protein induces alterations in cellular redox state (decrease in the NAD(+)/NADH ratio), which could influence the activity of SIRT1 and secondarily AMPK, then change the expression profile of glucose and lipid metabolism-related genes, thereby causing metabolism disorders of hepatocytes.	NAD	98-102	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	171-175
23673559-1	2013	Sirtuin 5 (SIRT5) is a nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase, belonging to the silent information regulator 2 (Sir2) family of sirtuin histone deacetylases (sirtuins).	NAD	58-61	sirtuin 5	Mus musculus	11-16
23825667-8	2013	Moreover, concomitant suppression of NAD-dependent deacetylase SIRT1 and AMPK is observed in atherosclerotic pigs, which leads to the proteolytic activation of SREBP-1 by diminishing the deacetylation and Ser-372 phosphorylation of SREBP-1.	NAD	37-40	protein kinase AMP-activated catalytic subunit alpha 1	Sus scrofa	73-77
23716697-3	2013	Here, we report that ADP-ribosylation of CtBP1-S/BARS by BFA occurs via a nonconventional mechanism that comprises two steps: (i) synthesis of a BFA-ADP-ribose conjugate by the ADP-ribosyl cyclase CD38 and (ii) covalent binding of the BFA-ADP-ribose conjugate into the CtBP1-S/BARS NAD(+)-binding pocket.	NAD	282-288	C-terminal binding protein 1	Homo sapiens	41-46
23716697-3	2013	Here, we report that ADP-ribosylation of CtBP1-S/BARS by BFA occurs via a nonconventional mechanism that comprises two steps: (i) synthesis of a BFA-ADP-ribose conjugate by the ADP-ribosyl cyclase CD38 and (ii) covalent binding of the BFA-ADP-ribose conjugate into the CtBP1-S/BARS NAD(+)-binding pocket.	NAD	282-288	C-terminal binding protein 1	Homo sapiens	49-53
23675962-7	2013	The addition of NADH to an aqueous solution of the met-Hb2-(HSA-LF)3 cluster reduced the inactive ferric Hb center to the functional ferrous Hb.	NAD	16-20	keratin 82	Homo sapiens	55-58
23435312-4	2013	Nicotinamide phosphoribosyltransferase (NAMPT/PBEF/visfatin, encoded by PBEF1) is a rate-limiting enzyme in NAD(+) biosynthesis from nicotinamide.	NAD	108-114	nicotinamide phosphoribosyltransferase	Homo sapiens	0-38
23435312-4	2013	Nicotinamide phosphoribosyltransferase (NAMPT/PBEF/visfatin, encoded by PBEF1) is a rate-limiting enzyme in NAD(+) biosynthesis from nicotinamide.	NAD	108-114	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
23435312-4	2013	Nicotinamide phosphoribosyltransferase (NAMPT/PBEF/visfatin, encoded by PBEF1) is a rate-limiting enzyme in NAD(+) biosynthesis from nicotinamide.	NAD	108-114	nicotinamide phosphoribosyltransferase	Homo sapiens	46-50
23435312-4	2013	Nicotinamide phosphoribosyltransferase (NAMPT/PBEF/visfatin, encoded by PBEF1) is a rate-limiting enzyme in NAD(+) biosynthesis from nicotinamide.	NAD	108-114	nicotinamide phosphoribosyltransferase	Homo sapiens	51-59
23435312-4	2013	Nicotinamide phosphoribosyltransferase (NAMPT/PBEF/visfatin, encoded by PBEF1) is a rate-limiting enzyme in NAD(+) biosynthesis from nicotinamide.	NAD	108-114	nicotinamide phosphoribosyltransferase	Homo sapiens	72-77
23435312-7	2013	APO866 is a specific PBEF1 inhibitor known to deplete cellular NAD(+).	NAD	63-69	nicotinamide phosphoribosyltransferase	Homo sapiens	21-26
22751110-7	2013	However, when extracellular signal-regulated kinase 1 and 2 (ERK 1/2) were activated by co-incubation with basement membrane extract or epidermal growth factor, induction of apoptosis by ERbeta agonists was repressed and DPN induced proliferation in a similar way as E2 or PPT.	NAD	221-224	mitogen-activated protein kinase 3	Mus musculus	14-59
22751110-7	2013	However, when extracellular signal-regulated kinase 1 and 2 (ERK 1/2) were activated by co-incubation with basement membrane extract or epidermal growth factor, induction of apoptosis by ERbeta agonists was repressed and DPN induced proliferation in a similar way as E2 or PPT.	NAD	221-224	mitogen-activated protein kinase 3	Mus musculus	61-68
23221771-5	2013	We recently reported that an intracellular NAD(+)-depleting agent, FK866, exerts its anti-MM effect by triggering autophagic cell death via transcriptional-dependent (transcription factor EB, TFEB) and -independent (PI3K-MTORC1) mechanisms.	NAD	43-49	transcription factor EB	Homo sapiens	192-196
23363239-1	2013	Human UDP-alpha-d-glucose 6-dehydrogenase (hUGDH) forms a hexamer that catalyzes the NAD(+)-dependent oxidation of UDP-alpha-d-glucose (UDG) to produce UDP-alpha-d-glucuronic acid.	NAD	85-91	UDP-glucose 6-dehydrogenase	Homo sapiens	43-48
23261716-7	2013	When NADPH was used, as compared to NADH, the reductions of CBCP-one by AKR1C1, AKR1C2 and AKR1C3 were 14-, 51- and 31-fold more efficient, respectively.	NAD	36-40	aldo-keto reductase family 1 member C2	Homo sapiens	80-86
23261716-7	2013	When NADPH was used, as compared to NADH, the reductions of CBCP-one by AKR1C1, AKR1C2 and AKR1C3 were 14-, 51- and 31-fold more efficient, respectively.	NAD	36-40	aldo-keto reductase family 1 member C3	Homo sapiens	91-97
23339632-2	2013	Results showed that diaphorase (DP) and lactate dehydrogenases (LDH) had distinct binding selectivity and preference over reduced and oxidized states of coenzyme NAD(H).	NAD	162-168	dihydrolipoamide dehydrogenase	Homo sapiens	20-30
23339632-2	2013	Results showed that diaphorase (DP) and lactate dehydrogenases (LDH) had distinct binding selectivity and preference over reduced and oxidized states of coenzyme NAD(H).	NAD	162-168	dihydrolipoamide dehydrogenase	Homo sapiens	32-34
23339632-3	2013	On the basis of that, DP and LDH were chosen as indicator enzymes to distinguish the specific state of surface-bound NAD(H).	NAD	117-123	dihydrolipoamide dehydrogenase	Homo sapiens	22-24
23321587-2	2013	In this research, azoreductase and glucose 1-dehydrogenase were coupled for both continuous generation of the cofactor NADH and azo dye removal.	NAD	119-123	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	35-58
23153509-2	2013	Nicotinamide phosphoribosyltransferase (NAMPT) is a key enzyme in the salvaging pathway for the synthesis of nicotinamide adenine dinucleotide (NAD(+)) that is involved in energy metabolism.	NAD	109-142	nicotinamide phosphoribosyltransferase	Homo sapiens	0-38
23153509-2	2013	Nicotinamide phosphoribosyltransferase (NAMPT) is a key enzyme in the salvaging pathway for the synthesis of nicotinamide adenine dinucleotide (NAD(+)) that is involved in energy metabolism.	NAD	109-142	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
23153509-2	2013	Nicotinamide phosphoribosyltransferase (NAMPT) is a key enzyme in the salvaging pathway for the synthesis of nicotinamide adenine dinucleotide (NAD(+)) that is involved in energy metabolism.	NAD	144-150	nicotinamide phosphoribosyltransferase	Homo sapiens	0-38
23153509-2	2013	Nicotinamide phosphoribosyltransferase (NAMPT) is a key enzyme in the salvaging pathway for the synthesis of nicotinamide adenine dinucleotide (NAD(+)) that is involved in energy metabolism.	NAD	144-150	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
24171767-1	2013	NAD+ biosynthesis through nicotinamide phosphoribosyltransferase (NAMPT) holds potential as a target for the treatment of inflammatory disorders due to NAD(+)"s role in immune cell signaling and metabolism.	NAD	152-158	nicotinamide phosphoribosyltransferase	Homo sapiens	66-71
23224332-6	2013	Coenzyme NAD or NADP could regulate the enzymatic thermostability, as well as the esterase activity.	NAD	9-12	esterase	Sulfurisphaera tokodaii str. 7	82-90
23536823-1	2013	Nicotinamide phosphoribosyltransferase (Nampt) is a rate-limiting enzyme in the mammalian NAD+ biosynthesis of a salvage pathway and exists in 2 known forms, intracellular Nampt (iNampt) and a secreted form, extracellular Nampt (eNampt).	NAD	90-94	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
23536823-1	2013	Nicotinamide phosphoribosyltransferase (Nampt) is a rate-limiting enzyme in the mammalian NAD+ biosynthesis of a salvage pathway and exists in 2 known forms, intracellular Nampt (iNampt) and a secreted form, extracellular Nampt (eNampt).	NAD	90-94	nicotinamide phosphoribosyltransferase	Homo sapiens	172-177
23536823-1	2013	Nicotinamide phosphoribosyltransferase (Nampt) is a rate-limiting enzyme in the mammalian NAD+ biosynthesis of a salvage pathway and exists in 2 known forms, intracellular Nampt (iNampt) and a secreted form, extracellular Nampt (eNampt).	NAD	90-94	nicotinamide phosphoribosyltransferase	Homo sapiens	172-177
23040397-4	2012	Glucose dehydrogenase was coated on a carbon electrode to catalyze glucose oxidation in the presence of NAD+ as a cofactor/mediator and methylene green as an electrocatalyst.	NAD	104-108	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	0-21
22992456-3	2012	We report that the NAD(+) biosynthetic enzyme, nicotinamide phosphoribosyltransferase (Nampt/PBEF/visfatin), mediates directionally persistent migration of vascular smooth muscle cells (SMCs).	NAD	19-25	nicotinamide phosphoribosyltransferase	Homo sapiens	47-85
22992456-3	2012	We report that the NAD(+) biosynthetic enzyme, nicotinamide phosphoribosyltransferase (Nampt/PBEF/visfatin), mediates directionally persistent migration of vascular smooth muscle cells (SMCs).	NAD	19-25	nicotinamide phosphoribosyltransferase	Homo sapiens	87-92
22992456-3	2012	We report that the NAD(+) biosynthetic enzyme, nicotinamide phosphoribosyltransferase (Nampt/PBEF/visfatin), mediates directionally persistent migration of vascular smooth muscle cells (SMCs).	NAD	19-25	nicotinamide phosphoribosyltransferase	Homo sapiens	93-97
22992456-3	2012	We report that the NAD(+) biosynthetic enzyme, nicotinamide phosphoribosyltransferase (Nampt/PBEF/visfatin), mediates directionally persistent migration of vascular smooth muscle cells (SMCs).	NAD	19-25	nicotinamide phosphoribosyltransferase	Homo sapiens	98-106
23262103-1	2012	Nicotinamide phosphoribosyltransferase (NAMPT), also known as pre-B cell colony-enhancing factor (PBEF) or visfatin, is a crucial rate-limiting enzyme of NAD biosynthetic pathway.	NAD	154-157	nicotinamide phosphoribosyltransferase	Homo sapiens	0-38
23262103-1	2012	Nicotinamide phosphoribosyltransferase (NAMPT), also known as pre-B cell colony-enhancing factor (PBEF) or visfatin, is a crucial rate-limiting enzyme of NAD biosynthetic pathway.	NAD	154-157	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
23262103-1	2012	Nicotinamide phosphoribosyltransferase (NAMPT), also known as pre-B cell colony-enhancing factor (PBEF) or visfatin, is a crucial rate-limiting enzyme of NAD biosynthetic pathway.	NAD	154-157	nicotinamide phosphoribosyltransferase	Homo sapiens	62-96
23262103-1	2012	Nicotinamide phosphoribosyltransferase (NAMPT), also known as pre-B cell colony-enhancing factor (PBEF) or visfatin, is a crucial rate-limiting enzyme of NAD biosynthetic pathway.	NAD	154-157	nicotinamide phosphoribosyltransferase	Homo sapiens	98-102
23262103-1	2012	Nicotinamide phosphoribosyltransferase (NAMPT), also known as pre-B cell colony-enhancing factor (PBEF) or visfatin, is a crucial rate-limiting enzyme of NAD biosynthetic pathway.	NAD	154-157	nicotinamide phosphoribosyltransferase	Homo sapiens	107-115
23203137-1	2012	Xanthine oxidoreductase (XOR) catalyzes the conversion of hypoxanthine to xanthine and xanthine to uric acid with concomitant reduction of either NAD+ or O(2).	NAD	146-150	xanthine dehydrogenase	Homo sapiens	0-23
23203137-1	2012	Xanthine oxidoreductase (XOR) catalyzes the conversion of hypoxanthine to xanthine and xanthine to uric acid with concomitant reduction of either NAD+ or O(2).	NAD	146-150	xanthine dehydrogenase	Homo sapiens	25-28
22776298-5	2012	[(3)H]-thymidine incorporation was also stimulated by the ERbeta agonist DPN and the ERalpha agonist PPT.	NAD	73-76	estrogen receptor 2	Homo sapiens	58-64
22993213-1	2012	Saccharomyces cerevisiae NDI1 codes for the internal mitochondrial ubiquinone oxidoreductase, which transfers electrons from NADH to ubiquinone in the respiratory chain.	NAD	125-129	NADH-ubiquinone reductase (H(+)-translocating) NDI1	Saccharomyces cerevisiae S288C	25-29
22955917-0	2012	Targeting NAD+ salvage pathway induces autophagy in multiple myeloma cells via mTORC1 and extracellular signal-regulated kinase (ERK1/2) inhibition.	NAD	10-14	CREB regulated transcription coactivator 1	Mus musculus	79-85
22955917-2	2012	Here we investigated the biologic role of a rate-limiting enzyme involved in NAD(+) synthesis, Nampt, in multiple myeloma (MM).	NAD	77-83	nicotinamide phosphoribosyltransferase	Homo sapiens	95-100
22955917-5	2012	Nampt knockdown by RNAi confirmed its pivotal role in maintenance of both MM cell viability and intracellular NAD(+) stores.	NAD	110-116	nicotinamide phosphoribosyltransferase	Homo sapiens	0-5
22503830-1	2012	The rates of NADH-supported superoxide/hydrogen peroxide production by membrane-bound bovine heart respiratory complex I, soluble pig heart dihydrolipoamide dehydrogenase (DLDH), and by accompanying operation of these enzymes in rat heart mitochondrial matrix were measured as a function of the pool of pyridine nucleotides and its redox state.	NAD	13-17	dihydrolipoamide dehydrogenase	Sus scrofa	172-176
22503830-4	2012	About half of the total NADH-supported H(2)O(2) production by permeabilized mitochondria in the absence of stimulating ammonium could be accounted for by DLDH activity.	NAD	24-28	dihydrolipoamide dehydrogenase	Sus scrofa	154-158
22377803-1	2012	Nicotinamide phosphoribosyltransferase (NAMPT), an enzyme involved in NAD biosynthesis, has recently been identified as a novel mediator of innate immunity.	NAD	70-73	nicotinamide phosphoribosyltransferase	Homo sapiens	0-38
22377803-1	2012	Nicotinamide phosphoribosyltransferase (NAMPT), an enzyme involved in NAD biosynthesis, has recently been identified as a novel mediator of innate immunity.	NAD	70-73	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
22740640-3	2012	or butylated hydroxylanisole (BHA) (0.45% in the diet) and of cytosolic NAD+-dependent ALDH activity.	NAD	72-76	aldehyde dehydrogenase family 1, subfamily A1	Mus musculus	87-91
22949654-5	2012	Here we present the crystal structures of Ndi1 in its substrate-free, NAD(+)- and ubiquinone- (UQ2) complexed states.	NAD	70-76	NADH-ubiquinone reductase (H(+)-translocating) NDI1	Saccharomyces cerevisiae S288C	42-46
22949654-7	2012	Crucially, the structures of the Ndi1-NAD(+) and Ndi1-UQ2 complexes show overlapping binding sites for the NAD(+) and quinone substrates.	NAD	38-44	NADH-ubiquinone reductase (H(+)-translocating) NDI1	Saccharomyces cerevisiae S288C	33-37
22949654-7	2012	Crucially, the structures of the Ndi1-NAD(+) and Ndi1-UQ2 complexes show overlapping binding sites for the NAD(+) and quinone substrates.	NAD	38-44	NADH-ubiquinone reductase (H(+)-translocating) NDI1	Saccharomyces cerevisiae S288C	49-53
22949654-7	2012	Crucially, the structures of the Ndi1-NAD(+) and Ndi1-UQ2 complexes show overlapping binding sites for the NAD(+) and quinone substrates.	NAD	107-113	NADH-ubiquinone reductase (H(+)-translocating) NDI1	Saccharomyces cerevisiae S288C	33-37
22949654-7	2012	Crucially, the structures of the Ndi1-NAD(+) and Ndi1-UQ2 complexes show overlapping binding sites for the NAD(+) and quinone substrates.	NAD	107-113	NADH-ubiquinone reductase (H(+)-translocating) NDI1	Saccharomyces cerevisiae S288C	49-53
22849721-3	2012	SIRT3 and SIRT5 are NAD-consuming enzymes that are potential therapeutic targets for the treatment of metabolic diseases and cancers.	NAD	20-23	sirtuin 5	Homo sapiens	10-15
22648686-2	2012	ALD6 encoding an aldehyde dehydrogenases of the indigenous yeast was replaced by a GPD1 and CUP1 gene cassette, which are responsible for NAD-dependent glycerol-3-phosphatase dehydrogenase and copper resistance, respectively.	NAD	138-141	aldehyde dehydrogenase (NADP(+)) ALD6	Saccharomyces cerevisiae S288C	0-4
22743824-1	2012	Sirtuin 6 (Sirt6), a mammalian Sir2 (silent information regulator-2) ortholog, is an NAD (+) -dependent histone deacetylase that modulates chromatin structure and genomic stability.	NAD	85-92	sirtuin 6	Homo sapiens	0-9
22743824-1	2012	Sirtuin 6 (Sirt6), a mammalian Sir2 (silent information regulator-2) ortholog, is an NAD (+) -dependent histone deacetylase that modulates chromatin structure and genomic stability.	NAD	85-92	sirtuin 6	Homo sapiens	11-16
22572242-9	2012	Low PDI activity of CYO1 was observed when NADPH or NADH was used as an electron donor.	NAD	52-56	prolyl 4-hydroxylase subunit beta	Homo sapiens	4-7
22572242-9	2012	Low PDI activity of CYO1 was observed when NADPH or NADH was used as an electron donor.	NAD	52-56	protein disulfide isomerase	Arabidopsis thaliana	20-24
22497727-2	2012	We report on characterizations of in situ regeneration of NADH via lipoamide dehydrogenase (LD)-catalyzed electron transfer reaction to regenerate NADH using UV-vis spectroelectrochemistry.	NAD	58-62	dihydrolipoamide dehydrogenase	Homo sapiens	67-90
22497727-2	2012	We report on characterizations of in situ regeneration of NADH via lipoamide dehydrogenase (LD)-catalyzed electron transfer reaction to regenerate NADH using UV-vis spectroelectrochemistry.	NAD	147-151	dihydrolipoamide dehydrogenase	Homo sapiens	67-90
22607208-3	2012	In the present study we show that GapC1 is a phosphorylating NAD-specific GAPDH with enzymatic activity strictly dependent on Cys(149).	NAD	61-64	glyceraldehyde-3-phosphate dehydrogenase C subunit 1	Arabidopsis thaliana	34-39
22722101-1	2012	Flavin reductase HpaC(St) catalyzes the reduction of free flavins using NADH or NADPH.	NAD	72-76	flavin reductase family protein	Sulfurisphaera tokodaii str. 7	0-16
22730426-3	2012	Here, we report that FIN4 encodes the chloroplastic enzyme ASPARTATE OXIDASE (AO), which catalyzes the first irreversible step in the de novo biosynthesis of NAD.	NAD	158-161	L-aspartate oxidase	Arabidopsis thaliana	21-25
22516612-6	2012	Structures of the 93% identical mouse P5CDH complexed with sulfate ion (1.3 A resolution), glutamate (1.5 A), and NAD(+) (1.5 A) were determined to obtain high-resolution views of the active site.	NAD	114-120	aldehyde dehydrogenase 4 family, member A1	Mus musculus	38-43
22661712-5	2012	ARTD15 features an alpha-helical domain that packs against its transferase domain without making direct contact with the NAD(+)-binding crevice or the donor loop.	NAD	121-127	poly(ADP-ribose) polymerase family member 16	Homo sapiens	0-6
22459323-2	2012	In bacteria and animals, GDH is a homohexamer allosterically regulated, whereas in plants NADH-GDH (EC 1.4.1.2) is also found as heterohexamer of alpha- and beta-subunits, but its regulation remains undefined.	NAD	90-94	glutamate dehydrogenase	Solanum lycopersicum	25-28
22459323-2	2012	In bacteria and animals, GDH is a homohexamer allosterically regulated, whereas in plants NADH-GDH (EC 1.4.1.2) is also found as heterohexamer of alpha- and beta-subunits, but its regulation remains undefined.	NAD	90-94	glutamate dehydrogenase	Solanum lycopersicum	95-98
22583019-0	2012	Substrates for efficient fluorometric screening employing the NAD-dependent sirtuin 5 lysine deacylase (KDAC) enzyme.	NAD	62-65	sirtuin 5	Homo sapiens	76-85
21975728-3	2012	Enzymes involved in NAD re-synthesis include nicotinamide phosphoribosyltransferase (NAMPT) and nicotinamide mononucleotide adenylyltransferase.	NAD	20-23	nicotinamide phosphoribosyltransferase	Homo sapiens	45-83
21975728-3	2012	Enzymes involved in NAD re-synthesis include nicotinamide phosphoribosyltransferase (NAMPT) and nicotinamide mononucleotide adenylyltransferase.	NAD	20-23	nicotinamide phosphoribosyltransferase	Homo sapiens	85-90
22406418-8	2012	In contrast, the ERbeta selective agonist DPN (100 pM) significantly reduced the Ca(2+)-influx (32%).	NAD	42-45	estrogen receptor 2 (beta)	Mus musculus	17-23
22430142-1	2012	Nicotinamide-phosphoribosyltransferase (NAMPT), induced under stress, converts nicotinamide (NA) to nicotinamide mononucleotide (NMN), which then reacts with ATP to regenerate NAD(+).	NAD	176-182	nicotinamide phosphoribosyltransferase	Homo sapiens	0-38
22430142-1	2012	Nicotinamide-phosphoribosyltransferase (NAMPT), induced under stress, converts nicotinamide (NA) to nicotinamide mononucleotide (NMN), which then reacts with ATP to regenerate NAD(+).	NAD	176-182	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
22430142-4	2012	The present study was designed to assess the significance of intracellular NAD(+) levels on the regulation of GADD45A expression.	NAD	75-81	growth arrest and DNA damage inducible alpha	Homo sapiens	110-117
22307295-3	2012	In Sinorhizobium meliloti bacteroids from alfalfa, NAD(+)-malic enzyme (DME) is required for N(2) fixation, and this activity is thought to be required for the anaplerotic synthesis of pyruvate.	NAD	51-57	NADP-dependent malic enzyme	Sinorhizobium fredii NGR234	72-75
22185573-0	2012	The human gene SLC25A17 encodes a peroxisomal transporter of coenzyme A, FAD and NAD+.	NAD	81-85	solute carrier family 25 member 17	Homo sapiens	15-23
22185573-4	2012	Its transport properties and kinetic parameters demonstrate that SLC25A17 is a transporter of CoA, FAD, FMN and AMP, and to a lesser extent of NAD+, PAP (adenosine 3",5"-diphosphate) and ADP.	NAD	143-147	solute carrier family 25 member 17	Homo sapiens	65-73
22209345-7	2012	Estradiol, and the specific estrogen receptor-beta agonist DPN, decreased current amplitude measured in the morning (AM), but had no effect on afternoon currents.	NAD	59-62	estrogen receptor 2 (beta)	Mus musculus	28-50
22209345-10	2012	The ER-beta agonist DPN did not mimic the effect of estradiol on DAPs, and the modulation of DAPs by estradiol was no longer present in cells from postreproductive animals.	NAD	20-23	estrogen receptor 2 (beta)	Mus musculus	4-11
22190494-6	2012	NAMPT is the rate-limiting enzyme of the NAD(+) salvage pathway and enhances SIRT1 activity by increasing the amount of NAD(+).	NAD	41-47	nicotinamide phosphoribosyltransferase	Homo sapiens	0-5
22190494-6	2012	NAMPT is the rate-limiting enzyme of the NAD(+) salvage pathway and enhances SIRT1 activity by increasing the amount of NAD(+).	NAD	120-126	nicotinamide phosphoribosyltransferase	Homo sapiens	0-5
22145797-6	2012	On the basis of new 1.65, 2.3, 1.9, and 2.2 A resolution crystal structures for XDH, XO, the NAD(+)- and NADH-complexed XDH, E(sq/hq) were calculated to better understand how the enzyme activates an ET from FeS-II to flavin.	NAD	93-99	xanthine dehydrogenase	Homo sapiens	80-83
22145797-6	2012	On the basis of new 1.65, 2.3, 1.9, and 2.2 A resolution crystal structures for XDH, XO, the NAD(+)- and NADH-complexed XDH, E(sq/hq) were calculated to better understand how the enzyme activates an ET from FeS-II to flavin.	NAD	93-99	xanthine dehydrogenase	Homo sapiens	120-123
22145797-6	2012	On the basis of new 1.65, 2.3, 1.9, and 2.2 A resolution crystal structures for XDH, XO, the NAD(+)- and NADH-complexed XDH, E(sq/hq) were calculated to better understand how the enzyme activates an ET from FeS-II to flavin.	NAD	105-109	xanthine dehydrogenase	Homo sapiens	80-83
22145797-6	2012	On the basis of new 1.65, 2.3, 1.9, and 2.2 A resolution crystal structures for XDH, XO, the NAD(+)- and NADH-complexed XDH, E(sq/hq) were calculated to better understand how the enzyme activates an ET from FeS-II to flavin.	NAD	105-109	xanthine dehydrogenase	Homo sapiens	120-123
22145797-9	2012	Instead, the positive charge of the NAD(+) ring, deprotonation of Asp429, and capping of the bulk surface of the flavin by the NAD(+) molecule all contribute to altering E(sq/hq) upon NAD(+) binding to XDH.	NAD	36-42	xanthine dehydrogenase	Homo sapiens	202-205
21979946-11	2012	This loss of p53 was regulated by MDM2-independent NADH quinone oxidoreductase 1-mediated protein degradation, likely due to the imbalance of flavin adenine dinucleotide/nicotinamide adenine dinucleotide in SDH(var+) cells.	NAD	170-203	serine dehydratase	Homo sapiens	207-210
22934941-1	2012	Nampt/Visfatin/PBEF is a primary, rate-limiting enzyme involved in NAD+ biosynthesis, which serves as a pivotal substance for proteins, and is required for cell growth, survival, DNA replication and repair and energy metabolism.	NAD	67-71	nicotinamide phosphoribosyltransferase	Homo sapiens	0-5
22934941-1	2012	Nampt/Visfatin/PBEF is a primary, rate-limiting enzyme involved in NAD+ biosynthesis, which serves as a pivotal substance for proteins, and is required for cell growth, survival, DNA replication and repair and energy metabolism.	NAD	67-71	nicotinamide phosphoribosyltransferase	Homo sapiens	6-14
22934941-1	2012	Nampt/Visfatin/PBEF is a primary, rate-limiting enzyme involved in NAD+ biosynthesis, which serves as a pivotal substance for proteins, and is required for cell growth, survival, DNA replication and repair and energy metabolism.	NAD	67-71	nicotinamide phosphoribosyltransferase	Homo sapiens	15-19
22934941-4	2012	APO866 and CHS-828 are recognized inhibitors of Nampt, known to block the intracellular and extracellular NAD+ synthesis pathway.	NAD	106-110	nicotinamide phosphoribosyltransferase	Homo sapiens	48-53
22684235-1	2012	Visfatin is a pleiotropic mediator which acts as growth factor, cytokine, enzyme involved in energy including nicotinamide adenine dinucleotide metabolism and has been recently demonstrated to exert several pro-inflammatory functions.	NAD	110-143	nicotinamide phosphoribosyltransferase	Homo sapiens	0-8
22089115-3	2012	Nicotinamide phosphoribosyltransferase (NAMPT) is a rate-limiting enzyme in nicotinamide adenine dinucleotide biosynthesis, and it regulates intracellular ATP levels in mammalian cells.	NAD	76-109	nicotinamide phosphoribosyltransferase	Homo sapiens	0-38
22089115-3	2012	Nicotinamide phosphoribosyltransferase (NAMPT) is a rate-limiting enzyme in nicotinamide adenine dinucleotide biosynthesis, and it regulates intracellular ATP levels in mammalian cells.	NAD	76-109	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
23430852-1	2012	Citrin plays a role in the transfer of NADH-reducing equivalent from cytosol to mitochondria as part of the malate-aspartate shuttle in liver.	NAD	39-43	solute carrier family 25 member 13	Homo sapiens	0-6
23226106-4	2012	This new phenotype is mediated by a new downstream target of Hiw: the NAD+ biosynthetic enzyme nicotinamide mononucleotide adenyltransferase (Nmnat), which acts in parallel to a previously known target of Hiw, the Wallenda dileucine zipper kinase (Wnd/DLK) MAPKKK.	NAD	70-74	highwire	Drosophila melanogaster	61-64
23226106-4	2012	This new phenotype is mediated by a new downstream target of Hiw: the NAD+ biosynthetic enzyme nicotinamide mononucleotide adenyltransferase (Nmnat), which acts in parallel to a previously known target of Hiw, the Wallenda dileucine zipper kinase (Wnd/DLK) MAPKKK.	NAD	70-74	highwire	Drosophila melanogaster	205-208
23226106-4	2012	This new phenotype is mediated by a new downstream target of Hiw: the NAD+ biosynthetic enzyme nicotinamide mononucleotide adenyltransferase (Nmnat), which acts in parallel to a previously known target of Hiw, the Wallenda dileucine zipper kinase (Wnd/DLK) MAPKKK.	NAD	70-74	mitogen-activated protein kinase kinase kinase 12	Mus musculus	252-255
23071504-1	2012	Nicotinamide phosphoribosyltransferase (NAMPT) is a key enzyme for nicotinamide adenine dinucleotide (NAD) biosynthesis, and can be found either intracellularly (iNAMPT) or extracellularly (eNAMPT).	NAD	67-100	nicotinamide phosphoribosyltransferase	Homo sapiens	0-38
23071504-1	2012	Nicotinamide phosphoribosyltransferase (NAMPT) is a key enzyme for nicotinamide adenine dinucleotide (NAD) biosynthesis, and can be found either intracellularly (iNAMPT) or extracellularly (eNAMPT).	NAD	67-100	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
23071504-1	2012	Nicotinamide phosphoribosyltransferase (NAMPT) is a key enzyme for nicotinamide adenine dinucleotide (NAD) biosynthesis, and can be found either intracellularly (iNAMPT) or extracellularly (eNAMPT).	NAD	102-105	nicotinamide phosphoribosyltransferase	Homo sapiens	0-38
23071504-1	2012	Nicotinamide phosphoribosyltransferase (NAMPT) is a key enzyme for nicotinamide adenine dinucleotide (NAD) biosynthesis, and can be found either intracellularly (iNAMPT) or extracellularly (eNAMPT).	NAD	102-105	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
23071504-6	2012	Application of recombinant NAMPT, mimicking the elevated serum NAMPT level, enhanced the susceptibility of cerebral endothelial cells to ischemic injury, while inhibition of iNAMPT by FK866, a specific inhibitor, reduced intracellular NAD level and induced neuronal death.	NAD	235-238	nicotinamide phosphoribosyltransferase	Homo sapiens	27-32
22033928-3	2011	It has been known that intracellular NAD(+) approaches ecto-CD38 via its export by connexin (Cx43) hemichannels, a component of gap junctions.	NAD	37-43	gap junction protein, alpha 3	Mus musculus	93-97
22033928-5	2011	Moreover, it has been unknown what physiological stimulation can trigger Cx43-mediated export of NAD(+).	NAD	97-103	gap junction protein, alpha 3	Mus musculus	73-77
22033928-7	2011	We also demonstrate that physiological stimulation such as Fcgamma receptor (FcgammaR) ligation induces calcium mobilization through three sequential steps, Cx43-mediated NAD(+) export, CD38-mediated generation of cADPR and Cx43-mediated cADPR import in J774 cells.	NAD	171-177	gap junction protein, alpha 3	Mus musculus	157-161
22190532-1	2011	Nicotinamide phosphoribosyl transferase (NAMPT) is the key enzyme for the synthesis of nicotinamide adenine dinucleotide (NAD), and also serves as a cytokine in mammalian cells.	NAD	87-120	nicotinamide phosphoribosyltransferase	Homo sapiens	0-39
22190532-1	2011	Nicotinamide phosphoribosyl transferase (NAMPT) is the key enzyme for the synthesis of nicotinamide adenine dinucleotide (NAD), and also serves as a cytokine in mammalian cells.	NAD	87-120	nicotinamide phosphoribosyltransferase	Homo sapiens	41-46
22190532-1	2011	Nicotinamide phosphoribosyl transferase (NAMPT) is the key enzyme for the synthesis of nicotinamide adenine dinucleotide (NAD), and also serves as a cytokine in mammalian cells.	NAD	122-125	nicotinamide phosphoribosyltransferase	Homo sapiens	0-39
22190532-1	2011	Nicotinamide phosphoribosyl transferase (NAMPT) is the key enzyme for the synthesis of nicotinamide adenine dinucleotide (NAD), and also serves as a cytokine in mammalian cells.	NAD	122-125	nicotinamide phosphoribosyltransferase	Homo sapiens	41-46
21844227-3	2011	While the macro domain of macroH2A1.1 can interact with NAD(+)-derived small molecules, such as poly(ADP-ribose), macroH2A1.2"s macro domain cannot.	NAD	56-62	macroH2A.1 histone	Mus musculus	26-35
21844227-3	2011	While the macro domain of macroH2A1.1 can interact with NAD(+)-derived small molecules, such as poly(ADP-ribose), macroH2A1.2"s macro domain cannot.	NAD	56-62	macroH2A.1 histone	Mus musculus	114-125
21844227-5	2011	Furthermore, reintroduction of macroH2A1.1 suppresses the proliferation of lung and cervical cancer cells in a manner that requires the ability of macroH2A1.1 to bind NAD(+)-derived metabolites.	NAD	167-173	macroH2A.1 histone	Mus musculus	31-40
21844227-5	2011	Furthermore, reintroduction of macroH2A1.1 suppresses the proliferation of lung and cervical cancer cells in a manner that requires the ability of macroH2A1.1 to bind NAD(+)-derived metabolites.	NAD	167-173	macroH2A.1 histone	Mus musculus	147-156
21865489-4	2011	Here, antisense suppression of CP12 in tobacco (Nicotiana tabacum) was observed to impact on NAD-induced PRK and GAPDH complex formation but had little effect on enzyme activity.	NAD	93-96	glyceraldehyde-3-phosphate dehydrogenase, cytosolic	Nicotiana tabacum	113-118
21309715-1	2011	BACKGROUND: Visfatin is a pleiotropic mediator that acts as growth factor, cytokine, and enzyme involved in energy including nicotinamide adenine dinucleotide metabolism and was recently demonstrated to exert several proinflammatory functions.	NAD	125-158	nicotinamide phosphoribosyltransferase	Homo sapiens	12-20
21730068-3	2011	To clarify the structural determinant underlying the high NADH kinase activity of Pos5 and its selectivity for NADH over NAD(+), we determined the tertiary structure of Pos5 complexed with NADH at a resolution of 2.0 A.	NAD	58-62	NADH kinase	Saccharomyces cerevisiae S288C	82-86
21730068-3	2011	To clarify the structural determinant underlying the high NADH kinase activity of Pos5 and its selectivity for NADH over NAD(+), we determined the tertiary structure of Pos5 complexed with NADH at a resolution of 2.0 A.	NAD	58-62	NADH kinase	Saccharomyces cerevisiae S288C	169-173
21730068-3	2011	To clarify the structural determinant underlying the high NADH kinase activity of Pos5 and its selectivity for NADH over NAD(+), we determined the tertiary structure of Pos5 complexed with NADH at a resolution of 2.0 A.	NAD	121-127	NADH kinase	Saccharomyces cerevisiae S288C	82-86
21730068-3	2011	To clarify the structural determinant underlying the high NADH kinase activity of Pos5 and its selectivity for NADH over NAD(+), we determined the tertiary structure of Pos5 complexed with NADH at a resolution of 2.0 A.	NAD	111-115	NADH kinase	Saccharomyces cerevisiae S288C	82-86
21730068-3	2011	To clarify the structural determinant underlying the high NADH kinase activity of Pos5 and its selectivity for NADH over NAD(+), we determined the tertiary structure of Pos5 complexed with NADH at a resolution of 2.0 A.	NAD	111-115	NADH kinase	Saccharomyces cerevisiae S288C	169-173
21730068-4	2011	Detailed analysis, including a comparison of the tertiary structure of Pos5 with the structures of human and bacterial NAD kinases, revealed that Arg-293 of Pos5, corresponding to His-351 of human NAD kinase, confers a positive charge on the surface of NADH-binding site, whereas the corresponding His residue does not.	NAD	119-122	NADH kinase	Saccharomyces cerevisiae S288C	157-161
21730068-4	2011	Detailed analysis, including a comparison of the tertiary structure of Pos5 with the structures of human and bacterial NAD kinases, revealed that Arg-293 of Pos5, corresponding to His-351 of human NAD kinase, confers a positive charge on the surface of NADH-binding site, whereas the corresponding His residue does not.	NAD	253-257	NADH kinase	Saccharomyces cerevisiae S288C	71-75
21730068-4	2011	Detailed analysis, including a comparison of the tertiary structure of Pos5 with the structures of human and bacterial NAD kinases, revealed that Arg-293 of Pos5, corresponding to His-351 of human NAD kinase, confers a positive charge on the surface of NADH-binding site, whereas the corresponding His residue does not.	NAD	253-257	NADH kinase	Saccharomyces cerevisiae S288C	157-161
21730068-8	2011	Thus, Arg-293 of Pos5 is a major determinant of NADH selectivity.	NAD	48-52	NADH kinase	Saccharomyces cerevisiae S288C	17-21
21502315-3	2011	Human UDP-glucose 6-dehydrogenase (hUGDH) catalyzes, in two NAD(+)-dependent steps without release of intermediate aldehyde, the biosynthetic oxidation of UDP-glucose (UDP-Glc) to UDP-GlcUA.	NAD	60-66	UDP-glucose 6-dehydrogenase	Homo sapiens	6-33
21502315-3	2011	Human UDP-glucose 6-dehydrogenase (hUGDH) catalyzes, in two NAD(+)-dependent steps without release of intermediate aldehyde, the biosynthetic oxidation of UDP-glucose (UDP-Glc) to UDP-GlcUA.	NAD	60-66	UDP-glucose 6-dehydrogenase	Homo sapiens	35-40
21502315-4	2011	Here, we present a structural characterization of the hUGDH reaction coordinate using crystal structures of the apoenzyme and ternary complexes of the enzyme bound with UDP-Glc/NADH and UDP-GlcUA/NAD(+).	NAD	177-181	UDP-glucose 6-dehydrogenase	Homo sapiens	54-59
21502315-4	2011	Here, we present a structural characterization of the hUGDH reaction coordinate using crystal structures of the apoenzyme and ternary complexes of the enzyme bound with UDP-Glc/NADH and UDP-GlcUA/NAD(+).	NAD	196-202	UDP-glucose 6-dehydrogenase	Homo sapiens	54-59
21502315-10	2011	Because thiohemiacetal intermediate accumulates at steady state under physiological reaction conditions, hUGDH inhibition might best explore ligand binding to the NAD(+) binding domain.	NAD	163-169	UDP-glucose 6-dehydrogenase	Homo sapiens	105-110
21550345-0	2011	Dissecting systemic control of metabolism and aging in the NAD World: the importance of SIRT1 and NAMPT-mediated NAD biosynthesis.	NAD	59-62	nicotinamide phosphoribosyltransferase	Homo sapiens	98-103
21550345-3	2011	Our studies on the mammalian NAD-dependent deacetylase SIRT1 and nicotinamide phosphoribosyltransferase (NAMPT)-mediated systemic NAD biosynthesis led us to propose a comprehensive model for the systemic regulatory network connecting metabolism and aging, termed the "NAD World".	NAD	29-32	nicotinamide phosphoribosyltransferase	Homo sapiens	65-103
21550345-3	2011	Our studies on the mammalian NAD-dependent deacetylase SIRT1 and nicotinamide phosphoribosyltransferase (NAMPT)-mediated systemic NAD biosynthesis led us to propose a comprehensive model for the systemic regulatory network connecting metabolism and aging, termed the "NAD World".	NAD	29-32	nicotinamide phosphoribosyltransferase	Homo sapiens	105-110
21550345-3	2011	Our studies on the mammalian NAD-dependent deacetylase SIRT1 and nicotinamide phosphoribosyltransferase (NAMPT)-mediated systemic NAD biosynthesis led us to propose a comprehensive model for the systemic regulatory network connecting metabolism and aging, termed the "NAD World".	NAD	130-133	nicotinamide phosphoribosyltransferase	Homo sapiens	65-103
21550345-3	2011	Our studies on the mammalian NAD-dependent deacetylase SIRT1 and nicotinamide phosphoribosyltransferase (NAMPT)-mediated systemic NAD biosynthesis led us to propose a comprehensive model for the systemic regulatory network connecting metabolism and aging, termed the "NAD World".	NAD	130-133	nicotinamide phosphoribosyltransferase	Homo sapiens	105-110
21550345-3	2011	Our studies on the mammalian NAD-dependent deacetylase SIRT1 and nicotinamide phosphoribosyltransferase (NAMPT)-mediated systemic NAD biosynthesis led us to propose a comprehensive model for the systemic regulatory network connecting metabolism and aging, termed the "NAD World".	NAD	130-133	nicotinamide phosphoribosyltransferase	Homo sapiens	65-103
21550345-3	2011	Our studies on the mammalian NAD-dependent deacetylase SIRT1 and nicotinamide phosphoribosyltransferase (NAMPT)-mediated systemic NAD biosynthesis led us to propose a comprehensive model for the systemic regulatory network connecting metabolism and aging, termed the "NAD World".	NAD	130-133	nicotinamide phosphoribosyltransferase	Homo sapiens	105-110
21550345-4	2011	In this article, I will discuss the importance of SIRT1 and NAMPT-mediated NAD biosynthesis in the NAD World and the system dynamics of this hierarchical network for the connection between metabolism and aging.	NAD	75-78	nicotinamide phosphoribosyltransferase	Homo sapiens	60-65
21550345-4	2011	In this article, I will discuss the importance of SIRT1 and NAMPT-mediated NAD biosynthesis in the NAD World and the system dynamics of this hierarchical network for the connection between metabolism and aging.	NAD	99-102	nicotinamide phosphoribosyltransferase	Homo sapiens	60-65
21543898-1	2011	During the last decade, it was established that the class III alcohol dehydrogenase (ADH3) enzyme, also known as glutathione-dependent formaldehyde dehydrogenase (FALDH; EC 1.2.1.1), catalyzes the NADH-dependent reduction of S-nitrosoglutathione (GSNO) and therefore was also designated as GSNO reductase.	NAD	197-201	alcohol dehydrogenase 5 (class III), chi polypeptide	Homo sapiens	85-89
21543898-1	2011	During the last decade, it was established that the class III alcohol dehydrogenase (ADH3) enzyme, also known as glutathione-dependent formaldehyde dehydrogenase (FALDH; EC 1.2.1.1), catalyzes the NADH-dependent reduction of S-nitrosoglutathione (GSNO) and therefore was also designated as GSNO reductase.	NAD	197-201	alcohol dehydrogenase 5 (class III), chi polypeptide	Homo sapiens	113-161
21543898-1	2011	During the last decade, it was established that the class III alcohol dehydrogenase (ADH3) enzyme, also known as glutathione-dependent formaldehyde dehydrogenase (FALDH; EC 1.2.1.1), catalyzes the NADH-dependent reduction of S-nitrosoglutathione (GSNO) and therefore was also designated as GSNO reductase.	NAD	197-201	alcohol dehydrogenase 5 (class III), chi polypeptide	Homo sapiens	163-168
21276780-0	2011	NADH fluorescence lifetime analysis of the effect of magnesium ions on ALDH2.	NAD	0-4	aldehyde dehydrogenase 2 family member	Homo sapiens	71-76
21276780-2	2011	Physiologic levels of Mg(2+) ions influence ALDH2 activity in part by increasing NADH binding affinity.	NAD	81-85	aldehyde dehydrogenase 2 family member	Homo sapiens	44-49
21276780-3	2011	Traditional fluorescence measurements monitor the blue shift of the NADH fluorescence spectrum to study ALDH2-NADH interactions.	NAD	68-72	aldehyde dehydrogenase 2 family member	Homo sapiens	104-109
21276780-3	2011	Traditional fluorescence measurements monitor the blue shift of the NADH fluorescence spectrum to study ALDH2-NADH interactions.	NAD	110-114	aldehyde dehydrogenase 2 family member	Homo sapiens	104-109
21276780-5	2011	We used this technique to investigate the effects of Mg(2+) on the ALDH2-NADH binding characteristics and enzyme catalysis.	NAD	73-77	aldehyde dehydrogenase 2 family member	Homo sapiens	67-72
21276780-6	2011	From the resolved free and bound NADH fluorescence signatures, the K(D) for NADH with ALDH2 ranged from 468 muM to 12 muM for Mg(2+) ion concentrations of 20 to 6000 muM, respectively.	NAD	33-37	aldehyde dehydrogenase 2 family member	Homo sapiens	86-91
21276780-6	2011	From the resolved free and bound NADH fluorescence signatures, the K(D) for NADH with ALDH2 ranged from 468 muM to 12 muM for Mg(2+) ion concentrations of 20 to 6000 muM, respectively.	NAD	76-80	aldehyde dehydrogenase 2 family member	Homo sapiens	86-91
21276780-12	2011	Furthermore, we observed distinct fluorescence signatures from multiple ALDH2-NADH complexes corresponding to free NADH, enzyme-bound NADH, and, potentially, an abortive NADH-enzyme-propanal complex (tau=11.2 ns).	NAD	78-82	aldehyde dehydrogenase 2 family member	Homo sapiens	72-77
21276780-12	2011	Furthermore, we observed distinct fluorescence signatures from multiple ALDH2-NADH complexes corresponding to free NADH, enzyme-bound NADH, and, potentially, an abortive NADH-enzyme-propanal complex (tau=11.2 ns).	NAD	115-119	aldehyde dehydrogenase 2 family member	Homo sapiens	72-77
21276780-12	2011	Furthermore, we observed distinct fluorescence signatures from multiple ALDH2-NADH complexes corresponding to free NADH, enzyme-bound NADH, and, potentially, an abortive NADH-enzyme-propanal complex (tau=11.2 ns).	NAD	115-119	aldehyde dehydrogenase 2 family member	Homo sapiens	72-77
21276780-12	2011	Furthermore, we observed distinct fluorescence signatures from multiple ALDH2-NADH complexes corresponding to free NADH, enzyme-bound NADH, and, potentially, an abortive NADH-enzyme-propanal complex (tau=11.2 ns).	NAD	115-119	aldehyde dehydrogenase 2 family member	Homo sapiens	72-77
21425834-6	2011	Using this system, we found that erastin increases permeability of VDAC2 liposomes to NADH in a manner that requires the amino-terminal region of VDAC2.	NAD	86-90	voltage dependent anion channel 2	Homo sapiens	67-72
21425834-6	2011	Using this system, we found that erastin increases permeability of VDAC2 liposomes to NADH in a manner that requires the amino-terminal region of VDAC2.	NAD	86-90	voltage dependent anion channel 2	Homo sapiens	146-151
21211508-2	2011	As the rate-limiting enzyme of the predominant NAD biosynthesis pathway in mammals, nicotinamide phosphoribosyltransferase (Nampt) regulates the cellular NAD level.	NAD	47-50	nicotinamide phosphoribosyltransferase	Homo sapiens	84-122
21211508-2	2011	As the rate-limiting enzyme of the predominant NAD biosynthesis pathway in mammals, nicotinamide phosphoribosyltransferase (Nampt) regulates the cellular NAD level.	NAD	47-50	nicotinamide phosphoribosyltransferase	Homo sapiens	124-129
21211508-2	2011	As the rate-limiting enzyme of the predominant NAD biosynthesis pathway in mammals, nicotinamide phosphoribosyltransferase (Nampt) regulates the cellular NAD level.	NAD	154-157	nicotinamide phosphoribosyltransferase	Homo sapiens	84-122
21211508-2	2011	As the rate-limiting enzyme of the predominant NAD biosynthesis pathway in mammals, nicotinamide phosphoribosyltransferase (Nampt) regulates the cellular NAD level.	NAD	154-157	nicotinamide phosphoribosyltransferase	Homo sapiens	124-129
21211508-3	2011	Tumor cells are more sensitive to the NAD levels, making them more susceptible to Nampt inhibition than their nontumorigenic counterparts.	NAD	38-41	nicotinamide phosphoribosyltransferase	Homo sapiens	82-87
21336366-1	2011	Due to the biological importance of nucleotides and related species, such as XNP (where X = adenosine (A), uridine (U), cytidine (C), guanosine (G), and N = mono, di, tri), FAD and NADH, the development of optical probes for these molecules has recently been an active area of research.	NAD	181-185	ATRX chromatin remodeler	Homo sapiens	77-80
21362626-8	2011	SIRT6 also lacks the conserved, highly flexible, NAD(+)-binding loop and instead contains a stable single helix.	NAD	49-55	sirtuin 6	Homo sapiens	0-5
21362626-9	2011	These differences led us to hypothesize that SIRT6, unlike all other studied sirtuins, would be able to bind NAD(+) in the absence of an acetylated substrate.	NAD	109-115	sirtuin 6	Homo sapiens	45-50
21362626-10	2011	Indeed, we found that SIRT6 binds NAD(+) with relatively high affinity (K(d) = 27 +- 1 muM) in the absence of an acetylated substrate.	NAD	34-40	sirtuin 6	Homo sapiens	22-27
21362626-12	2011	Collectively, these new insights imply a unique activating mechanism and/or the possibility that SIRT6 could act as an NAD(+) metabolite sensor.	NAD	119-125	sirtuin 6	Homo sapiens	97-102
21459329-2	2011	Here, we tested whether deletion of PARP-2, an alternative NAD(+)-consuming enzyme, impacts on NAD(+) bioavailability and SIRT1 activity.	NAD	59-65	poly (ADP-ribose) polymerase family, member 2	Mus musculus	36-42
21459329-2	2011	Here, we tested whether deletion of PARP-2, an alternative NAD(+)-consuming enzyme, impacts on NAD(+) bioavailability and SIRT1 activity.	NAD	95-101	poly (ADP-ribose) polymerase family, member 2	Mus musculus	36-42
21330015-1	2011	NAmPRTase (PBEF/Visfatin) plays a pivotal role in the salvage pathway of NAD(+) biosynthesis.	NAD	73-79	nicotinamide phosphoribosyltransferase	Homo sapiens	0-9
21330015-1	2011	NAmPRTase (PBEF/Visfatin) plays a pivotal role in the salvage pathway of NAD(+) biosynthesis.	NAD	73-79	nicotinamide phosphoribosyltransferase	Homo sapiens	11-15
21330015-1	2011	NAmPRTase (PBEF/Visfatin) plays a pivotal role in the salvage pathway of NAD(+) biosynthesis.	NAD	73-79	nicotinamide phosphoribosyltransferase	Homo sapiens	16-24
21330015-2	2011	NAmPRTase has been an attractive target for anti-cancer agents that induce apoptosis of tumor cells via a declining plasma NAD(+) level.	NAD	123-129	nicotinamide phosphoribosyltransferase	Homo sapiens	0-9
20956937-1	2011	Nicotinamide phosphoribosyltransferase (NAMPT) is a rate-limiting enzyme in regenerating nicotinamide adenine dinucleotide (NAD(+)) from nicotinamide in mammals.	NAD	124-130	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
20956937-2	2011	NAMPT has crucial roles for many cellular functions by regulating NAD(+)-dependent SIRT1 deacetylase.	NAD	66-72	nicotinamide phosphoribosyltransferase	Homo sapiens	0-5
21884623-1	2011	BACKGROUND: Pre-B-cell colony enhancing factor 1 gene (PBEF1) encodes nicotinamide phosphoribosyltransferase (NMPRTase), which catalyses the rate limiting step in the salvage pathway of NAD+ metabolism in mammalian cells.	NAD	186-190	nicotinamide phosphoribosyltransferase	Homo sapiens	12-48
21884623-1	2011	BACKGROUND: Pre-B-cell colony enhancing factor 1 gene (PBEF1) encodes nicotinamide phosphoribosyltransferase (NMPRTase), which catalyses the rate limiting step in the salvage pathway of NAD+ metabolism in mammalian cells.	NAD	186-190	nicotinamide phosphoribosyltransferase	Homo sapiens	55-60
21884623-1	2011	BACKGROUND: Pre-B-cell colony enhancing factor 1 gene (PBEF1) encodes nicotinamide phosphoribosyltransferase (NMPRTase), which catalyses the rate limiting step in the salvage pathway of NAD+ metabolism in mammalian cells.	NAD	186-190	nicotinamide phosphoribosyltransferase	Homo sapiens	70-108
21884623-1	2011	BACKGROUND: Pre-B-cell colony enhancing factor 1 gene (PBEF1) encodes nicotinamide phosphoribosyltransferase (NMPRTase), which catalyses the rate limiting step in the salvage pathway of NAD+ metabolism in mammalian cells.	NAD	186-190	nicotinamide phosphoribosyltransferase	Homo sapiens	110-118
21372389-7	2011	The elevated expressions of p22(phox) and Nox-4 proteins (reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase subunits) were significantly decreased after kangen-karyu treatments.	NAD	66-99	NADPH oxidase 4	Mus musculus	42-47
21381495-3	2011	Besides, it acts as Nicotinamide phosphoribosyl transferase (Nampt), an enzyme involved in the NAD+ salvage pathway.	NAD	95-99	nicotinamide phosphoribosyltransferase	Homo sapiens	20-59
21381495-3	2011	Besides, it acts as Nicotinamide phosphoribosyl transferase (Nampt), an enzyme involved in the NAD+ salvage pathway.	NAD	95-99	nicotinamide phosphoribosyltransferase	Homo sapiens	61-66
21484571-1	2011	Nicotinamide phosphoribosyltransferase Nicotinamide phosphoribosyltransferase (Nampt Nampt ) is a key nicotinamide adenine dinucleotide (NAD) NAD biosynthetic enzyme in mammals, converting nicotinamide nicotinamide into nicotinamide mononucleotide nicotinamide mononucleotide (NMN NMN ), an NAD intermediate.	NAD	102-135	nicotinamide phosphoribosyltransferase	Homo sapiens	79-84
21484571-1	2011	Nicotinamide phosphoribosyltransferase Nicotinamide phosphoribosyltransferase (Nampt Nampt ) is a key nicotinamide adenine dinucleotide (NAD) NAD biosynthetic enzyme in mammals, converting nicotinamide nicotinamide into nicotinamide mononucleotide nicotinamide mononucleotide (NMN NMN ), an NAD intermediate.	NAD	102-135	nicotinamide phosphoribosyltransferase	Homo sapiens	85-90
21484571-1	2011	Nicotinamide phosphoribosyltransferase Nicotinamide phosphoribosyltransferase (Nampt Nampt ) is a key nicotinamide adenine dinucleotide (NAD) NAD biosynthetic enzyme in mammals, converting nicotinamide nicotinamide into nicotinamide mononucleotide nicotinamide mononucleotide (NMN NMN ), an NAD intermediate.	NAD	137-140	nicotinamide phosphoribosyltransferase	Homo sapiens	79-84
21484571-1	2011	Nicotinamide phosphoribosyltransferase Nicotinamide phosphoribosyltransferase (Nampt Nampt ) is a key nicotinamide adenine dinucleotide (NAD) NAD biosynthetic enzyme in mammals, converting nicotinamide nicotinamide into nicotinamide mononucleotide nicotinamide mononucleotide (NMN NMN ), an NAD intermediate.	NAD	137-140	nicotinamide phosphoribosyltransferase	Homo sapiens	85-90
21484571-1	2011	Nicotinamide phosphoribosyltransferase Nicotinamide phosphoribosyltransferase (Nampt Nampt ) is a key nicotinamide adenine dinucleotide (NAD) NAD biosynthetic enzyme in mammals, converting nicotinamide nicotinamide into nicotinamide mononucleotide nicotinamide mononucleotide (NMN NMN ), an NAD intermediate.	NAD	142-145	nicotinamide phosphoribosyltransferase	Homo sapiens	79-84
21484571-1	2011	Nicotinamide phosphoribosyltransferase Nicotinamide phosphoribosyltransferase (Nampt Nampt ) is a key nicotinamide adenine dinucleotide (NAD) NAD biosynthetic enzyme in mammals, converting nicotinamide nicotinamide into nicotinamide mononucleotide nicotinamide mononucleotide (NMN NMN ), an NAD intermediate.	NAD	142-145	nicotinamide phosphoribosyltransferase	Homo sapiens	85-90
21484571-1	2011	Nicotinamide phosphoribosyltransferase Nicotinamide phosphoribosyltransferase (Nampt Nampt ) is a key nicotinamide adenine dinucleotide (NAD) NAD biosynthetic enzyme in mammals, converting nicotinamide nicotinamide into nicotinamide mononucleotide nicotinamide mononucleotide (NMN NMN ), an NAD intermediate.	NAD	142-145	nicotinamide phosphoribosyltransferase	Homo sapiens	79-84
21484571-1	2011	Nicotinamide phosphoribosyltransferase Nicotinamide phosphoribosyltransferase (Nampt Nampt ) is a key nicotinamide adenine dinucleotide (NAD) NAD biosynthetic enzyme in mammals, converting nicotinamide nicotinamide into nicotinamide mononucleotide nicotinamide mononucleotide (NMN NMN ), an NAD intermediate.	NAD	142-145	nicotinamide phosphoribosyltransferase	Homo sapiens	85-90
21484571-2	2011	First identified in humans as a cytokine cytokine pre-B-cell colony enhancing factor pre-B cell colony enhancing factor (PBEF PBEF ) and subsequently described as an insulin-mimetic hormone visfatin visfatin , Nampt has recently excited the scientific interest of researchers from diverse fields, including NAD biology, metabolic regulation, and inflammation.	NAD	307-310	nicotinamide phosphoribosyltransferase	Homo sapiens	210-215
21484571-3	2011	As an NAD biosynthetic enzyme, Nampt regulates the activity of NAD-consuming enzymes such as sirtuins sirtuins and influences a variety of metabolic and stress responses.	NAD	6-9	nicotinamide phosphoribosyltransferase	Homo sapiens	31-36
21484571-3	2011	As an NAD biosynthetic enzyme, Nampt regulates the activity of NAD-consuming enzymes such as sirtuins sirtuins and influences a variety of metabolic and stress responses.	NAD	63-66	nicotinamide phosphoribosyltransferase	Homo sapiens	31-36
21126600-3	2011	In the present study, the GPD1 gene, encoding NAD+-dependent glycerol-3-phosphate dehydrogenase in an industrial ethanol producing strain of S. cerevisiae, was deleted.	NAD	46-49	glycerol-3-phosphate dehydrogenase	Saccharomyces cerevisiae S288C	61-95
20818429-0	2010	Redox-dependent Brca1 transcriptional regulation by an NADH-sensor CtBP1.	NAD	55-59	C-terminal binding protein 1	Homo sapiens	67-72
20818429-4	2010	Additionally, the recruitment of CtBP1 to the Brca1 promoter is redox-dependent, that is, increased at high NADH levels in hypoxic conditions.	NAD	108-112	C-terminal binding protein 1	Homo sapiens	33-38
20818429-6	2010	Pharmacological disruption of CtBP1 binding to Brca1 promoter by the antioxidant Tempol, which reduces NADH levels, relieved CtBP1-mediated repression of Brca1, leading to increased DNA repair in HNSCC cells.	NAD	103-107	C-terminal binding protein 1	Homo sapiens	30-35
21106760-0	2010	Nicotinamide adenine dinucleotide (NAD)-regulated DNA methylation alters CCCTC-binding factor (CTCF)/cohesin binding and transcription at the BDNF locus.	NAD	0-33	CCCTC-binding factor	Mus musculus	73-93
21106760-0	2010	Nicotinamide adenine dinucleotide (NAD)-regulated DNA methylation alters CCCTC-binding factor (CTCF)/cohesin binding and transcription at the BDNF locus.	NAD	0-33	CCCTC-binding factor	Mus musculus	95-99
21106760-0	2010	Nicotinamide adenine dinucleotide (NAD)-regulated DNA methylation alters CCCTC-binding factor (CTCF)/cohesin binding and transcription at the BDNF locus.	NAD	35-38	CCCTC-binding factor	Mus musculus	73-93
21106760-0	2010	Nicotinamide adenine dinucleotide (NAD)-regulated DNA methylation alters CCCTC-binding factor (CTCF)/cohesin binding and transcription at the BDNF locus.	NAD	35-38	CCCTC-binding factor	Mus musculus	95-99
20926581-8	2010	The ERbeta selective agonist DPN, but not the ERalpha selective agonist 4,4",4"-(4-propyl-[1H]-pyrazole-1,3,5-triyl) trisphenol or other ERalpha-specific ligands, stimulated cell death.	NAD	29-32	estrogen receptor 2	Homo sapiens	4-10
20810270-2	2010	The bio-sniffer measures gaseous formaldehyde as fluorescence of nicotinamide adenine dinucleotide (NADH), which is the product of formaldehyde dehydrogenase (FALDH) reaction.	NAD	65-98	alcohol dehydrogenase 5 (class III), chi polypeptide	Homo sapiens	131-157
20810270-2	2010	The bio-sniffer measures gaseous formaldehyde as fluorescence of nicotinamide adenine dinucleotide (NADH), which is the product of formaldehyde dehydrogenase (FALDH) reaction.	NAD	65-98	alcohol dehydrogenase 5 (class III), chi polypeptide	Homo sapiens	159-164
20810270-2	2010	The bio-sniffer measures gaseous formaldehyde as fluorescence of nicotinamide adenine dinucleotide (NADH), which is the product of formaldehyde dehydrogenase (FALDH) reaction.	NAD	100-104	alcohol dehydrogenase 5 (class III), chi polypeptide	Homo sapiens	131-157
20810270-2	2010	The bio-sniffer measures gaseous formaldehyde as fluorescence of nicotinamide adenine dinucleotide (NADH), which is the product of formaldehyde dehydrogenase (FALDH) reaction.	NAD	100-104	alcohol dehydrogenase 5 (class III), chi polypeptide	Homo sapiens	159-164
20810270-5	2010	The excitation light was introduced to an optical fiber probe, and fluorescence emission of neighboring NADH, which was produced by applying formaldehyde vapor to the FALDH membrane, was concentrically measured with a photomultiplier tube.	NAD	104-108	alcohol dehydrogenase 5 (class III), chi polypeptide	Homo sapiens	167-172
20507824-7	2010	Then the oxidized state of DI was regenerated into its reduced native state by its natural substrate, nicotinamide adenine dinucleotide (NADH).	NAD	102-135	dihydrolipoamide dehydrogenase	Homo sapiens	27-29
20507824-7	2010	Then the oxidized state of DI was regenerated into its reduced native state by its natural substrate, nicotinamide adenine dinucleotide (NADH).	NAD	137-141	dihydrolipoamide dehydrogenase	Homo sapiens	27-29
20616185-9	2010	Human ALDH1B1 had an exclusive preference for NAD(+) as the cofactor and was catalytically active toward short- and medium-chain aliphatic aldehydes, aromatic aldehydes, and the products of lipid peroxidation, 4-hydroxynonenal and malondialdehyde.	NAD	46-52	aldehyde dehydrogenase 1 family member B1	Homo sapiens	6-13
20667834-6	2010	Current standard PAH activity assays are either indirect (NADH) or discontinuous due to substrate and product separation before detection.	NAD	58-62	phenylalanine hydroxylase	Homo sapiens	17-20
20518072-6	2010	We show in HeLa cells that NADH levels modulate the activities of two pivotal enzymes of sphingolipid metabolism: sphingosine kinase 1 (SK1) and neutral sphingomyelinase (nSMase).	NAD	27-31	sphingomyelin phosphodiesterase 2	Homo sapiens	145-169
20518072-6	2010	We show in HeLa cells that NADH levels modulate the activities of two pivotal enzymes of sphingolipid metabolism: sphingosine kinase 1 (SK1) and neutral sphingomyelinase (nSMase).	NAD	27-31	sphingomyelin phosphodiesterase 2	Homo sapiens	171-177
20518072-9	2010	Using plasma membranes isolated from cervical adenocarcinoma (HeLa) cells as well as purified proteins of both bacterial and human origin, we demonstrate that NADH inhibits SK1 and stimulates nSMase, while NAD(+) inhibits nSMase and has no effect on SK1.	NAD	159-163	sphingomyelin phosphodiesterase 2	Homo sapiens	192-198
20518072-9	2010	Using plasma membranes isolated from cervical adenocarcinoma (HeLa) cells as well as purified proteins of both bacterial and human origin, we demonstrate that NADH inhibits SK1 and stimulates nSMase, while NAD(+) inhibits nSMase and has no effect on SK1.	NAD	159-163	sphingomyelin phosphodiesterase 2	Homo sapiens	222-228
20647743-1	2010	Nampt/PBEF/visfatin is the rate-limiting enzyme that catalyzes the first step in NAD biosynthesis from nicotinamide and regulates growth, apoptosis and angiogenesis of mammalian cells.	NAD	81-84	nicotinamide phosphoribosyltransferase	Homo sapiens	6-10
20647743-1	2010	Nampt/PBEF/visfatin is the rate-limiting enzyme that catalyzes the first step in NAD biosynthesis from nicotinamide and regulates growth, apoptosis and angiogenesis of mammalian cells.	NAD	81-84	nicotinamide phosphoribosyltransferase	Homo sapiens	11-19
20616029-6	2010	FGF21 treatment increased cellular NAD(+) levels, leading to activation of SIRT1 and deacetylation of its downstream targets, peroxisome proliferator-activated receptor-gamma coactivator-1alpha (PGC-1alpha) and histone 3.	NAD	35-41	fibroblast growth factor 21	Mus musculus	0-5
20616029-6	2010	FGF21 treatment increased cellular NAD(+) levels, leading to activation of SIRT1 and deacetylation of its downstream targets, peroxisome proliferator-activated receptor-gamma coactivator-1alpha (PGC-1alpha) and histone 3.	NAD	35-41	peroxisome proliferative activated receptor, gamma, coactivator 1 alpha	Mus musculus	126-193
20616029-6	2010	FGF21 treatment increased cellular NAD(+) levels, leading to activation of SIRT1 and deacetylation of its downstream targets, peroxisome proliferator-activated receptor-gamma coactivator-1alpha (PGC-1alpha) and histone 3.	NAD	35-41	peroxisome proliferative activated receptor, gamma, coactivator 1 alpha	Mus musculus	195-205
20582794-4	2010	Glucose dehydrogenase was used for the regeneration of NADH and (15)NH(4)Cl as isotopically labelled material at 99 at.% (15)N. All reactions are inexpensive and easy to perform on a synthetically useful scale (1-10g) giving high yields of l-amino acids.	NAD	55-59	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	0-21
20190030-5	2010	Fasting serum glucose was measured using our laboratory reference method (LAB) and 2 glucose self-monitoring systems based on glucose dehydrogenase nicotinamide adenine dinucleotide (GDH-NAD) and GDH-PQQ respectively.	NAD	148-181	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	183-186
20121055-3	2010	With glucose dehydrogenase (GDH) as a model dehydrogenase-based recognition unit, electrochemical studies reveal that glucose is readily oxidized at the GDH/NAD(+)/MWCNT-modified electrode without addition of NAD(+) in the phosphate buffer.	NAD	157-163	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	5-26
20121055-3	2010	With glucose dehydrogenase (GDH) as a model dehydrogenase-based recognition unit, electrochemical studies reveal that glucose is readily oxidized at the GDH/NAD(+)/MWCNT-modified electrode without addition of NAD(+) in the phosphate buffer.	NAD	157-163	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	28-31
20121055-3	2010	With glucose dehydrogenase (GDH) as a model dehydrogenase-based recognition unit, electrochemical studies reveal that glucose is readily oxidized at the GDH/NAD(+)/MWCNT-modified electrode without addition of NAD(+) in the phosphate buffer.	NAD	157-163	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	153-156
20121055-3	2010	With glucose dehydrogenase (GDH) as a model dehydrogenase-based recognition unit, electrochemical studies reveal that glucose is readily oxidized at the GDH/NAD(+)/MWCNT-modified electrode without addition of NAD(+) in the phosphate buffer.	NAD	209-215	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	28-31
20121055-4	2010	The potential for the oxidation of glucose at the GDH/NAD(+)/MWCNT-modified electrode remains very close to that for NADH oxidation at the MWCNT-modified electrode, but it is more negative than those for the oxidation of glucose at the MWCNT-modified electrode and for NADH oxidation at a bare glassy carbon electrode.	NAD	54-60	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	50-53
20121055-4	2010	The potential for the oxidation of glucose at the GDH/NAD(+)/MWCNT-modified electrode remains very close to that for NADH oxidation at the MWCNT-modified electrode, but it is more negative than those for the oxidation of glucose at the MWCNT-modified electrode and for NADH oxidation at a bare glassy carbon electrode.	NAD	117-121	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	50-53
20121055-4	2010	The potential for the oxidation of glucose at the GDH/NAD(+)/MWCNT-modified electrode remains very close to that for NADH oxidation at the MWCNT-modified electrode, but it is more negative than those for the oxidation of glucose at the MWCNT-modified electrode and for NADH oxidation at a bare glassy carbon electrode.	NAD	269-273	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	50-53
20121055-7	2010	At the GDH/NAD(+)/MWCNT-based glucose biosensor, the current is linear with the concentration of glucose being within a concentration range from 10 to 300 microM with a limit of detection down to 4.81 microM (S/N = 3).	NAD	11-17	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	7-10
20175898-2	2010	In wild-type Saccharomyces cerevisiae, calorie restriction accomplished by glucose limitation extends replicative lifespan in a manner that depends on Sir2 and the NAD+ salvage enzymes, nicotinic acid phosphoribosyl transferase and nicotinamidase.	NAD	164-168	nicotinamidase	Saccharomyces cerevisiae S288C	232-246
19928762-8	2010	Moreover, we also found that AMPK activity mediated by resveratrol in cancer cells was due to inducing the expression of Sirtuin type 1 (SIRT1) via elevation in the cellular NAD(+)/NADH in ER-positive cells.	NAD	174-180	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	29-33
19928762-8	2010	Moreover, we also found that AMPK activity mediated by resveratrol in cancer cells was due to inducing the expression of Sirtuin type 1 (SIRT1) via elevation in the cellular NAD(+)/NADH in ER-positive cells.	NAD	181-185	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	29-33
20000467-9	2010	Our findings constitute the first evidence of the regulation of Complex II activity by the reversible acetylation of the SdhA subunit as a novel substrate of the NAD(+)-dependent deacetylase, SIRT3.	NAD	162-168	succinate dehydrogenase complex flavoprotein subunit A	Homo sapiens	121-125
19906643-4	2010	Alda-1 increased acetaldehyde oxidation by ALDH2*1 and ALDH2*2 approximately 1.5- and 6-fold, respectively, and stimulated the esterase activities of both enzymes to similar extent as the coenzyme NAD.	NAD	197-200	aldolase, fructose-bisphosphate A	Homo sapiens	0-4
19906643-6	2010	In the presence of 1 mM NAD, Alda-1 stimulated ALDH2*2-catalyzed ester hydrolysis 73-fold, whereas the NAD-stimulated activity of ALDH2*1 was inhibited because of 20-fold increased inhibitory potency of NAD in the presence of the drug.	NAD	24-27	aldolase, fructose-bisphosphate A	Homo sapiens	29-33
19906643-6	2010	In the presence of 1 mM NAD, Alda-1 stimulated ALDH2*2-catalyzed ester hydrolysis 73-fold, whereas the NAD-stimulated activity of ALDH2*1 was inhibited because of 20-fold increased inhibitory potency of NAD in the presence of the drug.	NAD	24-27	aldehyde dehydrogenase 2 family member	Homo sapiens	47-52
19906643-6	2010	In the presence of 1 mM NAD, Alda-1 stimulated ALDH2*2-catalyzed ester hydrolysis 73-fold, whereas the NAD-stimulated activity of ALDH2*1 was inhibited because of 20-fold increased inhibitory potency of NAD in the presence of the drug.	NAD	24-27	aldehyde dehydrogenase 2 family member	Homo sapiens	130-135
19906643-6	2010	In the presence of 1 mM NAD, Alda-1 stimulated ALDH2*2-catalyzed ester hydrolysis 73-fold, whereas the NAD-stimulated activity of ALDH2*1 was inhibited because of 20-fold increased inhibitory potency of NAD in the presence of the drug.	NAD	103-106	aldolase, fructose-bisphosphate A	Homo sapiens	29-33
19906643-6	2010	In the presence of 1 mM NAD, Alda-1 stimulated ALDH2*2-catalyzed ester hydrolysis 73-fold, whereas the NAD-stimulated activity of ALDH2*1 was inhibited because of 20-fold increased inhibitory potency of NAD in the presence of the drug.	NAD	103-106	aldehyde dehydrogenase 2 family member	Homo sapiens	130-135
19906643-6	2010	In the presence of 1 mM NAD, Alda-1 stimulated ALDH2*2-catalyzed ester hydrolysis 73-fold, whereas the NAD-stimulated activity of ALDH2*1 was inhibited because of 20-fold increased inhibitory potency of NAD in the presence of the drug.	NAD	103-106	aldolase, fructose-bisphosphate A	Homo sapiens	29-33
19906643-6	2010	In the presence of 1 mM NAD, Alda-1 stimulated ALDH2*2-catalyzed ester hydrolysis 73-fold, whereas the NAD-stimulated activity of ALDH2*1 was inhibited because of 20-fold increased inhibitory potency of NAD in the presence of the drug.	NAD	103-106	aldehyde dehydrogenase 2 family member	Homo sapiens	130-135
19906643-9	2010	The present results indicate that Alda-1 stimulates established ALDH2 activities by improving NAD binding but does not improve the GTN binding affinity of the Asian variant.	NAD	94-97	aldolase, fructose-bisphosphate A	Homo sapiens	34-38
19846757-5	2010	Interestingly, induction of polyploidy was completely prevented by modest overexpression of the NAD+ regenerating enzyme, nicotinamide phosphoribosyltransferase (Nampt).	NAD	96-99	nicotinamide phosphoribosyltransferase	Homo sapiens	122-160
19846757-5	2010	Interestingly, induction of polyploidy was completely prevented by modest overexpression of the NAD+ regenerating enzyme, nicotinamide phosphoribosyltransferase (Nampt).	NAD	96-99	nicotinamide phosphoribosyltransferase	Homo sapiens	162-167
19727706-8	2010	Glycerol is produced to dispose excess cytosolic reduced nicotinamide adenine dinucleotide (NADH), and the regulating step in the pathway is mediated by glycerol 3-phosphate dehydrogenase (encoded by GPD1 and GPD2 genes).	NAD	57-90	glycerol-3-phosphate dehydrogenase	Saccharomyces cerevisiae S288C	153-187
19727706-8	2010	Glycerol is produced to dispose excess cytosolic reduced nicotinamide adenine dinucleotide (NADH), and the regulating step in the pathway is mediated by glycerol 3-phosphate dehydrogenase (encoded by GPD1 and GPD2 genes).	NAD	92-96	glycerol-3-phosphate dehydrogenase	Saccharomyces cerevisiae S288C	153-187
20834161-2	2010	The electrochemical NAD+ recycling system was applied to glucose dehydrogenase (GDH) and to the recombinant formate dehydrogenase (RFDH) reactors.	NAD	20-24	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	57-78
20834161-2	2010	The electrochemical NAD+ recycling system was applied to glucose dehydrogenase (GDH) and to the recombinant formate dehydrogenase (RFDH) reactors.	NAD	20-24	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	80-83
20028851-3	2010	Several recent observations concur with this hypothesis and suggest that by regulating NAD availability, Nampt is able to control both cell viability and the inflammatory response.	NAD	87-90	nicotinamide phosphoribosyltransferase	Homo sapiens	105-110
19778564-0	2010	Nmnat2 delays axon degeneration in superior cervical ganglia dependent on its NAD synthesis activity.	NAD	78-81	nicotinamide nucleotide adenylyltransferase 2	Mus musculus	0-6
19916553-6	2009	The observed chemical shift changes upon addition of the native ligand NADH to nanodisc-embedded VDAC-1 resemble those of micelle-embedded VDAC-1, indicating a similar structure and function in the two membrane-mimicking environments.	NAD	71-75	voltage dependent anion channel 1	Homo sapiens	97-103
19916553-6	2009	The observed chemical shift changes upon addition of the native ligand NADH to nanodisc-embedded VDAC-1 resemble those of micelle-embedded VDAC-1, indicating a similar structure and function in the two membrane-mimicking environments.	NAD	71-75	voltage dependent anion channel 1	Homo sapiens	139-145
19729610-6	2009	Mice treated with the ERbeta-specific agonist, DPN had no effect on uterine weight but a 28% decrease in aortic lesion area in HSP27(o/e)apoE(-/-) compared to apoE(-/-) mice.	NAD	47-50	estrogen receptor 2 (beta)	Mus musculus	22-28
19289152-5	2009	In this review, I will follow the process of conceptual development from the heterochromatin island hypothesis to a novel, comprehensive concept of a systemic regulatory network for mammalian aging, named "NAD World," summarizing recent studies on the mammalian NAD-dependent deacetylase Sirt1 and nicotinamide phosphoribosyltransferase (Nampt)-mediated systemic NAD biosynthesis.	NAD	262-265	nicotinamide phosphoribosyltransferase	Homo sapiens	298-336
19506862-6	2009	Then, the genes encoding the NADH- and the NADPH-dependent HMF reductases, ADH1-S110P-Y295C and ADH6, respectively, were individually overexpressed in this background.	NAD	29-33	NADP-dependent alcohol dehydrogenase	Saccharomyces cerevisiae S288C	96-100
19448972-1	2009	Nicotinamide/nicotinic acid mononucleotide adenylyltransferase (NMNAT) has long been known as the master enzyme in NAD biosynthesis in living organisms.	NAD	115-118	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	0-62
19448972-1	2009	Nicotinamide/nicotinic acid mononucleotide adenylyltransferase (NMNAT) has long been known as the master enzyme in NAD biosynthesis in living organisms.	NAD	115-118	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	64-69
19448972-2	2009	A burst of investigations on NMNAT, going beyond enzymology, have paralleled increasing discoveries of key roles played by NAD homeostasis in a number or patho-physiological conditions.	NAD	123-126	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	29-34
19221895-4	2009	By the use of subtype preferential agonists and antagonists, we identified P2X(1), P2X(4), and P2X(7) receptors being engaged in the NAD(+)-induced rise in [Ca(2+)](i).	NAD	133-139	purinergic receptor P2X 4	Homo sapiens	83-89
19666485-4	2009	Alc1 ATPase and chromatin remodeling activities are strongly activated by Parp1 and its substrate NAD and require an intact macrodomain capable of binding poly(ADP-ribose).	NAD	98-101	chromodomain helicase DNA binding protein 1 like	Homo sapiens	0-4
19666527-1	2009	Nicotinamide phosphoribosyltransferase (NAMPT) is highly evolved to capture nicotinamide (NAM) and replenish the nicotinamide adenine dinucleotide (NAD(+)) pool during ADP-ribosylation and transferase reactions.	NAD	113-146	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
19666527-1	2009	Nicotinamide phosphoribosyltransferase (NAMPT) is highly evolved to capture nicotinamide (NAM) and replenish the nicotinamide adenine dinucleotide (NAD(+)) pool during ADP-ribosylation and transferase reactions.	NAD	148-155	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45
19460433-6	2009	GEN and DPN selectively increased luciferase activity in ERbeta-transfected cells at concentrations &lt; or =10 nM.	NAD	8-11	estrogen receptor 2	Homo sapiens	57-63
19653878-1	2009	Previously, we showed that the internal rotenone-insensitive nicotinamide adenine dinucleotide (NADH)-quinone oxidoreductase (NDI1) gene from Saccharomyces cerevisiae (baker"s yeast) can be successfully inserted into the mitochondria of mice and rats and the expressed enzyme was found to be fully functional.	NAD	61-94	NADH-ubiquinone reductase (H(+)-translocating) NDI1	Saccharomyces cerevisiae S288C	126-130
19653878-1	2009	Previously, we showed that the internal rotenone-insensitive nicotinamide adenine dinucleotide (NADH)-quinone oxidoreductase (NDI1) gene from Saccharomyces cerevisiae (baker"s yeast) can be successfully inserted into the mitochondria of mice and rats and the expressed enzyme was found to be fully functional.	NAD	96-100	NADH-ubiquinone reductase (H(+)-translocating) NDI1	Saccharomyces cerevisiae S288C	126-130
19506075-5	2009	The nucleotide co-factor NAD caused a pronounced increase in the rates of 1,2-glyceryl dinitrate formation by WT-ALDH2 but inhibited the reaction catalyzed by the E268Q mutant.	NAD	25-28	aldehyde dehydrogenase 2 family member	Homo sapiens	113-118
19351806-2	2009	Visfatin, a NAD biosynthetic enzyme, regulates the activity of the cellular survival factor, Sirt1.	NAD	12-15	nicotinamide phosphoribosyltransferase	Homo sapiens	0-8
18562442-8	2009	In experiment 3, administration of E(2) or DPN to ovariectomised wildtype, but not betaERKO, mice decreased immobility compared with vehicle administration, these data suggest that ERbeta may be required for some of the anti-depressant-like effects of E(2).	NAD	43-46	estrogen receptor 2 (beta)	Mus musculus	181-187
19299583-0	2009	Circadian clock feedback cycle through NAMPT-mediated NAD+ biosynthesis.	NAD	54-58	clock circadian regulator	Homo sapiens	10-15
19299583-0	2009	Circadian clock feedback cycle through NAMPT-mediated NAD+ biosynthesis.	NAD	54-58	nicotinamide phosphoribosyltransferase	Homo sapiens	39-44
19299583-2	2009	Here we report that both the rate-limiting enzyme in mammalian nicotinamide adenine dinucleotide (NAD+) biosynthesis, nicotinamide phosphoribosyltransferase (NAMPT), and levels of NAD+ display circadian oscillations that are regulated by the core clock machinery in mice.	NAD	63-96	clock circadian regulator	Homo sapiens	247-252
19299583-2	2009	Here we report that both the rate-limiting enzyme in mammalian nicotinamide adenine dinucleotide (NAD+) biosynthesis, nicotinamide phosphoribosyltransferase (NAMPT), and levels of NAD+ display circadian oscillations that are regulated by the core clock machinery in mice.	NAD	98-102	clock circadian regulator	Homo sapiens	247-252
19299583-4	2009	In turn, the circadian transcription factor CLOCK binds to and up-regulates Nampt, thus completing a feedback loop involving NAMPT/NAD+ and SIRT1/CLOCK:BMAL1.	NAD	131-135	clock circadian regulator	Homo sapiens	44-49
19299583-4	2009	In turn, the circadian transcription factor CLOCK binds to and up-regulates Nampt, thus completing a feedback loop involving NAMPT/NAD+ and SIRT1/CLOCK:BMAL1.	NAD	131-135	nicotinamide phosphoribosyltransferase	Homo sapiens	76-81
19299583-4	2009	In turn, the circadian transcription factor CLOCK binds to and up-regulates Nampt, thus completing a feedback loop involving NAMPT/NAD+ and SIRT1/CLOCK:BMAL1.	NAD	131-135	nicotinamide phosphoribosyltransferase	Homo sapiens	125-130
19354308-5	2009	Finally, nicotinamide adenine dinucleotide (NAD(+)), the third controlled input, is reduced under the action of glucose dehydrogenase to yield the optically detected signal.	NAD	9-42	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	112-133
19354308-5	2009	Finally, nicotinamide adenine dinucleotide (NAD(+)), the third controlled input, is reduced under the action of glucose dehydrogenase to yield the optically detected signal.	NAD	44-50	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	112-133
19221488-5	2009	We propose that the S-phase NAD(+)/NADH redox status constitutes a redox signaling, which along with the cyclin E/cdk2 signaling regulates histone expression and S-phase progression.	NAD	28-34	cyclin dependent kinase 2	Homo sapiens	114-118
19221488-5	2009	We propose that the S-phase NAD(+)/NADH redox status constitutes a redox signaling, which along with the cyclin E/cdk2 signaling regulates histone expression and S-phase progression.	NAD	35-39	cyclin dependent kinase 2	Homo sapiens	114-118
19018525-1	2009	The two homologous genes GPD1 and GPD2, encoding two isoenzymes of NAD(+)-dependent glycerol-3-phosphate dehydrogenase in industrial yeast Saccharomyces cerevisiae CICIMY0086, had been deleted.	NAD	67-73	glycerol-3-phosphate dehydrogenase	Saccharomyces cerevisiae S288C	84-118
19182797-0	2009	NAMPT is essential for the G-CSF-induced myeloid differentiation via a NAD(+)-sirtuin-1-dependent pathway.	NAD	71-77	nicotinamide phosphoribosyltransferase	Homo sapiens	0-5
19182797-5	2009	The molecular events triggered by NAMPT include NAD(+)-dependent sirtuin-1 activation, subsequent induction of CCAAT/enhancer binding protein-alpha and CCAAT/enhancer binding protein-beta, and, ultimately, upregulation of G-CSF synthesis and G-CSF receptor expression.	NAD	48-54	nicotinamide phosphoribosyltransferase	Homo sapiens	34-39
19139398-9	2009	This hypothesis was further supported by activity measurements of the purified enzymes: DauA catalyzes oxidative deamination of D-arginine into 2-ketoarginine and ammonia, and DauB is able to use 2-ketoarginine and ammonia as substrates and convert them into L-arginine in the presence of NADPH or NADH.	NAD	298-302	NAD(P)H-dependent anabolic L-arginine dehydrogenase DauB	Pseudomonas aeruginosa PAO1	176-180
19273250-0	2009	Therapeutic potential of SIRT1 and NAMPT-mediated NAD biosynthesis in type 2 diabetes.	NAD	50-53	nicotinamide phosphoribosyltransferase	Homo sapiens	35-40
19273250-2	2009	For the past several years, studies on the mammalian NAD-dependent protein deacetylase SIRT1 and systemic NAD biosynthesis mediated by nicotinamide phosphoribosyltransferase (NAMPT) have demonstrated that these two regulatory components together play a critical role in the regulation of glucose homeostasis, particularly in the regulation of glucose-stimulated insulin secretion in pancreatic beta cells.	NAD	53-56	nicotinamide phosphoribosyltransferase	Homo sapiens	135-173
19273250-2	2009	For the past several years, studies on the mammalian NAD-dependent protein deacetylase SIRT1 and systemic NAD biosynthesis mediated by nicotinamide phosphoribosyltransferase (NAMPT) have demonstrated that these two regulatory components together play a critical role in the regulation of glucose homeostasis, particularly in the regulation of glucose-stimulated insulin secretion in pancreatic beta cells.	NAD	53-56	nicotinamide phosphoribosyltransferase	Homo sapiens	175-180
19273250-2	2009	For the past several years, studies on the mammalian NAD-dependent protein deacetylase SIRT1 and systemic NAD biosynthesis mediated by nicotinamide phosphoribosyltransferase (NAMPT) have demonstrated that these two regulatory components together play a critical role in the regulation of glucose homeostasis, particularly in the regulation of glucose-stimulated insulin secretion in pancreatic beta cells.	NAD	106-109	nicotinamide phosphoribosyltransferase	Homo sapiens	135-173
19273250-2	2009	For the past several years, studies on the mammalian NAD-dependent protein deacetylase SIRT1 and systemic NAD biosynthesis mediated by nicotinamide phosphoribosyltransferase (NAMPT) have demonstrated that these two regulatory components together play a critical role in the regulation of glucose homeostasis, particularly in the regulation of glucose-stimulated insulin secretion in pancreatic beta cells.	NAD	106-109	nicotinamide phosphoribosyltransferase	Homo sapiens	175-180
19273250-4	2009	In this review article, the roles of SIRT1 and NAMPT-mediated systemic NAD biosynthesis in glucose homeostasis and the pathophysiology of type 2 diabetes will be summarized, and their potential as effective targets for the treatment and prevention of type 2 diabetes will be discussed.	NAD	71-74	nicotinamide phosphoribosyltransferase	Homo sapiens	47-52
19159355-3	2008	The VDAC1 purified by immunoprecipitation reduced FNQ in the presence of nicotinamide adenine dinucleotide (NADH) and produced H(2)O(2).	NAD	73-106	voltage dependent anion channel 1	Homo sapiens	4-9
19159355-3	2008	The VDAC1 purified by immunoprecipitation reduced FNQ in the presence of nicotinamide adenine dinucleotide (NADH) and produced H(2)O(2).	NAD	108-112	voltage dependent anion channel 1	Homo sapiens	4-9
19159355-4	2008	Blue native polyacrylamide gel electrophoresis demonstrated that the band that reduced FNQ NADH-dependently mainly included VDAC1.	NAD	91-95	voltage dependent anion channel 1	Homo sapiens	124-129
18762557-4	2008	We also find that among the NAD(+)-dependent class III deacetylases, genetic or pharmacological reduction of either Sir2 or Sirt2 provides neuroprotection to Htt-challenged animals and that even greater neuroprotection is achieved when Rpd3 and Sir2 are simultaneously reduced.	NAD	28-32	Sirtuin 2	Drosophila melanogaster	124-129
19073440-0	2008	Unregulated mitochondrial GSK3beta activity results in NADH: ubiquinone oxidoreductase deficiency.	NAD	55-59	glycogen synthase kinase 3 beta	Homo sapiens	26-34
19073440-3	2008	Here we selectively expressed constitutively active GSK3beta within the mitochondria and found that this enhanced the apoptosis signaling activated by the PD-mimetic NADH:ubiquinone oxidoreductase (complex I) inhibitors 1-methyl-4-phenylpyridinium ion (MPP+) and rotenone.	NAD	166-170	glycogen synthase kinase 3 beta	Homo sapiens	52-60
19073440-3	2008	Here we selectively expressed constitutively active GSK3beta within the mitochondria and found that this enhanced the apoptosis signaling activated by the PD-mimetic NADH:ubiquinone oxidoreductase (complex I) inhibitors 1-methyl-4-phenylpyridinium ion (MPP+) and rotenone.	NAD	166-170	hydroxysteroid 17-beta dehydrogenase 6	Homo sapiens	182-196
18823127-8	2008	NMN synthesis by NAMPT is powerfully inhibited by both NAD (+) ( K i = 0.14 muM) and NADH ( K i = 0.22 muM), an apparent regulatory feedback mechanism.	NAD	55-62	nicotinamide phosphoribosyltransferase	Homo sapiens	17-22
18823127-8	2008	NMN synthesis by NAMPT is powerfully inhibited by both NAD (+) ( K i = 0.14 muM) and NADH ( K i = 0.22 muM), an apparent regulatory feedback mechanism.	NAD	85-89	nicotinamide phosphoribosyltransferase	Homo sapiens	17-22
18939989-1	2008	BACKGROUND: Mono-ADP-ribosyltransferase (ART) 1 belongs to a family of mammalian ectoenzymes that catalyze the transfer of ADP-ribose from NAD+ to a target protein.	NAD	139-143	ADP-ribosyltransferase 3 (inactive)	Homo sapiens	12-39
18780747-4	2008	Overexpression of the nicotinamidase, Pnc1p, prevents inhibition of Sir2p by the excess NAM while maintaining the elevated NAD(+) concentration.	NAD	123-129	nicotinamidase	Saccharomyces cerevisiae S288C	22-36
18780747-4	2008	Overexpression of the nicotinamidase, Pnc1p, prevents inhibition of Sir2p by the excess NAM while maintaining the elevated NAD(+) concentration.	NAD	123-129	nicotinamidase	Saccharomyces cerevisiae S288C	38-43
18652836-4	2008	Using the selective ERbeta agonist, DPN (10nM), we show that activation of ERbeta rapidly increases phosphorylation levels of nNOS at Ser(1412) and NO production.	NAD	36-39	estrogen receptor 2	Homo sapiens	20-26
18652836-4	2008	Using the selective ERbeta agonist, DPN (10nM), we show that activation of ERbeta rapidly increases phosphorylation levels of nNOS at Ser(1412) and NO production.	NAD	36-39	estrogen receptor 2	Homo sapiens	75-81
18652836-4	2008	Using the selective ERbeta agonist, DPN (10nM), we show that activation of ERbeta rapidly increases phosphorylation levels of nNOS at Ser(1412) and NO production.	NAD	36-39	nitric oxide synthase 1	Homo sapiens	126-130
18685043-2	2008	The reduction of hydroxypyruvate to glycerate catalyzed by hydroxypyruvate reductase (HPR) in the peroxisomes is thought to be facilitated by the production of NADH by peroxisomal malate dehydrogenase (PMDH).	NAD	160-164	malate dehydrogenase	Arabidopsis thaliana	180-200
18599644-10	2008	Measurements of NAD(+) and NADH levels in sdp6 seedlings also suggest that NAD(+)/NADH homeostasis is altered, and this observation is consistent with the hypothesis that SDP6 participates in a mitochondrial G3P shuttle by cooperating with the cytosolic NAD-dependent GPDH protein GPDHC1.	NAD	16-22	FAD-dependent oxidoreductase family protein	Arabidopsis thaliana	42-46
18599644-10	2008	Measurements of NAD(+) and NADH levels in sdp6 seedlings also suggest that NAD(+)/NADH homeostasis is altered, and this observation is consistent with the hypothesis that SDP6 participates in a mitochondrial G3P shuttle by cooperating with the cytosolic NAD-dependent GPDH protein GPDHC1.	NAD	16-22	FAD-dependent oxidoreductase family protein	Arabidopsis thaliana	171-175
18599644-10	2008	Measurements of NAD(+) and NADH levels in sdp6 seedlings also suggest that NAD(+)/NADH homeostasis is altered, and this observation is consistent with the hypothesis that SDP6 participates in a mitochondrial G3P shuttle by cooperating with the cytosolic NAD-dependent GPDH protein GPDHC1.	NAD	27-31	FAD-dependent oxidoreductase family protein	Arabidopsis thaliana	42-46
18599644-10	2008	Measurements of NAD(+) and NADH levels in sdp6 seedlings also suggest that NAD(+)/NADH homeostasis is altered, and this observation is consistent with the hypothesis that SDP6 participates in a mitochondrial G3P shuttle by cooperating with the cytosolic NAD-dependent GPDH protein GPDHC1.	NAD	27-31	FAD-dependent oxidoreductase family protein	Arabidopsis thaliana	171-175
18599644-10	2008	Measurements of NAD(+) and NADH levels in sdp6 seedlings also suggest that NAD(+)/NADH homeostasis is altered, and this observation is consistent with the hypothesis that SDP6 participates in a mitochondrial G3P shuttle by cooperating with the cytosolic NAD-dependent GPDH protein GPDHC1.	NAD	75-81	FAD-dependent oxidoreductase family protein	Arabidopsis thaliana	42-46
18599644-10	2008	Measurements of NAD(+) and NADH levels in sdp6 seedlings also suggest that NAD(+)/NADH homeostasis is altered, and this observation is consistent with the hypothesis that SDP6 participates in a mitochondrial G3P shuttle by cooperating with the cytosolic NAD-dependent GPDH protein GPDHC1.	NAD	75-81	FAD-dependent oxidoreductase family protein	Arabidopsis thaliana	171-175
18599644-10	2008	Measurements of NAD(+) and NADH levels in sdp6 seedlings also suggest that NAD(+)/NADH homeostasis is altered, and this observation is consistent with the hypothesis that SDP6 participates in a mitochondrial G3P shuttle by cooperating with the cytosolic NAD-dependent GPDH protein GPDHC1.	NAD	82-86	FAD-dependent oxidoreductase family protein	Arabidopsis thaliana	42-46
18599644-10	2008	Measurements of NAD(+) and NADH levels in sdp6 seedlings also suggest that NAD(+)/NADH homeostasis is altered, and this observation is consistent with the hypothesis that SDP6 participates in a mitochondrial G3P shuttle by cooperating with the cytosolic NAD-dependent GPDH protein GPDHC1.	NAD	82-86	FAD-dependent oxidoreductase family protein	Arabidopsis thaliana	171-175
18599644-10	2008	Measurements of NAD(+) and NADH levels in sdp6 seedlings also suggest that NAD(+)/NADH homeostasis is altered, and this observation is consistent with the hypothesis that SDP6 participates in a mitochondrial G3P shuttle by cooperating with the cytosolic NAD-dependent GPDH protein GPDHC1.	NAD	16-19	FAD-dependent oxidoreductase family protein	Arabidopsis thaliana	42-46
18599644-10	2008	Measurements of NAD(+) and NADH levels in sdp6 seedlings also suggest that NAD(+)/NADH homeostasis is altered, and this observation is consistent with the hypothesis that SDP6 participates in a mitochondrial G3P shuttle by cooperating with the cytosolic NAD-dependent GPDH protein GPDHC1.	NAD	16-19	FAD-dependent oxidoreductase family protein	Arabidopsis thaliana	171-175
18617666-9	2008	NAD(+) repletion restored nDNA repair activity by inhibiting serine-specific phosphorylation of the essential BER enzymes AP endonuclease and DNA polymerase-beta.	NAD	0-6	DNA polymerase beta	Rattus norvegicus	142-161
18698584-5	2008	We then cloned two isogenes encoding putative NAD(+)-dependent glycerol 3-phosphate dehydrogenase (GPD) from Sm.	NAD	46-52	glycerol-3-phosphate dehydrogenase	Saccharomyces cerevisiae S288C	63-97
18698584-5	2008	We then cloned two isogenes encoding putative NAD(+)-dependent glycerol 3-phosphate dehydrogenase (GPD) from Sm.	NAD	46-52	glycerol-3-phosphate dehydrogenase	Saccharomyces cerevisiae S288C	99-102
18755977-7	2008	NMR measurements revealed the binding sites of VDAC-1 for the Bcl-2 protein Bcl-x(L), for reduced beta-nicotinamide adenine dinucleotide, and for cholesterol.	NAD	98-136	voltage dependent anion channel 1	Homo sapiens	47-53
18662537-4	2008	(2008) now demonstrate that the NAD(+)-dependent enzyme SIRT1 functions as a histone deacetylase that counteracts the activity of CLOCK.	NAD	32-38	clock circadian regulator	Homo sapiens	130-135
18485866-4	2008	They show that an altered NAD(+)/NADH ratio in response to glucose starvation regulates the silencing activity of eNoSC, a complex consisting of the NAD(+)-dependent histone deacetylase SIRT1, the histone methyltransferase SUV39H1, and a new protein called nucleomethylin (NML).	NAD	26-32	ribosomal RNA processing 8	Homo sapiens	257-271
18485866-4	2008	They show that an altered NAD(+)/NADH ratio in response to glucose starvation regulates the silencing activity of eNoSC, a complex consisting of the NAD(+)-dependent histone deacetylase SIRT1, the histone methyltransferase SUV39H1, and a new protein called nucleomethylin (NML).	NAD	26-32	ribosomal RNA processing 8	Homo sapiens	273-276
18485866-4	2008	They show that an altered NAD(+)/NADH ratio in response to glucose starvation regulates the silencing activity of eNoSC, a complex consisting of the NAD(+)-dependent histone deacetylase SIRT1, the histone methyltransferase SUV39H1, and a new protein called nucleomethylin (NML).	NAD	33-37	ribosomal RNA processing 8	Homo sapiens	257-271
18485866-4	2008	They show that an altered NAD(+)/NADH ratio in response to glucose starvation regulates the silencing activity of eNoSC, a complex consisting of the NAD(+)-dependent histone deacetylase SIRT1, the histone methyltransferase SUV39H1, and a new protein called nucleomethylin (NML).	NAD	33-37	ribosomal RNA processing 8	Homo sapiens	273-276
18485866-4	2008	They show that an altered NAD(+)/NADH ratio in response to glucose starvation regulates the silencing activity of eNoSC, a complex consisting of the NAD(+)-dependent histone deacetylase SIRT1, the histone methyltransferase SUV39H1, and a new protein called nucleomethylin (NML).	NAD	149-155	ribosomal RNA processing 8	Homo sapiens	257-271
18485866-4	2008	They show that an altered NAD(+)/NADH ratio in response to glucose starvation regulates the silencing activity of eNoSC, a complex consisting of the NAD(+)-dependent histone deacetylase SIRT1, the histone methyltransferase SUV39H1, and a new protein called nucleomethylin (NML).	NAD	149-155	ribosomal RNA processing 8	Homo sapiens	273-276
18728403-4	2008	Pre-B-cell colony enhancing factor 1 gene (PBEF1) encodes Nicotinamide phosphoribosyltransferase (NAmPRTase), which catalyses the rate limiting step in the salvage pathway of NAD metabolism in mammalian cells.	NAD	175-178	nicotinamide phosphoribosyltransferase	Homo sapiens	98-107
18477450-5	2008	Activated AMPK was required to promote GR-induced transcription of the NAD+ biosynthetic enzyme Nampt.	NAD	71-75	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	10-14
18252866-3	2008	Within the cell, PBEF functions as a nicotinamide phosphoribosyl transferase, the rate-limiting step in a salvage pathway of nicotinamide adenine dinucleotide (NAD) biosynthesis.	NAD	125-158	nicotinamide phosphoribosyltransferase	Homo sapiens	17-21
18252866-3	2008	Within the cell, PBEF functions as a nicotinamide phosphoribosyl transferase, the rate-limiting step in a salvage pathway of nicotinamide adenine dinucleotide (NAD) biosynthesis.	NAD	160-163	nicotinamide phosphoribosyltransferase	Homo sapiens	17-21
18201551-3	2008	Nicotinamide phosphoribosyltransferase (Nampt) is a crucial factor in the resynthesis of NAD, and thus in cancer cell survival.	NAD	89-92	nicotinamide phosphoribosyltransferase	Homo sapiens	0-38
18184656-3	2008	Given that CtBP1 function is regulated by NADH binding, we hypothesized that ACTH-stimulated changes in cellular pyridine nucleotide concentrations modulate the ability of CtBP1 to repress CYP17 transcription.	NAD	42-46	C-terminal binding protein 1	Homo sapiens	11-16
18184656-3	2008	Given that CtBP1 function is regulated by NADH binding, we hypothesized that ACTH-stimulated changes in cellular pyridine nucleotide concentrations modulate the ability of CtBP1 to repress CYP17 transcription.	NAD	42-46	C-terminal binding protein 1	Homo sapiens	172-177
18275811-0	2008	Bifunctional NMN adenylyltransferase/ADP-ribose pyrophosphatase: structure and function in bacterial NAD metabolism.	NAD	101-104	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	13-36
18230186-5	2008	Overexpression of p49/STRAP altered the intracellular level of NAD, and reduced the NAD/NADH ratio.	NAD	63-66	serine/threonine kinase receptor associated protein	Homo sapiens	22-27
18230186-5	2008	Overexpression of p49/STRAP altered the intracellular level of NAD, and reduced the NAD/NADH ratio.	NAD	84-87	serine/threonine kinase receptor associated protein	Homo sapiens	22-27
18230186-5	2008	Overexpression of p49/STRAP altered the intracellular level of NAD, and reduced the NAD/NADH ratio.	NAD	88-92	serine/threonine kinase receptor associated protein	Homo sapiens	22-27
18836232-3	2008	Its synthesis is the result of cyclooxygenase (COX) and prostaglandin E synthase (PGES) activities whereas NAD+-dependent 15 hydroxy-prostaglandin dehydrogenase (15-PGDH) is the key enzyme implicated in the catabolism of PGE2.	NAD	107-110	hydroxyprostaglandin dehydrogenase 15 (NAD)	Mus musculus	122-160
18039331-6	2008	Similar to the microsomal RDHs, RDH11, RDH12 and RDH14, RDH13 exhibits a much lower Km value for NADPH than for NADH and has a greater catalytic efficiency in the reductive than in the oxidative direction.	NAD	112-116	retinol dehydrogenase 12	Homo sapiens	39-44
18039331-6	2008	Similar to the microsomal RDHs, RDH11, RDH12 and RDH14, RDH13 exhibits a much lower Km value for NADPH than for NADH and has a greater catalytic efficiency in the reductive than in the oxidative direction.	NAD	112-116	retinol dehydrogenase 13	Homo sapiens	56-61
17673214-5	2007	With either NADH or NADPH, the membranal fraction of liver and duodenal mucosa converted dehydrocorticosterone (A) into corticosterone (B) with K(m) (1.1-8.7 microM) and V(max) (10-40 pmol/mg protein/min) values similar to those reported for mammalian 11 betaHSD1.	NAD	12-16	RNA, U1 small nuclear 1	Homo sapiens	242-263
17706244-5	2007	The fractional inhibition of the total NADH:CoQ(1) oxidoreductase by a saturating concentration of rotenone decreased sharply at CoQ(1) concentrations higher than 20 muM, which is indicative, but does not prove the involvement of a second CoQ(1) binding site at complex I.	NAD	39-43	decaprenyl diphosphate synthase subunit 1	Homo sapiens	44-50
17889652-4	2007	Increased Nampt provides protection against cell death and requires an intact mitochondrial NAD(+) salvage pathway as well as the mitochondrial NAD(+)-dependent deacetylases SIRT3 and SIRT4.	NAD	144-150	nicotinamide phosphoribosyltransferase	Homo sapiens	10-15
17516063-4	2007	Homology analysis and sequence alignment of amino acid sequence indicated that ADH1 and ADH3 of N. crassa contained a zinc-binding consensus sequence and a NAD(+)-binding motif and showed 54-75% identity with fungi ADHs.	NAD	156-162	alcohol dehydrogenase I	Neurospora crassa OR74A	79-83
17516063-5	2007	N. crassa ADH1 was expressed in E. coli to give a specific activity of 289 +/- 9 mU/mg using ethanol and NAD(+) as substrate and cofactor, respectively.	NAD	105-111	alcohol dehydrogenase I	Neurospora crassa OR74A	10-14
17516063-9	2007	N. crassa ADH1 was a primary alcohol dehydrogenase using cofactor NAD(+) preferably and possessed carboxylate ester-forming activity with short chain alcohols and aldehydes.	NAD	66-72	alcohol dehydrogenase I	Neurospora crassa OR74A	10-14
17440754-4	2007	While NADH efficiently reduced XD, only a great excess of NADH reduced XO.	NAD	6-10	xanthine dehydrogenase	Rattus norvegicus	31-33
17440754-5	2007	In agreement with reductive titration data, the XD specificity constant for NADH (8.73 +/- 1.36 microM(-1) min(-1)) was found to be higher than that of the XO specificity constant (1.07 +/- 0.09 microM(-1) min(-1)).	NAD	76-80	xanthine dehydrogenase	Rattus norvegicus	48-50
17587307-7	2007	Furthermore, nic2-1 seed had elevated levels of NAD, and germination was hypersensitive to methyl methanesulphonate (MMS), suggesting that PARP activity and DNA repair responses were impaired.	NAD	48-51	nicotinamidase 2	Arabidopsis thaliana	13-17
17543285-1	2007	Visfatin is a secretory protein which exerts insulin mimetic and proinflammatory effects, also functioning as an intracellular enzyme to produce NAD.	NAD	145-148	nicotinamide phosphoribosyltransferase	Homo sapiens	0-8
17098416-1	2007	A new formaldehyde-selective biosensor was constructed using NAD(+)- and glutathione-dependent recombinant formaldehyde dehydrogenase as a bio-recognition element immobilised on the surface of Si/SiO(2)/Si(3)N(4) structure.	NAD	61-67	alcohol dehydrogenase 5 (class III), chi polypeptide	Homo sapiens	107-133
17336418-8	2007	PPT/DPN reduced nitrate/nitrite production and iNOS mRNA in Kupffer cells following trauma-hemorrhage; however, these levels in DPN-treated animals remained higher than sham.	NAD	4-7	tachykinin, precursor 1	Rattus norvegicus	0-3
17336418-8	2007	PPT/DPN reduced nitrate/nitrite production and iNOS mRNA in Kupffer cells following trauma-hemorrhage; however, these levels in DPN-treated animals remained higher than sham.	NAD	128-131	tachykinin, precursor 1	Rattus norvegicus	0-3
17379634-7	2007	The NAD was abolished by both glibenclamide and PNU 37883A but was potentiated by CGRP.	NAD	4-7	calcitonin-related polypeptide alpha	Rattus norvegicus	82-86
17395143-4	2007	The NAD is then amplified using an enzyme cycling system driven by glucose dehydrogenase and diaphorase.	NAD	4-7	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	67-88
17395143-4	2007	The NAD is then amplified using an enzyme cycling system driven by glucose dehydrogenase and diaphorase.	NAD	4-7	dihydrolipoamide dehydrogenase	Homo sapiens	93-103
17175156-2	2007	The biosensor is based on the activity of glucose dehydrogenase (GDH) and diaphorase (DI) co-immobilized with NAD(+) into a carbon nanotube paste (CNTP) electrode modified with an osmium functionalized polymer.	NAD	110-116	dihydrolipoamide dehydrogenase	Homo sapiens	86-88
17175156-3	2007	This mediator was demonstrated to shuttle the electron transfer between the immobilized diaphorase and the CNTP electrode, thus, showing a good electrocatalytic activity towards NADH oxidation at potentials around +0.2V versus Ag AgCl, where interfering reactions are less prone to occur.	NAD	178-182	dihydrolipoamide dehydrogenase	Homo sapiens	88-98
17482543-2	2007	In eukaryotes, nicotinamide riboside is a newly discovered NAD(+) precursor that is converted to nicotinamide mononucleotide by specific nicotinamide riboside kinases, Nrk1 and Nrk2.	NAD	59-65	nicotinamide riboside kinase 1	Mus musculus	168-172
17402747-3	2007	Only the latter utilizes ITP efficiently in place of ATP, and while NMNH conversion to NADH by NMNAT1 and NMNAT3 occurs at similar rates, conversion by NMNAT2 is much slower.	NAD	87-91	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	95-101
17402747-3	2007	Only the latter utilizes ITP efficiently in place of ATP, and while NMNH conversion to NADH by NMNAT1 and NMNAT3 occurs at similar rates, conversion by NMNAT2 is much slower.	NAD	87-91	nicotinamide nucleotide adenylyltransferase 3	Homo sapiens	106-112
17310282-4	2007	Via the reverse of the PDC reaction, NADH and acetyl-CoA reductively acetylate lipoyl group of L2, which binds to the R domain and stimulates PDK2 activity by speeding up ADP dissociation.	NAD	37-41	pyruvate dehydrogenase kinase 2	Homo sapiens	142-146
17213189-2	2007	The two mammalian AGCs, aralar and citrin, are members of the malate-aspartate NADH shuttle.	NAD	79-83	solute carrier family 25 member 13	Homo sapiens	35-41
17200125-7	2007	The bound Q was slowly released from Ndi1 by treatment with NADH or dithionite under anaerobic conditions.	NAD	60-64	NADH-ubiquinone reductase (H(+)-translocating) NDI1	Saccharomyces cerevisiae S288C	37-41
17200125-8	2007	This release of Q was prevented when Ndi1 was kept in the reduced state by NADH.	NAD	75-79	NADH-ubiquinone reductase (H(+)-translocating) NDI1	Saccharomyces cerevisiae S288C	37-41
17200125-9	2007	When Ndi1 was incorporated into bovine heart submitochondrial particles, the Q-bound form, but not the Q-free form, established the NADH-linked respiratory activity, which was insensitive to piericidin A but inhibited by KCN.	NAD	132-136	NADH-ubiquinone reductase (H(+)-translocating) NDI1	Saccharomyces cerevisiae S288C	5-9
17157814-1	2007	In the present work, we have studied the kinetic properties of the catalytic domain of CtBP1, a co-repressor belonging to the d-2-hydroxyacid dehydrogenase family and known to reduce pyruvate in the presence of NADH.	NAD	211-215	C-terminal binding protein 1	Homo sapiens	87-92
17237342-6	2007	The two mammalian AGCs, aralar and citrin, are members of the malate-aspartate NADH shuttle, and citrin, the liver AGC, is also a member of the urea cycle.	NAD	79-83	solute carrier family 25 member 13	Homo sapiens	35-41
17126728-9	2006	At a high salt concentration, the nicotinamide adenine dinucleotide reduced (NADH)-GDH activity was stimulated concomitantly with the increasing NH(4)(+) contents and proteolysis activity in the leaves and roots.	NAD	77-81	glutamate dehydrogenase	Solanum lycopersicum	83-86
17194030-6	2006	NADH-stimulated oxidoreductase activity (25 microM NADH; 0.8mM NAD+) increased with sevoflurane.	NAD	0-4	hydroxysteroid 17-beta dehydrogenase 6	Homo sapiens	16-30
17194030-6	2006	NADH-stimulated oxidoreductase activity (25 microM NADH; 0.8mM NAD+) increased with sevoflurane.	NAD	63-67	hydroxysteroid 17-beta dehydrogenase 6	Homo sapiens	16-30
16901503-3	2006	Here, we describe the first crystal structure of visfatin in three different forms: apo and in complex with either nicotinamide mononucleotide (NMN) or the NAmPRTase inhibitor FK-866 which was developed as an anti-cancer agent, interferes with NAD biosynthesis, showing a particularly high specificity for NAmPRTase.	NAD	244-247	nicotinamide phosphoribosyltransferase	Homo sapiens	49-57
16967067-5	2006	The instruments used glucose dehydrogenase pyrroloquinolinequinone (GDH-PQQ), glucose dehydrogenase nicotinamide adenine dinucleotide (GDH- NAD), or glucose oxidase (GOx) methods.	NAD	140-143	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	135-138
16840720-6	2006	These results indicate that attenuation of BMP signaling can occur through modulation of CtBP-1 activity by hypoxia-induced changes in the NADH/NAD(+) ratio.	NAD	139-143	C-terminal binding protein 1	Homo sapiens	89-95
16840720-6	2006	These results indicate that attenuation of BMP signaling can occur through modulation of CtBP-1 activity by hypoxia-induced changes in the NADH/NAD(+) ratio.	NAD	144-150	C-terminal binding protein 1	Homo sapiens	89-95
16497729-4	2006	The acetylation of ERalpha by p300 is reversed by native cellular deacetylases, including trichostatin A-sensitive enzymes (i.e. class I and II deacetylases) and nicotinamide adenine dinucleotide-dependent/nicotinamide-sensitive enzymes (i.e. class III deacetylases, such as sirtuin 1).	NAD	162-195	E1A binding protein p300	Homo sapiens	30-34
16772165-2	2006	The Wlds protein is a fusion of nicotinamide mononucleotide adenyltransferase-1 (Nmnat1), an essential enzyme in the biosynthesis pathway of nicotinamide adenine dinucleotide (NAD), with the N-terminal 70 amino acids of the Ube4b ubiquitination assembly factor.	NAD	141-174	wallerian degeneration	Mus musculus	4-8
16772165-2	2006	The Wlds protein is a fusion of nicotinamide mononucleotide adenyltransferase-1 (Nmnat1), an essential enzyme in the biosynthesis pathway of nicotinamide adenine dinucleotide (NAD), with the N-terminal 70 amino acids of the Ube4b ubiquitination assembly factor.	NAD	176-179	wallerian degeneration	Mus musculus	4-8
16543240-3	2006	We have shown previously that the single subunit rotenone-insensitive NADH-quinone oxidoreductase (Ndi1) of Saccharomyces cerevisiae mitochondria can restore NADH oxidation in complex I-deficient mammalian cells.	NAD	70-74	NADH-ubiquinone reductase (H(+)-translocating) NDI1	Saccharomyces cerevisiae S288C	99-103
16580146-4	2006	CD38 is a multifunctional enzyme involved in the degradation of beta-nicotinamide adenine dinucleotide to ADP-ribose and cyclic ADP-ribose.	NAD	64-102	CD38 molecule	Canis lupus familiaris	0-4
16373280-5	2006	RESULTS: Rat esophageal samples produced ATRA from all-trans retinal in a NAD-dependent manner and the potential was significantly attenuated by phenetyl isothiocynate, an ALDH inhibitor, or acetaldehyde depending on the concentration used.	NAD	74-77	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	172-176
16292346-5	2005	This role of BARS requires its interaction with ARFGAP1, which is in turn regulated oppositely by p-coA and nicotinamide adenine dinucleotide, which act as cofactors of BARS.	NAD	108-141	C-terminal binding protein 1	Homo sapiens	13-17
16292346-5	2005	This role of BARS requires its interaction with ARFGAP1, which is in turn regulated oppositely by p-coA and nicotinamide adenine dinucleotide, which act as cofactors of BARS.	NAD	108-141	C-terminal binding protein 1	Homo sapiens	169-173
16373854-5	2005	Using mice that are completely deficient in gp91phox (a subunit protein of the superoxide producing nicotinamide adenine dinucleotide phosphate [NADPH] oxidase), we found that CH-enhanced PA constriction to ET-1 was completely blocked (decreases in mean [+/- SE] maximal isometric tension from 5.43 +/- 0.35 to 3.33 +/- 0.19 mN; n = 7; p &lt; 0.01).	NAD	100-133	cytochrome b-245, beta polypeptide	Mus musculus	44-52
16278810-4	2005	Compared to controls (n = 8), doxorubicin-exposed hearts (n = 6) showed low absolute enzyme activity of mtDNA-encoded nicotinamide adenine dinucleotide hydrogen dehydrogenase (NADH DH, 79% residual activity, p = 0.03) and cytochrome c oxidase (COX, 59% residual activity, p &lt; 0.001), but not of succinate dehydrogenase (SDH), which is encoded exclusively by nuclear DNA.	NAD	176-180	cytochrome c oxidase subunit 8A	Homo sapiens	244-247
16258009-8	2005	Exchanging NADP for NAD, reducing CP12, or reducing PRK were all conditions that prevented formation of the complex.	NAD	11-14	phosphoribulokinase	Arabidopsis thaliana	52-55
16216071-5	2005	All FNR variants show enhanced NADP+ and NAD+ binding, especially Tyr303Ser, which correlates with a noticeable improvement of NADH-dependent reactions.	NAD	41-45	ferredoxin reductase	Homo sapiens	4-7
16216071-5	2005	All FNR variants show enhanced NADP+ and NAD+ binding, especially Tyr303Ser, which correlates with a noticeable improvement of NADH-dependent reactions.	NAD	127-131	ferredoxin reductase	Homo sapiens	4-7
16081504-6	2005	We measured protein concentrations (recombinant human IL-1beta and recombinant human myoglobin) and quantified binding of cofactors (NADP+ and NAD+) to the enzyme glucose dehydrogenase.	NAD	143-147	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	163-184
16199199-7	2005	Citrin as a liver-type AGC plays a role in supplying aspartate to the cytosol for urea, protein and nucleotide synthesis by exchanging mitochondrial aspartate for cytosolic glutamate and proton, and transporting cytosolic NADH reducing equivalent to mitochondria as a member of malate aspartate shuttle essential for aerobic glycolysis.	NAD	222-226	solute carrier family 25 member 13	Homo sapiens	0-6
16199199-12	2005	Loss of citrin first cause deficiency of aspartate in the cytosol, which results in an increase in cytosolic NADH/NAD(+) ratio and then activation of fatty acid synthesis pathway to compensate the aberrant ratio.	NAD	109-113	solute carrier family 25 member 13	Homo sapiens	8-14
16199199-12	2005	Loss of citrin first cause deficiency of aspartate in the cytosol, which results in an increase in cytosolic NADH/NAD(+) ratio and then activation of fatty acid synthesis pathway to compensate the aberrant ratio.	NAD	114-120	solute carrier family 25 member 13	Homo sapiens	8-14
16128395-2	2005	Exposure of Acanthamoeba rhysodes cell lysate with SpvB and [32P]nicotinamide adenine dinucleotide (NAD) was here observed to result in labeling of a protein of 43 kDa that subsequently was identified as actin by immunoprecipitation.	NAD	65-98	virulence protein	Salmonella enterica	51-55
16013451-3	2005	Regular oscillatory patterns of oxygen consumption with period lengths characteristic of those observed for rates of NADH oxidation by ECTO-NOX proteins were observed to provide evidence for transfer of protons and electrons to reduce oxygen to water.	NAD	117-121	tripartite motif containing 33	Homo sapiens	135-139
15834423-5	2005	Moreover, CtBP1 blocks the accessibility of p300 to histones in an NADH-sensitive manner and thus represses p300-mediated histone acetylation and transcriptional activation.	NAD	67-71	C-terminal binding protein 1	Homo sapiens	10-15
15834423-5	2005	Moreover, CtBP1 blocks the accessibility of p300 to histones in an NADH-sensitive manner and thus represses p300-mediated histone acetylation and transcriptional activation.	NAD	67-71	E1A binding protein p300	Homo sapiens	44-48
15834423-6	2005	In addition, an NADH-nonresponsive, monomeric mutant, CtBP1 (G183V), was found to strongly repress p300-mediated transcriptional activation.	NAD	16-20	C-terminal binding protein 1	Homo sapiens	54-59
15834423-6	2005	In addition, an NADH-nonresponsive, monomeric mutant, CtBP1 (G183V), was found to strongly repress p300-mediated transcriptional activation.	NAD	16-20	E1A binding protein p300	Homo sapiens	99-103
15834423-7	2005	Thus, the dissociation of NADH from CtBP1 leads to the repression of p300-driven general transcriptional activity by CtBP1.	NAD	26-30	E1A binding protein p300	Homo sapiens	69-73
15834423-7	2005	Thus, the dissociation of NADH from CtBP1 leads to the repression of p300-driven general transcriptional activity by CtBP1.	NAD	26-30	C-terminal binding protein 1	Homo sapiens	117-122
15849307-4	2005	Heterologous expression of a barley HvUXS1 cDNA in Escherichia coli yields a soluble enzyme that converts UDP-d-glucuronate to UDP-D-xylose, is associated with a single molecule of bound NAD+, and is subject to feedback inhibition by UDP-D-xylose.	NAD	187-191	UXS1	Hordeum vulgare	36-42
15794939-2	2005	In this report, we describe a simple spectrophotometric assay to detect FAAH activity in vitro using the ability of the enzyme to hydrolyze oleamide and measuring the resultant production of ammonia with a NADH/NAD+-coupled enzyme reaction.	NAD	206-210	fatty-acid amide hydrolase-like	Rattus norvegicus	72-76
15794939-2	2005	In this report, we describe a simple spectrophotometric assay to detect FAAH activity in vitro using the ability of the enzyme to hydrolyze oleamide and measuring the resultant production of ammonia with a NADH/NAD+-coupled enzyme reaction.	NAD	211-215	fatty-acid amide hydrolase-like	Rattus norvegicus	72-76
15703174-7	2005	Indeed, PARP-1, in the presence of NAD(+), significantly decreased DFF40 activity on plasmid substrates.	NAD	35-41	DNA fragmentation factor subunit beta	Homo sapiens	67-72
15703174-9	2005	The inhibition of DFF40 activity in the presence of NAD(+) was reduced by co-incubation with poly(ADP-ribose) glycohydrolase and a PARP inhibitor.	NAD	52-58	DNA fragmentation factor subunit beta	Homo sapiens	18-23
15804366-9	2005	High levels of progesterone are synthesized by mitochondrial HSD because: 1) the requisite NAD+ cofactor for progesterone synthesis is provided directly by the mitochondria, rather than indirectly via the rate limiting malate-aspartate shuttle; and, 2) the end-product inhibition of P450scc by pregnenolone is eliminated because pregnenolone is converted to progesterone.	NAD	91-95	cytochrome P450, family 11, subfamily a, polypeptide 1	Mus musculus	283-290
15574419-6	2005	For mutant strains lacking IDP1, IDP2, and/or the mitochondrial NAD+-specific isocitrate dehydrogenase (IDH), metabolite measurements indicated that major cellular flux is through the IDH-catalyzed reaction in glucose-grown cells and through the IDP2-catalyzed reaction in cells grown with a nonfermentable carbon source (glycerol and lactate).	NAD	64-68	isocitrate dehydrogenase (NADP(+)) IDP2	Saccharomyces cerevisiae S288C	246-250
15557339-1	2005	In the yeast Saccharomyces cerevisiae, the most important systems for conveying excess cytosolic NADH to the mitochondrial respiratory chain are the external NADH dehydrogenases (Nde1p and Nde2p) and the glycerol-3-phosphate dehydrogenase shuttle.	NAD	97-101	glycerol-3-phosphate dehydrogenase	Saccharomyces cerevisiae S288C	204-238
15456401-0	2005	A novel NADPH:(bound) NADP+ reductase and NADH:(bound) NADP+ transhydrogenase function in bovine liver catalase.	NAD	42-46	catalase	Bos taurus	103-111
15677321-1	2005	NADH regulates the release of calcium from the endoplasmic reticulum by modulation of inositol 1,4,5-trisphosphate receptors (IP3R), accounting for the augmented calcium release of hypoxic cells.	NAD	0-4	inositol 1,4,5-trisphosphate receptor type 3	Homo sapiens	126-130
16247974-1	2005	NAD analogs modified at the ribose adenylyl moiety, named N-2"-MeAD and Na-2"-MeAD, were synthesized as ligands of pyridine nucleotide (NMN/NaMN) adenylyltransferase (NMNAT).	NAD	0-3	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	167-172
15611301-0	2005	Structure-function analysis of the yeast NAD+-dependent tRNA 2"-phosphotransferase Tpt1.	NAD	41-45	tRNA 2'-phosphotransferase	Saccharomyces cerevisiae S288C	83-87
15383625-12	2004	Using NAD+, the 3-hydroxymetabolites were efficiently oxidized by homogeneous recombinant AKR1C2 and AKR1C4.	NAD	6-10	aldo-keto reductase family 1 member C2	Homo sapiens	90-96
15491151-1	2004	Pyruvate dehydrogenase kinase 2 (PDK2) activity is stimulated by NADH and NADH plus acetyl-CoA via the reduction and reductive acetylation of the lipoyl groups of the dihydrolipoyl acetyltransferase (E2) component.	NAD	65-69	pyruvate dehydrogenase kinase 2	Homo sapiens	0-31
15491151-1	2004	Pyruvate dehydrogenase kinase 2 (PDK2) activity is stimulated by NADH and NADH plus acetyl-CoA via the reduction and reductive acetylation of the lipoyl groups of the dihydrolipoyl acetyltransferase (E2) component.	NAD	65-69	pyruvate dehydrogenase kinase 2	Homo sapiens	33-37
15491151-1	2004	Pyruvate dehydrogenase kinase 2 (PDK2) activity is stimulated by NADH and NADH plus acetyl-CoA via the reduction and reductive acetylation of the lipoyl groups of the dihydrolipoyl acetyltransferase (E2) component.	NAD	74-78	pyruvate dehydrogenase kinase 2	Homo sapiens	0-31
15491151-1	2004	Pyruvate dehydrogenase kinase 2 (PDK2) activity is stimulated by NADH and NADH plus acetyl-CoA via the reduction and reductive acetylation of the lipoyl groups of the dihydrolipoyl acetyltransferase (E2) component.	NAD	74-78	pyruvate dehydrogenase kinase 2	Homo sapiens	33-37
15210723-0	2004	Distinct intracellular localization of Gpd1p and Gpd2p, the two yeast isoforms of NAD+-dependent glycerol-3-phosphate dehydrogenase, explains their different contributions to redox-driven glycerol production.	NAD	82-85	glycerol-3-phosphate dehydrogenase	Saccharomyces cerevisiae S288C	97-131
15210723-2	2004	We here report that respiratory-deficient cells become strictly dependent on the Gpd2p isoform of the NAD(+)-linked glycerol-3-phosphate dehydrogenase (Gpd).	NAD	102-108	glycerol-3-phosphate dehydrogenase	Saccharomyces cerevisiae S288C	116-150
15212809-6	2004	On the other hand, the exposure of isolated hepatic mitochondria to CIPC reduced State 3 respiration with a FAD-linked substrate (succinate plus rotenone) and/or with a NAD+ -linked substrate (pyruvate plus malate), whereas State 3 respiration with ascorbate plus tetramethyl-p-phenylendiamine (cytochrome oxidase-linked respiration) was not affected markedly by CIPC.	NAD	169-173	CLOCK-interacting pacemaker	Rattus norvegicus	68-72
15336698-2	2004	PGs play a crucial role in mediating parturition events, and their synthesis and metabolism are regulated by cyclooxygenases (COXs) and NAD(+)-dependent 15-hydroxy-PG dehydrogenase (PGDH), respectively.	NAD	136-142	15-hydroxyprostaglandin dehydrogenase	Rattus norvegicus	153-180
15336698-2	2004	PGs play a crucial role in mediating parturition events, and their synthesis and metabolism are regulated by cyclooxygenases (COXs) and NAD(+)-dependent 15-hydroxy-PG dehydrogenase (PGDH), respectively.	NAD	136-142	15-hydroxyprostaglandin dehydrogenase	Rattus norvegicus	182-186
15236246-4	2004	Effective shuttling of the covalently bound NADH between LDH and GDH was achieved, such that regeneration cycles of NADH/NAD(+) were observed.	NAD	44-48	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	65-68
15236246-4	2004	Effective shuttling of the covalently bound NADH between LDH and GDH was achieved, such that regeneration cycles of NADH/NAD(+) were observed.	NAD	116-120	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	65-68
15236246-4	2004	Effective shuttling of the covalently bound NADH between LDH and GDH was achieved, such that regeneration cycles of NADH/NAD(+) were observed.	NAD	121-127	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	65-68
15126114-4	2004	Using three indicators of neuronal viability and survival, we demonstrated that both the ERalpha selective agonist PPT and the ERbeta selective agonist DPN protected hippocampal neurons against glutamate-induced cell death in a dose-dependent manner, with the maximal response occurring at 100 pM.	NAD	152-155	estrogen receptor 2	Homo sapiens	127-133
15044486-7	2004	We used crystal coordinates for Streptococcus pyogenes UGDH in complex with NAD+ cofactor and UDP-glucose substrate to generate a model of the enzyme active site.	NAD	76-80	UDP-glucose 6-dehydrogenase	Homo sapiens	55-59
15170127-2	2004	Characterization of the E71A mutant protein of p450nor highlights the existence of a unique mechanism for binding NADH that depends on the salt bridge network between Glu71, Arg64 and Asp88.	NAD	114-118	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	47-51
14724208-15	2004	Single channel recordings from RyRs incorporated into lipid bilayers revealed that NADH (2 mm) inhibited the activity of RyR channels by 84%.	NAD	83-87	ryanodine receptor 2	Rattus norvegicus	31-34
14724208-16	2004	However, NADH inhibition of RyR activity was O(2)(-).-independent.	NAD	9-13	ryanodine receptor 2	Rattus norvegicus	28-31
14724208-18	2004	The effect appears to be mediated by direct NADH inhibition of RyR channel activity and by indirect NADH inhibition (O(2)(-).	NAD	44-48	ryanodine receptor 2	Rattus norvegicus	63-66
15357287-2	2004	The purified INOS required NAD+ for the conversion of glucose-6-phosphate to inositol-1-phosphate.	NAD	27-31	myo-inositol-1-phosphate synthase	Drosophila melanogaster	13-17
14729974-3	2004	However, another NAD(+) salvage pathway component, Pnc1, modulates silencing independently of the NAD(+) concentration.	NAD	17-23	nicotinamidase	Saccharomyces cerevisiae S288C	51-55
14729974-3	2004	However, another NAD(+) salvage pathway component, Pnc1, modulates silencing independently of the NAD(+) concentration.	NAD	98-104	nicotinamidase	Saccharomyces cerevisiae S288C	51-55
14664579-1	2003	Xanthine dehydrogenase (XDH) from the bacterium Rhodobacter capsulatus catalyzes the hydroxylation of xanthine to uric acid with NAD(+) as the electron acceptor.	NAD	129-135	xanthine dehydrogenase	Homo sapiens	24-27
12925912-7	2003	Although it shows a higher overall identity to bovine aldehyde oxidase (AO; 54%) than to chicken XDH (51%), it has a NAD-binding domain that is specific to XDHs.	NAD	117-120	xanthine dehydrogenase	Gallus gallus	97-100
14534783-1	2003	The FDH1 gene of Candida boidinii encodes an NAD+-dependent formate dehydrogenase, which catalyzes the last reaction in the methanol dissimilation pathway.	NAD	45-48	formate dehydrogenase (NAD+)	Saccharomyces cerevisiae S288C	4-8
12912900-3	2003	A direct biochemical assay demonstrated that the POS5 gene product utilizes ATP to phosphorylate both NADH and NAD(+), with a twofold preference for NADH.	NAD	102-106	NADH kinase	Saccharomyces cerevisiae S288C	49-53
12912900-3	2003	A direct biochemical assay demonstrated that the POS5 gene product utilizes ATP to phosphorylate both NADH and NAD(+), with a twofold preference for NADH.	NAD	111-117	NADH kinase	Saccharomyces cerevisiae S288C	49-53
12912900-3	2003	A direct biochemical assay demonstrated that the POS5 gene product utilizes ATP to phosphorylate both NADH and NAD(+), with a twofold preference for NADH.	NAD	149-153	NADH kinase	Saccharomyces cerevisiae S288C	49-53
12928715-8	2003	NADH-TR staining was employed to distinguish nuclear bag1, nuclear bag2, and nuclear chain intrafusal muscle fibers.	NAD	0-4	BAG cochaperone 2	Rattus norvegicus	67-71
14565298-0	2003	Dinucleoside polyphosphate NAD analogs as potential NMN adenylyltransferase inhibitors.	NAD	27-30	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	52-75
12710131-6	2003	Our results suggest that versican expression may be of value for distinguishing NAD from benign melanocytic nevi and for distinguishing severe NAD from mild and moderate NAD.	NAD	143-146	versican	Homo sapiens	25-33
12534290-8	2003	Purified RoDH-4, stabilized by reconstitution into proteoliposomes, exhibits the apparent K(m) values for substrates and NAD(+) similar to those of the microsomal enzyme and oxidizes holo-CRBP with the catalytic efficiency (k(cat)/K(m)) of 59 min(-1) mM(-1).	NAD	121-127	retinol dehydrogenase 16	Homo sapiens	9-15
12361482-3	2002	L-threonine dehydrogenase (EC 1.1.1.103) is the first enzyme in the pathway and catalyses the reaction: L-threonine + NAD+ = 2-amino-3-ketobutyrate + NADH.	NAD	118-122	L-threonine dehydrogenase	Mus musculus	0-25
12361482-3	2002	L-threonine dehydrogenase (EC 1.1.1.103) is the first enzyme in the pathway and catalyses the reaction: L-threonine + NAD+ = 2-amino-3-ketobutyrate + NADH.	NAD	150-154	L-threonine dehydrogenase	Mus musculus	0-25
12393208-7	2002	These results suggest that fumarate reductase isoenzymes are required for the reoxidation of intracellular NADH under anaerobic conditions, but not aerobic conditions.	NAD	107-111	fumarate reductase	Saccharomyces cerevisiae S288C	27-45
12062199-7	2002	The changes in the NADH levels were followed by an increase in CBF.	NAD	19-23	CCAAT/enhancer binding protein zeta	Rattus norvegicus	63-66
11788603-2	2002	Nicotinamide/nicotinate mononucleotide (NMN/ NaMN)adenylyltransferase (NMNAT) is an indispensable enzyme in the biosynthesis of NAD(+) and NADP(+).	NAD	128-134	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	71-76
12069106-10	2002	This suggests that CoQ1 or menadione cytoprotection also involves the NQO1 catalysed reoxidation of NADH that accumulates as a result of complex I inhibition.	NAD	100-104	decaprenyl diphosphate synthase subunit 1	Homo sapiens	19-23
11751893-2	2002	Nicotinamide mononucleotide adenylyltransferase (NMNAT), a member of the nucleotidyltransferase alpha/beta-phosphodiesterases superfamily, catalyzes a universal step (NMN + ATP = NAD + PP(i)) in NAD biosynthesis.	NAD	179-182	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	0-47
11751893-2	2002	Nicotinamide mononucleotide adenylyltransferase (NMNAT), a member of the nucleotidyltransferase alpha/beta-phosphodiesterases superfamily, catalyzes a universal step (NMN + ATP = NAD + PP(i)) in NAD biosynthesis.	NAD	179-182	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	49-54
11939620-11	2002	CONCLUSION: We conclude that insulin increases cGMP production in VSMC with iNOS by raising the cell NADH/NAD+ redox state, which may increase the availability of iNOS-derived NO.	NAD	101-105	nitric oxide synthase 2	Canis lupus familiaris	163-167
11939620-11	2002	CONCLUSION: We conclude that insulin increases cGMP production in VSMC with iNOS by raising the cell NADH/NAD+ redox state, which may increase the availability of iNOS-derived NO.	NAD	106-110	nitric oxide synthase 2	Canis lupus familiaris	76-80
11901108-4	2002	Deletion of another NAD(+) salvage pathway gene called PNC1 caused a less severe silencing defect and did not significantly reduce the intracellular NAD(+) concentration.	NAD	20-26	nicotinamidase	Saccharomyces cerevisiae S288C	55-59
11901108-9	2002	We propose a model in which two components of the NAD(+) salvage pathway, Pnc1p and Npt1p, function together in recycling the nuclear nicotinamide generated by Sir2p deacetylase activity back into NAD(+).	NAD	50-56	nicotinamidase	Saccharomyces cerevisiae S288C	74-79
11901108-9	2002	We propose a model in which two components of the NAD(+) salvage pathway, Pnc1p and Npt1p, function together in recycling the nuclear nicotinamide generated by Sir2p deacetylase activity back into NAD(+).	NAD	197-203	nicotinamidase	Saccharomyces cerevisiae S288C	74-79
11785971-6	2002	The DFF45(-/-) cells regained the ability to fragment their DNA into 50-kb pieces in response to TNF, which resulted in a marked activation of PARP-1 and a concomitant depletion of intracellular NAD.	NAD	195-198	DNA fragmentation factor subunit alpha	Homo sapiens	4-9
11752792-1	2002	Nicotinamide mononucleotide adenylyltransferase catalyses the final step in the synthesis of nicotinamide-adenine dinucleotide (NAD(+)) by transferring the adenylyl moiety of ATP to nicotinamide mononucleotide (NMN) with the release of pyrophosphate.	NAD	93-126	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	0-47
11752792-1	2002	Nicotinamide mononucleotide adenylyltransferase catalyses the final step in the synthesis of nicotinamide-adenine dinucleotide (NAD(+)) by transferring the adenylyl moiety of ATP to nicotinamide mononucleotide (NMN) with the release of pyrophosphate.	NAD	128-134	nicotinamide nucleotide adenylyltransferase 1	Homo sapiens	0-47
11602597-1	2001	Connexin 43 (Cx43) hexameric hemichannels, recently demonstrated to mediate NAD(+) transport, functionally interact in the plasma membrane of several cells with the ectoenzyme CD38 that converts NAD(+) to the universal calcium mobilizer cyclic ADP-ribose (cADPR).	NAD	76-82	gap junction protein, alpha 3	Mus musculus	13-17
11602597-1	2001	Connexin 43 (Cx43) hexameric hemichannels, recently demonstrated to mediate NAD(+) transport, functionally interact in the plasma membrane of several cells with the ectoenzyme CD38 that converts NAD(+) to the universal calcium mobilizer cyclic ADP-ribose (cADPR).	NAD	195-201	gap junction protein, alpha 3	Mus musculus	13-17
11602597-2	2001	Here we demonstrate that functional uncoupling between CD38 and Cx43 in CD38-transfected 3T3 murine fibroblasts is paralleled by decreased [Ca(2+)](i) levels as a result of reduced intracellular conversion of NAD(+) to cADPR.	NAD	209-215	gap junction protein, alpha 3	Mus musculus	64-68
11602597-5	2001	Conversion of NAD(+)-permeable Cx43 to the phosphorylated, NAD(+)-impermeable form occurs via Ca(2+)-stimulated protein kinase C (PKC).	NAD	14-20	gap junction protein, alpha 3	Mus musculus	31-35
11602597-5	2001	Conversion of NAD(+)-permeable Cx43 to the phosphorylated, NAD(+)-impermeable form occurs via Ca(2+)-stimulated protein kinase C (PKC).	NAD	59-65	gap junction protein, alpha 3	Mus musculus	31-35
21669645-7	2001	Furthermore, the mature subunit exhibited a very high homology to the plastid-localized NAD-dependent malate dehydrogenase from Arabidopsis thaliana, which has a completely different transit peptide.	NAD	88-91	malate dehydrogenase	Arabidopsis thaliana	102-122
11708925-1	2001	Through an effort to develop novel ligands that have subtype selectivity for the estrogen receptors alpha (ERalpha) and beta (ERbeta), we have found that 2,3-bis(4-hydroxyphenyl)propionitrile (DPN) acts as an agonist on both ER subtypes, but has a 70-fold higher relative binding affinity and 170-fold higher relative potency in transcription assays with ERbeta than with ERalpha.	NAD	193-196	estrogen receptor 2	Homo sapiens	126-132
11708925-1	2001	Through an effort to develop novel ligands that have subtype selectivity for the estrogen receptors alpha (ERalpha) and beta (ERbeta), we have found that 2,3-bis(4-hydroxyphenyl)propionitrile (DPN) acts as an agonist on both ER subtypes, but has a 70-fold higher relative binding affinity and 170-fold higher relative potency in transcription assays with ERbeta than with ERalpha.	NAD	193-196	estrogen receptor 2	Homo sapiens	355-361
11708925-2	2001	To investigate the ERbeta affinity- and potency-selective character of this DPN further, we prepared a series of DPN analogues in which both the ligand core and the aromatic rings were modified by the repositioning of phenolic hydroxy groups and by the addition of alkyl substituents and nitrile groups.	NAD	76-79	estrogen receptor 2	Homo sapiens	19-25
11708925-5	2001	meso-2,3-Bis(4-hydroxyphenyl)succinonitrile and dl-2,3-bis(4-hydroxyphenyl)succinonitrile are among the highest ERbeta affinity-selective ligands, and they have an ERbeta potency selectivity that is equivalent to that of DPN.	NAD	221-224	estrogen receptor 2	Homo sapiens	112-118
11708925-5	2001	meso-2,3-Bis(4-hydroxyphenyl)succinonitrile and dl-2,3-bis(4-hydroxyphenyl)succinonitrile are among the highest ERbeta affinity-selective ligands, and they have an ERbeta potency selectivity that is equivalent to that of DPN.	NAD	221-224	estrogen receptor 2	Homo sapiens	164-170
11686930-5	2001	Fluorescence energy transfer studies also showed more binding of the reduced coenzyme (NADH) to GDH and the Lineweaver-Burk plots (with respect to NADH) indicate the existence of substrate inhibition in the presence of octyl glucoside.	NAD	87-91	glutamate dehydrogenase 1, mitochondrial	Bos taurus	96-99
11781695-1	2001	We report a novel point mutation in the gene for the mitochondrially encoded ND6 subunit of the NADH:ubiquinone oxidoreductase (complex I of the respiratory chain) in a patient with MELAS syndrome.	NAD	96-100	mitochondrially encoded NADH dehydrogenase 6	Homo sapiens	77-80
11396984-8	2001	In contrast, Ca(2+) reduced the [NADH] response to the ATPase addition, consistent with Ca(2+)-sensitive dehydrogenase activity (CaDH).	NAD	33-37	dynein axonemal heavy chain 8	Homo sapiens	55-61
11396984-10	2001	The addition of 172nM free Ca(2+)] ATPase increased mVo2 by 300% (P&lt;0.05, n=8) while deltapsi decreased by 14.9+/-0.1 mV without changes in [NADH] (P &gt; or =0.05, n=8), consistent with working heart preparations.	NAD	144-148	dynein axonemal heavy chain 8	Homo sapiens	35-41
11396984-11	2001	The addition of Ca(2+) and ATPase combined increased the mitochondrial ATP production rate with changes in deltapsi, NADH and [ADP], consistent with an activation of CaDH and F o /F(1)ATPase activity.	NAD	117-121	dynein axonemal heavy chain 8	Homo sapiens	27-33
11508269-9	2001	NAD inhibited anti-CD3 induced activation of splenic T cells in vitro and also retarded killing of beta-cell targets by NOD islet-reactive CD8 effectors in vitro at concentrations equal to or greater than 1 micromol/l.	NAD	0-3	CD3 antigen, epsilon polypeptide	Mus musculus	19-22
11274199-9	2001	These results demonstrate a paracrine process based on Cx43-mediated release of NAD(+), its CD38-catalyzed conversion to extracellular cADPR, and influx of this nucleotide into responsive cells to increase [Ca(2+)](i) and stimulate cell proliferation.	NAD	80-86	gap junction protein, alpha 3	Mus musculus	55-59
11390211-5	2001	With the electrocatalytically reduced product, dihydrolipoic acid, lipoamide dehydrogenase could reduce NAD(+) in 20% yield and thioredoxin reductase NADP(+) in 18.4% yield.	NAD	104-110	dihydrolipoamide dehydrogenase	Homo sapiens	67-90
11250901-5	2001	Consistent with acetylation of TIF-IB/SL1 being required for rDNA transcription, the NAD(+)-dependent histone deacetylase mSir2a deacetylates TAF(I)68 and represses Pol I transcription.	NAD	85-91	DNA polymerase iota	Homo sapiens	165-170
11306044-1	2001	Molecular dynamics (MD) simulation of the rat class 3 aldehyde dehydrogenase (ALDH) with nicotinamide dinucleotide (NAD) cofactors and explicit water molecules are reported.	NAD	89-114	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	54-76
11306044-1	2001	Molecular dynamics (MD) simulation of the rat class 3 aldehyde dehydrogenase (ALDH) with nicotinamide dinucleotide (NAD) cofactors and explicit water molecules are reported.	NAD	89-114	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	78-82
11306044-1	2001	Molecular dynamics (MD) simulation of the rat class 3 aldehyde dehydrogenase (ALDH) with nicotinamide dinucleotide (NAD) cofactors and explicit water molecules are reported.	NAD	116-119	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	54-76
11306044-1	2001	Molecular dynamics (MD) simulation of the rat class 3 aldehyde dehydrogenase (ALDH) with nicotinamide dinucleotide (NAD) cofactors and explicit water molecules are reported.	NAD	116-119	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	78-82
11306044-3	2001	Furthermore, the examination of the distance between the nucleophilic Cys-243 and the NAD cofactor reveal important fluctuations that could be linked to ALDH catalysis.	NAD	86-89	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	153-157
11029457-1	2001	Parallel activation of heart mitochondria NADH and ATP production by Ca(2+) has been shown to involve the Ca(2+)-sensitive dehydrogenases and the F(0)F(1)-ATPase.	NAD	42-46	ATP synthase F1 subunit epsilon	Homo sapiens	146-161
11163031-7	2001	We conclude that elimination of the reaction products (NADH, H(2)O(2) and O(2)) from the reaction mixture, and short incubation times, are necessary for accurate measurement of the XOR activities.	NAD	55-59	xanthine dehydrogenase	Homo sapiens	181-184
11080300-1	2000	We have previously shown that in Nicotiana sylvestris cytoplasmic male-sterile (CMS) mutants where the mtDNA lacks the nad7 gene coding for a subunit of respiratory Complex I (NADH:ubiquinone oxidoreductase, EC 1.6.5.3), glycine (Gly) oxidation was lower than in the wild type and insensitive to rotenone, suggesting Complex I dysfunction.	NAD	176-180	NADH dehydrogenase subunit 7	Nicotiana sylvestris	119-123
11011142-10	2000	Kinetic study of the NADase reaction revealed that the affinity of Rt6.1 for NAD and the rate of catalysis increased in the presence of DTT.	NAD	21-24	ADP-ribosyltransferase 2a	Mus musculus	67-72
10871622-5	2000	The second redox reaction occurring in retinal pigment epithelium, oxidation of 11-cis-retinol, which is largely catalyzed by abundantly expressed 11-cis-retinol dehydrogenase, is pro-S-specific to both 11-cis-retinol and NADH.	NAD	222-226	retinol dehydrogenase 5	Homo sapiens	147-175
11285859-6	2000	Because the method depends on the colorimetric determination of triose formed from fructose-1,6-diphosphate only by aldolase, glycerophosphate dehydrogenase/triosephosphate isomerase (GDH/TIM) and reduced nicotinamide adenine dinucleotide (NADH) which usually applied in multienzymatic method, are omitted in the modified method.	NAD	205-238	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	184-187
11285859-6	2000	Because the method depends on the colorimetric determination of triose formed from fructose-1,6-diphosphate only by aldolase, glycerophosphate dehydrogenase/triosephosphate isomerase (GDH/TIM) and reduced nicotinamide adenine dinucleotide (NADH) which usually applied in multienzymatic method, are omitted in the modified method.	NAD	240-244	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	184-187
10955999-4	2000	Cofactor displacement studies based on the reduced fluorescence intensity of free NADH versus that of enzyme-bound NADH revealed that both AMP and ATP decreased NADH-At-SSADH1 complex formation.	NAD	82-86	aldehyde dehydrogenase 5F1	Arabidopsis thaliana	169-175
10955999-4	2000	Cofactor displacement studies based on the reduced fluorescence intensity of free NADH versus that of enzyme-bound NADH revealed that both AMP and ATP decreased NADH-At-SSADH1 complex formation.	NAD	115-119	aldehyde dehydrogenase 5F1	Arabidopsis thaliana	169-175
10955999-12	2000	However, only ATP increased the dissociation constant of NAD(+) from SSADH.	NAD	57-63	aldehyde dehydrogenase 5F1	Arabidopsis thaliana	69-74
10955999-13	2000	This explains the reduced affinity of NAD(+)/NADH to At-SSADH1 in the presence of ATP, as revealed by enzymatic kinetics, and supports our model of feedback regulation of SSADH and the GABA shunt by ATP.	NAD	38-44	aldehyde dehydrogenase 5F1	Arabidopsis thaliana	56-62
10955999-13	2000	This explains the reduced affinity of NAD(+)/NADH to At-SSADH1 in the presence of ATP, as revealed by enzymatic kinetics, and supports our model of feedback regulation of SSADH and the GABA shunt by ATP.	NAD	38-44	aldehyde dehydrogenase 5F1	Arabidopsis thaliana	56-61
10955999-13	2000	This explains the reduced affinity of NAD(+)/NADH to At-SSADH1 in the presence of ATP, as revealed by enzymatic kinetics, and supports our model of feedback regulation of SSADH and the GABA shunt by ATP.	NAD	45-49	aldehyde dehydrogenase 5F1	Arabidopsis thaliana	56-62
10955999-13	2000	This explains the reduced affinity of NAD(+)/NADH to At-SSADH1 in the presence of ATP, as revealed by enzymatic kinetics, and supports our model of feedback regulation of SSADH and the GABA shunt by ATP.	NAD	45-49	aldehyde dehydrogenase 5F1	Arabidopsis thaliana	56-61
16232830-3	2000	During the glycerol-production phase, the NAD+-dependent glycerol-3-phosphate dehydrogenase (GPDH) activity of heat-shock-treated cells was much higher than that of control cells, suggesting that a higher GPDH activity enhances glycerol production.	NAD	42-45	glycerol-3-phosphate dehydrogenase	Saccharomyces cerevisiae S288C	57-91
16232830-3	2000	During the glycerol-production phase, the NAD+-dependent glycerol-3-phosphate dehydrogenase (GPDH) activity of heat-shock-treated cells was much higher than that of control cells, suggesting that a higher GPDH activity enhances glycerol production.	NAD	42-45	glycerol-3-phosphate dehydrogenase	Saccharomyces cerevisiae S288C	93-97
16232830-3	2000	During the glycerol-production phase, the NAD+-dependent glycerol-3-phosphate dehydrogenase (GPDH) activity of heat-shock-treated cells was much higher than that of control cells, suggesting that a higher GPDH activity enhances glycerol production.	NAD	42-45	glycerol-3-phosphate dehydrogenase	Saccharomyces cerevisiae S288C	205-209
11030089-8	2000	These observations are explained in terms of formation of a nickel-NADH complex with a higher affinity for binding to the regulatory site in GDH, as compared with the situation where nickel is not present.	NAD	67-71	glutamate dehydrogenase 1, mitochondrial	Bos taurus	141-144
11030089-9	2000	Such effects may be important for regulation of GDH and other NADH-utilizing enzymes.	NAD	62-66	glutamate dehydrogenase 1, mitochondrial	Bos taurus	48-51
10559215-4	1999	A small amount of NAD(+)-dependent retinaldehyde activity was associated with the E2 isozyme (product of aldh2 gene) of aldehyde dehydrogenase.	NAD	18-24	aldehyde dehydrogenase 2 family member	Homo sapiens	105-110
10567692-0	1999	The effect of iron limitation on glycerol production and expression of the isogenes for NAD(+)-dependent glycerol 3-phosphate dehydrogenase in Saccharomyces cerevisiae.	NAD	88-94	glycerol-3-phosphate dehydrogenase	Saccharomyces cerevisiae S288C	105-139
10419824-7	1999	Since the kinetic locking-on strategy is dependent on the target NAD(P)(+)-dependent dehydrogenase having an ordered sequential mechanism of substrate binding, the bioaffinity chromatographic behavior of bovine liver GDH using the locking-on tactic suggests that this enzyme has an ordered sequential mechanism of substrate binding under a variety of experimental conditions when NAD(+) is used as cofactor.	NAD	380-386	glutamate dehydrogenase 1, mitochondrial	Bos taurus	217-220
10387934-3	1999	Activity of quinolinate phosphoribosyltransferase (QAPRTase), one of the key enzymes in the Trp-NAD+ pathway, was increased by the PPs which caused significant increase in the hepatic NAD+.	NAD	96-100	quinolinate phosphoribosyltransferase	Rattus norvegicus	12-49
10387934-3	1999	Activity of quinolinate phosphoribosyltransferase (QAPRTase), one of the key enzymes in the Trp-NAD+ pathway, was increased by the PPs which caused significant increase in the hepatic NAD+.	NAD	96-100	quinolinate phosphoribosyltransferase	Rattus norvegicus	51-59
10387934-3	1999	Activity of quinolinate phosphoribosyltransferase (QAPRTase), one of the key enzymes in the Trp-NAD+ pathway, was increased by the PPs which caused significant increase in the hepatic NAD+.	NAD	184-188	quinolinate phosphoribosyltransferase	Rattus norvegicus	12-49
10387934-3	1999	Activity of quinolinate phosphoribosyltransferase (QAPRTase), one of the key enzymes in the Trp-NAD+ pathway, was increased by the PPs which caused significant increase in the hepatic NAD+.	NAD	184-188	quinolinate phosphoribosyltransferase	Rattus norvegicus	51-59
10354494-7	1999	The ADP/O ratios coupled to NADH oxidation were lowered from 2.4 to 1.8 by NDI1-transfection while the ADP/O ratios coupled to succinate oxidation (1.6) were not changed.	NAD	28-32	NADH-ubiquinone reductase (H(+)-translocating) NDI1	Saccharomyces cerevisiae S288C	75-79
10331651-6	1999	On the other hand, in a reconstituted reaction system, purified PARP from human placenta suppressed the pRB-phosphorylation activity in the presence of NAD and damaged DNA.	NAD	152-155	RB transcriptional corepressor 1	Homo sapiens	104-107
10575215-0	1999	Assignment of mitochondrial NAD(+)-specific isocitrate dehydrogenase beta subunit gene (IDH3B) to human chromosome band 20p13 by in situ hybridization and radiation hybrid mapping.	NAD	28-34	isocitrate dehydrogenase (NAD(+)) 3 non-catalytic subunit beta	Homo sapiens	88-93
9917322-1	1999	The enzyme used in the assay, formaldehyde dehydrogenase, is NAD+ dependent, and the assay measures the production of NADH by determining the increase in fluorescence at 460 nm.	NAD	62-66	alcohol dehydrogenase 5 (class III), chi polypeptide	Homo sapiens	31-57
9813015-1	1998	Photoaffinity labeling with [32P]nicotinamide 2-azidoadenosine dinucleotide (2N3NAD+) was used to identify the NAD+ binding site within two types of glutamate dehydrogenase isoproteins (GDH I and GDH II) isolated from bovine brain.	NAD	80-84	glucose dehydrogenase	Bos taurus	186-189
9813015-1	1998	Photoaffinity labeling with [32P]nicotinamide 2-azidoadenosine dinucleotide (2N3NAD+) was used to identify the NAD+ binding site within two types of glutamate dehydrogenase isoproteins (GDH I and GDH II) isolated from bovine brain.	NAD	80-84	glucose dehydrogenase	Bos taurus	196-199
9813015-10	1998	These results demonstrate selectivity of the photoprobe for the NAD+ binding site and suggest that the peptide identified using the photoprobe is located in the NAD+ binding domain of the brain GDH isoproteins.	NAD	64-68	glucose dehydrogenase	Bos taurus	194-197
9813015-10	1998	These results demonstrate selectivity of the photoprobe for the NAD+ binding site and suggest that the peptide identified using the photoprobe is located in the NAD+ binding domain of the brain GDH isoproteins.	NAD	161-165	glucose dehydrogenase	Bos taurus	194-197
9799522-2	1998	The oxidation-reduction potentials, Eox/EH2 (two-electron reduced enzyme), for yeast, Escherichia coli, and human glutathione reductase have been determined between pH 6.0 and 9.8 relative to the nonphysiological substrate couple NAD+/NADH and were found to be -237, -243, and -227 mV (+/-5 mV) at pH 7.0 and 20 degreesC, respectively.	NAD	230-234	glutathione-disulfide reductase	Homo sapiens	114-135
9799522-2	1998	The oxidation-reduction potentials, Eox/EH2 (two-electron reduced enzyme), for yeast, Escherichia coli, and human glutathione reductase have been determined between pH 6.0 and 9.8 relative to the nonphysiological substrate couple NAD+/NADH and were found to be -237, -243, and -227 mV (+/-5 mV) at pH 7.0 and 20 degreesC, respectively.	NAD	235-239	glutathione-disulfide reductase	Homo sapiens	114-135
9873629-1	1998	Electroenzymatic reduction of NAD+ to NADH for subsequent use in enzymatic synthesis has been carried out at carbon electrodes bearing lipoamide dehydrogenase (LiDH) immobilized under a Nafion film.	NAD	30-34	dihydrolipoamide dehydrogenase	Homo sapiens	135-158
9873629-1	1998	Electroenzymatic reduction of NAD+ to NADH for subsequent use in enzymatic synthesis has been carried out at carbon electrodes bearing lipoamide dehydrogenase (LiDH) immobilized under a Nafion film.	NAD	30-34	dihydrolipoamide dehydrogenase	Homo sapiens	160-164
9733747-3	1998	To investigate whether open reading frames YMR145c/NDE1 and YDL 085w/NDE2, which exhibit sequence similarity with NDI1, encode the latter enzyme, NADH-dependent mitochondrial respiration was assayed in wild-type S. cerevisiae and nde deletion mutants.	NAD	146-150	NADH-ubiquinone reductase (H(+)-translocating) NDI1	Saccharomyces cerevisiae S288C	114-118
10603952-2	1998	In crude membrane preparations from patients with terminal heart failure due to idiopathic dilated cardiomyopathy (DCM) and control hearts (NF), SERCA2 activity was measured with a NADH coupled assay.	NAD	181-185	ATPase sarcoplasmic/endoplasmic reticulum Ca2+ transporting 2	Homo sapiens	145-151
21644715-7	1998	Substrate cycling was realized via NADH/NAD(+) that, in conjunction with glucose dehydrogenase, regenerates glucose, the substrate in the glucose oxidase-catalyzed reaction.	NAD	35-39	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	73-94
21644715-7	1998	Substrate cycling was realized via NADH/NAD(+) that, in conjunction with glucose dehydrogenase, regenerates glucose, the substrate in the glucose oxidase-catalyzed reaction.	NAD	40-46	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	73-94
9696750-1	1998	The reoxidation of NADH generated in reactions within the mitochondrial matrix of Saccharomyces cerevisiae is catalyzed by an NADH dehydrogenase designated Ndi1p (C. A. M. Marres, S. de Vries, and L. A. Grivell, Eur.	NAD	19-23	NADH-ubiquinone reductase (H(+)-translocating) NDI1	Saccharomyces cerevisiae S288C	156-161
9706808-7	1998	Increased NADH selectively inhibited myocardial xanthine dehydrogenase in vitro.	NAD	10-14	xanthine dehydrogenase	Rattus norvegicus	48-70
9706808-8	1998	It was thus expected that a decrease of NADH might limit the production of reactive oxygen species through the recovery of xanthine dehydrogenase activity.	NAD	40-44	xanthine dehydrogenase	Rattus norvegicus	123-145
9620466-1	1998	NADH (reduced Coenzyme I)-cytochrome b5 reductase (b5R) is a multifunctional redox enzyme, whose deficiency causes recessive congenital methemoglobinemia.	NAD	0-4	cytochrome b5 reductase 3	Homo sapiens	51-54
9585000-14	1998	At d 21, decreased gene expression if ND-4L, SUC, and ANTI is associated with a decreased mitochondrial NAD+/NADH ratio.	NAD	104-108	NADH dehdrogenase 4L, mitochondrial	Rattus norvegicus	38-43
9585000-14	1998	At d 21, decreased gene expression if ND-4L, SUC, and ANTI is associated with a decreased mitochondrial NAD+/NADH ratio.	NAD	109-113	NADH dehdrogenase 4L, mitochondrial	Rattus norvegicus	38-43
9633649-4	1998	The apparent K(m)s for the glycerol dehydrogenase was 16-fold higher for the glycerol than that for the glyceraldehyde in the case of the glyceraldehyde-3-phosphate dehydrogenase and fourfold higher for the NAD+, providing an explanation for the shift of the glycerol flow toward 1,3-propanediol when cells were grown on glucose-glycerol mixtures.	NAD	207-211	gldA	Clostridium butyricum	27-49
9520374-5	1998	In addition, the potency of 29 rotenoids from cube insecticide for inhibiting NADH:ubiquinone oxidoreductase in vitro assayed with bovine heart electron transport particles satisfactorily predicts their potency in vivo in the induced ODC assay using noncytotoxic rotenoid concentrations with cultured MCF-7 human breast cancer cells (r = 0.86).	NAD	78-82	ornithine decarboxylase 1	Homo sapiens	234-237
9559543-10	1998	Our results also demonstrated that of the two isoforms of NAD-dependent glycerol 3-phosphate dehydrogenase, only the enzyme encoded by GPD1 appeared important for the shuttle, since the enhanced glycerol production that occurs in a gut2 delta strain proved dependent on GPD1 but not on GPD2.	NAD	58-61	glycerol-3-phosphate dehydrogenase	Saccharomyces cerevisiae S288C	232-236
9514863-1	1998	We tested the effect of the GTS1 gene of the yeast Saccharomyces cerevisiae on the cyanide-induced ultradian oscillation of the glycolytic metabolite NADH in cell suspension of strains with different copy numbers of the gene, that is, the wild-type, GTS1-disrupted and GTS1-overexpressing strains.	NAD	150-154	Gts1p	Saccharomyces cerevisiae S288C	28-32
9514081-6	1998	Each inhibited NAD-linked benzaldehyde oxidation catalyzed by ALDH-3s purified from human breast adenocarcinoma MCF-7/0/CAT cells (IC50 values were 16 and 0.75 microM, respectively) and human normal stomach mucosa (IC50 values were 202 and 5 microM, respectively).	NAD	15-18	aldehyde dehydrogenase 3 family member A1	Homo sapiens	62-68
9598055-0	1998	Enzyme activities leading to NAD synthesis in the erythrocytes of HPRT deficient subjects.	NAD	29-32	hypoxanthine phosphoribosyltransferase 1	Homo sapiens	66-70
9171333-0	1997	The two isoenzymes for yeast NAD+-dependent glycerol 3-phosphate dehydrogenase encoded by GPD1 and GPD2 have distinct roles in osmoadaptation and redox regulation.	NAD	29-33	glycerol-3-phosphate dehydrogenase	Saccharomyces cerevisiae S288C	44-78
9171333-1	1997	The two homologous genes GPD1 and GPD2 encode the isoenzymes of NAD-dependent glycerol 3-phosphate dehydrogenase in the yeast Saccharomyces cerevisiae.	NAD	64-67	glycerol-3-phosphate dehydrogenase	Saccharomyces cerevisiae S288C	78-112
9020087-1	1997	CD38 catalyzes not only the formation of cyclic ADP-ribose (cADPR) from NAD+ but also the hydrolysis of cADPR to ADP-ribose (ADPR), and ATP inhibits the hydrolysis (Takasawa, S., Tohgo, A., Noguchi, N., Koguma, T., Nata, K., Sugimoto, T., Yonekura, H., and Okamoto, H. (1993) J. Biol.	NAD	72-76	CD38 molecule	Homo sapiens	0-4
9193634-4	1997	Residues 39-46 of the active-site loop of the C-domain become disordered upon NAD-binding, suggesting a potential role for these residues in binding to elongation facor-2 (EF-2).	NAD	78-81	eukaryotic translation elongation factor 2	Homo sapiens	172-176
9193645-11	1997	Alignment of the deduced amino acid sequences of the mammalian transferases and the rodent RT6 enzymes, along with results from site-directed mutagenesis of the muscle enzyme, are consistent with the notion of a common mechanism of NAD binding and catalysis among ADP-ribosyltransferases.	NAD	232-235	ADP-ribosyltransferase 2, pseudogene	Homo sapiens	91-94
9040540-2	1997	Because PARP requires NAD as its substrate, we postulated that a deficiency of both folate and niacin would enhance the development of liver cancer in rats fed a diet deficient in methionine and choline.	NAD	22-25	poly (ADP-ribose) polymerase 1	Rattus norvegicus	8-12
9010772-5	1996	[32P]ADP-ribosylation of p33 occurred in the extracellular space, induced by the stimulus of A23187 or opsonized zymosan in the presence of [32P]NAD.	NAD	145-148	leukocyte cell derived chemotaxin 2	Gallus gallus	25-28
9001360-8	1996	These results indicate that the defects in the mitochondrial NADH- and NADPH-linked aquacobalamin reductases underlie cblC and cblA disorders, respectively.	NAD	61-65	Cbl proto-oncogene C	Homo sapiens	118-122
8915013-0	1996	NAD+-dependent internalization of the transmembrane glycoprotein CD38 in human Namalwa B cells.	NAD	0-4	CD38 molecule	Homo sapiens	65-69
8915013-4	1996	Incubation of CD38+ human Namalwa B cells with external NAD+ elicited extensive membrane down-regulation of CD38 and its internalization in non-clathrin-coated vesicles.	NAD	56-60	CD38 molecule	Homo sapiens	14-18
8915013-4	1996	Incubation of CD38+ human Namalwa B cells with external NAD+ elicited extensive membrane down-regulation of CD38 and its internalization in non-clathrin-coated vesicles.	NAD	56-60	CD38 molecule	Homo sapiens	108-112
8915013-5	1996	Since the internalized CD38 was demonstrated to be enzymatically active, this NAD+-dependent process is a hitherto unrecognized means for shifting cADPR metabolism from the cell surface to the intracellular environment.	NAD	78-82	CD38 molecule	Homo sapiens	23-27
8938587-3	1996	Two kinetically distinct isoforms of this enzyme have been characterized in both rodents and man; a low-affinity NADP(H)-dependent enzyme (11 beta-HSD1) which predominantly acts as an oxoreductase and, more recently, a high-affinity NAD-dependent uni-directional dehydrogenase (11 beta-HSD2).	NAD	113-116	hydroxysteroid 11-beta dehydrogenase 2	Homo sapiens	278-290
18629818-9	1996	Because the GDH needs beta-nicotinamide adenine dinucleotide (NAD(+)) as a cofactor, lactate dehydrogenase is used to regenerate NAD(+) from NADH by reducing pyruvate to (L)-lactate.	NAD	22-60	glutamate dehydrogenase 1	Homo sapiens	12-15
18629818-9	1996	Because the GDH needs beta-nicotinamide adenine dinucleotide (NAD(+)) as a cofactor, lactate dehydrogenase is used to regenerate NAD(+) from NADH by reducing pyruvate to (L)-lactate.	NAD	62-68	glutamate dehydrogenase 1	Homo sapiens	12-15
18629818-9	1996	Because the GDH needs beta-nicotinamide adenine dinucleotide (NAD(+)) as a cofactor, lactate dehydrogenase is used to regenerate NAD(+) from NADH by reducing pyruvate to (L)-lactate.	NAD	129-135	glutamate dehydrogenase 1	Homo sapiens	12-15
18629818-9	1996	Because the GDH needs beta-nicotinamide adenine dinucleotide (NAD(+)) as a cofactor, lactate dehydrogenase is used to regenerate NAD(+) from NADH by reducing pyruvate to (L)-lactate.	NAD	141-145	glutamate dehydrogenase 1	Homo sapiens	12-15
8751991-6	1996	In the modified assay, the enzyme formaldehyde dehydrogenase (FDH) and its co-factor, NAD+ are added in large excess during the exposure period so that any formaldehyde produced in the system is rapidly converted to formic acid which is not genotoxic.	NAD	86-90	alcohol dehydrogenase 5 (class III), chi polypeptide	Mus musculus	34-60
8751991-6	1996	In the modified assay, the enzyme formaldehyde dehydrogenase (FDH) and its co-factor, NAD+ are added in large excess during the exposure period so that any formaldehyde produced in the system is rapidly converted to formic acid which is not genotoxic.	NAD	86-90	alcohol dehydrogenase 5 (class III), chi polypeptide	Mus musculus	62-65
8751991-7	1996	An MTBE dose-responsive increase in the frequency of mutants and in cytotoxicity occurred without FDH present, and this effect was greatly reduced in the presence of FDH NAD+.	NAD	170-174	alcohol dehydrogenase 5 (class III), chi polypeptide	Mus musculus	166-169
8875451-8	1996	These findings suggest that up-regulation of the rat B13 mRNA expression after denervation plays an important role in the effective electron transfer from NADH to UQ-10 in skeletal muscle cells, resulting in restriction of lipid peroxidation and biological tissue damage.	NAD	155-159	NADH:ubiquinone oxidoreductase subunit A5	Homo sapiens	53-56
8663387-11	1996	The equilibrium dissociation constants of beta3 for NAD+ and NADH are 350-fold and 4000-fold higher, respectively, than those for beta1.	NAD	52-56	eukaryotic translation elongation factor 1 beta 2 pseudogene 2	Homo sapiens	42-47
8663387-11	1996	The equilibrium dissociation constants of beta3 for NAD+ and NADH are 350-fold and 4000-fold higher, respectively, than those for beta1.	NAD	61-65	eukaryotic translation elongation factor 1 beta 2 pseudogene 2	Homo sapiens	42-47
8679568-2	1996	PC is an allosteric activator that enhances NAD(H) binding to BDH.	NAD	44-50	3-hydroxybutyrate dehydrogenase 1	Homo sapiens	62-65
8679570-11	1996	Conditions known to increase the mitochondrial NADH/NAD+ ratio decreased CyP binding.	NAD	47-51	peptidylprolyl isomerase G	Homo sapiens	73-76
8679570-11	1996	Conditions known to increase the mitochondrial NADH/NAD+ ratio decreased CyP binding.	NAD	52-56	peptidylprolyl isomerase G	Homo sapiens	73-76
8782085-4	1996	The 11 beta-HSD activity in JEG-3 cell homogenates required NAD+ as cofactor with NADP+ ineffective and demonstrated a high affinity for cortisol (apparent Km 31 nM).	NAD	60-64	hydroxysteroid 11-beta dehydrogenase 2	Homo sapiens	4-11
8603696-0	1996	Streptozotocin, an inducer of NAD+ decrease, attenuates M-potassium current inhibition by ATP, bradykinin, angiotensin II, endothelin 1 and acetylcholine in NG108-15 cells.	NAD	30-34	endothelin 1	Mus musculus	123-135
8573568-2	1996	Specifically, the catalytic (C) domain of DT transfers the ADP-ribose group of NAD to elongation factor-2 (EF-2), rendering EF-2 inactive.	NAD	79-82	eukaryotic translation elongation factor 2	Homo sapiens	86-105
8573568-2	1996	Specifically, the catalytic (C) domain of DT transfers the ADP-ribose group of NAD to elongation factor-2 (EF-2), rendering EF-2 inactive.	NAD	79-82	eukaryotic translation elongation factor 2	Homo sapiens	107-111
8573568-3	1996	In order to investigate how the C-domain of DT binds NAD and catalyzes the ADP-ribosylation of EF-2, the crystal structure of DT in complex with NAD has been determined to 2.3 A resolution.	NAD	145-148	eukaryotic translation elongation factor 2	Homo sapiens	95-99
8573568-6	1996	Residues 39-46 of the active-site loop of the C-domain become disordered upon NAD binding, suggesting a potential role for this loop in the recognition of the ADP-ribose acceptor substrate, EF-2.	NAD	78-81	eukaryotic translation elongation factor 2	Homo sapiens	190-194
11666971-11	1996	The substrate-induced enzymatic perturbation of electron density at C-4 of NAD(+) quantitatively accounts for its increase in reactivity at the active site, but the perturbation at N-1 is less closely correlated with reactivity.	NAD	75-81	complement C4A (Rodgers blood group)	Homo sapiens	68-71
8538347-8	1996	NAD-dependent 11 beta-HSD activity was severely attenuated in the stillbirth placenta compared with control placental tissue, and no 11 beta-HSD immunostaining was observed in this placenta with antisera derived against a C-terminal 11 beta-HSD2 peptide sequence.	NAD	0-3	hydroxysteroid 11-beta dehydrogenase 2	Homo sapiens	14-21
8530456-2	1995	CD38 is a lymphocyte differentiation antigen which has recently been shown to be a bifunctional enzyme that can synthesize cADPR from NAD+ as well as hydrolyze cADPR to ADP-ribose.	NAD	134-138	CD38 molecule	Homo sapiens	0-4
8547170-3	1995	In the kidney it is the NAD dependent high affinity isoform (11 beta-HSD2) which is thought to endow specificity on the receptor.	NAD	24-27	hydroxysteroid 11-beta dehydrogenase 2	Homo sapiens	61-73
8653076-0	1995	The reducing ability of iron chelates by NADH-cytochrome B5 reductase or cytochrome B5 responsible for NADH-supported lipid peroxidation.	NAD	41-45	cytochrome b5 type A	Homo sapiens	46-59
7641178-1	1995	We have used two different approaches to study the consequences of NAD/poly(ADP-ribose) deficiency on p53 expression and its activity in V79-derived cell lines.	NAD	67-70	cellular tumor antigen p53	Cricetulus griseus	102-105
7641178-3	1995	In a second approach, we have used a cell line that is deficient in NAD/pADPR metabolism due to unavailability of NAD, the substrate for PARP.	NAD	68-71	poly [ADP-ribose] polymerase 1	Cricetulus griseus	137-141
7657650-5	1995	NAD(+)-activated CuBP has high SAHH enzymatic activity.	NAD	0-6	S-adenosylhomocysteine hydrolase	Mus musculus	17-21
7657650-5	1995	NAD(+)-activated CuBP has high SAHH enzymatic activity.	NAD	0-6	adenosylhomocysteinase	Homo sapiens	31-35
7619835-6	1995	Biophys Acta 974 (1989) 311-320), which predicts that Complex I is a heterodimer with promoter B, containing FMN and Fe-S clusters 1-4 in stiochiometric amounts, catalyzing NADH oxidation at pH 8, and Protomer A, containing FMN and Fe-S clusters 2, 4, catalyzing NAD(P)H oxidation at pH 6.5.	NAD	173-177	formin 1	Homo sapiens	109-112
7619835-6	1995	Biophys Acta 974 (1989) 311-320), which predicts that Complex I is a heterodimer with promoter B, containing FMN and Fe-S clusters 1-4 in stiochiometric amounts, catalyzing NADH oxidation at pH 8, and Protomer A, containing FMN and Fe-S clusters 2, 4, catalyzing NAD(P)H oxidation at pH 6.5.	NAD	173-177	formin 1	Homo sapiens	224-227
7763246-1	1995	The coenzyme binding site of NAD(+)-dependent 3-isopropylmalate dehydrogenase from Thermus thermophilus was analyzed by chemical modification and site-directed mutagenesis, and His273 of the enzyme was identified to be involved in the coenzyme binding.	NAD	29-35	3-isopropylmalate dehydrogenase	Thermus thermophilus HB8	46-77
7744774-10	1995	However, failure of sodium borohydride to reduce the bound NAD in the NBS-inactivated epimerase suggests that the reactive tryptophans are close to the coenzyme.	NAD	59-62	nibrin	Homo sapiens	70-73
7744774-11	1995	Tryptophan fluorescence lifetime values of 1.9 and 3.9 ns for the native and 3.5 ns for the NBS-modified epimerase, complemented by a linear Stern-Volmer plot (effective Stern-Volmer constant = 2.85 M-1) of acrylamide quenching, suggest that the two key tryptophans are buried close to an intrinsic quencher, presumably NAD.	NAD	320-323	nibrin	Homo sapiens	92-95
7763299-5	1995	The rate of NAD+ deletion induced by tert-butyl hydroperoxide (500 microM) and 2,3-dimethoxy-1,4-naphthoquinone (50 microM) was reduced by preincubating the hepatocytes for 1 hr with either 3-aminobenzamide (20 mM), nicotinamide (10 mM) or theophylline (7.5 mM), potent inhibitors of poly(ADP-ribose)polymerase.	NAD	12-16	poly (ADP-ribose) polymerase 1	Rattus norvegicus	284-310
7763299-9	1995	These results suggest that during oxidative stress, NAD+ is hydrolysed to nicotinamide, possibly by the activation of poly(ADP-ribose)polymerase and that the depletion of NAD+ is independent of the increase in NADP+.	NAD	52-56	poly (ADP-ribose) polymerase 1	Rattus norvegicus	118-144
7607668-0	1995	Molecular cloning and characterization of the active human mitochondrial NADH:ubiquinone oxidoreductase 24-kDa gene (NDUFV2) and its pseudogene.	NAD	73-77	NADH:ubiquinone oxidoreductase core subunit V2	Homo sapiens	117-123
7869031-9	1995	It is known that CD38 catalyzes nicotinamide adenine dinucleotide (NAD+) hydrolysis into cyclic ADP-ribose (cADPR) and ADPR.	NAD	32-65	CD38 molecule	Homo sapiens	17-21
7869031-9	1995	It is known that CD38 catalyzes nicotinamide adenine dinucleotide (NAD+) hydrolysis into cyclic ADP-ribose (cADPR) and ADPR.	NAD	67-71	CD38 molecule	Homo sapiens	17-21
7803457-6	1994	By comparison with xanthine dehydrogenase it can be predicted that the molybdenum cofactor binds to the large subunit of CODH, the small subunit of CODH contains the iron-sulphur centers and the medium subunit binds FAD/NAD+.	NAD	220-224	rosy	Drosophila melanogaster	19-41
7982936-6	1994	The overall reaction catalyzed by CD38 is the formation of ADP-ribose and nicotinamide from NAD+, identical to that catalyzed by NADase.	NAD	92-96	CD38 molecule	Homo sapiens	34-38
7898455-2	1994	The enzyme transfers ADP-ribose from NAD to elongation factor 2, inactivating the factor and thus inhibiting in vitro protein synthesis.	NAD	37-40	eukaryotic translation elongation factor 2	Homo sapiens	44-63
8060361-2	1994	When CD38, purified to homogeneity from human erythrocyte membranes, was incubated with NAD+ or beta-mercaptoethanol, extensive aggregation took place.	NAD	88-92	CD38 molecule	Homo sapiens	5-9
8060361-4	1994	Extensive and stable CD38 self-aggregation was shown by, i) SDS-PAGE and autoradiography of the [32P]NAD(+)-incubated CD38, ii) SDS-PAGE followed by immunochemical detection of CD38 on the transblots, iii) direct electron microscopy on negatively stained CD38 samples.	NAD	101-107	CD38 molecule	Homo sapiens	21-25
8060361-4	1994	Extensive and stable CD38 self-aggregation was shown by, i) SDS-PAGE and autoradiography of the [32P]NAD(+)-incubated CD38, ii) SDS-PAGE followed by immunochemical detection of CD38 on the transblots, iii) direct electron microscopy on negatively stained CD38 samples.	NAD	101-107	CD38 molecule	Homo sapiens	118-122
8060361-4	1994	Extensive and stable CD38 self-aggregation was shown by, i) SDS-PAGE and autoradiography of the [32P]NAD(+)-incubated CD38, ii) SDS-PAGE followed by immunochemical detection of CD38 on the transblots, iii) direct electron microscopy on negatively stained CD38 samples.	NAD	101-107	CD38 molecule	Homo sapiens	118-122
8060361-4	1994	Extensive and stable CD38 self-aggregation was shown by, i) SDS-PAGE and autoradiography of the [32P]NAD(+)-incubated CD38, ii) SDS-PAGE followed by immunochemical detection of CD38 on the transblots, iii) direct electron microscopy on negatively stained CD38 samples.	NAD	101-107	CD38 molecule	Homo sapiens	118-122
7520697-9	1994	A 1 mM concentration of NADPH or NADH greatly increased the extent of double-strand breakage by 0.01 microM FeBlm, suggesting roles for cytochrome P450 or cytochrome b5 reductase in strand breakage.	NAD	33-37	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	136-151
7882155-2	1994	In this study, we propose that domain III, common to the hsp60s and hsp70s is also found in the hsp90s and adopts a beta-alpha-beta Rossmann-folded structure which is encountered in the NAD-binding domain of dehydrogenases.	NAD	186-189	heat shock protein 90 alpha family class A member 1	Homo sapiens	96-101
8041359-0	1994	The 42.5 kDa subunit of the NADH: ubiquinone oxidoreductase (complex I) in higher plants is encoded by the mitochondrial nad7 gene.	NAD	28-32	nad7	Triticum aestivum	121-125
7920253-1	1994	The primary structure of bovine liver UDP-glucose dehydrogenase (UDPGDH), a hexameric, NAD(+)-linked enzyme, has been determined at the protein level.	NAD	87-93	UDP-glucose 6-dehydrogenase	Bos taurus	38-63
7920253-1	1994	The primary structure of bovine liver UDP-glucose dehydrogenase (UDPGDH), a hexameric, NAD(+)-linked enzyme, has been determined at the protein level.	NAD	87-93	UDP-glucose 6-dehydrogenase	Bos taurus	65-71
8020473-0	1994	A few amino acid substitutions are responsible for the higher thermostability of a novel NAD(+)-dependent bacillar alcohol dehydrogenase.	NAD	89-95	Alcohol dehydrogenase	Escherichia coli	115-136
8020473-1	1994	The gene adh-hT encoding a thermostable and thermophilic NAD(+)-dependent alcohol dehydrogenase (ADH) from the novel and more thermophilic Bacillus stearothermophilus LLD-R strain was cloned and its nucleotide sequence determined.	NAD	57-63	Alcohol dehydrogenase	Escherichia coli	9-12
8020473-1	1994	The gene adh-hT encoding a thermostable and thermophilic NAD(+)-dependent alcohol dehydrogenase (ADH) from the novel and more thermophilic Bacillus stearothermophilus LLD-R strain was cloned and its nucleotide sequence determined.	NAD	57-63	Alcohol dehydrogenase	Escherichia coli	74-95
8020473-1	1994	The gene adh-hT encoding a thermostable and thermophilic NAD(+)-dependent alcohol dehydrogenase (ADH) from the novel and more thermophilic Bacillus stearothermophilus LLD-R strain was cloned and its nucleotide sequence determined.	NAD	57-63	Alcohol dehydrogenase	Escherichia coli	97-100
8135539-2	1994	At first and in the unique but obligatory presence of NAD, the NAD kinase acts almost instantaneously as an oxido-reductase (probably coupled with the transformation of NAD to NADH).	NAD	54-57	NAD kinase	Homo sapiens	63-73
8135539-2	1994	At first and in the unique but obligatory presence of NAD, the NAD kinase acts almost instantaneously as an oxido-reductase (probably coupled with the transformation of NAD to NADH).	NAD	176-180	NAD kinase	Homo sapiens	63-73
8132465-5	1994	In vitro experiments showed that ArcB phosphorylation is enhanced by pyruvate, D-lactate, acetate, and NADH, the concentrations of which are likely to increase with the lack of an effective exogenous electron sink.	NAD	103-107	hypothetical protein	Escherichia coli	33-37
8299570-1	1994	3 beta-Hydroxy-5-ene-steroid dehydrogenase/delta 5-delta 4-isomerase (3 beta HSD) is a NAD(+)-dependent membrane-bound enzyme that catalyzes the oxidation of delta 5-3 beta-hydroxysteroids to delta 4-3-keto structures during adrenal, gonadal, and placental steroidogenesis.	NAD	87-93	3 beta-hydroxysteroid dehydrogenase/Delta 5-->4-isomerase	Bos taurus	70-80
8299570-5	1994	In contrast, mitochondrial 3 beta HSD used matrix space NAD+, was inhibited by reduction of intramitochondrial NAD(P)+, and was insensitive to mersalyl.	NAD	56-60	3 beta-hydroxysteroid dehydrogenase/Delta 5-->4-isomerase	Bos taurus	27-37
8299570-10	1994	Both groups of submitochondrial particles required exogenous NAD+ for 3 beta HSD activity, indicating that the active site faced the medium (the particles were everted), and the contained NAD+ was inside the particles.	NAD	61-65	3 beta-hydroxysteroid dehydrogenase/Delta 5-->4-isomerase	Bos taurus	70-80
8299570-10	1994	Both groups of submitochondrial particles required exogenous NAD+ for 3 beta HSD activity, indicating that the active site faced the medium (the particles were everted), and the contained NAD+ was inside the particles.	NAD	188-192	3 beta-hydroxysteroid dehydrogenase/Delta 5-->4-isomerase	Bos taurus	70-80
8299570-11	1994	However, 3 beta HSD activity was increased 12-140% in particles that contained NAD+.	NAD	79-83	3 beta-hydroxysteroid dehydrogenase/Delta 5-->4-isomerase	Bos taurus	9-19
8299570-14	1994	Mitochondrial 3 beta HSD activity may be enhanced by oxidation of intermembrane space NADH via an active rotenone- and antimycin-a-insensitive NADH oxidase.	NAD	86-90	3 beta-hydroxysteroid dehydrogenase/Delta 5-->4-isomerase	Bos taurus	14-24
8258350-1	1993	The extracellular domain of the lymphocyte surface antigen CD38 has been recently shown to share a high sequence homology with a nicotinamide adenine dinucleotide (NAD+)-specific hydrolyzing enzyme cloned from the ovotestis of the gastropod Aplysia (E. States, D.J., Walseth, T.F., Lee, H. C., Trends Biochem.	NAD	129-162	CD38 molecule	Homo sapiens	59-63
8258350-1	1993	The extracellular domain of the lymphocyte surface antigen CD38 has been recently shown to share a high sequence homology with a nicotinamide adenine dinucleotide (NAD+)-specific hydrolyzing enzyme cloned from the ovotestis of the gastropod Aplysia (E. States, D.J., Walseth, T.F., Lee, H. C., Trends Biochem.	NAD	164-168	CD38 molecule	Homo sapiens	59-63
8258350-5	1993	In agreement with this finding, we present here evidence that CD38-overexpressing T cells, such as human thymocytes and cells from the human HPB-ALL T cell line, exhibit a NAD(+)-hydrolyzing enzymatic activity present on the outer surface of the cell membrane.	NAD	172-178	CD38 molecule	Homo sapiens	62-66
8258350-8	1993	Moreover, CD38 immunoprecipitates from thymocytes behave as an authentic NAD+ glycohydrolase enzyme: it transforms NAD+ stoichiometrically into nicotinamide plus adenosine 5"-diphosphoribose.	NAD	73-76	CD38 molecule	Homo sapiens	10-14
8258350-8	1993	Moreover, CD38 immunoprecipitates from thymocytes behave as an authentic NAD+ glycohydrolase enzyme: it transforms NAD+ stoichiometrically into nicotinamide plus adenosine 5"-diphosphoribose.	NAD	73-77	CD38 molecule	Homo sapiens	10-14
8258350-9	1993	Altogether these results strongly support the assumption that CD38 is actually a lymphocyte-specific NAD(+)-hydrolyzing enzyme, a finding that give new prospects to understand the in vivo function of this cell membrane protein.	NAD	101-107	CD38 molecule	Homo sapiens	62-66
8216372-1	1993	The product formed from 4-nitroquinoline 1-oxide (4NQO), a potent carcinogen, by the action of mouse NADH:4NQO nitroreductase NR-1 was directly identified as 4-hydroxyaminoquinoline 1-oxide (4HAQO) by high performance liquid chromatography analyses in two systems.	NAD	101-105	glutamate receptor, ionotropic, NMDA1 (zeta 1)	Mus musculus	126-130
8217828-5	1993	Vitamin K epoxide reductase activity stimulated by NADH/lipoamide and microsomal lipoamide dehydrogenase activity showed higher inter-subject variability than the reductase activity by itself.	NAD	51-55	vitamin K epoxide reductase complex subunit 1	Homo sapiens	0-27
8336204-1	1993	The niacin cofactor, NAD, is the substrate for poly(ADP-ribose) polymerase, an enzyme associated with DNA repair.	NAD	21-24	poly (ADP-ribose) polymerase 1	Rattus norvegicus	47-74
8336204-5	1993	The hepatic poly(ADP-ribose) polymerase activity was decreased in one experiment when mean hepatic NAD concentrations were 0.60 and 0.51 mumol/g at d 34 and d 60, respectively, compared with 0.77 and 0.80 mumol/g in pair-fed controls.	NAD	99-102	poly (ADP-ribose) polymerase 1	Rattus norvegicus	12-39
8475096-4	1993	The PARP protein of 994 amino acids contains two zinc-finger motifs and an NAD-binding motif, which are conserved among different species.	NAD	75-78	Poly-(ADP-ribose) polymerase	Drosophila melanogaster	4-8
8428969-2	1993	This was shown in experiments in which oxygen consumption was measured during redox cycling of the altered myoglobin in the presence of ascorbate or an enzymatic reducing system containing diaphorase and NADH.	NAD	204-208	myoglobin	Homo sapiens	107-116
8416969-2	1993	The stereochemistry and kinetics for hydrogen transfer to the catalytically essential NAD+ of S-adenosylhomocysteine hydrolase (SAHase) have been determined for selected adenosine analogues.	NAD	86-90	adenosylhomocysteinase	Homo sapiens	94-126
8416969-2	1993	The stereochemistry and kinetics for hydrogen transfer to the catalytically essential NAD+ of S-adenosylhomocysteine hydrolase (SAHase) have been determined for selected adenosine analogues.	NAD	86-90	adenosylhomocysteinase	Homo sapiens	128-134
8416969-3	1993	Reduced SAHase (ENADH), which was made by reconstituting apoSAHase with NADH, stereospecifically transferred the pro-R hydrogen of NADH to 3"-ketoadenosine, a proposed reaction intermediate.	NAD	17-21	adenosylhomocysteinase	Homo sapiens	8-14
8416969-3	1993	Reduced SAHase (ENADH), which was made by reconstituting apoSAHase with NADH, stereospecifically transferred the pro-R hydrogen of NADH to 3"-ketoadenosine, a proposed reaction intermediate.	NAD	72-76	adenosylhomocysteinase	Homo sapiens	8-14
1441742-5	1992	For example, in the present study colonies were screened for the presence of elongation factor 2 (EF-2) that can be [32P]ADP-ribosylated by diphtheria toxin and [32P]NAD+.	NAD	166-170	elongation factor 2	Saccharomyces cerevisiae S288C	77-96
1441742-5	1992	For example, in the present study colonies were screened for the presence of elongation factor 2 (EF-2) that can be [32P]ADP-ribosylated by diphtheria toxin and [32P]NAD+.	NAD	166-170	elongation factor 2	Saccharomyces cerevisiae S288C	98-102
1508955-1	1992	NAD(+)-dependent 15-hydroxyprostaglandin dehydrogenase (15-PGDH) is a key enzyme involved in the catabolism of the prostaglandins.	NAD	0-6	15-hydroxyprostaglandin dehydrogenase	Homo sapiens	56-63
16668941-6	1992	The purified cytochrome c reductase, which had a major size of 43 kilodaltons, was inhibited by polyclonal antibodies for maize leaf NADH:nitrate reductase and bound these antibodies when blotted to nitrocellulose.	NAD	133-137	nitrate reductase [NADH] 1	Zea mays	138-155
16668941-7	1992	Ultraviolet and visible spectra of oxidized and NADH-reduced recombinant cytochrome c reductase were nearly identical with those of maize leaf NADH:nitrate reductase.	NAD	48-52	nitrate reductase [NADH] 1	Zea mays	148-165
1502256-1	1992	The specific activity of NAD(+)-dependent 15-hydroxyprostaglandin dehydrogenase (PGDH) was found to increase in the ovaries of pregnant and pseudopregnant rabbits.	NAD	25-31	15-hydroxyprostaglandin dehydrogenase	Homo sapiens	81-85
1350433-2	1992	An enzyme layer composed of glutamate dehydrogenase (GDH) and glutamate-pyruvate transaminase (GPT) is used to produce reduced nicotinamide adenine dinucleotide (NADH) at the tip of a fiber-optic probe.	NAD	127-160	glutamate dehydrogenase 1	Homo sapiens	28-51
1350433-2	1992	An enzyme layer composed of glutamate dehydrogenase (GDH) and glutamate-pyruvate transaminase (GPT) is used to produce reduced nicotinamide adenine dinucleotide (NADH) at the tip of a fiber-optic probe.	NAD	127-160	glutamate dehydrogenase 1	Homo sapiens	53-56
1350433-2	1992	An enzyme layer composed of glutamate dehydrogenase (GDH) and glutamate-pyruvate transaminase (GPT) is used to produce reduced nicotinamide adenine dinucleotide (NADH) at the tip of a fiber-optic probe.	NAD	162-166	glutamate dehydrogenase 1	Homo sapiens	28-51
1350433-2	1992	An enzyme layer composed of glutamate dehydrogenase (GDH) and glutamate-pyruvate transaminase (GPT) is used to produce reduced nicotinamide adenine dinucleotide (NADH) at the tip of a fiber-optic probe.	NAD	162-166	glutamate dehydrogenase 1	Homo sapiens	53-56
1350433-4	1992	GDH catalyzes the formation of NADH, and GPT drives the GDH reaction by removing a reaction product and regenerating glutamate.	NAD	31-35	glutamate dehydrogenase 1	Homo sapiens	0-3
1635910-2	1992	This is due to the presence of large quantities of the NAD(+)-linked 15-hydroxy-prostaglandin dehydrogenase (PGDH type I; EC 1.1.1.141).	NAD	55-61	15-hydroxyprostaglandin dehydrogenase	Homo sapiens	109-113
1612526-1	1992	Localization of NAD(+)-dependent 15-hydroxy prostaglandin dehydrogenase (type I-PGDH) may influence local concentrations of bioactive eicosanoids within intrauterine tissues.	NAD	16-22	15-hydroxyprostaglandin dehydrogenase	Homo sapiens	80-84
1959619-0	1991	Electron transfer properties of NADH:ubiquinone reductase in the ND1/3460 and the ND4/11778 mutations of the Leber hereditary optic neuroretinopathy (LHON).	NAD	32-36	mitochondrially encoded NADH dehydrogenase 4	Homo sapiens	82-85
1959619-6	1991	However, in isolated mitochondria with the ND4 mutation, the rate of oxidation of NAD-linked substrates, but not of succinate, was significantly decreased.	NAD	82-85	mitochondrially encoded NADH dehydrogenase 4	Homo sapiens	43-46
1896463-1	1991	The three-dimensional structure of human beta 1 beta 1 alcohol dehydrogenase (ADH; EC 1.1.1.1) complexed with NAD+ has been determined by x-ray crystallography to 3.0-A resolution.	NAD	110-114	alcohol dehydrogenase 1A (class I), alpha polypeptide	Homo sapiens	78-81
1782265-6	1991	The control coefficient for ANT is higher, while that of proton leakage is lower at the same relative rates of respiration with NAD-dependent substrates compared with succinate.	NAD	128-131	solute carrier family 25 member 6	Homo sapiens	28-31
2071302-7	1991	Stabilization of IL-2-PE40 at 37 degrees C for the continuous administration by pumps was achieved by adding NAD, the substrate for the enzyme portion of the chimeric toxin.	NAD	109-112	interleukin 2	Rattus norvegicus	17-21
2264826-4	1990	The cytochrome b5 was reduced in the membrane preparations by NADH, demonstrating the presence of an NADH: cytochrome b5 reductase; NADPH was a less effective donor.	NAD	62-66	cytochrome b5 type A	Homo sapiens	4-17
2264826-4	1990	The cytochrome b5 was reduced in the membrane preparations by NADH, demonstrating the presence of an NADH: cytochrome b5 reductase; NADPH was a less effective donor.	NAD	62-66	cytochrome b5 type A	Homo sapiens	107-120
2264826-4	1990	The cytochrome b5 was reduced in the membrane preparations by NADH, demonstrating the presence of an NADH: cytochrome b5 reductase; NADPH was a less effective donor.	NAD	101-105	cytochrome b5 type A	Homo sapiens	4-17
2264826-4	1990	The cytochrome b5 was reduced in the membrane preparations by NADH, demonstrating the presence of an NADH: cytochrome b5 reductase; NADPH was a less effective donor.	NAD	101-105	cytochrome b5 type A	Homo sapiens	107-120
2264826-7	1990	The addition of oleoyl-CoA to the NADH-reduced membranes resulted in the CN(-)-sensitive partial re-oxidation of cytochrome b5, indicating that electrons from NADH were transferred to the site of desaturation via this cytochrome.	NAD	34-38	cytochrome b5 type A	Homo sapiens	113-126
2264826-7	1990	The addition of oleoyl-CoA to the NADH-reduced membranes resulted in the CN(-)-sensitive partial re-oxidation of cytochrome b5, indicating that electrons from NADH were transferred to the site of desaturation via this cytochrome.	NAD	159-163	cytochrome b5 type A	Homo sapiens	113-126
2264826-8	1990	The delta 12-desaturase in safflower, therefore, is CN(-)-sensitive and appears to require cytochrome b5 and NADH: cytochrome b5 reductase for activity.	NAD	109-113	cytochrome b5 type A	Homo sapiens	115-128
2121277-0	1990	Characterization and reconstitution of a cell free system for NAD(+)-dependent deoxyhypusine formation on the 18 kDa eIF-4D precursor.	NAD	62-68	eukaryotic translation initiation factor 5A	Homo sapiens	117-123
2369123-10	1990	In the presence of Triton X-100, divalent cations were inhibitory in NADH-dependent cytochrome b5 reduction, and in contrast, stimulative in NADPH-dependent reaction.	NAD	69-73	cytochrome b5 type A	Homo sapiens	84-97
2369123-11	1990	These findings suggest that the activation of cytochrome b5 reduction by divalent cations in the NADH system is mainly due to an increasing accessibility of the substrate, and in the NADPH system, in addition to this, a direct effect of divalent cations on NADPH-cytochrome P450 reductase is also involved.	NAD	97-101	cytochrome b5 type A	Homo sapiens	46-59
2372048-5	1990	These metabolites participate in the glutamate dehydrogenase (GDH) reaction, which, based on a number of assumptions, theoretically enables calculation of the mitochondrial redox state as follows (brackets indicate concentrations): [NAD+]/[NADH] = ([NH+4] [2-OG])/[( Glu]Kapp), where Kapp is the apparent equilibrium constant for GDH.	NAD	233-237	glutamate dehydrogenase 1	Homo sapiens	37-60
2372048-5	1990	These metabolites participate in the glutamate dehydrogenase (GDH) reaction, which, based on a number of assumptions, theoretically enables calculation of the mitochondrial redox state as follows (brackets indicate concentrations): [NAD+]/[NADH] = ([NH+4] [2-OG])/[( Glu]Kapp), where Kapp is the apparent equilibrium constant for GDH.	NAD	233-237	glutamate dehydrogenase 1	Homo sapiens	62-65
2372048-5	1990	These metabolites participate in the glutamate dehydrogenase (GDH) reaction, which, based on a number of assumptions, theoretically enables calculation of the mitochondrial redox state as follows (brackets indicate concentrations): [NAD+]/[NADH] = ([NH+4] [2-OG])/[( Glu]Kapp), where Kapp is the apparent equilibrium constant for GDH.	NAD	240-244	glutamate dehydrogenase 1	Homo sapiens	37-60
2372048-5	1990	These metabolites participate in the glutamate dehydrogenase (GDH) reaction, which, based on a number of assumptions, theoretically enables calculation of the mitochondrial redox state as follows (brackets indicate concentrations): [NAD+]/[NADH] = ([NH+4] [2-OG])/[( Glu]Kapp), where Kapp is the apparent equilibrium constant for GDH.	NAD	240-244	glutamate dehydrogenase 1	Homo sapiens	62-65
2372048-5	1990	These metabolites participate in the glutamate dehydrogenase (GDH) reaction, which, based on a number of assumptions, theoretically enables calculation of the mitochondrial redox state as follows (brackets indicate concentrations): [NAD+]/[NADH] = ([NH+4] [2-OG])/[( Glu]Kapp), where Kapp is the apparent equilibrium constant for GDH.	NAD	240-244	glutamate dehydrogenase 1	Homo sapiens	330-333
16667591-3	1990	Two forms of NR were identified, an NADH monospecific NR found mainly in the 1cm root tip and an NAD(P)H bispecific NR found predominantly in mature regions of the root.	NAD	36-40	nitrate reductase [NADH] 1	Zea mays	13-15
2107882-7	1990	These observations suggest that replacement of Pro-127 causes a significant conformation change in the nucleotide-binding domain that affects electron transport from NADH to cytochrome b5.	NAD	166-170	cytochrome b5 type A	Homo sapiens	174-187
2341026-2	1990	Furthermore, the activation of PLA2 induced by the H-toxin was enhanced in the presence of NAD.	NAD	91-94	phospholipase A2	Oryctolagus cuniculus	31-35
33805250-10	2021	Based on the in vivo, ex vivo, and molecular evaluations, we identified that the deletion of Kvbeta2 altered the cardiac pathophysiology mediated by SLC41a3 and altered the NAD (nicotinamide adenine dinucleotide)-dependent gene responses.	NAD	173-176	potassium voltage-gated channel, shaker-related subfamily, beta member 2	Mus musculus	93-100
33805250-10	2021	Based on the in vivo, ex vivo, and molecular evaluations, we identified that the deletion of Kvbeta2 altered the cardiac pathophysiology mediated by SLC41a3 and altered the NAD (nicotinamide adenine dinucleotide)-dependent gene responses.	NAD	178-211	potassium voltage-gated channel, shaker-related subfamily, beta member 2	Mus musculus	93-100
34619358-1	2022	Malate dehydrogenase (MDH) catalyzes the conversion of NAD+ and malate to NADH and oxaloacetate in the citric acid cycle.	NAD	55-59	Malate dehydrogenase	Caenorhabditis elegans	0-20
34619358-1	2022	Malate dehydrogenase (MDH) catalyzes the conversion of NAD+ and malate to NADH and oxaloacetate in the citric acid cycle.	NAD	55-59	Malate dehydrogenase	Caenorhabditis elegans	22-25
34619358-1	2022	Malate dehydrogenase (MDH) catalyzes the conversion of NAD+ and malate to NADH and oxaloacetate in the citric acid cycle.	NAD	74-78	Malate dehydrogenase	Caenorhabditis elegans	0-20
34619358-1	2022	Malate dehydrogenase (MDH) catalyzes the conversion of NAD+ and malate to NADH and oxaloacetate in the citric acid cycle.	NAD	74-78	Malate dehydrogenase	Caenorhabditis elegans	22-25
34619358-5	2022	In steady-state enzyme kinetics assays, we measured KM values for oxaloacetate of 54 and 52 muM and KM values for NADH of 61 and 107 muM for MDH-1 and MDH-2, respectively.	NAD	114-118	Malate dehydrogenase	Caenorhabditis elegans	141-146
34896700-1	2022	CD38 is a single-pass transmembrane enzyme catalyzing the synthesis of two nucleotide second messengers, cyclic ADP-ribose (cADPR) from NAD and nicotinic acid adenine dinucleotide phosphate (NAADP) from NADP.	NAD	136-139	CD38 molecule	Homo sapiens	0-4
34494892-9	2022	The authors discuss a critical but under-appreciated trifecta of CD38-mediated NAD+ metabolism, aging, and COVID-19 immune response and speculate that the CD38/NAD+ axis is a promising therapeutic target for this disease (2).	NAD	79-83	CD38 molecule	Homo sapiens	65-69
34494892-9	2022	The authors discuss a critical but under-appreciated trifecta of CD38-mediated NAD+ metabolism, aging, and COVID-19 immune response and speculate that the CD38/NAD+ axis is a promising therapeutic target for this disease (2).	NAD	160-164	CD38 molecule	Homo sapiens	65-69
34928817-0	2021	NAD+ improved experimental autoimmune encephalomyelitis by regulating SIRT1 to inhibit PI3K/Akt/mTOR signaling pathway.	NAD	0-4	sirtuin 1	Mus musculus	70-75
34928817-0	2021	NAD+ improved experimental autoimmune encephalomyelitis by regulating SIRT1 to inhibit PI3K/Akt/mTOR signaling pathway.	NAD	0-4	mechanistic target of rapamycin kinase	Mus musculus	96-100
34928817-1	2021	OBJECTIVE: To investigate the effect of NAD+ on thymus autophagy in experimental autoimmune encephalomyelitis (EAE) mice through SIRT1.	NAD	40-44	sirtuin 1	Mus musculus	129-134
34928817-10	2021	RESULTS: Enrichment analysis showed PI3K-Akt-mTOR and autophagy pathway were main terms in EAE diseases, and the relationship between NAD+ and SIRT1.	NAD	134-138	mechanistic target of rapamycin kinase	Mus musculus	45-49
34928817-10	2021	RESULTS: Enrichment analysis showed PI3K-Akt-mTOR and autophagy pathway were main terms in EAE diseases, and the relationship between NAD+ and SIRT1.	NAD	134-138	sirtuin 1	Mus musculus	143-148
34928817-11	2021	The activation of p-PI3K, p-Akt and p-mTOR were the highest in the EAE group consistent with decreased P62, Beclin1, LC-3A/B and SIRT1, and NAD+ reversed these results, furthermore SIRT1 inhibitor: SIRT-IN3 weakened the NAD+" effects in both in vivo and in vitro experiments.	NAD	140-144	sirtuin 1	Mus musculus	181-186
34928817-11	2021	The activation of p-PI3K, p-Akt and p-mTOR were the highest in the EAE group consistent with decreased P62, Beclin1, LC-3A/B and SIRT1, and NAD+ reversed these results, furthermore SIRT1 inhibitor: SIRT-IN3 weakened the NAD+" effects in both in vivo and in vitro experiments.	NAD	220-224	sirtuin 1	Mus musculus	181-186
34928817-13	2021	CONCLUSIONS: NAD+ exerted a protective effect on EAE mice by inhibiting PI3K/Akt/mTOR signaling pathway through SIRT1 in TECs, and prevented EAE mice from sustained damage.	NAD	13-17	mechanistic target of rapamycin kinase	Mus musculus	81-85
34928817-13	2021	CONCLUSIONS: NAD+ exerted a protective effect on EAE mice by inhibiting PI3K/Akt/mTOR signaling pathway through SIRT1 in TECs, and prevented EAE mice from sustained damage.	NAD	13-17	sirtuin 1	Mus musculus	112-117
34938344-0	2021	Jian-Pi-Yi-Shen Formula Alleviates Chronic Kidney Disease in Two Rat Models by Modulating QPRT/NAD+/SIRT3/Mitochondrial Dynamics Pathway.	NAD	95-99	sirtuin 3	Rattus norvegicus	100-105
34938344-11	2021	In addition, CKD rats exhibited suppressed QPRT/NAD+/SIRT3 signal, increased mitochondrial fission, and decreased mitochondrial fusion.	NAD	48-52	sirtuin 3	Rattus norvegicus	53-58
34950703-4	2021	We have previously reported that in unstressed cardiomyocytes exogenous NAD+ resulted in a time and dose dependent decrease in O-GlcNAc levels.	NAD	72-76	O-linked N-acetylglucosamine (GlcNAc) transferase	Homo sapiens	127-135
34950703-6	2021	Using glucose deprivation as a model system in an immortalized human ventricular cell line, we examined the influence of extracellular NAD+ on cellular O-GlcNAc levels and ER stress in the presence and absence of glucose.	NAD	135-139	O-linked N-acetylglucosamine (GlcNAc) transferase	Homo sapiens	152-160
34950703-7	2021	We found that NAD+ completely blocked the increase in O-GlcNAc induced by glucose deprivation and suppressed the activation of ER stress.	NAD	14-18	O-linked N-acetylglucosamine (GlcNAc) transferase	Homo sapiens	54-62
34925016-3	2021	Sirtuin2 (Sirt2), a nicotinamide adenine dinucleotide (NAD)-dependent deacetylase, has been proved to be involved in the fibrosis and inflammation in the liver, kidney and heart.	NAD	20-53	sirtuin 2	Homo sapiens	0-8
34925016-3	2021	Sirtuin2 (Sirt2), a nicotinamide adenine dinucleotide (NAD)-dependent deacetylase, has been proved to be involved in the fibrosis and inflammation in the liver, kidney and heart.	NAD	20-53	sirtuin 2	Homo sapiens	10-15
34925016-3	2021	Sirtuin2 (Sirt2), a nicotinamide adenine dinucleotide (NAD)-dependent deacetylase, has been proved to be involved in the fibrosis and inflammation in the liver, kidney and heart.	NAD	55-58	sirtuin 2	Homo sapiens	0-8
34925016-3	2021	Sirtuin2 (Sirt2), a nicotinamide adenine dinucleotide (NAD)-dependent deacetylase, has been proved to be involved in the fibrosis and inflammation in the liver, kidney and heart.	NAD	55-58	sirtuin 2	Homo sapiens	10-15
34975119-0	2021	Nicotinamide adenine dinucleotide promotes synaptic plasticity gene expression through regulation N-methyl-D-aspartate receptor/Ca2+/Erk1/2 pathway.	NAD	0-33	glutamate receptor, ionotropic, NMDA1 (zeta 1)	Mus musculus	98-127
34975119-2	2021	To explore the contribution and the underlying mechanisms of NADH regulating synaptic plasticity, here, we examined NADH"s effect on immediate-early response genes (IEGs) expressions, including C-Fos and Arc in primary cultured cortical neurons and the frontal cortex of mouse brain.	NAD	61-65	FBJ osteosarcoma oncogene	Mus musculus	194-199
34975119-2	2021	To explore the contribution and the underlying mechanisms of NADH regulating synaptic plasticity, here, we examined NADH"s effect on immediate-early response genes (IEGs) expressions, including C-Fos and Arc in primary cultured cortical neurons and the frontal cortex of mouse brain.	NAD	116-120	FBJ osteosarcoma oncogene	Mus musculus	194-199
34975119-3	2021	Our results showed that NADH promoted IEGs expression and that the C-Fos and Arc levels are increased in primary cultured cortical neurons, which is almost completely blocked by N-methyl-D-aspartate receptor (NMDAR) inhibitor, MK-801.	NAD	24-28	FBJ osteosarcoma oncogene	Mus musculus	67-72
34975119-3	2021	Our results showed that NADH promoted IEGs expression and that the C-Fos and Arc levels are increased in primary cultured cortical neurons, which is almost completely blocked by N-methyl-D-aspartate receptor (NMDAR) inhibitor, MK-801.	NAD	24-28	glutamate receptor, ionotropic, NMDA1 (zeta 1)	Mus musculus	178-207
34975119-3	2021	Our results showed that NADH promoted IEGs expression and that the C-Fos and Arc levels are increased in primary cultured cortical neurons, which is almost completely blocked by N-methyl-D-aspartate receptor (NMDAR) inhibitor, MK-801.	NAD	24-28	glutamate receptor, ionotropic, NMDA1 (zeta 1)	Mus musculus	209-214
34975119-4	2021	Moreover, NADH significantly increased intracellular Ca2+ levels and the phosphorylation of Erk1/2, a downstream molecule of the NMDAR.	NAD	10-14	glutamate receptor, ionotropic, NMDA1 (zeta 1)	Mus musculus	129-134
34975119-6	2021	In conclusion, this study indicates that NADH can promote the expression of synaptic plasticity-related IEGs through the NMDAR/Ca2+/Erk1/2 pathway, which provides a new way to understand the regulatory role of NADH in synaptic plasticity.	NAD	41-45	glutamate receptor, ionotropic, NMDA1 (zeta 1)	Mus musculus	121-126
34975119-6	2021	In conclusion, this study indicates that NADH can promote the expression of synaptic plasticity-related IEGs through the NMDAR/Ca2+/Erk1/2 pathway, which provides a new way to understand the regulatory role of NADH in synaptic plasticity.	NAD	210-214	glutamate receptor, ionotropic, NMDA1 (zeta 1)	Mus musculus	121-126
34666225-9	2021	A similar discrepancy between protein expression and enzymatic activity was observed for NAD-degrading CD38 on SLE B cells.	NAD	89-92	CD38 molecule	Homo sapiens	103-107
34619528-8	2021	Doxorubicin and IR caused metabolic changes with nicotinamide adenine dinucleotide depletion and ensuing mitochondrial stunning (reversible mitochondria dysfunction without showing any cell death under ATP depletion) via p90RSK-ERK5 modulation and poly (ADP-ribose) polymerase (PARP) activation, which formed a nucleus-mitochondria positive feedback loop.	NAD	49-82	ribosomal protein S6 kinase A1	Homo sapiens	221-227
34803499-10	2021	More importantly, Ex527 (Sirt1 inhibitor) and 3-TYP (Sirt3 inhibitor) significantly enhanced OA-induced lipid accumulation and oxidative stress in CD38-/- primary hepatocytes, suggesting that the anti-lipid accumulation of CD38 deficiency might be dependent on NAD/Sirtuins-mediated enhancement of FAA beta-oxidation and suppression of oxidative stress in hepatocytes.	NAD	261-264	sirtuin 1	Mus musculus	25-30
34803499-10	2021	More importantly, Ex527 (Sirt1 inhibitor) and 3-TYP (Sirt3 inhibitor) significantly enhanced OA-induced lipid accumulation and oxidative stress in CD38-/- primary hepatocytes, suggesting that the anti-lipid accumulation of CD38 deficiency might be dependent on NAD/Sirtuins-mediated enhancement of FAA beta-oxidation and suppression of oxidative stress in hepatocytes.	NAD	261-264	sirtuin 3	Mus musculus	53-58
34618304-6	2022	The effects of reduced nicotinamide adenine dinucleotide (NADH), an antioxidant compound, on purified ACE activity were also researched.	NAD	23-56	angiotensin-converting enzyme	Ovis aries	102-105
34618304-6	2022	The effects of reduced nicotinamide adenine dinucleotide (NADH), an antioxidant compound, on purified ACE activity were also researched.	NAD	58-62	angiotensin-converting enzyme	Ovis aries	102-105
34618304-7	2022	NADH on ACE activity showed an inhibition effect.	NAD	0-4	angiotensin-converting enzyme	Ovis aries	8-11
34464722-5	2021	ERbeta agonists DPN and ERB-041 attenuated P2X7R expression in macrophages from colitis rats and in a murine macrophage cell line (RAW264.7) in response to either lipopolysaccharide (LPS) or adenosine triphosphate (ATP).	NAD	16-19	estrogen receptor 2	Rattus norvegicus	0-6
34429771-5	2021	Sirtuin 2 (SIRT2), a primarily cytosolic nicotinamide adenine dinucleotide-dependent class III protein deacetylase, has been shown to catalyze the removal of acetyl groups from a wide range of proteins, including tubulin, ribonucleotide reductase regulatory subunit M2 and glucose-6-phosphate dehydrogenase.	NAD	41-74	sirtuin 2	Homo sapiens	0-9
34429771-5	2021	Sirtuin 2 (SIRT2), a primarily cytosolic nicotinamide adenine dinucleotide-dependent class III protein deacetylase, has been shown to catalyze the removal of acetyl groups from a wide range of proteins, including tubulin, ribonucleotide reductase regulatory subunit M2 and glucose-6-phosphate dehydrogenase.	NAD	41-74	sirtuin 2	Homo sapiens	11-16
34495320-2	2021	Here, we used Drosophila to identify whether cardiac Nmnat/NAD+/SIR2 pathways activation could mediate endurance exercise resistance to lipotoxic cardiomyopathy.	NAD	59-63	Nicotinamide mononucleotide adenylyltransferase	Drosophila melanogaster	53-58
34495320-2	2021	Here, we used Drosophila to identify whether cardiac Nmnat/NAD+/SIR2 pathways activation could mediate endurance exercise resistance to lipotoxic cardiomyopathy.	NAD	59-63	Sirtuin 1	Drosophila melanogaster	64-68
34495320-3	2021	The results showed that endurance exercise activated the cardiac Nmnat/NAD+/SIR2/FOXO pathway and Nmnat/NAD+/SIR2/PGC-1alpha pathway, including up-regulating cardiac Nmnat, SIR2, FOXO, PGC-1alpha expression, SOD activity, and NAD+ level, and it prevented HFD-induced or cardiac Nmnat knock-down-induced cardiac lipid accumulation, MDA content and fibrillation increase, and fractional shortening decrease.	NAD	226-230	Nicotinamide mononucleotide adenylyltransferase	Drosophila melanogaster	98-103
34495320-3	2021	The results showed that endurance exercise activated the cardiac Nmnat/NAD+/SIR2/FOXO pathway and Nmnat/NAD+/SIR2/PGC-1alpha pathway, including up-regulating cardiac Nmnat, SIR2, FOXO, PGC-1alpha expression, SOD activity, and NAD+ level, and it prevented HFD-induced or cardiac Nmnat knock-down-induced cardiac lipid accumulation, MDA content and fibrillation increase, and fractional shortening decrease.	NAD	226-230	Nicotinamide mononucleotide adenylyltransferase	Drosophila melanogaster	278-283
34495320-4	2021	Cardiac Nmnat overexpression also activated heart Nmnat/NAD+/SIR2 pathways and resisted HFD-induced cardiac malfunction, but it could not protect against HFD-induced lifespan reduction and locomotor impairment.	NAD	56-60	Nicotinamide mononucleotide adenylyltransferase	Drosophila melanogaster	8-13
34495320-6	2021	Therefore, current results confirmed that cardiac Nmnat/NAD+/SIR2 pathways were important antagonists of HFD-induced lipotoxic cardiomyopathy.	NAD	56-60	Nicotinamide mononucleotide adenylyltransferase	Drosophila melanogaster	50-55
34495320-6	2021	Therefore, current results confirmed that cardiac Nmnat/NAD+/SIR2 pathways were important antagonists of HFD-induced lipotoxic cardiomyopathy.	NAD	56-60	Sirtuin 1	Drosophila melanogaster	61-65
34497121-4	2021	Here, we report that levels of NAD+ are reduced and markers of inflammation increased in the brains of APP/PS1 mutant transgenic mice with beta-amyloid pathology.	NAD	31-35	presenilin 1	Mus musculus	107-110
34497121-5	2021	Treatment of APP/PS1 mutant mice with the NAD+ precursor nicotinamide riboside (NR) for 5 mo increased brain NAD+ levels, reduced expression of proinflammatory cytokines, and decreased activation of microglia and astrocytes.	NAD	42-46	presenilin 1	Mus musculus	17-20
34497121-5	2021	Treatment of APP/PS1 mutant mice with the NAD+ precursor nicotinamide riboside (NR) for 5 mo increased brain NAD+ levels, reduced expression of proinflammatory cytokines, and decreased activation of microglia and astrocytes.	NAD	109-113	presenilin 1	Mus musculus	17-20
34564436-0	2021	KLF15 Regulates Oxidative Stress Response in Cardiomyocytes through NAD.	NAD	68-71	Kruppel-like factor 15	Rattus norvegicus	0-5
34564436-7	2021	The resultant SIRT3-dependent hyperacetylation and the inactivation of mitochondrial antioxidants can be rescued by MnSOD mimetics or NAD+ precursors.	NAD	134-138	sirtuin 3	Rattus norvegicus	14-19
34564436-8	2021	Collectively, these findings suggest that KLF15 regulates cardiac ROS clearance through the regulation of NAD+ levels.	NAD	106-110	Kruppel-like factor 15	Rattus norvegicus	42-47
34378958-0	2021	An NAD-Specific 6-Hydroxy-3-Succinoyl-Semialdehyde-Pyridine Dehydrogenase from Nicotine-Degrading Agrobacterium tumefaciens Strain S33.	NAD	3-6	hydroxyacid dehydrogenase	Agrobacterium tumefaciens	60-73
34174704-10	2021	NAD+ intervention decreased pro-inflammatory cytokine mRNA and pro-apoptotic protein expression and enhanced anti-inflammatory cytokine mRNA expression and the SIRT1 signaling in the optic nerve and retina and regulated the Th1/Th17/Tregs immune response in the spleen.	NAD	0-4	sirtuin 1	Mus musculus	160-165
34174704-11	2021	In addition, EX-527 reversed the therapeutic effect of NAD+ on EAE, suggesting that NAD+ prevented MS-triggered ON by activating the SIRT1 signaling pathway.	NAD	55-59	sirtuin 1	Mus musculus	133-138
34174704-11	2021	In addition, EX-527 reversed the therapeutic effect of NAD+ on EAE, suggesting that NAD+ prevented MS-triggered ON by activating the SIRT1 signaling pathway.	NAD	84-88	sirtuin 1	Mus musculus	133-138
34723263-3	2021	Unexpectedly, photoinduced cleavage of DNA by C60-PEG 1 was much higher than that by C70-PEG 2 and 3 with higher absorption intensity, especially in the presence of an electron donor (NADH).	NAD	184-188	paternally expressed 3	Homo sapiens	85-100
34343089-4	2021	Using a transgenic model, we demonstrate that high levels of mice cardiomyocyte mtDNA damage cause a reduction in NAD+ levels due to extreme DNA repair activity, causing impaired activation of NAD+-dependent SIRT3.	NAD	114-118	sirtuin 3	Mus musculus	208-213
34343089-4	2021	Using a transgenic model, we demonstrate that high levels of mice cardiomyocyte mtDNA damage cause a reduction in NAD+ levels due to extreme DNA repair activity, causing impaired activation of NAD+-dependent SIRT3.	NAD	193-197	sirtuin 3	Mus musculus	208-213
34344935-4	2021	To establish the evolutionary history and divergence time of NAD-dependent IDH, we examined transcriptomic data from 195 eukaryotes (mostly animals).	NAD	61-64	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	75-78
34341193-1	2021	In many prokaryotes, the first step of threonine metabolism is catalysed by the enzyme threonine dehydrogenase (TDH), which uses NAD+ to oxidize its substrate to 2-amino-3-ketobutyrate.	NAD	129-133	L-threonine dehydrogenase (pseudogene)	Homo sapiens	112-115
34156979-5	2021	Mechanistically, Esrrg-deficient Treg cells presented with dysregulated mitochondria with decreased oxygen consumption as well as ATP and NAD+ production.	NAD	138-142	estrogen-related receptor gamma	Mus musculus	17-22
34112762-1	2021	CD38 is the main enzyme for nicotinamide adenine dinucleotide (NAD) degradation in mammalian cells.	NAD	28-61	CD38 molecule	Homo sapiens	0-4
34112762-1	2021	CD38 is the main enzyme for nicotinamide adenine dinucleotide (NAD) degradation in mammalian cells.	NAD	63-66	CD38 molecule	Homo sapiens	0-4
34766147-4	2021	Supplementing NAD+ intermediates can activate sirtuin deacylases (SIRT1-SIRT7), which regulates the benefits of exercise and dietary restriction, reduce the level of intracellular oxidative stress, and improve mitochondrial function, thereby reversing cell senescence.	NAD	14-18	sirtuin 1	Mus musculus	66-71
34108853-1	2021	As a type of nicotinamide adenine dinucleotide (NAD+)-dependent deacetylases, sirtuin 2 (SIRT2) is predominantly found in the cytoplasm of cells in the central nervous system (CNS), suggesting its potential role in neurological disorders.	NAD	13-46	sirtuin 2	Homo sapiens	78-87
34108853-1	2021	As a type of nicotinamide adenine dinucleotide (NAD+)-dependent deacetylases, sirtuin 2 (SIRT2) is predominantly found in the cytoplasm of cells in the central nervous system (CNS), suggesting its potential role in neurological disorders.	NAD	13-46	sirtuin 2	Homo sapiens	89-94
34108853-1	2021	As a type of nicotinamide adenine dinucleotide (NAD+)-dependent deacetylases, sirtuin 2 (SIRT2) is predominantly found in the cytoplasm of cells in the central nervous system (CNS), suggesting its potential role in neurological disorders.	NAD	48-51	sirtuin 2	Homo sapiens	78-87
34108853-1	2021	As a type of nicotinamide adenine dinucleotide (NAD+)-dependent deacetylases, sirtuin 2 (SIRT2) is predominantly found in the cytoplasm of cells in the central nervous system (CNS), suggesting its potential role in neurological disorders.	NAD	48-51	sirtuin 2	Homo sapiens	89-94
35367825-1	2022	The mitochondrial enzyme SIRT3 is an NAD+-dependent deacetylase important in cell metabolism, and a decline in its protein expression or activity has been linked with insulin resistance in obesity, ageing and type 2 diabetes.	NAD	37-40	sirtuin 3	Mus musculus	25-30
35287177-9	2022	Plasma neuroexosomal NADH ubiquinone oxidoreductase core subunit S3 (NDUFS3) and succinate dehydrogenase complex subunit B (SDHB) levels were significantly lower in T2DM patients with AD dementia and progressive MCI than in cognitively normal subjects (P < 0.001 for both groups).	NAD	21-25	NADH:ubiquinone oxidoreductase core subunit S3	Homo sapiens	69-75
35622273-10	2022	Estrogen and DPN also led to GFAP upregulation in OVX mice.	NAD	13-16	glial fibrillary acidic protein	Mus musculus	29-33
35622273-11	2022	However, the effect of estrogen and DPN in activating astrocytes was lost in Ndrg2 knockout OVX mice and primary cultured astrocytes, but partially retained in conditional knockdown OVX mice.	NAD	36-39	N-myc downstream regulated gene 2	Mus musculus	77-82
35622273-12	2022	Most importantly, we found that the neuroprotective effects of E2 and DPN against cerebral ischemic injury were lost in Ndrg2 knockout OVX mice but partially retained in conditional knockdown OVX mice.	NAD	70-73	N-myc downstream regulated gene 2	Mus musculus	120-125
35630420-2	2022	GAPDHs differ in cofactor specificity and use NAD+, NADP+, or both cofactors, reducing them to NADH and NADPH, respectively.	NAD	95-99	Aldehyde dehydrogenase	Escherichia coli	46-49
35499760-5	2022	Mechanistically, loss of BCAT1 increased the NAD+/NADH ratio but impaired oxidative phosphorylation, mTORC1 activity, and nucleotide biosynthesis.	NAD	45-49	branched chain amino acid transaminase 1	Homo sapiens	25-30
35499760-5	2022	Mechanistically, loss of BCAT1 increased the NAD+/NADH ratio but impaired oxidative phosphorylation, mTORC1 activity, and nucleotide biosynthesis.	NAD	50-54	branched chain amino acid transaminase 1	Homo sapiens	25-30
35561022-3	2022	Sirtuin-1 (Sirt1), a NAD-dependent deacetylase, regulates cellular metabolic activity and activation of this protein has been associated with vasoprotection in aged mice.	NAD	21-24	sirtuin 1	Mus musculus	0-9
35561022-3	2022	Sirtuin-1 (Sirt1), a NAD-dependent deacetylase, regulates cellular metabolic activity and activation of this protein has been associated with vasoprotection in aged mice.	NAD	21-24	sirtuin 1	Mus musculus	11-16
35473926-4	2022	At the same time, the light-activated Os2 induces photocatalytic oxidation of endogenous 1,4-dihydronicotinamide adenine dinucleotide in living cancer cells, leading to ferroptosis, which is mediated by glutathione degradation, lipid peroxide accumulation and down-regulation of glutathione peroxidase 4.	NAD	89-133	glutathione peroxidase 4	Mus musculus	279-303
35517822-4	2022	One of the most striking characteristics of NQO2 is that it uses conventional dihydronicotinamide cosubstrates, NADH and NADPH, extremely inefficiently, raising questions about an enzymatic function in cells.	NAD	112-116	N-ribosyldihydronicotinamide:quinone reductase 2	Homo sapiens	44-48
35517822-8	2022	Like the mammalian enzymes, the reptile and bird NQO2 were efficient catalysts with the small and synthetic cosubstrate N-benzyl-1,4-dihydronicotinamide but were inefficient in their use of NADH and NADPH.	NAD	190-194	N-ribosyldihydronicotinamide:quinone reductase 2	Homo sapiens	49-53
35457121-2	2022	Cyclic ADP-ribose (cADPR), synthesized from NAD+ by ADP-ribosyl cyclase family proteins, such as the mammalian cluster of differentiation 38 (CD38), is important for intracellular Ca2+ mobilization for cell functioning.	NAD	44-48	CD38 molecule	Homo sapiens	142-146
35397003-8	2022	To test the functional significance of these findings, we ectopically expressed wild-type alpha-synuclein in retinoic acid-differentiated dopaminergic SH-SY5Y cells which resulted in decreased levels of NMNAT3 protein plus a neurite pathology which could be rescued by FK866, an inhibitor of nicotinamide phosphoribosyltransferase that acts as a key enzyme in the regulation of NAD+ synthesis.	NAD	378-382	synuclein alpha	Homo sapiens	90-105
35397003-10	2022	These findings identify alterations in the NAD+ biosynthetic pathway as a pathogenic mechanism underlying alpha-synuclein mediated synaptopathy.	NAD	43-47	synuclein alpha	Homo sapiens	106-121
35419389-4	2022	Here, we identify PPARalpha as a deacetylation target of the NAD-dependent deacetylase sirtuin-1 (SIRT1) and link this to the decrease in PPARalpha protein levels in undernourished liver.	NAD	61-64	sirtuin 1	Mus musculus	98-103
35085893-5	2022	The co-treatment of alpha-syn/MPP+ can cause aberrant mitochondrial homeostasis to diminish the concentration of the coenzyme nicotinamide adenine dinucleotide (NAD+), mediate accumulation of ac-alpha-tubulin, and induce mitochondrial perinuclear aggregation, navigating the co-localization of NLRP3 and apoptosis-associated speck-like protein containing a CARD domain (ASC).	NAD	126-159	synuclein, alpha	Mus musculus	20-29
35085893-5	2022	The co-treatment of alpha-syn/MPP+ can cause aberrant mitochondrial homeostasis to diminish the concentration of the coenzyme nicotinamide adenine dinucleotide (NAD+), mediate accumulation of ac-alpha-tubulin, and induce mitochondrial perinuclear aggregation, navigating the co-localization of NLRP3 and apoptosis-associated speck-like protein containing a CARD domain (ASC).	NAD	161-165	synuclein, alpha	Mus musculus	20-29
35085893-5	2022	The co-treatment of alpha-syn/MPP+ can cause aberrant mitochondrial homeostasis to diminish the concentration of the coenzyme nicotinamide adenine dinucleotide (NAD+), mediate accumulation of ac-alpha-tubulin, and induce mitochondrial perinuclear aggregation, navigating the co-localization of NLRP3 and apoptosis-associated speck-like protein containing a CARD domain (ASC).	NAD	161-165	NLR family, pyrin domain containing 3	Mus musculus	294-299
35213221-6	2022	NAD binds to FMN in HydB, and electrons from H2 via HydA to a HydB (4Fe-4S) cluster enable the FMN to reduce NAD.	NAD	0-3	formin 1	Homo sapiens	13-16
35213221-6	2022	NAD binds to FMN in HydB, and electrons from H2 via HydA to a HydB (4Fe-4S) cluster enable the FMN to reduce NAD.	NAD	0-3	formin 1	Homo sapiens	95-98
35213221-6	2022	NAD binds to FMN in HydB, and electrons from H2 via HydA to a HydB (4Fe-4S) cluster enable the FMN to reduce NAD.	NAD	109-112	formin 1	Homo sapiens	13-16
35213221-6	2022	NAD binds to FMN in HydB, and electrons from H2 via HydA to a HydB (4Fe-4S) cluster enable the FMN to reduce NAD.	NAD	109-112	formin 1	Homo sapiens	95-98
35168992-7	2022	The glucose- induced high NADH/NAD+ ratio upregulates the hypoxia-inducible factor-1 gene, which stimulates not only the glucose transporter-1 gene, but also many profibrotic genes like TGFbeta, VEGF, PAI-1 and CTGF, all known to be involved in the development of peritoneal fibrosis.	NAD	26-30	serpin family E member 1	Homo sapiens	201-206
35168992-7	2022	The glucose- induced high NADH/NAD+ ratio upregulates the hypoxia-inducible factor-1 gene, which stimulates not only the glucose transporter-1 gene, but also many profibrotic genes like TGFbeta, VEGF, PAI-1 and CTGF, all known to be involved in the development of peritoneal fibrosis.	NAD	31-35	serpin family E member 1	Homo sapiens	201-206
34637412-14	2022	In addition, nicotinamide adenine dinucleotide+ treatment activated the Sirtuin3 pathway, down-regulating acetylated-NDUFA9 in the isolated mitochondria protein.	NAD	13-46	sirtuin 3	Rattus norvegicus	72-80
34637412-14	2022	In addition, nicotinamide adenine dinucleotide+ treatment activated the Sirtuin3 pathway, down-regulating acetylated-NDUFA9 in the isolated mitochondria protein.	NAD	13-46	NADH:ubiquinone oxidoreductase subunit A9	Rattus norvegicus	117-123
35013907-2	2022	The NAD-dependent deacetylase protein Sirtuin 3 (SIRT3) regulates mitochondrial oxidative stress response and neuroinflammation.	NAD	4-7	sirtuin 3	Mus musculus	38-47
35013907-2	2022	The NAD-dependent deacetylase protein Sirtuin 3 (SIRT3) regulates mitochondrial oxidative stress response and neuroinflammation.	NAD	4-7	sirtuin 3	Mus musculus	49-54
34981667-12	2022	Mechanistically, mitochondrial fission increased the acetylation level of sterol regulatory element-binding protein 1 (SREBP1) and peroxisome proliferator-activated receptor coactivator 1 alpha (PGC-1alpha) by suppressing nicotinamide adenine dinucleotide (NAD+)/Sirtuin 1 (SIRT1) signaling.	NAD	257-261	sterol regulatory element binding transcription factor 1	Homo sapiens	74-117
34981667-12	2022	Mechanistically, mitochondrial fission increased the acetylation level of sterol regulatory element-binding protein 1 (SREBP1) and peroxisome proliferator-activated receptor coactivator 1 alpha (PGC-1alpha) by suppressing nicotinamide adenine dinucleotide (NAD+)/Sirtuin 1 (SIRT1) signaling.	NAD	257-261	sterol regulatory element binding transcription factor 1	Homo sapiens	119-125
2573605-5	1989	The Km values of the patients" GDH for alpha-ketoglutarate, glutamate, NADH, and NADPH were significantly increased as compared to GDH obtained from normal and neurologic control subjects.	NAD	71-75	glutamate dehydrogenase 1	Homo sapiens	31-34
2673038-6	1989	Inhibition studies with S-NADH and butanol indicate that the NADH-BDH follows an ordered bibi mechanism with kinetic constants of 4.86 s-1, 0.18 mM, and 16 mM for Kcat, KNADH, and Kbutyraldehyde, respectively.	NAD	26-30	bdhA	Clostridium acetobutylicum ATCC 824	61-69
2497737-5	1989	GL alpha was [32P]ADP-ribosylated in the presence of pertussis toxin and [32P]NAD+.	NAD	78-82	GLA	Bos taurus	0-8
2742824-1	1989	3-Hydroxybutyrate dehydrogenase (BDH) is a lecithin-requiring mitochondrial enzyme which catalyzes the interconversion of 3-hydroxybutyrate and acetoacetate with NAD(H) as coenzyme.	NAD	162-168	3-hydroxybutyrate dehydrogenase 1	Homo sapiens	33-36
2742824-8	1989	Apparent dissociation constants for binding of NADH to BDH are approximately 10 microM and approximately 37 microM for BDH activated by bilayer and soluble lecithin, respectively.	NAD	47-51	3-hydroxybutyrate dehydrogenase 1	Homo sapiens	55-58
2742824-8	1989	Apparent dissociation constants for binding of NADH to BDH are approximately 10 microM and approximately 37 microM for BDH activated by bilayer and soluble lecithin, respectively.	NAD	47-51	3-hydroxybutyrate dehydrogenase 1	Homo sapiens	119-122
2930468-4	1989	When further NADH binds to E-X-CO-NMe2 its fluorescence is enhanced over 4 times more than when it binds to unmodified enzyme; this fluorescence is completely unaffected by high propionaldehyde concentration and only slightly affected by p-nitrobenzaldehyde.	NAD	13-17	NME/NM23 nucleoside diphosphate kinase 2	Homo sapiens	34-38
2930468-6	1989	The rate of dissociation of E-X-CO-NMe2.NADH is biphasic (k 3.4 and 1.8 min-1) and is considerably lower than that of E.NADH; the presence of Mg2+ slows the process even more (k 0.47 and 0.37 min-1).	NAD	40-44	NME/NM23 nucleoside diphosphate kinase 2	Homo sapiens	35-39
2930468-6	1989	The rate of dissociation of E-X-CO-NMe2.NADH is biphasic (k 3.4 and 1.8 min-1) and is considerably lower than that of E.NADH; the presence of Mg2+ slows the process even more (k 0.47 and 0.37 min-1).	NAD	120-124	NME/NM23 nucleoside diphosphate kinase 2	Homo sapiens	35-39
3137923-0	1988	The opposite effect of bivalent cations on cytochrome b5 reduction by NADH:cytochrome b5 reductase and NADPH:cytochrome c reductase.	NAD	70-74	cytochrome b5 type A	Homo sapiens	43-56
3137923-0	1988	The opposite effect of bivalent cations on cytochrome b5 reduction by NADH:cytochrome b5 reductase and NADPH:cytochrome c reductase.	NAD	70-74	cytochrome b5 type A	Homo sapiens	75-88
3137923-1	1988	The effects of bivalent cations on cytochrome b5 reduction by NADH:cytochrome b5 reductase and NADPH:cytochrome c reductase were studied with the proteinase-solubilized enzymes.	NAD	62-66	cytochrome b5 type A	Homo sapiens	35-48
3137923-2	1988	Cytochrome b5 reduction by NADH:cytochrome b5 reductase was strongly inhibited by CaCl2 or MgCl2.	NAD	27-31	cytochrome b5 type A	Homo sapiens	0-13
3137923-2	1988	Cytochrome b5 reduction by NADH:cytochrome b5 reductase was strongly inhibited by CaCl2 or MgCl2.	NAD	27-31	cytochrome b5 type A	Homo sapiens	32-45
2434494-2	1987	The activity of the thrice extracted particle (AE-P3) in ATP-driven NAD+ reduction by succinate and the 32Pi-ATP exchange activity were substantially stimulated, 8-fold and 5-fold, respectively, by purified FB.	NAD	68-72	distal membrane arm assembly component 2 like	Bos taurus	207-209
3545081-3	1987	A NADH-dependent hydroxypyruvate reductase was purified 130-fold from Chlamydomonas to a specific activity of 18 mumol NADH oxidized X min-1 X mg protein-1.	NAD	2-6	uncharacterized protein	Chlamydomonas reinhardtii	17-42
3545081-3	1987	A NADH-dependent hydroxypyruvate reductase was purified 130-fold from Chlamydomonas to a specific activity of 18 mumol NADH oxidized X min-1 X mg protein-1.	NAD	119-123	uncharacterized protein	Chlamydomonas reinhardtii	17-42
3545081-7	1987	NADH-dependent glyoxylate reductase activity copurified with the hydroxypyruvate reductase.	NAD	0-4	uncharacterized protein	Chlamydomonas reinhardtii	65-90
3097018-1	1986	The enzyme rhodanese (thiosulfate sulfurtransferase; EC 2.8.1.1) is inactivated with a half-time of approximately 3 min when incubated with 50 mM NADH.	NAD	146-150	thiosulfate sulfurtransferase	Homo sapiens	22-51
16665101-6	1986	These results were taken to indicate that bromphenol blue and NADH donated electrons to nitrate reductase at different sites.	NAD	62-66	nitrate reductase [NADH] 1	Zea mays	88-105
16665101-7	1986	When monoclonal antibodies prepared against corn and squash nitrate reductases were used to inhibit the nitrate reductase activities supported by NADH, bromphenol blue, and methyl viologen, differential inhibition was found which tended to indicate that the three electron donors were interacting with the enzyme at different sites.	NAD	146-150	nitrate reductase [NADH] 1	Zea mays	60-77
3015963-0	1986	Functional domains of assimilatory NADH:nitrate reductase from Chlorella.	NAD	35-39	nitrate reductase [NADH] 1	Zea mays	40-57
3015963-2	1986	Besides the reduction of nitrate by NADH, nitrate reductase also catalyzes the partial activities NADH:cytochrome c reductase, NADH:ferricyanide reductase, and reduced methyl viologen:nitrate reductase.	NAD	36-40	nitrate reductase [NADH] 1	Zea mays	42-59
3015963-2	1986	Besides the reduction of nitrate by NADH, nitrate reductase also catalyzes the partial activities NADH:cytochrome c reductase, NADH:ferricyanide reductase, and reduced methyl viologen:nitrate reductase.	NAD	36-40	nitrate reductase [NADH] 1	Zea mays	184-201
3015963-2	1986	Besides the reduction of nitrate by NADH, nitrate reductase also catalyzes the partial activities NADH:cytochrome c reductase, NADH:ferricyanide reductase, and reduced methyl viologen:nitrate reductase.	NAD	98-102	nitrate reductase [NADH] 1	Zea mays	42-59
3015963-2	1986	Besides the reduction of nitrate by NADH, nitrate reductase also catalyzes the partial activities NADH:cytochrome c reductase, NADH:ferricyanide reductase, and reduced methyl viologen:nitrate reductase.	NAD	98-102	nitrate reductase [NADH] 1	Zea mays	184-201
3015963-8	1986	These results are consistent with a structure-function model of nitrate reductase which has the following features: FAD/NADH-binding domains exposed on the surface of the molecule, a protease-sensitive hinge region which connects the nitrate-reducing and NADH dehydrogenase moieties, and the quaternary structure maintained via association sites on the heme/molybdenum domain.	NAD	120-124	nitrate reductase [NADH] 1	Zea mays	64-81
3015904-2	1986	It was shown that there is no direct electron transfer between the cytochrome and dopamine beta-hydroxylase, but that in the presence of ascorbate, turnover of dopamine beta-hydroxylase causes an oxidation of the cytochrome, which is partially reversed by the action of the mitochondrial NADH:A-.	NAD	288-292	dopamine beta-hydroxylase	Homo sapiens	160-185
3015904-7	1986	The data are consistent with a model in which cytochrome b561, by reacting with ascorbate or ascorbate free radical on either side of the granule membrane, could couple the ascorbate-consuming reaction of the dopamine beta-hydroxylase inside the chromaffin granule to the ascorbate-regenerating reaction of the NADH:A-.	NAD	311-315	dopamine beta-hydroxylase	Homo sapiens	209-234
3015905-7	1986	These data provide direct experimental evidence for the hypothesis that the adrenal medullary mitochondrial NADH:ascorbate radical oxidoreductase could drive the re-reduction of ascorbate free radical generated inside the chromaffin granule by the turnover of dopamine beta-hydroxylase, without the ascorbate radical ever having to leave the granule.	NAD	108-112	dopamine beta-hydroxylase	Homo sapiens	260-285
3015206-8	1986	A dimeric model of the enzyme is proposed in which one protomer, containing FMN and the Fe-S clusters 1-4 in stoichiometric amounts, is responsible for NADH oxidation at pH 8.	NAD	152-156	formin 1	Homo sapiens	76-79
3711040-1	1986	The catalytic properties of a new type of dihydropteridine reductase, NADPH-specific dihydropteridine reductase [EC 1.6.99.10], from bovine liver, were studied and compared with those of the previously characterized enzyme, NADH-specific dihydropteridine reductase [EC 1.6.99.7].	NAD	224-228	quinoid dihydropteridine reductase	Bos taurus	42-68
3711040-1	1986	The catalytic properties of a new type of dihydropteridine reductase, NADPH-specific dihydropteridine reductase [EC 1.6.99.10], from bovine liver, were studied and compared with those of the previously characterized enzyme, NADH-specific dihydropteridine reductase [EC 1.6.99.7].	NAD	224-228	quinoid dihydropteridine reductase	Bos taurus	85-111
3711040-1	1986	The catalytic properties of a new type of dihydropteridine reductase, NADPH-specific dihydropteridine reductase [EC 1.6.99.10], from bovine liver, were studied and compared with those of the previously characterized enzyme, NADH-specific dihydropteridine reductase [EC 1.6.99.7].	NAD	224-228	quinoid dihydropteridine reductase	Bos taurus	85-111
3711040-2	1986	With quinonoid-dihydro-6-methylpterin, approximate Km values of NADPH-specific dihydropteridine reductase for NADPH and NADH were estimated to be 1.4 micron and 2,900 microns, respectively.	NAD	120-124	quinoid dihydropteridine reductase	Bos taurus	79-105
2850270-1	1986	Cardiac mitochondrial NADH dehydrogenase (Cytochrome c reductase, EC1.6.99.3) catalyses the reduction of ferricytochrome c to ferrocytochrome c by NADH.	NAD	22-26	Susceptibility to lysis by alloreactive natural killer cells	Homo sapiens	66-69
2996930-5	1985	This work reports on the capacity of an NAD analog, the nicotinamide 1-N6-ethenoadenine dinucleotide (epsilon NAD), to be a substrate of diphtheria toxin fragment A in the transferring reaction of the fluorescent moiety, the epsilon ADP-ribose, to the EF-2.	NAD	40-43	eukaryotic translation elongation factor 2	Homo sapiens	252-256
2996930-5	1985	This work reports on the capacity of an NAD analog, the nicotinamide 1-N6-ethenoadenine dinucleotide (epsilon NAD), to be a substrate of diphtheria toxin fragment A in the transferring reaction of the fluorescent moiety, the epsilon ADP-ribose, to the EF-2.	NAD	110-113	eukaryotic translation elongation factor 2	Homo sapiens	252-256
4052045-9	1985	Variability in the specific activity of preparations of S-adenosylhomocysteine hydrolase was related to the NAD+/NADH ratio of the preparation.	NAD	108-112	adenosylhomocysteinase	Homo sapiens	56-88
4052045-9	1985	Variability in the specific activity of preparations of S-adenosylhomocysteine hydrolase was related to the NAD+/NADH ratio of the preparation.	NAD	113-117	adenosylhomocysteinase	Homo sapiens	56-88
3162018-2	1985	Pyruvate kinase and lactate dehydrogenase were used to link adenosine diphosphate formation to oxidation of nicotinamide adenine dinucleotide which was followed by the change in absorption at 340 nm.	NAD	108-141	pyruvate kinase PKLR	Oryctolagus cuniculus	0-15
3985993-6	1985	The NAD analogs of tiazofurin and selenazofurin were inhibitors of L1210 IMP dehydrogenase (IMP:NAD oxidoreductase, EC 1.2.1.14), and both showed uncompetitive inhibition with respect to NAD having Kii values of 5.7 X 10(-8)M and 3.3 X 10(-8)M respectively.	NAD	4-7	inositol monophosphatase 1	Homo sapiens	73-76
3985993-6	1985	The NAD analogs of tiazofurin and selenazofurin were inhibitors of L1210 IMP dehydrogenase (IMP:NAD oxidoreductase, EC 1.2.1.14), and both showed uncompetitive inhibition with respect to NAD having Kii values of 5.7 X 10(-8)M and 3.3 X 10(-8)M respectively.	NAD	4-7	inositol monophosphatase 1	Homo sapiens	92-114
3985993-6	1985	The NAD analogs of tiazofurin and selenazofurin were inhibitors of L1210 IMP dehydrogenase (IMP:NAD oxidoreductase, EC 1.2.1.14), and both showed uncompetitive inhibition with respect to NAD having Kii values of 5.7 X 10(-8)M and 3.3 X 10(-8)M respectively.	NAD	96-99	inositol monophosphatase 1	Homo sapiens	73-76
3967007-6	1985	A relation between the increase of exogenous NADH oxidation and phospholipase A2 activity in liver mitochondria is discussed.	NAD	45-49	phospholipase A2 group IB	Rattus norvegicus	64-80
2981686-3	1985	At low NAD concentrations the enzyme can poly(ADP-ribosyl)ate histones H1 and H1, H2A, A2A, and H2B.	NAD	7-10	H2B clustered histone 21	Homo sapiens	96-99
2981686-5	1985	Furthermore we have observed hyper ADP-ribosylation of histone H2B at NAD concentrations of 10 microM suggesting that histone H2B can undergo the same type of ADP-ribosylation pattern as histone H1.	NAD	70-73	H2B clustered histone 21	Homo sapiens	63-66
2981686-5	1985	Furthermore we have observed hyper ADP-ribosylation of histone H2B at NAD concentrations of 10 microM suggesting that histone H2B can undergo the same type of ADP-ribosylation pattern as histone H1.	NAD	70-73	H2B clustered histone 21	Homo sapiens	126-129
4052167-1	1985	Since cytosolic malate dehydrogenase has been shown to play a role in the regulation of liver cytosolic [NAD+]/[NADH] redox state during ethanol metabolism, it is possible that differences in this enzyme could cause differences in response to ethanol.	NAD	105-109	malate dehydrogenase 1	Homo sapiens	6-36
4052167-1	1985	Since cytosolic malate dehydrogenase has been shown to play a role in the regulation of liver cytosolic [NAD+]/[NADH] redox state during ethanol metabolism, it is possible that differences in this enzyme could cause differences in response to ethanol.	NAD	112-116	malate dehydrogenase 1	Homo sapiens	6-36
6527187-9	1984	The inhibition of diphtheria toxin was NAD+ dependent, suggesting that ADP-ribosylation of EF-2 could be the cause of the inhibition as it is in mammalian cell lines.	NAD	39-43	eukaryotic translation elongation factor 2	Homo sapiens	91-95
6208195-4	1984	Electron transport of C-32 sterol demethylation can be fully supported by very low concentrations of NADPH (approximately 10 microM) only in the presence of saturating concentrations of NADH (approximately 200 microM) suggesting involvement of cytochrome b5-dependent electron transfer in addition to the NADPH-supported pathway.	NAD	186-190	chemokine like factor	Homo sapiens	22-26
6502134-4	1984	This bacterial GDH was predominantly NAD+-linked, but was able to utilize both NADP+ and NADPH at 4% of the rates with NAD+ and NADH, respectively.	NAD	37-41	glutamate dehydrogenase 1	Homo sapiens	15-18
6502134-4	1984	This bacterial GDH was predominantly NAD+-linked, but was able to utilize both NADP+ and NADPH at 4% of the rates with NAD+ and NADH, respectively.	NAD	119-123	glutamate dehydrogenase 1	Homo sapiens	15-18
6502134-4	1984	This bacterial GDH was predominantly NAD+-linked, but was able to utilize both NADP+ and NADPH at 4% of the rates with NAD+ and NADH, respectively.	NAD	128-132	glutamate dehydrogenase 1	Homo sapiens	15-18
6380584-1	1984	The kinetics of the reduction of quinonoid 2-amino-4-hydroxy-6, 7-dimethyldihydropteridine (DMPH2) catalyzed by bovine liver dihydropteridine reductase were examined with NADH, (S)-NADD, (S)-NADT, and [3H]-NADH as substrates.	NAD	171-175	quinoid dihydropteridine reductase	Bos taurus	125-151
6380584-1	1984	The kinetics of the reduction of quinonoid 2-amino-4-hydroxy-6, 7-dimethyldihydropteridine (DMPH2) catalyzed by bovine liver dihydropteridine reductase were examined with NADH, (S)-NADD, (S)-NADT, and [3H]-NADH as substrates.	NAD	206-210	quinoid dihydropteridine reductase	Bos taurus	125-151
6143754-13	1984	The erythrocyte transferase also catalyzed the NAD-dependent inactivation of glutamine synthetase purified from chicken heart; 0.60 mol of ADP-ribose was transferred per mol of enzyme, resulting in a 95% inactivation.	NAD	47-50	glutamate-ammonia ligase	Gallus gallus	77-97
6707013-10	1984	In [alpha, beta-dehydro-Trp 15]beta-globin, the fluorescence was exceptionally intense, the fluorescence yield being comparable to that of NADH.	NAD	139-143	hemoglobin subunit beta	Homo sapiens	31-42
6356985-9	1983	The latter two probably represent functional groups in the free enzyme; pK1 may represent a functional group in the enzyme-NAD+ complex.	NAD	123-127	pyruvate kinase L/R	Rattus norvegicus	72-75
18551483-1	1983	Oocystis sp., a unicellular green alga, contained two glutamate dehydrogenase isoenzymes: one was specific for NADH and the other for NADPH.	NAD	111-115	glutamate dehydrogenase 1	Homo sapiens	54-77
18551483-2	1983	Activity staining after gel electrophoresis indicated that one component in NADH-GDH was not specific for the cofactor and three components in NADPH-GDH.	NAD	76-80	glutamate dehydrogenase 1	Homo sapiens	81-84
18551483-2	1983	Activity staining after gel electrophoresis indicated that one component in NADH-GDH was not specific for the cofactor and three components in NADPH-GDH.	NAD	76-80	glutamate dehydrogenase 1	Homo sapiens	149-152
18551483-5	1983	There was a sharp increase in NADPH-GDH activity following the exhaustion of ammonia from the medium but NADH-GDH activity remained unchanged.	NAD	105-109	glutamate dehydrogenase 1	Homo sapiens	110-113
6882460-7	1983	The observation that NADH supports the reduction of folate and dihydrofolate but not MTX binding suggests that natural resistance to MTX could exist if NADH replaces NADPH as the main cofactor for DHFR.	NAD	21-25	dihydrofolate reductase	Homo sapiens	197-201
6882460-7	1983	The observation that NADH supports the reduction of folate and dihydrofolate but not MTX binding suggests that natural resistance to MTX could exist if NADH replaces NADPH as the main cofactor for DHFR.	NAD	152-156	dihydrofolate reductase	Homo sapiens	197-201
6850553-2	1983	Direct EF-2 quantification is obtained by a modification of the method of the diphtheria toxin-catalyzed transfer of (14C)ADP-ribose from (14C)NAD+ to the enzyme.	NAD	143-147	eukaryotic translation elongation factor 2	Mus musculus	7-11
6759120-5	1982	Lys10 mutants displayed NAD-reducing activity, whereas lys9 mutants retained some carboxylating activity.	NAD	24-27	homoisocitrate dehydrogenase	Saccharomyces cerevisiae S288C	0-5
6811590-4	1982	In systems containing cytochrome and reductase, the rate of NADH oxidation exceeded that of NADPH oxidation, indicating that reduced cytochrome b5 is an effective electron donor for prostaglandin H2 formation, enhancing both the initial rate and the extent of the reaction.	NAD	60-64	cytochrome b5 type A	Homo sapiens	133-146
7127739-1	1982	Determination of lactate dehydrogenase (LDH) activity in the SMAC (Technicon) is based on the change in NADH absorbance between two flow cells.	NAD	104-108	diablo IAP-binding mitochondrial protein	Homo sapiens	61-65
7085595-3	1982	Reconstitution of deficient particles with FB restores ATP-dependent proton translocation and oxonol binding but has little effect on oxonol binding supported by respiratory substrates.l In contrast, low levels of oligomycin stimulate oxonol binding supported by either ATP or NADH.	NAD	277-281	distal membrane arm assembly component 2 like	Bos taurus	43-45
7073766-6	1982	There was a synergistic effect in the presence of NADPH and NADH for both hexa- and pentachloroethane.	NAD	60-64	hexosaminidase subunit alpha	Homo sapiens	74-78
6275889-6	1982	NADH oxidation, both in intact and in water-treated mitochondria, is 90% inhibited by mersalyl, an inhibitor of the outer membrane NADH-cytochrome b5 reductase, and 10% inhibited by rotenone.	NAD	0-4	cytochrome b5 type A	Homo sapiens	136-149
6275889-10	1982	It is concluded that (i) oxidation of exogenous NADH in the presence of cytochrome c proceeds mostly through NADH-cytochrome b5 reductase and cytochrome b5 on the outer membrane and then through cytochrome oxidase via the cytochrome c shuttle, and (ii) ATP synthesis during oxidation of exogenous NADH is partly due to oxidation of endogenous substrates and partly to operation of cytochrome oxidase receiving electrons from the outer membrane via cytochrome c.	NAD	48-52	cytochrome b5 type A	Homo sapiens	114-127
6275889-10	1982	It is concluded that (i) oxidation of exogenous NADH in the presence of cytochrome c proceeds mostly through NADH-cytochrome b5 reductase and cytochrome b5 on the outer membrane and then through cytochrome oxidase via the cytochrome c shuttle, and (ii) ATP synthesis during oxidation of exogenous NADH is partly due to oxidation of endogenous substrates and partly to operation of cytochrome oxidase receiving electrons from the outer membrane via cytochrome c.	NAD	48-52	cytochrome b5 type A	Homo sapiens	142-155
6275889-10	1982	It is concluded that (i) oxidation of exogenous NADH in the presence of cytochrome c proceeds mostly through NADH-cytochrome b5 reductase and cytochrome b5 on the outer membrane and then through cytochrome oxidase via the cytochrome c shuttle, and (ii) ATP synthesis during oxidation of exogenous NADH is partly due to oxidation of endogenous substrates and partly to operation of cytochrome oxidase receiving electrons from the outer membrane via cytochrome c.	NAD	109-113	cytochrome b5 type A	Homo sapiens	114-127
6460012-7	1981	However, most ChE deposits occurred in intrafusal fiber regions that displayed the greatest NADH-TR variability.	NAD	92-96	butyrylcholinesterase	Homo sapiens	14-17
7034720-1	1981	NADH--cytochrome b5 reductase and cytochrome b5 associated with slow-muscle sarcoplasmic reticulum and liver microsomal fraction were identified with discrete protein bands of molecular weights 33000 and 16700 by polyacrylamide-gel electrophoresis.	NAD	0-4	cytochrome b5 type A	Homo sapiens	6-19
7034720-1	1981	NADH--cytochrome b5 reductase and cytochrome b5 associated with slow-muscle sarcoplasmic reticulum and liver microsomal fraction were identified with discrete protein bands of molecular weights 33000 and 16700 by polyacrylamide-gel electrophoresis.	NAD	0-4	cytochrome b5 type A	Homo sapiens	34-47
6263333-4	1981	These bands shifted to 590 and 430 nm, respectively, in CO difference spectra, NADPH, NADH and ascorbate reduced the cytochrome through added horse heart cytochrome c as electron mediator.	NAD	86-90	cytochrome c, somatic	Equus caballus	154-166
7305938-7	1981	In the enzyme-NADH complex the reaction of diethyl pyrocarbonate was controlled by two groups with pKa 6.8 and 7.9.	NAD	14-18	protein kinase cAMP-activated catalytic subunit alpha	Sus scrofa	99-102
7008786-1	1980	A number of reactive dichlorotriazine dyes specifically and irreversibly inactivate pig heart lactate dehydrogenase, yeast glucose 6-phosphate dehydrogenase and yeast hexokinase at sites competitive with NAD+, NADP+, and ATP respectively.	NAD	204-208	hexokinase	Saccharomyces cerevisiae S288C	167-177
6246954-1	1980	Human placenta contains a thermostable, cytosolic NADH-diaphorase which is different from the other diaphorases and which we designate as diaphorase P. It is specific for NADH and reduces artificial substrates such as dichlorophenol and tetrazolium derivatives, but not natural substrates such as methemoglobin, cytochrome b5 or lipoate.	NAD	50-54	cytochrome b5 type A	Homo sapiens	312-325
16661130-12	1980	Inactivation of corn leaf NR by rice inactivator was inhibited by the simultaneous addition of NADH, but rice inactivator-inactivated corn leaf NR could not be reactivated by NADH.	NAD	95-99	nitrate reductase [NADH] 1	Zea mays	26-28
230779-2	1979	The effects of coenzyme NAD and related compounds on the electrophoretic properties of the human ADH isozymes have been examined by the technique of affinity electrophoresis.	NAD	24-27	alcohol dehydrogenase 1C (class I), gamma polypeptide	Homo sapiens	97-100
227369-8	1979	In these conditions oxidation of NADH and succinate by way of cytochrome b and cytochrome a/a(3) occurs without the mediation of cytochrome c.	NAD	33-37	MEXAM1_RS00595	Methylobacterium extorquens AM1	62-74
735712-1	1978	The activity of NADPH- and NADH-dependent erythrocyte glutathione reductase was determined in rats with Morris 5123 hepatoma at different stages of tumor development (10, 20, 30 and 40 days after transplantation).	NAD	27-31	glutathione-disulfide reductase	Rattus norvegicus	54-75
689031-1	1978	Conditions are described whereby the ADP-ribosylation (from NAD+) of reticulocyte elongation factor EF-2, catalyzed by diphtheria toxin, is essentially complete and whereby the reverse of this process may be carried out with recovery of 60--70% of the original EF-2 activity.	NAD	60-64	eukaryotic translation elongation factor 2	Homo sapiens	100-104
197387-2	1977	Drosophila XDH exhibits ordered binding for substrate and NAD+, analogous to the corresponding enzymes from vertebrate sources.	NAD	58-62	rosy	Drosophila melanogaster	11-14
197387-3	1977	The wild-type enzyme exhibits a Km for xanthine of 2.4 X 10(-5) M, and for NAD+ of 4.0 X 10(-5) M. XDH purified from a genetic variant exhibiting elevated levels of enzyme activity has similar kinetic constants.	NAD	75-79	rosy	Drosophila melanogaster	99-102
199521-1	1977	Carboquone was found to greatly stimulate the aerobic NADH oxidation in the presence of both the partially purified NADH-cytochrome b5 reductase and cytochrome b5 prepared from hepatic microsomes by acting as an electron carrier from cytochrome b5 to molecular oxygen.	NAD	54-58	cytochrome b5 type A	Homo sapiens	121-134
849463-6	1977	Finally, results of nicotinamide-adenine dinucleotide-binding measurements suggest that tryptophan 153 would be concerned with the elongation factor 2 binding site or with the catalytic site itself.	NAD	20-53	eukaryotic translation elongation factor 2	Homo sapiens	131-150
188760-1	1977	Previous studies showed that Pseudomonas aeruginosa exotoxin A (PA toxin) catalyzes nicotinamide adenine dinucleotide (NAD)-dependent inhibition of protein synthesis in a rabbit reticulocyte lysate and transfer of radioactivity from [14C]adenine-labeled NAD to a protein having the same molecular weight as elongation factor 2 (EF-2) (B.H.	NAD	84-117	eukaryotic translation elongation factor 2	Homo sapiens	307-326
188760-1	1977	Previous studies showed that Pseudomonas aeruginosa exotoxin A (PA toxin) catalyzes nicotinamide adenine dinucleotide (NAD)-dependent inhibition of protein synthesis in a rabbit reticulocyte lysate and transfer of radioactivity from [14C]adenine-labeled NAD to a protein having the same molecular weight as elongation factor 2 (EF-2) (B.H.	NAD	84-117	eukaryotic translation elongation factor 2	Mus musculus	328-332
188760-1	1977	Previous studies showed that Pseudomonas aeruginosa exotoxin A (PA toxin) catalyzes nicotinamide adenine dinucleotide (NAD)-dependent inhibition of protein synthesis in a rabbit reticulocyte lysate and transfer of radioactivity from [14C]adenine-labeled NAD to a protein having the same molecular weight as elongation factor 2 (EF-2) (B.H.	NAD	119-122	eukaryotic translation elongation factor 2	Homo sapiens	307-326
188760-1	1977	Previous studies showed that Pseudomonas aeruginosa exotoxin A (PA toxin) catalyzes nicotinamide adenine dinucleotide (NAD)-dependent inhibition of protein synthesis in a rabbit reticulocyte lysate and transfer of radioactivity from [14C]adenine-labeled NAD to a protein having the same molecular weight as elongation factor 2 (EF-2) (B.H.	NAD	119-122	eukaryotic translation elongation factor 2	Mus musculus	328-332
177419-0	1976	The reduced nicotinamide adenine dinucleotide-activated phosphoenolpyruvate carboxylase from Pseudomonas MA.	NAD	12-45	phosphoenolpyruvate carboxykinase 1	Homo sapiens	56-87
177074-3	1976	In the first place a stimulation of succinate- and NADH-consuming, antimycin-A-sensitive respiration, which reaches a maximal value at low cytochrome c concentrations, has been found.	NAD	51-55	cytochrome c	Solanum tuberosum	139-151
177074-4	1976	In the second place, at higher concentrations of cytochrome c a stimulation of NADH-consuming respiration occurs, which is antimycin-A-resistant, but KCN-sensitive.	NAD	79-83	cytochrome c	Solanum tuberosum	49-61
235894-1	1975	A quantitative estimation of cytochrome b5 content in the NADPH- and NADH-oxidation chains.	NAD	69-73	cytochrome b5 type A	Homo sapiens	29-42
178010-1	1975	When the diamines putrescine, cadaverine, cystamine and lanthionamine are oxidized by purified pig kidney diamine oxidase in the presence of NADH and either liver or yeast crystalline alcohol dehydrogenase, NADH is oxidized.	NAD	141-145	amine oxidase copper containing 1	Sus scrofa	106-121
178010-1	1975	When the diamines putrescine, cadaverine, cystamine and lanthionamine are oxidized by purified pig kidney diamine oxidase in the presence of NADH and either liver or yeast crystalline alcohol dehydrogenase, NADH is oxidized.	NAD	207-211	amine oxidase copper containing 1	Sus scrofa	106-121
186944-5	1975	Our studies have shown that the isoenzymes of LDH which are richer in H subunits have a higher affinity for deamino-NAD and deamino-NADH than for NAD and NADH.	NAD	116-119	lactate dehydrogenase C	Rattus norvegicus	46-49
186944-5	1975	Our studies have shown that the isoenzymes of LDH which are richer in H subunits have a higher affinity for deamino-NAD and deamino-NADH than for NAD and NADH.	NAD	132-136	lactate dehydrogenase C	Rattus norvegicus	46-49
4345437-0	1972	Interactions between NADH-cytochrome b5 reductase and cytochrome b5 preparations purified from liver microsomes.	NAD	21-25	cytochrome b5 type A	Homo sapiens	26-39
4345437-0	1972	Interactions between NADH-cytochrome b5 reductase and cytochrome b5 preparations purified from liver microsomes.	NAD	21-25	cytochrome b5 type A	Homo sapiens	54-67
16657416-3	1970	NADH oxidation was slightly stimulated by cytochrome c, ATP, and ADP; succinate oxidation was markedly increased by ATP, slightly by ADP and cytochrome c; and malate oxidation required the addition of NAD(+) NADH oxidation is inhibited weakly by amytal, completely by antimycin A and KCN, but not by rotenone.	NAD	0-4	cytochrome c	Vigna radiata	42-54
5702582-2	1968	Reactivation of NADH coenzyme-Q-1 reductase activity in diethyl ether and phospholipase-A treated heart-muscle preparations.	NAD	16-20	phospholipase A and acyltransferase 1	Homo sapiens	74-89
4379240-0	1965	Effect of CCl4, dimethylnitrosamine, and thioacetamide on hepatic DPNH and TPNH cytochrome C reductase.	NAD	66-70	C-C motif chemokine ligand 4	Homo sapiens	10-14
33028985-7	2021	Consequently, Tan-IIA reduced glycolysis and protected the activity of Sirtuin2 (Sirt2), an NAD+-dependent protein deacetylase, by raising the ratio of NAD+/NADH in activated macrophages.	NAD	92-96	sirtuin 2	Mus musculus	71-79
33028985-7	2021	Consequently, Tan-IIA reduced glycolysis and protected the activity of Sirtuin2 (Sirt2), an NAD+-dependent protein deacetylase, by raising the ratio of NAD+/NADH in activated macrophages.	NAD	92-96	sirtuin 2	Mus musculus	81-86
33028985-7	2021	Consequently, Tan-IIA reduced glycolysis and protected the activity of Sirtuin2 (Sirt2), an NAD+-dependent protein deacetylase, by raising the ratio of NAD+/NADH in activated macrophages.	NAD	157-161	sirtuin 2	Mus musculus	71-79
33028985-7	2021	Consequently, Tan-IIA reduced glycolysis and protected the activity of Sirtuin2 (Sirt2), an NAD+-dependent protein deacetylase, by raising the ratio of NAD+/NADH in activated macrophages.	NAD	157-161	sirtuin 2	Mus musculus	81-86
33795425-1	2021	BACKGROUND: The activation of NAD+-dependent deacetylase, Sirt1, by the administration of nicotinamide mononucleotide (NMN) ameliorates various aging-related diseases.	NAD	30-33	sirtuin 1	Mus musculus	58-63
33485900-4	2021	As a sensing or consuming enzyme of the poly (ADP-ribose) polymerase 1 (PARP1), the cyclic ADP-ribose (cADPR) synthases (CD38 and CD157), and sirtuin protein deacetylases (sirtuins, SIRTs), NAD+ participates in several key processes in cardiovascular disease.	NAD	190-194	CD38 molecule	Homo sapiens	121-125
33609723-8	2021	The NAD+ precursor nicotinamide mononucleotide and the poly ADP-ribose polymerase (PARP1) inhibitor olaparib also exerted anti-senescent effects by activating SIRT1.	NAD	4-8	sirtuin 1	Mus musculus	159-164
33577950-1	2021	Nicotinamide adenine dinucleotide (NAD+) is an essential coenzyme involved in numerous physiological processes.	NAD	0-33	Aldehyde dehydrogenase	Escherichia coli	35-38
33754067-16	2021	Conclusions: The findings from this research for the first time demonstrate that NAD+-boosting therapy reverses NAFLD by regulating SIRT2-deppendent Fndc5 deacetylation and deubiquitination, which results in a stimulation of Fndc5/irisin, a novel exerkine.	NAD	81-85	sirtuin 2	Mus musculus	132-137
33754067-16	2021	Conclusions: The findings from this research for the first time demonstrate that NAD+-boosting therapy reverses NAFLD by regulating SIRT2-deppendent Fndc5 deacetylation and deubiquitination, which results in a stimulation of Fndc5/irisin, a novel exerkine.	NAD	81-85	fibronectin type III domain containing 5	Mus musculus	149-154
33754067-16	2021	Conclusions: The findings from this research for the first time demonstrate that NAD+-boosting therapy reverses NAFLD by regulating SIRT2-deppendent Fndc5 deacetylation and deubiquitination, which results in a stimulation of Fndc5/irisin, a novel exerkine.	NAD	81-85	fibronectin type III domain containing 5	Mus musculus	225-230
33754067-17	2021	These results suggest that Fndc5/irisin may be a potential nexus between physical exercise and NAD+-boosting therapy in metabolic pathophysiology.	NAD	95-99	fibronectin type III domain containing 5	Mus musculus	27-32
33541361-3	2021	The NAD-dependent deacetylase protein Sirtuin 3 (SIRT3) is located in the mitochondria and regulates mitochondrial function.	NAD	4-7	sirtuin 3	Mus musculus	38-47
33327751-3	2021	SIRT3 (sirtuin-3), a NAD-dependent deacetylase, is sensitive to metabolic status and mediates adaptation responses.	NAD	21-24	sirtuin 3	Mus musculus	0-5
33327751-3	2021	SIRT3 (sirtuin-3), a NAD-dependent deacetylase, is sensitive to metabolic status and mediates adaptation responses.	NAD	21-24	sirtuin 3	Mus musculus	7-16
33246154-1	2021	17beta-Hydroxysteroid dehydrogenase type 2 (17beta-HSD2) catalyzes the conversion of highly active estrogens and androgens into their less active forms using NAD+ as cofactor.	NAD	158-162	hydroxysteroid 17-beta dehydrogenase 2	Homo sapiens	0-42
33246154-1	2021	17beta-Hydroxysteroid dehydrogenase type 2 (17beta-HSD2) catalyzes the conversion of highly active estrogens and androgens into their less active forms using NAD+ as cofactor.	NAD	158-162	hydroxysteroid 17-beta dehydrogenase 2	Homo sapiens	44-55
33246154-7	2021	For this, the first homology model of 17beta-HSD2 in complex with NAD+ and 17beta-estradiol was built, using a multi-fragment "patchwork" approach.	NAD	66-70	hydroxysteroid 17-beta dehydrogenase 2	Homo sapiens	38-49
32710757-1	2021	BACKGROUND: IDH-mutant tumors exhibit an altered metabolic state and are critically dependent upon nicotinamide adenine dinucleotide (NAD+) for cellular survival.	NAD	99-132	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	12-15
32710757-1	2021	BACKGROUND: IDH-mutant tumors exhibit an altered metabolic state and are critically dependent upon nicotinamide adenine dinucleotide (NAD+) for cellular survival.	NAD	134-138	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	12-15
33521859-7	2021	By integrating into the NAD+ synthesis pathway, chirons could directly catalyze the NAD+ rate-limiting reaction and probably impact two energy metabolism genes (nmnat1 and naprt) to be under positive selection in Danioninae fishes.	NAD	24-28	nicotinamide nucleotide adenylyltransferase 1	Danio rerio	161-167
33479917-4	2021	Importantly, CD38 stimulation with NAD accelerated ATP production along with increasing glutathione reductase (GR) and dipicolinic acid (DPA) in intracellular mitochondria.	NAD	35-38	glutathione-disulfide reductase	Rattus norvegicus	88-109
33479917-4	2021	Importantly, CD38 stimulation with NAD accelerated ATP production along with increasing glutathione reductase (GR) and dipicolinic acid (DPA) in intracellular mitochondria.	NAD	35-38	glutathione-disulfide reductase	Rattus norvegicus	111-113
33303985-0	2021	Author Correction: Senescent cells promote tissue NAD+ decline during ageing via the activation of CD38+ macrophages.	NAD	50-54	CD38 molecule	Homo sapiens	99-103
33271294-3	2021	The seminal observation that the fungicide-derivative fadrozole blunted steroidogenesis has led to develop several agents to inhibit aldosterone synthase (AS, CYP11B2), the mitochondrial NADH-dependent enzyme that is necessary for aldosterone biosynthesis.	NAD	187-191	cytochrome P450 family 11 subfamily B member 2	Homo sapiens	133-153
33271294-3	2021	The seminal observation that the fungicide-derivative fadrozole blunted steroidogenesis has led to develop several agents to inhibit aldosterone synthase (AS, CYP11B2), the mitochondrial NADH-dependent enzyme that is necessary for aldosterone biosynthesis.	NAD	187-191	cytochrome P450 family 11 subfamily B member 2	Homo sapiens	159-166
32527186-7	2021	The activity-based assay uses an alpha-NAD+, anomer of beta-NAD+, which is accepted as a substrate by MacroD1, MacroD2, and ARH3 due to its resemblance to the protein-linked ADP-ribose.	NAD	55-64	ADP-ribosylserine hydrolase	Homo sapiens	124-128
33300786-4	2020	The NADH oxidase encoding gene nox was inserted into the locus of the lactate dehydrogenase encoding gene ldhD in the genome of K. oxytoca to simultaneously block lactate production and regenerate NAD+.	NAD	197-201	2-hydroxyacid dehydrogenase	Klebsiella oxytoca	70-91
33424902-4	2020	The difficulty to isolate ProDH in active form has led several researchers to erroneously report proline-dependent NAD+ reduction at pH 10 as ProDH activity.	NAD	115-119	proline dehydrogenase 1	Homo sapiens	26-31
33424902-4	2020	The difficulty to isolate ProDH in active form has led several researchers to erroneously report proline-dependent NAD+ reduction at pH 10 as ProDH activity.	NAD	115-119	proline dehydrogenase 1	Homo sapiens	142-147
33424902-6	2020	ProDH does not use NAD+ as electron acceptor but can be assayed with the artificial electron acceptor 2,6-dichlorophenolindophenol (DCPIP) after detergent-mediated solubilization or enrichment of mitochondria.	NAD	19-23	proline dehydrogenase 1	Homo sapiens	0-5
33297334-6	2020	Moreover, the NADH-stabilized 26S PC is efficient in degrading intrinsically disordered protein (IDP) substrates that might not require ATP-dependent unfolding, such as p27, Tau, c-Fos and more.	NAD	14-18	microtubule associated protein tau	Homo sapiens	174-177
33385109-0	2021	Targeting CD38-dependent NAD+ metabolism to mitigate multiple organ fibrosis.	NAD	25-29	CD38 molecule	Homo sapiens	10-14
33385109-2	2021	Age-related pathologies are associated with organismal decline in nicotinamide adenine dinucleotide (NAD+) that is due to dysregulation of NAD+ homeostasis and involves the NADase CD38.	NAD	66-99	CD38 molecule	Homo sapiens	180-184
33385109-2	2021	Age-related pathologies are associated with organismal decline in nicotinamide adenine dinucleotide (NAD+) that is due to dysregulation of NAD+ homeostasis and involves the NADase CD38.	NAD	101-105	CD38 molecule	Homo sapiens	180-184
33385109-3	2021	We now show that CD38 is upregulated in patients with diffuse cutaneous SSc, and CD38 levels in the skin associate with molecular fibrosis signatures, as well as clinical fibrosis scores, while expression of key NAD+-synthesizing enzymes is unaltered.	NAD	212-216	CD38 molecule	Homo sapiens	17-21
31710686-8	2020	Mechanistically, both niacin and nicotinamide supplementation increased nicotinamide adenine dinucleotide (NAD+) levels and NAD+-dependent Sirt1 activity, which were reduced in AAA tissues.	NAD	124-127	sirtuin 1	Mus musculus	139-144
32672888-1	2020	We have discovered the sirtuin rearranging ligands (SirReals) as a novel class of highly potent and selective inhibitors of the NAD+-dependent lysine deacetylase sirtuin 2 (Sirt2).	NAD	128-131	sirtuin 2	Homo sapiens	162-171
32672888-1	2020	We have discovered the sirtuin rearranging ligands (SirReals) as a novel class of highly potent and selective inhibitors of the NAD+-dependent lysine deacetylase sirtuin 2 (Sirt2).	NAD	128-131	sirtuin 2	Homo sapiens	173-178
33329591-1	2020	CD38 is a molecule that can act as an enzyme, with NAD-depleting and intracellular signaling activity, or as a receptor with adhesive functions.	NAD	51-54	CD38 molecule	Homo sapiens	0-4
33329591-4	2020	The role of CD38 in immune cells ranges from modulating cell differentiation to effector functions during inflammation, where CD38 may regulate cell recruitment, cytokine release, and NAD availability.	NAD	184-187	CD38 molecule	Homo sapiens	12-16
33329591-4	2020	The role of CD38 in immune cells ranges from modulating cell differentiation to effector functions during inflammation, where CD38 may regulate cell recruitment, cytokine release, and NAD availability.	NAD	184-187	CD38 molecule	Homo sapiens	126-130
33163999-3	2020	SORDH is an enzyme involved in carbohydrate metabolism converting sorbitol, the sugar alcohol form of glucose, into fructose, with NAD+ as a cofactor being simultaneously reduced to NADH.	NAD	131-135	sorbitol dehydrogenase	Bos taurus	0-5
33163999-3	2020	SORDH is an enzyme involved in carbohydrate metabolism converting sorbitol, the sugar alcohol form of glucose, into fructose, with NAD+ as a cofactor being simultaneously reduced to NADH.	NAD	182-186	sorbitol dehydrogenase	Bos taurus	0-5
32935380-3	2020	Supplementation with the NAD precursor, nicotinamide riboside, and CD38 inhibition improved NAD homeostasis, thereby alleviating telomere damage, defective mitochondrial biosynthesis and clearance, cell growth retardation, and cellular senescence of DC fibroblasts.	NAD	92-95	CD38 molecule	Homo sapiens	67-71
33139340-1	2020	Tumors mutated in IDH1 tend to have lower levels of the essential substrate NAD+.	NAD	76-80	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	18-22
31340681-3	2020	Sirtuin 3 (SIRT3), an NAD-dependent deacetylase, plays a central role in maintaining cellular metabolic homeostasis.	NAD	22-25	sirtuin 3	Mus musculus	0-9
31340681-3	2020	Sirtuin 3 (SIRT3), an NAD-dependent deacetylase, plays a central role in maintaining cellular metabolic homeostasis.	NAD	22-25	sirtuin 3	Mus musculus	11-16
32941246-1	2020	PURPOSE OF REVIEW: Here we review recent literature on the emerging role of nicotinamide adenine dinucleotide (NAD) metabolism and its dysfunction via the enzyme CD38 in the pathogenesis of rheumatologic diseases.	NAD	76-109	CD38 molecule	Homo sapiens	162-166
32941246-1	2020	PURPOSE OF REVIEW: Here we review recent literature on the emerging role of nicotinamide adenine dinucleotide (NAD) metabolism and its dysfunction via the enzyme CD38 in the pathogenesis of rheumatologic diseases.	NAD	111-114	CD38 molecule	Homo sapiens	162-166
32941246-2	2020	We evaluate the potential of targeting CD38 to ameliorate NAD-related metabolic imbalance and tissue dysfunction in the treatment of systemic sclerosis (SSc), systemic lupus erythematous (SLE), and rheumatoid arthritis (RA).	NAD	58-61	CD38 molecule	Homo sapiens	39-43
32941246-4	2020	In particular, recent studies implicate increased activity of CD38, one of the main enzymes in NAD catabolism, in the pathogenesis of persistent systemic fibrosis in SSc, and increased susceptibility of SLE patients to infections.	NAD	95-98	CD38 molecule	Homo sapiens	62-66
32941246-6	2020	SUMMARY: Recent studies identify potential therapeutic approaches for boosting NAD to treat rheumatologic diseases including SSc, RA, and SLE, with particular attention to inhibition of CD38 enzymatic activity as a target.	NAD	79-82	CD38 molecule	Homo sapiens	186-190
32965071-6	2020	Reagents targeting the NAD+ -dependent deacetylase activity of SIRT2 would be beneficial for inhibiting tumor lymphangiogenesis and treating other hypoxia-related diseases.	NAD	23-26	sirtuin 2	Homo sapiens	63-68
33199925-2	2020	NAD+ decline can be partially prevented by knockout of the enzyme CD38.	NAD	0-4	CD38 molecule	Homo sapiens	66-70
33199925-7	2020	Finally, blocking the ecto-enzymatic activity of CD38 can increase NAD+ through a nicotinamide mononucleotide (NMN)-dependent process.	NAD	67-71	CD38 molecule	Homo sapiens	49-53
33199925-8	2020	Our findings demonstrate that senescence-induced inflammation promotes accumulation of CD38 in immune cells that, through its ecto-enzymatic activity, decreases levels of NMN and NAD+.	NAD	179-183	CD38 molecule	Homo sapiens	87-91
33053837-4	2020	In this study, DUSP22 is used to investigate the importance of the DPN-triloop interaction in active site formation.	NAD	67-70	dual specificity phosphatase 22	Homo sapiens	15-21
32933349-7	2022	We noted that HTT null cardiomyocytes showed diminished intracellular ATP (4.9 +- 0.5; 6.7 +- 0.4 nmol/mg protein HTT KO vs. SCR) and NAD+ (0.9 +- 0.1; 1.6 +- 0.1 nmol/mg HTT KO vs. SCR).	NAD	134-138	huntingtin	Mus musculus	14-17
32664470-8	2020	We find LRE1 to be an effective inducer of a mitohormetic response based on all parameters tested, a phenomenon that appears to require the activity of the NAD+-dependent sirtuin deacylase (SirT3) and the subsequent deacetylation of mitochondrial proteins.	NAD	156-160	sirtuin 3	Rattus norvegicus	190-195
32289286-6	2020	Overexpression of APP/PS1 impaired learning and memory of mice; produced more senile plaques, disrupted membranes, and resulted in broken or absent cristae of mitochondria in the brain; decreased levels of A disintegrin and metallopeptidase domain 10, beta-secretase 2, 8-oxoguanine DNA glycosylase-1, PGC-1alpha, and NAD+; and increased levels of beta-secretase 1 and apoptosis.	NAD	318-322	presenilin 1	Mus musculus	22-25
32380185-4	2020	The production of reactive oxygen species (ROS) induces DNA damage and the consequent PARP-1 activation, which depletes NAD+ and ATP, resulting in brain injury.	NAD	120-124	poly (ADP-ribose) polymerase 1	Rattus norvegicus	86-92
32519817-4	2020	We further demonstrated that the NAD-dependent protein deacetylase, SIRT7, and the FOXO4 transcription factor acted as endogenous brakes for GLS1 expression, which are inhibited by TGF-beta.	NAD	33-36	glutaminase	Homo sapiens	141-145
32319590-5	2020	Liquid chromatography-tandem mass spectrometry and bioinformatic analyses revealed that differentially abundant proteins in CD38-overexpressed cervical cancer cells (CaSki-CD38 and HeLa-CD38) are predominantly involved in glycolytic pathways, oxidative phosphorylation and the NAD/NADH metabolic process.	NAD	277-280	CD38 molecule	Homo sapiens	124-128
32319590-5	2020	Liquid chromatography-tandem mass spectrometry and bioinformatic analyses revealed that differentially abundant proteins in CD38-overexpressed cervical cancer cells (CaSki-CD38 and HeLa-CD38) are predominantly involved in glycolytic pathways, oxidative phosphorylation and the NAD/NADH metabolic process.	NAD	277-280	CD38 molecule	Homo sapiens	172-176
32319590-5	2020	Liquid chromatography-tandem mass spectrometry and bioinformatic analyses revealed that differentially abundant proteins in CD38-overexpressed cervical cancer cells (CaSki-CD38 and HeLa-CD38) are predominantly involved in glycolytic pathways, oxidative phosphorylation and the NAD/NADH metabolic process.	NAD	277-280	CD38 molecule	Homo sapiens	172-176
32319590-5	2020	Liquid chromatography-tandem mass spectrometry and bioinformatic analyses revealed that differentially abundant proteins in CD38-overexpressed cervical cancer cells (CaSki-CD38 and HeLa-CD38) are predominantly involved in glycolytic pathways, oxidative phosphorylation and the NAD/NADH metabolic process.	NAD	281-285	CD38 molecule	Homo sapiens	124-128
32319590-5	2020	Liquid chromatography-tandem mass spectrometry and bioinformatic analyses revealed that differentially abundant proteins in CD38-overexpressed cervical cancer cells (CaSki-CD38 and HeLa-CD38) are predominantly involved in glycolytic pathways, oxidative phosphorylation and the NAD/NADH metabolic process.	NAD	281-285	CD38 molecule	Homo sapiens	172-176
32319590-5	2020	Liquid chromatography-tandem mass spectrometry and bioinformatic analyses revealed that differentially abundant proteins in CD38-overexpressed cervical cancer cells (CaSki-CD38 and HeLa-CD38) are predominantly involved in glycolytic pathways, oxidative phosphorylation and the NAD/NADH metabolic process.	NAD	281-285	CD38 molecule	Homo sapiens	172-176
32065636-0	2020	Down-regulation of a Mitochondrial NAD+ Transporter (NDT2) Alters Seed Production and Germination in Arabidopsis.	NAD	35-38	NAD+ transporter 2	Arabidopsis thaliana	53-57
32065636-2	2020	We previously characterized the Arabidopsis thaliana gene (At1g25380), named AtNDT2, encoding a protein located in the mitochondrial inner membrane, which imports NAD+ from the cytosol using ADP and AMP as counter-exchange substrates for NAD+.	NAD	163-166	NAD+ transporter 2	Arabidopsis thaliana	77-83
32065636-2	2020	We previously characterized the Arabidopsis thaliana gene (At1g25380), named AtNDT2, encoding a protein located in the mitochondrial inner membrane, which imports NAD+ from the cytosol using ADP and AMP as counter-exchange substrates for NAD+.	NAD	238-241	NAD+ transporter 2	Arabidopsis thaliana	77-83
32065636-7	2020	Furthermore, flowers and seedlings of NDT2 mutants displayed up-regulation of de novo and salvage pathway genes encoding for NAD+ biosynthesis enzymes, demonstrating the transcriptional control mediated by NDT2 activity over these genes.	NAD	125-128	NAD+ transporter 2	Arabidopsis thaliana	38-42
32065636-7	2020	Furthermore, flowers and seedlings of NDT2 mutants displayed up-regulation of de novo and salvage pathway genes encoding for NAD+ biosynthesis enzymes, demonstrating the transcriptional control mediated by NDT2 activity over these genes.	NAD	125-128	NAD+ transporter 2	Arabidopsis thaliana	206-210
32065636-8	2020	Taken together, our results suggest that NDT2 expression is fundamental for maintaining NAD+ balance among organelles that modulate metabolism, physiology and developmental processes of heterotrophic tissues.	NAD	88-91	NAD+ transporter 2	Arabidopsis thaliana	41-45
32056076-8	2020	The transcriptional footprint of NMN treatment indicates that increased NAD+ levels promote SIRT1 activation in the neurovascular unit, as demonstrated by analysis of upstream regulators of differentially expressed genes as well as analysis of the expression of known SIRT1-dependent genes.	NAD	72-75	sirtuin 1	Mus musculus	92-97
32180563-4	2020	METHODS: Here we report that the oxidoreductase cytochrome b5 reductase 3 (Cyb5r3) links FoxO1 signaling to beta-cell stimulus/secretion coupling by regulating mitochondrial function, reactive oxygen species generation, and nicotinamide actin dysfunction (NAD)/reduced nicotinamide actin dysfunction (NADH) ratios.	NAD	301-305	forkhead box O1	Mus musculus	89-94
31932322-1	2020	The enzyme Tpt1 removes an internal RNA 2"-PO4 via a two-step reaction in which: (i) the 2"-PO4 attacks NAD+ to form an RNA-2"-phospho-(ADP-ribose) intermediate and nicotinamide; and (ii) transesterification of the ADP-ribose O2"" to the RNA 2"-phosphodiester yields 2"-OH RNA and ADP-ribose-1"",2""-cyclic phosphate.	NAD	104-108	tumor protein, translationally-controlled 1	Homo sapiens	11-15
32142284-1	2020	Deoxyhypusine synthase (DHPS) utilizes spermidine and NAD as cofactors to incorporate a hypusine modification into the eukaryotic translation initiation factor 5A (eIF5A).	NAD	54-57	eukaryotic translation initiation factor 5A	Homo sapiens	119-162
32142284-1	2020	Deoxyhypusine synthase (DHPS) utilizes spermidine and NAD as cofactors to incorporate a hypusine modification into the eukaryotic translation initiation factor 5A (eIF5A).	NAD	54-57	eukaryotic translation initiation factor 5A	Homo sapiens	164-169
31932479-1	2020	The NAD-dependent histone deacetylase sirtuin 2 (SIRT2) plays critical roles in mitosis and cell cycle progression and recently was shown to suppress tumor growth and to be down-regulated in several types of cancers.	NAD	4-7	sirtuin 2	Homo sapiens	38-47
31932479-1	2020	The NAD-dependent histone deacetylase sirtuin 2 (SIRT2) plays critical roles in mitosis and cell cycle progression and recently was shown to suppress tumor growth and to be down-regulated in several types of cancers.	NAD	4-7	sirtuin 2	Homo sapiens	49-54
31838391-6	2020	Moreover, our results showed that NAD+ insufficiency is responsible for BDE-47-mediated mitophagy defect and mitochondrial dysfunction in mouse livers, which was associated with suppression of Sirt3/FoxO3a/PINK1 signaling.	NAD	34-37	sirtuin 3	Mus musculus	193-198
31838391-6	2020	Moreover, our results showed that NAD+ insufficiency is responsible for BDE-47-mediated mitophagy defect and mitochondrial dysfunction in mouse livers, which was associated with suppression of Sirt3/FoxO3a/PINK1 signaling.	NAD	34-37	PTEN induced putative kinase 1	Mus musculus	206-211
31586008-9	2020	Altering NADH and NADPH metabolism using drug strategies and IDH1 mutations resulted in significant changes in 64Cu-ATSM signal under normoxic conditions.	NAD	9-13	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	61-65
32061543-2	2020	Recently, Katsuyama et al., demonstrated that the CD38/NAD/Sirtuin1/EZH2 axis reduces cytolytic CD8+ T cell function and might be targeted to overcome incidence of infections.	NAD	55-58	CD38 molecule	Homo sapiens	50-54
32103017-4	2020	We demonstrate that the NAD+-dependent deacylase SIRT2 removes the myristoyl group, and our evidence suggests that NMT prefers the GTP-bound while SIRT2 prefers the GDP-bound ARF6.	NAD	24-28	sirtuin 2	Homo sapiens	49-54
32103017-4	2020	We demonstrate that the NAD+-dependent deacylase SIRT2 removes the myristoyl group, and our evidence suggests that NMT prefers the GTP-bound while SIRT2 prefers the GDP-bound ARF6.	NAD	24-28	sirtuin 2	Homo sapiens	147-152
32103017-4	2020	We demonstrate that the NAD+-dependent deacylase SIRT2 removes the myristoyl group, and our evidence suggests that NMT prefers the GTP-bound while SIRT2 prefers the GDP-bound ARF6.	NAD	24-28	ADP ribosylation factor 6	Homo sapiens	175-179
32017914-15	2020	However, EX-527(inhibitor of SIRT1) decreased NAD+/NADH ratio and increased acetyl-p53 levels, and abolished the cardioprotective effects of taurine on mice subjected to TAC and increased apoptosis and oxidative stress.	NAD	46-50	sirtuin 1	Mus musculus	29-34
32017914-15	2020	However, EX-527(inhibitor of SIRT1) decreased NAD+/NADH ratio and increased acetyl-p53 levels, and abolished the cardioprotective effects of taurine on mice subjected to TAC and increased apoptosis and oxidative stress.	NAD	51-55	sirtuin 1	Mus musculus	29-34
31773269-3	2020	This interaction leads to the formation of one-electron reduced cobalamin, cob(II)alamin, and proceeds via water substitution on aquacobalamin by NADH and further decomposition of NADH-Co(III) complex to cob(II)alamin and NADH +.	NAD	146-150	metabolism of cobalamin associated B	Homo sapiens	64-67
31773269-3	2020	This interaction leads to the formation of one-electron reduced cobalamin, cob(II)alamin, and proceeds via water substitution on aquacobalamin by NADH and further decomposition of NADH-Co(III) complex to cob(II)alamin and NADH +.	NAD	180-192	metabolism of cobalamin associated B	Homo sapiens	64-67
31773269-3	2020	This interaction leads to the formation of one-electron reduced cobalamin, cob(II)alamin, and proceeds via water substitution on aquacobalamin by NADH and further decomposition of NADH-Co(III) complex to cob(II)alamin and NADH +.	NAD	180-192	metabolism of cobalamin associated B	Homo sapiens	75-78
31773269-3	2020	This interaction leads to the formation of one-electron reduced cobalamin, cob(II)alamin, and proceeds via water substitution on aquacobalamin by NADH and further decomposition of NADH-Co(III) complex to cob(II)alamin and NADH +.	NAD	180-184	metabolism of cobalamin associated B	Homo sapiens	64-67
31773269-3	2020	This interaction leads to the formation of one-electron reduced cobalamin, cob(II)alamin, and proceeds via water substitution on aquacobalamin by NADH and further decomposition of NADH-Co(III) complex to cob(II)alamin and NADH +.	NAD	180-184	metabolism of cobalamin associated B	Homo sapiens	75-78
31936501-4	2020	Here, we found that agc1Delta yeasts decreased fat utilization, impaired NADH balance in peroxisomes, and decreased chronological lifespan.	NAD	73-77	citrin	Saccharomyces cerevisiae S288C	20-24
31936501-5	2020	The activation of GPD1-mediated NAD+ regeneration in peroxisomes by GPD1 over-expression or activation of the malate-oxaloacetate NADH peroxisomal shuttle, by increasing flux in this NADH shuttle and over-expression of MDH3, resulted in lifespan extension of agc1Delta yeasts.	NAD	32-35	citrin	Saccharomyces cerevisiae S288C	259-263
31936501-5	2020	The activation of GPD1-mediated NAD+ regeneration in peroxisomes by GPD1 over-expression or activation of the malate-oxaloacetate NADH peroxisomal shuttle, by increasing flux in this NADH shuttle and over-expression of MDH3, resulted in lifespan extension of agc1Delta yeasts.	NAD	110-134	citrin	Saccharomyces cerevisiae S288C	259-263
31936501-5	2020	The activation of GPD1-mediated NAD+ regeneration in peroxisomes by GPD1 over-expression or activation of the malate-oxaloacetate NADH peroxisomal shuttle, by increasing flux in this NADH shuttle and over-expression of MDH3, resulted in lifespan extension of agc1Delta yeasts.	NAD	130-134	citrin	Saccharomyces cerevisiae S288C	259-263
31936501-7	2020	The effect of PEX34-mediated longevity required the presence of the GPD1-mediated NADH peroxisomal shuttle, which was independent of the presence of the peroxisomal malate-oxaloacetate NADH shuttle and PEX34-induced peroxisome proliferation.	NAD	82-86	Pex34p	Saccharomyces cerevisiae S288C	14-19
31936501-7	2020	The effect of PEX34-mediated longevity required the presence of the GPD1-mediated NADH peroxisomal shuttle, which was independent of the presence of the peroxisomal malate-oxaloacetate NADH shuttle and PEX34-induced peroxisome proliferation.	NAD	165-189	Pex34p	Saccharomyces cerevisiae S288C	14-19
31691304-7	2020	Importantly, genetic deficiencies in several metabolite repair enzymes lead to "inborn errors of metabolite repair", such as L-2-hydroxyglutaric aciduria, D-2-hydroxyglutaric aciduria, "ubiquitous glucose-6-phosphatase" (G6PC3) deficiency, the neutropenia present in Glycogen Storage Disease type Ib or defects in the enzymes that repair the hydrated forms of NADH or NADPH.	NAD	360-364	glucose-6-phosphatase catalytic subunit 3	Homo sapiens	221-226
31878234-6	2019	When intracellular NAD+ was increased by a mutation of pme-1 (poly (ADP-ribose) metabolism enzyme 1) or by pretreatment with NAD+ in the medium, the lifespan extension ability of NA disappeared.	NAD	19-22	protein phosphatase methylesterase 1	Homo sapiens	55-60
31578871-7	2019	The calcification and downregulated Klotho protein levels induced by salusin-beta were restored by ROS scavenger NAC, DPI (an inhibitor of flavin-containing enzyme, including NAD(P)H oxidase), or gene knockdown of NOX-2, p22phox or p47phox, but were not affected by NOX-1 and NOX-4 knockdown.	NAD	175-182	Klotho	Rattus norvegicus	36-42
31578871-11	2019	CONCLUSION: Salusin-beta regulates VC through activation of NAD(P)H/ROS mediated Klotho downregulation, suggesting that salusin-beta may be a novel target for treatment of VC.	NAD	60-67	Klotho	Rattus norvegicus	81-87
31847204-3	2019	As an ectoenzyme, CD38 functions as a metabolic sensor catalyzing the extracellular conversion of NAD+ to the immunosuppressive factor adenosine (ADO).	NAD	98-101	CD38 molecule	Homo sapiens	18-22
31598701-5	2019	Pyruvate represses histone gene expression by inducing the expression of NAD+ biosynthesis enzyme, nicotinamide phosphoribosyltransferase (NAMPT) via myocyte enhancer factor 2C (MEF2C), which then increases NAD+ levels and activates the histone deacetylase activity of SIRT1.	NAD	207-210	myocyte enhancer factor 2C	Homo sapiens	150-176
31598701-5	2019	Pyruvate represses histone gene expression by inducing the expression of NAD+ biosynthesis enzyme, nicotinamide phosphoribosyltransferase (NAMPT) via myocyte enhancer factor 2C (MEF2C), which then increases NAD+ levels and activates the histone deacetylase activity of SIRT1.	NAD	207-210	myocyte enhancer factor 2C	Homo sapiens	178-183
31538237-6	2019	The homozygous missense variant in the NAD+-binding domain of MDH1 led to severely diminished MDH protein expression.	NAD	39-43	malate dehydrogenase 1	Homo sapiens	62-66
31538237-6	2019	The homozygous missense variant in the NAD+-binding domain of MDH1 led to severely diminished MDH protein expression.	NAD	39-43	malate dehydrogenase 1	Homo sapiens	62-65
31702813-6	2019	The administration of NAD+ alleviated the spatial learning and memory of APP/PS1 mice and reduced senile plaques.	NAD	22-26	presenilin 1	Mus musculus	77-80
31649033-4	2019	Notably, GSNO reductase (GSNOR, Adh5) accounts for most NADH-dependent GSNOR activity, whereas NADPH-dependent GSNOR activity is largely unaccounted for (CBR1 mediates a minor portion).	NAD	56-60	alcohol dehydrogenase 5 (class III), chi polypeptide	Mus musculus	71-76
31783629-4	2019	Furthermore, CD38 metabolizes extracellular NAD+, generating ADPR and cyclic ADPR.	NAD	44-48	CD38 molecule	Homo sapiens	13-17
31754102-5	2019	NAD+ repletion restores NAD+ metabolic profiles and improves mitochondrial quality through DCT-1 and ULK-1-dependent mitophagy.	NAD	0-4	solute carrier family 36 member 1	Homo sapiens	91-96
31465774-0	2019	Functions of aryl hydrocarbon receptor (AHR) and CD38 in NAD metabolism and nonalcoholic steatohepatitis (NASH).	NAD	57-60	CD38 molecule	Homo sapiens	49-53
31465774-2	2019	AHR targets of the latter function are PARPs/ARTs and CD38 that are regulating glucose and lipid metabolism via NAD-dependent sirtuins.	NAD	112-115	CD38 molecule	Homo sapiens	54-58
31465774-7	2019	However, these proteins are also involved in protection against inflammation and CD38-mediated age-related decreased NAD levels that may be responsible for neurodegeneration.	NAD	117-120	CD38 molecule	Homo sapiens	81-85
31590397-0	2019	Ginsenoside Rb1 Attenuates High Glucose-Induced Oxidative Injury via the NAD-PARP-SIRT Axis in Rat Retinal Capillary Endothelial Cells.	NAD	73-76	poly (ADP-ribose) polymerase 1	Rattus norvegicus	77-81
31636635-2	2019	There, high extracellular levels of nucleotides, mainly NAD+ and ATP, are catabolized by different ectonucleotidases, which can be divided in two families according to substrate specificity: on one side those that metabolize NAD+, including CD38, CD157, and CD203a; on the other, those that convert ATP, namely CD39 (and other ENTPDases) and CD73.	NAD	56-60	CD38 molecule	Homo sapiens	241-245
31636635-2	2019	There, high extracellular levels of nucleotides, mainly NAD+ and ATP, are catabolized by different ectonucleotidases, which can be divided in two families according to substrate specificity: on one side those that metabolize NAD+, including CD38, CD157, and CD203a; on the other, those that convert ATP, namely CD39 (and other ENTPDases) and CD73.	NAD	56-60	ectonucleoside triphosphate diphosphohydrolase 1	Homo sapiens	311-315
31636635-2	2019	There, high extracellular levels of nucleotides, mainly NAD+ and ATP, are catabolized by different ectonucleotidases, which can be divided in two families according to substrate specificity: on one side those that metabolize NAD+, including CD38, CD157, and CD203a; on the other, those that convert ATP, namely CD39 (and other ENTPDases) and CD73.	NAD	225-229	CD38 molecule	Homo sapiens	241-245
31636635-2	2019	There, high extracellular levels of nucleotides, mainly NAD+ and ATP, are catabolized by different ectonucleotidases, which can be divided in two families according to substrate specificity: on one side those that metabolize NAD+, including CD38, CD157, and CD203a; on the other, those that convert ATP, namely CD39 (and other ENTPDases) and CD73.	NAD	225-229	ectonucleoside triphosphate diphosphohydrolase 1	Homo sapiens	311-315
31607329-9	2019	After treatment, the expressions of TLR2, TLR4, TLR6 and HMGB in CR and NAD groups was significantly lower than that before treatment (P<0.05), while the expressions levels of TLR2, TLR4, TLR6 and HMGB in AD and RD groups were no statistically significant different from those before treatment (P<0.05); the expressions levels of TLR2, TLR4, TLR6 and HMGB in dealth group all were higher than those in survival group (P<0.05).	NAD	72-75	toll like receptor 4	Homo sapiens	42-46
31763496-1	2019	BACKGROUND: Sirtuin 1 (SIRT1) is a NAD+-dependent enzyme that has important roles in many biological processes involved in aging, including cell growth and repair, inflammation, and energy regulation.	NAD	35-38	sirtuin 1	Mus musculus	12-21
31763496-1	2019	BACKGROUND: Sirtuin 1 (SIRT1) is a NAD+-dependent enzyme that has important roles in many biological processes involved in aging, including cell growth and repair, inflammation, and energy regulation.	NAD	35-38	sirtuin 1	Mus musculus	23-28
31510043-5	2019	We recently identified and characterized a new class of nicotinamide adenine dinucleotide-dependent deacetylase isoform 2 of sirtuin protein (SIRT2) inhibitors that can be utilized as cytotoxic agents based on an S-trityl-l-histidine scaffold.	NAD	56-89	sirtuin 2	Homo sapiens	142-147
32624970-2	2019	In this study, E. coli MEC697 (MG1655 nadR nudC mazG) maintained a larger pool of NAD(H) compared to the wild-type control, and also accumulated lower concentrations of acetate when grown in batch culture on glucose.	NAD	82-88	RNA decapping hydrolase	Escherichia coli str. K-12 substr. MG1655	43-47
30936015-4	2019	The radioactivity of [32P]NAD+ was incorporated into human ADH1 by human poly(ADP-ribose) polymerase 1 in vitro, but was not incorporated when heat-inactivated PARP1 or a PARP inhibitor, 3-aminobenzamide, was used.	NAD	26-30	alcohol dehydrogenase 1A (class I), alpha polypeptide	Homo sapiens	59-63
31140145-10	2019	Enzyme annotation of the family and superfamily revealed that it encodes to five structural clusters and coding to enzymes NAD(P)H oxidase (H2O2-forming) (EC:1.6.3.1), Ferric-chelate reductase (NADH) (EC: 1.16.1.7), Peroxidase (EC: 1.11.1.7), Ribose-phosphate diphosphokinase (EC: 2.7.6.1).	NAD	194-198	peroxidase-like	Triticum aestivum	216-226
31474877-3	2019	SIRT3 is an NAD+-dependent deacetylase primarily located inside mitochondria, and reports on the effect of chronic alcohol exposure on liver SIRT3 expression are scarce.	NAD	12-15	sirtuin 3	Mus musculus	0-5
31184932-0	2019	Exogenous H2S reduces the acetylation levels of mitochondrial respiratory enzymes via regulating the NAD+-SIRT3 pathway in cardiac tissues of db/db mice.	NAD	101-105	sirtuin 3	Mus musculus	106-111
31415077-9	2019	The replenishment of NMN or NAD+ partially slowed down corneal nerve fiber degeneration, reduced the epithelial defect in denervated mice, and improved apoptosis induction in FK866-treated cells by restoring the activation levels of SIRT1, AKT, and CREB.	NAD	28-32	sirtuin 1	Mus musculus	233-238
33365629-3	2019	Excluding tRNA sequences, sequence divergence rate was lowest in rRNA genes and highest in genes encoding NADH (specifically ND1, ND2, ND3) and the control region.	NAD	106-110	mitochondrially encoded NADH dehydrogenase 3	Homo sapiens	135-138
29981012-6	2019	We measured the two-photon excitation fluorescence (TPEF) signal of nicotinamide adenine dinucleotide hydride (NADH) and elastin and second harmonic generation (SHG) signal of collagen on 10 ex vivo healthy control and BCC skin samples and compared the images by different quantitative image analysis methods.	NAD	111-115	transmembrane protein with EGF like and two follistatin like domains 2	Homo sapiens	52-56
31144814-0	2019	Identification of Diketopiperazine-Containing 2-Anilinobenzamides as Potent Sirtuin 2 (SIRT2)-Selective Inhibitors Targeting the "Selectivity Pocket", Substrate-Binding Site, and NAD+-Binding Site.	NAD	179-183	sirtuin 2	Mus musculus	76-85
31144814-0	2019	Identification of Diketopiperazine-Containing 2-Anilinobenzamides as Potent Sirtuin 2 (SIRT2)-Selective Inhibitors Targeting the "Selectivity Pocket", Substrate-Binding Site, and NAD+-Binding Site.	NAD	179-183	sirtuin 2	Mus musculus	87-92
31144814-5	2019	Inhibition of SIRT2 by 53 was mediated by the formation of a 53-ADP-ribose conjugate, suggesting that 53 is a mechanism-based inhibitor targeting the "selectivity pocket", substrate-binding site, and NAD+-binding site.	NAD	200-204	sirtuin 2	Mus musculus	14-19
31242212-1	2019	Activation of SIRT1, an NAD+-dependent protein deacetylase, ameliorates muscular pathophysiology of delta-sarcoglycan-deficient TO-2 hamsters and dystrophin-deficient mdx mice.	NAD	24-27	sirtuin 1	Mus musculus	14-19
30909324-6	2019	To sum up, our data indicate a role for NMNAT2 in controlling redox homeostasis during oocyte maturation and uncover that NMNAT2- NAD+ -SIRT1 is an important pathway mediating the effects of maternal age on oocyte developmental competence.	NAD	130-134	sirtuin 1	Mus musculus	136-141
31140365-8	2019	In turn, increased CD38 expression is believed to be the key modulator of lowered NAD+ levels with aging in mammals.	NAD	82-86	CD38 molecule	Homo sapiens	19-23
30975470-0	2019	The NADase CD38 is induced by factors secreted from senescent cells providing a potential link between senescence and age-related cellular NAD+ decline.	NAD	139-143	CD38 molecule	Homo sapiens	11-15
30975470-2	2019	We have recently identified CD38 as a central regulator involved in tissue NAD+ decline during the aging process.	NAD	75-79	CD38 molecule	Homo sapiens	28-32
30975470-9	2019	Our data suggest a link between cellular senescence and NAD+ decline in which SASP-mediated upregulation of CD38 can disrupt cellular NAD+ homeostasis.	NAD	56-60	CD38 molecule	Homo sapiens	108-112
30975470-9	2019	Our data suggest a link between cellular senescence and NAD+ decline in which SASP-mediated upregulation of CD38 can disrupt cellular NAD+ homeostasis.	NAD	134-138	CD38 molecule	Homo sapiens	108-112
31281500-15	2019	CD38 is a member of the NAD+ glycohydrolase family that catalyzes the cyclization of extracellular NAD+ to intracellular cADPR.	NAD	24-28	CD38 molecule	Homo sapiens	0-4
31281500-17	2019	Thus, endocytosis involving isolated mitochondria internalization was mediated by NAD+-CD38-cADPR-Ca2+ signaling.	NAD	82-86	CD38 molecule	Homo sapiens	87-91
31281500-21	2019	Conclusion: These findings suggested that starvation-induced endocytosis via NAD+-CD38-cADPR-Ca2+ signaling could be a new mechanism of mitochondrial transplantation to rescue aerobic respiration and attenuate the Warburg effect.	NAD	77-81	CD38 molecule	Homo sapiens	82-86
30779909-6	2019	CD38 is involved in extra- and intracellular NAD degradation but acts also as differentiation marker.	NAD	45-48	CD38 molecule	Homo sapiens	0-4
30885568-3	2019	In this paper, we developed inhibitors of nicotinamide adenine dinucleotide-dependent deacetylase isoform 2 of Sirtuin protein (SIRT2), based on HPH-1Trt/HPH-2Trt, and aimed to generate new anti-cancer drugs.	NAD	42-75	sirtuin 2	Homo sapiens	128-133
30836176-1	2019	17beta-Hydroxysteroid dehydrogenase type 14 (17beta-HSD14) catalyzes the conversion of highly active estrogens and androgens into their less active oxidized forms in presence of NAD+ as cofactor.	NAD	178-182	hydroxysteroid 17-beta dehydrogenase 14	Homo sapiens	0-57
31068926-4	2019	At neutral and acidic pH, CD38 catalyzes the extracellular conversion of NAD+ to regulators of calcium signaling.	NAD	73-77	CD38 molecule	Homo sapiens	26-30
31068926-5	2019	The initial disassembly of NAD+ is also followed by adenosinergic activity, if CD38 is operating in the presence of CD203a and CD73 nucleotidases.	NAD	27-31	CD38 molecule	Homo sapiens	79-83
30907577-1	2019	The sodium-pumping NADH:quinone oxidoreductase (Na+-NQR) is a bacterial enzyme that oxidizes NADH, reduces ubiquinone, and translocates Na+ across the membrane.	NAD	19-23	crystallin zeta	Homo sapiens	24-46
30907577-1	2019	The sodium-pumping NADH:quinone oxidoreductase (Na+-NQR) is a bacterial enzyme that oxidizes NADH, reduces ubiquinone, and translocates Na+ across the membrane.	NAD	93-97	crystallin zeta	Homo sapiens	24-46
30617135-5	2019	RESULTS: beta-Lap administration after IR treatment hyperactivated PARP, greatly lowered NAD+/ATP levels, and increased double-strand break (DSB) lesions over time in vitro.	NAD	89-93	LAP	Homo sapiens	14-17
30617135-8	2019	PK/PD responses confirm that IR + beta-lap treatments hyperactivate PARP activity, greatly lower NAD+/ATP levels, and dramatically inhibit DSB repair in exposed NQO1+ cancer tissue, whereas low NQO1 levels and high levels of catalase in associated normal tissue were protective.	NAD	97-101	LAP	Homo sapiens	39-42
30971927-5	2019	Such evodiamine-mediated increases in NLRP3 activation and pyroptosis were attenuated by activators of alpha-tubulin deacetylase, resveratrol and NAD+, or dynein-specific inhibitor ciliobrevin A.	NAD	146-150	NLR family, pyrin domain containing 3	Mus musculus	38-43
30901919-1	2019	Nicotinamide mononucleotide adenylyltransferase (NMNAT), a key enzyme for NAD+ synthesis, is well known for its activity in neuronal survival and attenuation of Wallerian degeneration.	NAD	74-78	Nicotinamide mononucleotide adenylyltransferase	Drosophila melanogaster	49-54
29295624-7	2019	The NAD+ deficiency in the diseases and aging results from not only poly(ADP-ribose) polymerase-1 (PARP-1) activation but also decreased nicotinamide phosphoribosyltransferase (Nampt) activity and increased CD38 activity.	NAD	4-8	CD38 molecule	Homo sapiens	207-211
30616888-2	2019	Sirtuin 2 (SIRT2) is an NAD-dependent deacetylase that regulates cellular response to oxidative stress, however, its role in NIHL remains poorly understood.	NAD	24-27	sirtuin 2	Homo sapiens	0-9
30616888-2	2019	Sirtuin 2 (SIRT2) is an NAD-dependent deacetylase that regulates cellular response to oxidative stress, however, its role in NIHL remains poorly understood.	NAD	24-27	sirtuin 2	Homo sapiens	11-16
30504209-5	2019	Analyses of d-LDH activity in MR-1 and the ldhA deletion mutant confirmed that LdhA functions as an NADH-dependent d-LDH that catalyzes the reduction of pyruvate to d-lactate.	NAD	100-104	2-hydroxyacid dehydrogenase	Shewanella oneidensis MR-1	79-83
30504209-8	2019	These results indicate that LdhA-Dld serves as a bypass of NDH in electron transfer from NADH to quinones.	NAD	89-93	2-hydroxyacid dehydrogenase	Shewanella oneidensis MR-1	28-32
30504209-8	2019	These results indicate that LdhA-Dld serves as a bypass of NDH in electron transfer from NADH to quinones.	NAD	89-93	NAD(P)/FAD-dependent oxidoreductase	Shewanella oneidensis MR-1	59-62
30504209-9	2019	Our findings suggest that the LdhA-Dld system manages intracellular redox balance by utilizing d-lactate as a temporal electron sink under electron acceptor-limited conditions.IMPORTANCE NADH-dependent LDHs are conserved among diverse organisms and contribute to NAD+ regeneration in lactic acid fermentation.	NAD	187-191	2-hydroxyacid dehydrogenase	Shewanella oneidensis MR-1	30-34
30504209-9	2019	Our findings suggest that the LdhA-Dld system manages intracellular redox balance by utilizing d-lactate as a temporal electron sink under electron acceptor-limited conditions.IMPORTANCE NADH-dependent LDHs are conserved among diverse organisms and contribute to NAD+ regeneration in lactic acid fermentation.	NAD	263-267	2-hydroxyacid dehydrogenase	Shewanella oneidensis MR-1	30-34
30504209-11	2019	Here, we show that LdhA (an NADH-dependent d-LDH) works in concert with Dld (a quinone-dependent d-LDH) to transfer electrons from NADH to quinones during sugar catabolism in S. oneidensis MR-1.	NAD	28-32	2-hydroxyacid dehydrogenase	Shewanella oneidensis MR-1	19-23
30504209-11	2019	Here, we show that LdhA (an NADH-dependent d-LDH) works in concert with Dld (a quinone-dependent d-LDH) to transfer electrons from NADH to quinones during sugar catabolism in S. oneidensis MR-1.	NAD	131-135	2-hydroxyacid dehydrogenase	Shewanella oneidensis MR-1	19-23
30644400-4	2019	Here we report a 1.4 A crystal structure of Tpt1 in a product-mimetic complex with ADP-ribose-1""-phosphate in the NAD+ site and pAp in the RNA site.	NAD	115-119	tumor protein, translationally-controlled 1	Homo sapiens	44-48
29634344-2	2019	NAD+ depletion may occur in response to either excessive DNA damage due to free radical or ultraviolet attack, resulting in significant poly(ADP-ribose) polymerase (PARP) activation and a high turnover and subsequent depletion of NAD+, and/or chronic immune activation and inflammatory cytokine production resulting in accelerated CD38 activity and decline in NAD+ levels.	NAD	0-4	CD38 molecule	Homo sapiens	331-335
30597885-3	2018	To exploit this vulnerability, we treated glioma and fibrosarcoma cells that harbor an IDH1 mutation with an inhibitor of nicotinamide adenine dinucleotide (NAD+) salvage pathway, FK866, and observed decreased viability in these cells.	NAD	122-155	isocitrate dehydrogenase 1 (NADP+), soluble	Mus musculus	87-91
30597885-3	2018	To exploit this vulnerability, we treated glioma and fibrosarcoma cells that harbor an IDH1 mutation with an inhibitor of nicotinamide adenine dinucleotide (NAD+) salvage pathway, FK866, and observed decreased viability in these cells.	NAD	157-161	isocitrate dehydrogenase 1 (NADP+), soluble	Mus musculus	87-91
30631755-8	2018	NAD also serves as a substrate for poly(ADP-ribose) polymerase (PARP), sirtuin, and NAD gylycohydrolase (CD38 and CD157); thus, NAD regulates DNA repair, gene expression, and stress response through these enzymes.	NAD	0-3	CD38 molecule	Homo sapiens	105-109
30631755-8	2018	NAD also serves as a substrate for poly(ADP-ribose) polymerase (PARP), sirtuin, and NAD gylycohydrolase (CD38 and CD157); thus, NAD regulates DNA repair, gene expression, and stress response through these enzymes.	NAD	84-87	CD38 molecule	Homo sapiens	105-109
30295421-1	2018	SIRT1 is an NAD+ -dependent deacetylase that functions in a variety of cells and tissues to mitigate age-associated diseases.	NAD	12-15	sirtuin 1	Mus musculus	0-5
29869077-2	2018	As the members of the nicotinamide adenine dinucleotide-dependent family of histone deacetylases, class I sirtuin genes (including SIRT1, SIRT2 and SIRT3) play crucial roles in regulating lipid metabolism, cellular growth and metabolism, suggesting that they are potential candidate genes affecting body measurement traits in animals.	NAD	22-55	sirtuin 3	Bos taurus	148-153
30223149-3	2018	Compound 3q exhibited H-bonding interactions with Tyr158, Thr196 and co-factor NAD+ that binds the active site of InhA.	NAD	79-83	NADH-dependent enoyl-[ACP] reductase	Mycobacterium tuberculosis H37Rv	114-118
29654491-1	2018	Sirtuin 2 (SIRT2) is a family member of nicotinamide adenine dinucleotide (NAD+)-dependent deacetylases which appears to have detrimental roles in an array of neurological disorders such as Parkinson"s disease (PD) and Huntington"s disease (HD).	NAD	40-73	sirtuin 2	Mus musculus	0-9
29654491-1	2018	Sirtuin 2 (SIRT2) is a family member of nicotinamide adenine dinucleotide (NAD+)-dependent deacetylases which appears to have detrimental roles in an array of neurological disorders such as Parkinson"s disease (PD) and Huntington"s disease (HD).	NAD	40-73	sirtuin 2	Mus musculus	11-16
29654491-1	2018	Sirtuin 2 (SIRT2) is a family member of nicotinamide adenine dinucleotide (NAD+)-dependent deacetylases which appears to have detrimental roles in an array of neurological disorders such as Parkinson"s disease (PD) and Huntington"s disease (HD).	NAD	75-78	sirtuin 2	Mus musculus	0-9
29654491-1	2018	Sirtuin 2 (SIRT2) is a family member of nicotinamide adenine dinucleotide (NAD+)-dependent deacetylases which appears to have detrimental roles in an array of neurological disorders such as Parkinson"s disease (PD) and Huntington"s disease (HD).	NAD	75-78	sirtuin 2	Mus musculus	11-16
29897845-2	2018	The objective of our study is to identify the mechanisms of renal mitochondrial oxidative stress, focusing on Sirt3, which is nicotinamide adenine dinucleotide (NAD+; oxidized NAD)-dependent deacetylase in mitochondria.	NAD	126-159	sirtuin 3	Rattus norvegicus	110-115
29897845-2	2018	The objective of our study is to identify the mechanisms of renal mitochondrial oxidative stress, focusing on Sirt3, which is nicotinamide adenine dinucleotide (NAD+; oxidized NAD)-dependent deacetylase in mitochondria.	NAD	161-165	sirtuin 3	Rattus norvegicus	110-115
30585266-5	2018	The lower NADH level in atrophic nonunion tissues disrupted CtBP2 dimerization and enhanced the blockage of the accessibility of the p300-Runx2 complex to the promoters of a series of bone-related target genes, such as OSC, ALPL, COL1A1, IBSP, SPP1 and MMP13.	NAD	10-14	secreted phosphoprotein 1	Homo sapiens	244-248
30102915-2	2018	Sirtuins, including SIRT2, detect the redox state via the NAD+/NADH ratio to regulate mitochondrial function via, in part, AMP-activated protein kinase (AMPK) and peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1alpha).	NAD	58-62	sirtuin 2	Mus musculus	20-25
30102915-2	2018	Sirtuins, including SIRT2, detect the redox state via the NAD+/NADH ratio to regulate mitochondrial function via, in part, AMP-activated protein kinase (AMPK) and peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1alpha).	NAD	63-67	sirtuin 2	Mus musculus	20-25
30179595-5	2018	NAD (a selective 5-HT1A antagonist) was microinjected into the CA1 region of the hippocampus at the doses of 2.5 and 5 mug/1 mul.	NAD	0-3	carbonic anhydrase 1	Rattus norvegicus	63-66
30327366-6	2018	PARP activation causes depletion of its substrate, nicotinamide adenine dinucleotide (NAD+) and subsequent loss of Adenosine Tri-Phosphate (ATP), and we found that adding ATP or nicotinamide (a precursor in the synthesis of NAD+) could rescue the observed phenotypes.	NAD	51-84	Poly-(ADP-ribose) polymerase	Drosophila melanogaster	0-4
30327366-6	2018	PARP activation causes depletion of its substrate, nicotinamide adenine dinucleotide (NAD+) and subsequent loss of Adenosine Tri-Phosphate (ATP), and we found that adding ATP or nicotinamide (a precursor in the synthesis of NAD+) could rescue the observed phenotypes.	NAD	86-90	Poly-(ADP-ribose) polymerase	Drosophila melanogaster	0-4
30327366-6	2018	PARP activation causes depletion of its substrate, nicotinamide adenine dinucleotide (NAD+) and subsequent loss of Adenosine Tri-Phosphate (ATP), and we found that adding ATP or nicotinamide (a precursor in the synthesis of NAD+) could rescue the observed phenotypes.	NAD	224-228	Poly-(ADP-ribose) polymerase	Drosophila melanogaster	0-4
29309913-5	2018	In addition, we examined the effects of hypoxia on cytoplasmic and mitochondrial redox status, whole-cell energetics, the activity of the mitochondrial NAD+-dependent deacetylase SIRT3, and electron transport chain complex activities to determine if there is an association between hypoxia-induced metabolic disturbances, protein acetylation, and mitochondrial function.	NAD	152-156	sirtuin 3	Danio rerio	179-184
30114477-3	2018	In this study, we provide evidence that NAD(P)H:quinone oxidoreductase 1 (NQO1) interacts with and activates SIRT2 in an NAD-dependent manner.	NAD	40-43	sirtuin 2	Homo sapiens	109-114
30144531-4	2018	In HFD feeding or fasting state, hepatic gluconeogenesis and fatty acid oxidation induced SirT1 expression due to the increased nicotinamide adenine dinucleotide+ (NAD+) contents.	NAD	128-161	sirtuin 1	Mus musculus	90-95
30144531-4	2018	In HFD feeding or fasting state, hepatic gluconeogenesis and fatty acid oxidation induced SirT1 expression due to the increased nicotinamide adenine dinucleotide+ (NAD+) contents.	NAD	164-168	sirtuin 1	Mus musculus	90-95
30144531-5	2018	Baicalin reduces endogenous glucose production via suppression of hepatic gluconeogenesis and decreased SirT1 induction via reducing NAD+ accumulation in an energy-sensing way.	NAD	133-137	sirtuin 1	Mus musculus	104-109
30158377-9	2018	The addition of NAD+ in the cell culture supernatant had no significant effect on the polarization of M1 but increased the M2 polarization and the expression levels of IL-10 and IL-1ra.	NAD	16-20	interleukin 1 receptor antagonist	Homo sapiens	178-184
30283350-3	2018	An alternative pathway for NAD biosynthesis has been described for the nicotinamide riboside vitamin B3 precursor used by the NMRK kinases, including the striated muscle-specific NMRK2.	NAD	27-30	nicotinamide riboside kinase 2	Mus musculus	179-184
30283350-14	2018	Although NMRK2 seems to be predominantly dispensable to maintain global NAD levels in heart and skeletal muscle, we demonstrated a maladaptive metabolic response to exercise in cardiac and skeletal muscle, showing that NMRK2 has a specific and restricted role in NAD signaling compared to the NAMPT pathway.	NAD	263-266	nicotinamide riboside kinase 2	Mus musculus	219-224
30228292-1	2018	The NAD+-dependent lysine deacetylase, Sirtuin 1 (SIRT1), plays a central role in metabolic regulation.	NAD	4-8	sirtuin 1	Mus musculus	39-48
30228292-1	2018	The NAD+-dependent lysine deacetylase, Sirtuin 1 (SIRT1), plays a central role in metabolic regulation.	NAD	4-8	sirtuin 1	Mus musculus	50-55
30096284-3	2018	We found that ERalpha and/or ERbeta activation using their agonists (0.5 mg/kg E2, PPT or DPN) ameliorate memory impairment in the Morris water maze (MWM) and Y-maze tests and suppress apoptosis as evidenced by decreased caspase-3 activity and increased ratio of Bcl-2/Bax.	NAD	90-93	estrogen receptor 1 (alpha)	Mus musculus	14-21
30112426-1	2018	CD38 is a multifunctional enzyme involved in calcium signaling and Nicotinamide Adenine Dinucleotide (NAD+) metabolism.	NAD	67-100	CD38 molecule	Homo sapiens	0-4
30112426-1	2018	CD38 is a multifunctional enzyme involved in calcium signaling and Nicotinamide Adenine Dinucleotide (NAD+) metabolism.	NAD	102-106	CD38 molecule	Homo sapiens	0-4
30112426-2	2018	Through its major activity, the hydrolysis of NAD+, CD38 helps maintain the appropriate levels of this molecule for all NAD+-dependent metabolic processes to occur.	NAD	46-50	CD38 molecule	Homo sapiens	52-56
30112426-2	2018	Through its major activity, the hydrolysis of NAD+, CD38 helps maintain the appropriate levels of this molecule for all NAD+-dependent metabolic processes to occur.	NAD	120-124	CD38 molecule	Homo sapiens	52-56
30112426-3	2018	Due to current advances and studies relating NAD+ decline and the development of multiple age-related conditions and diseases, CD38 gained importance in both basic science and clinical settings.	NAD	45-49	CD38 molecule	Homo sapiens	127-131
29972782-1	2018	SIRT3 is a nicotinamide adenine dinucleotide (NAD+)-dependent mitochondrial protein deacetylase purported to influence metabolism through post-translational modification of metabolic enzymes.	NAD	11-44	sirtuin 3	Mus musculus	0-5
29972782-1	2018	SIRT3 is a nicotinamide adenine dinucleotide (NAD+)-dependent mitochondrial protein deacetylase purported to influence metabolism through post-translational modification of metabolic enzymes.	NAD	46-50	sirtuin 3	Mus musculus	0-5
29603199-10	2018	Furthermore, deacetylation of CypD at Lys residue by sirtuin 3 (SIRT3) caused its dissociation from ANT, contributing to an increase in mPT threshold in NAD+ -pretreated animals.	NAD	153-157	sirtuin 3	Rattus norvegicus	53-62
29603199-10	2018	Furthermore, deacetylation of CypD at Lys residue by sirtuin 3 (SIRT3) caused its dissociation from ANT, contributing to an increase in mPT threshold in NAD+ -pretreated animals.	NAD	153-157	sirtuin 3	Rattus norvegicus	64-69
29768224-1	2018	p-Hydroxyphenylacetate 3-hydroxylase component 1 (C1) is a useful enzyme for generating reduced flavin and NAD+ intermediates.	NAD	107-111	heterogeneous nuclear ribonucleoprotein C	Homo sapiens	50-52
29217642-6	2018	RESULTS: We observed a 30% loss in levels of NAD+ in the murine failing heart of both DCM and transverse aorta constriction mice that was accompanied by a decrease in expression of the nicotinamide phosphoribosyltransferase enzyme that recycles the nicotinamide precursor, whereas the nicotinamide riboside kinase 2 (NMRK2) that phosphorylates the nicotinamide riboside precursor is increased, to a higher level in the DCM (40-fold) than in transverse aorta constriction (4-fold).	NAD	45-49	nicotinamide riboside kinase 2	Mus musculus	285-315
29217642-6	2018	RESULTS: We observed a 30% loss in levels of NAD+ in the murine failing heart of both DCM and transverse aorta constriction mice that was accompanied by a decrease in expression of the nicotinamide phosphoribosyltransferase enzyme that recycles the nicotinamide precursor, whereas the nicotinamide riboside kinase 2 (NMRK2) that phosphorylates the nicotinamide riboside precursor is increased, to a higher level in the DCM (40-fold) than in transverse aorta constriction (4-fold).	NAD	45-49	nicotinamide riboside kinase 2	Mus musculus	317-322
29217642-8	2018	We show that the Nmrk2 gene is an AMP-activated protein kinase and peroxisome proliferator-activated receptor alpha responsive gene that is activated by energy stress and NAD+ depletion in isolated rat cardiomyocytes.	NAD	171-175	peroxisome proliferator activated receptor alpha	Rattus norvegicus	67-115
29535219-1	2018	Label-free nonlinear optical microscopy (NLOM) based on two-photon excited fluorescence (TPEF) from cofactors nicotinamide adenine dinucleotide (NADH) and flavin adenine dinucleotide (FAD+) is widely used for high-resolution cellular redox imaging.	NAD	110-143	transmembrane protein with EGF like and two follistatin like domains 2	Homo sapiens	89-93
29535219-1	2018	Label-free nonlinear optical microscopy (NLOM) based on two-photon excited fluorescence (TPEF) from cofactors nicotinamide adenine dinucleotide (NADH) and flavin adenine dinucleotide (FAD+) is widely used for high-resolution cellular redox imaging.	NAD	145-149	transmembrane protein with EGF like and two follistatin like domains 2	Homo sapiens	89-93
29398136-11	2018	Thus, the Nampt/NAD+ system for Npt2 regulation and cellular shifts to tissues such as the liver play an important role in generating daily oscillation of plasma inorganic phosphate levels.	NAD	16-20	solute carrier family 34 (sodium phosphate), member 1	Mus musculus	32-36
29795347-5	2018	The mART catalytic site is composed of an alpha-helical lobe (AHL) that, together with the mART core, creates a chamber for NAD+ binding and ADP-ribosylation of ubiquitin.	NAD	124-128	ADP-ribosyltransferase 2b	Mus musculus	4-8
29795347-5	2018	The mART catalytic site is composed of an alpha-helical lobe (AHL) that, together with the mART core, creates a chamber for NAD+ binding and ADP-ribosylation of ubiquitin.	NAD	124-128	ADP-ribosyltransferase 2b	Mus musculus	91-95
29438976-1	2018	Glutamate dehydrogenase (Gdh) plays a central role in ammonia detoxification by catalysing reversible oxidative deamination of l-glutamate into alpha-ketoglutarate using NAD+ or NADP+ as cofactor.	NAD	170-174	glutamate dehydrogenase 1	Homo sapiens	25-28
29311229-13	2018	GPD1, an enzyme involved in the mitochondrial oxidation of cytosolic NADH, was overexpressed in Meishan.	NAD	69-73	glycerol-3-phosphate dehydrogenase 1	Sus scrofa	0-4
29086002-0	2018	CTNNB1-mutated melanocytic lesions with DPN like features: a distinct subtype of melanocytic tumors?	NAD	40-43	catenin beta 1	Homo sapiens	0-6
29769837-3	2018	Alternatively, ADO can be generated starting from NAD+, which is metabolized by the concerted action of CD38, CD203a/PC-1, and CD73.	NAD	50-54	CD38 molecule	Homo sapiens	104-108
29570999-5	2018	Treatment of mice with the NAD+ booster nicotinamide mononucleotide (NMN) improves blood flow and increases endurance in elderly mice by promoting SIRT1-dependent increases in capillary density, an effect augmented by exercise or increasing the levels of hydrogen sulfide (H2S), a DR mimetic and regulator of endothelial NAD+ levels.	NAD	27-31	sirtuin 1	Mus musculus	147-152
29570999-5	2018	Treatment of mice with the NAD+ booster nicotinamide mononucleotide (NMN) improves blood flow and increases endurance in elderly mice by promoting SIRT1-dependent increases in capillary density, an effect augmented by exercise or increasing the levels of hydrogen sulfide (H2S), a DR mimetic and regulator of endothelial NAD+ levels.	NAD	321-325	sirtuin 1	Mus musculus	147-152
29567766-1	2018	In BRAFV600E melanoma cells, a global metabolomic analysis discloses a decrease in nicotinamide adenine dinucleotide (NAD+) levels upon PLX4032 treatment that is conveyed by a STAT5 inhibition and a transcriptional regulation of the nicotinamide phosphoribosyltransferase (NAMPT) gene.	NAD	83-116	signal transducer and activator of transcription 5A	Homo sapiens	176-181
29567766-1	2018	In BRAFV600E melanoma cells, a global metabolomic analysis discloses a decrease in nicotinamide adenine dinucleotide (NAD+) levels upon PLX4032 treatment that is conveyed by a STAT5 inhibition and a transcriptional regulation of the nicotinamide phosphoribosyltransferase (NAMPT) gene.	NAD	118-122	signal transducer and activator of transcription 5A	Homo sapiens	176-181
29449409-4	2018	Finally, we show that overexpression of the full-length AFMID isoform leads to a higher NAD+ level, lower DNA-damage response, and slower cell growth in HepG2 cells.	NAD	88-92	arylformamidase	Homo sapiens	56-61
29452638-3	2018	We found that impaired utilization of reduced nicotinamide adenine dinucleotide (NADH) by the mitochondrial respiratory chain leads to cytosolic reductive carboxylation of glutamine as a new mechanism for cytosol-confined NADH recycling supported by malate dehydrogenase 1 (MDH1).	NAD	46-79	malate dehydrogenase 1	Homo sapiens	250-272
29452638-3	2018	We found that impaired utilization of reduced nicotinamide adenine dinucleotide (NADH) by the mitochondrial respiratory chain leads to cytosolic reductive carboxylation of glutamine as a new mechanism for cytosol-confined NADH recycling supported by malate dehydrogenase 1 (MDH1).	NAD	46-79	malate dehydrogenase 1	Homo sapiens	274-278
29452638-3	2018	We found that impaired utilization of reduced nicotinamide adenine dinucleotide (NADH) by the mitochondrial respiratory chain leads to cytosolic reductive carboxylation of glutamine as a new mechanism for cytosol-confined NADH recycling supported by malate dehydrogenase 1 (MDH1).	NAD	81-85	malate dehydrogenase 1	Homo sapiens	250-272
29452638-3	2018	We found that impaired utilization of reduced nicotinamide adenine dinucleotide (NADH) by the mitochondrial respiratory chain leads to cytosolic reductive carboxylation of glutamine as a new mechanism for cytosol-confined NADH recycling supported by malate dehydrogenase 1 (MDH1).	NAD	81-85	malate dehydrogenase 1	Homo sapiens	274-278
29452638-3	2018	We found that impaired utilization of reduced nicotinamide adenine dinucleotide (NADH) by the mitochondrial respiratory chain leads to cytosolic reductive carboxylation of glutamine as a new mechanism for cytosol-confined NADH recycling supported by malate dehydrogenase 1 (MDH1).	NAD	222-226	malate dehydrogenase 1	Homo sapiens	250-272
29452638-3	2018	We found that impaired utilization of reduced nicotinamide adenine dinucleotide (NADH) by the mitochondrial respiratory chain leads to cytosolic reductive carboxylation of glutamine as a new mechanism for cytosol-confined NADH recycling supported by malate dehydrogenase 1 (MDH1).	NAD	222-226	malate dehydrogenase 1	Homo sapiens	274-278
29228209-1	2018	The ectodomain of the plasma membrane ectoenzyme CD38 functions as both an NAD glycohydrolase and an ADP-ribosyl cyclase by catalyzing, respectively, the conversion of NAD to nicotinamide and ADP-ribose or cyclic ADP-ribose.	NAD	75-78	CD38 molecule	Homo sapiens	49-53
28970254-7	2018	In addition, supplementing NAD+ directly or increasing NAD+ concentration with silybin could maintain the activity of SIRT2.	NAD	27-31	sirtuin 2	Mus musculus	118-123
28970254-7	2018	In addition, supplementing NAD+ directly or increasing NAD+ concentration with silybin could maintain the activity of SIRT2.	NAD	55-59	sirtuin 2	Mus musculus	118-123
28168426-3	2018	We observed that NAD+ metabolism is altered in sporadic Parkinson"s disease patient-derived cells, which contributes to Sirtuin-2 activation and subsequent decrease in acetylated-alpha-tubulin levels.	NAD	17-21	sirtuin 2	Homo sapiens	120-129
28168426-3	2018	We observed that NAD+ metabolism is altered in sporadic Parkinson"s disease patient-derived cells, which contributes to Sirtuin-2 activation and subsequent decrease in acetylated-alpha-tubulin levels.	NAD	17-21	tubulin alpha 1b	Homo sapiens	179-192
29378070-1	2018	Nicotinamide phosphoribosyltransferase (NAMPT) has been investigated as a target for oncology because it catalyzes a rate-limiting step in cellular energy metabolism to produce nicotinamide adenine dinucleotide.	NAD	177-210	nicotinamide phosphoribosyltransferase 1	Danio rerio	0-38
29378070-1	2018	Nicotinamide phosphoribosyltransferase (NAMPT) has been investigated as a target for oncology because it catalyzes a rate-limiting step in cellular energy metabolism to produce nicotinamide adenine dinucleotide.	NAD	177-210	nicotinamide phosphoribosyltransferase 1	Danio rerio	40-45
30146805-8	2018	The mRNA expression of E-cadherin and vimentin, and the activated ERK1/2 were significantly increased after 1.0 nmol/L FK866 treatment for 72 h. The pretreatment with nicotinamide adenine dinucleotide (NAD) precursor nicotinamide mononucleotide(1.0 mmol/L) or ERK1/2 inhibitor U0126 (10.0 mumol/L) reversed the up-regulation of E-cadherin and vimentin expression induced by FK866.	NAD	167-200	vimentin	Homo sapiens	38-46
30146805-8	2018	The mRNA expression of E-cadherin and vimentin, and the activated ERK1/2 were significantly increased after 1.0 nmol/L FK866 treatment for 72 h. The pretreatment with nicotinamide adenine dinucleotide (NAD) precursor nicotinamide mononucleotide(1.0 mmol/L) or ERK1/2 inhibitor U0126 (10.0 mumol/L) reversed the up-regulation of E-cadherin and vimentin expression induced by FK866.	NAD	167-200	vimentin	Homo sapiens	343-351
29189472-0	2018	SIRT2 and Akt mediate NAD+-induced and NADH-induced increases in the intracellular ATP levels of BV2 microglia under basal conditions.	NAD	22-26	sirtuin 2	Mus musculus	0-5
29189472-0	2018	SIRT2 and Akt mediate NAD+-induced and NADH-induced increases in the intracellular ATP levels of BV2 microglia under basal conditions.	NAD	39-43	sirtuin 2	Mus musculus	0-5
29189472-4	2018	We found that both NAD and NADH significantly increased the intracellular ATP levels of BV2 microglia, which were attenuated by SIRT2 siRNA, the SIRT2 inhibitor AGK2, and the phosphatidylinositol 3-kinase/Akt inhibitor LY294002.	NAD	19-22	sirtuin 2	Mus musculus	128-133
29189472-4	2018	We found that both NAD and NADH significantly increased the intracellular ATP levels of BV2 microglia, which were attenuated by SIRT2 siRNA, the SIRT2 inhibitor AGK2, and the phosphatidylinositol 3-kinase/Akt inhibitor LY294002.	NAD	19-22	sirtuin 2	Mus musculus	145-150
29189472-4	2018	We found that both NAD and NADH significantly increased the intracellular ATP levels of BV2 microglia, which were attenuated by SIRT2 siRNA, the SIRT2 inhibitor AGK2, and the phosphatidylinositol 3-kinase/Akt inhibitor LY294002.	NAD	27-31	sirtuin 2	Mus musculus	128-133
29189472-4	2018	We found that both NAD and NADH significantly increased the intracellular ATP levels of BV2 microglia, which were attenuated by SIRT2 siRNA, the SIRT2 inhibitor AGK2, and the phosphatidylinositol 3-kinase/Akt inhibitor LY294002.	NAD	27-31	sirtuin 2	Mus musculus	145-150
29189472-5	2018	Our study has also suggested that SIRT2 mediates the NAD-induced and NADH-induced increase in Akt phosphorylation in BV2 microglia.	NAD	53-56	sirtuin 2	Mus musculus	34-39
29189472-5	2018	Our study has also suggested that SIRT2 mediates the NAD-induced and NADH-induced increase in Akt phosphorylation in BV2 microglia.	NAD	69-73	sirtuin 2	Mus musculus	34-39
29189472-6	2018	Collectively, our study has suggested that SIRT2 mediates both NAD-induced and NADH-induced increases in the intracellular ATP levels of BV2 microglia by modulating Akt phosphorylation.	NAD	63-66	sirtuin 2	Mus musculus	43-48
29189472-6	2018	Collectively, our study has suggested that SIRT2 mediates both NAD-induced and NADH-induced increases in the intracellular ATP levels of BV2 microglia by modulating Akt phosphorylation.	NAD	79-83	sirtuin 2	Mus musculus	43-48
29040168-11	2018	MicroRNA-21 knockout blocked these favorable effects of isoflurane, whereas endothelial nitric-oxide synthase knockout had no effect on the expression of microRNA-21 but blocked the inhibitory effect of isoflurane preconditioning on nicotinamide adenine dinucleotide.	NAD	233-266	nitric oxide synthase 3, endothelial cell	Mus musculus	76-109
29145149-2	2018	SIRT2, an NAD+-dependent sirtuin deacetylase, is involved in modulating macrophage polarization.	NAD	10-14	sirtuin 2	Mus musculus	0-5
29614635-5	2018	Emerging evidence points towards a dominant mechanism in which innate immune receptors, such as Toll like receptor 4, activate nicotinamide adenine dinucleotide phosphate (NADPH) oxidases to produce reactive oxygen species (ROS) which in turn enables downstream pro-inflammatory signaling and subsequent endothelial activation.	NAD	127-160	toll like receptor 4	Homo sapiens	96-116
29807573-2	2018	Indeed, upon genotoxic stress, CCAR2, phosphorylated by the apical DDR kinases ATM and ATR, increases its binding to the NAD+-dependent histone deacetylase SIRT1 and inhibits SIRT1 activity.	NAD	121-125	cell cycle and apoptosis regulator 2	Homo sapiens	31-36
29807573-2	2018	Indeed, upon genotoxic stress, CCAR2, phosphorylated by the apical DDR kinases ATM and ATR, increases its binding to the NAD+-dependent histone deacetylase SIRT1 and inhibits SIRT1 activity.	NAD	121-125	ATM serine/threonine kinase	Homo sapiens	79-82
29423066-3	2018	Silent information regulator transcript-1 (SIRT1), an NAD-dependent deacetylase, inhibits the release of inflammatory cytokines.	NAD	54-57	sirtuin 1	Mus musculus	43-48
29239724-4	2017	Sirtuin 2 (SIRT2), one of the mammalian nicotinamide adenine dinucleotide (NAD)-dependent lysine deacylases, catalyzes the removal of fatty acylation from K-Ras4a.	NAD	40-73	sirtuin 2	Homo sapiens	0-9
29239724-4	2017	Sirtuin 2 (SIRT2), one of the mammalian nicotinamide adenine dinucleotide (NAD)-dependent lysine deacylases, catalyzes the removal of fatty acylation from K-Ras4a.	NAD	40-73	sirtuin 2	Homo sapiens	11-16
29239724-4	2017	Sirtuin 2 (SIRT2), one of the mammalian nicotinamide adenine dinucleotide (NAD)-dependent lysine deacylases, catalyzes the removal of fatty acylation from K-Ras4a.	NAD	75-78	sirtuin 2	Homo sapiens	0-9
29239724-4	2017	Sirtuin 2 (SIRT2), one of the mammalian nicotinamide adenine dinucleotide (NAD)-dependent lysine deacylases, catalyzes the removal of fatty acylation from K-Ras4a.	NAD	75-78	sirtuin 2	Homo sapiens	11-16
28625351-2	2017	The tolerance mechanisms involved in the strain might have existed through the upregulation of genes involved in NAD(H)/NADP(H) cofactors generations (ALD6, ZWF1, GND1), membrane robustness for efflux pump (YOR1, PDR5, TPO3) and cation/polyamine transport (TPO3).	NAD	113-119	glucose-6-phosphate dehydrogenase	Saccharomyces cerevisiae S288C	157-161
28625351-2	2017	The tolerance mechanisms involved in the strain might have existed through the upregulation of genes involved in NAD(H)/NADP(H) cofactors generations (ALD6, ZWF1, GND1), membrane robustness for efflux pump (YOR1, PDR5, TPO3) and cation/polyamine transport (TPO3).	NAD	113-119	spermine transporter	Saccharomyces cerevisiae S288C	219-223
28625351-2	2017	The tolerance mechanisms involved in the strain might have existed through the upregulation of genes involved in NAD(H)/NADP(H) cofactors generations (ALD6, ZWF1, GND1), membrane robustness for efflux pump (YOR1, PDR5, TPO3) and cation/polyamine transport (TPO3).	NAD	113-119	spermine transporter	Saccharomyces cerevisiae S288C	257-261
29184112-8	2017	Both proteins were verified as targets of ARTC2.1 in vitro using a radiolabeling assay with 32P-NAD+ as substrate.	NAD	96-100	ADP-ribosyltransferase 2b	Mus musculus	42-47
28973994-1	2017	Nicotinamide adenine dinucleotide (NAD+) homeostasis is emerging as a key player in the pathogenesis of non-alcoholic fatty liver disease (NAFLD) and is tightly linked to the SIRT1/5"-AMP-activated protein kinase (AMPK) pathway.	NAD	0-33	sirtuin 1	Mus musculus	175-180
28973994-1	2017	Nicotinamide adenine dinucleotide (NAD+) homeostasis is emerging as a key player in the pathogenesis of non-alcoholic fatty liver disease (NAFLD) and is tightly linked to the SIRT1/5"-AMP-activated protein kinase (AMPK) pathway.	NAD	35-39	sirtuin 1	Mus musculus	175-180
28950020-6	2017	These findings are consistent with the TQ-dependent re-oxidation of NADH to NAD+, which stimulates glucose and fatty acid oxidation and activation of SIRT-1-dependent pathways.	NAD	68-72	sirtuin 1	Mus musculus	150-156
28950020-6	2017	These findings are consistent with the TQ-dependent re-oxidation of NADH to NAD+, which stimulates glucose and fatty acid oxidation and activation of SIRT-1-dependent pathways.	NAD	76-80	sirtuin 1	Mus musculus	150-156
28709706-2	2017	Kidney 11beta-hydroxysteroid dehydrogenase 2 (11beta-HSD2) is an NAD+-dependent oxidase that inactivates glucocorticoid cortisol (human) or corticosterone (rodents) into biologically inert 11 keto glucocorticoids.	NAD	65-68	hydroxysteroid 11-beta dehydrogenase 2	Homo sapiens	7-44
28709706-2	2017	Kidney 11beta-hydroxysteroid dehydrogenase 2 (11beta-HSD2) is an NAD+-dependent oxidase that inactivates glucocorticoid cortisol (human) or corticosterone (rodents) into biologically inert 11 keto glucocorticoids.	NAD	65-68	hydroxysteroid 11-beta dehydrogenase 2	Homo sapiens	46-57
28671679-7	2017	Consistently, cytosolic nicotinamide mononucleotide adenylyltransferase 2 (NMNAT-2) and nicotinamide adenine dinucleotide (NAD)-glycohydrolase CD38 sequentially catalyzed the synthesis of 2"-deoxy-ADPR from nicotinamide mononucleotide (NMN) and 2"-deoxy-ATP in vitro.	NAD	88-121	CD38 molecule	Homo sapiens	143-147
28894448-1	2017	Sirtuin 2 (SIRT2) is one of the seven members of the family of NAD+-dependent histone deacetylases.	NAD	63-66	sirtuin 2	Mus musculus	0-9
28894448-1	2017	Sirtuin 2 (SIRT2) is one of the seven members of the family of NAD+-dependent histone deacetylases.	NAD	63-66	sirtuin 2	Mus musculus	11-16
28684630-1	2017	RATIONALE: Clinical studies have shown that Sirt3 (Sirtuin 3) expression declines by 40% by 65 years of age paralleling the increased incidence of hypertension and metabolic conditions further inactivate Sirt3 because of increased NADH (nicotinamide adenine dinucleotide, reduced form) and acetyl-CoA levels.	NAD	231-235	sirtuin 3	Mus musculus	44-49
28684630-1	2017	RATIONALE: Clinical studies have shown that Sirt3 (Sirtuin 3) expression declines by 40% by 65 years of age paralleling the increased incidence of hypertension and metabolic conditions further inactivate Sirt3 because of increased NADH (nicotinamide adenine dinucleotide, reduced form) and acetyl-CoA levels.	NAD	231-235	sirtuin 3	Mus musculus	51-60
28684630-1	2017	RATIONALE: Clinical studies have shown that Sirt3 (Sirtuin 3) expression declines by 40% by 65 years of age paralleling the increased incidence of hypertension and metabolic conditions further inactivate Sirt3 because of increased NADH (nicotinamide adenine dinucleotide, reduced form) and acetyl-CoA levels.	NAD	231-235	sirtuin 3	Mus musculus	204-209
28684630-1	2017	RATIONALE: Clinical studies have shown that Sirt3 (Sirtuin 3) expression declines by 40% by 65 years of age paralleling the increased incidence of hypertension and metabolic conditions further inactivate Sirt3 because of increased NADH (nicotinamide adenine dinucleotide, reduced form) and acetyl-CoA levels.	NAD	237-270	sirtuin 3	Mus musculus	44-49
28684630-1	2017	RATIONALE: Clinical studies have shown that Sirt3 (Sirtuin 3) expression declines by 40% by 65 years of age paralleling the increased incidence of hypertension and metabolic conditions further inactivate Sirt3 because of increased NADH (nicotinamide adenine dinucleotide, reduced form) and acetyl-CoA levels.	NAD	237-270	sirtuin 3	Mus musculus	51-60
28684630-1	2017	RATIONALE: Clinical studies have shown that Sirt3 (Sirtuin 3) expression declines by 40% by 65 years of age paralleling the increased incidence of hypertension and metabolic conditions further inactivate Sirt3 because of increased NADH (nicotinamide adenine dinucleotide, reduced form) and acetyl-CoA levels.	NAD	237-270	sirtuin 3	Mus musculus	204-209
28862956-2	2017	The nicotinamide adenine dinucleotide-dependent deacetylase Sirtuin 3 (SIRT3) has the potential to modulate angiogenesis, but this has not been confirmed.	NAD	4-37	sirtuin 3	Mus musculus	60-69
28862956-2	2017	The nicotinamide adenine dinucleotide-dependent deacetylase Sirtuin 3 (SIRT3) has the potential to modulate angiogenesis, but this has not been confirmed.	NAD	4-37	sirtuin 3	Mus musculus	71-76
29137352-6	2017	The mitochondrial dysfunction-associated senescence in pups was accompanied by a drop in NAD+/NADH ratio and alteration in the NAD+-dependent enzymes PARP1 and SIRT1.	NAD	127-131	sirtuin 1	Mus musculus	160-165
28779137-5	2017	NAD+ intervention significantly reduced the incidence of spontaneous recurrent seizure (SRS) and abnormal electroencephalogram (EEG) activity, rescued contextual fear memory formation, reduced neuronal loss in the CA1 region of the hippocampus at SRS stage.	NAD	0-4	carbonic anhydrase 1	Mus musculus	214-217
28779137-6	2017	Furthermore, exogenous supply of NAD+ distinctly reversed the seizure-induced depletion of endogenous NAD+, reduced neuronal apoptosis in the CA1 region of the hippocampus, and reversed the augmented Acp53/p53 ratio at the early stage of epileptogenesis.	NAD	33-37	carbonic anhydrase 1	Mus musculus	142-145
28779137-6	2017	Furthermore, exogenous supply of NAD+ distinctly reversed the seizure-induced depletion of endogenous NAD+, reduced neuronal apoptosis in the CA1 region of the hippocampus, and reversed the augmented Acp53/p53 ratio at the early stage of epileptogenesis.	NAD	33-37	transformation related protein 53, pseudogene	Mus musculus	202-205
28246130-3	2017	In this study, we found that, compared with the kidneys of 3-month-old mice, the kidneys of 20-month-old mice expressed reduced levels of the renal protective molecule sirtuin 1 (SIRT1) and its cofactor NAD+ Supplementation with nicotinamide mononucleotide (NMN), an NAD+ precursor, restored renal SIRT1 activity and NAD+ content in 20-month-old mice and further increased both in 3-month-old mice.	NAD	267-271	sirtuin 1	Mus musculus	168-177
28246130-3	2017	In this study, we found that, compared with the kidneys of 3-month-old mice, the kidneys of 20-month-old mice expressed reduced levels of the renal protective molecule sirtuin 1 (SIRT1) and its cofactor NAD+ Supplementation with nicotinamide mononucleotide (NMN), an NAD+ precursor, restored renal SIRT1 activity and NAD+ content in 20-month-old mice and further increased both in 3-month-old mice.	NAD	267-271	sirtuin 1	Mus musculus	179-184
28246130-3	2017	In this study, we found that, compared with the kidneys of 3-month-old mice, the kidneys of 20-month-old mice expressed reduced levels of the renal protective molecule sirtuin 1 (SIRT1) and its cofactor NAD+ Supplementation with nicotinamide mononucleotide (NMN), an NAD+ precursor, restored renal SIRT1 activity and NAD+ content in 20-month-old mice and further increased both in 3-month-old mice.	NAD	267-271	sirtuin 1	Mus musculus	168-177
28246130-3	2017	In this study, we found that, compared with the kidneys of 3-month-old mice, the kidneys of 20-month-old mice expressed reduced levels of the renal protective molecule sirtuin 1 (SIRT1) and its cofactor NAD+ Supplementation with nicotinamide mononucleotide (NMN), an NAD+ precursor, restored renal SIRT1 activity and NAD+ content in 20-month-old mice and further increased both in 3-month-old mice.	NAD	267-271	sirtuin 1	Mus musculus	179-184
28319892-7	2017	The 10+16 MAPT mutation is also associated with lower mitochondrial NADH levels, partially supressed complex I-driven respiration, and lower ATP production by oxidative phosphorylation, with cells relying on glycolysis to maintain ATP levels.	NAD	68-72	microtubule associated protein tau	Homo sapiens	10-14
28724806-3	2017	A putative mechanism of NAD+ therapeutic action exists via activation of the mitochondrial NAD+-dependent protein deacetylase sirtuin 3 (SIRT3).	NAD	24-28	sirtuin 3	Mus musculus	126-135
28724806-3	2017	A putative mechanism of NAD+ therapeutic action exists via activation of the mitochondrial NAD+-dependent protein deacetylase sirtuin 3 (SIRT3).	NAD	24-28	sirtuin 3	Mus musculus	137-142
28724806-3	2017	A putative mechanism of NAD+ therapeutic action exists via activation of the mitochondrial NAD+-dependent protein deacetylase sirtuin 3 (SIRT3).	NAD	24-27	sirtuin 3	Mus musculus	126-135
28724806-3	2017	A putative mechanism of NAD+ therapeutic action exists via activation of the mitochondrial NAD+-dependent protein deacetylase sirtuin 3 (SIRT3).	NAD	24-27	sirtuin 3	Mus musculus	137-142
28497908-7	2017	The human and plants mARC proteins require a Cytochrome b5 (Cytb5) and a Cytochrome b5 reductase (Cytb5-R) to form an electron transfer chain from NADH to the NHC.	NAD	147-151	cytochrome b5 type A	Homo sapiens	45-58
28497908-7	2017	The human and plants mARC proteins require a Cytochrome b5 (Cytb5) and a Cytochrome b5 reductase (Cytb5-R) to form an electron transfer chain from NADH to the NHC.	NAD	147-151	cytochrome b5 type A	Homo sapiens	60-65
28497908-7	2017	The human and plants mARC proteins require a Cytochrome b5 (Cytb5) and a Cytochrome b5 reductase (Cytb5-R) to form an electron transfer chain from NADH to the NHC.	NAD	147-151	cytochrome b5 type A	Homo sapiens	73-86
28497908-7	2017	The human and plants mARC proteins require a Cytochrome b5 (Cytb5) and a Cytochrome b5 reductase (Cytb5-R) to form an electron transfer chain from NADH to the NHC.	NAD	147-151	cytochrome b5 type A	Homo sapiens	98-103
28559281-8	2017	Supplementation with kynurenine pathway intermediates also boosted NAD+ levels and partially reversed NAD+-dependent phenotypes caused by mutation of pnc-1, which encodes a nicotinamidase required for NAD+ salvage biosynthesis, demonstrating contribution of de novo synthesis to NAD+ homeostasis.	NAD	102-106	Isochorismatase domain-containing protein	Caenorhabditis elegans	150-155
28559281-8	2017	Supplementation with kynurenine pathway intermediates also boosted NAD+ levels and partially reversed NAD+-dependent phenotypes caused by mutation of pnc-1, which encodes a nicotinamidase required for NAD+ salvage biosynthesis, demonstrating contribution of de novo synthesis to NAD+ homeostasis.	NAD	102-106	Isochorismatase domain-containing protein	Caenorhabditis elegans	150-155
28559281-8	2017	Supplementation with kynurenine pathway intermediates also boosted NAD+ levels and partially reversed NAD+-dependent phenotypes caused by mutation of pnc-1, which encodes a nicotinamidase required for NAD+ salvage biosynthesis, demonstrating contribution of de novo synthesis to NAD+ homeostasis.	NAD	102-106	Isochorismatase domain-containing protein	Caenorhabditis elegans	150-155
28506746-0	2017	The NAD+-dependent deacetylase, Bifidobacterium longum Sir2 in response to oxidative stress by deacetylating SigH (sigmaH) and FOXO3a in Bifidobacterium longum and HEK293T cell respectively.	NAD	4-7	sirtuin 2	Homo sapiens	55-59
28506746-1	2017	Silent information regulator 2 (Sir2) enzymes which catalyze NAD+-dependent protein/histone deacetylation.	NAD	61-64	sirtuin 2	Homo sapiens	32-36
28429368-1	2017	ARALAR/AGC1 (aspartate-glutamate mitochondrial carrier 1) is an important component of the NADH malate-aspartate shuttle (MAS).	NAD	91-95	aggrecan	Mus musculus	7-11
28429368-1	2017	ARALAR/AGC1 (aspartate-glutamate mitochondrial carrier 1) is an important component of the NADH malate-aspartate shuttle (MAS).	NAD	91-95	mitochondrial carrier 1	Mus musculus	33-56
27766571-7	2017	Strong correlation has been proved between the expression levels of HDAC4 and SIRT6 (r = 0.722 in full cohort and r = 0.794 in AML), that confirms the recently suggested cooperation between NAD+-independent and NAD+-dependent HDAC enzymes in leukemia.	NAD	190-194	histone deacetylase 4	Homo sapiens	68-73
27766571-7	2017	Strong correlation has been proved between the expression levels of HDAC4 and SIRT6 (r = 0.722 in full cohort and r = 0.794 in AML), that confirms the recently suggested cooperation between NAD+-independent and NAD+-dependent HDAC enzymes in leukemia.	NAD	211-215	histone deacetylase 4	Homo sapiens	68-73
28495134-0	2017	Reevaluating the role of IDO1: Examining NAD+ metabolism in inflammation.	NAD	41-45	indoleamine 2,3-dioxygenase 1	Homo sapiens	25-29
28592850-6	2017	Moreover, we confirmed that the increase of cellular NAD+ by NQO1 enzymatic action using the substrate beta-Lapachone suppressed caerulein-induced AP with down-regulating TLR4-mediated inflammasome signalling, and thereby reducing the inflammatory responses and pancreatic cell death.	NAD	53-57	toll like receptor 4	Homo sapiens	171-175
28537485-3	2017	Decreased NAD+ levels with age reduce SIRT1 function and reduce the mitochondrial unfolded protein response, which can be overcome by NR supplementation.	NAD	10-14	sirtuin 1	Mus musculus	38-43
28536482-0	2017	NAD+ loss, a new player in AhR biology: prevention of thymus atrophy and hepatosteatosis by NAD+ repletion.	NAD	0-4	aryl hydrocarbon receptor 1 alpha	Gallus gallus	27-30
28536482-0	2017	NAD+ loss, a new player in AhR biology: prevention of thymus atrophy and hepatosteatosis by NAD+ repletion.	NAD	92-96	aryl hydrocarbon receptor 1 alpha	Gallus gallus	27-30
28533555-3	2017	Scopolin decreased the Km of SIRT1 for p53 and nicotinamide adenine dinucleotide without altering Vmax in a cell-free system.	NAD	47-80	sirtuin 1	Mus musculus	29-34
28881659-1	2017	SIRT1, a highly conserved NAD+-dependent protein deacetylase, plays a pivotal role in the pathogenesis and therapy of atherosclerosis (AS).	NAD	26-29	sirtuin 1	Mus musculus	0-5
28254441-6	2017	Moreover, the EPA+DHA mixture activated SIRT1 signaling by enhancing mRNA level of nicotinamide phosphoribosyltransferase (NAMPT), cellular NAD+ level, SIRT1 protein deacetylase activity, and SIRT1 mRNA levels in LPS-stimulated MG6.	NAD	140-144	sirtuin 1	Mus musculus	40-45
27396440-11	2017	Cytochrome c oxidase subunit IV (COXIV) and NADH:ubiquinone oxidoreductase subunit A9 (NDUFA9) were more abundant in type I than type II fibres (P &lt; 0.05) but training did not increase the content of COXIV, NDUFA9 or MFN2 in either fibre type (P &gt; 0.05).	NAD	44-48	NADH:ubiquinone oxidoreductase subunit A9	Homo sapiens	87-93
28450888-5	2017	RESULTS: GPD2 encodes one of two S. cerevisiae isoenzymes of NAD+-dependent glycerol-3-phosphate dehydrogenase (G3PDH).	NAD	61-64	glycerol-3-phosphate dehydrogenase (NAD(+)) GPD2	Saccharomyces cerevisiae S288C	9-13
28445509-5	2017	SIRT2 is a member of sirtuin family, NAD(+)-dependent class III deacetylases.	NAD	37-43	sirtuin 2	Homo sapiens	0-5
28240897-4	2017	Their mechanism of inhibition is uncompetitive toward both the peptide substrate and NAD+, and the crystal structure of a 1,2,4-oxadiazole analog in complex with Sirt2 and ADP-ribose reveals its orientation in a still unexplored subcavity useful for further inhibitor development.	NAD	85-89	sirtuin 2	Homo sapiens	162-167
28286128-4	2017	Based on potent SIRT2-specific inhibitors we developed, here we report crystal structures of SIRT2 in complexes with a thiomyristoyl lysine peptide-based inhibitor and carba-NAD or NAD.	NAD	174-177	sirtuin 2	Homo sapiens	16-21
28286128-4	2017	Based on potent SIRT2-specific inhibitors we developed, here we report crystal structures of SIRT2 in complexes with a thiomyristoyl lysine peptide-based inhibitor and carba-NAD or NAD.	NAD	174-177	sirtuin 2	Homo sapiens	93-98
27474445-2	2017	SIRT1, a NAD dependent protein deacetylase, has been implicated in the pathogenesis of neurodegeneration in neurological diseases including MS. We have studied the role of SIRT1 in experimental autoimmune encephalomyelitis (EAE) and found evidence for a neuroprotective role.	NAD	9-12	sirtuin 1	Mus musculus	0-5
27989687-1	2017	BACKGROUND: The reduced form of nicotinamide adenine dinucleotide (NADH) increases in cardiomyopathy, activates protein kinase C (PKC), up-regulates mitochondrial reactive oxygen species (mitoROS), and down-regulates the cardiac Na+ channel (NaV1.5).	NAD	32-65	sodium voltage-gated channel alpha subunit 5	Homo sapiens	242-248
27989687-1	2017	BACKGROUND: The reduced form of nicotinamide adenine dinucleotide (NADH) increases in cardiomyopathy, activates protein kinase C (PKC), up-regulates mitochondrial reactive oxygen species (mitoROS), and down-regulates the cardiac Na+ channel (NaV1.5).	NAD	67-71	sodium voltage-gated channel alpha subunit 5	Homo sapiens	242-248
27989687-2	2017	OBJECTIVE: The purpose of this study was to determine how NADH signals down-regulation of NaV1.5.	NAD	58-62	sodium voltage-gated channel alpha subunit 5	Homo sapiens	90-96
28053092-2	2017	We previously reported that the inhibition of the NAD-dependent histone deacetylase (HDAC) SIRT2 induces granulocytic differentiation in leukemia cells, suggesting the involvement of protein acetylation in ATRA-induced leukemia cell differentiation.	NAD	50-53	sirtuin 2	Homo sapiens	91-96
28211546-7	2017	Prolactin caused no significant change in IGF-1 levels and an increase in IGF-2 in HKCs correlating with an increase in ATP and NADH levels.	NAD	128-132	insulin like growth factor 2	Homo sapiens	74-79
28011627-0	2017	Enhancing NAD+ salvage metabolism is neuroprotective in a PINK1 model of Parkinson"s disease.	NAD	10-14	PTEN-induced putative kinase 1	Drosophila melanogaster	58-63
28011627-4	2017	We found alterations in NAD+ salvage metabolism in Drosophila pink1 mutants and showed that a diet supplemented with the NAD+ precursor nicotinamide rescued mitochondrial defects and protected neurons from degeneration.	NAD	24-28	PTEN-induced putative kinase 1	Drosophila melanogaster	62-67
27864727-4	2017	Acetylation was reversed by the deacetylase Sirtuin 3 in the presence of NAD+.	NAD	73-77	sirtuin 3	Rattus norvegicus	44-53
27923678-5	2017	In the presence of NADH and flavin reductase, 1 molecule of flavin nucleotide is sufficient to reduce about 100 molecules of the mitoNEET [2Fe-2S] clusters in 4min under aerobic conditions.	NAD	19-23	CDGSH iron sulfur domain 1	Homo sapiens	129-137
29104319-4	2017	We also evaluated the effectiveness of coenzymes of two of the microsomal reductases, NADPH as a coenzyme of POR, and NADH as a coenzyme of NADH:cytochrome b5 reductase, to mediate ellipticine oxidation in these enzyme systems.	NAD	118-122	cytochrome b5 type A	Homo sapiens	145-158
29104319-4	2017	We also evaluated the effectiveness of coenzymes of two of the microsomal reductases, NADPH as a coenzyme of POR, and NADH as a coenzyme of NADH:cytochrome b5 reductase, to mediate ellipticine oxidation in these enzyme systems.	NAD	140-144	cytochrome b5 type A	Homo sapiens	145-158
29104319-10	2017	In the presence of NADPH or NADH, cytochrome b5 stimulated the CYP3A4-mediated oxidation of ellipticine, but the stimulation effect differed for individual ellipticine metabolites.	NAD	28-32	cytochrome b5 type A	Homo sapiens	34-47
29104319-12	2017	The results demonstrate that cytochrome b5 plays a dual role in the CYP3A4-catalyzed oxidation of ellipticine: (1) cytochrome b5 mediates CYP3A4 catalytic activities by donating the first and second electron to this enzyme in its catalytic cycle, indicating that NADH:cytochrome b5 reductase can substitute NADPH-dependent POR in this enzymatic reaction and (2) cytochrome b5 can act as an allosteric modifier of the CYP3A4 oxygenase.	NAD	263-267	cytochrome b5 type A	Homo sapiens	29-42
29104319-12	2017	The results demonstrate that cytochrome b5 plays a dual role in the CYP3A4-catalyzed oxidation of ellipticine: (1) cytochrome b5 mediates CYP3A4 catalytic activities by donating the first and second electron to this enzyme in its catalytic cycle, indicating that NADH:cytochrome b5 reductase can substitute NADPH-dependent POR in this enzymatic reaction and (2) cytochrome b5 can act as an allosteric modifier of the CYP3A4 oxygenase.	NAD	263-267	cytochrome b5 type A	Homo sapiens	115-128
29104319-12	2017	The results demonstrate that cytochrome b5 plays a dual role in the CYP3A4-catalyzed oxidation of ellipticine: (1) cytochrome b5 mediates CYP3A4 catalytic activities by donating the first and second electron to this enzyme in its catalytic cycle, indicating that NADH:cytochrome b5 reductase can substitute NADPH-dependent POR in this enzymatic reaction and (2) cytochrome b5 can act as an allosteric modifier of the CYP3A4 oxygenase.	NAD	263-267	cytochrome b5 type A	Homo sapiens	115-128
29104319-12	2017	The results demonstrate that cytochrome b5 plays a dual role in the CYP3A4-catalyzed oxidation of ellipticine: (1) cytochrome b5 mediates CYP3A4 catalytic activities by donating the first and second electron to this enzyme in its catalytic cycle, indicating that NADH:cytochrome b5 reductase can substitute NADPH-dependent POR in this enzymatic reaction and (2) cytochrome b5 can act as an allosteric modifier of the CYP3A4 oxygenase.	NAD	263-267	cytochrome b5 type A	Homo sapiens	115-128
27453987-1	2016	A novel fluorescent label-free "turn-on" NAD(+) and adenosine triphosphate (ATP) biosensing strategy is proposed by fully exploiting ligation triggered Nanocluster Beacon (NCB).	NAD	41-47	ubiquitin like 5	Homo sapiens	164-170
27875273-1	2016	Sirtuin 2 (SIRT2) is an NAD-dependent deacetylase known to regulate microtubule dynamics and cell cycle progression.	NAD	24-27	sirtuin 2	Homo sapiens	0-9
27875273-1	2016	Sirtuin 2 (SIRT2) is an NAD-dependent deacetylase known to regulate microtubule dynamics and cell cycle progression.	NAD	24-27	sirtuin 2	Homo sapiens	11-16
27929535-4	2016	GLS1 remarkably contributes to ATP production through transferring cytosolic NADH into mitochondria via malate-aspartate shuttle by supply of glutamate in NSCLC.	NAD	77-81	glutaminase	Homo sapiens	0-4
27686254-3	2016	This process catalyzes the NAD+-dependent synthesis of polymers of ADP-ribose (PAR) and their subsequent attachment to target proteins by PARPs.	NAD	27-31	poly (ADP-ribose) polymerase 1	Rattus norvegicus	138-143
27771463-1	2016	Silent mating type information regulation 2 homolog 1 (SIRT1), a NAD-dependent deacetylase, mediates cellular processes involved in gene silencing and aging.	NAD	65-68	sirtuin 1	Mus musculus	55-60
27451147-12	2016	Decreased levels of oxaloacetate in cells with knockdown of SLC25A22 reduced regeneration of oxidized nicotinamide adenine dinucleotide and reduced nicotinamide adenine dinucleotide phosphate.	NAD	102-135	solute carrier family 25 member 22	Homo sapiens	60-68
27552971-2	2016	Mice engineered to express additional copies of SIRT1 or SIRT6, or treated with sirtuin-activating compounds (STACs) such as resveratrol and SRT2104 or with NAD+ precursors, have improved organ function, physical endurance, disease resistance and longevity.	NAD	157-161	sirtuin 1	Mus musculus	48-53
27681422-7	2016	We further demonstrate that the NAD(+)-dependent mitochondrial deacylases SIRT3 and SIRT5 play important roles in retinal homeostasis and that NAD(+) deficiency causes SIRT3 dysfunction.	NAD	32-38	sirtuin 3	Mus musculus	74-79
27519409-5	2016	These include the following: (i) GDH2 encoding NAD-dependent glutamate dehydrogenase; (ii) AAT1 and AAT2 encoding mitochondrial and cytosolic aspartate aminotransferases, respectively; (iii) MDH1 and MDH2 encoding mitochondrial and cytosolic malate dehydrogenases, respectively; and (iv) GLN1 encoding glutamine synthetase.	NAD	47-50	glutamate dehydrogenase (NAD(+))	Saccharomyces cerevisiae S288C	33-37
27466185-6	2016	NDUFAF6 encodes NADH:ubiquinone oxidoreductase complex assembly factor 6, also known as C8ORF38.	NAD	16-20	NADH:ubiquinone oxidoreductase complex assembly factor 6	Homo sapiens	0-7
27466185-6	2016	NDUFAF6 encodes NADH:ubiquinone oxidoreductase complex assembly factor 6, also known as C8ORF38.	NAD	16-20	NADH:ubiquinone oxidoreductase complex assembly factor 6	Homo sapiens	88-95
27622334-5	2016	In cancer cells preferentially to normal cells, lactate dehydrogenase B (LDHB), catalyzing the conversion of lactate and NAD(+) to pyruvate, NADH and H(+), controls lysosomal acidification, vesicle maturation, and intracellular proteolysis.	NAD	121-127	lactate dehydrogenase B	Homo sapiens	48-71
27622334-5	2016	In cancer cells preferentially to normal cells, lactate dehydrogenase B (LDHB), catalyzing the conversion of lactate and NAD(+) to pyruvate, NADH and H(+), controls lysosomal acidification, vesicle maturation, and intracellular proteolysis.	NAD	121-127	lactate dehydrogenase B	Homo sapiens	73-77
27622334-5	2016	In cancer cells preferentially to normal cells, lactate dehydrogenase B (LDHB), catalyzing the conversion of lactate and NAD(+) to pyruvate, NADH and H(+), controls lysosomal acidification, vesicle maturation, and intracellular proteolysis.	NAD	141-145	lactate dehydrogenase B	Homo sapiens	48-71
27622334-5	2016	In cancer cells preferentially to normal cells, lactate dehydrogenase B (LDHB), catalyzing the conversion of lactate and NAD(+) to pyruvate, NADH and H(+), controls lysosomal acidification, vesicle maturation, and intracellular proteolysis.	NAD	141-145	lactate dehydrogenase B	Homo sapiens	73-77
27378422-3	2016	Sirtuin1 (Sirt1) is a nicotinamide adenine dinucleotide (NAD(+))-dependent deacetylase, which is reported to be involved in improving osteogenesis.	NAD	22-55	sirtuin 1	Mus musculus	0-8
27378422-3	2016	Sirtuin1 (Sirt1) is a nicotinamide adenine dinucleotide (NAD(+))-dependent deacetylase, which is reported to be involved in improving osteogenesis.	NAD	22-55	sirtuin 1	Mus musculus	10-15
27378422-3	2016	Sirtuin1 (Sirt1) is a nicotinamide adenine dinucleotide (NAD(+))-dependent deacetylase, which is reported to be involved in improving osteogenesis.	NAD	57-61	sirtuin 1	Mus musculus	0-8
27378422-3	2016	Sirtuin1 (Sirt1) is a nicotinamide adenine dinucleotide (NAD(+))-dependent deacetylase, which is reported to be involved in improving osteogenesis.	NAD	57-61	sirtuin 1	Mus musculus	10-15
27505350-3	2016	It has been shown that cyt c plays a catalytic role in the transfer of two reducing equivalents from NADH to Pt(IV) species.	NAD	101-105	cytochrome c, somatic	Equus caballus	23-28
26804254-8	2016	RONS may activate LKB1 through Sestrin2 and SIRT1 (NAD(+)/NADH.H(+)-dependent deacetylase).	NAD	51-57	serine/threonine kinase 11	Homo sapiens	18-22
26804254-8	2016	RONS may activate LKB1 through Sestrin2 and SIRT1 (NAD(+)/NADH.H(+)-dependent deacetylase).	NAD	58-62	serine/threonine kinase 11	Homo sapiens	18-22
27449933-3	2016	In this study, we hypothesized that NAD-dependent deacetylase sirtuin-3 (SIRT3), an important regulator of cell metabolism, protects pancreatic beta-cells from ER stress-mediated apoptosis.	NAD	36-39	sirtuin 3	Rattus norvegicus	62-71
27449933-3	2016	In this study, we hypothesized that NAD-dependent deacetylase sirtuin-3 (SIRT3), an important regulator of cell metabolism, protects pancreatic beta-cells from ER stress-mediated apoptosis.	NAD	36-39	sirtuin 3	Rattus norvegicus	73-78
27348016-3	2016	CD38 catalyzes beta-NAD into cyclic ADP ribose (cADPR), which could elevate the intracellular Ca by Ca-permeable channels for oxytocin secretion.	NAD	15-23	CD38 molecule	Homo sapiens	0-4
27348016-10	2016	CD38 agonists (beta-NAD, cADPR) and antagonist (8-Br-cADPR) could increase or reduce the oxytocin release, respectively.	NAD	15-23	CD38 molecule	Homo sapiens	0-4
27404282-10	2016	They suggest that NADH-dependent CBR can replace NADPH-dependent POR in the P450 1A1-catalyzed metabolism of BaP.	NAD	18-22	prohibitin 2	Homo sapiens	109-112
27339462-0	2016	alpha7 Nicotinic Acetylcholine Receptor Relieves Angiotensin II-Induced Senescence in Vascular Smooth Muscle Cells by Raising Nicotinamide Adenine Dinucleotide-Dependent SIRT1 Activity.	NAD	126-159	cholinergic receptor, nicotinic, alpha polypeptide 7	Mus musculus	0-39
27339462-0	2016	alpha7 Nicotinic Acetylcholine Receptor Relieves Angiotensin II-Induced Senescence in Vascular Smooth Muscle Cells by Raising Nicotinamide Adenine Dinucleotide-Dependent SIRT1 Activity.	NAD	126-159	sirtuin 1	Mus musculus	170-175
27339462-11	2016	CONCLUSIONS: Our results demonstrate that activation of alpha7nAChR alleviates Ang II-induced VSMC senescence through promoting NAD(+)-SIRT1 pathway, suggesting that alpha7nAChR may be a potential therapeutic target for the treatment of Ang II-associated vascular aging disorders.	NAD	128-134	cholinergic receptor, nicotinic, alpha polypeptide 7	Mus musculus	56-67
27339462-11	2016	CONCLUSIONS: Our results demonstrate that activation of alpha7nAChR alleviates Ang II-induced VSMC senescence through promoting NAD(+)-SIRT1 pathway, suggesting that alpha7nAChR may be a potential therapeutic target for the treatment of Ang II-associated vascular aging disorders.	NAD	128-134	sirtuin 1	Mus musculus	135-140
27339462-11	2016	CONCLUSIONS: Our results demonstrate that activation of alpha7nAChR alleviates Ang II-induced VSMC senescence through promoting NAD(+)-SIRT1 pathway, suggesting that alpha7nAChR may be a potential therapeutic target for the treatment of Ang II-associated vascular aging disorders.	NAD	128-134	cholinergic receptor, nicotinic, alpha polypeptide 7	Mus musculus	166-177
27362750-1	2016	17beta-HSD14 is a SDR enzyme able to oxidize estradiol and 5-androstenediol using NAD(+).	NAD	82-88	hydroxysteroid 17-beta dehydrogenase 14	Homo sapiens	0-12
27107935-9	2016	Cycloheximide blocked the DPN-induced upregulation of non-phosphorylated beta-catenin, suggesting de novo synthesis of this protein.	NAD	26-29	catenin beta 1	Homo sapiens	73-85
27404390-5	2016	During ethanol metabolism, a low NAD(+)/NADH ratio repressed NAD-dependent deacetylase sirtuin 1 (SIRT1) activity, concomitantly resulting in increased acetylated PPARgamma with high transcriptional activity.	NAD	33-39	sirtuin 1	Mus musculus	87-96
27404390-5	2016	During ethanol metabolism, a low NAD(+)/NADH ratio repressed NAD-dependent deacetylase sirtuin 1 (SIRT1) activity, concomitantly resulting in increased acetylated PPARgamma with high transcriptional activity.	NAD	33-39	sirtuin 1	Mus musculus	98-103
27404390-5	2016	During ethanol metabolism, a low NAD(+)/NADH ratio repressed NAD-dependent deacetylase sirtuin 1 (SIRT1) activity, concomitantly resulting in increased acetylated PPARgamma with high transcriptional activity.	NAD	40-44	sirtuin 1	Mus musculus	87-96
27404390-5	2016	During ethanol metabolism, a low NAD(+)/NADH ratio repressed NAD-dependent deacetylase sirtuin 1 (SIRT1) activity, concomitantly resulting in increased acetylated PPARgamma with high transcriptional activity.	NAD	40-44	sirtuin 1	Mus musculus	98-103
27449624-0	2016	Phylogenomic Analysis of Type 1 NADH:Quinone Oxidoreductase.	NAD	32-36	crystallin zeta	Homo sapiens	37-59
27181414-4	2016	My research and others" suggest that the SIRT1-liver kinase B1-AMPK cascade creates positive feedback through nicotinamide adenine dinucleotide synthesis to help cells cope with metabolic stress.	NAD	110-143	serine/threonine kinase 11	Homo sapiens	47-62
27304496-3	2016	(2016) implicate CD38 in the decline of NAD(+) during aging, with implications for combating age-related diseases.	NAD	40-46	CD38 molecule	Homo sapiens	17-21
27304511-0	2016	CD38 Dictates Age-Related NAD Decline and Mitochondrial Dysfunction through an SIRT3-Dependent Mechanism.	NAD	26-29	CD38 molecule	Homo sapiens	0-4
27304511-3	2016	Here we demonstrate that expression and activity of the NADase CD38 increase with aging and that CD38 is required for the age-related NAD decline and mitochondrial dysfunction via a pathway mediated at least in part by regulation of SIRT3 activity.	NAD	56-59	CD38 molecule	Homo sapiens	63-67
27304511-4	2016	We also identified CD38 as the main enzyme involved in the degradation of the NAD precursor nicotinamide mononucleotide (NMN) in vivo, indicating that CD38 has a key role in the modulation of NAD-replacement therapy for aging and metabolic diseases.	NAD	78-81	CD38 molecule	Homo sapiens	19-23
27304511-4	2016	We also identified CD38 as the main enzyme involved in the degradation of the NAD precursor nicotinamide mononucleotide (NMN) in vivo, indicating that CD38 has a key role in the modulation of NAD-replacement therapy for aging and metabolic diseases.	NAD	78-81	CD38 molecule	Homo sapiens	151-155
27304511-4	2016	We also identified CD38 as the main enzyme involved in the degradation of the NAD precursor nicotinamide mononucleotide (NMN) in vivo, indicating that CD38 has a key role in the modulation of NAD-replacement therapy for aging and metabolic diseases.	NAD	192-195	CD38 molecule	Homo sapiens	19-23
27304511-4	2016	We also identified CD38 as the main enzyme involved in the degradation of the NAD precursor nicotinamide mononucleotide (NMN) in vivo, indicating that CD38 has a key role in the modulation of NAD-replacement therapy for aging and metabolic diseases.	NAD	192-195	CD38 molecule	Homo sapiens	151-155
26485210-6	2016	The NAD-consuming proteins, including sirtuins, poly-ADP-ribose polymerases (PARPs), and CD38, may contribute to the regulatory effects of NAMPT-NAD axis in these cells and vascular repair.	NAD	4-7	CD38 molecule	Homo sapiens	89-93
26485210-6	2016	The NAD-consuming proteins, including sirtuins, poly-ADP-ribose polymerases (PARPs), and CD38, may contribute to the regulatory effects of NAMPT-NAD axis in these cells and vascular repair.	NAD	145-148	CD38 molecule	Homo sapiens	89-93
27300321-1	2016	Two-photon excited fluorescence (TPEF) imaging of the cellular cofactors nicotinamide adenine dinucleotide and oxidized flavin adenine dinucleotide is widely used to measure cellular metabolism, both in normal and pathological cells and tissues.	NAD	73-106	transmembrane protein with EGF like and two follistatin like domains 2	Homo sapiens	33-37
26921398-9	2016	MAIN RESULTS AND THE ROLE OF CHANCE: Our studies produced the first apoenzyme crystal structures for human and mouse GAPDHS and a 1.73 A crystal structure for NAD(+)-bound human GAPDHS, facilitating the identification of unique structural features of this sperm isozyme.	NAD	159-165	glyceraldehyde-3-phosphate dehydrogenase, spermatogenic	Homo sapiens	178-184
26704979-3	2016	Here we showed that the human Dicer protein interacts with SIRT7, an NAD(+)-dependent H3K18Ac (acetylated lysine 18 of histone H3) deacetylase, and holds a proportion of SIRT7 in the cytoplasm.	NAD	69-75	dicer 1, ribonuclease III	Homo sapiens	30-35
27098689-1	2016	UNLABELLED: ARALAR/AGC1/Slc25a12, the aspartate-glutamate carrier from brain mitochondria, is the regulatory step in the malate-aspartate NADH shuttle, MAS.	NAD	138-142	aggrecan	Mus musculus	19-23
26986569-10	2016	The amide exhibited noncompetitive Sirt2 inhibition against the NAD+ (Ki = 9.8 muM) and showed competitive inhibition against the peptide substrate (Ki = 5.3 muM).	NAD	64-68	sirtuin 2	Homo sapiens	35-40
26707577-3	2016	Nicotinamide adenine dinucleotide (NAD(+)/NADH) is a major coenzyme for oxidoreduction reactions in energy metabolism; it has recently emerged as a signalling molecule with a broad range of activities, ranging from calcium (Ca(2+)) signalling (CD38 ectoenzyme) to the epigenetic regulation of gene expression involved in the oxidative stress response, catabolic metabolism and mitochondrial biogenesis (sirtuins, poly[adenosine diphosphate-ribose] polymerases [PARPs]).	NAD	0-33	CD38 molecule	Homo sapiens	244-248
26707577-3	2016	Nicotinamide adenine dinucleotide (NAD(+)/NADH) is a major coenzyme for oxidoreduction reactions in energy metabolism; it has recently emerged as a signalling molecule with a broad range of activities, ranging from calcium (Ca(2+)) signalling (CD38 ectoenzyme) to the epigenetic regulation of gene expression involved in the oxidative stress response, catabolic metabolism and mitochondrial biogenesis (sirtuins, poly[adenosine diphosphate-ribose] polymerases [PARPs]).	NAD	35-41	CD38 molecule	Homo sapiens	244-248
26707577-3	2016	Nicotinamide adenine dinucleotide (NAD(+)/NADH) is a major coenzyme for oxidoreduction reactions in energy metabolism; it has recently emerged as a signalling molecule with a broad range of activities, ranging from calcium (Ca(2+)) signalling (CD38 ectoenzyme) to the epigenetic regulation of gene expression involved in the oxidative stress response, catabolic metabolism and mitochondrial biogenesis (sirtuins, poly[adenosine diphosphate-ribose] polymerases [PARPs]).	NAD	42-46	CD38 molecule	Homo sapiens	244-248
26998043-5	2016	Therefore, the aim of the present study was to investigate the in vitro impact of metformin on cell viability and the expression levels of nicotinamide adenine dinucleotide phosphate (NAPDH) oxidase (p22phox), a major enzyme in reactive oxygen species generation, and the three antioxidative enzymes superoxide dismutase (SOD), glutathione peroxidase (GPx) and catalase (CAT) in monocytes/macrophages derived from 10 healthy volunteers.	NAD	139-172	cytochrome b-245 alpha chain	Homo sapiens	200-207
26660500-4	2016	We have previously shown that human CD38 exhibits a higher preference towards the hydrolysis of NAD(+) to form linear ADPR while Aplysia ADP-ribosyl cyclase prefers cyclizing NAD(+) to form cADPR.	NAD	96-102	CD38 molecule	Homo sapiens	36-40
26660500-4	2016	We have previously shown that human CD38 exhibits a higher preference towards the hydrolysis of NAD(+) to form linear ADPR while Aplysia ADP-ribosyl cyclase prefers cyclizing NAD(+) to form cADPR.	NAD	175-181	CD38 molecule	Homo sapiens	36-40
26660500-6	2016	We also determined the X-ray crystallographic structures of porcine CD38 and were able to observe conformational flexibility at the base of the active site of the enzyme which allow the NAD(+) reaction intermediate to adopt conformations resulting in both hydrolysis and cyclization forming linear ADPR and cADPR respectively.	NAD	186-192	CD38 molecule	Homo sapiens	68-72
26647771-1	2016	SIRT2, one of nicotinamide adenine dinucleotide (NAD+)-dependent class III histone deacetylase family proteins, has been found to be involved in the proliferation and survival of acute myeloid leukemia (AML) cells.	NAD	14-47	sirtuin 2	Homo sapiens	0-5
26647771-1	2016	SIRT2, one of nicotinamide adenine dinucleotide (NAD+)-dependent class III histone deacetylase family proteins, has been found to be involved in the proliferation and survival of acute myeloid leukemia (AML) cells.	NAD	49-53	sirtuin 2	Homo sapiens	0-5
27725455-1	2016	SIRT2 is a member of the human sirtuin family of proteins and possesses nicotinamide adenine dinucleotide (NAD)-dependent lysine deacetylase activity.	NAD	72-105	sirtuin 2	Homo sapiens	0-5
27725455-1	2016	SIRT2 is a member of the human sirtuin family of proteins and possesses nicotinamide adenine dinucleotide (NAD)-dependent lysine deacetylase activity.	NAD	107-110	sirtuin 2	Homo sapiens	0-5
26001219-7	2016	Use of a pan-sirtuin inhibitor and shRNA-mediated protein knockdown led us to uncover a role for the NAD(+)-dependent family of sirtuins, and in particular for SIRT2 and SIRT5, in the regulation of the necroptotic cell death program.	NAD	101-107	sirtuin 2	Mus musculus	160-165
27423864-1	2016	The NAD(+)-dependent deacetylase SIRT1 plays key roles in numerous cellular processes including DNA repair, gene transcription, cell differentiation, and metabolism.	NAD	4-10	sirtuin 1	Mus musculus	33-38
26620281-7	2015	Deacetylation of GKRP is effected by the NAD(+)-dependent, class III histone deacetylase SIRT2, which is inhibited by nicotinamide.	NAD	41-47	sirtuin 2	Mus musculus	89-94
26618989-0	2015	Nmnat1-Rbp7 Is a Conserved Fusion-Protein That Combines NAD+ Catalysis of Nmnat1 with Subcellular Localization of Rbp7.	NAD	56-60	nicotinamide nucleotide adenylyltransferase 1	Danio rerio	0-6
26618989-0	2015	Nmnat1-Rbp7 Is a Conserved Fusion-Protein That Combines NAD+ Catalysis of Nmnat1 with Subcellular Localization of Rbp7.	NAD	56-60	nicotinamide nucleotide adenylyltransferase 1	Danio rerio	74-80
26618989-6	2015	Further, we describe a novel nmnat1-rbp7 transcript encoding a fusion of Rbp7 and the NAD+ (Nicotinamide adenine dinucleotide) synthesizing enzyme Nmnat1.	NAD	86-90	nicotinamide nucleotide adenylyltransferase 1	Danio rerio	29-35
26618989-6	2015	Further, we describe a novel nmnat1-rbp7 transcript encoding a fusion of Rbp7 and the NAD+ (Nicotinamide adenine dinucleotide) synthesizing enzyme Nmnat1.	NAD	86-90	nicotinamide nucleotide adenylyltransferase 1	Danio rerio	147-153
26618989-6	2015	Further, we describe a novel nmnat1-rbp7 transcript encoding a fusion of Rbp7 and the NAD+ (Nicotinamide adenine dinucleotide) synthesizing enzyme Nmnat1.	NAD	92-125	nicotinamide nucleotide adenylyltransferase 1	Danio rerio	29-35
26618989-6	2015	Further, we describe a novel nmnat1-rbp7 transcript encoding a fusion of Rbp7 and the NAD+ (Nicotinamide adenine dinucleotide) synthesizing enzyme Nmnat1.	NAD	92-125	nicotinamide nucleotide adenylyltransferase 1	Danio rerio	147-153
26618989-8	2015	Injection experiments in zebrafish further revealed that Nmnat1-Rbp7a and Nmnat1 have similar NAD+ catalyzing activities but a different subcellular localization.	NAD	94-98	nicotinamide nucleotide adenylyltransferase 1	Danio rerio	57-63
26618989-8	2015	Injection experiments in zebrafish further revealed that Nmnat1-Rbp7a and Nmnat1 have similar NAD+ catalyzing activities but a different subcellular localization.	NAD	94-98	nicotinamide nucleotide adenylyltransferase 1	Danio rerio	74-80
26463129-1	2015	Two novel compounds, pyridopyrimidines (1) and naphthyridines (2) were identified as potent inhibitors of bacterial NAD(+)-dependent DNA ligase (Lig) A in a fragment screening.	NAD	116-122	ubiquitin conjugating enzyme E2 K	Homo sapiens	137-143
26463129-1	2015	Two novel compounds, pyridopyrimidines (1) and naphthyridines (2) were identified as potent inhibitors of bacterial NAD(+)-dependent DNA ligase (Lig) A in a fragment screening.	NAD	116-122	ubiquitin conjugating enzyme E2 K	Homo sapiens	145-148
26432643-8	2015	Surprisingly, constitutive redistribution of NAD(+) from the cytosol to the mitochondria by stable expression of the Arabidopsis thaliana mitochondrial NAD(+) transporter NDT2 in HEK293 cells resulted in dramatic growth retardation and a metabolic shift from oxidative phosphorylation to glycolysis, despite the elevated mitochondrial NAD(+) levels.	NAD	45-51	NAD+ transporter 2	Arabidopsis thaliana	171-175
26432643-8	2015	Surprisingly, constitutive redistribution of NAD(+) from the cytosol to the mitochondria by stable expression of the Arabidopsis thaliana mitochondrial NAD(+) transporter NDT2 in HEK293 cells resulted in dramatic growth retardation and a metabolic shift from oxidative phosphorylation to glycolysis, despite the elevated mitochondrial NAD(+) levels.	NAD	152-158	NAD+ transporter 2	Arabidopsis thaliana	171-175
26716738-8	2015	Recently a-NAD(P)H oxidase/anomerase activity of renalase, which also pomotes oxidative conversion of b-NADH isomers inhibiting activity of NAD-dependent dehydrogenases, has been described.	NAD	104-108	renalase, FAD dependent amine oxidase	Homo sapiens	49-57
26002966-2	2015	AKR1C34 and AKR1C35 similarly oxidized various xenobiotic alicyclic alcohols using NAD(+), but differed in their substrate specificity for hydroxysteroids and inhibitor sensitivity.	NAD	83-89	aldo-keto reductase family 1 member C13-like	Mesocricetus auratus	12-19
26481044-7	2015	These results support a novel, important role for Nampt-mediated NAD(+) biosynthesis in LTD and in the function of GluN2B-containing NMDARs.	NAD	65-71	glutamate receptor, ionotropic, NMDA2B (epsilon 2)	Mus musculus	115-121
26089537-4	2015	The contribution of the ADO-generating ectoenzymes in the regulatory response was shown by: 1) selective inhibition of the enzymatic activities of CD39, CD73, and CD38; 2) the ability of suppressor T cells to convert exogenously added ATP and NAD(+) to ADO; and 3) a positive correlation between ectoenzyme expression, ADO levels, and suppression abilities.	NAD	243-249	5' nucleotidase, ecto	Mus musculus	153-157
26219913-1	2015	NAD(+) kinase (NADK) is the only known cytosolic enzyme that converts NAD(+) to NADP(+), which is subsequently reduced to NADPH.	NAD	0-6	NAD kinase	Homo sapiens	15-19
26287518-1	2015	Activation of Sirtuin1 (Sirt1), an nicotinamide adenine dinucleotide oxidized-dependent deacetylase, by natural or synthetic compounds like resveratrol, SRT2104, or SRT3025 attenuates the loss of bone mass caused by ovariectomy, aging, or unloading in mice.	NAD	35-68	sirtuin 1	Mus musculus	14-22
26287518-1	2015	Activation of Sirtuin1 (Sirt1), an nicotinamide adenine dinucleotide oxidized-dependent deacetylase, by natural or synthetic compounds like resveratrol, SRT2104, or SRT3025 attenuates the loss of bone mass caused by ovariectomy, aging, or unloading in mice.	NAD	35-68	sirtuin 1	Mus musculus	24-29
26211444-8	2015	Also, reduction of NAD-dependent deacetylase sirtuin-3 (SIRT-3)/proline hydroxylase-2 (PHD-2) signaling pathway was evaluated.	NAD	19-22	sirtuin 3	Rattus norvegicus	56-62
26393653-5	2015	CD38, the main mammalian enzyme that hydrolyzes NAD+, belongs to the ectoenzymatic network generating intracellular Ca(2+)-active metabolites.	NAD	48-52	CD38 molecule	Homo sapiens	0-4
26376991-1	2015	BACKGROUND: Sirtuin-1 (SirT1), a nicotinamide adenine dinucleotide(+)-dependent deacetylase, is a key enzyme in the cellular response to metabolic, inflammatory, and oxidative stresses; however, the role of endogenous SirT1 in the vasculature has not been fully elucidated.	NAD	33-66	sirtuin 1	Mus musculus	12-21
26376991-1	2015	BACKGROUND: Sirtuin-1 (SirT1), a nicotinamide adenine dinucleotide(+)-dependent deacetylase, is a key enzyme in the cellular response to metabolic, inflammatory, and oxidative stresses; however, the role of endogenous SirT1 in the vasculature has not been fully elucidated.	NAD	33-66	sirtuin 1	Mus musculus	23-28
26376991-1	2015	BACKGROUND: Sirtuin-1 (SirT1), a nicotinamide adenine dinucleotide(+)-dependent deacetylase, is a key enzyme in the cellular response to metabolic, inflammatory, and oxidative stresses; however, the role of endogenous SirT1 in the vasculature has not been fully elucidated.	NAD	33-66	sirtuin 1	Mus musculus	218-223
26033245-5	2015	Enhanced NAD levels were associated with deacetylation of p53 and Nfkappab indicating increased activation of Sirt1.	NAD	9-12	transformation related protein 53, pseudogene	Mus musculus	58-61
26033245-5	2015	Enhanced NAD levels were associated with deacetylation of p53 and Nfkappab indicating increased activation of Sirt1.	NAD	9-12	sirtuin 1	Mus musculus	110-115
26049000-4	2015	The reaction catalyzed defines renalase as an oxidase, one that harvests two electrons from either 2-dihydroNAD(P) or 6-dihydroNAD(P) to form beta-NAD(P)(+) and hydrogen peroxide.	NAD	142-150	renalase, FAD dependent amine oxidase	Homo sapiens	31-39
25446886-3	2015	Cyt-b5 can augment the 17,20-lyase activity of CYP17A1 by promoting the interaction of CYP17A1 and POR; enhance the 16-ene-synthase activity of CYP17A1 by acting as an electron donor; and enhance the activity of 3betaHSD by increasing the affinity of 3betaHSD for its cofactor NAD(+).	NAD	277-283	cytochrome b5 type A	Homo sapiens	0-6
26016690-9	2015	This bacterial form of renalase has the same substrate specificity profile as that of human renalase but, in terms of binding constant (K(d)), shows a marked preference for substrates derived from beta-NAD+.	NAD	197-206	renalase, FAD dependent amine oxidase	Homo sapiens	23-31
26016690-9	2015	This bacterial form of renalase has the same substrate specificity profile as that of human renalase but, in terms of binding constant (K(d)), shows a marked preference for substrates derived from beta-NAD+.	NAD	197-206	renalase, FAD dependent amine oxidase	Homo sapiens	92-100
26016690-12	2015	We also offer the first structures of a renalase in complex with catalytically relevant ligands beta-NAD+ and beta-NADH (the latter being an analogue of the substrate(s)).	NAD	96-105	renalase, FAD dependent amine oxidase	Homo sapiens	40-48
26016690-12	2015	We also offer the first structures of a renalase in complex with catalytically relevant ligands beta-NAD+ and beta-NADH (the latter being an analogue of the substrate(s)).	NAD	110-119	renalase, FAD dependent amine oxidase	Homo sapiens	40-48
25839883-1	2015	Class I sirtuin genes including SIRT1, SIRT2 and SIRT3, are members of the nicotinamide adenine dinucleotide (NAD)-dependent family of histone deacetylases, and play essential roles in senescence, metabolism, and apoptosis.	NAD	75-108	sirtuin 3	Bos taurus	49-54
25839883-1	2015	Class I sirtuin genes including SIRT1, SIRT2 and SIRT3, are members of the nicotinamide adenine dinucleotide (NAD)-dependent family of histone deacetylases, and play essential roles in senescence, metabolism, and apoptosis.	NAD	110-113	sirtuin 3	Bos taurus	49-54
25938585-3	2015	Sirtuins are a family of seven NAD+-dependent deacetylases (Sirt1-7), which are involved in multiple cellular processes and are emerging as important regulators in oocytes and embryos.	NAD	31-34	sirtuin 1	Mus musculus	60-67
25835215-3	2015	PARP-1 overactivation implies increased energy demands, worsening the metabolic failure and depleting further NAD(+) availability.	NAD	110-116	poly (ADP-ribose) polymerase 1	Rattus norvegicus	0-6
25830335-8	2015	Mice lacking the NAD-dependent deacetylase SIRT3 fail to induce mitochondrial and anti-inflammatory elements of the signature in response to CR, suggesting a potential mechanism involving SIRT3.	NAD	17-20	sirtuin 3	Mus musculus	43-48
25830335-8	2015	Mice lacking the NAD-dependent deacetylase SIRT3 fail to induce mitochondrial and anti-inflammatory elements of the signature in response to CR, suggesting a potential mechanism involving SIRT3.	NAD	17-20	sirtuin 3	Mus musculus	188-193
24681946-8	2015	Moreover, a pharmacological agent that increased the intracellular NAD(+)/NADH ratio led to the degradation of HIF-1alpha by increasing SIRT2-mediated deacetylation and subsequent hydroxylation.	NAD	67-73	sirtuin 2	Homo sapiens	136-141
24681946-8	2015	Moreover, a pharmacological agent that increased the intracellular NAD(+)/NADH ratio led to the degradation of HIF-1alpha by increasing SIRT2-mediated deacetylation and subsequent hydroxylation.	NAD	74-78	sirtuin 2	Homo sapiens	136-141
25834895-0	2010	Discovery of two small molecule inhibitors, ML387 and ML388, of human NAD(+)-dependent 15-hydroxyprostaglandin dehydrogenase The central role of hydroxyprostaglandin dehydrogenase(HPGD) is to inactivate prostaglandins such as prostaglandin E2 (PGE2) or prostaglandin D2 (PGD2).	NAD	70-76	15-hydroxyprostaglandin dehydrogenase	Homo sapiens	180-184
24469059-4	2015	Using a focused RNA interference library for genes involved in epigenetic regulation, we identify sirtuin2 (SIRT2), an NAD(+)-dependent deacetylase, as a modulator of the response to EGFR inhibitors in colon and lung cancer.	NAD	119-125	sirtuin 2	Homo sapiens	98-106
24469059-4	2015	Using a focused RNA interference library for genes involved in epigenetic regulation, we identify sirtuin2 (SIRT2), an NAD(+)-dependent deacetylase, as a modulator of the response to EGFR inhibitors in colon and lung cancer.	NAD	119-125	sirtuin 2	Homo sapiens	108-113
25543138-6	2015	Furthermore, we demonstrate that single-cell metabolic heterogeneity within the basal cell layer correlates with the circadian clock and that diurnal fluctuations in NADH/NAD+ ratio are Bmal1 dependent.	NAD	166-170	aryl hydrocarbon receptor nuclear translocator-like	Mus musculus	186-191
25543138-6	2015	Furthermore, we demonstrate that single-cell metabolic heterogeneity within the basal cell layer correlates with the circadian clock and that diurnal fluctuations in NADH/NAD+ ratio are Bmal1 dependent.	NAD	171-175	aryl hydrocarbon receptor nuclear translocator-like	Mus musculus	186-191
26598832-9	2015	The nutritional levels of niacin such as blood and liver NAD concentrations were also lower in the qprt(-/-) mice than in the qprt(+/+) and the qprt(+/-) mice.	NAD	57-60	quinolinate phosphoribosyltransferase	Mus musculus	99-103
26075037-2	2015	Sirtuins (silent information regulator 2 (Sir2) proteins), NAD(+) dependent enzymes with deacetylase and/or mono-ADP-ribosyltransferase activity, are emerging as key antiaging molecules and regulators in many diseases.	NAD	59-65	sirtuin 2	Homo sapiens	10-40
26075037-2	2015	Sirtuins (silent information regulator 2 (Sir2) proteins), NAD(+) dependent enzymes with deacetylase and/or mono-ADP-ribosyltransferase activity, are emerging as key antiaging molecules and regulators in many diseases.	NAD	59-65	sirtuin 2	Homo sapiens	42-46
25354921-5	2015	Surprisingly, tamoxifen, an estrogen receptor antagonist used for breast cancer treatment, increased the activity and decreased the Km for NAD(+) by about twofold in ALDH1A1.	NAD	139-145	aldehyde dehydrogenase 1 family member A1	Homo sapiens	166-173
25392530-2	2014	Airway epithelial cells express arginine-specific ADP ribosyltransferase (ART)-1, a GPI-anchored ART that transfers ADP-ribose from NAD to arginines 14 and 24 of HNP-1.	NAD	132-135	HNP1	Homo sapiens	162-167
25598664-0	2014	Scant Extracellular NAD Cleaving Activity of Human Neutrophils is Down-Regulated by fMLP via FPRL1.	NAD	20-23	formyl peptide receptor 2	Homo sapiens	93-98
25429139-6	2014	Hypoxia produced PARP1-dependent depletion of nicotinamide adenine dinucleotide (NAD(+)) and inhibition of the NAD(+)-dependent class III histone deactelyase (HDAC) sirtuin-1 (SIRT1).	NAD	111-117	sirtuin 1	Mus musculus	165-174
25064694-4	2014	Here, we have found that a 24h-long exposure to slightly decreased ambient fractional concentration of oxygen (20% oxygen), which is an equivalent to oxygen tension at 350m above sea level, significantly increased levels of SUR2A in the heart despite that this drop of oxygen did not affect levels of O2, CO2 and hematocrit in the blood or myocardial levels of ATP, lactate and NAD/NADH/NAD(+).	NAD	378-381	ATP-binding cassette, sub-family C (CFTR/MRP), member 9	Mus musculus	224-229
25064694-4	2014	Here, we have found that a 24h-long exposure to slightly decreased ambient fractional concentration of oxygen (20% oxygen), which is an equivalent to oxygen tension at 350m above sea level, significantly increased levels of SUR2A in the heart despite that this drop of oxygen did not affect levels of O2, CO2 and hematocrit in the blood or myocardial levels of ATP, lactate and NAD/NADH/NAD(+).	NAD	382-386	ATP-binding cassette, sub-family C (CFTR/MRP), member 9	Mus musculus	224-229
24814981-0	2014	Regulation of SIRT2-dependent alpha-tubulin deacetylation by cellular NAD levels.	NAD	70-73	sirtuin 2	Homo sapiens	14-19
24814981-0	2014	Regulation of SIRT2-dependent alpha-tubulin deacetylation by cellular NAD levels.	NAD	70-73	tubulin alpha 1b	Homo sapiens	30-43
24814981-2	2014	The acetylation reaction is catalyzed by alpha-tubulin N-acetyltransferase and the modification can be reversed by either the NAD-independent class II histone deacetylase HDAC6 or the NAD-dependent deacetylase SIRT2.	NAD	126-129	tubulin alpha 1b	Homo sapiens	41-54
24814981-2	2014	The acetylation reaction is catalyzed by alpha-tubulin N-acetyltransferase and the modification can be reversed by either the NAD-independent class II histone deacetylase HDAC6 or the NAD-dependent deacetylase SIRT2.	NAD	126-129	sirtuin 2	Homo sapiens	210-215
24814981-2	2014	The acetylation reaction is catalyzed by alpha-tubulin N-acetyltransferase and the modification can be reversed by either the NAD-independent class II histone deacetylase HDAC6 or the NAD-dependent deacetylase SIRT2.	NAD	184-187	tubulin alpha 1b	Homo sapiens	41-54
24814981-2	2014	The acetylation reaction is catalyzed by alpha-tubulin N-acetyltransferase and the modification can be reversed by either the NAD-independent class II histone deacetylase HDAC6 or the NAD-dependent deacetylase SIRT2.	NAD	184-187	sirtuin 2	Homo sapiens	210-215
24814981-3	2014	In this study, we assessed to what extent cellular NAD levels are involved in the regulation of the alpha-tubulin acetylation state.	NAD	51-54	tubulin alpha 1b	Homo sapiens	100-113
25001863-6	2014	We tested this concept in septic mice, using the highly specific SIRT1 inhibitor EX-527, a small molecule that closes the NAD+ binding site of SIRT1.	NAD	122-126	sirtuin 1	Mus musculus	65-70
25001863-6	2014	We tested this concept in septic mice, using the highly specific SIRT1 inhibitor EX-527, a small molecule that closes the NAD+ binding site of SIRT1.	NAD	122-126	sirtuin 1	Mus musculus	143-148
25001863-11	2014	Our findings reveal that modifying the SIRT1 NAD+ axis may provide a novel way to treat sepsis in its hypoinflammatory phase.	NAD	45-49	sirtuin 1	Mus musculus	39-44
25051436-6	2014	In mice, DPN (EC50 0.85) increased Slit3 mRNA concentrations compared with hormone-depleted and 17beta-estradiol-treated (EC50 0.1) animals and decreased the density of nerves but not vessels in endometriosis lesions.	NAD	9-12	slit guidance ligand 3	Mus musculus	35-40
25044690-3	2014	FoxO1 is a transcription factor regulated by insulin signaling that is deacetylated by Sirt1, a nicotinamide adenine dinucleotide- (NAD(+) -) dependent deacetylase.	NAD	96-129	forkhead box O1	Mus musculus	0-5
25044690-3	2014	FoxO1 is a transcription factor regulated by insulin signaling that is deacetylated by Sirt1, a nicotinamide adenine dinucleotide- (NAD(+) -) dependent deacetylase.	NAD	96-129	sirtuin 1	Mus musculus	87-92
25203508-3	2014	Here we provide a structural explanation for the stability of the heterotetramer from the crystal structure with NAD(+) and NADP(+) bound to the HSD17B8 and CBR4 subunits, respectively, and show that the catalytic activity of the NADPH- and ACP-dependent CBR4 subunit is crucial for a functional HsKAR.	NAD	113-119	carbonyl reductase 4	Homo sapiens	157-161
25203508-3	2014	Here we provide a structural explanation for the stability of the heterotetramer from the crystal structure with NAD(+) and NADP(+) bound to the HSD17B8 and CBR4 subunits, respectively, and show that the catalytic activity of the NADPH- and ACP-dependent CBR4 subunit is crucial for a functional HsKAR.	NAD	113-119	carbonyl reductase 4	Homo sapiens	255-259
25038521-7	2014	In this regard, the GHRH-GH-IGF-1/Insulin, TOR-S6K1,NAD(+)-Sirtuin, P53, Klotho and APOE pathways have been linked to processes associated with age-related diseases, including cancer, cardiovascular disease, diabetes, osteoporosis, and neurodegenerative diseases, all of which directly influence health in aging, and represent key targets in anti-aging therapy.	NAD	52-58	gamma-glutamyl hydrolase	Homo sapiens	20-22
24842953-2	2014	C-terminal-binding protein 1 (CtBP1) is a transcription repressor of tumor suppressor genes and is activated by NADH binding.	NAD	112-116	C-terminal binding protein 1	Mus musculus	0-28
24842953-2	2014	C-terminal-binding protein 1 (CtBP1) is a transcription repressor of tumor suppressor genes and is activated by NADH binding.	NAD	112-116	C-terminal binding protein 1	Mus musculus	30-35
24880552-1	2014	Anthocyanidin reductase (ANR) is an NADPH-/NADH-dependent enzyme that transfers two hydrides to anthocyanidins to produce three types of isomeric flavan-3-ols.	NAD	43-47	anthocyanidin reductase ((2S)-flavan-3-ol-forming)	Vitis vinifera	25-28
24687991-1	2014	The sirtuins (SIRTs; SIRT1-7) are a family of NAD(+)-dependent enzymes that dynamically regulate cellular physiology.	NAD	46-52	sirtuin 1	Mus musculus	21-28
24994116-3	2014	EMT-induced CS-like cells (HMLERshEcad) and isogenic parental cells (HMLERshCntrol) were simultaneously screened for their ability to generate energy-rich NADH when cultured in a standardized high-throughput metabolic phenotyping platform comprising &gt;350 wells that were pre-loaded with different carbohydrates/starches, alcohols, fatty acids, ketones, carboxylic acids, amino acids, and bi-amino acids.	NAD	155-159	IL2 inducible T cell kinase	Homo sapiens	0-3
24967705-6	2014	High levels of CD38 reduced intracellular nicotinamide adenine dinucleotide (NAD+) levels and blocked acquired resistance by inhibiting the activity of the NAD+-dependent SIRT1 deacetylase that we have previously shown to promote resistance in CML cells by facilitating error-prone DNA damage repair.	NAD	42-75	CD38 molecule	Homo sapiens	15-19
24967705-6	2014	High levels of CD38 reduced intracellular nicotinamide adenine dinucleotide (NAD+) levels and blocked acquired resistance by inhibiting the activity of the NAD+-dependent SIRT1 deacetylase that we have previously shown to promote resistance in CML cells by facilitating error-prone DNA damage repair.	NAD	77-81	CD38 molecule	Homo sapiens	15-19
24967705-6	2014	High levels of CD38 reduced intracellular nicotinamide adenine dinucleotide (NAD+) levels and blocked acquired resistance by inhibiting the activity of the NAD+-dependent SIRT1 deacetylase that we have previously shown to promote resistance in CML cells by facilitating error-prone DNA damage repair.	NAD	156-160	CD38 molecule	Homo sapiens	15-19
24959710-2	2014	Silent information regulator 1 (sir2 or SIRT1), a NAD-dependent deacetylase, plays complex systemic roles in a variety of processes through deacetylating acetylated histone and other specific substrates.	NAD	50-53	sirtuin 1	Mus musculus	32-36
24959710-2	2014	Silent information regulator 1 (sir2 or SIRT1), a NAD-dependent deacetylase, plays complex systemic roles in a variety of processes through deacetylating acetylated histone and other specific substrates.	NAD	50-53	sirtuin 1	Mus musculus	40-45
24748594-3	2014	Silent information regulator of transcription 3 (SIRT3), the major mitochondrial NAD(+)-dependent lysine deacetylase, regulates a variety of functions, and its inhibition may disrupt mitochondrial function to impact recovery from IR injury.	NAD	81-87	sirtuin 3	Rattus norvegicus	49-54
24905194-1	2014	Nicotinamide phosphoribosyltransferase (Nampt), the rate-limiting enzyme for nicotinamide adenine dinucleotide (NAD+) synthesis, and Sirt1, an NAD+-dependent histone deacetylase, protect the heart against ischemia/reperfusion (I/R).	NAD	112-116	sirtuin 1	Mus musculus	133-138
24814483-0	2014	NAD(+)-dependent activation of Sirt1 corrects the phenotype in a mouse model of mitochondrial disease.	NAD	0-6	sirtuin 1	Mus musculus	31-36
24814483-4	2014	As NAD(+) boosts the activity of Sirtuin1 and other sirtuins, intracellular levels of NAD(+) play a key role in the homeostatic control of mitochondrial function by the metabolic status of the cell.	NAD	3-9	sirtuin 1	Mus musculus	33-41
24814483-4	2014	As NAD(+) boosts the activity of Sirtuin1 and other sirtuins, intracellular levels of NAD(+) play a key role in the homeostatic control of mitochondrial function by the metabolic status of the cell.	NAD	86-92	sirtuin 1	Mus musculus	33-41
24814483-5	2014	We show here that supplementation with nicotinamide riboside, a natural NAD(+) precursor, or reduction of NAD(+) consumption by inhibiting the poly(ADP-ribose) polymerases, leads to marked improvement of the respiratory chain defect and exercise intolerance of the Sco2 knockout/knockin mouse, a mitochondrial disease model characterized by impaired cytochrome c oxidase biogenesis.	NAD	106-112	SCO2 cytochrome c oxidase assembly protein	Mus musculus	265-269
23113554-4	2014	Cytochrome b5 reductase is involved in the transfer of reducing equivalents from the physiological electron donor, NADH, via an FAD domain to the small molecules of cytochrome b5.	NAD	115-119	cytochrome b5 type A	Homo sapiens	165-178
24875183-5	2014	Sirtuin family member SIRT1 was found to interact with and deacetylate FOXA2, the latter process being dependent on the NAD+-binding catalytic site of SIRT1.	NAD	120-124	sirtuin 1	Mus musculus	22-27
24875183-5	2014	Sirtuin family member SIRT1 was found to interact with and deacetylate FOXA2, the latter process being dependent on the NAD+-binding catalytic site of SIRT1.	NAD	120-124	sirtuin 1	Mus musculus	151-156
24622975-7	2014	Furthermore, Akt2 knockout displayed upregulated apoptotic protein markers (Bax, caspase-3, caspase-9, and caspace-12) and mitochondrial damage (reduced aconitase activity and NAD(+), elevated cytochrome-c release from mitochondria) along with reduced phosphorylation of PTEN, Akt, and GSK3beta in the absence of changes in pan protein expression, the effects of which were abolished or significantly ameliorated by H2S treatment.	NAD	176-182	thymoma viral proto-oncogene 2	Mus musculus	13-17
24760190-2	2014	Hydroxyprostaglandin dehydrogenase 15-(nicotinamide adenine dinucleotide) (15-PGDH, HPGD) is down-regulated in colorectal cancers and functions as a metabolic antagonist of PTGS2.	NAD	39-72	15-hydroxyprostaglandin dehydrogenase	Homo sapiens	75-82
24743600-3	2014	Expression of the NAD-dependent deacetylase Sirtuin-3 is down-regulated in GK rats compared to normoglycemic Brown Norway (BN) rats.	NAD	18-21	sirtuin 3	Rattus norvegicus	44-53
24719103-0	2014	ArfGAP3 is a component of the photoreceptor synaptic ribbon complex and forms an NAD(H)-regulated, redox-sensitive complex with RIBEYE that is important for endocytosis.	NAD	81-87	ADP-ribosylation factor GTPase activating protein 3	Mus musculus	0-7
24719103-9	2014	ArfGAP3 binds to RIBEYE(B)-domain in an NAD(H)-dependent manner.	NAD	40-46	ADP-ribosylation factor GTPase activating protein 3	Mus musculus	0-7
24719103-10	2014	The interaction is redox sensitive because NADH is more efficient than the oxidized NAD(+) in promoting ArfGAP3-RIBEYE interaction.	NAD	43-47	ADP-ribosylation factor GTPase activating protein 3	Mus musculus	104-111
24719103-10	2014	The interaction is redox sensitive because NADH is more efficient than the oxidized NAD(+) in promoting ArfGAP3-RIBEYE interaction.	NAD	84-90	ADP-ribosylation factor GTPase activating protein 3	Mus musculus	104-111
24699644-0	2014	The first crystal structure of NAD-dependent 3-dehydro-2-deoxy-D-gluconate dehydrogenase from Thermus thermophilus HB8.	NAD	31-34	2-hydroxyacid dehydrogenase	Thermus thermophilus HB8	75-88
24292505-7	2014	Extracellular NAD(+) inhibited proteasome-dependent degradation of Mcl-1 upstream of caspase activation and, furthermore, suppressed Bax translocation to the mitochondria and attenuated both dissipation of mitochondrial transmembrane potential (DeltaPsim) and cytochrome c release from the mitochondria into the cytosol.	NAD	14-20	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	67-72
24292505-8	2014	Finally, we found that extracellular NAD(+) inhibited spontaneous activation of caspase-9, but not caspase-8, and the pro-survival effect of extracellular NAD(+) was abrogated by the inhibitor of caspase-9, but not by the inhibitor of caspase-8.	NAD	37-43	caspase 9	Homo sapiens	80-89
24292505-8	2014	Finally, we found that extracellular NAD(+) inhibited spontaneous activation of caspase-9, but not caspase-8, and the pro-survival effect of extracellular NAD(+) was abrogated by the inhibitor of caspase-9, but not by the inhibitor of caspase-8.	NAD	37-43	caspase 9	Homo sapiens	196-205
24292505-8	2014	Finally, we found that extracellular NAD(+) inhibited spontaneous activation of caspase-9, but not caspase-8, and the pro-survival effect of extracellular NAD(+) was abrogated by the inhibitor of caspase-9, but not by the inhibitor of caspase-8.	NAD	155-161	caspase 9	Homo sapiens	80-89
24292505-8	2014	Finally, we found that extracellular NAD(+) inhibited spontaneous activation of caspase-9, but not caspase-8, and the pro-survival effect of extracellular NAD(+) was abrogated by the inhibitor of caspase-9, but not by the inhibitor of caspase-8.	NAD	155-161	caspase 9	Homo sapiens	196-205
24292505-9	2014	Together, these results demonstrate that extracellular NAD(+) inhibits neutrophil apoptosis via P2Y11 receptor and cAMP/PKA pathway by regulating Mcl-1 level, Bax targeting to the mitochondria and mitochondrial apoptotic pathway.	NAD	55-61	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	146-151
24374551-1	2014	AIMS/HYPOTHESIS: Obesity is associated with ageing and increased energy intake, while restriction of energy intake improves health and longevity in multiple organisms; the NAD(+)-dependent deacetylase sirtuin 1 (SIRT1) is implicated in this process.	NAD	172-178	sirtuin 1	Mus musculus	212-217
24647961-4	2014	The nicotinamide adenine dinucleotide-dependent deacetylase sirtuin type 3 (SirT3) coordinates mitochondrial energy production and redox homeostasis.	NAD	4-37	sirtuin 3	Mus musculus	60-74
24647961-4	2014	The nicotinamide adenine dinucleotide-dependent deacetylase sirtuin type 3 (SirT3) coordinates mitochondrial energy production and redox homeostasis.	NAD	4-37	sirtuin 3	Mus musculus	76-81
24203696-2	2014	Here, we present for the first time that SIRT2, a nicotinamide adenine dinucleotide (NAD)-dependent deacetylase, regulates ciliogenesis and centrosome amplification.	NAD	50-83	sirtuin 2	Homo sapiens	41-46
24203696-2	2014	Here, we present for the first time that SIRT2, a nicotinamide adenine dinucleotide (NAD)-dependent deacetylase, regulates ciliogenesis and centrosome amplification.	NAD	85-88	sirtuin 2	Homo sapiens	41-46
24212099-1	2014	Release of NAD(+) during preparation of murine lymphocytes causes enzymatic ADP-ribosylation of cell-surface proteins on T cells, catalyzed by toxin-related ecto-ADP-ribosyltransferase, ARTC2.	NAD	11-17	ADP-ribosyltransferase 2b	Mus musculus	186-191
24572426-0	2014	Retraction: The NAD-dependent deacetylase SIRT2 is required for programmed necrosis.	NAD	16-19	sirtuin 2	Homo sapiens	42-47
24573134-2	2014	Silent information regulator transcript-1 (SIRT1), an NAD-dependent deacetylase, mediates NF-kappaB deacetylation, and inhibits its function.	NAD	54-57	sirtuin 1	Mus musculus	0-41
24573134-2	2014	Silent information regulator transcript-1 (SIRT1), an NAD-dependent deacetylase, mediates NF-kappaB deacetylation, and inhibits its function.	NAD	54-57	sirtuin 1	Mus musculus	43-48
24586202-6	2014	Since two-pore domain K(+) channels regulate the resting membrane potentials of numerous cell types, we suggest that the SUP-18 IYD regulates the activity of the SUP-9 channel using NADH as a coenzyme and thus couples the metabolic state of muscle cells to muscle membrane excitability.	NAD	182-186	Iodotyrosine dehalogenase 1 homolog	Caenorhabditis elegans	121-127
24551254-6	2014	The apo-form of human SIRT2 and the same structure solved in complex with its co-substrate NAD(+) allowed the modeling of TcSir2rp1 in the open and closed conformational states.	NAD	91-97	sirtuin 2	Homo sapiens	22-27
24293653-4	2014	We discovered that poly(ADP-ribose) synthesis catalysed by PARP1 at the sites of unrepaired SBs activates ARF transcription through a protein signalling cascade, including the NAD(+)-dependent deacetylase SIRT1 and the transcription factor E2F1.	NAD	176-182	E2F transcription factor 1	Homo sapiens	240-244
24293653-5	2014	Our data suggest that poly(ADP-ribose) synthesis at the sites of SBs initiates DNA damage signal transduction by reducing the cellular concentration of NAD(+), thus down-regulating SIRT1 activity and consequently activating E2F1-dependent ARF transcription.	NAD	152-158	E2F transcription factor 1	Homo sapiens	224-228
24056172-3	2014	E2 and the ESR2-selective agonist DPN, but not PPT, increased, in a PI3K and CREB-dependent manner, the expression of CDKN1B and the transcription factors GATA-1 and DMRT1.	NAD	34-37	estrogen receptor 2	Rattus norvegicus	11-15
24056172-3	2014	E2 and the ESR2-selective agonist DPN, but not PPT, increased, in a PI3K and CREB-dependent manner, the expression of CDKN1B and the transcription factors GATA-1 and DMRT1.	NAD	34-37	cAMP responsive element binding protein 1	Rattus norvegicus	77-81
24056172-3	2014	E2 and the ESR2-selective agonist DPN, but not PPT, increased, in a PI3K and CREB-dependent manner, the expression of CDKN1B and the transcription factors GATA-1 and DMRT1.	NAD	34-37	cyclin-dependent kinase inhibitor 1B	Rattus norvegicus	118-124
24473773-3	2014	MacroH2A1.1 binds with high affinity O-acetyl ADP ribose, a small metabolite produced by the reaction catalysed by NAD+-dependent deacetylase SIRT1, whereas macroH2A1.2 is unable to do so.	NAD	115-119	sirtuin 1	Mus musculus	142-147
24078189-2	2014	Ammonia is produced from the enzymatic reactions between Gly and GDH with NAD(+) in phosphate buffer medium.	NAD	74-80	glutamate dehydrogenase 1	Homo sapiens	65-68
24848420-4	2014	However, the complexity of these systems due to the need of electron transfer from nicotinamide adenine dinucleotide (phosphate) (NAD(P)H) via redox partner proteins for the initial hydroxylation step limits a broader technical implementation of CYP enzymes.	NAD	83-116	peptidylprolyl isomerase G	Homo sapiens	246-249
24025713-7	2014	However, we identified a role for the NAD degradation pathway mediated by the NADase CD38 on the sensitivity to Nampt inhibition.	NAD	38-41	CD38 molecule	Homo sapiens	85-89
24145018-1	2014	Clostridium difficile produces an NAD-specific glutamate dehydrogenase (GDH), which converts l-glutamate into alpha-ketoglutarate through an irreversible reaction.	NAD	34-37	glutamate dehydrogenase 1	Homo sapiens	72-75
23761034-3	2014	In many organisms this holds also for glutamate dehydrogenases (GDH), NAD(+)-dependent for glutamate oxidation, NADP(+)-dependent for fixing ammonia.	NAD	70-76	glutamate dehydrogenase 1	Homo sapiens	64-67
23761034-5	2014	It has been suggested that GDH in mitochondria reacts only with NADP(H), the NAD(+) reaction being an in vitro artefact.	NAD	77-83	glutamate dehydrogenase 1	Homo sapiens	27-30
23761034-6	2014	However, contrary evidence suggests mitochondrial GDH not only reacts with NAD(+) but maintains equilibrium using the same pool as accessed by beta-hydroxybutyrate dehydrogenase.	NAD	75-81	glutamate dehydrogenase 1	Homo sapiens	50-53
24144881-9	2013	Responses to ADP, MRS-2365 and beta-NAD were absent in PDGFRalpha(+) cells from P2ry1((-/-)) mice, but responses to ATP were retained.	NAD	31-39	purinergic receptor P2Y, G-protein coupled 1	Mus musculus	80-85
24216102-0	2013	Large changes in NAD levels associated with CD38 expression during HL-60 cell differentiation.	NAD	17-20	CD38 molecule	Homo sapiens	44-48
24216102-2	2013	One such enzyme is CD38 which, alongside synthesising Ca(2+)-releasing second messengers and acting as a cell surface receptor, has also been suggested to play a key role in NAD(+) homeostasis.	NAD	174-180	CD38 molecule	Homo sapiens	19-23
24216102-4	2013	We have exploited the HL-60 cell line as a model of inducible CD38 expression, to investigate CD38-mediated regulation intracellular NAD(+) levels and the consequences of changes in NAD(+) levels on cell physiology.	NAD	133-139	CD38 molecule	Homo sapiens	94-98
24216102-5	2013	Intracellular NAD(+) levels fell with increasing CD38 expression and this was reversed with the CD38 inhibitor, kuromanin confirming the key role of CD38 in NAD(+) homeostasis.	NAD	14-20	CD38 molecule	Homo sapiens	49-53
24216102-5	2013	Intracellular NAD(+) levels fell with increasing CD38 expression and this was reversed with the CD38 inhibitor, kuromanin confirming the key role of CD38 in NAD(+) homeostasis.	NAD	14-20	CD38 molecule	Homo sapiens	96-100
24216102-5	2013	Intracellular NAD(+) levels fell with increasing CD38 expression and this was reversed with the CD38 inhibitor, kuromanin confirming the key role of CD38 in NAD(+) homeostasis.	NAD	14-20	CD38 molecule	Homo sapiens	96-100
24216102-5	2013	Intracellular NAD(+) levels fell with increasing CD38 expression and this was reversed with the CD38 inhibitor, kuromanin confirming the key role of CD38 in NAD(+) homeostasis.	NAD	157-163	CD38 molecule	Homo sapiens	96-100
24216102-5	2013	Intracellular NAD(+) levels fell with increasing CD38 expression and this was reversed with the CD38 inhibitor, kuromanin confirming the key role of CD38 in NAD(+) homeostasis.	NAD	157-163	CD38 molecule	Homo sapiens	96-100
24216102-6	2013	We also measured the consequences of CD38 expression during the differentiation on a number of functions linked to NAD(+) and we show that some but not all NAD(+)-dependent processes are significantly affected by the lowered NAD(+) levels.	NAD	115-121	CD38 molecule	Homo sapiens	37-41
24216102-6	2013	We also measured the consequences of CD38 expression during the differentiation on a number of functions linked to NAD(+) and we show that some but not all NAD(+)-dependent processes are significantly affected by the lowered NAD(+) levels.	NAD	156-162	CD38 molecule	Homo sapiens	37-41
24216102-6	2013	We also measured the consequences of CD38 expression during the differentiation on a number of functions linked to NAD(+) and we show that some but not all NAD(+)-dependent processes are significantly affected by the lowered NAD(+) levels.	NAD	156-162	CD38 molecule	Homo sapiens	37-41
24047466-2	2013	Mice deficient in sirtuin (Sirt) 3, a nicotinamide adenine dinucleotide-dependent mitochondrial deacetylase, demonstrate enhanced left ventricular hypertrophy after aortic banding, whereas cells from these mice reportedly exhibit augmented hypoxia-induced ROS signaling and hypoxia-inducible factor (HIF)-1 activation.	NAD	38-71	sirtuin 3	Mus musculus	27-34
24278448-3	2013	Activated PARP-1 consumes cytosolic NAD, and because NAD is required for glycolysis, hypoglycemia-induced PARP-1 activation may render cells unable to use glucose even when glucose availability is restored.	NAD	36-39	poly (ADP-ribose) polymerase 1	Rattus norvegicus	10-16
23876293-2	2013	IDH3 is mitochondrial, uses NAD(H) and was believed to be the IDH that supports the citric acid cycle.	NAD	28-34	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	0-3
23995837-4	2013	Here, we report that TR-mediated transcriptional activation of PCK1 and G6PC in human hepatic cells and mouse liver was FoxO1-dependent and furthermore required FoxO1 deacetylation by the NAD(+)-dependent deacetylase, SirT1.	NAD	188-194	phosphoenolpyruvate carboxykinase 1	Homo sapiens	63-67
23995837-4	2013	Here, we report that TR-mediated transcriptional activation of PCK1 and G6PC in human hepatic cells and mouse liver was FoxO1-dependent and furthermore required FoxO1 deacetylation by the NAD(+)-dependent deacetylase, SirT1.	NAD	188-194	forkhead box O1	Mus musculus	161-166
23794046-6	2013	When they were respectively co-expressed with ALD4, an ALDH from S. cerevisiae, the activities of ALD4 were significantly elevated compared with that expressing ALD4 alone, suggesting that the regenerated NAD(+) enhanced the activity of ALD4.	NAD	205-211	aldehyde dehydrogenase (NADP(+)) ALD4	Saccharomyces cerevisiae S288C	46-50
23794046-6	2013	When they were respectively co-expressed with ALD4, an ALDH from S. cerevisiae, the activities of ALD4 were significantly elevated compared with that expressing ALD4 alone, suggesting that the regenerated NAD(+) enhanced the activity of ALD4.	NAD	205-211	aldehyde dehydrogenase (NADP(+)) ALD4	Saccharomyces cerevisiae S288C	98-102
23794046-6	2013	When they were respectively co-expressed with ALD4, an ALDH from S. cerevisiae, the activities of ALD4 were significantly elevated compared with that expressing ALD4 alone, suggesting that the regenerated NAD(+) enhanced the activity of ALD4.	NAD	205-211	aldehyde dehydrogenase (NADP(+)) ALD4	Saccharomyces cerevisiae S288C	98-102
23794046-6	2013	When they were respectively co-expressed with ALD4, an ALDH from S. cerevisiae, the activities of ALD4 were significantly elevated compared with that expressing ALD4 alone, suggesting that the regenerated NAD(+) enhanced the activity of ALD4.	NAD	205-211	aldehyde dehydrogenase (NADP(+)) ALD4	Saccharomyces cerevisiae S288C	98-102
23794046-8	2013	This study not only reveals the reliance of ALD4 activity on NAD(+) availability but also provides a method for regulating the dha regulon.	NAD	61-67	aldehyde dehydrogenase (NADP(+)) ALD4	Saccharomyces cerevisiae S288C	44-48
23931755-5	2013	Decreased NAD(+)/NADH ratio by complex I deficiency inhibited Sirt3 activity, leading to an increase in protein acetylation and sensitization of the permeability transition in mitochondria (mPTP).	NAD	10-16	sirtuin 3	Mus musculus	62-67
23931755-5	2013	Decreased NAD(+)/NADH ratio by complex I deficiency inhibited Sirt3 activity, leading to an increase in protein acetylation and sensitization of the permeability transition in mitochondria (mPTP).	NAD	17-21	sirtuin 3	Mus musculus	62-67
23922874-8	2013	In addition, over expression of miR-26b strongly inhibited LoVo cell survival and invasion, an effect partially abrogated by the addition of NAD.	NAD	141-144	microRNA 26b	Homo sapiens	32-39
23786618-3	2013	In one of the adult fibroblast strains evaluated, these changes in procollagen-1 and NAD(+)/NADH in response to the complex of bioactives were in parallel with increased expression of mRNA biomarkers related primarily to dermal matrix and basement membrane structure, including COL1A1, COL3A1, COL5A1, COL14A1, ELN and LOXL2, in addition to SOD2, NAMPT and TGFBR3; MMP1 was decreased in expression.	NAD	85-91	collagen type III alpha 1 chain	Homo sapiens	286-292
23786618-3	2013	In one of the adult fibroblast strains evaluated, these changes in procollagen-1 and NAD(+)/NADH in response to the complex of bioactives were in parallel with increased expression of mRNA biomarkers related primarily to dermal matrix and basement membrane structure, including COL1A1, COL3A1, COL5A1, COL14A1, ELN and LOXL2, in addition to SOD2, NAMPT and TGFBR3; MMP1 was decreased in expression.	NAD	85-91	collagen type XIV alpha 1 chain	Homo sapiens	302-309
23786618-3	2013	In one of the adult fibroblast strains evaluated, these changes in procollagen-1 and NAD(+)/NADH in response to the complex of bioactives were in parallel with increased expression of mRNA biomarkers related primarily to dermal matrix and basement membrane structure, including COL1A1, COL3A1, COL5A1, COL14A1, ELN and LOXL2, in addition to SOD2, NAMPT and TGFBR3; MMP1 was decreased in expression.	NAD	85-91	matrix metallopeptidase 1	Homo sapiens	365-369
23786618-3	2013	In one of the adult fibroblast strains evaluated, these changes in procollagen-1 and NAD(+)/NADH in response to the complex of bioactives were in parallel with increased expression of mRNA biomarkers related primarily to dermal matrix and basement membrane structure, including COL1A1, COL3A1, COL5A1, COL14A1, ELN and LOXL2, in addition to SOD2, NAMPT and TGFBR3; MMP1 was decreased in expression.	NAD	92-96	collagen type III alpha 1 chain	Homo sapiens	286-292
23786618-3	2013	In one of the adult fibroblast strains evaluated, these changes in procollagen-1 and NAD(+)/NADH in response to the complex of bioactives were in parallel with increased expression of mRNA biomarkers related primarily to dermal matrix and basement membrane structure, including COL1A1, COL3A1, COL5A1, COL14A1, ELN and LOXL2, in addition to SOD2, NAMPT and TGFBR3; MMP1 was decreased in expression.	NAD	92-96	collagen type XIV alpha 1 chain	Homo sapiens	302-309
23786618-3	2013	In one of the adult fibroblast strains evaluated, these changes in procollagen-1 and NAD(+)/NADH in response to the complex of bioactives were in parallel with increased expression of mRNA biomarkers related primarily to dermal matrix and basement membrane structure, including COL1A1, COL3A1, COL5A1, COL14A1, ELN and LOXL2, in addition to SOD2, NAMPT and TGFBR3; MMP1 was decreased in expression.	NAD	92-96	matrix metallopeptidase 1	Homo sapiens	365-369
23548750-14	2013	Our study suggests that some fungal IDO enzymes function in tryptophan metabolism and NAD(+) supply.	NAD	86-92	indoleamine 2,3-dioxygenase 1	Homo sapiens	36-39
23548750-15	2013	In contrast, other IDO enzymes do not possess sufficient Trp-metabolising capacity to supply NAD(+).	NAD	93-99	indoleamine 2,3-dioxygenase 1	Homo sapiens	19-22
23673559-1	2013	Sirtuin 5 (SIRT5) is a nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase, belonging to the silent information regulator 2 (Sir2) family of sirtuin histone deacetylases (sirtuins).	NAD	58-61	sirtuin 1	Mus musculus	104-134
23673559-1	2013	Sirtuin 5 (SIRT5) is a nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase, belonging to the silent information regulator 2 (Sir2) family of sirtuin histone deacetylases (sirtuins).	NAD	58-61	sirtuin 1	Mus musculus	136-140
23846805-2	2013	In massive DNA damage, PARP is overactivated, exhausting nicotinamide adenine dinucleotide and leading to cell death.	NAD	57-90	poly (ADP-ribose) polymerase 1	Rattus norvegicus	23-27
23435875-3	2013	In this study, E. coli SZ420 was further engineered for reduction of xylose to xylitol by (1) deleting the alcohol dehydrogenase gene (adhE) to divert NADH from the ethanol pathway; (2) deleting the glucose-specific PTS permease gene (ptsG) to eliminate catabolite repression and allow simultaneous uptake of glucose and xylose; (3) cloning the aldose reductase gene (xylI) of Candida boidinii to reduce xylose to xylitol.	NAD	151-155	Alcohol dehydrogenase	Escherichia coli	107-128
23825667-8	2013	Moreover, concomitant suppression of NAD-dependent deacetylase SIRT1 and AMPK is observed in atherosclerotic pigs, which leads to the proteolytic activation of SREBP-1 by diminishing the deacetylation and Ser-372 phosphorylation of SREBP-1.	NAD	37-40	SREBP-1	Sus scrofa	160-167
23825667-8	2013	Moreover, concomitant suppression of NAD-dependent deacetylase SIRT1 and AMPK is observed in atherosclerotic pigs, which leads to the proteolytic activation of SREBP-1 by diminishing the deacetylation and Ser-372 phosphorylation of SREBP-1.	NAD	37-40	SREBP-1	Sus scrofa	232-239
23420347-1	2013	Glutamate dehydrogenase (GDH) uses ammonia to reversibly convert alpha-ketoglutarate to glutamate using NADP(H) and NAD(H) as cofactors.	NAD	116-122	glutamate dehydrogenase 1	Homo sapiens	0-23
23420347-1	2013	Glutamate dehydrogenase (GDH) uses ammonia to reversibly convert alpha-ketoglutarate to glutamate using NADP(H) and NAD(H) as cofactors.	NAD	116-122	glutamate dehydrogenase 1	Homo sapiens	25-28
23597945-4	2013	In addition, we demonstrated that the Myc/HIF-1-targeted glyceraldehyde-3-phosphate dehydrogenase (GAPDH) catalyzing a key step producing the NADH cofactor, activates the Akt pathway, thereby upregulating expression of the anti-apoptotic Bcl-xL.	NAD	142-146	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	38-41
24020004-1	2013	SIRT1 is a NAD(+)-dependent protein deacetylase that has a very large number of established protein substrates and an equally impressive list of biological functions thought to be regulated by its activity.	NAD	11-15	sirtuin 1	Mus musculus	0-5
23261716-7	2013	When NADPH was used, as compared to NADH, the reductions of CBCP-one by AKR1C1, AKR1C2 and AKR1C3 were 14-, 51- and 31-fold more efficient, respectively.	NAD	36-40	aldo-keto reductase family 1 member C1	Homo sapiens	72-78
23264732-4	2013	Although the nicotinamide mononucleotide adenylyltransferase (Nmnat1) portion of Wld(S) is required, we found that its nicotinamide adenine dinucleotide (NAD(+)) enzyme activity and the Wld(S) N-terminus (N70) are dispensable, unlike axotomy models of neurodegeneration.	NAD	119-152	Nicotinamide mononucleotide adenylyltransferase	Drosophila melanogaster	62-68
23264732-4	2013	Although the nicotinamide mononucleotide adenylyltransferase (Nmnat1) portion of Wld(S) is required, we found that its nicotinamide adenine dinucleotide (NAD(+)) enzyme activity and the Wld(S) N-terminus (N70) are dispensable, unlike axotomy models of neurodegeneration.	NAD	154-161	Nicotinamide mononucleotide adenylyltransferase	Drosophila melanogaster	62-68
23442855-5	2013	The ME-R model is able to simulate: i), the shape and order of magnitude of H(2)O(2) emission and dose-response kinetics observed after treatment with inhibitors of the GSH or Trx scavenging systems and ii), steady and transient behavior of DeltaPsi(m) and NADH after single or repetitive pulses of substrate- or uncoupler-elicited energetic-redox transitions.	NAD	257-261	thioredoxin	Homo sapiens	176-179
23832361-2	2013	We investigated in this study the effect of phytol, a phytochemical known as a peroxisome proliferator-activated receptor alpha (PPARalpha) ligand, on NAD synthesis and ACMSD expression in rats.	NAD	151-154	peroxisome proliferator activated receptor alpha	Rattus norvegicus	79-127
23511477-4	2013	The unexpected observation of nicotinamide adenine dinucleotide located at the carbohydrate-binding site expands our knowledge of the sugar-binding specificity of galectin-8.	NAD	30-63	galectin 8	Homo sapiens	163-173
23460848-9	2013	In addition, lactate dehydrogenase A and malate dehydrogenase 1 partially associate with human liver peroxisomes and enzyme activity profiles support the idea that NAD(+) becomes regenerated during fatty acid beta-oxidation by alternative shuttling processes in human peroxisomes involving lactate dehydrogenase and/or malate dehydrogenase.	NAD	164-170	malate dehydrogenase 1	Homo sapiens	41-63
23201684-0	2012	The NAD-dependent deacetylase SIRT2 is required for programmed necrosis.	NAD	4-7	sirtuin 2	Mus musculus	30-35
23201684-4	2012	Here, we show that the NAD-dependent deacetylase SIRT2 binds constitutively to RIP3 and that deletion or knockdown of SIRT2 prevents formation of the RIP1-RIP3 complex in mice.	NAD	23-26	sirtuin 2	Mus musculus	49-54
23201684-4	2012	Here, we show that the NAD-dependent deacetylase SIRT2 binds constitutively to RIP3 and that deletion or knockdown of SIRT2 prevents formation of the RIP1-RIP3 complex in mice.	NAD	23-26	sirtuin 2	Mus musculus	118-123
23141294-8	2012	More importantly, DHTKD1 silencing was found to lead to impaired energy production, evidenced by decreased ATP, total NAD(+) and NADH, and NADH levels.	NAD	118-124	dehydrogenase E1 and transketolase domain containing 1	Homo sapiens	18-24
23141294-8	2012	More importantly, DHTKD1 silencing was found to lead to impaired energy production, evidenced by decreased ATP, total NAD(+) and NADH, and NADH levels.	NAD	129-133	dehydrogenase E1 and transketolase domain containing 1	Homo sapiens	18-24
23141294-8	2012	More importantly, DHTKD1 silencing was found to lead to impaired energy production, evidenced by decreased ATP, total NAD(+) and NADH, and NADH levels.	NAD	139-143	dehydrogenase E1 and transketolase domain containing 1	Homo sapiens	18-24
23096014-4	2012	We previously showed these mechanisms are also involved in Zn(2+) neurotoxicity and are attenuated by nicotinamide- or pyruvate-induced restoration of NAD(+) concentrations, Zn(2+) restriction, or inhibition of Sir2 proteins.	NAD	151-157	sirtuin 1	Mus musculus	211-215
23160044-6	2012	BCL6 triggered exclusion of the co-activator Mastermind-like 1 and recruitment of the NAD(+)-dependent deacetylase Sirt1, which was required for BCL6-dependent neurogenesis.	NAD	86-92	sirtuin 1	Mus musculus	115-120
23285706-10	2012	Kinetic parameters (Km, Vmax) of recombinant ALDH1A1 towards several aliphatic and aromatic aldehydes occurring in food products (vanillin, citral, furfural, cinnamaldehyde, anisaldehyde, benzaldehyde and trans-hexenal) were determined by measuring the increase of NADH fluorescence after adding various concentrations of aldehyde substrates.	NAD	265-269	aldehyde dehydrogenase 1 family member A1	Homo sapiens	45-52
22465856-0	2012	Insights into the mechanism of electron transfer and sodium translocation of the Na(+)-pumping NADH:quinone oxidoreductase.	NAD	95-99	crystallin zeta	Homo sapiens	100-122
22750529-5	2012	In hippocampal slices of a Rett mouse model (Mecp2(-/y)) we detected an increased FAD/NADH baseline-ratio indicating intensified oxidization.	NAD	86-90	methyl CpG binding protein 2	Mus musculus	45-50
22648686-2	2012	ALD6 encoding an aldehyde dehydrogenases of the indigenous yeast was replaced by a GPD1 and CUP1 gene cassette, which are responsible for NAD-dependent glycerol-3-phosphatase dehydrogenase and copper resistance, respectively.	NAD	138-141	metallothionein CUP1	Saccharomyces cerevisiae S288C	92-96
22743824-1	2012	Sirtuin 6 (Sirt6), a mammalian Sir2 (silent information regulator-2) ortholog, is an NAD (+) -dependent histone deacetylase that modulates chromatin structure and genomic stability.	NAD	85-92	sirtuin 2	Homo sapiens	31-35
22743824-1	2012	Sirtuin 6 (Sirt6), a mammalian Sir2 (silent information regulator-2) ortholog, is an NAD (+) -dependent histone deacetylase that modulates chromatin structure and genomic stability.	NAD	85-92	sirtuin 2	Homo sapiens	37-67
22819213-3	2012	The biosynthesis, transport, and catabolism of NAD and its key intermediates play an important role in the regulation of NAD-consuming mediators, such as sirtuins, poly-ADP-ribose polymerases, and CD38/157 ectoenzymes, in intra- and extracellular compartments.	NAD	47-50	CD38 molecule	Homo sapiens	197-201
22819213-3	2012	The biosynthesis, transport, and catabolism of NAD and its key intermediates play an important role in the regulation of NAD-consuming mediators, such as sirtuins, poly-ADP-ribose polymerases, and CD38/157 ectoenzymes, in intra- and extracellular compartments.	NAD	121-124	CD38 molecule	Homo sapiens	197-201
22932127-5	2012	SIRT2, an NAD-dependent class III histone deacetylase, contributes to H4-K16Ac deacetylation and DNA compaction in human fibroblast cell lines that assemble striking senescence-associated heterochromatin foci (SAHFs).	NAD	10-13	sirtuin 2	Homo sapiens	0-5
22904041-6	2012	In the first part of this review, we describe the role of NADH and NADPH as electron donors for NADPH oxidases (Noxs), glutathione (GSH), and thioredoxin (Trx) systems in cellular redox regulation.	NAD	58-62	thioredoxin	Homo sapiens	142-153
22904041-6	2012	In the first part of this review, we describe the role of NADH and NADPH as electron donors for NADPH oxidases (Noxs), glutathione (GSH), and thioredoxin (Trx) systems in cellular redox regulation.	NAD	58-62	thioredoxin	Homo sapiens	155-158
22863012-3	2012	Here we report that gain of function of the NAD-dependent deacetylase SirT1 or loss of function of its endogenous inhibitor Deleted in breast cancer-1 (Dbc1) promote "browning" of WAT by deacetylating peroxisome proliferator-activated receptor (Ppar)-gamma on Lys268 and Lys293.	NAD	44-47	cell cycle and apoptosis regulator 2	Homo sapiens	152-156
22564706-2	2012	In fungi, the primary role of IDO is to supply nicotinamide adenine dinucleotide (NAD(+)) via the kynurenine pathway.	NAD	47-80	indoleamine 2,3-dioxygenase 1	Homo sapiens	30-33
22564706-2	2012	In fungi, the primary role of IDO is to supply nicotinamide adenine dinucleotide (NAD(+)) via the kynurenine pathway.	NAD	82-88	indoleamine 2,3-dioxygenase 1	Homo sapiens	30-33
22700961-2	2012	We reported previously that switching from the early to the late acute inflammatory response following TLR4 stimulation depends on NAD(+) activation of deacetylase sirtuin 1 (SirT1).	NAD	131-137	toll like receptor 4	Homo sapiens	103-107
22669083-2	2012	Following the injection of NADH at different concentrations, we obtained different electrical signals from a semiconductor characterization system mimicking biological catalysis of NADH dehydrogenase (CoI).	NAD	27-31	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	201-204
22669083-5	2012	In the presence of NADH, electrons transferred to phenazine derivant through SWCNT, by analogous means of the electron transport chain formed by a series of iron-sulfur (FeS) clusters in CoI.	NAD	19-23	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	187-190
22270613-9	2012	The measurement of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, superoxide dismutase (SOD), malondialdehyde (MDA), and caspase-3 activity levels showed that LIF attenuated the high glucose-induced decreased level of SOD and elevated level of NADPH oxidase, MDA and caspase-3 activity.	NAD	19-52	LIF interleukin 6 family cytokine	Homo sapiens	173-176
22547068-2	2012	NAD(+)-derived Ca(2+)-mobilizing second messengers, produced by CD38, play a pivotal role in T cell activation.	NAD	0-6	CD38 molecule	Homo sapiens	64-68
22456698-6	2012	RESULTS: ALA increased the NAD(+)/NADH ratio to enhance SIRT1 activity and production in C(2)C(12) myotubes.	NAD	27-33	sirtuin 1	Mus musculus	56-61
22456698-6	2012	RESULTS: ALA increased the NAD(+)/NADH ratio to enhance SIRT1 activity and production in C(2)C(12) myotubes.	NAD	34-38	sirtuin 1	Mus musculus	56-61
21975728-7	2012	Moreover, APO866 strongly decreased the production of reactive oxygen species (ROS), increased surface expression of the NAD-consuming enzyme CD38, and modified the production of selective eicosanoids.	NAD	121-124	CD38 molecule	Homo sapiens	142-146
22654783-1	2012	Resveratrol is a naturally occurring polyphenol that activates SIRT1, an NAD-dependent deacetylase.	NAD	73-76	sirtuin 1	Mus musculus	63-68
22383490-2	2012	The purinergic receptor P2X7 is upstream of the nod-like receptor family, pryin domain containing-3 (NLRP3) inflammasome in immune cells and is activated by ATP and NAD that serve as damage-associated molecular patterns.	NAD	165-168	NLR family, pyrin domain containing 3	Mus musculus	101-106
22352983-3	2012	Several studies have indicated that TBI-induced neuronal death arises in part due to excessive activation of poly(ADP-ribose) polymerase-1 (PARP-1), which results in nicotinamide adenine dinucleotide (NAD+) depletion and subsequent energy failure.	NAD	166-199	poly (ADP-ribose) polymerase 1	Rattus norvegicus	109-138
22352983-3	2012	Several studies have indicated that TBI-induced neuronal death arises in part due to excessive activation of poly(ADP-ribose) polymerase-1 (PARP-1), which results in nicotinamide adenine dinucleotide (NAD+) depletion and subsequent energy failure.	NAD	166-199	poly (ADP-ribose) polymerase 1	Rattus norvegicus	140-146
22352983-3	2012	Several studies have indicated that TBI-induced neuronal death arises in part due to excessive activation of poly(ADP-ribose) polymerase-1 (PARP-1), which results in nicotinamide adenine dinucleotide (NAD+) depletion and subsequent energy failure.	NAD	201-205	poly (ADP-ribose) polymerase 1	Rattus norvegicus	109-138
22352983-3	2012	Several studies have indicated that TBI-induced neuronal death arises in part due to excessive activation of poly(ADP-ribose) polymerase-1 (PARP-1), which results in nicotinamide adenine dinucleotide (NAD+) depletion and subsequent energy failure.	NAD	201-205	poly (ADP-ribose) polymerase 1	Rattus norvegicus	140-146
22352983-6	2012	The intranasal administration of NAD+ (20 mg/kg) immediately after TBI protected neurons in CA1, CA3, and dentate gyrus of the hippocampus, but not in the cortex.	NAD	33-37	carbonic anhydrase 1	Rattus norvegicus	92-95
22416140-5	2012	Previously, we demonstrated that the NAD(+)-dependent deacetylase SIRT3 was essential for the prevention of age-related hearing loss in mice fed a calorically restricted diet.	NAD	37-43	sirtuin 3	Mus musculus	66-71
21706162-5	2012	The decrease in NAMPT mRNA levels was accompanied by an increase in NADH levels, thereby decreasing the NAD(+)/H ratio.	NAD	68-72	nicotinamide phosphoribosyltransferase 1	Danio rerio	16-21
21706162-5	2012	The decrease in NAMPT mRNA levels was accompanied by an increase in NADH levels, thereby decreasing the NAD(+)/H ratio.	NAD	104-110	nicotinamide phosphoribosyltransferase 1	Danio rerio	16-21
22236458-1	2012	CD38 (EC 3.2.2.6, NAD(+)-glycohydrolase) is a multifunctional enzyme catalyzing the synthesis and hydrolysis of cyclic ADP-ribose from NAD(+) to ADP-ribose.	NAD	18-24	CD38 molecule	Homo sapiens	0-4
22306819-0	2012	NAD-dependent histone deacetylase, SIRT1, plays essential roles in the maintenance of hematopoietic stem cells.	NAD	0-3	sirtuin 1	Mus musculus	35-40
22010850-4	2012	In the present study, we show that the malate-aspartate NADH shuttle is impaired in Saccharomyces cerevisiae frataxin-deficient cells (Deltayfh1) due to decreased activity of cytosolic and mitochondrial isoforms of malate dehydrogenase and to complete inactivation of the mitochondrial aspartate aminotransferase (Aat1).	NAD	56-60	aspartate transaminase AAT1	Saccharomyces cerevisiae S288C	314-318
22204321-5	2012	For examples, the key NAD(+)-dependent enzymes SIRT1 and SIRT2 have been indicated to strongly affect the pathological changes of PD and AD; PARP-1 inhibition can profoundly reduce the brain injury in the animal models of multiple neurological diseases; and administration of either NAD(+) or nicotinamide can also decrease ischemic brain damage.	NAD	283-289	sirtuin 2	Homo sapiens	57-62
22186418-7	2012	Both areas showed elevated c-fos mRNA expression with S-DPN treatment in the WT but not betaERKO females.	NAD	56-59	FBJ osteosarcoma oncogene	Mus musculus	27-32
22190494-4	2012	Activation of a conditional c-MYC allele induced increased levels of SIRT1 protein, NAD(+), and nicotinamide-phosphoribosyltransferase (NAMPT) mRNA in several cell types.	NAD	84-90	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	28-33
21909679-3	2012	In this study, S. cerevisiae was engineered to investigate the effects of the sole and double disruption of NADH-dependent glycerol-3-phosphate dehydrogenase 1 (GPD1) and NADPH-requiring glutamate dehydrogenase 1 (GDH1) on the production of glycerol and ethanol from glucose.	NAD	108-112	glutamate dehydrogenase (NADP(+)) GDH1	Saccharomyces cerevisiae S288C	214-218
22052482-9	2012	Mammalian GDH exhibits negative cooperativity with respect to binding of NAD and NADPH coenzyme molecules, activation by ADP, and inhibition by GTP.	NAD	73-76	glutamate dehydrogenase 1	Homo sapiens	10-13
22848454-3	2012	Gating of murine P2X7 can be induced by the soluble ligand ATP, as well as by NAD(+)-dependent ADP-ribosylation of arginine 125, a posttranslational protein modification catalyzed by the toxin-related ecto-enzymes ART2.1 and ART2.2.	NAD	78-84	ADP-ribosyltransferase 2b	Mus musculus	225-231
22153507-6	2011	This study also provides insight into how the GAPDH-CP12 complex is dissociated by a high NADP(H)/NAD(H) ratio.	NAD	98-104	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	52-56
21901281-4	2011	One of its potential targets is the NAD(+)-dependent deacetylase sirtuin 1.	NAD	36-42	sirtuin 1	Mus musculus	65-74
21127968-7	2011	Treatment of cells with 100 nM fulvestrant (estrogen receptor antagonist) prior to addition of PPT, DPN, or estrogen significantly decreased their ability to prevent cell death, indicating involvement of estrogen receptor (ER) in providing PPT, DPN, or estrogen mediated cytoprotection.	NAD	245-248	estrogen receptor 1	Rattus norvegicus	44-61
21127968-7	2011	Treatment of cells with 100 nM fulvestrant (estrogen receptor antagonist) prior to addition of PPT, DPN, or estrogen significantly decreased their ability to prevent cell death, indicating involvement of estrogen receptor (ER) in providing PPT, DPN, or estrogen mediated cytoprotection.	NAD	245-248	estrogen receptor 1	Rattus norvegicus	204-221
21127968-7	2011	Treatment of cells with 100 nM fulvestrant (estrogen receptor antagonist) prior to addition of PPT, DPN, or estrogen significantly decreased their ability to prevent cell death, indicating involvement of estrogen receptor (ER) in providing PPT, DPN, or estrogen mediated cytoprotection.	NAD	245-248	estrogen receptor 1	Rattus norvegicus	223-225
21596782-5	2011	DBC1 was recently shown to function as a negative regulator of the NAD-dependent protein deacetylase SIRT1.	NAD	67-70	cell cycle and apoptosis regulator 2	Homo sapiens	0-4
21730068-1	2011	NAD kinase catalyzes the phosphorylation of NAD(+) to synthesize NADP(+), whereas NADH kinase catalyzes conversion of NADH to NADPH.	NAD	44-50	NAD kinase	Homo sapiens	0-10
21730068-1	2011	NAD kinase catalyzes the phosphorylation of NAD(+) to synthesize NADP(+), whereas NADH kinase catalyzes conversion of NADH to NADPH.	NAD	82-86	NAD kinase	Homo sapiens	0-10
21730068-4	2011	Detailed analysis, including a comparison of the tertiary structure of Pos5 with the structures of human and bacterial NAD kinases, revealed that Arg-293 of Pos5, corresponding to His-351 of human NAD kinase, confers a positive charge on the surface of NADH-binding site, whereas the corresponding His residue does not.	NAD	253-257	NAD kinase	Homo sapiens	119-129
21593185-3	2011	The nicotinamide adenine dinucleotide-dependent protein deacetylase SIRT1 decreases apoptosis through deacetylating of p53, and resveratrol is known as an activator of SIRT1.	NAD	4-37	sirtuin 1	Mus musculus	68-73
21593185-3	2011	The nicotinamide adenine dinucleotide-dependent protein deacetylase SIRT1 decreases apoptosis through deacetylating of p53, and resveratrol is known as an activator of SIRT1.	NAD	4-37	transformation related protein 53, pseudogene	Mus musculus	119-122
21502369-3	2011	beta-Lapachone (betaL), a well-known substrate of NAD(P)H:quinone oxidoreductase (NQO1), increases the cellular NAD(+)/NADH ratio via the activation of NQO1.	NAD	112-118	crystallin zeta	Homo sapiens	58-80
21421831-1	2011	Sirtuins, the mammalian homologs of the silent information regulator 2 gene of Saccharomyces cerevisiae, are members of the NAD(+)-dependent family of histone deacetylases.	NAD	124-130	sirtuin 2	Homo sapiens	40-70
20862513-3	2011	To improve cofactor regeneration, in the present study we overexpressed an NAD(+)-dependent aldehyde dehydrogenase in the recombinant strain.	NAD	75-81	Aldehyde dehydrogenase	Escherichia coli	92-114
20862513-4	2011	To this end, an aldehyde dehydrogenase AldHk homologous to E. coli AldH but with NAD(+)-dependent propionaldehyde dehydrogenase activity was identified in K. pneumoniae.	NAD	81-87	Aldehyde dehydrogenase	Escherichia coli	16-38
21524995-4	2011	In this study, we engineered a novel soluble form of CD38 that can be efficiently expressed in the cytosol and use cytosolic NAD as a substrate to produce cADPR intracellularly.	NAD	125-128	CD38 molecule	Homo sapiens	53-57
21478149-5	2011	Recent studies on the NAD synthesis enzyme nicotinamide mononucleotide adenylyltransferase (NMNAT) have uncovered a novel neuronal maintenance and protective function against activity-, injury-, or misfolded protein-induced degeneration in Drosophila and in mammalian neurons.	NAD	22-25	Nicotinamide mononucleotide adenylyltransferase	Drosophila melanogaster	92-97
21334188-6	2011	Further modification with the enzyme, GLUD leads to effective amperometric biosensing of alpha-KG through monitoring of the NADH consumption.	NAD	124-128	glutamate dehydrogenase 1	Homo sapiens	38-42
21366264-8	2011	This mutation led to a loss of activity for NADPH and NADH, indicating the crucial role of this residue in maintaining the algal GAPDH structure.	NAD	54-58	uncharacterized protein	Chlamydomonas reinhardtii	129-134
21459329-1	2011	SIRT1 is a NAD(+)-dependent enzyme that affects metabolism by deacetylating key transcriptional regulators of energy expenditure.	NAD	11-17	sirtuin 1	Mus musculus	0-5
21459330-2	2011	The fact that NAD(+) levels control SIRT1 activity confers a hypothetical basis for the design of new strategies to activate SIRT1 by increasing NAD(+) availability.	NAD	14-20	sirtuin 1	Mus musculus	36-41
21459330-2	2011	The fact that NAD(+) levels control SIRT1 activity confers a hypothetical basis for the design of new strategies to activate SIRT1 by increasing NAD(+) availability.	NAD	14-20	sirtuin 1	Mus musculus	125-130
21459330-2	2011	The fact that NAD(+) levels control SIRT1 activity confers a hypothetical basis for the design of new strategies to activate SIRT1 by increasing NAD(+) availability.	NAD	145-151	sirtuin 1	Mus musculus	36-41
21459330-2	2011	The fact that NAD(+) levels control SIRT1 activity confers a hypothetical basis for the design of new strategies to activate SIRT1 by increasing NAD(+) availability.	NAD	145-151	sirtuin 1	Mus musculus	125-130
21284999-2	2011	A recent cancer genome-sequencing project revealed that more than 70% of low-grade gliomas bear mutations in one of two NAD(+)-dependent isocitrate dehydrogenase enzymes, namely, IDH1 and IDH2.	NAD	120-126	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	179-183
21411645-3	2011	SIRT1 is an nicotinamide adenine dinucleotide responsive deacetylase serving diverse adaptive responses to metabolic challenges, yet this metabolic rheostat may be downregulated under conditions of significant oxidative stress.	NAD	12-45	sirtuin 1	Mus musculus	0-5
21282379-5	2011	However, gp91(phox) and p22(phox) reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase subunits are dispensable for inflammatory cytokine production, indicating that NADPH oxidases are not the source of proinflammatory ROS.	NAD	42-75	calcineurin like EF-hand protein 1	Homo sapiens	24-27
21735612-0	2010	Potent and selective inhibitors of NAD(+)-dependent 15-hydroxyprostaglandin dehydrogenase (HPGD) 15-hydroxyprostaglandin dehydrogenase (15-PGDH; HPGD) is the key enzyme for the inactivation of prostaglandins, and thus regulates processes such as inflammation or proliferation.	NAD	35-41	15-hydroxyprostaglandin dehydrogenase	Homo sapiens	91-95
21735612-0	2010	Potent and selective inhibitors of NAD(+)-dependent 15-hydroxyprostaglandin dehydrogenase (HPGD) 15-hydroxyprostaglandin dehydrogenase (15-PGDH; HPGD) is the key enzyme for the inactivation of prostaglandins, and thus regulates processes such as inflammation or proliferation.	NAD	35-41	15-hydroxyprostaglandin dehydrogenase	Homo sapiens	145-149
21390132-10	2011	Remarkably, the viability requirement for Lig3 can be circumvented by targeting Lig1 to the mitochondria or expressing Chlorella virus DNA ligase, the minimal eukaryal nick-sealing enzyme, or Escherichia coli LigA, an NAD(+)-dependent ligase.	NAD	218-224	DNA ligase 3	Homo sapiens	42-46
21165558-0	2011	Genomic organization and localization of the NAD-dependent histone deacetylase gene sirtuin 3 (Sirt3) in the mouse.	NAD	45-48	sirtuin 3	Mus musculus	84-93
21165558-0	2011	Genomic organization and localization of the NAD-dependent histone deacetylase gene sirtuin 3 (Sirt3) in the mouse.	NAD	45-48	sirtuin 3	Mus musculus	95-100
21165558-1	2011	Sirtuin 3 (SIRT3) is a nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase, which belongs to the Silent information regulator 2 (Sir2) family of histone deacetylases (sirtuin HDACs).	NAD	23-56	sirtuin 3	Mus musculus	0-9
21165558-1	2011	Sirtuin 3 (SIRT3) is a nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase, which belongs to the Silent information regulator 2 (Sir2) family of histone deacetylases (sirtuin HDACs).	NAD	23-56	sirtuin 3	Mus musculus	11-16
21165558-1	2011	Sirtuin 3 (SIRT3) is a nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase, which belongs to the Silent information regulator 2 (Sir2) family of histone deacetylases (sirtuin HDACs).	NAD	23-56	sirtuin 1	Mus musculus	108-138
21165558-1	2011	Sirtuin 3 (SIRT3) is a nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase, which belongs to the Silent information regulator 2 (Sir2) family of histone deacetylases (sirtuin HDACs).	NAD	23-56	sirtuin 1	Mus musculus	140-144
21212137-7	2011	In theca-interstitial cells the expression of hydroxyprostaglandin dehydrogenase 15-(nicotinamide adenine dinucleotide) (Hpgd) was also inhibited by NFIL3 overexpression.	NAD	85-118	15-hydroxyprostaglandin dehydrogenase	Homo sapiens	121-125
21134381-2	2011	When NAD is used as substrate, CD38 predominantly hydrolyzes it to ADP-ribose, with a trace amount of cyclic ADP-ribose produced through cyclization of the substrate.	NAD	5-8	CD38 molecule	Homo sapiens	31-35
20844277-1	2011	Human sirtuin (SIRT) 1 and SIRT2, which possess nicotinamide adenosine dinucleotide (NAD(+))-dependent deacetylase activity, exhibit anti-inflammatory actions.	NAD	85-91	sirtuin 2	Homo sapiens	27-32
21059157-1	2011	We previously reported that sirtuin 2 (SIRT2), a mammalian member of the NAD+-dependent protein deacetylases, participates in mitotic regulation, specifically, in efficient mitotic cell death caused by the spindle checkpoint.	NAD	73-76	sirtuin 2	Homo sapiens	28-37
21059157-1	2011	We previously reported that sirtuin 2 (SIRT2), a mammalian member of the NAD+-dependent protein deacetylases, participates in mitotic regulation, specifically, in efficient mitotic cell death caused by the spindle checkpoint.	NAD	73-76	sirtuin 2	Homo sapiens	39-44
21030595-4	2010	DBC1 has been previously identified as a regulator of some nuclear receptors, the methyltransferase SUV39H1, and the NAD-dependent deacetylase SIRT1.	NAD	117-120	sirtuin 1	Mus musculus	143-148
21106760-0	2010	Nicotinamide adenine dinucleotide (NAD)-regulated DNA methylation alters CCCTC-binding factor (CTCF)/cohesin binding and transcription at the BDNF locus.	NAD	0-33	brain derived neurotrophic factor	Mus musculus	142-146
21106760-0	2010	Nicotinamide adenine dinucleotide (NAD)-regulated DNA methylation alters CCCTC-binding factor (CTCF)/cohesin binding and transcription at the BDNF locus.	NAD	35-38	brain derived neurotrophic factor	Mus musculus	142-146
21106760-3	2010	Here, we found that lowering NAD levels in mouse primary cortical neurons led to decreased activity-dependent BDNF expression.	NAD	29-32	brain derived neurotrophic factor	Mus musculus	110-114
21106760-4	2010	The altered BDNF transcription occurred independently of Sirt or Parp activities; instead, low NAD levels promoted increased DNA methylation of the activity-dependent BDNF promoter.	NAD	95-98	brain derived neurotrophic factor	Mus musculus	167-171
21106760-7	2010	Because BDNF is critical for neuronal function, these results suggest that age- or nutrition-associated declines in NAD levels as well as deficits in cohesin function associated with disease modulate BDNF expression and could contribute to cognitive impairment.	NAD	116-119	brain derived neurotrophic factor	Mus musculus	200-204
20975043-0	2010	Extracellular NAD+ shapes the Foxp3+ regulatory T cell compartment through the ART2-P2X7 pathway.	NAD	14-18	forkhead box P3	Mus musculus	30-35
20975043-2	2010	Nicotinamide adenine dinucleotide (NAD(+)) released during cell damage or inflammation results in ART2.2-mediated ADP-ribosylation of the cytolytic P2X7 receptor on T cells.	NAD	0-33	ADP-ribosyltransferase 2b	Mus musculus	98-104
20975043-2	2010	Nicotinamide adenine dinucleotide (NAD(+)) released during cell damage or inflammation results in ART2.2-mediated ADP-ribosylation of the cytolytic P2X7 receptor on T cells.	NAD	35-42	ADP-ribosyltransferase 2b	Mus musculus	98-104
20975043-3	2010	We show that T reg cells express the ART2.2 enzyme and high levels of P2X7 and that T reg cells can be depleted by intravenous injection of NAD(+).	NAD	140-146	ADP-ribosyltransferase 2b	Mus musculus	37-43
20975043-6	2010	We demonstrate that T reg cells can be protected from the deleterious effects of NAD(+) by an inhibitory ART2.2-specific single domain antibody.	NAD	81-87	ADP-ribosyltransferase 2b	Mus musculus	105-111
21103071-1	2010	SIRT1, a homolog of yeast Sir2, is a type III NAD(+) dependent histone and protein deacetylase.	NAD	46-52	sirtuin 1	Mus musculus	0-5
20857515-8	2010	Here we demonstrated that overexpression of Nmnat2 in M-cells significantly delayed axon degeneration in vivo, and disruption of the NAD synthesis activity of Nmnat2 markedly attenuated its axon-protective function.	NAD	133-136	nicotinamide nucleotide adenylyltransferase 2	Danio rerio	159-165
20677216-2	2010	SIRT3 possesses NAD(+)-dependent protein deacetylase activity.	NAD	16-22	sirtuin 3	Mus musculus	0-5
20699658-2	2010	Recently, 15-hydroxyprostaglandin dehydrogenase [NAD+] (15-PGDH), the key enzyme in prostaglandin degradation, was found to be down-regulated in human gastric cancer tissues, but little is known about its role in gastric tumorigenesis.	NAD	49-53	15-hydroxyprostaglandin dehydrogenase	Homo sapiens	59-63
20687591-3	2010	On the basis of the available X-ray structures of S-adenosylhomocysteine hydrolases (SAHHs), free energy simulations employing the MM-GBSA approach were applied to predict residues important to the differential cofactor binding properties of human and trypanosomal SAHHs (Hs-SAHH and Tc-SAHH), within 5 A of the cofactor NAD(+)/NADH binding site.	NAD	321-327	adenosylhomocysteinase	Homo sapiens	85-89
20687591-3	2010	On the basis of the available X-ray structures of S-adenosylhomocysteine hydrolases (SAHHs), free energy simulations employing the MM-GBSA approach were applied to predict residues important to the differential cofactor binding properties of human and trypanosomal SAHHs (Hs-SAHH and Tc-SAHH), within 5 A of the cofactor NAD(+)/NADH binding site.	NAD	328-332	adenosylhomocysteinase	Homo sapiens	85-89
20518072-6	2010	We show in HeLa cells that NADH levels modulate the activities of two pivotal enzymes of sphingolipid metabolism: sphingosine kinase 1 (SK1) and neutral sphingomyelinase (nSMase).	NAD	27-31	sphingosine kinase 1	Homo sapiens	114-134
20518072-6	2010	We show in HeLa cells that NADH levels modulate the activities of two pivotal enzymes of sphingolipid metabolism: sphingosine kinase 1 (SK1) and neutral sphingomyelinase (nSMase).	NAD	27-31	sphingosine kinase 1	Homo sapiens	136-139
20518072-9	2010	Using plasma membranes isolated from cervical adenocarcinoma (HeLa) cells as well as purified proteins of both bacterial and human origin, we demonstrate that NADH inhibits SK1 and stimulates nSMase, while NAD(+) inhibits nSMase and has no effect on SK1.	NAD	159-163	sphingosine kinase 1	Homo sapiens	173-176
20518072-9	2010	Using plasma membranes isolated from cervical adenocarcinoma (HeLa) cells as well as purified proteins of both bacterial and human origin, we demonstrate that NADH inhibits SK1 and stimulates nSMase, while NAD(+) inhibits nSMase and has no effect on SK1.	NAD	159-163	sphingosine kinase 1	Homo sapiens	250-253
20074616-1	2010	Sirt1 is a NAD-dependent deacetylase that has been shown as a link between energy metabolism and aging.	NAD	11-14	sirtuin 1	Mus musculus	0-5
20668706-1	2010	BACKGROUND: SIRT1, a NAD-dependent deacetylase, has diverse roles in a variety of organs such as regulation of endocrine function and metabolism.	NAD	21-24	sirtuin 1	Mus musculus	12-17
20616029-6	2010	FGF21 treatment increased cellular NAD(+) levels, leading to activation of SIRT1 and deacetylation of its downstream targets, peroxisome proliferator-activated receptor-gamma coactivator-1alpha (PGC-1alpha) and histone 3.	NAD	35-41	sirtuin 1	Mus musculus	75-80
20237298-5	2010	Here we show that 2-hydroxy naphthyl derivatives, a previously identified subclass of NAD(+) analog inhibitors of sirtuin 2 (SIRT2), are direct gamma-secretase inhibitors.	NAD	86-92	sirtuin 2	Homo sapiens	114-123
20237298-5	2010	Here we show that 2-hydroxy naphthyl derivatives, a previously identified subclass of NAD(+) analog inhibitors of sirtuin 2 (SIRT2), are direct gamma-secretase inhibitors.	NAD	86-92	sirtuin 2	Homo sapiens	125-130
20595232-5	2010	We demonstrate here a conserved role for orthologs of the NAD(+)-dependent deacetylase SIRT1 in metazoans in down-regulation of SREBP orthologs during fasting, resulting in inhibition of lipid synthesis and fat storage.	NAD	58-64	sirtuin 1	Mus musculus	87-92
20470215-1	2010	CD38 is an ecto-enzyme that hydrolyzes NAD.	NAD	39-42	CD38 molecule	Homo sapiens	0-4
20093189-7	2010	Furthermore, the oxidoreductase activity in the reverse reaction indicated that the soluble recombinant BmDLDH produced at lower growth temperature was able to catalyze the lipoamide-dependent oxidation of NADH.	NAD	206-210	dihydrolipoamide dehydrogenase	Bombyx mori	104-110
20381466-8	2010	Four days later, animals were administered the ERbeta agonist S-DPN or vehicle (with four daily sc injections).	NAD	62-67	estrogen receptor 2	Rattus norvegicus	47-53
20640790-5	2010	The large majority of the substrate NAD is hydrolyzed to ADPR while the conversion of NAD to cADPR is not the dominant reaction catalyzed by wild-type human CD38.	NAD	36-39	CD38 molecule	Homo sapiens	157-161
20640790-5	2010	The large majority of the substrate NAD is hydrolyzed to ADPR while the conversion of NAD to cADPR is not the dominant reaction catalyzed by wild-type human CD38.	NAD	86-89	CD38 molecule	Homo sapiens	157-161
20148352-2	2010	CR induces an increase in the NAD(+)/NADH ratio in cells and results in activation of SIRT1, an NAD(+)-dependent protein deacetylase that is thought to be a metabolic master switch linked to the modulation of lifespans.	NAD	30-36	sirtuin 1	Mus musculus	86-91
20148352-2	2010	CR induces an increase in the NAD(+)/NADH ratio in cells and results in activation of SIRT1, an NAD(+)-dependent protein deacetylase that is thought to be a metabolic master switch linked to the modulation of lifespans.	NAD	37-41	sirtuin 1	Mus musculus	86-91
20148352-10	2010	A 24-h fasting in mice increased mRNA and protein expression of both SIRT1 and PPARalpha in the livers, where the NAD(+) levels increased with increasing nicotinamide phosphoribosyltransferase (NAMPT) activity in the NAD(+) salvage pathway.	NAD	114-120	sirtuin 1	Mus musculus	69-74
20148352-10	2010	A 24-h fasting in mice increased mRNA and protein expression of both SIRT1 and PPARalpha in the livers, where the NAD(+) levels increased with increasing nicotinamide phosphoribosyltransferase (NAMPT) activity in the NAD(+) salvage pathway.	NAD	217-223	sirtuin 1	Mus musculus	69-74
20148352-11	2010	Treatment of Hepa1-6 cells in a low glucose medium conditions with NAD(+) or NADH showed that the mRNA expression of both SIRT1 and PPARalpha can be enhanced by addition of NAD(+), and decreased by increasing NADH levels.	NAD	67-73	sirtuin 1	Mus musculus	122-127
20148352-11	2010	Treatment of Hepa1-6 cells in a low glucose medium conditions with NAD(+) or NADH showed that the mRNA expression of both SIRT1 and PPARalpha can be enhanced by addition of NAD(+), and decreased by increasing NADH levels.	NAD	77-81	sirtuin 1	Mus musculus	122-127
20148352-11	2010	Treatment of Hepa1-6 cells in a low glucose medium conditions with NAD(+) or NADH showed that the mRNA expression of both SIRT1 and PPARalpha can be enhanced by addition of NAD(+), and decreased by increasing NADH levels.	NAD	173-179	sirtuin 1	Mus musculus	122-127
20148352-11	2010	Treatment of Hepa1-6 cells in a low glucose medium conditions with NAD(+) or NADH showed that the mRNA expression of both SIRT1 and PPARalpha can be enhanced by addition of NAD(+), and decreased by increasing NADH levels.	NAD	209-213	sirtuin 1	Mus musculus	122-127
20463219-5	2010	We show that the flexible hinge 2 linker region of RIBEYE(B) domain that connects the nicotinamide adenine dinucleotide (NADH)-binding subdomain with the substrate-binding subdomain (SBD) binds to the C terminus of GCAP2.	NAD	86-119	guanylate cyclase activator 1B	Homo sapiens	215-220
20463219-5	2010	We show that the flexible hinge 2 linker region of RIBEYE(B) domain that connects the nicotinamide adenine dinucleotide (NADH)-binding subdomain with the substrate-binding subdomain (SBD) binds to the C terminus of GCAP2.	NAD	121-125	guanylate cyclase activator 1B	Homo sapiens	215-220
20463219-6	2010	We demonstrate that the RIBEYE-GCAP2 interaction is induced by the binding of NADH to RIBEYE.	NAD	78-82	guanylate cyclase activator 1B	Homo sapiens	31-36
20219674-3	2010	Using NAD(+), 11beta-HSD2 from testicular microsomes oxidized 11-OHT with apparent K(m) 56+/-4nM and V(max) 55+/-6pmol/h/mgprotein values.	NAD	6-12	hydroxysteroid 11-beta dehydrogenase 2	Homo sapiens	14-25
20490902-8	2010	NADH was used as a coenzyme by rat kidney GR but with a lower efficiency (32.7%) than NADPH.	NAD	0-4	glutathione-disulfide reductase	Rattus norvegicus	42-44
20097881-1	2010	Mutations of nicotinamide adenine dinucleotide phosphate-dependent isocitrate dehydrogenase gene (IDH1) have been identified in patients with gliomas.	NAD	13-46	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	98-102
19908284-1	2010	The mitochondrial aspartate-glutamate carriers (AGC) aralar (SLC25A12) and citrin (SLC25A13) are components of the malate aspartate shuttle (MAS), a major intracellular pathway to transfer reducing equivalents from NADH to the mitochondrial matrix.	NAD	215-219	solute carrier family 25 (mitochondrial carrier, adenine nucleotide translocator), member 13	Mus musculus	75-81
19908284-1	2010	The mitochondrial aspartate-glutamate carriers (AGC) aralar (SLC25A12) and citrin (SLC25A13) are components of the malate aspartate shuttle (MAS), a major intracellular pathway to transfer reducing equivalents from NADH to the mitochondrial matrix.	NAD	215-219	solute carrier family 25 (mitochondrial carrier, adenine nucleotide translocator), member 13	Mus musculus	83-91
19592035-6	2010	Doses of 1mg/kg of either PPT (ER-alpha agonist) or DPN (ER-beta agonist) were administered to 12 OVX rats for 6 d postoperatively, whereas all other animals received vehicle.	NAD	52-55	estrogen receptor 2	Rattus norvegicus	57-64
20122899-1	2010	Poly(ADP-ribose) polymerase-1 (PARP-1), a nuclear enzyme that catalyzes the NAD(+)-dependent addition of ADP-ribose polymers on a variety of nuclear proteins, has been shown to be associated with the nuclear matrix.	NAD	76-82	poly (ADP-ribose) polymerase 1	Rattus norvegicus	0-29
20122899-1	2010	Poly(ADP-ribose) polymerase-1 (PARP-1), a nuclear enzyme that catalyzes the NAD(+)-dependent addition of ADP-ribose polymers on a variety of nuclear proteins, has been shown to be associated with the nuclear matrix.	NAD	76-82	poly (ADP-ribose) polymerase 1	Rattus norvegicus	31-37
19940131-4	2010	NAD treatment blocked the activation of pro-hypertrophic Akt1 signaling, and augmented the activity of anti-hypertrophic LKB1-AMPK signaling in the heart, which prevented subsequent induction of mTOR-mediated protein synthesis.	NAD	0-3	mechanistic target of rapamycin kinase	Mus musculus	195-199
19940131-5	2010	By using gene knock-out and transgenic mouse models of SIRT3 and SIRT1, we showed that the anti-hypertrophic effects of exogenous NAD are mediated through activation of SIRT3, but not SIRT1.	NAD	130-133	sirtuin 3	Mus musculus	55-60
19940131-5	2010	By using gene knock-out and transgenic mouse models of SIRT3 and SIRT1, we showed that the anti-hypertrophic effects of exogenous NAD are mediated through activation of SIRT3, but not SIRT1.	NAD	130-133	sirtuin 1	Mus musculus	65-70
19940131-5	2010	By using gene knock-out and transgenic mouse models of SIRT3 and SIRT1, we showed that the anti-hypertrophic effects of exogenous NAD are mediated through activation of SIRT3, but not SIRT1.	NAD	130-133	sirtuin 3	Mus musculus	169-174
19727706-8	2010	Glycerol is produced to dispose excess cytosolic reduced nicotinamide adenine dinucleotide (NADH), and the regulating step in the pathway is mediated by glycerol 3-phosphate dehydrogenase (encoded by GPD1 and GPD2 genes).	NAD	57-90	glycerol-3-phosphate dehydrogenase (NAD(+)) GPD2	Saccharomyces cerevisiae S288C	209-213
19727706-8	2010	Glycerol is produced to dispose excess cytosolic reduced nicotinamide adenine dinucleotide (NADH), and the regulating step in the pathway is mediated by glycerol 3-phosphate dehydrogenase (encoded by GPD1 and GPD2 genes).	NAD	92-96	glycerol-3-phosphate dehydrogenase (NAD(+)) GPD2	Saccharomyces cerevisiae S288C	209-213
19727706-9	2010	We expressed NADH oxidase in S. cerevisiae under the control of the GPD2 promoter to modulate the decrease in cytosolic NADH to the right level where the heterologous enzyme does not compete with oxidative phosphorylation while at the same time, decreasing glycerol production.	NAD	13-17	glycerol-3-phosphate dehydrogenase (NAD(+)) GPD2	Saccharomyces cerevisiae S288C	68-72
20798531-9	2010	DPN mainly inhibited PHE and KCl contraction, suggesting an interaction between ERbeta and Ca(2+) channels.	NAD	0-3	estrogen receptor 2	Rattus norvegicus	80-86
19745225-2	2009	Two mitochondrial carrier family members, here named AtNDT1 and AtNDT2, exhibit high structural similarities to the mitochondrial nicotinamide adenine dinucleotide (NAD(+)) carrier ScNDT1 from bakers" yeast.	NAD	130-163	NAD+ transporter 1	Arabidopsis thaliana	53-59
19745225-2	2009	Two mitochondrial carrier family members, here named AtNDT1 and AtNDT2, exhibit high structural similarities to the mitochondrial nicotinamide adenine dinucleotide (NAD(+)) carrier ScNDT1 from bakers" yeast.	NAD	130-163	NAD+ transporter 2	Arabidopsis thaliana	64-70
19745225-2	2009	Two mitochondrial carrier family members, here named AtNDT1 and AtNDT2, exhibit high structural similarities to the mitochondrial nicotinamide adenine dinucleotide (NAD(+)) carrier ScNDT1 from bakers" yeast.	NAD	165-172	NAD+ transporter 1	Arabidopsis thaliana	53-59
19745225-2	2009	Two mitochondrial carrier family members, here named AtNDT1 and AtNDT2, exhibit high structural similarities to the mitochondrial nicotinamide adenine dinucleotide (NAD(+)) carrier ScNDT1 from bakers" yeast.	NAD	165-172	NAD+ transporter 2	Arabidopsis thaliana	64-70
19745225-3	2009	Expression of AtNDT1 or AtNDT2 restores mitochondrial NAD(+) transport activity in a yeast mutant lacking ScNDT.	NAD	54-60	NAD+ transporter 1	Arabidopsis thaliana	14-20
19745225-3	2009	Expression of AtNDT1 or AtNDT2 restores mitochondrial NAD(+) transport activity in a yeast mutant lacking ScNDT.	NAD	54-60	NAD+ transporter 2	Arabidopsis thaliana	24-30
19619667-5	2009	However, since disruption of GDH1 impairs the ammonia utilization, simultaneous over-expression of the NADH-dependent glutamate dehydrogenase encoded by GDH2 was also considered in this study.	NAD	103-107	glutamate dehydrogenase (NAD(+))	Saccharomyces cerevisiae S288C	153-157
19745168-3	2009	OBJECTIVE: Therefore, we tested whether NAD(H) could regulate human cardiac sodium channels (Na(v)1.5).	NAD	40-46	immunoglobulin lambda variable 2-18	Homo sapiens	93-101
19506862-1	2009	Industrial Saccharomyces cerevisiae strains able to utilize xylose have been constructed by overexpression of XYL1 and XYL2 genes encoding the NADPH-preferring xylose reductase (XR) and the NAD(+)-dependent xylitol dehydrogenase (XDH), respectively, from Pichia stipitis.	NAD	190-196	D-xylulose reductase XYL2	Saccharomyces cerevisiae S288C	119-123
19221895-4	2009	By the use of subtype preferential agonists and antagonists, we identified P2X(1), P2X(4), and P2X(7) receptors being engaged in the NAD(+)-induced rise in [Ca(2+)](i).	NAD	133-139	purinergic receptor P2X 1	Homo sapiens	75-81
19691144-3	2009	Mitochondrial ME2 uses either NAD or NADP as a cofactor, has a high Km for malate and is allosterically activated by fumarate and inhibited by ATP.	NAD	30-33	malic enzyme 2	Rattus norvegicus	14-17
19457063-5	2009	Our results suggest that the change in aspartate-glutamate homeostasis is due to a decreased availability of NADH for cytosolic malate dehydrogenase and thus reduced malate-aspartate shuttle activity in neurons using beta-hydroxybutyrate.	NAD	109-113	malate dehydrogenase 1	Homo sapiens	118-148
19513971-2	2009	Poly (ADP-Ribose) polymerase (PARP-1) overactivation leads to massive NAD(+) consumption and ATP depletion with induction of cellular necrosis under high reactive oxygen species.	NAD	70-76	poly (ADP-ribose) polymerase 1	Rattus norvegicus	0-28
19513971-2	2009	Poly (ADP-Ribose) polymerase (PARP-1) overactivation leads to massive NAD(+) consumption and ATP depletion with induction of cellular necrosis under high reactive oxygen species.	NAD	70-76	poly (ADP-ribose) polymerase 1	Rattus norvegicus	30-36
19286518-0	2009	Circadian control of the NAD+ salvage pathway by CLOCK-SIRT1.	NAD	25-29	sirtuin 1	Mus musculus	55-60
19286518-2	2009	We have shown that the core circadian regulator, CLOCK, is a histone acetyltransferase whose activity is counterbalanced by the nicotinamide adenine dinucleotide (NAD+)-dependent histone deacetylase SIRT1.	NAD	128-161	sirtuin 1	Mus musculus	199-204
19286518-2	2009	We have shown that the core circadian regulator, CLOCK, is a histone acetyltransferase whose activity is counterbalanced by the nicotinamide adenine dinucleotide (NAD+)-dependent histone deacetylase SIRT1.	NAD	163-167	sirtuin 1	Mus musculus	199-204
19286518-4	2009	CLOCK:BMAL1 regulates the circadian expression of NAMPT (nicotinamide phosphoribosyltransferase), an enzyme that provides a rate-limiting step in the NAD+ salvage pathway.	NAD	150-154	aryl hydrocarbon receptor nuclear translocator-like	Mus musculus	6-11
19188449-1	2009	The NAD(+)-dependent histone deacetylase hSirT1 regulates cell survival and stress responses by inhibiting p53-, NF-kappaB-, and E2F1-dependent transcription.	NAD	4-10	E2F transcription factor 1	Homo sapiens	129-133
19284563-3	2009	The NAD+-dependent protein deacetylase SIRT1 has been implicated as one of the key downstream regulators of CR in yeast, rodents, and humans.	NAD	4-7	sirtuin 1	Mus musculus	39-44
19194776-3	2009	NDUFV2, located on 18p11.31-p11.2, encodes an important subunit of mitochondrial NADH (complex I).	NAD	81-85	NADH:ubiquinone oxidoreductase core subunit V2	Homo sapiens	0-6
19060927-1	2009	Sirtuin 1 (Sirt1) and Sirtuin 2 (Sirt2) belong to the family of NAD+ (nicotinamide adenine dinucleotide-positive)-dependent class III histone deacetylases and are involved in regulating lifespan.	NAD	64-68	sirtuin 2	Homo sapiens	22-31
19060927-1	2009	Sirtuin 1 (Sirt1) and Sirtuin 2 (Sirt2) belong to the family of NAD+ (nicotinamide adenine dinucleotide-positive)-dependent class III histone deacetylases and are involved in regulating lifespan.	NAD	64-68	sirtuin 2	Homo sapiens	33-38
19060927-1	2009	Sirtuin 1 (Sirt1) and Sirtuin 2 (Sirt2) belong to the family of NAD+ (nicotinamide adenine dinucleotide-positive)-dependent class III histone deacetylases and are involved in regulating lifespan.	NAD	70-103	sirtuin 2	Homo sapiens	22-31
19060927-1	2009	Sirtuin 1 (Sirt1) and Sirtuin 2 (Sirt2) belong to the family of NAD+ (nicotinamide adenine dinucleotide-positive)-dependent class III histone deacetylases and are involved in regulating lifespan.	NAD	70-103	sirtuin 2	Homo sapiens	33-38
19057515-6	2009	RESULTS: In the injured artery, superoxide anion production and expression of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase subunits p47(phox) and Rac-1 were markedly increased, together with expression of monocyte chemotactic protein-1 (MCP-1) and tumor necrosis factor (TNF)-alpha.	NAD	78-111	milk fat globule EGF and factor V/VIII domain containing	Mus musculus	147-156
19018525-1	2009	The two homologous genes GPD1 and GPD2, encoding two isoenzymes of NAD(+)-dependent glycerol-3-phosphate dehydrogenase in industrial yeast Saccharomyces cerevisiae CICIMY0086, had been deleted.	NAD	67-73	glycerol-3-phosphate dehydrogenase (NAD(+)) GPD2	Saccharomyces cerevisiae S288C	34-38
19038292-5	2009	Overexpression of Glrx2 completely prevents DOX-induced decreases in NAD- and FAD-linked state 3 respiration and respiratory control ratio (RCR) in heart mitochondria at days 1 and 5 of treatment.	NAD	69-72	glutaredoxin 2 (thioltransferase)	Mus musculus	18-23
19148549-0	2009	Chromosomal characterization and localization of the NAD+-dependent histone deacetylase gene sirtuin 1 in the mouse.	NAD	53-57	sirtuin 1	Mus musculus	93-102
19182797-0	2009	NAMPT is essential for the G-CSF-induced myeloid differentiation via a NAD(+)-sirtuin-1-dependent pathway.	NAD	71-77	colony stimulating factor 3	Homo sapiens	27-32
19182797-2	2009	Intracellular NAMPT and NAD(+) amounts in myeloid cells, as well as plasma NAMPT and NAD(+) levels, were increased by G-CSF treatment of both healthy volunteers and individuals with congenital neutropenia.	NAD	24-30	colony stimulating factor 3	Homo sapiens	118-123
19182797-2	2009	Intracellular NAMPT and NAD(+) amounts in myeloid cells, as well as plasma NAMPT and NAD(+) levels, were increased by G-CSF treatment of both healthy volunteers and individuals with congenital neutropenia.	NAD	85-91	colony stimulating factor 3	Homo sapiens	118-123
19182797-7	2009	These results reveal a decisive role of the NAD(+) metabolic pathway in G-CSF-triggered myelopoiesis.	NAD	44-50	colony stimulating factor 3	Homo sapiens	72-77
18762557-4	2008	We also find that among the NAD(+)-dependent class III deacetylases, genetic or pharmacological reduction of either Sir2 or Sirt2 provides neuroprotection to Htt-challenged animals and that even greater neuroprotection is achieved when Rpd3 and Sir2 are simultaneously reduced.	NAD	28-32	Sirtuin 1	Drosophila melanogaster	116-120
18762557-4	2008	We also find that among the NAD(+)-dependent class III deacetylases, genetic or pharmacological reduction of either Sir2 or Sirt2 provides neuroprotection to Htt-challenged animals and that even greater neuroprotection is achieved when Rpd3 and Sir2 are simultaneously reduced.	NAD	28-32	huntingtin	Drosophila melanogaster	158-161
18722353-2	2008	Sirt proteins are mammalian members of the Sir2 family of NAD+ (nicotinamide adenine dinucleotide)-dependent protein deacetylases.	NAD	58-62	sirtuin 2	Homo sapiens	43-47
18722353-2	2008	Sirt proteins are mammalian members of the Sir2 family of NAD+ (nicotinamide adenine dinucleotide)-dependent protein deacetylases.	NAD	64-97	sirtuin 2	Homo sapiens	43-47
18940667-0	2008	Covalent and noncovalent intermediates of an NAD utilizing enzyme, human CD38.	NAD	45-48	CD38 molecule	Homo sapiens	73-77
18940667-3	2008	Using X-ray crystallography, we show that human CD38, an NAD-utilizing enzyme, is capable of catalyzing the cleavage reactions through both covalent and noncovalent intermediates, depending on the substrate used.	NAD	57-60	CD38 molecule	Homo sapiens	48-52
18940667-6	2008	Our structural results favor the proposal of a noncovalent intermediate during normal enzymatic utilization of NAD by human CD38 and provide structural insights into the design of covalent and noncovalent inhibitors targeting NAD-utilization pathways.	NAD	111-114	CD38 molecule	Homo sapiens	124-128
18940667-6	2008	Our structural results favor the proposal of a noncovalent intermediate during normal enzymatic utilization of NAD by human CD38 and provide structural insights into the design of covalent and noncovalent inhibitors targeting NAD-utilization pathways.	NAD	226-229	CD38 molecule	Homo sapiens	124-128
18780747-3	2008	We have determined that high concentrations of NAM in the growth medium elevate the intracellular NAD(+) concentration through a mechanism that is partially dependent on NPT1, an important gene in the Preiss-Handler NAD(+) salvage pathway.	NAD	98-104	nicotinate phosphoribosyltransferase	Saccharomyces cerevisiae S288C	170-174
18780747-3	2008	We have determined that high concentrations of NAM in the growth medium elevate the intracellular NAD(+) concentration through a mechanism that is partially dependent on NPT1, an important gene in the Preiss-Handler NAD(+) salvage pathway.	NAD	216-222	nicotinate phosphoribosyltransferase	Saccharomyces cerevisiae S288C	170-174
18828915-8	2008	We find that deletion of BNA2 and NPT1, which is also involved in NAD+ synthesis, suppresses the temperature sensitivity of cdc13-1 strains, indicating that NAD+ metabolism may be linked to telomere end protection.	NAD	66-70	nicotinate phosphoribosyltransferase	Saccharomyces cerevisiae S288C	34-38
18828915-8	2008	We find that deletion of BNA2 and NPT1, which is also involved in NAD+ synthesis, suppresses the temperature sensitivity of cdc13-1 strains, indicating that NAD+ metabolism may be linked to telomere end protection.	NAD	157-161	nicotinate phosphoribosyltransferase	Saccharomyces cerevisiae S288C	34-38
18982432-3	2008	The NADH oxidation domain harbouring the FMN cofactor is connected via a chain of iron-sulfur clusters to the ubiquinone reduction site that is located in a large pocket formed by the PSST- and 49-kDa subunits of complex I.	NAD	4-8	formin 1	Homo sapiens	41-44
18978034-0	2008	The Arabidopsis onset of leaf death5 mutation of quinolinate synthase affects nicotinamide adenine dinucleotide biosynthesis and causes early ageing.	NAD	78-111	quinolinate synthase	Arabidopsis thaliana	49-69
18978034-3	2008	Here, we show that OLD5 encodes quinolinate synthase (QS), a key enzyme in the de novo synthesis of NAD.	NAD	100-103	quinolinate synthase	Arabidopsis thaliana	19-23
18978034-3	2008	Here, we show that OLD5 encodes quinolinate synthase (QS), a key enzyme in the de novo synthesis of NAD.	NAD	100-103	quinolinate synthase	Arabidopsis thaliana	32-52
18978034-6	2008	The old5 mutation causes increased NAD steady state levels that coincide with increased activity of enzymes in the NAD salvage pathway.	NAD	35-38	quinolinate synthase	Arabidopsis thaliana	4-8
18978034-6	2008	The old5 mutation causes increased NAD steady state levels that coincide with increased activity of enzymes in the NAD salvage pathway.	NAD	115-118	quinolinate synthase	Arabidopsis thaliana	4-8
18619469-2	2008	Next, Sir2/3/4 proteins propagate across these loci as histones are deacetylated by the NAD(+)-dependent histone deacetylase Sir2p, ultimately resulting in the cessation of transcription and in the loss of SET1- and DOT1-dependent methylation of histone H3 within silent chromatin.	NAD	88-94	histone methyltransferase SET1	Saccharomyces cerevisiae S288C	206-210
18752667-5	2008	Given that increased levels of nicotinamide adenine dinucleotide (NAD) via deletion of CD38 have been shown to prevent high fat diet induced obesity in mice in a SIRT-1 dependent fashion we explored the possibility of directly applying NAD to zebrafish.	NAD	66-69	sirtuin 1	Mus musculus	162-168
18662547-0	2008	The NAD+-dependent deacetylase SIRT1 modulates CLOCK-mediated chromatin remodeling and circadian control.	NAD	4-8	sirtuin 1	Mus musculus	31-36
18662547-4	2008	We show that the HDAC activity of the NAD(+)-dependent SIRT1 enzyme is regulated in a circadian manner, correlating with rhythmic acetylation of BMAL1 and H3 Lys9/Lys14 at circadian promoters.	NAD	38-44	sirtuin 1	Mus musculus	55-60
18662547-4	2008	We show that the HDAC activity of the NAD(+)-dependent SIRT1 enzyme is regulated in a circadian manner, correlating with rhythmic acetylation of BMAL1 and H3 Lys9/Lys14 at circadian promoters.	NAD	38-44	aryl hydrocarbon receptor nuclear translocator-like	Mus musculus	145-150
18470990-0	2008	Deep tunneling dominates the biologically important hydride transfer reaction from NADH to FMN in morphinone reductase.	NAD	83-87	formin 1	Homo sapiens	91-94
18438860-2	2008	PGE2 synthesis under inflammatory conditions is catalyzed by cyclooxygenase 2 and microsomal PGE synthase 1 (mPGES-1), whereas NAD+-dependent 15-hydroxy-PG dehydrogenase (15-PGDH) is the key enzyme implicated in PGE2 catabolism.	NAD	127-131	15-hydroxyprostaglandin dehydrogenase	Homo sapiens	142-169
18438860-2	2008	PGE2 synthesis under inflammatory conditions is catalyzed by cyclooxygenase 2 and microsomal PGE synthase 1 (mPGES-1), whereas NAD+-dependent 15-hydroxy-PG dehydrogenase (15-PGDH) is the key enzyme implicated in PGE2 catabolism.	NAD	127-131	15-hydroxyprostaglandin dehydrogenase	Homo sapiens	171-178
18393535-3	2008	The S-adenosyl- l-homocysteine (AdoHcy) hydrolases (SAHH) from Homo sapiens (Hs-SAHH) and from the parasite Trypanosoma cruzi (Tc-SAHH) are very similar in structure and catalytic properties but differ in the kinetics and thermodynamics of association and dissociation of the cofactor NAD (+).	NAD	285-292	adenosylhomocysteinase	Homo sapiens	52-56
18393535-4	2008	The binding of NAD (+) and NADH in SAHH appears structurally to be mediated by helix 18, formed by seven residues near the C-terminus of the adjacent subunit.	NAD	15-22	adenosylhomocysteinase	Homo sapiens	35-39
18393535-4	2008	The binding of NAD (+) and NADH in SAHH appears structurally to be mediated by helix 18, formed by seven residues near the C-terminus of the adjacent subunit.	NAD	27-31	adenosylhomocysteinase	Homo sapiens	35-39
18393535-8	2008	Association of NAD (+) with Hs-SAHH, Hs-18Pf-SAHH, Tc-18Hs-SAHH, and Tc-SAHH exhibited biphasic kinetics for all enzymes.	NAD	15-22	adenosylhomocysteinase	Homo sapiens	31-35
18393535-8	2008	Association of NAD (+) with Hs-SAHH, Hs-18Pf-SAHH, Tc-18Hs-SAHH, and Tc-SAHH exhibited biphasic kinetics for all enzymes.	NAD	15-22	adenosylhomocysteinase	Homo sapiens	45-49
18393535-8	2008	Association of NAD (+) with Hs-SAHH, Hs-18Pf-SAHH, Tc-18Hs-SAHH, and Tc-SAHH exhibited biphasic kinetics for all enzymes.	NAD	15-22	adenosylhomocysteinase	Homo sapiens	45-49
18393535-8	2008	Association of NAD (+) with Hs-SAHH, Hs-18Pf-SAHH, Tc-18Hs-SAHH, and Tc-SAHH exhibited biphasic kinetics for all enzymes.	NAD	15-22	adenosylhomocysteinase	Homo sapiens	45-49
18249187-1	2008	Sirt2 is a mammalian member of the Sirtuin family of NAD(+) (nicotinamide adenine dinucleotide)-dependent protein deacetylases.	NAD	53-59	sirtuin 2	Homo sapiens	0-5
17932938-3	2008	We present a microscopic description of the structure and dynamics of the substrate-free, NAD(+)-bound SAHH in solution, based on a 15-ns molecular dynamics simulation in explicit solvent.	NAD	90-96	adenosylhomocysteinase	Homo sapiens	103-107
18296641-0	2008	A role for the NAD-dependent deacetylase Sirt1 in the regulation of autophagy.	NAD	15-18	sirtuin 1	Mus musculus	41-46
18296641-1	2008	We demonstrate a role for the NAD-dependent deacetylase Sirt1 in the regulation of autophagy.	NAD	30-33	sirtuin 1	Mus musculus	56-61
18296641-6	2008	In vitro, Sirt1 can, in an NAD-dependent fashion, directly deacetylate these components.	NAD	27-30	sirtuin 1	Mus musculus	10-15
18328572-8	2008	Interestingly, the ERbeta agonist, DPN significantly decreased IL-1beta following LPS treatment in young adult-derived microglia.	NAD	35-38	estrogen receptor 2	Rattus norvegicus	19-25
18039331-6	2008	Similar to the microsomal RDHs, RDH11, RDH12 and RDH14, RDH13 exhibits a much lower Km value for NADPH than for NADH and has a greater catalytic efficiency in the reductive than in the oxidative direction.	NAD	112-116	retinol dehydrogenase 11	Homo sapiens	32-37
18039331-6	2008	Similar to the microsomal RDHs, RDH11, RDH12 and RDH14, RDH13 exhibits a much lower Km value for NADPH than for NADH and has a greater catalytic efficiency in the reductive than in the oxidative direction.	NAD	112-116	retinol dehydrogenase 14	Homo sapiens	49-54
18046409-2	2007	SIRT1, an NAD+-dependent deacetylase, is a principal modulator of pathways downstream of calorie restriction that produce beneficial effects on glucose homeostasis and insulin sensitivity.	NAD	10-13	sirtuin 1	Mus musculus	0-5
17855339-5	2007	Overexpression of NADK resulted in a 4-5-fold increase in the NADPH, but not NADP(+), concentration, although the recombinant enzyme phosphorylated preferentially NAD(+).	NAD	163-169	NAD kinase	Homo sapiens	18-22
17964573-0	2007	Role of NAD binding and catalytic residues in the C-terminal binding protein corepressor.	NAD	8-11	C-terminal Binding Protein	Drosophila melanogaster	50-76
17964573-4	2007	The NAD mutant, similar to a dimerization mutant, is expressed at low levels, indicating that binding of NAD/NADH may affect CtBP stability.	NAD	4-7	C-terminal Binding Protein	Drosophila melanogaster	125-129
17964573-4	2007	The NAD mutant, similar to a dimerization mutant, is expressed at low levels, indicating that binding of NAD/NADH may affect CtBP stability.	NAD	105-108	C-terminal Binding Protein	Drosophila melanogaster	125-129
17964573-4	2007	The NAD mutant, similar to a dimerization mutant, is expressed at low levels, indicating that binding of NAD/NADH may affect CtBP stability.	NAD	109-113	C-terminal Binding Protein	Drosophila melanogaster	125-129
17766683-1	2007	Poly(ADP-ribose)polymerases (PARP-1 and -2) are activated by DNA strand breaks to synthesize protein-bound ADP-ribose polymers from NAD+.	NAD	132-136	poly (ADP-ribose) polymerase 1	Rattus norvegicus	29-42
17913880-9	2007	Responses to beta-NAD and inhibitory junction potentials are blocked by the P2Y1-selective antagonist, MRS2179, and the nonselective P2 receptor antagonists, pyridoxal phosphate 6-azophenyl-2",4"-disulfonic acid and suramin.	NAD	13-21	purinergic receptor P2Y1	Homo sapiens	76-80
17726514-1	2007	The human NAD+-dependent protein deacetylase SIRT2 resides predominantly in the cytoplasm where it functions as a tubulin deacetylase.	NAD	10-14	sirtuin 2	Homo sapiens	45-50
17591776-2	2007	Citrin also plays a role in transporting cytosolic NADH reducing equivalents into mitochondria as a component of the malate-aspartate shuttle.	NAD	51-55	solute carrier family 25 (mitochondrial carrier, adenine nucleotide translocator), member 13	Mus musculus	0-6
17560549-0	2007	Resveratrol abolishes resistance to axonal degeneration in slow Wallerian degeneration (WldS) mice: activation of SIRT2, an NAD-dependent tubulin deacetylase.	NAD	124-127	sirtuin 2	Mus musculus	114-119
17560549-5	2007	This promoting effect on tubulin deacetylation was mimicked by NAD, suggesting the involvement of SIRT2, an NAD-dependent tubulin deacetylase.	NAD	63-66	sirtuin 2	Mus musculus	98-103
17560549-5	2007	This promoting effect on tubulin deacetylation was mimicked by NAD, suggesting the involvement of SIRT2, an NAD-dependent tubulin deacetylase.	NAD	108-111	sirtuin 2	Mus musculus	98-103
17538025-3	2007	CtBP1/BARS is an NAD-binding protein that becomes ribosylated when cells are exposed to BFA.	NAD	17-20	C-terminal binding protein 1	Mus musculus	0-5
17538025-3	2007	CtBP1/BARS is an NAD-binding protein that becomes ribosylated when cells are exposed to BFA.	NAD	17-20	C-terminal binding protein 1	Mus musculus	6-10
17452319-0	2007	Characterization of Arabidopsis thaliana SufE2 and SufE3: functions in chloroplast iron-sulfur cluster assembly and Nad synthesis.	NAD	116-119	quinolinate synthase	Arabidopsis thaliana	51-56
17452319-12	2007	We conclude that SufE3 is the NadA enzyme of A. thaliana, involved in a critical step during NAD biosynthesis.	NAD	93-96	quinolinate synthase	Arabidopsis thaliana	17-22
17531229-6	2007	NADH and NADPH, but not NAD or NADP, can also replace NTP, suggesting that the NAD(P)H-binding-pocket configuration of the GDH contacts the RNA.	NAD	0-4	glutamate dehydrogenase 1	Homo sapiens	123-126
17531229-6	2007	NADH and NADPH, but not NAD or NADP, can also replace NTP, suggesting that the NAD(P)H-binding-pocket configuration of the GDH contacts the RNA.	NAD	0-3	glutamate dehydrogenase 1	Homo sapiens	123-126
17267199-6	2007	In connection with the oxidation of nicotinamide adenine dinucleotide (NADH), excellent electrocatalytic activities were observed at MB/CNT/GCE compared with MB/GP modified glassy carbon electrode (MB/GP/GCE).	NAD	36-69	aminomethyltransferase	Homo sapiens	140-143
17482543-2	2007	In eukaryotes, nicotinamide riboside is a newly discovered NAD(+) precursor that is converted to nicotinamide mononucleotide by specific nicotinamide riboside kinases, Nrk1 and Nrk2.	NAD	59-65	nicotinamide riboside kinase 2	Mus musculus	177-181
17164398-10	2007	Since CD38 is an ectoenzyme, we suggest that the modulation of extracellular NAD(+) metabolism likely serves as a unique mechanism to coordinate the fate of cells within a local environment.	NAD	77-83	CD38 molecule	Homo sapiens	6-10
17430113-6	2007	Approaches to cell specific therapeutic IDO induction with NAD precursor supplementation to prevent the collateral non-T cell pathogenesis due to chronic TNFalpha-IDO activated tryptophan depletion in autoimmune diseases are reviewed.	NAD	59-62	indoleamine 2,3-dioxygenase 1	Homo sapiens	40-43
17430113-6	2007	Approaches to cell specific therapeutic IDO induction with NAD precursor supplementation to prevent the collateral non-T cell pathogenesis due to chronic TNFalpha-IDO activated tryptophan depletion in autoimmune diseases are reviewed.	NAD	59-62	indoleamine 2,3-dioxygenase 1	Homo sapiens	163-166
17213189-0	2007	Ca2+ Activation kinetics of the two aspartate-glutamate mitochondrial carriers, aralar and citrin: role in the heart malate-aspartate NADH shuttle.	NAD	134-138	solute carrier family 25 (mitochondrial carrier, adenine nucleotide translocator), member 13	Mus musculus	91-97
17197703-0	2007	Nucleocytoplasmic shuttling of the NAD+-dependent histone deacetylase SIRT1.	NAD	35-39	sirtuin 1	Mus musculus	70-75
16909107-1	2007	We previously identified SIRT2, an nicotinamide adenine dinucleotide (NAD)-dependent tubulin deacetylase, as a protein downregulated in gliomas and glioma cell lines, which are characterized by aneuploidy.	NAD	35-68	sirtuin 2	Homo sapiens	25-30
16909107-1	2007	We previously identified SIRT2, an nicotinamide adenine dinucleotide (NAD)-dependent tubulin deacetylase, as a protein downregulated in gliomas and glioma cell lines, which are characterized by aneuploidy.	NAD	70-73	sirtuin 2	Homo sapiens	25-30
17305476-1	2007	The extrahepatic enzyme indoleamine 2,3-dioxygenase (IDO) catalyzes tryptophan degradation in the first and rate-limiting step towards biosynthesis of the central metabolic co-factor nicotinamide adenine dinucleotide (NAD).	NAD	183-216	indoleamine 2,3-dioxygenase 1	Homo sapiens	53-56
17305476-1	2007	The extrahepatic enzyme indoleamine 2,3-dioxygenase (IDO) catalyzes tryptophan degradation in the first and rate-limiting step towards biosynthesis of the central metabolic co-factor nicotinamide adenine dinucleotide (NAD).	NAD	218-221	indoleamine 2,3-dioxygenase 1	Homo sapiens	53-56
16736046-1	2007	Previous neuron and glial cell culture studies of excessive poly (ADP-ribose) polymerase (PARP-1) activation found NAD(+) depletion, glycolytic arrest, and cell death that could be avoided by exogenous tricarboxylic acid cycle (TCA) metabolites, especially pyruvate (pyr).	NAD	115-121	poly (ADP-ribose) polymerase 1	Rattus norvegicus	60-88
16736046-1	2007	Previous neuron and glial cell culture studies of excessive poly (ADP-ribose) polymerase (PARP-1) activation found NAD(+) depletion, glycolytic arrest, and cell death that could be avoided by exogenous tricarboxylic acid cycle (TCA) metabolites, especially pyruvate (pyr).	NAD	115-121	poly (ADP-ribose) polymerase 1	Rattus norvegicus	90-96
16889625-4	2007	The C terminus (amino acids 234-453) encodes a 14-3-3-dependent ADP-ribosyltransferase domain which transfers ADP-ribose from NAD onto substrates such as the Ras GTPases and vimentin.	NAD	126-129	vimentin	Homo sapiens	174-182
17336131-11	2007	The transcriptional regulatory activity of CtBP is modulated by the nuclear NADH/NAD+ ratio and hence appears to be influenced by the metabolic status of the cell.	NAD	76-80	C-terminal Binding Protein	Drosophila melanogaster	43-47
17336131-11	2007	The transcriptional regulatory activity of CtBP is modulated by the nuclear NADH/NAD+ ratio and hence appears to be influenced by the metabolic status of the cell.	NAD	81-85	C-terminal Binding Protein	Drosophila melanogaster	43-47
21469509-2	2007	Previous research indicates that the cytotoxicity caused by CCl4 may be mediated by the rapid induction of PARP-1, a nuclear repair enzyme, which results in celluar depletion of NAD+ and ATP.	NAD	178-182	C-C motif chemokine ligand 4	Homo sapiens	60-64
18084894-4	2007	Consequently, the NADH oxidase-Prx system catalyzes the reduction of both oxygen and hydrogen peroxide to water with NADH as the preferred electron donor.	NAD	18-22	periaxin	Homo sapiens	31-34
18084894-5	2007	The NADH oxidase-Prx system is widely distributed in aerobically growing bacteria lacking a respiratory chain and catalase, and plays an important role not only in scavenging hydroperoxides but also in regenerating NAD in these bacteria.	NAD	4-7	periaxin	Homo sapiens	17-20
17380200-8	2006	Finally, crosstalk between CD38 and other NAD(+) utilizing enzymes such as ART2, SIRT1, and PARP-1 impacts NAD(+) homeostasis, inflammation, and immunity.	NAD	42-48	sirtuin 1	Mus musculus	81-86
17380200-8	2006	Finally, crosstalk between CD38 and other NAD(+) utilizing enzymes such as ART2, SIRT1, and PARP-1 impacts NAD(+) homeostasis, inflammation, and immunity.	NAD	107-113	sirtuin 1	Mus musculus	81-86
17041593-4	2006	This reduced expression is mediated by the transcription factor NRSF, which recruits the NADH-binding co-repressor CtBP to generate a repressive chromatin environment around the BDNF promoter.	NAD	89-93	RE1-silencing transcription factor	Rattus norvegicus	64-68
16959573-1	2006	Sir2 is an NAD-dependent deacetylase that connects metabolism with longevity in yeast, flies, and worms.	NAD	11-14	sirtuin 1	Mus musculus	0-4
16959573-3	2006	We show that SIRT4 is a mitochondrial enzyme that uses NAD to ADP-ribosylate and downregulate glutamate dehydrogenase (GDH) activity.	NAD	55-58	sirtuin 4	Mus musculus	13-18
16840720-6	2006	These results indicate that attenuation of BMP signaling can occur through modulation of CtBP-1 activity by hypoxia-induced changes in the NADH/NAD(+) ratio.	NAD	139-143	bone morphogenetic protein 1	Homo sapiens	43-46
16840720-6	2006	These results indicate that attenuation of BMP signaling can occur through modulation of CtBP-1 activity by hypoxia-induced changes in the NADH/NAD(+) ratio.	NAD	144-150	bone morphogenetic protein 1	Homo sapiens	43-46
16687393-3	2006	During attempts to understand the mode of regulation of H2A.z, we found that overexpression of silent information regulator 2alpha (Sir2alpha) specifically induced down-regulation of H2A.z via NAD-dependent activity.	NAD	193-196	H2A.Z variant histone 1	Homo sapiens	56-61
16687393-3	2006	During attempts to understand the mode of regulation of H2A.z, we found that overexpression of silent information regulator 2alpha (Sir2alpha) specifically induced down-regulation of H2A.z via NAD-dependent activity.	NAD	193-196	H2A.Z variant histone 1	Homo sapiens	183-188
16730329-10	2006	We postulated that CD38 is the major NADase in mammalian cells and that it regulates intracellular NAD levels.	NAD	37-40	CD38 molecule	Homo sapiens	19-23
16380372-3	2006	The structure of human DHRS6 was determined at a resolution of 1.8 A in complex with NAD(H) and reveals a tetrameric organization with a short chain dehydrogenases/reductase-typical folding pattern.	NAD	85-91	3-hydroxybutyrate dehydrogenase 2	Homo sapiens	23-28
16579765-3	2006	PROCEDURES: Induced superoxide production by reduced nicotinamide adenine dinucleotides (NAD[P]H; ie, reduced nicotinamide adenine dinucleotide [NADH] and reduced nicotinamide adenine dinucleotide phosphate [NADPH]) was measured by use of a nitroblue tetrazolium (NBT) reduction assay on whole spermatozoa and a cytochrome c reduction assay on isolated membrane fractions of spermatozoa.	NAD	53-87	cytochrome c, somatic	Equus caballus	312-324
16579765-3	2006	PROCEDURES: Induced superoxide production by reduced nicotinamide adenine dinucleotides (NAD[P]H; ie, reduced nicotinamide adenine dinucleotide [NADH] and reduced nicotinamide adenine dinucleotide phosphate [NADPH]) was measured by use of a nitroblue tetrazolium (NBT) reduction assay on whole spermatozoa and a cytochrome c reduction assay on isolated membrane fractions of spermatozoa.	NAD	53-86	cytochrome c, somatic	Equus caballus	312-324
16403805-6	2006	Similar modifications in mRNA levels were mimicked for some of the genes (including pttg1) by 1 mm nicotinamide adenine dinucleotide (NAD).	NAD	99-132	PTTG1 regulator of sister chromatid separation, securin	Homo sapiens	84-89
16403805-6	2006	Similar modifications in mRNA levels were mimicked for some of the genes (including pttg1) by 1 mm nicotinamide adenine dinucleotide (NAD).	NAD	134-137	PTTG1 regulator of sister chromatid separation, securin	Homo sapiens	84-89
16291748-10	2006	Consistently with Ndt1p localization and its function as a NAD+ transporter, cells lacking NDT1 had reduced levels of NAD+ and NADH in their mitochondria and reduced activity of mitochondrial NAD+-requiring enzymes.	NAD	59-63	NAD+ transporter	Saccharomyces cerevisiae S288C	18-23
16291748-10	2006	Consistently with Ndt1p localization and its function as a NAD+ transporter, cells lacking NDT1 had reduced levels of NAD+ and NADH in their mitochondria and reduced activity of mitochondrial NAD+-requiring enzymes.	NAD	59-63	NAD+ transporter	Saccharomyces cerevisiae S288C	91-95
16291748-10	2006	Consistently with Ndt1p localization and its function as a NAD+ transporter, cells lacking NDT1 had reduced levels of NAD+ and NADH in their mitochondria and reduced activity of mitochondrial NAD+-requiring enzymes.	NAD	127-131	NAD+ transporter	Saccharomyces cerevisiae S288C	91-95
16291748-10	2006	Consistently with Ndt1p localization and its function as a NAD+ transporter, cells lacking NDT1 had reduced levels of NAD+ and NADH in their mitochondria and reduced activity of mitochondrial NAD+-requiring enzymes.	NAD	118-122	NAD+ transporter	Saccharomyces cerevisiae S288C	91-95
16291748-12	2006	The delta ndt1 delta ndt2 double mutant exhibited lower mitochondrial NAD+ and NADH levels than the single deletants and a more pronounced delay in growth on nonfermentable carbon sources.	NAD	70-74	NAD+ transporter	Saccharomyces cerevisiae S288C	10-14
16291748-12	2006	The delta ndt1 delta ndt2 double mutant exhibited lower mitochondrial NAD+ and NADH levels than the single deletants and a more pronounced delay in growth on nonfermentable carbon sources.	NAD	79-83	NAD+ transporter	Saccharomyces cerevisiae S288C	10-14
16291748-13	2006	The main role of Ndt1p and Ndt2p is to import NAD+ into mitochondria by unidirectional transport or by exchange with intramitochondrially generated (d)AMP and (d)GMP.	NAD	46-50	NAD+ transporter	Saccharomyces cerevisiae S288C	17-22
16720433-5	2006	This mechanism, dubbed "NAD-induced cell death" or NICD, is initiated when ART2 ADP-ribosylates the cytolytic P2X7 purinergic receptor, inducing formation of a cation channel, opening of a nonselective pore, shedding of CD62L from the cell surface, exposure of phosphatidylserine on the outer leaflet of the plasma membrane, breakdown of the mitochondrial membrane potential, and DNA-fragmentation.	NAD	24-27	selectin L	Homo sapiens	220-225
16720433-7	2006	In the extracellular environment, the signaling function of NAD is terminated by NAD-degrading ectoenzymes such as CD38.	NAD	60-63	CD38 molecule	Homo sapiens	115-119
16720433-7	2006	In the extracellular environment, the signaling function of NAD is terminated by NAD-degrading ectoenzymes such as CD38.	NAD	81-84	CD38 molecule	Homo sapiens	115-119
16384941-4	2006	Production of fluorescent reduced nicotinamide adenine dinucleotide (NADH) was used to measure enzymatic activity of mutant IMPDH1 proteins.	NAD	34-67	inosine monophosphate dehydrogenase 1	Homo sapiens	124-130
16384941-4	2006	Production of fluorescent reduced nicotinamide adenine dinucleotide (NADH) was used to measure enzymatic activity of mutant IMPDH1 proteins.	NAD	69-73	inosine monophosphate dehydrogenase 1	Homo sapiens	124-130
16242668-6	2005	ERalpha agonist PPT induced the same suppressive effect as that induced by estradiol on the density of thorns, but ERbeta agonist DPN did not affect the density of thorns.	NAD	130-133	estrogen receptor 2	Rattus norvegicus	115-121
16198644-6	2005	For the oxidation of glyoxylate, K(M) values were 0.18 mM and 0.26 mM for LDHA and LDHB respectively with NAD+ as cofactor.	NAD	106-110	lactate dehydrogenase B	Homo sapiens	83-87
16373854-5	2005	Using mice that are completely deficient in gp91phox (a subunit protein of the superoxide producing nicotinamide adenine dinucleotide phosphate [NADPH] oxidase), we found that CH-enhanced PA constriction to ET-1 was completely blocked (decreases in mean [+/- SE] maximal isometric tension from 5.43 +/- 0.35 to 3.33 +/- 0.19 mN; n = 7; p &lt; 0.01).	NAD	100-133	endothelin 1	Mus musculus	207-211
16258009-6	2005	GapA, a bispecific NAD(P)-dependent dehydrogenase, specifically formed a binary complex with oxidized CP12 when bound to NAD.	NAD	19-22	CP12 domain-containing protein 2	Arabidopsis thaliana	102-106
16258009-8	2005	Exchanging NADP for NAD, reducing CP12, or reducing PRK were all conditions that prevented formation of the complex.	NAD	11-14	CP12 domain-containing protein 2	Arabidopsis thaliana	34-38
16112812-7	2005	Inhibitors of PKA, PKC, and PTK also prevented the AR induced by LPC or NADH, suggesting the involvement of these kinases in the process.	NAD	72-76	protein tyrosine kinase 2 beta	Homo sapiens	28-31
16154098-2	2005	We show that the forkhead protein FoxO1 protects beta cells against oxidative stress by forming a complex with the promyelocytic leukemia protein Pml and the NAD-dependent deacetylase Sirt1 to activate expression of NeuroD and MafA, two Insulin2 (Ins2) gene transcription factors.	NAD	158-161	PML nuclear body scaffold	Homo sapiens	146-149
16154098-2	2005	We show that the forkhead protein FoxO1 protects beta cells against oxidative stress by forming a complex with the promyelocytic leukemia protein Pml and the NAD-dependent deacetylase Sirt1 to activate expression of NeuroD and MafA, two Insulin2 (Ins2) gene transcription factors.	NAD	158-161	MAF bZIP transcription factor A	Homo sapiens	227-231
16187535-4	2005	Mercury supply increased the NADH-GDH activity in the presence of NH4NO3, but to a lesser extent than in the absence of NH4NO3.	NAD	29-33	glutamate dehydrogenase 1	Homo sapiens	34-37
16187535-10	2005	It has been suggested that Hg activates the NADH-GDH enzyme in the bean leaf segments by binding to thiol groups of protein and pronounced increase in activity by Hg suggests a possible role of enzyme under Hg-stress.	NAD	44-48	glutamate dehydrogenase 1	Homo sapiens	49-52
16012755-7	2005	In contrast, mammalian SIRT1 was found to bind to FOXO4, catalyze its deacetylation in an NAD-dependent manner, and thereby increase its transactivation activity.	NAD	90-93	forkhead box O4	Homo sapiens	50-55
15795221-4	2005	Here we report the three-dimensional structure of Gal10p in complex with NAD(+), UDP-glucose, and beta-D-galactose determined to 1.85-A resolution.	NAD	73-79	bifunctional UDP-glucose 4-epimerase/aldose 1-epimerase	Saccharomyces cerevisiae S288C	50-56
15795229-1	2005	Members of the Sir2 family of NAD-dependent protein deacetylases regulate diverse cellular processes including aging, gene silencing, and cellular differentiation.	NAD	30-33	sirtuin 1	Mus musculus	15-19
15900217-3	2005	The enzyme coded by Aldh2(2) has a four- to five-fold lower affinity for NAD than that coded by Aldh2(1).	NAD	73-76	aldehyde dehydrogenase 2 family member	Rattus norvegicus	20-25
15900217-3	2005	The enzyme coded by Aldh2(2) has a four- to five-fold lower affinity for NAD than that coded by Aldh2(1).	NAD	73-76	aldehyde dehydrogenase 2 family member	Rattus norvegicus	96-101
15728189-8	2005	CC3 provides an example of the adaptation of a metabolic enzyme fold to include a regulatory role, as also seen in the case of the NADH-binding co-repressor CtBP.	NAD	131-135	HIV-1 Tat interactive protein 2	Homo sapiens	0-3
15657180-3	2005	After the release of NAD from cells, ART2.2 ADP-ribosylates the P2X7 purinoceptor, lymphocyte function-associated antigen (LFA-1), and other membrane.	NAD	21-24	ADP-ribosyltransferase 2b	Mus musculus	37-43
15657180-3	2005	After the release of NAD from cells, ART2.2 ADP-ribosylates the P2X7 purinoceptor, lymphocyte function-associated antigen (LFA-1), and other membrane.	NAD	21-24	integrin alpha L	Mus musculus	123-128
15574424-1	2005	Cyclic ADP-ribose (cADPR) is an intracellular calcium mobilizer generated from NAD(+) by the ADP-ribosyl cyclases CD38 and BST-1.	NAD	79-85	CD38 molecule	Homo sapiens	114-118
15361073-1	2005	The extracellular domain of integrin alpha7 is ADP-ribosylated by an arginine-specific ecto-ADP-ribosyltransferase after adding exogenous NAD+ to intact C2C12 skeletal muscle cells.	NAD	138-142	integrin alpha 7	Mus musculus	28-43
15389540-5	2005	We demonstrated that specific inhibition of poly(ADP-ribose) polymerase activity via 3-aminobenzamide (3ABA) or NAD+ deprivation prevents FGF2-mediated uPA mRNA over-expression and cell-associated plasminogen activator (PA) production in GM7373 endothelial cell line.	NAD	112-116	plasminogen activator, urokinase	Bos taurus	152-155
15494407-2	2004	Aralar1 and citrin are two isoforms of the mitochondrial aspartate/glutamate carrier, one key constituent of the malate-aspartate NADH shuttle.	NAD	130-134	solute carrier family 25 member 12	Rattus norvegicus	0-7
15566299-1	2004	Type 2 human sirtuin (SIRT2) is a NAD(+)-dependent cytoplasmic protein that is colocalized with HDAC6 on microtubules.	NAD	34-40	sirtuin 2	Homo sapiens	22-27
15273247-8	2004	We propose that GDH is one target of action of sulfite, leading to a decrease in alpha-ketoglutarate and a diminished flux through the tricarboxylic acid cycle accompanied by a decrease in NADH through the mitochondrial electron transport chain, a decreased MMP, and a decrease in ATP synthesis.	NAD	189-193	glutamate dehydrogenase 1	Homo sapiens	16-19
15210723-0	2004	Distinct intracellular localization of Gpd1p and Gpd2p, the two yeast isoforms of NAD+-dependent glycerol-3-phosphate dehydrogenase, explains their different contributions to redox-driven glycerol production.	NAD	82-85	glycerol-3-phosphate dehydrogenase (NAD(+)) GPD2	Saccharomyces cerevisiae S288C	49-54
15210723-2	2004	We here report that respiratory-deficient cells become strictly dependent on the Gpd2p isoform of the NAD(+)-linked glycerol-3-phosphate dehydrogenase (Gpd).	NAD	102-108	glycerol-3-phosphate dehydrogenase (NAD(+)) GPD2	Saccharomyces cerevisiae S288C	81-86
15269219-1	2004	Sir2 (silent information regulator 2) enzymes catalyze a unique protein deacetylation reaction that requires the coenzyme NAD(+) and produces nicotinamide and a newly discovered metabolite, O-acetyl-ADP-ribose (OAADPr).	NAD	122-128	sirtuin 2	Homo sapiens	0-4
15269219-1	2004	Sir2 (silent information regulator 2) enzymes catalyze a unique protein deacetylation reaction that requires the coenzyme NAD(+) and produces nicotinamide and a newly discovered metabolite, O-acetyl-ADP-ribose (OAADPr).	NAD	122-128	sirtuin 2	Homo sapiens	6-36
15269219-3	2004	Here we examine the role of NAD(+) metabolites/derivatives and salvage pathway intermediates as activators, inhibitors, or coenzyme substrates of Sir2 enzymes in vitro.	NAD	28-34	sirtuin 2	Homo sapiens	146-150
15269219-5	2004	Sir2 enzymes showed an exquisite selectivity for the nicotinamide base coenzyme, with the most dramatic losses in binding affinity/reactivity resulting from relatively minor changes in the nicotinamide ring, either by reduction, as in NADH, or by converting the amide to its acid analogue.	NAD	235-239	sirtuin 2	Homo sapiens	0-4
15269219-11	2004	We propose that changes in both free nicotinamide and free NAD(+) afford the greatest contribution to cellular activity of Sir2 enzymes but with nicotinamide having a more dramatic effect during smaller fluctuations in concentration.	NAD	59-65	sirtuin 2	Homo sapiens	123-127
15274642-1	2004	The Silent information regulator 2 (Sir2) family of enzymes consists of NAD(+)-dependent histone/protein deacetylases that tightly couple the hydrolysis of NAD(+) and the deacetylation of an acetylated substrate to form nicotinamide, the deacetylated product, and the novel metabolite O-acetyl-ADP-ribose (OAADPR).	NAD	72-78	sirtuin 2	Homo sapiens	4-34
15274642-1	2004	The Silent information regulator 2 (Sir2) family of enzymes consists of NAD(+)-dependent histone/protein deacetylases that tightly couple the hydrolysis of NAD(+) and the deacetylation of an acetylated substrate to form nicotinamide, the deacetylated product, and the novel metabolite O-acetyl-ADP-ribose (OAADPR).	NAD	72-78	sirtuin 2	Homo sapiens	36-40
15274642-1	2004	The Silent information regulator 2 (Sir2) family of enzymes consists of NAD(+)-dependent histone/protein deacetylases that tightly couple the hydrolysis of NAD(+) and the deacetylation of an acetylated substrate to form nicotinamide, the deacetylated product, and the novel metabolite O-acetyl-ADP-ribose (OAADPR).	NAD	156-162	sirtuin 2	Homo sapiens	4-34
15274642-1	2004	The Silent information regulator 2 (Sir2) family of enzymes consists of NAD(+)-dependent histone/protein deacetylases that tightly couple the hydrolysis of NAD(+) and the deacetylation of an acetylated substrate to form nicotinamide, the deacetylated product, and the novel metabolite O-acetyl-ADP-ribose (OAADPR).	NAD	156-162	sirtuin 2	Homo sapiens	36-40
15274642-4	2004	Bisubstrate kinetic analysis indicates that Sir2 enzymes follow a sequential mechanism, where both the acetylated substrate and NAD(+) must bind to form a ternary complex, prior to any catalytic step.	NAD	128-134	sirtuin 2	Homo sapiens	44-48
15207836-3	2004	Assays were performed in purified brain cell nuclei to determine Parp activity by incorporation of radiolabeled ADP-ribose moieties from nicotinamide adenine dinucleotide (NAD+) into nuclear proteins.	NAD	137-170	poly (ADP-ribose) polymerase 1	Rattus norvegicus	65-69
15207836-3	2004	Assays were performed in purified brain cell nuclei to determine Parp activity by incorporation of radiolabeled ADP-ribose moieties from nicotinamide adenine dinucleotide (NAD+) into nuclear proteins.	NAD	172-176	poly (ADP-ribose) polymerase 1	Rattus norvegicus	65-69
15207836-6	2004	RESULTS: Parp activity but not NAD-glycohydrolase (NADase) was stimulated by 21% in diabetes vs. control while lowering effects of diabetes on NAD+ and ATP levels were observed.	NAD	143-147	poly (ADP-ribose) polymerase 1	Rattus norvegicus	9-13
15207836-10	2004	The mechanism of brain disorders seems to be at least partially connected with a decrease in cellular content and altered subcellular distribution of Parp substrate, NAD+, which, in turn, results in a reduction of ATP level that leads to a total failure of oxidative metabolism.	NAD	166-170	poly (ADP-ribose) polymerase 1	Rattus norvegicus	150-154
15986701-2	2004	A bacterial flavoprotein, putidaredoxin reductase (PdR), was activated and shown to be capable of catalyzing the electron transport from NADH to electron-carrier proteins such as cytochrome b5 (tCyt-b5) and putidaredoxin (Pdx) in reverse micelles.	NAD	137-141	cytochrome b5 type A	Homo sapiens	179-192
15147502-3	2004	PARP is activated following DNA damage and may lead to cell death via NAD+ and ATP depletion.	NAD	70-74	poly (ADP-ribose) polymerase 1	Rattus norvegicus	0-4
15147502-5	2004	Acute ammonia intoxication increases PARP content twofold in brain cells nuclei.NAD+ content decreased by 55% in rats injected with ammonia.	NAD	80-84	poly (ADP-ribose) polymerase 1	Rattus norvegicus	37-41
15024000-3	2004	Activity of the recombinant human MIP synthase purified from Escherichia coli was optimal at pH 8.0 at 37 degrees C and exhibited K(m) values of 0.57 mm and 8 microm for glucose 6-phosphate and NAD(+), respectively.	NAD	194-200	inositol-3-phosphate synthase 1	Homo sapiens	34-46
17903964-5	2004	Although a 2-mm depth of mechanical impact caused a drastic decrease in NAD-linked electron transfer activities and energy-coupling capacities in brain mitochondria of nontransgenic mice, the decrease in mitochondrial function was completely prevented by overexpression of Gpx1 in Gpx1 transgenic mice.	NAD	72-75	glutathione peroxidase 1	Mus musculus	273-277
14684747-3	2004	Here we present the structure of MIP synthase in complex with NAD(+) and a high-affinity inhibitor, 2-deoxy-d-glucitol 6-(E)-vinylhomophosphonate.	NAD	62-68	inositol-3-phosphate synthase 1	Homo sapiens	33-45
15050973-2	2004	GDH catalyzes the oxidative deamination of glutamate to alpha-ketoglutarate plus ammonia, using NAD or NADP as co-factor.	NAD	96-99	glutamate dehydrogenase 1	Homo sapiens	0-3
14729974-2	2004	The NAD(+) salvage pathway protein, Npt1, regulates Sir2-mediated processes by maintaining a sufficiently high intracellular NAD(+) concentration.	NAD	4-10	nicotinate phosphoribosyltransferase	Saccharomyces cerevisiae S288C	36-40
14729974-2	2004	The NAD(+) salvage pathway protein, Npt1, regulates Sir2-mediated processes by maintaining a sufficiently high intracellular NAD(+) concentration.	NAD	125-131	nicotinate phosphoribosyltransferase	Saccharomyces cerevisiae S288C	36-40
14986171-2	2004	ALDH4 is a mitochondrial-matrix NAD+-dependent enzyme catalyzing the second step of the proline degradation pathway.	NAD	32-36	aldehyde dehydrogenase 3 family member B1	Homo sapiens	0-5
12969868-0	2003	Nicotinamide adenine dinucleotide (phosphate) reduced:quinone oxidoreductase and glutathione S-transferase M1 polymorphisms and childhood asthma.	NAD	0-33	crystallin zeta	Homo sapiens	54-76
12969868-1	2003	Nicotinamide adenine dinucleotide (phosphate) reduced:quinone oxidoreductase (NQO1) and glutathione S-transferase (GST) M1 are phase II enzymes important in response to oxidative stress, such as occurs during exposure to ozone.	NAD	0-33	crystallin zeta	Homo sapiens	54-76
12969868-1	2003	Nicotinamide adenine dinucleotide (phosphate) reduced:quinone oxidoreductase (NQO1) and glutathione S-transferase (GST) M1 are phase II enzymes important in response to oxidative stress, such as occurs during exposure to ozone.	NAD	0-33	glutathione S-transferase kappa 1	Homo sapiens	115-118
15090235-9	2003	The optimized procedure revealed (3)H-DPN affinity constants at the MOR that were consistent with results obtained using filtration methods (K(D) (SPA) = 1.89 +/- 0.24 nM, K(D) (filtration) = 1.88 +/- 0.35 nM).	NAD	38-41	opioid receptor mu 1	Homo sapiens	68-71
14554197-2	2003	The NADPH-dependent glutamate dehydrogenase encoded by GDH1, which accounts for a major fraction of the NADPH consumption during growth on ammonium, was deleted, and alternative pathways for ammonium assimilation were overexpressed: GDH2 (NADH-consuming) or GLN1 and GLT1 (the GS-GOGAT system).	NAD	239-243	glutamate dehydrogenase (NADP(+)) GDH1	Saccharomyces cerevisiae S288C	55-59
12972620-10	2003	Transcript array analysis shows that reduction in cellular NAD(+) levels preferentially affects Hst1p-regulated genes in comparison to genes regulated with other NAD(+)-dependent deacetylases (Sir2p, Hst2p, Hst3p, and Hst4p).	NAD	59-65	NAD-dependent histone deacetylase HST3	Saccharomyces cerevisiae S288C	207-212
12963490-3	2003	As a rate-limiting enzyme, IDO regulates tryptophan catabolism via the kynurenine pathway producing a series of metabolic precursors (some of which are neurotoxic) before complete oxidation to the essential pyridine nucleotide NAD.	NAD	227-230	indoleamine 2,3-dioxygenase 1	Homo sapiens	27-30
12963490-6	2003	We investigated the hypothesis that IDO activity is directly involved in maintenance of intracellular [NAD] in activated astroglial cells through control of de novo synthesis.	NAD	103-106	indoleamine 2,3-dioxygenase 1	Homo sapiens	36-39
12963490-8	2003	Inhibition of IDO activity with either 6-chloro-D-tryptophan (competitive inhibition), or 3-ethoxy beta-carboline (non-competitive inhibition) resulted in a dose-dependent decrease in IDO activity that correlated directly with decreasing [NAD] (R(2)=0.92 and 0.81, respectively).	NAD	239-242	indoleamine 2,3-dioxygenase 1	Homo sapiens	14-17
12963490-8	2003	Inhibition of IDO activity with either 6-chloro-D-tryptophan (competitive inhibition), or 3-ethoxy beta-carboline (non-competitive inhibition) resulted in a dose-dependent decrease in IDO activity that correlated directly with decreasing [NAD] (R(2)=0.92 and 0.81, respectively).	NAD	239-242	indoleamine 2,3-dioxygenase 1	Homo sapiens	184-187
12963490-9	2003	These results support the hypothesis that one important consequence of increasing IDO activity in astroglial cells during inflammation is to maintain NAD levels through de novo synthesis from tryptophan.	NAD	150-153	indoleamine 2,3-dioxygenase 1	Homo sapiens	82-85
14523559-4	2003	Due to the NAD+ dependency, Sir2 might be the link between metabolic activity and histone/protein acetylation.	NAD	11-15	sirtuin 1	Mus musculus	28-32
12899610-2	2003	The Sir2 enzymes are NAD(+)-dependent protein deacetylases that influence gene expression by forming deacetylated proteins, nicotinamide and 2"-O-acetyl-ADPR.	NAD	21-25	sirtuin 1	Mus musculus	4-8
12893989-3	2003	The University of Chile rat lines UChA (low drinkers) and UChB (high drinkers) display differences in the relative K(m) for NAD+ of mitochondrial aldehyde dehydrogenase (ALDH2) but no V(max) differences.	NAD	124-128	aldehyde dehydrogenase 2 family member	Rattus norvegicus	132-168
12893989-3	2003	The University of Chile rat lines UChA (low drinkers) and UChB (high drinkers) display differences in the relative K(m) for NAD+ of mitochondrial aldehyde dehydrogenase (ALDH2) but no V(max) differences.	NAD	124-128	aldehyde dehydrogenase 2 family member	Rattus norvegicus	170-175
12893989-5	2003	We investigated whether there are differences in the coding regions of ALDH2 cDNA in these lines and whether the Aldh2 genotype predicts the phenotype of alcohol consumption and the K(m) of ALDH2 for NAD+.	NAD	200-204	aldehyde dehydrogenase 2 family member	Rattus norvegicus	190-195
12893989-11	2003	Rats of different Aldh2 genotypes displayed marked phenotypic differences in both ethanol consumption (g/kg/day; means +/- SE): (Aldh21/Aldh21) = 5.7 +/- 0.2, (Aldh22/Aldh22) = 0.9 +/- 0.2 and (Aldh23/Aldh23) = 4.6 +/- 0.2; and K(m)s for NAD+ of 43 +/- 3 microm, 132 +/- 13 microm and 41 +/- 2 microm, respectively (Aldh22 versus Aldh21 or Aldh23; P &lt; 0.0001 for both phenotypes).	NAD	238-242	aldehyde dehydrogenase 2 family member	Rattus norvegicus	18-23
12893989-12	2003	Overall, the data show that alleles of Aldh2 strongly segregate with the phenotype of ethanol consumption and the relative K(m) for NAD+ of ALDH2.	NAD	132-136	aldehyde dehydrogenase 2 family member	Rattus norvegicus	39-44
12893989-12	2003	Overall, the data show that alleles of Aldh2 strongly segregate with the phenotype of ethanol consumption and the relative K(m) for NAD+ of ALDH2.	NAD	132-136	aldehyde dehydrogenase 2 family member	Rattus norvegicus	140-145
12887926-3	2003	Surprisingly, p38 represents a nuclear form of glyceraldehyde-3-phosphate dehydrogenase, and binding to Oct-1, as well as OCA-S function, is stimulated by NAD(+) but inhibited by NADH.	NAD	155-161	POU class 2 homeobox 1	Homo sapiens	104-109
12887926-3	2003	Surprisingly, p38 represents a nuclear form of glyceraldehyde-3-phosphate dehydrogenase, and binding to Oct-1, as well as OCA-S function, is stimulated by NAD(+) but inhibited by NADH.	NAD	179-183	POU class 2 homeobox 1	Homo sapiens	104-109
12834903-1	2003	Poly(ADP-ribose) is synthesized from nicotinamide adenine dinucleotide (NAD(+)) by poly(ADP-ribose) polymerase (PARP) and degraded by poly(ADP-ribose) glycohydrolase (PARG).	NAD	37-70	poly (ADP-ribose) polymerase 1	Rattus norvegicus	83-110
12834903-1	2003	Poly(ADP-ribose) is synthesized from nicotinamide adenine dinucleotide (NAD(+)) by poly(ADP-ribose) polymerase (PARP) and degraded by poly(ADP-ribose) glycohydrolase (PARG).	NAD	37-70	poly (ADP-ribose) polymerase 1	Rattus norvegicus	112-116
12834903-1	2003	Poly(ADP-ribose) is synthesized from nicotinamide adenine dinucleotide (NAD(+)) by poly(ADP-ribose) polymerase (PARP) and degraded by poly(ADP-ribose) glycohydrolase (PARG).	NAD	37-70	poly (ADP-ribose) glycohydrolase	Rattus norvegicus	134-165
12834903-1	2003	Poly(ADP-ribose) is synthesized from nicotinamide adenine dinucleotide (NAD(+)) by poly(ADP-ribose) polymerase (PARP) and degraded by poly(ADP-ribose) glycohydrolase (PARG).	NAD	37-70	poly (ADP-ribose) glycohydrolase	Rattus norvegicus	167-171
12834903-1	2003	Poly(ADP-ribose) is synthesized from nicotinamide adenine dinucleotide (NAD(+)) by poly(ADP-ribose) polymerase (PARP) and degraded by poly(ADP-ribose) glycohydrolase (PARG).	NAD	72-78	poly (ADP-ribose) polymerase 1	Rattus norvegicus	83-110
12834903-1	2003	Poly(ADP-ribose) is synthesized from nicotinamide adenine dinucleotide (NAD(+)) by poly(ADP-ribose) polymerase (PARP) and degraded by poly(ADP-ribose) glycohydrolase (PARG).	NAD	72-78	poly (ADP-ribose) polymerase 1	Rattus norvegicus	112-116
12834903-1	2003	Poly(ADP-ribose) is synthesized from nicotinamide adenine dinucleotide (NAD(+)) by poly(ADP-ribose) polymerase (PARP) and degraded by poly(ADP-ribose) glycohydrolase (PARG).	NAD	72-78	poly (ADP-ribose) glycohydrolase	Rattus norvegicus	134-165
12714601-7	2003	The extent of phosphorylation of both FDH and PDH was strongly decreased by NAD+, formate, and pyruvate, indicating that reversible phosphorylation of FDH and PDHs was regulated in a similar fashion.	NAD	76-80	formate dehydrogenase, mitochondrial	Solanum tuberosum	38-41
12714601-7	2003	The extent of phosphorylation of both FDH and PDH was strongly decreased by NAD+, formate, and pyruvate, indicating that reversible phosphorylation of FDH and PDHs was regulated in a similar fashion.	NAD	76-80	formate dehydrogenase, mitochondrial	Solanum tuberosum	151-154
12903798-6	2003	After adding appropriate amount of NAD+ to the hypoxia treated cardiac muscle specimen, PAGE showed the subbands of four isoymes (LDH2-LDH5) reduced or even totally disappeared in the isozyme patterns.	NAD	35-39	lactate dehydrogenase B	Mus musculus	130-134
12693930-4	2003	It has a better-defined NAD binding site than those of related mammalian ALDH1 enzymes with the cofactor bound in the "hydride transfer" position in all four monomers with small differences about the dimer dyads.	NAD	24-27	aldehyde dehydrogenase 1 family member A1	Homo sapiens	73-78
12693930-8	2003	The structure not only gives a view of a "natural mutant" of ALDH1 illustrating the adaptive conflict that can arise in multifunctional proteins, but also provides a well-ordered NAD binding site structure for this class of enzymes with important roles in development and health.	NAD	179-182	aldehyde dehydrogenase 1 family member A1	Homo sapiens	61-66
12631263-6	2003	Thioredoxin efficiently protects the complexes from self-inactivation during catalysis at low NAD+.	NAD	94-98	thioredoxin	Homo sapiens	0-11
12631263-10	2003	It is suggested that this side-effect of the 2-oxo acid oxidation at low NAD+in vivo would be overcome by cooperation of mitochondrial thioredoxin and the thioredoxin-dependent peroxidase, SP-22.	NAD	73-77	thioredoxin 2	Homo sapiens	121-146
12631263-10	2003	It is suggested that this side-effect of the 2-oxo acid oxidation at low NAD+in vivo would be overcome by cooperation of mitochondrial thioredoxin and the thioredoxin-dependent peroxidase, SP-22.	NAD	73-77	thioredoxin	Homo sapiens	135-146
12571358-1	2003	Sir2 is an NAD-dependent histone deacetylase required for transcriptional silencing.	NAD	11-14	Sirtuin 1	Drosophila melanogaster	0-4
12571358-8	2003	With this hyperacetylated histone-DNA complex, we observed potent (50- to 100-fold) NAD-dependent transcriptional repression by purified dSir2.	NAD	84-87	Sirtuin 1	Drosophila melanogaster	137-142
12571358-10	2003	We also found that dSir2 mediates the formation of a nuclease-resistant fast-sedimenting histone-DNA complex in an NAD-dependent manner.	NAD	115-118	Sirtuin 1	Drosophila melanogaster	19-24
12517959-5	2003	Overexpression of EGR-1 induces down-regulation of copper-zinc superoxide dismutase and manganese superoxide dismutase and stimulates the generation of reactive oxygen species (ROS) via the NADH/NADPH-oxidase system.	NAD	190-194	early growth response 1	Homo sapiens	18-23
15206738-2	2003	The breaks induce DNA repair involving the activation of poly(ADP-ribose) polymerase (PARP), which uses NAD+ as a substrate.	NAD	104-108	poly (ADP-ribose) polymerase 1	Rattus norvegicus	57-84
15206738-2	2003	The breaks induce DNA repair involving the activation of poly(ADP-ribose) polymerase (PARP), which uses NAD+ as a substrate.	NAD	104-108	poly (ADP-ribose) polymerase 1	Rattus norvegicus	86-90
15206738-5	2003	We subsequently proposed that maintenance of the NAD+ level is essential for the synthesis and secretion of insulin, and presented a unifying model for beta-cell damage and its prevention (The Okamoto model), in which PARP activation plays an essential role.	NAD	49-53	poly (ADP-ribose) polymerase 1	Rattus norvegicus	218-222
12381719-7	2002	Both proteins were 2-3-fold more active than wild-type reductase with NADH in reconstitution assays with cytochrome P-450 1A2 and with squalene monooxygenase.	NAD	70-74	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	105-125
12445818-6	2002	We found that HOBIT human osteoblastic cells, which are known to express ADP-ribosyl cyclase/CD38 activity, respond to micromolar concentrations of extracellular NAD(+) with oscillatory increases of the cytosolic Ca(2+) concentration.	NAD	162-168	CD38 molecule	Homo sapiens	93-97
12460669-0	2002	Transmembrane topology of the NuoL, M and N subunits of NADH:quinone oxidoreductase and their homologues among membrane-bound hydrogenases and bona fide antiporters.	NAD	56-60	crystallin zeta	Homo sapiens	61-83
12460669-1	2002	Nicotinamide adenine dinucleotide-reduced form (NADH):quinone oxidoreductase (respiratory Complex I), F420H2 oxidoreductase and complex, membrane-bound NiFe-hydrogenase contain protein subunits homologous to a certain type of bona fide antiporters.	NAD	0-33	crystallin zeta	Homo sapiens	54-76
12460669-1	2002	Nicotinamide adenine dinucleotide-reduced form (NADH):quinone oxidoreductase (respiratory Complex I), F420H2 oxidoreductase and complex, membrane-bound NiFe-hydrogenase contain protein subunits homologous to a certain type of bona fide antiporters.	NAD	48-52	crystallin zeta	Homo sapiens	54-76
12450807-5	2002	Both NADH and NADPH were effective as electron donors for His-tagged CarAd.	NAD	5-9	carAd	Pseudomonas resinovorans	69-74
12450807-6	2002	However, since the k(cat)/K(m) for NADH is 22.3-fold higher than that for NADPH in the 2,6-dichlorophenolindophenol reductase assay, NADH was supposed to be the physiological electron donor of CarAd.	NAD	35-39	carAd	Pseudomonas resinovorans	193-198
12450807-6	2002	However, since the k(cat)/K(m) for NADH is 22.3-fold higher than that for NADPH in the 2,6-dichlorophenolindophenol reductase assay, NADH was supposed to be the physiological electron donor of CarAd.	NAD	133-137	carAd	Pseudomonas resinovorans	193-198
12450807-7	2002	In the presence of NADH, His-tagged CarAc was reduced by His-tagged CarAd.	NAD	19-23	carAd	Pseudomonas resinovorans	68-73
12411406-2	2002	In the presence of genotoxic stress poly(ADP-ribose) polymerase-1 (PARP-1) leads to NAD(+) and ATP depletion, participating in the pathogenesis of several disorders including inflammation.	NAD	84-90	poly (ADP-ribose) polymerase 1	Rattus norvegicus	36-65
12411406-2	2002	In the presence of genotoxic stress poly(ADP-ribose) polymerase-1 (PARP-1) leads to NAD(+) and ATP depletion, participating in the pathogenesis of several disorders including inflammation.	NAD	84-90	poly (ADP-ribose) polymerase 1	Rattus norvegicus	67-73
12467981-0	2002	Role of dihydrolipoyl dehydrogenase (E3) and a novel E3-binding protein in the NADH sensitivity of the pyruvate dehydrogenase complex from anaerobic mitochondria of the parasitic nematode, Ascaris suum.	NAD	79-83	epididymal protein 3B	Rattus norvegicus	37-39
12467981-0	2002	Role of dihydrolipoyl dehydrogenase (E3) and a novel E3-binding protein in the NADH sensitivity of the pyruvate dehydrogenase complex from anaerobic mitochondria of the parasitic nematode, Ascaris suum.	NAD	79-83	epididymal protein 3B	Rattus norvegicus	53-55
12467981-3	2002	Therefore, we have cloned cDNAs encoding E3 and a novel anaerobic-specific E3-binding protein (E3BP) that lacks the terminal lipoyl domain found in E3BPs from yeast and mammals, and functionally expressed E3 and E3 mutants designed to have decreased dimer stability on the assumption that the binding of E3 to an anaerobic-specific E3BP might stabilize the E3 dimer interface and decrease E3 sensitivity to NADH inhibition.	NAD	407-411	epididymal protein 3B	Rattus norvegicus	41-43
12467981-3	2002	Therefore, we have cloned cDNAs encoding E3 and a novel anaerobic-specific E3-binding protein (E3BP) that lacks the terminal lipoyl domain found in E3BPs from yeast and mammals, and functionally expressed E3 and E3 mutants designed to have decreased dimer stability on the assumption that the binding of E3 to an anaerobic-specific E3BP might stabilize the E3 dimer interface and decrease E3 sensitivity to NADH inhibition.	NAD	407-411	epididymal protein 3B	Rattus norvegicus	75-77
12467981-3	2002	Therefore, we have cloned cDNAs encoding E3 and a novel anaerobic-specific E3-binding protein (E3BP) that lacks the terminal lipoyl domain found in E3BPs from yeast and mammals, and functionally expressed E3 and E3 mutants designed to have decreased dimer stability on the assumption that the binding of E3 to an anaerobic-specific E3BP might stabilize the E3 dimer interface and decrease E3 sensitivity to NADH inhibition.	NAD	407-411	epididymal protein 3B	Rattus norvegicus	75-77
12467981-3	2002	Therefore, we have cloned cDNAs encoding E3 and a novel anaerobic-specific E3-binding protein (E3BP) that lacks the terminal lipoyl domain found in E3BPs from yeast and mammals, and functionally expressed E3 and E3 mutants designed to have decreased dimer stability on the assumption that the binding of E3 to an anaerobic-specific E3BP might stabilize the E3 dimer interface and decrease E3 sensitivity to NADH inhibition.	NAD	407-411	epididymal protein 3B	Rattus norvegicus	75-77
12467981-3	2002	Therefore, we have cloned cDNAs encoding E3 and a novel anaerobic-specific E3-binding protein (E3BP) that lacks the terminal lipoyl domain found in E3BPs from yeast and mammals, and functionally expressed E3 and E3 mutants designed to have decreased dimer stability on the assumption that the binding of E3 to an anaerobic-specific E3BP might stabilize the E3 dimer interface and decrease E3 sensitivity to NADH inhibition.	NAD	407-411	epididymal protein 3B	Rattus norvegicus	75-77
12467981-3	2002	Therefore, we have cloned cDNAs encoding E3 and a novel anaerobic-specific E3-binding protein (E3BP) that lacks the terminal lipoyl domain found in E3BPs from yeast and mammals, and functionally expressed E3 and E3 mutants designed to have decreased dimer stability on the assumption that the binding of E3 to an anaerobic-specific E3BP might stabilize the E3 dimer interface and decrease E3 sensitivity to NADH inhibition.	NAD	407-411	epididymal protein 3B	Rattus norvegicus	75-77
12467981-3	2002	Therefore, we have cloned cDNAs encoding E3 and a novel anaerobic-specific E3-binding protein (E3BP) that lacks the terminal lipoyl domain found in E3BPs from yeast and mammals, and functionally expressed E3 and E3 mutants designed to have decreased dimer stability on the assumption that the binding of E3 to an anaerobic-specific E3BP might stabilize the E3 dimer interface and decrease E3 sensitivity to NADH inhibition.	NAD	407-411	epididymal protein 3B	Rattus norvegicus	75-77
12467981-4	2002	As predicted, the mutants exhibited decreased thermal stability, increased sensitivity to NADH and the binding of E3(Y18F) to the E3-depleted core of the pig heart PDC increased E3 activity and decreased E3 sensitivity to NADH inhibition.	NAD	222-226	epididymal protein 3B	Rattus norvegicus	114-116
12467981-4	2002	As predicted, the mutants exhibited decreased thermal stability, increased sensitivity to NADH and the binding of E3(Y18F) to the E3-depleted core of the pig heart PDC increased E3 activity and decreased E3 sensitivity to NADH inhibition.	NAD	222-226	epididymal protein 3B	Rattus norvegicus	130-132
12467981-4	2002	As predicted, the mutants exhibited decreased thermal stability, increased sensitivity to NADH and the binding of E3(Y18F) to the E3-depleted core of the pig heart PDC increased E3 activity and decreased E3 sensitivity to NADH inhibition.	NAD	222-226	epididymal protein 3B	Rattus norvegicus	130-132
12467981-4	2002	As predicted, the mutants exhibited decreased thermal stability, increased sensitivity to NADH and the binding of E3(Y18F) to the E3-depleted core of the pig heart PDC increased E3 activity and decreased E3 sensitivity to NADH inhibition.	NAD	222-226	epididymal protein 3B	Rattus norvegicus	130-132
12467981-5	2002	However, although the free A. suum E3 was less sensitive to NADH inhibition than the pig heart E3, both E3s were significantly more sensitive to NADH inhibition when assayed with dihydrolipoamide than their corresponding PDCs assayed with pyruvate.	NAD	60-64	epididymal protein 3B	Rattus norvegicus	35-37
12361715-2	2002	Specific removal of factor B from well-coupled bovine heart submitochondrial particles (SMP) results in uncoupling and the loss of ATP-driven membrane potential formation and reverse electron transfer from succinate to NAD.	NAD	219-222	distal membrane arm assembly component 2 like	Bos taurus	20-28
12183365-1	2002	Poly(ADP-ribose) polymerase (PARP) is a major NAD-dependent modifying enzyme that mediates important steps in DNA repair, transcription, and apoptosis, but its role during development is poorly understood.	NAD	46-49	Poly-(ADP-ribose) polymerase	Drosophila melanogaster	0-27
12086602-1	2002	Yeast SIR2 is a NAD+-dependent histone deacetylase required for heterochromatic silencing at telomeres, rDNA, and mating-type loci.	NAD	16-19	Sirtuin 1	Drosophila melanogaster	6-10
11935028-1	2002	The conserved Sir2 family of proteins has protein deacetylase activity that is dependent on NAD (the oxidized form of nicotinamide adenine dinucleotide).	NAD	92-95	sirtuin 2	Homo sapiens	14-18
11935028-1	2002	The conserved Sir2 family of proteins has protein deacetylase activity that is dependent on NAD (the oxidized form of nicotinamide adenine dinucleotide).	NAD	118-151	sirtuin 2	Homo sapiens	14-18
11901108-2	2002	Mutations in the NAD(+) salvage gene NPT1 weaken all three forms of silencing and also cause a reduction in the intracellular NAD(+) level.	NAD	17-23	nicotinate phosphoribosyltransferase	Saccharomyces cerevisiae S288C	37-41
11901108-2	2002	Mutations in the NAD(+) salvage gene NPT1 weaken all three forms of silencing and also cause a reduction in the intracellular NAD(+) level.	NAD	126-132	nicotinate phosphoribosyltransferase	Saccharomyces cerevisiae S288C	37-41
11901108-8	2002	In contrast, Myc-tagged Npt1p was highly concentrated in the nucleus in approximately 40% of the cells, indicating that NAD(+) salvage occurs in the nucleus in a significant fraction of cells.	NAD	120-126	nicotinate phosphoribosyltransferase	Saccharomyces cerevisiae S288C	24-29
11901108-9	2002	We propose a model in which two components of the NAD(+) salvage pathway, Pnc1p and Npt1p, function together in recycling the nuclear nicotinamide generated by Sir2p deacetylase activity back into NAD(+).	NAD	50-56	nicotinate phosphoribosyltransferase	Saccharomyces cerevisiae S288C	84-89
11901108-9	2002	We propose a model in which two components of the NAD(+) salvage pathway, Pnc1p and Npt1p, function together in recycling the nuclear nicotinamide generated by Sir2p deacetylase activity back into NAD(+).	NAD	197-203	nicotinate phosphoribosyltransferase	Saccharomyces cerevisiae S288C	84-89
11875050-15	2002	Several classes of drugs are known to affect IMPDH isoenzymes, including nucleotide and NAD analogs, suggesting that small-molecule therapy may be available, one day, for RP10 patients.	NAD	88-91	inosine monophosphate dehydrogenase 1	Homo sapiens	171-175
11942325-8	2002	O2- at the concentration of 18 micromol/l NADH and 4 micromol/l PMS can downregulate EGF and EGF mRNA expression.	NAD	42-46	epidermal growth factor	Homo sapiens	85-88
11942325-8	2002	O2- at the concentration of 18 micromol/l NADH and 4 micromol/l PMS can downregulate EGF and EGF mRNA expression.	NAD	42-46	epidermal growth factor	Homo sapiens	93-96
11788419-3	2002	The goal of the present study was to examine the effects of NADH and NADPH that are commonly used to stimulate NAD(P)H oxidase activity, on superoxide levels and cerebral vascular tone.	NAD	60-64	NADPH oxidase 1	Oryctolagus cuniculus	111-126
11788419-11	2002	These data suggest that NADH- and NADPH-induced changes in cerebral vascular tone are mediated by superoxide, produced by a flavin-containing enzyme, most likely NAD(P)H oxidase, but not xanthine oxidase or nitric oxide synthase.	NAD	24-28	NADPH oxidase 1	Oryctolagus cuniculus	162-177
11999706-2	2002	An excessive PARP activation may result in a depletion of intracellular NAD+ and ATP, hence cell suffering and, ultimately, cell death.	NAD	72-76	poly (ADP-ribose) polymerase 1	Rattus norvegicus	13-17
11562373-3	2001	The GDH2-encoded NAD(+)-dependent glutamate dehydrogenase degrades glutamate producing ammonium and alpha-ketoglutarate.	NAD	17-23	glutamate dehydrogenase (NAD(+))	Saccharomyces cerevisiae S288C	4-8
11696370-2	2001	We observed (i) NAD-dependent enzyme activity and mRNA for 11beta-HSD2, but not 11beta-HSD1, (ii) increasing 11beta-HSD2 activity with increasing degree of differentiation and (iii) a concentration-dependent down-regulation by TNF-alpha, phorbol myristate acetate (PMA) or glucose of activity and mRNA of 11beta-HSD2.	NAD	16-19	hydroxysteroid 11-beta dehydrogenase 2	Homo sapiens	59-70
11604236-4	2001	Ishikawa cells contain an NAD dependent enzyme migrating at 41 kDa on Western blots, consistent with the presence of the glucocorticoid-inactivating enzyme 11 beta HSD2, while the NADP dependent 11 beta HSD1 is barely detectable.	NAD	26-29	hydroxysteroid 11-beta dehydrogenase 2	Homo sapiens	121-168
11606183-4	2001	The enhanced poly(ADP-ribose) polymerase activity observed in PC12 cells was paralleled by a significant decline in NAD+ content and both events were prevented by treatments suppressing formation of peroxynitrite.	NAD	116-120	poly (ADP-ribose) polymerase 1	Rattus norvegicus	13-40
11513738-2	2001	CD38 is endowed with two different activities: it is a signal transduction molecule and an ectoenzyme that converts NAD(+) into ADP-ribose (NAD(+) glycohydrolase activity) and small proportions of cADP-ribose (cADPR; ADP-ribosyl cyclase activity), a calcium-mobilizing metabolite, which, ultimately, can also be hydrolysed (cADPR hydrolase activity).	NAD	116-122	CD38 molecule	Homo sapiens	0-4
11513738-4	2001	In the present study we wanted to test whether the CD38-cADPR complex is kinetically competent in the conversion of NAD(+) into the reaction product ADP-ribose.	NAD	116-122	CD38 molecule	Homo sapiens	51-55
11513738-6	2001	Analysis of the kinetic parameters measured for the CD38/NAD(+) glycohydrolase-catalysed hydrolysis of 2"-deoxy-2"-aminoribo-NAD(+) and ADP-cyclo[N1,C1"]-2"-deoxy-2"-aminoribose (slowly hydrolysable analogues of NAD(+) and cADPR respectively) ruled out that the CD38-cADPR complex can accumulate under steady-state conditions.	NAD	57-63	CD38 molecule	Homo sapiens	52-56
11513738-6	2001	Analysis of the kinetic parameters measured for the CD38/NAD(+) glycohydrolase-catalysed hydrolysis of 2"-deoxy-2"-aminoribo-NAD(+) and ADP-cyclo[N1,C1"]-2"-deoxy-2"-aminoribose (slowly hydrolysable analogues of NAD(+) and cADPR respectively) ruled out that the CD38-cADPR complex can accumulate under steady-state conditions.	NAD	57-63	CD38 molecule	Homo sapiens	262-266
11513738-12	2001	267, 3056-3064], we believe that the Michaelis CD38-NAD(+) complex could play such a role instead.	NAD	52-58	CD38 molecule	Homo sapiens	47-51
11488932-2	2001	The enzyme was a hexamer consisting of 30 kDa subunits and utilized ATP or other nucleoside triphosphates as phosphoryl donors for the phosphorylation of NAD, most efficiently at pH 7.5 and 60 degrees C. The enzyme could not use inorganic polyphosphates as phosphoryl donors and was designated as ATP-NAD kinase.	NAD	154-157	NAD kinase	Escherichia coli str. K-12 substr. MG1655	301-311
11427894-2	2001	The 1.7 A crystal structure of the 323 amino acid catalytic core of human SIRT2, a homolog of yeast Sir2, reveals an NAD-binding domain, which is a variant of the Rossmann fold, and a smaller domain composed of a helical module and a zinc-binding module.	NAD	117-120	sirtuin 2	Homo sapiens	74-79
11350929-5	2001	Purified GDH was ADP-ribosylated in a cysteine residue in the presence of the mitochondrial activity that transferred the ADP-ribose from NAD+ onto the acceptor site.	NAD	138-142	glutamate dehydrogenase 1	Homo sapiens	9-12
11250901-5	2001	Consistent with acetylation of TIF-IB/SL1 being required for rDNA transcription, the NAD(+)-dependent histone deacetylase mSir2a deacetylates TAF(I)68 and represses Pol I transcription.	NAD	85-91	sirtuin 1	Mus musculus	122-128
11568445-3	2001	The GPX1 protection was associated with attenuation of NADPH and NADH oxidation, protein carbonyl and F(2)-isoprostanes formation, and alanine transaminase release in various tissues, and was irreplaceable by high levels of dietary vitamin E or other selenoproteins.	NAD	65-69	glutathione peroxidase 1	Mus musculus	4-8
11501263-4	2001	However, for several pathological situations, which include massive DNA injury (brain ischemia for example), excessive activation of PARP can deplete stores of nicotinamide adenine dinucleotide (NAD+), the PARP substrate, which, with the subsequent ATP depletion, leads to cell death.	NAD	160-193	poly (ADP-ribose) polymerase 1	Rattus norvegicus	206-210
11501263-4	2001	However, for several pathological situations, which include massive DNA injury (brain ischemia for example), excessive activation of PARP can deplete stores of nicotinamide adenine dinucleotide (NAD+), the PARP substrate, which, with the subsequent ATP depletion, leads to cell death.	NAD	195-199	poly (ADP-ribose) polymerase 1	Rattus norvegicus	133-137
11104695-1	2000	Deoxyhypusine synthase catalyses the NAD-dependent transfer of the butylamine moiety from the polyamine, spermidine, to a specific lysine residue of a single cellular protein, eukaryotic translation-initiation factor 5A (eIF5A) precursor.	NAD	37-40	eukaryotic translation initiation factor 5A	Homo sapiens	176-219
11104695-1	2000	Deoxyhypusine synthase catalyses the NAD-dependent transfer of the butylamine moiety from the polyamine, spermidine, to a specific lysine residue of a single cellular protein, eukaryotic translation-initiation factor 5A (eIF5A) precursor.	NAD	37-40	eukaryotic translation initiation factor 5A	Homo sapiens	221-226
11104695-6	2000	Although [(3)H]NAD binding to the enzyme occurred in the absence of spermidine, its affinity for the enzyme was markedly enhanced by spermidine, GC(7) and also by the eIF5A precursor.	NAD	15-18	eukaryotic translation initiation factor 5A	Homo sapiens	167-172
11104695-8	2000	The dependence of spermidine binding on NAD and the modulation of binding of NAD by spermidine and the eIF5A precursor suggest intricate relationships between the binding of cofactor and the substrates, and provide new insights into the reaction mechanism.	NAD	40-43	eukaryotic translation initiation factor 5A	Homo sapiens	103-108
11104695-8	2000	The dependence of spermidine binding on NAD and the modulation of binding of NAD by spermidine and the eIF5A precursor suggest intricate relationships between the binding of cofactor and the substrates, and provide new insights into the reaction mechanism.	NAD	77-80	eukaryotic translation initiation factor 5A	Homo sapiens	103-108
11123803-1	2000	Plant cytochrome b5 reductases (b5R) are assumed to be part of an ER-associated redox chain that oxidizes NADH to provide electrons via cytochrome b5 (cyt b5) to ER-associated fatty acyl desaturase and related hydroxylases, as in mammalian cells.	NAD	106-110	cytochrome b5 type A	Homo sapiens	6-19
11123803-1	2000	Plant cytochrome b5 reductases (b5R) are assumed to be part of an ER-associated redox chain that oxidizes NADH to provide electrons via cytochrome b5 (cyt b5) to ER-associated fatty acyl desaturase and related hydroxylases, as in mammalian cells.	NAD	106-110	cytochrome b5 type A	Homo sapiens	136-149
11123803-1	2000	Plant cytochrome b5 reductases (b5R) are assumed to be part of an ER-associated redox chain that oxidizes NADH to provide electrons via cytochrome b5 (cyt b5) to ER-associated fatty acyl desaturase and related hydroxylases, as in mammalian cells.	NAD	106-110	cytochrome b5 type A	Homo sapiens	151-157
10933785-3	2000	A rapid two-step affinity purification yields active HH-Histag-BDH (and six mutants) with high specific activity ( approximately 130 micromol of NAD(+) reduced.min(-1).mg(-1)).	NAD	145-151	3-hydroxybutyrate dehydrogenase 1	Homo sapiens	63-66
10933785-5	2000	The HH-Histag-BDH-PC complex (and HH-BDH derived therefrom by enterokinase cleavage) has apparent Michaelis constants (K(m) values) for NAD(+), NADH, (R)-3-hydroxybutyrate (HOB), and acetoacetate (AcAc) similar to those for bovine heart or rat liver BDH.	NAD	136-142	3-hydroxybutyrate dehydrogenase 1	Homo sapiens	14-17
10933785-5	2000	The HH-Histag-BDH-PC complex (and HH-BDH derived therefrom by enterokinase cleavage) has apparent Michaelis constants (K(m) values) for NAD(+), NADH, (R)-3-hydroxybutyrate (HOB), and acetoacetate (AcAc) similar to those for bovine heart or rat liver BDH.	NAD	136-142	3-hydroxybutyrate dehydrogenase 1	Homo sapiens	37-40
10777496-5	2000	During the exposure of activated T cells to NAD, the CD38 is modified by ecto-mono-ADP-ribosyltransferases (ecto-mono-ADPRTs) specific for cysteine and arginine residues.	NAD	44-47	CD38 molecule	Homo sapiens	53-57
10841563-4	2000	The yeast NPT1 gene, encoding an important NAD(+) synthesis enzyme, is required for rDNA and telomeric silencing and contributes to silencing of the HM loci.	NAD	43-49	nicotinate phosphoribosyltransferase	Saccharomyces cerevisiae S288C	10-14
10887283-3	2000	A significant part of the activity of nuclear NMN-adenylyltransferase, a key enzyme for biosynthesis of NAD (the substrate of poly(ADP-ribose)-polymerase), has been found in the nuclear matrix.	NAD	104-107	poly (ADP-ribose) polymerase 1	Rattus norvegicus	126-153
10734052-7	2000	Upon addition of the eIF5A precursor, utilization of the enzyme-bound NADH for reduction of the eIF5A-imine intermediate to deoxyhypusine was reflected by a rapid decrease in the NADH fluorescence, indicating a transient hydride transfer mechanism as an integral part of the reaction.	NAD	70-74	eukaryotic translation initiation factor 5A	Homo sapiens	21-26
10734052-7	2000	Upon addition of the eIF5A precursor, utilization of the enzyme-bound NADH for reduction of the eIF5A-imine intermediate to deoxyhypusine was reflected by a rapid decrease in the NADH fluorescence, indicating a transient hydride transfer mechanism as an integral part of the reaction.	NAD	70-74	eukaryotic translation initiation factor 5A	Homo sapiens	96-101
10734052-7	2000	Upon addition of the eIF5A precursor, utilization of the enzyme-bound NADH for reduction of the eIF5A-imine intermediate to deoxyhypusine was reflected by a rapid decrease in the NADH fluorescence, indicating a transient hydride transfer mechanism as an integral part of the reaction.	NAD	179-183	eukaryotic translation initiation factor 5A	Homo sapiens	21-26
10734052-7	2000	Upon addition of the eIF5A precursor, utilization of the enzyme-bound NADH for reduction of the eIF5A-imine intermediate to deoxyhypusine was reflected by a rapid decrease in the NADH fluorescence, indicating a transient hydride transfer mechanism as an integral part of the reaction.	NAD	179-183	eukaryotic translation initiation factor 5A	Homo sapiens	96-101
10734052-8	2000	The number of NADH molecules bound approached four/enzyme tetramer; not all of the bound NADH was available for reduction of the eIF5A-imine intermediate.	NAD	14-18	eukaryotic translation initiation factor 5A	Homo sapiens	129-134
10734052-8	2000	The number of NADH molecules bound approached four/enzyme tetramer; not all of the bound NADH was available for reduction of the eIF5A-imine intermediate.	NAD	89-93	eukaryotic translation initiation factor 5A	Homo sapiens	129-134
10739349-4	2000	GDH activity was NAD-dependent in some psychrophilic strains.	NAD	17-20	glutamate dehydrogenase 1	Homo sapiens	0-3
10601238-1	1999	To understand the interactions and functional role of each of the three mitochondrial NAD(+)-dependent isocitrate dehydrogenase (IDH) subunits (alpha, beta, and gamma), we have characterized human cDNAs encoding two beta isoforms (beta(1) and beta(2)) and the gamma subunit.	NAD	86-92	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	129-132
10607407-2	1999	The inactivation was partially prevented by preincubation of the GDH isoproteins with 2-oxoglutarate or NADH.	NAD	104-108	glutamate dehydrogenase 1	Homo sapiens	65-68
10580118-1	1999	Low (C(1/2) = 1.5 x 10(-7) M) concentrations of horse cytochrome c strongly inhibit H(2)O(2) production by rat heart mitochondria under conditions of reverse electron transfer from succinate to NAD(+).	NAD	194-200	cytochrome c, somatic	Equus caballus	54-66
10559215-3	1999	Moreover, in both organs the major NAD(+)-dependent retinaldehyde activity copurified with the propionaldehyde and octanaldehyde activities; in both organs the major NAD(+)-dependent retinaldehyde activity was associated with the E1 isozyme (coded for by aldh1 gene) of human aldehyde dehydrogenase.	NAD	166-172	aldehyde dehydrogenase 1 family member A1	Homo sapiens	255-260
10569643-10	1999	Ischemia-reperfusion by ROS overproduction and increasing DNA breaks activates PARP leading to accelerated NAD+ catabolism, impaired energy metabolism, and cell damage.	NAD	107-111	poly (ADP-ribose) polymerase 1	Rattus norvegicus	79-83
10637772-5	1999	Rat blood also exhibited the carbonyl reductase activity in the presence of NADH or NADPH, but to a lesser extent.	NAD	76-80	dehydrogenase/reductase 4	Rattus norvegicus	29-47
10555195-7	1999	While monitoring the various parameters until complete recovery was reached, we found high correlation between the CBF and the NADH during occlusion as well as during the reperfusion period.	NAD	127-131	CCAAT enhancer binding protein zeta	Homo sapiens	115-118
10477767-1	1999	The multifunctional ADP-ribosyl cyclase, CD38, catalyzes the cyclization of NAD(+) to cyclic ADP-ribose (cADPr).	NAD	76-82	CD38 molecule	Homo sapiens	41-45
10477767-7	1999	The ADP-ribosyl cyclase activity of osteoclastic CD38 was next demonstrated by its ability to cyclize the NAD(+) surrogate, NGD(+), to its fluorescent derivative cGDP-ribose.	NAD	106-112	CD38 molecule	Homo sapiens	49-53
10477767-9	1999	CD38 activation by an agonist antibody (A10) in the presence of substrate (NAD(+)) triggered a cytosolic Ca(2+) signal.	NAD	75-81	CD38 molecule	Homo sapiens	0-4
11228745-5	1999	In VSMC transfected with antisense p22phox to attenuate NADH/NADPH oxidase expression, arachidonic acid is unable to stimulate NADH/NADPH-dependent superoxide production.	NAD	56-60	calcineurin like EF-hand protein 1	Homo sapiens	35-38
10383895-2	1999	We speculate that other loci that determine response to oxidative stress, such as NAD(H):quinone oxidoreductase (NQO1) are candidates.	NAD	82-88	crystallin zeta	Homo sapiens	89-111
10387934-7	1999	These data suggested that regulation of the key enzymes in the Trp-NAD+ pathway was associated with PPAR-alpha directly or indirectly, and as a consequence the hepatic NAD+ was increased by PPs.	NAD	67-71	peroxisome proliferator activated receptor alpha	Rattus norvegicus	100-110
10387934-7	1999	These data suggested that regulation of the key enzymes in the Trp-NAD+ pathway was associated with PPAR-alpha directly or indirectly, and as a consequence the hepatic NAD+ was increased by PPs.	NAD	168-172	peroxisome proliferator activated receptor alpha	Rattus norvegicus	100-110
10334203-5	1999	Using 32P-5"-end-labeled DNA fragments obtained from human p53 tumor suppressor gene and c-Ha-ras-1 protooncogene, we showed that PBQ plus NADH, and also PHQ, induced DNA damage frequently at thymine residues, in the presence of Cu(II).	NAD	139-143	HRas proto-oncogene, GTPase	Homo sapiens	89-99
10199955-2	1999	Upon DNA damage PARP binds to DNA strand breaks and transfers ADP-ribose residues from NAD+ to acceptor proteins and to ADP-ribosyl protein adducts.	NAD	87-91	Poly-(ADP-ribose) polymerase	Drosophila melanogaster	16-20
10068448-3	1999	A recent study has revealed that CD38 in Namalwa B cells undergoes internalization upon exposure to external NAD+.	NAD	109-113	CD38 molecule	Homo sapiens	33-37
10068454-6	1999	Second, incubation of assembled desmin filaments with mono-ADP-ribosyltransferase and NAD+ results in disassembly of the filaments.	NAD	86-90	desmin	Homo sapiens	32-38
9973315-0	1999	Ligand-induced internalization of CD38 results in intracellular Ca2+ mobilization: role of NAD+ transport across cell membranes.	NAD	91-95	CD38 molecule	Homo sapiens	34-38
9973315-5	1999	Moreover, CD38 was reported to undergo a selective and extensive internalization through non clathrin-coated endocytotic vesicles upon incubating CD38(+) cells with either NAD+ or thiol compounds: these endocytotic vesicles can convert cytosolic NAD into cADPR despite an asymmetric unfavorable orientation that makes the active site of CD38 intravesicular.	NAD	172-176	CD38 molecule	Homo sapiens	10-14
9973315-5	1999	Moreover, CD38 was reported to undergo a selective and extensive internalization through non clathrin-coated endocytotic vesicles upon incubating CD38(+) cells with either NAD+ or thiol compounds: these endocytotic vesicles can convert cytosolic NAD into cADPR despite an asymmetric unfavorable orientation that makes the active site of CD38 intravesicular.	NAD	172-175	CD38 molecule	Homo sapiens	10-14
9973315-8	1999	This unknown intracellular trafficking of NAD+ and cADPR based on two distinctive and specific transmembrane carriers for either nucleotide can affect the intracellular calcium homeostasis in CD38(+) cells.	NAD	42-46	CD38 molecule	Homo sapiens	192-196
10721074-4	1999	The results strongly suggest that the hepatic NAD increase might be caused by transcription of genes coding the key enzymes of the Trp-NAD pathway via PPAR.	NAD	46-49	peroxisome proliferator activated receptor alpha	Rattus norvegicus	151-155
10721074-4	1999	The results strongly suggest that the hepatic NAD increase might be caused by transcription of genes coding the key enzymes of the Trp-NAD pathway via PPAR.	NAD	135-138	peroxisome proliferator activated receptor alpha	Rattus norvegicus	151-155
10432444-2	1999	CD38 is a member of an emerging family of cytosolic and membrane-bound enzymes whose substrate is nicotinamide adenine dinucleotide (NAD), a coenzyme ubiquitously distributed in nature.	NAD	98-131	CD38 molecule	Homo sapiens	0-4
10432444-2	1999	CD38 is a member of an emerging family of cytosolic and membrane-bound enzymes whose substrate is nicotinamide adenine dinucleotide (NAD), a coenzyme ubiquitously distributed in nature.	NAD	133-136	CD38 molecule	Homo sapiens	0-4
9794804-0	1998	Inhibition of the intrinsic NAD+ glycohydrolase activity of CD38 by carbocyclic NAD analogues.	NAD	28-31	CD38 molecule	Homo sapiens	60-64
9806760-10	1998	Likewise, CD38-reconstituted proteoliposomes were active in concentrating NAD+ (NGD+) -derived cADPR (cGDPR) inside the vesicle compartment.	NAD	74-78	CD38 molecule	Homo sapiens	10-14
9806760-13	1998	In CD38 sense- but not in antisense-transfected HeLa cells, externally added NAD+ resulted in significant, transient increases in cytosolic calcium.	NAD	77-81	CD38 molecule	Homo sapiens	3-7
9744810-1	1998	CD38, a type II transmembrane glycoprotein, behaves as a catalytically active transporter responsible for ectocellular generation of cyclic ADP-ribose (cADPR) from NAD+ and for subsequent influx of cADPR across membranes [Franco, L., Guida, L., Bruzzone, S., Zocchi, E., Usai, C. and De Flora, A.	NAD	164-168	CD38 molecule	Homo sapiens	0-4
9675145-6	1998	Stimulation of vessels with NADH (200 microM) increased CLA enhanced chemiluminescence, which was inhibited by low concentrations of superoxide dismutase (20U/ml).	NAD	28-32	selectin P ligand	Homo sapiens	56-59
9723880-2	1998	The results demonstrated a predominant expression of the NAD-dependent dehydrogenase isoform (11beta-HSD2) over the NADP-dependent oxoreductase (11beta-HSD1).	NAD	57-60	hydroxysteroid 11-beta dehydrogenase 2	Homo sapiens	94-105
9741047-0	1998	Rat testis mitochondrial aldehyde dehydrogenase: kinetic evidence for a direct reaction between capronaldehyde and enzyme-bound NAD+ in the presence of Mg2+ ions.	NAD	128-132	aldehyde dehydrogenase 2 family member	Rattus norvegicus	11-47
9654134-1	1998	The effect of platelet stimulation on the subcellular localization of CD38, a membrane glycoprotein that catalyses the synthesis of cyclic ADP-ribose from beta-NAD+ was investigated.	NAD	155-164	CD38 molecule	Homo sapiens	70-74
9605319-7	1998	Michaelis constants for NADPH, NADH, and pyruvate, of approximately 3.5 microM, 19.0 microM, and 1.5 mM, respectively, were comparable to those reported for the native VanH (Bugg TDH et al., 1991, Biochemistry 30:10408-10415).	NAD	31-35	VanH protein	Enterococcus faecium	168-172
9558358-3	1998	MLCK activity was determined by measuring the rate of formation of one of the reaction products, ADP, in a coupled enzymatic assay by continuous fluorimetric monitoring of NADH removal in 100 microM CaCl2 at ionic strength 0.15 M, pH 7.0 and 21 degreesC.	NAD	172-176	myosin light chain kinase	Homo sapiens	0-4
9787766-3	1998	At pH 7.4 and 25 degrees C, the major and minor components of the E3 isozyme catalyzed the reaction with Vmax of 1.1 and 0.8 mumol NADH min-1 mg-1 protein, respectively, compared to 0.067 and 0.060 mumol NADH min-1 mg-1 protein for the E1 and E2 isozymes, respectively.	NAD	131-135	small nucleolar RNA, H/ACA box 73A	Homo sapiens	236-245
9586947-6	1998	NADH was as effective as NADPH in promoting microsomal AZT reduction, raising the possibility of cytochrome b5 (b5) involvement.	NAD	0-4	cytochrome b5 type A	Homo sapiens	97-110
9586947-8	1998	Upon reconstitution, human liver b5 plus NADH:b5 reductase and CYP2C9 plus NADPH:P450 reductase were both effective catalysts of AZT reduction, which was also supported when CYP2A6 or CYP2E1 was substituted for CYP2C9.	NAD	41-45	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	211-217
9559543-10	1998	Our results also demonstrated that of the two isoforms of NAD-dependent glycerol 3-phosphate dehydrogenase, only the enzyme encoded by GPD1 appeared important for the shuttle, since the enhanced glycerol production that occurs in a gut2 delta strain proved dependent on GPD1 but not on GPD2.	NAD	58-61	glycerol-3-phosphate dehydrogenase (NAD(+)) GPD2	Saccharomyces cerevisiae S288C	286-290
9291187-2	1997	NAD-dependent 11beta-HSD is expressed at high levels in the distal nephron and contributes to mineralocorticoid specificity in that region.	NAD	0-3	hydroxysteroid 11-beta dehydrogenase 2	Homo sapiens	14-24
9291187-3	1997	The present studies determined whether N-glycosylation is necessary for the activity of NAD-dependent 11beta-HSD (11beta-HSD2).	NAD	88-91	hydroxysteroid 11-beta dehydrogenase 2	Homo sapiens	102-112
9291187-3	1997	The present studies determined whether N-glycosylation is necessary for the activity of NAD-dependent 11beta-HSD (11beta-HSD2).	NAD	88-91	hydroxysteroid 11-beta dehydrogenase 2	Homo sapiens	114-125
9384521-2	1997	In addition, an NADH-dependent 15-ketoprostaglandin delta13-reductase (15-PGDH) activity was determined in the brain and eye tissue of some species.	NAD	16-20	15-hydroxyprostaglandin dehydrogenase	Homo sapiens	71-78
9148900-1	1997	CD38, a lymphocyte differentiation antigen, is also a bifunctional enzyme catalyzing the synthesis of cyclic ADP-ribose (cADPR) from NAD+ and its hydrolysis to ADP-ribose (ADPR).	NAD	133-137	CD38 molecule	Homo sapiens	0-4
9148900-2	1997	An additional enzymatic activity of CD38 shared by monofunctional ADP-ribosyl cyclase from Aplysia californica is the exchange of the base group of NAD+ (nicotinamide) with various nucleophiles.	NAD	148-152	CD38 molecule	Homo sapiens	36-40
9148900-3	1997	Both human CD38 (either recombinant or purified from erythrocyte membranes) and Aplysia cyclase were found to catalyze the exchange of ADPR with the nicotinamide group of NAD+ leading to the formation of a dimeric ADPR ((ADPR)2).	NAD	171-175	CD38 molecule	Homo sapiens	11-15
9148900-4	1997	The dimeric structure of the enzymatic product, which was generated by recombinant CD38 and by CD38(+) Namalwa cells from as low as 10 microM NAD+, was demonstrated using specific enzyme treatments (dinucleotide pyrophosphatase and 5"-nucleotidase) and mass spectrometry analyses of the resulting products.	NAD	142-146	CD38 molecule	Homo sapiens	83-87
9148900-4	1997	The dimeric structure of the enzymatic product, which was generated by recombinant CD38 and by CD38(+) Namalwa cells from as low as 10 microM NAD+, was demonstrated using specific enzyme treatments (dinucleotide pyrophosphatase and 5"-nucleotidase) and mass spectrometry analyses of the resulting products.	NAD	142-146	CD38 molecule	Homo sapiens	95-99
9171333-0	1997	The two isoenzymes for yeast NAD+-dependent glycerol 3-phosphate dehydrogenase encoded by GPD1 and GPD2 have distinct roles in osmoadaptation and redox regulation.	NAD	29-33	glycerol-3-phosphate dehydrogenase (NAD(+)) GPD2	Saccharomyces cerevisiae S288C	99-103
9171333-1	1997	The two homologous genes GPD1 and GPD2 encode the isoenzymes of NAD-dependent glycerol 3-phosphate dehydrogenase in the yeast Saccharomyces cerevisiae.	NAD	64-67	glycerol-3-phosphate dehydrogenase (NAD(+)) GPD2	Saccharomyces cerevisiae S288C	34-38
9171333-11	1997	In addition, GPD2 is induced under aerobic conditions by the addition of bisulfite which causes NADH accumulation by inhibiting the final, reductive step in ethanol fermentation and this induction is reversed by addition of acetaldehyde.	NAD	96-100	glycerol-3-phosphate dehydrogenase (NAD(+)) GPD2	Saccharomyces cerevisiae S288C	13-17
18966751-3	1997	The amperometric determination is based on the electrochemical detection of NADH which is generated in the enzymatic reaction of ethanol with NAD(+) under catalysis of ADH.	NAD	142-148	aldo-keto reductase family 1 member A1	Homo sapiens	77-80
9328141-1	1997	Poly(ADP-ribose) polymerase (PADPRP), which uses NAD to synthesize ADP-ribose polymers, is activated by DNA strand breaks and mediates cellular responses to DNA damage.	NAD	49-52	poly (ADP-ribose) polymerase family, member 1	Mus musculus	0-27
9328141-1	1997	Poly(ADP-ribose) polymerase (PADPRP), which uses NAD to synthesize ADP-ribose polymers, is activated by DNA strand breaks and mediates cellular responses to DNA damage.	NAD	49-52	poly (ADP-ribose) polymerase family, member 1	Mus musculus	29-35
9328141-2	1997	The consequences of low cellular NAD levels in a cell line deficient in nicotinamide mononucleotide adenylyltransferase (NMNAT), an enzyme essential for NAD biosynthesis, were investigated by assessing NAD metabolism and DNA repair after treatment with alkylating agents.	NAD	33-36	nicotinamide nucleotide adenylyltransferase 1	Mus musculus	121-126
9328141-2	1997	The consequences of low cellular NAD levels in a cell line deficient in nicotinamide mononucleotide adenylyltransferase (NMNAT), an enzyme essential for NAD biosynthesis, were investigated by assessing NAD metabolism and DNA repair after treatment with alkylating agents.	NAD	153-156	nicotinamide nucleotide adenylyltransferase 1	Mus musculus	121-126
9328141-2	1997	The consequences of low cellular NAD levels in a cell line deficient in nicotinamide mononucleotide adenylyltransferase (NMNAT), an enzyme essential for NAD biosynthesis, were investigated by assessing NAD metabolism and DNA repair after treatment with alkylating agents.	NAD	153-156	nicotinamide nucleotide adenylyltransferase 1	Mus musculus	121-126
9328141-13	1997	These data demonstrate that modest decreases in cellular NAD levels can sensitize cells to alkylating agents and PADPRP inhibitors.	NAD	57-60	poly (ADP-ribose) polymerase family, member 1	Mus musculus	113-119
8981030-5	1997	The amount of NADH- or succinate-reducible cytochrome b in the presence of cyanide was strongly decreased, but could be recovered by the addition of antimycin.	NAD	14-18	mitochondrially encoded cytochrome b	Homo sapiens	43-55
9001360-8	1996	These results indicate that the defects in the mitochondrial NADH- and NADPH-linked aquacobalamin reductases underlie cblC and cblA disorders, respectively.	NAD	61-65	metabolism of cobalamin associated A	Homo sapiens	127-131
8917627-2	1996	The most direct tactic has been the use of immobilised analogues of the following, usually enzyme-specific substrates, e.g., lactate/pyruvate in the case of lactate dehydrogenase for which NAD+ is the leading substrate.	NAD	189-193	LDH	Bos taurus	157-178
8917627-4	1996	The locking-on strategy reverses the tactic by using the more accessible immobilised leading substrate, immobilised NAD+, as adsorbent with soluble analogues of the enzyme-specific ligands (e.g., lactate in the case of lactate dehydrogenase) providing a substantial reinforcement of biospecific adsorption sufficient to effect adsorptive selection of an enzyme from a group of enzymes such as the NAD(+)-specific enzymes.	NAD	116-120	LDH	Bos taurus	219-240
9183651-9	1996	SNP increased the amount of radioisotopic labeled glyceraldehyde-3 phosphate dehydrogenase (GAPDH) in the presence of [32P]NAD and inhibited the enzyme activity.	NAD	123-126	glyceraldehyde-3-phosphate dehydrogenase	Mus musculus	50-90
9183651-9	1996	SNP increased the amount of radioisotopic labeled glyceraldehyde-3 phosphate dehydrogenase (GAPDH) in the presence of [32P]NAD and inhibited the enzyme activity.	NAD	123-126	glyceraldehyde-3-phosphate dehydrogenase	Mus musculus	92-97
9183651-10	1996	The results suggested that SNP-induced cell death is partly due to the NO-induced inhibition of GAPDH, perhaps by stimulating the binding of NAD to GAPDH.	NAD	141-144	glyceraldehyde-3-phosphate dehydrogenase	Mus musculus	96-101
9183651-10	1996	The results suggested that SNP-induced cell death is partly due to the NO-induced inhibition of GAPDH, perhaps by stimulating the binding of NAD to GAPDH.	NAD	141-144	glyceraldehyde-3-phosphate dehydrogenase	Mus musculus	148-153
8782397-2	1996	Expression of (S)-mandelate dehydrogenase (MDH), BFDC, NAD(+)-dependent benzaldehyde dehydrogenase (BDH) and NADP(+)-dependent BDH in the MR-lacking mutant was not affected by the insertion, and it was inducible similarly to the wild type strain.	NAD	55-61	benzaldehyde dehydrogenase	Pseudomonas putida	72-98
8782397-2	1996	Expression of (S)-mandelate dehydrogenase (MDH), BFDC, NAD(+)-dependent benzaldehyde dehydrogenase (BDH) and NADP(+)-dependent BDH in the MR-lacking mutant was not affected by the insertion, and it was inducible similarly to the wild type strain.	NAD	55-61	benzaldehyde dehydrogenase	Pseudomonas putida	100-103
8665935-5	1996	Experiments carried out with purified GraP-DH or CNBr fragments of GraP-DH indicated that binding to the ICAM-1 matrix was mediated by the C-terminal domain of GraP-DH, containing the binding site of the cofactor NAD+, and that NAD+ could compete with this binding.	NAD	213-217	glyceraldehyde-3-phosphate dehydrogenase	Rattus norvegicus	67-74
8665935-5	1996	Experiments carried out with purified GraP-DH or CNBr fragments of GraP-DH indicated that binding to the ICAM-1 matrix was mediated by the C-terminal domain of GraP-DH, containing the binding site of the cofactor NAD+, and that NAD+ could compete with this binding.	NAD	213-217	intercellular adhesion molecule 1	Rattus norvegicus	105-111
8665935-5	1996	Experiments carried out with purified GraP-DH or CNBr fragments of GraP-DH indicated that binding to the ICAM-1 matrix was mediated by the C-terminal domain of GraP-DH, containing the binding site of the cofactor NAD+, and that NAD+ could compete with this binding.	NAD	213-217	glyceraldehyde-3-phosphate dehydrogenase	Rattus norvegicus	67-74
8665935-5	1996	Experiments carried out with purified GraP-DH or CNBr fragments of GraP-DH indicated that binding to the ICAM-1 matrix was mediated by the C-terminal domain of GraP-DH, containing the binding site of the cofactor NAD+, and that NAD+ could compete with this binding.	NAD	228-232	glyceraldehyde-3-phosphate dehydrogenase	Rattus norvegicus	67-74
8665935-5	1996	Experiments carried out with purified GraP-DH or CNBr fragments of GraP-DH indicated that binding to the ICAM-1 matrix was mediated by the C-terminal domain of GraP-DH, containing the binding site of the cofactor NAD+, and that NAD+ could compete with this binding.	NAD	228-232	intercellular adhesion molecule 1	Rattus norvegicus	105-111
8665935-5	1996	Experiments carried out with purified GraP-DH or CNBr fragments of GraP-DH indicated that binding to the ICAM-1 matrix was mediated by the C-terminal domain of GraP-DH, containing the binding site of the cofactor NAD+, and that NAD+ could compete with this binding.	NAD	228-232	glyceraldehyde-3-phosphate dehydrogenase	Rattus norvegicus	67-74
8665935-6	1996	Using a series of ICAM-1 C-terminal truncated peptides, we could demonstrate that (a) the nitric-oxide-induced covalent linkage of NAD+ to GraP-DH was impaired by these peptides, (b) the glycolytic activity of GraP-DH was drastically inhibited by a truncated peptide containing the 15 C-terminal residues, (c) nitric oxide appeared to prevent this inhibition.	NAD	131-135	intercellular adhesion molecule 1	Rattus norvegicus	18-24
8665935-6	1996	Using a series of ICAM-1 C-terminal truncated peptides, we could demonstrate that (a) the nitric-oxide-induced covalent linkage of NAD+ to GraP-DH was impaired by these peptides, (b) the glycolytic activity of GraP-DH was drastically inhibited by a truncated peptide containing the 15 C-terminal residues, (c) nitric oxide appeared to prevent this inhibition.	NAD	131-135	glyceraldehyde-3-phosphate dehydrogenase	Rattus norvegicus	139-146
8665935-6	1996	Using a series of ICAM-1 C-terminal truncated peptides, we could demonstrate that (a) the nitric-oxide-induced covalent linkage of NAD+ to GraP-DH was impaired by these peptides, (b) the glycolytic activity of GraP-DH was drastically inhibited by a truncated peptide containing the 15 C-terminal residues, (c) nitric oxide appeared to prevent this inhibition.	NAD	131-135	glyceraldehyde-3-phosphate dehydrogenase	Rattus norvegicus	210-217
8647136-1	1996	The NAD(P)H:flavin oxidoreductase (NADPH:riboflavin oxidoreductase) from Escherichia coli, Fre, is a monomer of 26.1 kDa, which catalyzes the reduction of free flavins by NADPH or NADH.	NAD	180-184	oxidoreductase	Escherichia coli	19-33
8647136-1	1996	The NAD(P)H:flavin oxidoreductase (NADPH:riboflavin oxidoreductase) from Escherichia coli, Fre, is a monomer of 26.1 kDa, which catalyzes the reduction of free flavins by NADPH or NADH.	NAD	180-184	oxidoreductase	Escherichia coli	52-66
8600980-14	1996	These results indicate that P-450, and to a lesser extent, cytochrome b5, play a role in the ferritin-dependent increase in formation of reactive oxygen species with either NADPH or NADH, most likely reflecting the requirement of these enzymes for microsomal production of superoxide anion.	NAD	182-186	cytochrome b5 type A	Rattus norvegicus	59-72
8604044-5	1996	Blockade of this effect by 2-deoxyglucose and inhibition of glyceraldehyde-3-phosphate dehydrogenase implicates enhanced glycolytic production of NADH in the Ca2+ stimulation.	NAD	146-150	glyceraldehyde-3-phosphate dehydrogenase	Rattus norvegicus	60-100
8604044-7	1996	These findings indicate that direct regulation of IP3R by NADH is responsible for elevated cytoplasmic [Ca2+] occurring in the earliest phase of hypoxia.	NAD	58-62	inositol 1,4,5-trisphosphate receptor, type 1	Rattus norvegicus	50-54
8567127-9	1996	This activity was also distinct from xanthine oxidoreductase and NADH-cytochrome b5 reductase, 2 other enzymes that catalyze metabolic activation of MMC, because the unique activity was not inhibited by allopurinol (an inhibitor of xanthine oxidoreductase) and its activity was the same with NADH and NADPH (cytochrome b5 reductase is specific to NADH).	NAD	292-296	cytochrome b5 reductase 2	Homo sapiens	65-96
8924602-2	1996	The rat hepatic microsomal aldehyde dehydrogenase (mALDH) metabolizes aliphatic and aromatic aldehydes to the corresponding acids with NAD as the optimal cofactor.	NAD	135-138	aldehyde dehydrogenase 3 family, member A2	Rattus norvegicus	16-49
8547174-3	1995	The 3 beta-HSD isoenzymes prefer NAD+ to NADP+ as cofactor with the exception of the rat liver type III and mouse kidney type IV, which both prefer NADPH as cofactor for their specific 3-ketosteroid reductase activity due to the presence of Tyr36 in the rat type III and of Phe36 in mouse type IV enzymes instead of Asp36 found in other 3 beta-HSD isoenzymes.	NAD	33-37	hydroxy-delta-5-steroid dehydrogenase, 3 beta- and steroid delta-isomerase 1	Homo sapiens	4-14
7592744-9	1995	The synergistic activation was inhibited by C3 exoenzyme-catalyzed ADP-ribosylation of recombinant isoprenylated rhoA p21 in a NAD-dependent manner.	NAD	127-130	KRAS proto-oncogene, GTPase	Rattus norvegicus	118-121
8673015-1	1995	In vitro experiments are reported showing that NAD(P)H:(quinone acceptor) oxidoreductase (QR), purified from Glycine max seedlings, reduces Leu- and Met-enkephalin-tyrosinase oxidation products, in the presence of NADH or NADPH.	NAD	214-218	tyrosinase	Homo sapiens	164-174
7576049-1	1995	CD38 is an ectoenzyme that utilizes NAD+ and is expressed by many cells of hematopoietic origin.	NAD	36-40	CD38 antigen	Mus musculus	0-4
7822839-3	1994	The resulting NAD was measured by using a redox enzymatic recycling system of alcohol dehydrogenase, diaphorase and iodonitrotetrazolium as chromogen.	NAD	14-17	aldo-keto reductase family 1 member A1	Homo sapiens	78-99
7734152-4	1994	These conditions permit us to demonstrate NADH channelling from malate dehydrogenase to complex I using the competing reaction test.	NAD	42-46	malic enzyme 1	Homo sapiens	64-84
15299357-1	1994	A binary complex of dihydropteridine reductase and NADH crystallizes in the space group C2, with a = 222.2, b = 46.5, c = 95.3 A and beta = 101.1 degrees.	NAD	51-55	quinoid dihydropteridine reductase	Rattus norvegicus	20-46
7873098-12	1994	The presence of NAD(+)-dependent D-lactate dehydrogenase is characteristic of representatives of the genus Haloarcula, which possess only low activities of NAD(+)-independent L- and D-lactate dehydrogenases, if at all.	NAD	16-20	lactate dehydrogenase D	Homo sapiens	33-56
7873098-12	1994	The presence of NAD(+)-dependent D-lactate dehydrogenase is characteristic of representatives of the genus Haloarcula, which possess only low activities of NAD(+)-independent L- and D-lactate dehydrogenases, if at all.	NAD	16-22	lactate dehydrogenase D	Homo sapiens	33-56
8068673-10	1994	It was found that compounds 1 and 3 inactivated 3 alpha-HSD only in the presence of NAD+.	NAD	84-88	aldo-keto reductase family 1, member C14	Rattus norvegicus	48-59
8078764-3	1994	The deduced amino acid sequence of the nad9 gene product has significant similarity to the nuclear-encoded 30 kDa subunit of the bovine and Neurospora NADH:ubiquinone oxidoreductase (complex I) and to the chloroplast ndhJ gene product.	NAD	151-155	nad9	Triticum aestivum	39-43
8044789-7	1994	When N3 cells with deficiency of poly(ADP-ribose) synthesis due to NAD deficiency are shifted to complete, nicotinamide-containing medium, they restore their NAD content, undergo a decrease in GRP78 levels, and regain sensitivity to VP-16.	NAD	67-70	endoplasmic reticulum chaperone BiP	Cricetulus griseus	193-198
7882155-2	1994	In this study, we propose that domain III, common to the hsp60s and hsp70s is also found in the hsp90s and adopts a beta-alpha-beta Rossmann-folded structure which is encountered in the NAD-binding domain of dehydrogenases.	NAD	186-189	heat shock protein family D (Hsp60) member 1	Homo sapiens	57-62
7882155-2	1994	In this study, we propose that domain III, common to the hsp60s and hsp70s is also found in the hsp90s and adopts a beta-alpha-beta Rossmann-folded structure which is encountered in the NAD-binding domain of dehydrogenases.	NAD	186-189	heat shock protein family A (Hsp70) member 4	Homo sapiens	68-73
8045900-9	1994	The second ORF coded for a protein of 335 amino acids that displayed 45 to 60% identity to the NAD-dependent glyceraldehyde-3-phosphate dehydrogenase (GAP) family of enzymes.	NAD	95-98	glyceraldehyde-3-phosphate dehydrogenase	Pseudomonas aeruginosa PAO1	109-149
8045900-9	1994	The second ORF coded for a protein of 335 amino acids that displayed 45 to 60% identity to the NAD-dependent glyceraldehyde-3-phosphate dehydrogenase (GAP) family of enzymes.	NAD	95-98	glyceraldehyde-3-phosphate dehydrogenase	Pseudomonas aeruginosa PAO1	151-154
8045900-10	1994	The NAD-dependent GAP gene on the P. aeruginosa chromosome was previously unmapped.	NAD	4-7	glyceraldehyde-3-phosphate dehydrogenase	Pseudomonas aeruginosa PAO1	18-21
7520100-8	1994	In addition, an increase in the Km value for NAD utilization by IMPDH was observed in p210 bcr-abl transformed cells, but this increase was within the range of resident NAD concentrations observed in the cells.	NAD	45-48	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	91-98
7520100-8	1994	In addition, an increase in the Km value for NAD utilization by IMPDH was observed in p210 bcr-abl transformed cells, but this increase was within the range of resident NAD concentrations observed in the cells.	NAD	169-172	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	91-98
8218174-0	1993	NAD-dependent methylenetetrahydrofolate dehydrogenase-methenyltetrahydrofolate cyclohydrolase is the mammalian homolog of the mitochondrial enzyme encoded by the yeast MIS1 gene.	NAD	0-3	trifunctional formate-tetrahydrofolate ligase/methenyltetrahydrofolate cyclohydrolase/methylenetetrahydrofolate dehydrogenase MIS1	Saccharomyces cerevisiae S288C	168-172
8218174-5	1993	The human NAD-dependent bifunctional enzyme has a 44% amino acid sequence identity with the dehydrogenase-cyclohydrolase domain of the yeast mitochondrial NADP-dependent trifunctional enzyme encoded by the MIS1 gene, compared to 37% identity with the corresponding domain of the cytosolic trifunctional enzyme.	NAD	10-13	trifunctional formate-tetrahydrofolate ligase/methenyltetrahydrofolate cyclohydrolase/methylenetetrahydrofolate dehydrogenase MIS1	Saccharomyces cerevisiae S288C	206-210
8216369-4	1993	58C80 hydroxylation in human liver microsomes was dependent on either NADPH or NADH, with the activity supported by NADH being 35% of that supported by NADPH.	NAD	116-120	2,4-dienoyl-CoA reductase 1	Homo sapiens	70-75
8369340-1	1993	The sequence pattern CxxCxnGxCxxxGxmGCPP, thus far found in the small subunits from 21 different nickel hydrogenases, appears also to be present in the PSST polypeptide from NADH:ubiquinone oxidoreductase (Complex I) of beef-heart mitochondria.	NAD	174-178	NADH:ubiquinone oxidoreductase core subunit S7	Homo sapiens	152-156
8237468-1	1993	We have developed a chemiluminescent flow injection method for analysis of bile acid, glucose and ATP using the chemiluminescent assay of NADH using 1-methoxy-5-methylphenazinium methyl sulphate (1-MPMS)/isoluminol(IL)/microperoxidase (m-POD) system and immobilized enzyme reactors such as 3 alpha-hydroxysteroid dehydrogenase, glucose-dehydrogenase, hexokinase and glucose-6-phosphate dehydrogenase.	NAD	138-142	glucose-6-phosphate dehydrogenase	Homo sapiens	366-399
8344929-0	1993	Photoaffinity labeling of human placental NAD(+)-linked 15-hydroxyprostaglandin dehydrogenase with [alpha-32P]2N3NAD+.	NAD	42-48	carbonyl reductase 1	Homo sapiens	56-93
8344929-4	1993	Using the photoaffinity analog of NAD+, [alpha-32P]nicotinamide-2-azidoadenine dinucleotide, we have identified a peptide in the adenine ring binding domain of the NAD+ binding site of 15-hydroxyprostaglandin dehydrogenase.	NAD	34-38	carbonyl reductase 1	Homo sapiens	185-222
8344929-4	1993	Using the photoaffinity analog of NAD+, [alpha-32P]nicotinamide-2-azidoadenine dinucleotide, we have identified a peptide in the adenine ring binding domain of the NAD+ binding site of 15-hydroxyprostaglandin dehydrogenase.	NAD	164-168	carbonyl reductase 1	Homo sapiens	185-222
8266745-3	1993	Recently we have been investigating the practical application of this methodology to the estimation of kinetic parameters for the closed two enzyme system of aspartate aminotransferase (AAT) and malate dehydrogenase (MDH) (Fisher 1990a; Fisher 1990b; Bennett and Fisher, 1990): aspartate + alpha-ketoglutamate &lt;--&gt; glutamate + oxaloacetate; oxaloacetate + NADH &lt;--&gt; malate + NAD.	NAD	362-366	malic enzyme 1	Homo sapiens	195-215
8266745-3	1993	Recently we have been investigating the practical application of this methodology to the estimation of kinetic parameters for the closed two enzyme system of aspartate aminotransferase (AAT) and malate dehydrogenase (MDH) (Fisher 1990a; Fisher 1990b; Bennett and Fisher, 1990): aspartate + alpha-ketoglutamate &lt;--&gt; glutamate + oxaloacetate; oxaloacetate + NADH &lt;--&gt; malate + NAD.	NAD	362-366	malic enzyme 1	Homo sapiens	217-220
8266745-3	1993	Recently we have been investigating the practical application of this methodology to the estimation of kinetic parameters for the closed two enzyme system of aspartate aminotransferase (AAT) and malate dehydrogenase (MDH) (Fisher 1990a; Fisher 1990b; Bennett and Fisher, 1990): aspartate + alpha-ketoglutamate &lt;--&gt; glutamate + oxaloacetate; oxaloacetate + NADH &lt;--&gt; malate + NAD.	NAD	362-365	malic enzyme 1	Homo sapiens	195-215
8266745-3	1993	Recently we have been investigating the practical application of this methodology to the estimation of kinetic parameters for the closed two enzyme system of aspartate aminotransferase (AAT) and malate dehydrogenase (MDH) (Fisher 1990a; Fisher 1990b; Bennett and Fisher, 1990): aspartate + alpha-ketoglutamate &lt;--&gt; glutamate + oxaloacetate; oxaloacetate + NADH &lt;--&gt; malate + NAD.	NAD	362-365	malic enzyme 1	Homo sapiens	217-220
8316213-1	1993	Tobacco plants were genetically transformed to generate antisense RNA from a gene construct comprised of a full-length cucumber NADH-dependent hydroxypyruvate reductase (HPR) cDNA placed in reverse orientation between the cauliflower mosaic virus 35S promoter and a nopaline synthase termination/polyadenylation signal sequence.	NAD	128-132	glycerate dehydrogenase	Cucumis sativus	143-168
8316213-1	1993	Tobacco plants were genetically transformed to generate antisense RNA from a gene construct comprised of a full-length cucumber NADH-dependent hydroxypyruvate reductase (HPR) cDNA placed in reverse orientation between the cauliflower mosaic virus 35S promoter and a nopaline synthase termination/polyadenylation signal sequence.	NAD	128-132	glycerate dehydrogenase	Cucumis sativus	170-173
16348915-7	1993	When NADH was used as an electron donor, at first cytochrome b in the cell extract was reduced, and then molybdenum blue was formed.	NAD	5-9	mitochondrially encoded cytochrome b	Homo sapiens	50-62
1471148-10	1992	MIC induced twofold delay in the onset of anerobiosis, and cytochrome b reduction in SMP with NADH in vitro confirms inhibition of electron transport at complex I region.	NAD	94-98	cytochrome b, mitochondrial	Rattus norvegicus	59-71
1527087-2	1992	An NAD-dependent rat liver cytosolic dehydrogenase accepted as substrate retinal generated in situ by microsomes from retinol bound to excess CRBP (cellular retinol binding protein, type I).	NAD	3-6	retinol binding protein 1	Rattus norvegicus	142-146
1527087-2	1992	An NAD-dependent rat liver cytosolic dehydrogenase accepted as substrate retinal generated in situ by microsomes from retinol bound to excess CRBP (cellular retinol binding protein, type I).	NAD	3-6	retinol binding protein 1	Rattus norvegicus	148-180
1325441-4	1992	Although rapid NADH-coupled turnover requires all three protein components, three less complex systems are also functional: System I, NADH, O2, reductase, and MMOH; System II, H2O2 and oxidized MMOH; System III, MMOH reduced nonenzymatically by 2e- and then exposed to O2 (single turnover).	NAD	15-19	immunoglobulin kappa variable 1D-39	Homo sapiens	140-153
1426532-5	1992	Addition of NAD+ or EDTA to either enzyme resulted in a protective effect on GAPDH activity.	NAD	12-16	glyceraldehyde-3-phosphate dehydrogenase	Bos taurus	77-82
1512561-6	1992	While the Km of the TyrA* dehydrogenase for NAD+ remained unaltered, the Km for prephenate was fourfold greater and the Vmax was almost twofold greater than observed for the parental T-protein dehydrogenase.	NAD	44-48	AL522_RS20385	Pantoea agglomerans	26-39
1631094-1	1992	The structure of a binary complex of dihydropteridine reductase [DHPR; NAD(P)H:6,7-dihydropteridine oxidoreductase, EC 1.6.99.7] with its cofactor, NADH, has been solved and refined to a final R factor of 15.4% by using 2.3 A diffraction data.	NAD	148-152	quinoid dihydropteridine reductase	Rattus norvegicus	37-63
1631094-1	1992	The structure of a binary complex of dihydropteridine reductase [DHPR; NAD(P)H:6,7-dihydropteridine oxidoreductase, EC 1.6.99.7] with its cofactor, NADH, has been solved and refined to a final R factor of 15.4% by using 2.3 A diffraction data.	NAD	148-152	quinoid dihydropteridine reductase	Rattus norvegicus	65-69
1631094-2	1992	DHPR is an alpha/beta protein with a Rossmann-type dinucleotide fold for NADH binding.	NAD	73-77	quinoid dihydropteridine reductase	Rattus norvegicus	0-4
1631094-5	1992	DHPR is structurally and mechanistically distinct from dihydrofolate reductase, appearing to more closely resemble certain nicotinamide dinucleotide-requiring flavin-dependent enzymes, such as glutathione reductase.	NAD	123-148	quinoid dihydropteridine reductase	Rattus norvegicus	0-4
1599930-1	1992	We have measured the frequency of the carbon-hydrogen stretching mode of the pro-R and pro-S C4-H bonds of NADH in solution and when bound to pig heart lactate (LDH) or mitochondrial malate (mMDH) dehydrogenases.	NAD	107-111	malate dehydrogenase 2, NAD (mitochondrial)	Mus musculus	191-195
1599930-5	1992	The fact that the frequency of the pro-R hydrogen is not significantly affected during complex formation suggests that the rate enhancements for reaction of substrate with NADH brought about by both pig heart LDH and mMDH apparently do not involve either stabilization or destabilization of the pro-R hydrogen of NADH in enzyme-coenzyme binary complexes, in agreement with previous chemical studies.	NAD	172-176	malate dehydrogenase 2, NAD (mitochondrial)	Mus musculus	217-221
1597188-6	1992	Incubation of PG-9-KR with prostaglandin F2 alpha and NAD+ leads to the preferential formation of 15-keto prostaglandin F2 alpha rather than prostaglandin E2.	NAD	54-58	carbonyl reductase [NADPH] 1	Sus scrofa	14-21
1577005-7	1992	In addition, the enzyme is able to catalyze electron transfer from NADH to various other electron acceptors (methylene blue, cytochrome c, p-nitroblue tetrazolium, 2,6-dichloroindophenol and potassium ferricyanide), even in the absence of flavin shuttles.	NAD	67-71	sulfur oxidation c-type cytochrome SoxA	Thermus thermophilus HB8	125-137
1348935-0	1992	ADPRibosylation of chicken red cell tubulin and inhibition of microtubule self-assembly in vitro by the NAD(+)-dependent avian ADPRibosyl transferase.	NAD	104-110	ADP-ribosyltransferase 1 like 3	Gallus gallus	127-149
1552368-3	1992	By mixing the purified cytochrome b5 with cytochrome b5 reductase, cob(II)alamin was immediately formed from aquacobalamin and NADH.	NAD	127-131	cytochrome b5 type A	Rattus norvegicus	23-36
1552368-3	1992	By mixing the purified cytochrome b5 with cytochrome b5 reductase, cob(II)alamin was immediately formed from aquacobalamin and NADH.	NAD	127-131	cytochrome b5 type A	Rattus norvegicus	42-55
1552368-4	1992	These results provide evidence that the NADH-linked aquacobalamin reductase activity is derived from the cytochrome b5/cytochrome b5 reductase complex in rat liver microsomes.	NAD	40-44	cytochrome b5 type A	Rattus norvegicus	105-118
1552368-4	1992	These results provide evidence that the NADH-linked aquacobalamin reductase activity is derived from the cytochrome b5/cytochrome b5 reductase complex in rat liver microsomes.	NAD	40-44	cytochrome b5 type A	Rattus norvegicus	119-132
1741380-2	1992	We used FLIM to create lifetime images of NADH when free in solution and when bound to malate dehydrogenase.	NAD	42-46	malic enzyme 1	Homo sapiens	87-107
1612526-1	1992	Localization of NAD(+)-dependent 15-hydroxy prostaglandin dehydrogenase (type I-PGDH) may influence local concentrations of bioactive eicosanoids within intrauterine tissues.	NAD	16-22	carbonyl reductase 1	Homo sapiens	33-71
1834689-4	1991	To facilitate the determination of 3 beta HSD activity, an abbreviated technique was developed that consisted in the use of [3 alpha-3H]dehydroepiandrosterone [( 3 alpha-3H]DHEA) as the substrate and NAD+ as the cofactor.	NAD	200-204	hydroxy-delta-5-steroid dehydrogenase, 3 beta- and steroid delta-isomerase 1	Homo sapiens	35-45
2059213-0	1991	Regulation of synthesis and activity of NAD(+)-dependent 15-hydroxy-prostaglandin dehydrogenase (15-PGDH) by dexamethasone and phorbol ester in human erythroleukemia (HEL) cells.	NAD	40-46	carbonyl reductase 1	Homo sapiens	57-95
2059213-0	1991	Regulation of synthesis and activity of NAD(+)-dependent 15-hydroxy-prostaglandin dehydrogenase (15-PGDH) by dexamethasone and phorbol ester in human erythroleukemia (HEL) cells.	NAD	40-46	carbonyl reductase 1	Homo sapiens	97-104
1750672-4	1991	Total CO2 was determined as bicarbonate/carbonate by monitoring the oxidation of NADH at 340 nm using the coupled assay of phosphoenolpyruvate carboxylase (EC 4.1.1.31) and malate dehydrogenase (EC 1.1.1.37).	NAD	81-85	phosphoenolpyruvate carboxykinase 1	Rattus norvegicus	123-154
1943056-2	1991	Both the Syva EMIT st Urine Ethyl Alcohol Assay and the Sigma Diagnostics Alcohol in Urine Assay, which utilize the reduction of nicotinamide adenine dinucleotide (NAD) to NADH associated with the oxidation of ethanol in the presence of alcohol dehydrogenase (ADH), were adapted to spectrophotometrically determine ethanol concentration.	NAD	129-162	aldo-keto reductase family 1 member A1	Homo sapiens	237-258
1943056-2	1991	Both the Syva EMIT st Urine Ethyl Alcohol Assay and the Sigma Diagnostics Alcohol in Urine Assay, which utilize the reduction of nicotinamide adenine dinucleotide (NAD) to NADH associated with the oxidation of ethanol in the presence of alcohol dehydrogenase (ADH), were adapted to spectrophotometrically determine ethanol concentration.	NAD	129-162	aldo-keto reductase family 1 member A1	Homo sapiens	173-176
1943056-2	1991	Both the Syva EMIT st Urine Ethyl Alcohol Assay and the Sigma Diagnostics Alcohol in Urine Assay, which utilize the reduction of nicotinamide adenine dinucleotide (NAD) to NADH associated with the oxidation of ethanol in the presence of alcohol dehydrogenase (ADH), were adapted to spectrophotometrically determine ethanol concentration.	NAD	164-167	aldo-keto reductase family 1 member A1	Homo sapiens	237-258
1943056-2	1991	Both the Syva EMIT st Urine Ethyl Alcohol Assay and the Sigma Diagnostics Alcohol in Urine Assay, which utilize the reduction of nicotinamide adenine dinucleotide (NAD) to NADH associated with the oxidation of ethanol in the presence of alcohol dehydrogenase (ADH), were adapted to spectrophotometrically determine ethanol concentration.	NAD	164-167	aldo-keto reductase family 1 member A1	Homo sapiens	173-176
2025219-4	1991	The data demonstrate that PBG deaminase and protoporphyrinogen oxidase activities rise rapidly and early, in comparison with ferrochelatase activity, which rises more slowly, and coproporphyrinogen oxidase activity, which decreases by 60% within 24 h of induction before returning to initial levels by 72 h. NADH:ferric iron reductase activity increases slightly, but is always present at levels higher than needed for haem synthesis.	NAD	308-312	hydroxymethylbilane synthase	Mus musculus	26-39
1650254-6	1991	The enzyme has an apparent molecular mass of 29 kDa, a Km for NAD of 0.7 mM, and a turnover rate of approximately 27,000 mol NAD.min-1.mol enzyme-1 at 30 degrees C. Monoclonal antibodies were generated to the NADase.	NAD	62-65	ADP-ribosyl cyclase/cyclic ADP-ribose hydrolase	Aplysia californica	209-215
1650254-6	1991	The enzyme has an apparent molecular mass of 29 kDa, a Km for NAD of 0.7 mM, and a turnover rate of approximately 27,000 mol NAD.min-1.mol enzyme-1 at 30 degrees C. Monoclonal antibodies were generated to the NADase.	NAD	125-128	ADP-ribosyl cyclase/cyclic ADP-ribose hydrolase	Aplysia californica	209-215
1989987-3	1991	Immunochemical levels of IDP1 were found to vary in inverse proportion with those of mitochondrial NAD(H)-specific isocitrate dehydrogenase in cells grown with glucose or with acetate as a carbon source.	NAD	99-105	isocitrate dehydrogenase (NADP(+)) IDP1	Saccharomyces cerevisiae S288C	25-29
2264826-4	1990	The cytochrome b5 was reduced in the membrane preparations by NADH, demonstrating the presence of an NADH: cytochrome b5 reductase; NADPH was a less effective donor.	NAD	101-105	2,4-dienoyl-CoA reductase 1	Homo sapiens	132-137
2240085-1	1990	Biochemical studies have shown the presence of type I oxidized nicotinamide-adenine dinucleotide-dependent 15-hydroxyprostaglandin dehydrogenase in human fetal membranes, decidua, and placenta.	NAD	63-96	carbonyl reductase 1	Homo sapiens	107-144
2202600-2	1990	Benzyl alcohol dehydrogenase catalyses the oxidation of benzyl alcohol to benzaldehyde with the concomitant reduction of NAD+; the reaction is reversible.	NAD	121-125	benzyl alcohol dehydrogenase	Pseudomonas putida	0-28
2121286-3	1990	Incubation of purified GTP-binding protein from rat brain (Go-protein) with membranes and erythrocyte cytoplasm in the presence of [32P]NAD resulted in the label incorporation into the Go-protein alpha-subunit.	NAD	136-139	RAS like proto-oncogene B	Rattus norvegicus	23-42
2123732-5	1990	Following treatment of these cells with 2 mM benzamide, an inhibitor of the NAD(+)-utilizing enzyme poly(ADP-ribose) polymerase, NAD+ levels slowly increased up to about 160% of control levels after 3 hours.	NAD	76-82	poly (ADP-ribose) polymerase family, member 1	Mus musculus	100-127
2123732-5	1990	Following treatment of these cells with 2 mM benzamide, an inhibitor of the NAD(+)-utilizing enzyme poly(ADP-ribose) polymerase, NAD+ levels slowly increased up to about 160% of control levels after 3 hours.	NAD	129-133	poly (ADP-ribose) polymerase family, member 1	Mus musculus	100-127
2367567-3	1990	When GPDH containing about 1 mol NAD per mol of tetramer is incubated with acrylamide (0.01-0.1 M), the tryptophan emission of GPDH, initially quenched by acrylamide, slowly increases to a value exceeding that recorded before the addition of acrylamide.	NAD	33-36	glyceraldehyde-3-phosphate dehydrogenase	Oryctolagus cuniculus	5-9
2367567-3	1990	When GPDH containing about 1 mol NAD per mol of tetramer is incubated with acrylamide (0.01-0.1 M), the tryptophan emission of GPDH, initially quenched by acrylamide, slowly increases to a value exceeding that recorded before the addition of acrylamide.	NAD	33-36	glyceraldehyde-3-phosphate dehydrogenase	Oryctolagus cuniculus	127-131
2367567-4	1990	This effect is not observed in apoenzyme solutions, indicating that the enhancement of fluorescence results from the dissociation of some NAD from the acrylamide treated GPDH.	NAD	138-141	glyceraldehyde-3-phosphate dehydrogenase	Oryctolagus cuniculus	170-174
2367567-5	1990	Acrylamide inactivates GPDH but 1 mM NAD protects the enzyme from inactivation.	NAD	37-40	glyceraldehyde-3-phosphate dehydrogenase	Oryctolagus cuniculus	23-27
2157416-3	1990	By some criteria including its high sensitivity to mersalyl, and its relatively high specificity for NADPH compared to NADH, the rabbit neutrophil NADPH cytochrome c reductase resembled NADPH-cytochrome P-450 reductase.	NAD	119-123	NADPH--cytochrome P450 reductase	Oryctolagus cuniculus	186-218
2183647-2	1990	The assay measures NADH production at 340 nm after initiation of the reaction with rabbit liver 3-hydroxyisobutyrate dehydrogenase (EC 1.1.1.31).	NAD	19-23	3-hydroxyisobutyrate dehydrogenase	Oryctolagus cuniculus	96-130
1710590-1	1990	Calf thymus DNA was incubated with bleomycin and FeCl3 in the presence of isolated rat liver microsomal NADH-cytochrome b5 reductase, cytochrome b5 and NADH which catalyze redox cycling of the bleomycin-Fe-complex.	NAD	104-108	cytochrome b5 type A	Rattus norvegicus	109-122
33779856-3	2021	SIRT1 (silent information regulator 1) is an NAD-dependent deacetylase.	NAD	45-48	sirtuin 1	Homo sapiens	0-5
33779856-3	2021	SIRT1 (silent information regulator 1) is an NAD-dependent deacetylase.	NAD	45-48	sirtuin 1	Homo sapiens	7-37
33763166-4	2021	The results showed that NADH:ubiquinone oxidoreductase core subunit S1- (Ndufs1-) dependent mitochondrial dysfunction plays a key role in pressure overload-induced CH.	NAD	24-28	NADH:ubiquinone oxidoreductase core subunit S1	Rattus norvegicus	73-79
34990970-4	2022	Electrons are typically supplied by NADH via a rubredoxin reductase (AlkT) to a rubredoxin (AlkG) to AlkB, although alternative electron transfer partners have been observed.	NAD	36-40	alkB homolog 1, histone H2A dioxygenase	Homo sapiens	101-105
34619358-5	2022	In steady-state enzyme kinetics assays, we measured KM values for oxaloacetate of 54 and 52 muM and KM values for NADH of 61 and 107 muM for MDH-1 and MDH-2, respectively.	NAD	114-118	putative malate dehydrogenase, mitochondrial	Caenorhabditis elegans	151-156
34966665-2	2021	NADH: ubiquinone oxidoreductase subunit C1 (NDUFC1), which is an accessory subunit of the NADH dehydrogenase (complex I), is responsible for the transportation of electrons from NADH to the respiratory chain essential for the oxidative phosphorylation.	NAD	178-182	NADH:ubiquinone oxidoreductase subunit C1	Homo sapiens	44-50
34878972-2	2021	Here, we show that deletion of the nuclear-localized NAD+ synthase nicotinamide mononucleotide adenylyltransferase-1 (NMNAT1) in the developing murine retina causes early and severe degeneration of photoreceptors and select inner retinal neurons via multiple distinct cell death pathways.	NAD	53-57	nicotinamide nucleotide adenylyltransferase 1	Mus musculus	67-116
34878972-2	2021	Here, we show that deletion of the nuclear-localized NAD+ synthase nicotinamide mononucleotide adenylyltransferase-1 (NMNAT1) in the developing murine retina causes early and severe degeneration of photoreceptors and select inner retinal neurons via multiple distinct cell death pathways.	NAD	53-57	nicotinamide nucleotide adenylyltransferase 1	Mus musculus	118-124
34637964-1	2021	Cluster of differentiation (CD) 38, a major enzyme for nicotinamide adenine dinucleotide (NAD+) degradation, plays a key role in inflammation.	NAD	55-88	CD38 antigen	Mus musculus	0-34
34531546-4	2021	Furthermore, ROF significantly enhanced the lysosomal function, as evidenced by the increased levels of mature cathepsin D (CTSD) and lysosomal-associated membrane protein 1 (LAMP1) through increasing NAD+/NADH and the expression of sirtuin 1 (SIRT1).	NAD	201-205	cathepsin D	Mus musculus	111-122
34887866-2	2021	Sirtuin 1 (SIRT1), a member of the class III family of nicotinamide adenine dinucleotide (NAD+)-dependent histone deacetylases, has been reported to participate in the progression of several diseases.	NAD	55-88	sirtuin 1	Homo sapiens	0-9
34887866-2	2021	Sirtuin 1 (SIRT1), a member of the class III family of nicotinamide adenine dinucleotide (NAD+)-dependent histone deacetylases, has been reported to participate in the progression of several diseases.	NAD	55-88	sirtuin 1	Homo sapiens	11-16
34887866-2	2021	Sirtuin 1 (SIRT1), a member of the class III family of nicotinamide adenine dinucleotide (NAD+)-dependent histone deacetylases, has been reported to participate in the progression of several diseases.	NAD	90-94	sirtuin 1	Homo sapiens	0-9
34887866-2	2021	Sirtuin 1 (SIRT1), a member of the class III family of nicotinamide adenine dinucleotide (NAD+)-dependent histone deacetylases, has been reported to participate in the progression of several diseases.	NAD	90-94	sirtuin 1	Homo sapiens	11-16
34757706-1	2021	Sirt1, a member of the sirtuins family, is a nicotinamide adenosine dinucleotide (NAD+)-dependent deacetylase.	NAD	82-86	sirtuin 1	Homo sapiens	0-5
34374810-6	2021	This was confirmed in vitro, as the interaction of FhHDM-1 with the NOD-derived beta-cell line, NIT-1, resulted in increased levels of phosphorylated Akt, increased NADH and NADPH and reduced activity of the NAD-dependent DNA nick sensor, poly(ADP-ribose) polymerase (PARP-1).	NAD	208-211	nitrilase 1	Mus musculus	96-101
34374810-6	2021	This was confirmed in vitro, as the interaction of FhHDM-1 with the NOD-derived beta-cell line, NIT-1, resulted in increased levels of phosphorylated Akt, increased NADH and NADPH and reduced activity of the NAD-dependent DNA nick sensor, poly(ADP-ribose) polymerase (PARP-1).	NAD	208-211	poly (ADP-ribose) polymerase family, member 1	Mus musculus	239-266
34374810-6	2021	This was confirmed in vitro, as the interaction of FhHDM-1 with the NOD-derived beta-cell line, NIT-1, resulted in increased levels of phosphorylated Akt, increased NADH and NADPH and reduced activity of the NAD-dependent DNA nick sensor, poly(ADP-ribose) polymerase (PARP-1).	NAD	208-211	poly (ADP-ribose) polymerase family, member 1	Mus musculus	268-274
34803499-10	2021	More importantly, Ex527 (Sirt1 inhibitor) and 3-TYP (Sirt3 inhibitor) significantly enhanced OA-induced lipid accumulation and oxidative stress in CD38-/- primary hepatocytes, suggesting that the anti-lipid accumulation of CD38 deficiency might be dependent on NAD/Sirtuins-mediated enhancement of FAA beta-oxidation and suppression of oxidative stress in hepatocytes.	NAD	261-264	CD38 antigen	Mus musculus	223-227
34803499-11	2021	In conclusion, we demonstrated that CD38 deficiency protected mice from HFD-induced NAFLD by reducing lipid accumulation and suppressing oxidative stress via activating NAD/Sirtuins signaling pathways.	NAD	169-172	CD38 antigen	Mus musculus	36-40
34493542-2	2021	CD38 shows increased expression in the cuprizone and experimental autoimmune encephalomyelitis models of demyelination; in addition, CD38 is the main nicotinamide adenine dinucleotide (NAD+)-depleting enzyme in the CNS.	NAD	150-183	CD38 antigen	Mus musculus	0-4
34493542-2	2021	CD38 shows increased expression in the cuprizone and experimental autoimmune encephalomyelitis models of demyelination; in addition, CD38 is the main nicotinamide adenine dinucleotide (NAD+)-depleting enzyme in the CNS.	NAD	150-183	CD38 antigen	Mus musculus	133-137
34493542-2	2021	CD38 shows increased expression in the cuprizone and experimental autoimmune encephalomyelitis models of demyelination; in addition, CD38 is the main nicotinamide adenine dinucleotide (NAD+)-depleting enzyme in the CNS.	NAD	185-189	CD38 antigen	Mus musculus	0-4
34493542-2	2021	CD38 shows increased expression in the cuprizone and experimental autoimmune encephalomyelitis models of demyelination; in addition, CD38 is the main nicotinamide adenine dinucleotide (NAD+)-depleting enzyme in the CNS.	NAD	185-189	CD38 antigen	Mus musculus	133-137
34493542-5	2021	We demonstrate that CD38-catalytically inactive mice are substantially protected from high fat-induced NAD+ depletion, oligodendrocyte loss, oxidative damage, and astrogliosis.	NAD	103-107	CD38 antigen	Mus musculus	20-24
34493542-6	2021	A CD38 inhibitor, 78c, increased NAD+ and attenuated neuroinflammatory changes induced by saturated fat applied to astrocyte cultures.	NAD	33-37	CD38 antigen	Mus musculus	2-6
34493542-11	2021	Our findings suggest high fat diet impairs oligodendrocyte survival and differentiation through astrocyte-linked mechanisms mediated by the NAD+ase CD38 and highlight CD38 inhibitors as potential therapeutic candidates to improve myelin regeneration.SIGNIFICANCE STATEMENTMyelin disturbances and oligodendrocyte loss can leave axons vulnerable leading to permanent neurologic deficits.	NAD	140-144	CD38 antigen	Mus musculus	148-152
34493542-13	2021	We demonstrate that restoring nicotinamide adenine dinucleotide (NAD+) levels via genetic inactivation of CD38 can overcome these effects.	NAD	30-63	CD38 antigen	Mus musculus	106-110
34493542-13	2021	We demonstrate that restoring nicotinamide adenine dinucleotide (NAD+) levels via genetic inactivation of CD38 can overcome these effects.	NAD	65-69	CD38 antigen	Mus musculus	106-110
34645816-8	2021	Sirt1 activity, dependent on the cytoplasmic glycolysis product NAD+, directly interacts with p107, impeding its mitochondrial localization.	NAD	64-68	sirtuin 1	Homo sapiens	0-5
34364937-1	2021	Sirtuin-1 (SIRT1) as a NAD + -dependent Class III protein deacetylase, involves in longevity and various cellular physiological processes.	NAD	23-26	sirtuin 1	Homo sapiens	0-9
34364937-1	2021	Sirtuin-1 (SIRT1) as a NAD + -dependent Class III protein deacetylase, involves in longevity and various cellular physiological processes.	NAD	23-26	sirtuin 1	Homo sapiens	11-16
34436591-1	2021	Sirtuin 1 (SIRT1), an NAD-dependent protein deacetylase, plays a central role in the control of lipid metabolism in non-ruminants.	NAD	22-25	sirtuin 1	Bos taurus	0-9
34436591-1	2021	Sirtuin 1 (SIRT1), an NAD-dependent protein deacetylase, plays a central role in the control of lipid metabolism in non-ruminants.	NAD	22-25	sirtuin 1	Bos taurus	11-16
34478713-4	2021	Utilising NAD+, the ecto-enzyme adenosine diphosphate (ADP) ribosyl transferase 2.2 (ART2.2) catalyzes the addition of ADP-ribosyl groups onto arginine residues of CD8alpha or beta chains and alters the interaction between the MHC and TCR complexes.	NAD	10-14	CD8a molecule	Homo sapiens	164-172
34478713-4	2021	Utilising NAD+, the ecto-enzyme adenosine diphosphate (ADP) ribosyl transferase 2.2 (ART2.2) catalyzes the addition of ADP-ribosyl groups onto arginine residues of CD8alpha or beta chains and alters the interaction between the MHC and TCR complexes.	NAD	10-14	major histocompatibility complex, class I, C	Homo sapiens	227-230
34478713-6	2021	Here, we show that ADP-ribosylation of CD8 facilitates the binding of the liver-restricted non-classical MHC, H2-Q10, independent of the associated TCR or presented peptide, and propose that this highly regulated binding imposes an additional inhibitory leash on the activation of CD8-expressing cells in the presence of NAD+.	NAD	321-325	CD8a molecule	Homo sapiens	39-42
34478713-6	2021	Here, we show that ADP-ribosylation of CD8 facilitates the binding of the liver-restricted non-classical MHC, H2-Q10, independent of the associated TCR or presented peptide, and propose that this highly regulated binding imposes an additional inhibitory leash on the activation of CD8-expressing cells in the presence of NAD+.	NAD	321-325	major histocompatibility complex, class I, C	Homo sapiens	105-108
34478713-6	2021	Here, we show that ADP-ribosylation of CD8 facilitates the binding of the liver-restricted non-classical MHC, H2-Q10, independent of the associated TCR or presented peptide, and propose that this highly regulated binding imposes an additional inhibitory leash on the activation of CD8-expressing cells in the presence of NAD+.	NAD	321-325	CD8a molecule	Homo sapiens	281-284
34358533-3	2021	Phytochemicals exhibit biphasic dose responses on cancer cells, activating at low dose, signaling pathways resulting in upregulation of vitagenes, as in the case of the Nrf2 pathway upregulated by hydroxytyrosol (HT) or curcumin and NAD/NADH-sirtuin-1 activated by resveratrol.	NAD	233-236	sirtuin 1	Homo sapiens	242-251
34358533-3	2021	Phytochemicals exhibit biphasic dose responses on cancer cells, activating at low dose, signaling pathways resulting in upregulation of vitagenes, as in the case of the Nrf2 pathway upregulated by hydroxytyrosol (HT) or curcumin and NAD/NADH-sirtuin-1 activated by resveratrol.	NAD	237-241	sirtuin 1	Homo sapiens	242-251
34663976-5	2021	In the nucleus, the altered PHGDH activity restricts NAD+ level and compartmentally repressed NAD+-dependent PARP1 activity for poly(ADP-ribosyl)ation of c-Jun, thereby leading to impaired c-Jun transcriptional activity linked to cell growth inhibition.	NAD	94-97	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	154-159
34663976-5	2021	In the nucleus, the altered PHGDH activity restricts NAD+ level and compartmentally repressed NAD+-dependent PARP1 activity for poly(ADP-ribosyl)ation of c-Jun, thereby leading to impaired c-Jun transcriptional activity linked to cell growth inhibition.	NAD	94-97	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	189-194
34310047-6	2021	We employ the alcohol dehydrogenase (ADH) and coenzyme I (NAD + ) for methanol catalytic dehydrogenation at low temperature, which could generate formaldehyde and reductive coenzyme I (NADH).	NAD	58-63	aldo-keto reductase family 1 member A1	Homo sapiens	14-35
34310047-6	2021	We employ the alcohol dehydrogenase (ADH) and coenzyme I (NAD + ) for methanol catalytic dehydrogenation at low temperature, which could generate formaldehyde and reductive coenzyme I (NADH).	NAD	58-63	aldo-keto reductase family 1 member A1	Homo sapiens	37-40
34310047-6	2021	We employ the alcohol dehydrogenase (ADH) and coenzyme I (NAD + ) for methanol catalytic dehydrogenation at low temperature, which could generate formaldehyde and reductive coenzyme I (NADH).	NAD	185-189	aldo-keto reductase family 1 member A1	Homo sapiens	14-35
34310047-6	2021	We employ the alcohol dehydrogenase (ADH) and coenzyme I (NAD + ) for methanol catalytic dehydrogenation at low temperature, which could generate formaldehyde and reductive coenzyme I (NADH).	NAD	185-189	aldo-keto reductase family 1 member A1	Homo sapiens	37-40
34547231-2	2021	report a novel metabolic cycle, which they name HTC, that converts NADH into the key antioxidant factor NADPH.	NAD	67-71	2,4-dienoyl-CoA reductase 1	Homo sapiens	104-109
34564436-6	2021	Mechanistically, we found that KLF15 deficiency leads to reduced amounts of the rate-limiting NAD+ salvage enzyme NAMPT and to NAD+ deficiency.	NAD	94-98	nicotinamide phosphoribosyltransferase	Rattus norvegicus	114-119
34622167-6	2021	The metabolism of NAD+ is an important contributor to Sirt1 activity in this context.	NAD	18-22	sirtuin 1	Danio rerio	54-59
34378958-5	2021	It was found that Ald catalyzes the NAD-specific dehydrogenation of 6-hydroxy-3-succinoyl-semialdehyde-pyridine to 6-hydroxy-3-succinoylpyridine.	NAD	36-39	AWN88_RS16050	Agrobacterium tumefaciens	18-21
34378958-6	2021	With the nonhydroxylated analog 3-succinoyl-semialdehyde-pyridine (SAP) as a substrate, Ald had a specific activity of 10.05 U/mg at pH 9.0 and apparent Km values of around 58.68 muM and 0.41 mM for SAP and NAD+, respectively.	NAD	207-211	AWN88_RS16050	Agrobacterium tumefaciens	88-91
34378958-16	2021	Similar to the known aldehyde dehydrogenase, the NAD-specific homodimeric enzyme presents a broad substrate range with high activity in alkaline and low-salt-containing buffers.	NAD	49-52	AWN88_RS16050	Agrobacterium tumefaciens	21-43
34435784-1	2021	This study utilizes the FMN-dependent NADH:quinone oxidoreductase from Pseudomonas aeruginosa PAO1 to investigate the effect of introducing an active site negative charge on the flavin absorption spectrum both in the absence and presence of a long-range electrostatic potential coming from solution ions.	NAD	38-42	quinone oxidoreductase	Pseudomonas aeruginosa PAO1	43-65
34418332-1	2021	BACKGROUND: Nicotinamide phosphoribosyltransferase (Nampt/Visfatin/PBEF) acts both as an enzyme in the nicotinamide adenine dinucleotide (NAD) synthesis pathway as well as an extracellular hormone (eNampt).	NAD	103-136	nicotinamide phosphoribosyltransferase	Rattus norvegicus	52-57
34418332-1	2021	BACKGROUND: Nicotinamide phosphoribosyltransferase (Nampt/Visfatin/PBEF) acts both as an enzyme in the nicotinamide adenine dinucleotide (NAD) synthesis pathway as well as an extracellular hormone (eNampt).	NAD	103-136	nicotinamide phosphoribosyltransferase	Rattus norvegicus	58-66
34418332-1	2021	BACKGROUND: Nicotinamide phosphoribosyltransferase (Nampt/Visfatin/PBEF) acts both as an enzyme in the nicotinamide adenine dinucleotide (NAD) synthesis pathway as well as an extracellular hormone (eNampt).	NAD	103-136	nicotinamide phosphoribosyltransferase	Rattus norvegicus	67-71
34418332-1	2021	BACKGROUND: Nicotinamide phosphoribosyltransferase (Nampt/Visfatin/PBEF) acts both as an enzyme in the nicotinamide adenine dinucleotide (NAD) synthesis pathway as well as an extracellular hormone (eNampt).	NAD	138-141	nicotinamide phosphoribosyltransferase	Rattus norvegicus	52-57
34418332-1	2021	BACKGROUND: Nicotinamide phosphoribosyltransferase (Nampt/Visfatin/PBEF) acts both as an enzyme in the nicotinamide adenine dinucleotide (NAD) synthesis pathway as well as an extracellular hormone (eNampt).	NAD	138-141	nicotinamide phosphoribosyltransferase	Rattus norvegicus	58-66
34418332-1	2021	BACKGROUND: Nicotinamide phosphoribosyltransferase (Nampt/Visfatin/PBEF) acts both as an enzyme in the nicotinamide adenine dinucleotide (NAD) synthesis pathway as well as an extracellular hormone (eNampt).	NAD	138-141	nicotinamide phosphoribosyltransferase	Rattus norvegicus	67-71
34233924-7	2021	However, DLST loss significantly suppressed NADH production and impaired OXPHOS, leading to growth arrest and apoptosis of neuroblastoma cells.	NAD	44-48	dihydrolipoamide S-succinyltransferase	Homo sapiens	9-13
34130151-1	2021	Supplement of nicotinamide mononucleotide (NMN), the direct precursor of nicotinamide adenine dinucleotide (NAD+) has gained prominence due to the significant anti-aging potentials of nicotinamide phosphoribosyltransferas (NAMPT)/NAD+ signaling.	NAD	73-106	nicotinamide phosphoribosyltransferase	Rattus norvegicus	223-228
34130151-1	2021	Supplement of nicotinamide mononucleotide (NMN), the direct precursor of nicotinamide adenine dinucleotide (NAD+) has gained prominence due to the significant anti-aging potentials of nicotinamide phosphoribosyltransferas (NAMPT)/NAD+ signaling.	NAD	108-112	nicotinamide phosphoribosyltransferase	Rattus norvegicus	223-228
34130151-1	2021	Supplement of nicotinamide mononucleotide (NMN), the direct precursor of nicotinamide adenine dinucleotide (NAD+) has gained prominence due to the significant anti-aging potentials of nicotinamide phosphoribosyltransferas (NAMPT)/NAD+ signaling.	NAD	230-234	nicotinamide phosphoribosyltransferase	Rattus norvegicus	223-228
34174704-8	2021	NAD+ intervention relieved inflammatory infiltration and CD3+ and CD4+ cell infiltration and decreased the number and activation of microglia and astrocytes in the optic nerve.	NAD	0-4	CD4 antigen	Mus musculus	66-69
34434488-3	2021	Previous studies have found that small extracellular vesicles (sEVs) secreted by adipocytes (Adipo-sEVs) or adipose tissue are abundant in nicotinamide phosphoribosyltransferase (NAMPT), which is the key NAD+ biosynthetic enzyme in mammals.	NAD	204-208	nicotinamide phosphoribosyltransferase	Rattus norvegicus	139-177
34434488-3	2021	Previous studies have found that small extracellular vesicles (sEVs) secreted by adipocytes (Adipo-sEVs) or adipose tissue are abundant in nicotinamide phosphoribosyltransferase (NAMPT), which is the key NAD+ biosynthetic enzyme in mammals.	NAD	204-208	nicotinamide phosphoribosyltransferase	Rattus norvegicus	179-184
34379994-2	2021	Sirtuin 1 (SIRT1) is an NAD + dependent protein deacetylase with a critical function in the regulation of glucose/lipid metabolism, insulin resistance, inflammation, oxidative stress, and mitochondrial function.	NAD	24-27	sirtuin 1	Homo sapiens	0-9
34379994-2	2021	Sirtuin 1 (SIRT1) is an NAD + dependent protein deacetylase with a critical function in the regulation of glucose/lipid metabolism, insulin resistance, inflammation, oxidative stress, and mitochondrial function.	NAD	24-27	sirtuin 1	Homo sapiens	11-16
34723263-3	2021	Unexpectedly, photoinduced cleavage of DNA by C60-PEG 1 was much higher than that by C70-PEG 2 and 3 with higher absorption intensity, especially in the presence of an electron donor (NADH).	NAD	184-188	mesoderm specific transcript	Homo sapiens	50-55
34343089-1	2021	Poly(ADP-ribose) polymerase (PARP) enzymes initiate (mt)DNA repair mechanisms and use nicotinamide adenine dinucleotide (NAD+) as energy source.	NAD	86-119	poly (ADP-ribose) polymerase family, member 1	Mus musculus	0-27
34343089-1	2021	Poly(ADP-ribose) polymerase (PARP) enzymes initiate (mt)DNA repair mechanisms and use nicotinamide adenine dinucleotide (NAD+) as energy source.	NAD	86-119	poly (ADP-ribose) polymerase family, member 1	Mus musculus	29-33
34343089-1	2021	Poly(ADP-ribose) polymerase (PARP) enzymes initiate (mt)DNA repair mechanisms and use nicotinamide adenine dinucleotide (NAD+) as energy source.	NAD	121-125	poly (ADP-ribose) polymerase family, member 1	Mus musculus	0-27
34343089-1	2021	Poly(ADP-ribose) polymerase (PARP) enzymes initiate (mt)DNA repair mechanisms and use nicotinamide adenine dinucleotide (NAD+) as energy source.	NAD	121-125	poly (ADP-ribose) polymerase family, member 1	Mus musculus	29-33
34343089-2	2021	Prolonged PARP activity can drain cellular NAD+ reserves, leading to de-regulation of important molecular processes.	NAD	43-47	poly (ADP-ribose) polymerase family, member 1	Mus musculus	10-14
34097876-0	2021	SIRT1-dependent restoration of NAD+ homeostasis after increased extracellular NAD+ exposure.	NAD	31-35	sirtuin 1	Homo sapiens	0-5
34097876-0	2021	SIRT1-dependent restoration of NAD+ homeostasis after increased extracellular NAD+ exposure.	NAD	78-82	sirtuin 1	Homo sapiens	0-5
34097876-8	2021	Interestingly, silencing the NAD+-sensor enzyme SIRT1 prevented eNAD+-dependent transcriptional repression of CD73, Slc12a8, and NRK1, as well as iNAD+ resetting.	NAD	29-33	sirtuin 1	Homo sapiens	48-53
34234670-1	2021	Silent information regulator 2-related enzyme 1 (SIRT1) is an NAD+-dependent class III deacetylase and a key component of the cellular metabolic sensing pathway.	NAD	62-65	sirtuin 1	Homo sapiens	0-47
34234670-1	2021	Silent information regulator 2-related enzyme 1 (SIRT1) is an NAD+-dependent class III deacetylase and a key component of the cellular metabolic sensing pathway.	NAD	62-65	sirtuin 1	Homo sapiens	49-54
34234670-2	2021	The requirement of NAD+ for SIRT1 activity led us to assume that NQO1, an NADH oxidoreductase producing NAD+, regulates SIRT1 activity.	NAD	19-23	sirtuin 1	Homo sapiens	28-33
34234670-2	2021	The requirement of NAD+ for SIRT1 activity led us to assume that NQO1, an NADH oxidoreductase producing NAD+, regulates SIRT1 activity.	NAD	19-23	sirtuin 1	Homo sapiens	120-125
34234670-2	2021	The requirement of NAD+ for SIRT1 activity led us to assume that NQO1, an NADH oxidoreductase producing NAD+, regulates SIRT1 activity.	NAD	104-108	sirtuin 1	Homo sapiens	28-33
34234670-2	2021	The requirement of NAD+ for SIRT1 activity led us to assume that NQO1, an NADH oxidoreductase producing NAD+, regulates SIRT1 activity.	NAD	104-108	sirtuin 1	Homo sapiens	120-125
34112762-7	2021	In conclusion, our findings demonstrated that CD38 and its associated intracellular NAD decline are critical for Ang II-induced VSMC senescence and vascular remodeling.	NAD	84-87	CD38 antigen	Mus musculus	46-50
32414855-7	2021	Interestingly, gene expression and metabolomic profiling revealed that ALDH1A2 supported glycolysis and the TCA cycle, accompanied by NADH production, by affecting multiple metabolic enzymes to promote ATP production.	NAD	134-138	aldehyde dehydrogenase 1 family member A2	Homo sapiens	71-78
34766147-4	2021	Supplementing NAD+ intermediates can activate sirtuin deacylases (SIRT1-SIRT7), which regulates the benefits of exercise and dietary restriction, reduce the level of intracellular oxidative stress, and improve mitochondrial function, thereby reversing cell senescence.	NAD	14-18	sirtuin 7	Mus musculus	72-77
34108855-4	2021	Here, we show that low NAD+ in cultured cells promotes PER2 to be retained in the cytoplasm through the NAD+/SIRT1 axis, which leads to the attenuated amplitude of Bmal1 promoter-driven luciferase oscillation.	NAD	23-27	period circadian regulator 2	Homo sapiens	55-59
34108855-4	2021	Here, we show that low NAD+ in cultured cells promotes PER2 to be retained in the cytoplasm through the NAD+/SIRT1 axis, which leads to the attenuated amplitude of Bmal1 promoter-driven luciferase oscillation.	NAD	23-27	sirtuin 1	Homo sapiens	109-114
34108855-4	2021	Here, we show that low NAD+ in cultured cells promotes PER2 to be retained in the cytoplasm through the NAD+/SIRT1 axis, which leads to the attenuated amplitude of Bmal1 promoter-driven luciferase oscillation.	NAD	23-27	aryl hydrocarbon receptor nuclear translocator like	Homo sapiens	164-169
34108855-4	2021	Here, we show that low NAD+ in cultured cells promotes PER2 to be retained in the cytoplasm through the NAD+/SIRT1 axis, which leads to the attenuated amplitude of Bmal1 promoter-driven luciferase oscillation.	NAD	104-108	period circadian regulator 2	Homo sapiens	55-59
34108855-4	2021	Here, we show that low NAD+ in cultured cells promotes PER2 to be retained in the cytoplasm through the NAD+/SIRT1 axis, which leads to the attenuated amplitude of Bmal1 promoter-driven luciferase oscillation.	NAD	104-108	sirtuin 1	Homo sapiens	109-114
34108855-4	2021	Here, we show that low NAD+ in cultured cells promotes PER2 to be retained in the cytoplasm through the NAD+/SIRT1 axis, which leads to the attenuated amplitude of Bmal1 promoter-driven luciferase oscillation.	NAD	104-108	aryl hydrocarbon receptor nuclear translocator like	Homo sapiens	164-169
34194700-7	2021	The optimised chemo-bio catalysts are then used to supply NADH to an alcohol dehydrogenase for enantioselective (>99% ee) ketone reductions, leading to high cofactor turnover numbers and Pd and NAD+ reductase activities of 441 h-1 and 2347 h-1, respectively.	NAD	58-62	aldo-keto reductase family 1 member A1	Homo sapiens	69-90
35436671-1	2022	Sirtuin belongs to a family of coenzyme nicotinamide adenine dinucleotide (NAD+)-dependent histone deacetylases, which could be classified as seven isoforms (SIRT1-SIRT7).	NAD	75-79	sirtuin 1	Homo sapiens	158-163
35616339-6	2022	Sirtuins (SIRT1-SIRT7) are a highly conserved family of nicotinamide adenine dinucleotide (NAD+)-dependent deacetylases, protecting cells from metabolic stress by deacetylating vital proteins associated with lipid metabolism.	NAD	56-89	sirtuin 1	Homo sapiens	10-15
35616339-6	2022	Sirtuins (SIRT1-SIRT7) are a highly conserved family of nicotinamide adenine dinucleotide (NAD+)-dependent deacetylases, protecting cells from metabolic stress by deacetylating vital proteins associated with lipid metabolism.	NAD	56-89	sirtuin 7	Homo sapiens	16-21
35616339-6	2022	Sirtuins (SIRT1-SIRT7) are a highly conserved family of nicotinamide adenine dinucleotide (NAD+)-dependent deacetylases, protecting cells from metabolic stress by deacetylating vital proteins associated with lipid metabolism.	NAD	91-95	sirtuin 1	Homo sapiens	10-15
35616339-6	2022	Sirtuins (SIRT1-SIRT7) are a highly conserved family of nicotinamide adenine dinucleotide (NAD+)-dependent deacetylases, protecting cells from metabolic stress by deacetylating vital proteins associated with lipid metabolism.	NAD	91-95	sirtuin 7	Homo sapiens	16-21
34994384-10	2022	Moreover, it was demonstrated that H2S derived from CBS activated SIRT1 via increasing the NAD +/NADH ratio and promoting the phosphorylation of SIRT1.	NAD	91-96	sirtuin 1	Homo sapiens	66-71
34994384-10	2022	Moreover, it was demonstrated that H2S derived from CBS activated SIRT1 via increasing the NAD +/NADH ratio and promoting the phosphorylation of SIRT1.	NAD	97-101	sirtuin 1	Homo sapiens	66-71
35545049-0	2022	The lactate-NAD+ axis activates cancer-associated fibroblasts by downregulating p62.	NAD	12-16	nucleoporin 62	Homo sapiens	80-83
35545049-3	2022	Here we show that tumor-secreted lactate downregulates p62 transcriptionally through a mechanism involving reduction of the NAD+/NADH ratio, which impairs poly(ADP-ribose)-polymerase 1 (PARP-1) activity.	NAD	124-128	nucleoporin 62	Homo sapiens	55-58
35545049-3	2022	Here we show that tumor-secreted lactate downregulates p62 transcriptionally through a mechanism involving reduction of the NAD+/NADH ratio, which impairs poly(ADP-ribose)-polymerase 1 (PARP-1) activity.	NAD	129-133	nucleoporin 62	Homo sapiens	55-58
35545049-5	2022	Importantly, restoring p62 levels in CAFs by NAD+ renders CAFs less active.	NAD	45-49	nucleoporin 62	Homo sapiens	23-26
35500221-4	2022	Transcriptional profiling revealed that this oxidative phenotype was driven by IFNgamma-induced reprogramming of NAD+ metabolism, which is dependent on nicotinamide phosphoribosyltransferase (NAMPT)-mediated NAD+ salvage to generate NADH and NADPH for oxidation by mitochondrial complex I and NADPH oxidase, respectively.	NAD	113-117	2,4-dienoyl-CoA reductase 1	Homo sapiens	293-298
35150808-2	2022	Heat shock response (HSR) was altered in the absence of the NAD-dependent glycerol 3-phosphate dehydrogenase (Gpd1).	NAD	60-63	glycerol-3-phosphate dehydrogenase (NAD(+)) GPD1	Saccharomyces cerevisiae S288C	110-114
35150861-6	2022	Besides, Rd strengthened the interaction between AMPK and SIRT1 by increasing NAD+/NADH levels and LKB1 deacetylation in endothelial cells.	NAD	78-82	sirtuin 1	Homo sapiens	58-63
35150861-6	2022	Besides, Rd strengthened the interaction between AMPK and SIRT1 by increasing NAD+/NADH levels and LKB1 deacetylation in endothelial cells.	NAD	83-87	sirtuin 1	Homo sapiens	58-63
35504207-4	2022	Elevated PARP-1 activity triggered a cascade of molecular events, including PAR polymer release from the nucleus and the nicotinamide adenine dinucleotide (NAD+) and ATP depletion.	NAD	121-154	poly (ADP-ribose) polymerase family, member 1	Mus musculus	9-15
35504207-4	2022	Elevated PARP-1 activity triggered a cascade of molecular events, including PAR polymer release from the nucleus and the nicotinamide adenine dinucleotide (NAD+) and ATP depletion.	NAD	156-160	poly (ADP-ribose) polymerase family, member 1	Mus musculus	9-15
35137552-0	2022	NAD+ ameliorates endotoxin-induced acute kidney injury in a sirtuin1-dependent manner via GSK-3beta/Nrf2 signalling pathway.	NAD	0-4	sirtuin 1	Homo sapiens	60-68
35137552-3	2022	Sirtuin 1 (SIRT1) is an NAD+ -dependent deacetylase associated with renal protection and acute stress resistance.	NAD	24-27	sirtuin 1	Homo sapiens	0-9
35137552-3	2022	Sirtuin 1 (SIRT1) is an NAD+ -dependent deacetylase associated with renal protection and acute stress resistance.	NAD	24-27	sirtuin 1	Homo sapiens	11-16
35137552-6	2022	We also found that the protection of NAD+ is associated with SIRT1 expressions and performs in a SIRT1-dependent manner.	NAD	37-41	sirtuin 1	Homo sapiens	61-66
35137552-6	2022	We also found that the protection of NAD+ is associated with SIRT1 expressions and performs in a SIRT1-dependent manner.	NAD	37-41	sirtuin 1	Homo sapiens	97-102
35134563-6	2022	ATP and NADH, derivatives of adenosine, inhibit insulin signaling inside cells by downregulation of activities of AMPK and SIRT1, respectively.	NAD	8-12	sirtuin 1	Homo sapiens	123-128
35369299-4	2022	Sirtuin 3 (SIRT3) is one of the seven mammalian sirtuins (SIRT1 to SIRT7), with NAD+ dependent deacetylase activity.	NAD	80-83	sirtuin 1	Homo sapiens	58-63
35369299-4	2022	Sirtuin 3 (SIRT3) is one of the seven mammalian sirtuins (SIRT1 to SIRT7), with NAD+ dependent deacetylase activity.	NAD	80-83	sirtuin 7	Homo sapiens	67-72
35359990-5	2022	We also summarize factors that influence SIRT1 activity including the NAD+/NADH ratio, SIRT1 binding partners, and post-translational modifications.	NAD	70-74	sirtuin 1	Homo sapiens	41-46
34981410-1	2022	Betaine aldehyde dehydrogenase (BADH EC 1.2.1.8) catalyzes the irreversible oxidation of betaine aldehyde to glycine betaine using NAD+ as a coenzyme.	NAD	131-135	aldehyde dehydrogenase 7 family member A1	Homo sapiens	0-30
35296520-4	2022	Reduction of the cytoplasmic and mitochondrial NAD+/NADH ratio consequent to CoQ10 deficit can be expected to decrease the activity of these deacetylases by lessening availability of their obligate substrate NAD+ The increased oxidant production induced by CoQ10 deficiency can decrease the stability of Sirt1 protein by complementary mechanisms.	NAD	47-51	sirtuin 1	Homo sapiens	304-309
35296520-4	2022	Reduction of the cytoplasmic and mitochondrial NAD+/NADH ratio consequent to CoQ10 deficit can be expected to decrease the activity of these deacetylases by lessening availability of their obligate substrate NAD+ The increased oxidant production induced by CoQ10 deficiency can decrease the stability of Sirt1 protein by complementary mechanisms.	NAD	52-56	sirtuin 1	Homo sapiens	304-309
35296520-4	2022	Reduction of the cytoplasmic and mitochondrial NAD+/NADH ratio consequent to CoQ10 deficit can be expected to decrease the activity of these deacetylases by lessening availability of their obligate substrate NAD+ The increased oxidant production induced by CoQ10 deficiency can decrease the stability of Sirt1 protein by complementary mechanisms.	NAD	208-212	sirtuin 1	Homo sapiens	304-309
35182418-0	2022	MIB-626, an Oral Formulation of a Microcrystalline Unique Polymorph of beta-Nicotinamide Mononucleotide, Increases Circulating Nicotinamide Adenine Dinucleotide and its Metabolome in Middle-aged and Older Adults.	NAD	127-160	MIB E3 ubiquitin protein ligase 1	Homo sapiens	0-3
35182418-9	2022	MIB-626 treatment was associated with substantial dose-related increases in blood NAD levels.	NAD	82-85	MIB E3 ubiquitin protein ligase 1	Homo sapiens	0-3
35182418-13	2022	CONCLUSIONS: MIB-626 1000-mg once daily or twice daily regimens were safe and associated with substantial dose-related increases in blood NAD levels and its metabolome.	NAD	138-141	MIB E3 ubiquitin protein ligase 1	Homo sapiens	13-16
35013907-3	2022	TREM2 deficiency impairs the denovo synthesis pathway of NAD+.	NAD	57-61	triggering receptor expressed on myeloid cells 2	Mus musculus	0-5
35153673-2	2022	Synaptic ribbons are largely composed of RIBEYE, a protein containing an N-terminal A-domain and a carboxyterminal B-domain that is identical with CtBP2, a NAD(H)-binding transcriptional co-repressor.	NAD	156-162	C-terminal binding protein 2	Mus musculus	147-152
34981667-12	2022	Mechanistically, mitochondrial fission increased the acetylation level of sterol regulatory element-binding protein 1 (SREBP1) and peroxisome proliferator-activated receptor coactivator 1 alpha (PGC-1alpha) by suppressing nicotinamide adenine dinucleotide (NAD+)/Sirtuin 1 (SIRT1) signaling.	NAD	222-255	sirtuin 1	Homo sapiens	263-272
34981667-12	2022	Mechanistically, mitochondrial fission increased the acetylation level of sterol regulatory element-binding protein 1 (SREBP1) and peroxisome proliferator-activated receptor coactivator 1 alpha (PGC-1alpha) by suppressing nicotinamide adenine dinucleotide (NAD+)/Sirtuin 1 (SIRT1) signaling.	NAD	222-255	sirtuin 1	Homo sapiens	274-279
2478270-5	1989	High c-myc expression at this site coincides with expression of the NADH-dependent, cytosolic form of glycerol-3-phosphate dehydrogenase (GPDH).	NAD	68-72	glycerol phosphate dehydrogenase 2, mitochondrial	Mus musculus	102-136
2478270-5	1989	High c-myc expression at this site coincides with expression of the NADH-dependent, cytosolic form of glycerol-3-phosphate dehydrogenase (GPDH).	NAD	68-72	glycerol phosphate dehydrogenase 2, mitochondrial	Mus musculus	138-142
2546610-0	1989	Catalytic mechanism and interactions of NAD+ with glyceraldehyde-3-phosphate dehydrogenase: correlation of EPR data and enzymatic studies.	NAD	40-44	glyceraldehyde-3-phosphate dehydrogenase	Oryctolagus cuniculus	50-90
2930199-6	1989	Inactivation of NAD+-free apo-GAPDH by 1 showed simple pseudo-first-order kinetics.	NAD	16-20	glyceraldehyde-3-phosphate dehydrogenase	Oryctolagus cuniculus	30-35
2540809-10	1989	Both of the reconstituted proteins were found to be capable of transferring electrons to cytochrome c in a reconstituted system dependent on NADH and cytochrome b5 reductase, thus stimulating the activity of native cytochrome b5.	NAD	141-145	cytochrome b5 type A	Rattus norvegicus	215-228
3194395-6	1988	(ii) The koff for NADH from its GPDH complex is 60 sec-1 rather than 9.4 sec-1 in Tris.HCl buffer (pH 7.4) at 25 degrees C. With this value one can explain kcat = 50 sec-1 for LDH-catalyzed hydrogenation of pyruvate with GPDH-bound NADH as coenzyme.	NAD	18-22	secretory blood group 1, pseudogene	Homo sapiens	51-56
3194395-6	1988	(ii) The koff for NADH from its GPDH complex is 60 sec-1 rather than 9.4 sec-1 in Tris.HCl buffer (pH 7.4) at 25 degrees C. With this value one can explain kcat = 50 sec-1 for LDH-catalyzed hydrogenation of pyruvate with GPDH-bound NADH as coenzyme.	NAD	18-22	secretory blood group 1, pseudogene	Homo sapiens	73-78
3194395-6	1988	(ii) The koff for NADH from its GPDH complex is 60 sec-1 rather than 9.4 sec-1 in Tris.HCl buffer (pH 7.4) at 25 degrees C. With this value one can explain kcat = 50 sec-1 for LDH-catalyzed hydrogenation of pyruvate with GPDH-bound NADH as coenzyme.	NAD	18-22	secretory blood group 1, pseudogene	Homo sapiens	73-78
3194395-6	1988	(ii) The koff for NADH from its GPDH complex is 60 sec-1 rather than 9.4 sec-1 in Tris.HCl buffer (pH 7.4) at 25 degrees C. With this value one can explain kcat = 50 sec-1 for LDH-catalyzed hydrogenation of pyruvate with GPDH-bound NADH as coenzyme.	NAD	232-236	secretory blood group 1, pseudogene	Homo sapiens	51-56
3194395-6	1988	(ii) The koff for NADH from its GPDH complex is 60 sec-1 rather than 9.4 sec-1 in Tris.HCl buffer (pH 7.4) at 25 degrees C. With this value one can explain kcat = 50 sec-1 for LDH-catalyzed hydrogenation of pyruvate with GPDH-bound NADH as coenzyme.	NAD	232-236	secretory blood group 1, pseudogene	Homo sapiens	73-78
3194395-6	1988	(ii) The koff for NADH from its GPDH complex is 60 sec-1 rather than 9.4 sec-1 in Tris.HCl buffer (pH 7.4) at 25 degrees C. With this value one can explain kcat = 50 sec-1 for LDH-catalyzed hydrogenation of pyruvate with GPDH-bound NADH as coenzyme.	NAD	232-236	secretory blood group 1, pseudogene	Homo sapiens	73-78
16666409-5	1988	Cells grown on ammonium, instead of nitrate as nitrogen source, had a higher total cellular activity of the NADH-dependent glutamate synthase (+95%) and glutamate dehydrogenase (+33%) but less activity of glutamine synthetase (-10%).	NAD	108-112	uncharacterized protein	Chlamydomonas reinhardtii	205-225
3243781-1	1988	D-Lactate in biological samples was converted into the hydrazone of pyruvate in the presence of D-lactate dehydrogenase, an NADH-reoxidation system using diaphorase, DL-6,8-thioctamide and hydrazine.	NAD	124-128	lactate dehydrogenase D	Homo sapiens	96-119
3404995-4	1988	The cofactor dependence of EH was studied showing that NADPH is a better substrate for the enzyme than NADH.	NAD	103-107	2,4-dienoyl-CoA reductase 1	Homo sapiens	55-60
3395364-0	1988	Interaction of a photolabile NADH analog with rat liver dihydropteridine reductase.	NAD	29-33	quinoid dihydropteridine reductase	Rattus norvegicus	56-82
3276685-13	1988	The second question investigated was whether the known inhibition by acetyl-CoA of binding of NADH, an allosteric inhibitor of E. coli citrate synthase, occurs heterotropically, as an indirect result of acetyl-CoA binding at the active site, or directly, by competition at the allosteric NADH binding site.	NAD	94-98	citrate synthase	Sus scrofa	135-151
3276518-8	1988	Association of GAPD with mono- and polyribosomes can be prevented by a low concentration (10 microM) of NADH, but not NAD+.	NAD	104-108	glyceraldehyde-3-phosphate dehydrogenase	Oryctolagus cuniculus	15-19
3148319-4	1988	Also, the decrease in the cellular NAD+ content in these cells after irradiation was more pronounced than in LY-R cells; this may indicate an increased ADPRP activity upon infliction of DNA damage, or a difference in poly(ADP-ribose) turnover.	NAD	35-39	poly (ADP-ribose) polymerase family, member 1	Mus musculus	152-157
3170237-3	1988	Glutathione and NADH (10 mM) were the most effective antioxidants tested, causing a significant decrease in the rate of methemoglobin formation at 37 degrees C for periods of up to 50 hours.	NAD	16-20	hemoglobin subunit gamma 2	Homo sapiens	120-133
3170237-5	1988	In addition, NADH and glutathione were found to reduce methemoglobin levels to 10% over a period of 100 hours in a sample of human hemoglobin that had been stored at 4 degrees C for one year and had 60% methemoglobin.	NAD	13-17	hemoglobin subunit gamma 2	Homo sapiens	55-68
3170237-5	1988	In addition, NADH and glutathione were found to reduce methemoglobin levels to 10% over a period of 100 hours in a sample of human hemoglobin that had been stored at 4 degrees C for one year and had 60% methemoglobin.	NAD	13-17	hemoglobin subunit gamma 2	Homo sapiens	203-216
3320042-9	1987	Activity of fatty alcohol:NAD+ oxidoreductase, which catalyzes the oxidation of hexadecanol to palmitic acid, was inhibited by palmitoyl-CoA and NADH, but not by palmitic acid.	NAD	145-149	thioredoxin reductase 1	Homo sapiens	31-45
3435530-1	1987	The rate of 3-phosphoglycerate kinase reaction carried out under the conditions of saturating substrate concentrations (10 mM 3-phosphoglycerate, 3 mM ATP) and 0.2 mM NADH is increased in the presence of glyceraldehyde-3-phosphate dehydrogenase.	NAD	167-171	glyceraldehyde-3-phosphate dehydrogenase	Oryctolagus cuniculus	204-244
3620115-6	1987	The enzymatic properties of mMDH (specific activity, Km for oxaloacetate and NADH) in the absence and in the presence of PEG 6000 are indistinguishable.	NAD	77-81	malate dehydrogenase 2, NAD (mitochondrial)	Mus musculus	28-32
3690017-11	1987	At the same time ATP and NAD (the substrate of pADP-RP) concentrations dropped and nicotinamide accumulated extracellularly.	NAD	25-28	poly (ADP-ribose) polymerase family, member 1	Mus musculus	47-54
3595610-1	1987	On- and off-velocity constants for NADH and NAD+ binding to liver alcohol dehydrogenase in the pH range 10-12 have been determined by stopped-flow kinetic methods.	NAD	35-39	aldo-keto reductase family 1 member A1	Homo sapiens	66-87
3595610-1	1987	On- and off-velocity constants for NADH and NAD+ binding to liver alcohol dehydrogenase in the pH range 10-12 have been determined by stopped-flow kinetic methods.	NAD	44-48	aldo-keto reductase family 1 member A1	Homo sapiens	66-87
16665497-5	1987	All three NRs showed similar spectra with absorption maxima at 413 and 273 nanometers in the oxidized state, and with the characteristics of a cytochrome b type heme upon reduction with NADH (absorption maxima at 556, 527, and 424 nanometers).	NAD	186-190	LOC100797098	Glycine max	143-155
3116769-1	1987	After administration into rats of folic acid at a dose of 25 mg/kg within 14 days activities of NADPH-cytochrome P-450 and NADH-cytochrome b5 reductases, content of cytochromes P-450 and b5 as well as the rates of NADPH and NADH oxidation were increased in liver microsomes.	NAD	123-127	cytochrome b5 type A	Rattus norvegicus	128-141
3569292-0	1987	Electrostatic effects of bound NADH and NAD+ on ionizing groups in liver alcohol dehydrogenase.	NAD	31-35	aldo-keto reductase family 1 member A1	Homo sapiens	73-94
3569292-0	1987	Electrostatic effects of bound NADH and NAD+ on ionizing groups in liver alcohol dehydrogenase.	NAD	40-44	aldo-keto reductase family 1 member A1	Homo sapiens	73-94
3303039-5	1987	Mouse lung CBR exhibited optimal activity at pH 5.0; a preference for NADPH as coenzyme, although reactive with NADH at an order of magnitude higher concentration; poor activity as an ADH, but was strongly inhibited by 4-methyl pyrazole; and was inhibited by quercitin, dithiothreitol and p-OH-mercuribenzoate, but was insensitive to valproate or sorbinil.	NAD	112-116	carbonyl reductase 1	Mus musculus	11-14
3803575-3	1986	NADH-supported reduction of cytochrome b5 was also inhibited by propylthiouracil in the reconstituted system consisting of cytochrome b5 and partially purified NADH-cytochrome b5 reductase.	NAD	0-4	cytochrome b5 type A	Rattus norvegicus	28-41
3803575-3	1986	NADH-supported reduction of cytochrome b5 was also inhibited by propylthiouracil in the reconstituted system consisting of cytochrome b5 and partially purified NADH-cytochrome b5 reductase.	NAD	0-4	cytochrome b5 type A	Rattus norvegicus	123-136
3803575-3	1986	NADH-supported reduction of cytochrome b5 was also inhibited by propylthiouracil in the reconstituted system consisting of cytochrome b5 and partially purified NADH-cytochrome b5 reductase.	NAD	0-4	cytochrome b5 type A	Rattus norvegicus	123-136
3789735-0	1986	Microenvironment of the enzyme-bound NADH is different in lobster and pig muscle glyceraldehyde-3-phosphate dehydrogenase microcrystals.	NAD	37-41	glyceraldehyde-3-phosphate dehydrogenase	Sus scrofa	81-121
2875734-3	1986	However, the rebound crosslinked ATPase differed from the native enzyme in lacking the ability to restore NADH oxidation - and ATP hydrolysis-dependent quenching of the fluorescence of quinacrine to ATPase-stripped membrane vesicles.	NAD	106-110	ATPase	Escherichia coli	33-39
2875734-3	1986	However, the rebound crosslinked ATPase differed from the native enzyme in lacking the ability to restore NADH oxidation - and ATP hydrolysis-dependent quenching of the fluorescence of quinacrine to ATPase-stripped membrane vesicles.	NAD	106-110	ATPase	Escherichia coli	199-205
3729995-5	1986	Preincubation of the incubation mixture with NADH and NMTT resulted in inhibition of carboxylase activity when either vitamin KH2 or [vitamin K + NADH] was the substrate.	NAD	45-49	potassium voltage-gated channel modifier subfamily G member 1	Rattus norvegicus	126-129
3089221-7	1986	Severe depression of dGTP pools consequent to NAD and ATP depletion may provide a metabolic pathway for rapidly stopping DNA synthesis as a consequence of DNA damage and the activation of poly(ADP-ribose) polymerase.	NAD	46-49	poly (ADP-ribose) polymerase family, member 1	Mus musculus	188-215
3707618-4	1986	A two step pathway for the formation of this adduct was proposed involving first the production of oct-1-en-3-ol by NADPH dependent mixed function oxidases and secondly a NADP or NAD linked oxidation, independent of cytochrome P-450, to yield the putative reactive intermediate oct-1-en-3-one.	NAD	116-119	solute carrier family 22 member 1	Rattus norvegicus	99-104
3707618-4	1986	A two step pathway for the formation of this adduct was proposed involving first the production of oct-1-en-3-ol by NADPH dependent mixed function oxidases and secondly a NADP or NAD linked oxidation, independent of cytochrome P-450, to yield the putative reactive intermediate oct-1-en-3-one.	NAD	116-119	solute carrier family 22 member 1	Rattus norvegicus	278-283
3015753-3	1986	With NADH, however, strong O2- production was induced by Con A and Cyt B.	NAD	5-9	cytochrome b, mitochondrial	Rattus norvegicus	67-72
3015753-4	1986	2) FUT-175 at 10(-6) and 10(-5) M inhibited O2- production in rat PMN induced by Con A and Cyt B with NADH in a concentration-dependent manner.	NAD	102-106	cytochrome b, mitochondrial	Rattus norvegicus	91-96
4044607-7	1985	The biphasic relationship can be explained by the influence of the NADH/NAD+ ratio on the near-equilibrium reactions catalyzed by glyceraldehyde-3-phosphate dehydrogenase and malate dehydrogenase in the hepatocyte cytosol.	NAD	67-71	glyceraldehyde-3-phosphate dehydrogenase	Rattus norvegicus	130-170
4044607-7	1985	The biphasic relationship can be explained by the influence of the NADH/NAD+ ratio on the near-equilibrium reactions catalyzed by glyceraldehyde-3-phosphate dehydrogenase and malate dehydrogenase in the hepatocyte cytosol.	NAD	72-76	glyceraldehyde-3-phosphate dehydrogenase	Rattus norvegicus	130-170
4044607-8	1985	By shifting the equilibrium of the glyceraldehyde-3-phosphate dehydrogenase reaction, a rise in the NADH/NAD+ ratio decreases the concentration of 3-phosphoglycerate which, because of the linkage of 3-phosphoglycerate to phosphoenolpyruvate through two near-equilibrium reactions, reduces the concentration of phosphoenolpyruvate and therefore causes a decline in flux through pyruvate kinase.	NAD	100-104	glyceraldehyde-3-phosphate dehydrogenase	Rattus norvegicus	35-75
4044607-8	1985	By shifting the equilibrium of the glyceraldehyde-3-phosphate dehydrogenase reaction, a rise in the NADH/NAD+ ratio decreases the concentration of 3-phosphoglycerate which, because of the linkage of 3-phosphoglycerate to phosphoenolpyruvate through two near-equilibrium reactions, reduces the concentration of phosphoenolpyruvate and therefore causes a decline in flux through pyruvate kinase.	NAD	105-109	glyceraldehyde-3-phosphate dehydrogenase	Rattus norvegicus	35-75
3840037-2	1985	NADH-specific diaphorase activity is also present in membrane fractions rich in oxidoreductase activity.	NAD	0-4	thioredoxin reductase 1	Homo sapiens	80-94
3931630-6	1985	They show high enrichment and exclusive localization of the endoplasmic-reticulum marker NADH:cytochrome c reductase, and they sequester Ca2+ by an ATP-dependent process, reaching steady-state values in 10-12 min.	NAD	89-93	carbonic anhydrase 2	Homo sapiens	137-140
18553714-5	1985	Low concentration (50 muM) of NAD was also effective for the stabilization of malate dehydrogenase.	NAD	30-33	malic enzyme 1	Homo sapiens	78-98
6489918-4	1984	Furthermore, the rate of the NADH-depending lathosterol 5-desaturation in the reconstitution system, was proportional to the concentration either of the terminal desaturase, cytochrome b5, or NADH-cytochrome b5 reductase, under conditions in which other enzymes were present in excess.	NAD	29-33	cytochrome b5 type A	Rattus norvegicus	174-187
6489918-4	1984	Furthermore, the rate of the NADH-depending lathosterol 5-desaturation in the reconstitution system, was proportional to the concentration either of the terminal desaturase, cytochrome b5, or NADH-cytochrome b5 reductase, under conditions in which other enzymes were present in excess.	NAD	29-33	cytochrome b5 type A	Rattus norvegicus	197-210
6144544-11	1984	Poly(ADP-ribose) polymerase from Ehrlich ascites tumor cell nuclei accepted NAD[S] as a substrate but the reaction was significantly slower and approached saturation at much lower values than with NAD.	NAD	76-79	poly (ADP-ribose) polymerase family, member 1	Mus musculus	0-27
6698613-4	1984	Alternatively, treatment with base released D-lactate (beta-elimination), which was identified fluorimetrically by reduction of NAD to NADH with D-lactate dehydrogenase.	NAD	135-139	lactate dehydrogenase D	Homo sapiens	145-168
6425273-4	1984	Addition of NADH to the NADPH-supported oxygenase assay system enhanced both steroid oxygenase activities, and addition of the antibody against cytochrome b5 decreased the NADH-caused stimulation of steroid 17 alpha-hydroxylase and C-17-C-20 lyase activities.	NAD	172-176	cytochrome b5 type A	Rattus norvegicus	144-157
6366529-2	1984	Upon incubating emodin with the hepatic S9 derived from PCB-pretreated rats, this anthraquinone exhibited mutagenicity in the presence of NADPH or NADH, and this enzymatic activation, maximal at pH 7.0 and occurring in the microsomes, was induced by the pretreatment of rats with PCB, 3-methyl-cholanthrene or phenobarbital and was inhibited by alpha-naphthoflavone, SKF 525A and carbon monoxide.	NAD	147-151	pyruvate carboxylase	Rattus norvegicus	56-59
6317378-2	1983	Protection by NADH is strengthened by removal of cytochrome c from the submitochondrial particles and by antimycin A but abolished by rotenone.	NAD	14-18	cytochrome c	Sus scrofa	49-61
6137972-8	1983	DPR in adrenals and brain was found to be a NADH-dependent type.	NAD	44-48	quinoid dihydropteridine reductase	Rattus norvegicus	0-3
6871163-1	1983	Transferred nuclear Overhauser enhancement was used to examine the conformation of NAD+ and NADP+ bound to glucose-6-phosphate dehydrogenase and glutamate dehydrogenase and of NAD+ bound to lactate dehydrogenase.	NAD	83-87	glucose-6-phosphate dehydrogenase	Homo sapiens	107-140
6305359-3	1983	NADH-synergistic effect decreased in parallel with the decrease of the ratio of cytochrome b5/cytochrome P-450 in liver microsomes.	NAD	0-4	cytochrome b5 type A	Rattus norvegicus	80-93
6190435-3	1983	When ruthenium red is added to block efflux via this pathway, high rates of Ca2+ efflux can still be induced by an uncoupler, provided either NADH is oxidized or mitochondrial adenine nucleotide pools are depleted by prior treatment.	NAD	142-146	carbonic anhydrase 2	Homo sapiens	76-79
6834391-5	1983	The omicron-quinone 7b has a rather low inhibitory effect against L1210 leukemia cell multiplication but acts as an electron carrier and dramatically augments the oxygen consumption in xanthine oxidase-NADH and rat liver microsomes-NADPH systems.	NAD	202-206	xanthine dehydrogenase	Mus musculus	185-201
6848515-7	1983	This pair could also provide an explanation for the relatively stronger binding by cytoplasmic malate dehydrogenase and lactate dehydrogenase of NADH versus NAD.	NAD	145-149	malic enzyme 1	Homo sapiens	95-115
6848515-7	1983	This pair could also provide an explanation for the relatively stronger binding by cytoplasmic malate dehydrogenase and lactate dehydrogenase of NADH versus NAD.	NAD	145-148	malic enzyme 1	Homo sapiens	95-115
6316379-1	1983	The reactions of oxidation of NADH by Dopa and Dopamine-melanins show inhibition with low quantities of Superoxide dismutase, the enzyme which catalyzes the reaction: O2- + O2- + 2H+ leads to H2O2 + O2 and which has been used as an indicator of the involvement of superoxide ions in many biochemical systems.	NAD	30-34	immunoglobulin kappa variable 1D-39	Homo sapiens	192-201
6817789-0	1982	Local conformational changes induced by successive nicotinamide adenine dinucleotide binding to dissociable tetrameric D-glyceraldehyde-3-phosphate dehydrogenase.	NAD	51-84	glyceraldehyde-3-phosphate dehydrogenase	Sus scrofa	119-161
6817789-3	1982	The binding of NAD to dehydrogenase-FITC complex partially reverts the quenching caused by the binding of dye to apo-GAPD.	NAD	15-18	glyceraldehyde-3-phosphate dehydrogenase	Sus scrofa	117-121
6817789-11	1982	The specific fluorescence intensity and the fluorescence anisotropy of fluorescent dye labeled apo-GAPD and GAPD saturated with NAD are also dependent on enzyme concentration.	NAD	128-131	glyceraldehyde-3-phosphate dehydrogenase	Sus scrofa	99-103
6817789-11	1982	The specific fluorescence intensity and the fluorescence anisotropy of fluorescent dye labeled apo-GAPD and GAPD saturated with NAD are also dependent on enzyme concentration.	NAD	128-131	glyceraldehyde-3-phosphate dehydrogenase	Sus scrofa	108-112
6806275-6	1982	Thus, microsomal cytochrome P-450 appears to be reduced via two independent pathways of electron transport from NADH; the biphasic reduction occurs via cytochrome P-450 reductase while the slower monophasic reduction occurs via cytochrome b5.	NAD	112-116	cytochrome b5 type A	Rattus norvegicus	228-241
6954534-1	1982	Extensive amino acid sequence homology has been found between nine tryptic peptides of pig heart lipoamide dehydrogenase (NADH:lipoamide oxidoreductase, EC 1.6.4.3] and the sequence of human erythrocyte glutathione reductase [NAD(P)H:glutathione oxidoreductase, EC 1.6.4.2].	NAD	122-125	thioredoxin reductase 1	Homo sapiens	137-151
6954534-1	1982	Extensive amino acid sequence homology has been found between nine tryptic peptides of pig heart lipoamide dehydrogenase (NADH:lipoamide oxidoreductase, EC 1.6.4.3] and the sequence of human erythrocyte glutathione reductase [NAD(P)H:glutathione oxidoreductase, EC 1.6.4.2].	NAD	122-125	thioredoxin reductase 1	Homo sapiens	246-260
6119752-7	1981	It is concluded that bromotrichloromethane and 1,2-dibromo-1,2-dichloroethane stimulate hepatic microsomal electron transfer from NADH via cytochrome b-5 by interacting with cytochrome P-450 and with stearate desaturase.	NAD	130-134	cytochrome b5 type A	Rattus norvegicus	139-153
7028733-2	1981	Aspartate is converted to oxalacetate by glutamate-oxalacetate transaminase, and the resulting oxalacetate is converted to malate by the NADH, NAD+ oxidoreductase enzyme malate dehydrogenase.	NAD	137-141	oxidoreductase	Escherichia coli	148-162
7028119-1	1981	The binding of dimers of nicotinamide adenine dinucleotide, (NAD)2, to lactate, malate and alcohol dehydrogenase has been studied by the fluorescence quenching technique.	NAD	25-58	aldo-keto reductase family 1 member A1	Homo sapiens	91-112
7281897-0	1981	[Half-of-the-sites reactivity of glyceraldehyde-3 phosphate dehydrogenase from rabbit muscle with structural analogs of NAD (author"s transl)].	NAD	120-123	glyceraldehyde-3-phosphate dehydrogenase	Oryctolagus cuniculus	33-73
6788036-4	1981	We have shown than ADH (Alcohol: NAD oxidoreductase, E.C.1.1.1.1) also oxidizes L(+)-lactate or D(-)-lactate with the NAD, while LDH oxidizes ethanol.	NAD	33-36	Lactate dehydrogenase	Drosophila melanogaster	129-132
6252782-1	1980	The activities of the enzymes catalyzing in the early steps in prostaglandin metabolism (the nicotinamide adenine dinucleotide [NAD]-linked 15-hydroxyprostaglandin dehydrogenase, the nicotinamide adenine dinucleotide phosphate [NADP]-linked 15-hydroxyprostaglandin dehydrogenase, and the 15-ketoprostaglandin delta 13 reductase) were measured in homogenates of term placenta.	NAD	93-126	carbonyl reductase 1	Homo sapiens	140-177
6252782-1	1980	The activities of the enzymes catalyzing in the early steps in prostaglandin metabolism (the nicotinamide adenine dinucleotide [NAD]-linked 15-hydroxyprostaglandin dehydrogenase, the nicotinamide adenine dinucleotide phosphate [NADP]-linked 15-hydroxyprostaglandin dehydrogenase, and the 15-ketoprostaglandin delta 13 reductase) were measured in homogenates of term placenta.	NAD	128-131	carbonyl reductase 1	Homo sapiens	140-177
6774753-1	1980	Three homozygous allelic forms (alpha GPDHf, alpha GPDHm and alpha GPDHs) of NAD+-dependent glycerol-3-phosphate dehydrogenase (sn-glycerol-3-phosphate:NAD+ 2-oxidoreductase, EC 1.1.1.8) of Drosophila virilis were purified to homogeneity and their biochemical properties were compared.	NAD	77-80	glycerol-3-phosphate dehydrogenase [NAD(+)], cytoplasmic	Drosophila virilis	92-126
6786276-2	1980	The addition of NADH gave similar stimulation of both aniline parahydroxylation and NADPH-cytochrome P450 reductase activity in the presence of aniline.	NAD	16-20	cytochrome p450 oxidoreductase	Rattus norvegicus	84-115
6786276-3	1980	It is proposed that the increase in aniline metabolism with NADH is due to an increase in the NADPH-cytochrome P450 reductase activity which is rate limiting in microsomes from both phenobarbital and untreated rats.	NAD	60-64	cytochrome p450 oxidoreductase	Rattus norvegicus	94-125
6108211-4	1980	The immobilised-IMP analogues displayed specificity for the inosine-nucleotide-dependent enzyme, IMP dehydrogenase (IMP:NAD+ oxidoreductase, EC 1.2.1.14) but not for the NAD+-dependent enzymes, L-alanine and L-acetate dehydrogenases.	NAD	120-124	oxidoreductase	Escherichia coli	125-139
7390994-1	1980	A reconstituted system containing a form of cytochrome P-450, cytochrome b5, NADPH-cytochrome P-450 reductase, and NADH-cytochrome b5 reductase, all purified from rabbit liver microsomes, could catalyze O-demethylation of p-nitroanisole in the presence of both NADPH and NADH.	NAD	115-119	cytochrome b5	Oryctolagus cuniculus	120-133
6246954-1	1980	Human placenta contains a thermostable, cytosolic NADH-diaphorase which is different from the other diaphorases and which we designate as diaphorase P. It is specific for NADH and reduces artificial substrates such as dichlorophenol and tetrazolium derivatives, but not natural substrates such as methemoglobin, cytochrome b5 or lipoate.	NAD	50-54	hemoglobin subunit gamma 2	Homo sapiens	297-310
6250824-2	1980	Alkylation at the N-1 position of the adenine moiety of NAD+, ADP or ATP with 2,3-epoxypropyl acrylate, followed by polymerization with or without acrylamide at pH 8, gave water-soluble polymers of NAD+ and ADP where the alkyl chain was located at the exocyclic adenine C-6 amino group.	NAD	56-60	LOW QUALITY PROTEIN: complement component C6	Oryctolagus cuniculus	270-273
94928-2	1979	The liberated glucose is determined specifically by the hexokinase/glucose-6-phosphate dehydrogenase (NAD+-dependent) method+ by addition of pyruvate, lactate dehydrogenase and ATP.	NAD	102-106	glucose-6-phosphate dehydrogenase	Homo sapiens	67-100
230779-4	1979	Incorporation of NAD, NADH or AMP into a starch-gel matrix leads to retardation in the cathodal mobilities of the gamma 2 gamma 2 and alpha alpha isozymes, but not the beta 1 beta 1 and gamma 1 gamma 1 isozymes.	NAD	17-20	UDP-GlcNAc:betaGal beta-1,3-N-acetylglucosaminyltransferase 2	Homo sapiens	175-181
508300-6	1979	It is concluded that, in the newborn rat in vivo, hepatic fatty acids oxidation can increase the gluconeogenic flux by providing the acetyl-CoA necessary for the reaction catalysed by pyruvate carboxylase and the reducing equivalents (NADH) to displace the reversible reaction catalysed by glyceraldehyde 3-phosphate dehydrogenase in the direction of gluconeogenesis.	NAD	235-239	glyceraldehyde-3-phosphate dehydrogenase	Rattus norvegicus	290-330
220211-10	1979	The remaining nicotinamide mononucleotide accumulates extracellularly and will support the growth of nadA pncB mutants which cannot utilize the nicotinamide resulting from the major pathway of NAD degradation.	NAD	193-196	nicotinate phosphoribosyltransferase	Salmonella enterica subsp. enterica serovar Typhimurium str. LT2	106-110
37557-4	1979	With NAD+ as electron acceptor a different profile in the pKM xanthine plot is obtained for chicken liver xanthine dehydrogenase.	NAD	5-9	pyruvate kinase, liver and RBC	Gallus gallus	58-61
217734-0	1979	Recycling by a second enzyme of NAD covalently bound to alcohol dehydrogenase.	NAD	32-35	aldo-keto reductase family 1 member A1	Homo sapiens	56-77
220964-11	1979	The kinetics of cytochrome b reduction by NADH were measured in mixtures containing 2 mol of Complex III/mol of Complex I.	NAD	42-46	cytochrome b	Bos taurus	16-28
233819-2	1979	The time course of the probe absorption spectrum red shift induced by ATP or NADH injection into a suspension of submitochondrial particles in a dye solution is biphasic, consisting of a faster process described by a second-order rate law with k2 approximately 3 x 10(5) M-1 sec-1.	NAD	77-81	secretory blood group 1, pseudogene	Homo sapiens	275-280
212320-1	1978	A functional NAD molecule was immobilized at the active site of Alcohol dehydrogenase within a proteic membrane.	NAD	13-16	aldo-keto reductase family 1 member A1	Homo sapiens	64-85
29040-1	1978	The interactions of a homogeneous preparation of rat liver dihydropteridine reductase with NADH, NADPH, NAD+, NADP+, and the 1-N6-ethenoadenine derivative of NAD+ have been investigated by fluorescence titration, circular dichroism, equilibrium dialysis, Sephadex G-25 chromatography, and polyacrylamide gel electrophoresis.	NAD	91-95	quinoid dihydropteridine reductase	Rattus norvegicus	59-85
29040-1	1978	The interactions of a homogeneous preparation of rat liver dihydropteridine reductase with NADH, NADPH, NAD+, NADP+, and the 1-N6-ethenoadenine derivative of NAD+ have been investigated by fluorescence titration, circular dichroism, equilibrium dialysis, Sephadex G-25 chromatography, and polyacrylamide gel electrophoresis.	NAD	104-108	quinoid dihydropteridine reductase	Rattus norvegicus	59-85
29040-1	1978	The interactions of a homogeneous preparation of rat liver dihydropteridine reductase with NADH, NADPH, NAD+, NADP+, and the 1-N6-ethenoadenine derivative of NAD+ have been investigated by fluorescence titration, circular dichroism, equilibrium dialysis, Sephadex G-25 chromatography, and polyacrylamide gel electrophoresis.	NAD	158-162	quinoid dihydropteridine reductase	Rattus norvegicus	59-85
737227-8	1978	Combined effect of Ca2+ and phospholipase D on outer and inner NADH oxidation pathway manifests differently.	NAD	63-67	carbonic anhydrase 2	Homo sapiens	19-22
27359-5	1978	All essential features of the transient-state kinetics of alcohol oxidation by NAD+ in the liver alcohol dehydrogenase system can be qualitatively and quantitatively explained in view of the compulsory-order mechanism in the proposed scheme.	NAD	79-83	aldo-keto reductase family 1 member A1	Homo sapiens	97-118
204355-1	1978	NAD recycling in the collagen membrane was investigated as follows: (1) Alcohol dehydrogenase and lactate dehydrogenase were co-immobilized in the collagen membrane and the rate of lactate production by immobilized enzymes was compared with that of free enzymes by using free NAD.	NAD	0-3	aldo-keto reductase family 1 member A1	Homo sapiens	72-93
24622-3	1978	Antibodies to NADH-cytochrome b5 reductase [EC 1.6.2.2] and cytochrome b5 inhibited NADH-dependent lipid peroxidation in the presence of ADP-Fe, whereas the antibody against NADPH-cytochrome c reductase [EC 1.6.2.4] showed no inhibition.	NAD	14-18	cytochrome b5 type A	Rattus norvegicus	19-32
24622-4	1978	These oberservations suggest that the electron from NADH was supplied to the lipid peroxidation reaction via NADH-cytochrome b5 reductase and cytochrome b5.	NAD	52-56	cytochrome b5 type A	Rattus norvegicus	114-127
24622-4	1978	These oberservations suggest that the electron from NADH was supplied to the lipid peroxidation reaction via NADH-cytochrome b5 reductase and cytochrome b5.	NAD	52-56	cytochrome b5 type A	Rattus norvegicus	142-155
32437-0	1978	Isolation and partial characterization of human erythrocyte membrane NADH: (acceptor) oxidoreductase.	NAD	69-73	thioredoxin reductase 1	Homo sapiens	86-100
32437-1	1978	The NADH: (acceptor) oxidoreductase (EC 1.6.99.3) was isolated from human erythrocyte ghosts by a procedure including Triton X-100 solubilization, affinity chromatography on an NAD+-Sepharose 4B column, ammonium sulfate precipitation, and isoelectric focusing.	NAD	4-8	thioredoxin reductase 1	Homo sapiens	21-35
32437-1	1978	The NADH: (acceptor) oxidoreductase (EC 1.6.99.3) was isolated from human erythrocyte ghosts by a procedure including Triton X-100 solubilization, affinity chromatography on an NAD+-Sepharose 4B column, ammonium sulfate precipitation, and isoelectric focusing.	NAD	177-181	thioredoxin reductase 1	Homo sapiens	21-35
32437-5	1978	The pH optimum was 6.8 and the isoelectric point, pI, was 6.6 The oxidoreductase has a specificity for NADH as a cofactor.	NAD	103-107	thioredoxin reductase 1	Homo sapiens	66-80
32437-13	1978	We suggest that the membrane-bound NADH: (acceptor) oxidoreductase might be a transmembrane protein.	NAD	35-39	thioredoxin reductase 1	Homo sapiens	52-66
13132-1	1977	The NADH-dependent stearoyl CoA desaturase of hepatic microsomes (EC 1.14.99.5) is an enzyme system consisting of cytochrome b5 reductase (EC 1.6.2.2), cytochrome b5, and the terminal desaturase.	NAD	4-8	stearoyl-CoA desaturase	Rattus norvegicus	19-42
1007618-1	1976	In apples, L-malate was significantly less when estimated by titration with NaOH than by spectrophotometry after enzymatic reduction of NAD+ with malate dehydrogenase.	NAD	136-140	malate dehydrogenase	Malus domestica	146-166
10108-8	1976	among these NAD analogues, 3-acetyl NXD gives the highest HBD activity, especially in the M4 preparation.	NAD	12-15	HBD	Homo sapiens	58-61
10108-12	1976	As to HBD activity, the content of LDH subunit having HBD activity has been estimated by determing the enzyme activity under conditions in which either 300 mM 2-hydroxybutyrate with 3-acetyl NXD or 15 mM 2-hydroxybutyrate with NAD are employed.	NAD	227-230	HBD	Homo sapiens	54-57
8453-2	1976	The three purified proteins which are required for microsomal stearyl-CoA desaturation, NADH-cytochrome b5 reductase, cytochrome b5, and desaturase, have been combined with egg lecithin or dimyristyl lecithin vesicles to reconstruct a functional electron transport system capable of utilizing NADH and O2 in the desaturation of stearyl-CoA.	NAD	88-92	cytochrome b5 type A	Rattus norvegicus	93-106
9276-2	1976	The synthesis and purification of the 8-azidoadenine analogs of NAD+ (azido-NAD+) and FAD (AZIDO-FAD) from 8-azidoadenosine 5"-phosphate and NMN+ or FMN, respectively, is described.	NAD	64-68	FA complementation group D2	Homo sapiens	91-100
938666-4	1976	Acid-labile amide-bound ammonia of elastin was quantitated after hydrolysis of the insoluble protein with 2 M HC1 by incubating aliquots of microdistilled hydrolysates with glutamate dehydrogenase, excess alpha-ketoglutarate, and reduced nicotinamide adenine dinucleotide and measuring the resultant decrease in A340 due to oxidation of the dinucleotide cofactor.	NAD	238-271	elastin	Homo sapiens	35-42
176283-4	1976	In the third phase, membrane basal adenylate cyclase is activated by MCAF in the presence of NAD.	NAD	93-96	chemokine (C-C motif) ligand 2	Mus musculus	69-73
2388-1	1976	The molar absorptivity of NADH at 340 nm has been determined by an indirect procedure in which high-purity glucose is phosphorylated by ATP in the presence of hexokinase, coupled to oxidation of the glucose-6-phosphate by NAD+ in the presence of glucose-6-phosphate dehydrogenase.	NAD	26-30	glucose-6-phosphate dehydrogenase	Homo sapiens	246-279
12937-4	1976	The results indicated that two different enzymes were involved in the NAD- and NADP-IDH activities.	NAD	70-73	isocitrate dehydrogenase (NAD(+)) 3 non-catalytic subunit gamma	Rattus norvegicus	84-87
6615-1	1976	The oxidoreductase inhibitor was prepared from NAD in alkaline solution, and purified chromatographically.	NAD	47-50	thioredoxin reductase 1	Homo sapiens	4-18
6616-1	1976	The oxidoreductase inhibitor is not formed from NADH as previously thought, but only from NAD under alkaline conditions.	NAD	48-52	thioredoxin reductase 1	Homo sapiens	4-18
175045-10	1975	In contrast to the reoxidation of beta-NADH-reduced cytochrome b5, the process was largely monophasic when cytochrome b5 was reduced with alpha-NADH.	NAD	34-43	cytochrome b5 type A	Rattus norvegicus	52-65
175045-10	1975	In contrast to the reoxidation of beta-NADH-reduced cytochrome b5, the process was largely monophasic when cytochrome b5 was reduced with alpha-NADH.	NAD	34-43	cytochrome b5 type A	Rattus norvegicus	107-120
239968-4	1975	The Km"s for NADPH and NADH were 8.6 +/- 4.6 muM and 0.83 +/- 0.30 mM, respectively, suggesting that NADPH is the physiological electron donor in this system.	NAD	23-27	2,4-dienoyl-CoA reductase 1	Homo sapiens	101-106
164884-0	1975	Interaction of reduced nicotinamide adenine dinucleotide with beef heart s-malate dehydrogenase.	NAD	23-56	malic enzyme 1	Homo sapiens	75-95
164884-1	1975	The interaction of NADH with s-malate dehydrogenase isolated from beef heart was studied in 20 mM potassium phosphate (pH 6.9)-1 mM EDTA, with forced dialysis, fluorescence, and temperature-jump techniques.	NAD	19-23	malic enzyme 1	Homo sapiens	31-51
170082-6	1975	The biphasic reduction of cytochrome b was observed over a wide temperature range (0--30 degrees C), with succinate of NADH as electron donors and with phosphorylating particles or coupled rat-heart mitochondria.	NAD	119-123	cytochrome b, mitochondrial	Rattus norvegicus	26-38
167554-5	1975	ADH catalyses interconversion of a large variety of saturated and unsaturated aliphatic and aromatic alcohols and the corresponding aldehydes and ketones utilizing NAD(H).	NAD	164-170	aldo-keto reductase family 1 member A1	Homo sapiens	0-3
4399579-0	1971	Decreased thermal stability of alcohol dehydrogenase in the presence of oxidized nicotinamide-adenine dinucleotide or oxidized nicotinamide-adenine dinucleotide phosphate.	NAD	81-114	aldo-keto reductase family 1 member A1	Homo sapiens	31-52
5784224-1	1969	A study of the subcellular localization of the nicotinamide adenine dinucleotide (NADH)-3-(4, 3-dimethylthiazolyl-2)-2,5-diphenyltetrazolium bromide (MTT) oxido-reductase systems in Mycobacterium was presented.	NAD	47-80	thioredoxin reductase 1	Homo sapiens	155-170
4304229-0	1969	The effect of deuterium oxide on the fluorescence of reduced nicotinamide adenine dinucleotide free in solution and in complexes with liver alcohol dehydrogenase.	NAD	61-94	aldo-keto reductase family 1 member A1	Homo sapiens	140-161
4304739-0	1968	Inhibitory effect of lysolecithin on electron transfer from NADH to cytochrome b.	NAD	60-64	mitochondrially encoded cytochrome b	Homo sapiens	68-80
16695946-6	1968	Hemolysates prepared from both normal erythrocytes and from erythrocytes deficient in glucose-6-phosphate dehydrogenase activity were able to reduce oxidized glutathione in the presence of added lactate and NAD.	NAD	207-210	glucose-6-phosphate dehydrogenase	Homo sapiens	86-119
4385354-0	1967	[Studies on the kinetics of microsomal NADH:semidehydroascorbate oxidoreductase].	NAD	39-43	thioredoxin reductase 1	Homo sapiens	65-80
14335764-1	1964	NADH AND NADPH OXIDASES AS WELL AS NADP REACTIVE LACTATE OXIDOREDUCTASE IN RED BLOOD CELLS].	NAD	0-4	thioredoxin reductase 1	Homo sapiens	57-71
14057355-1	1963	Experiments with analogs of the coenzyme nicotinamide adenine dinucleotide demonstrate that the molecular forms of malate dehydrogenase in Euglena vary with the nutritional environment.	NAD	41-74	malic enzyme 1	Homo sapiens	115-135
33907836-3	2021	Sirtuin 1 (SIRT1) is a NAD+-dependent deacetylase that regulates several bioactive substances, and the present study aimed to identify the role of SIRT1/AMP-activated protein kinase (AMPK) signaling in RCC progression.	NAD	23-26	sirtuin 1	Homo sapiens	0-9
33907836-3	2021	Sirtuin 1 (SIRT1) is a NAD+-dependent deacetylase that regulates several bioactive substances, and the present study aimed to identify the role of SIRT1/AMP-activated protein kinase (AMPK) signaling in RCC progression.	NAD	23-26	sirtuin 1	Homo sapiens	11-16
33907836-3	2021	Sirtuin 1 (SIRT1) is a NAD+-dependent deacetylase that regulates several bioactive substances, and the present study aimed to identify the role of SIRT1/AMP-activated protein kinase (AMPK) signaling in RCC progression.	NAD	23-26	protein kinase AMP-activated non-catalytic subunit beta 1	Homo sapiens	183-187
34052293-7	2021	Protein level of nuclear factor erythroid 2-related factor 2 (Nrf2), haem oxygenase-1 (HO1) and nicotinamide adenine dinucleotide phosphate quinone oxidoreductase 1 (NQO1) was evaluated by immunohistochemistry staining and western blotting.	NAD	96-129	NAD(P)H dehydrogenase, quinone 1	Mus musculus	166-170
33709122-0	2021	Mutant NMNAT1 leads to a retina-specific decrease of NAD+ accompanied by increased poly(ADP-ribose) in a mouse model of NMNAT1-associated retinal degeneration.	NAD	53-57	nicotinamide nucleotide adenylyltransferase 1	Mus musculus	7-13
33709122-1	2021	Nicotinamide mononucleotide adenylyltransferase 1 (NMNAT1) is required for nuclear NAD+ biosynthesis in all nucleated cells, and despite its functional ubiquity, mutations in this gene lead to an isolated retinal degeneration.	NAD	83-87	nicotinamide nucleotide adenylyltransferase 1	Mus musculus	0-49
33709122-1	2021	Nicotinamide mononucleotide adenylyltransferase 1 (NMNAT1) is required for nuclear NAD+ biosynthesis in all nucleated cells, and despite its functional ubiquity, mutations in this gene lead to an isolated retinal degeneration.	NAD	83-87	nicotinamide nucleotide adenylyltransferase 1	Mus musculus	51-57
33709122-3	2021	Using a mouse model of NMNAT1-associated retinal degeneration that harbors the p.Val9Met mutation, we tested the hypothesis that decreased function of mutant NMNAT1 has a greater effect on the levels of NAD+ in the retina than elsewhere in the body.	NAD	203-207	nicotinamide nucleotide adenylyltransferase 1	Mus musculus	158-164
33991007-7	2021	ATP, ADP and AMP as well as NAD+ , NADH, NADP+ and NADPH directly interact with CIRBP, involving both the folded RNA-recognition motif and the disordered RG/RGG region.	NAD	28-32	2,4-dienoyl-CoA reductase 1	Homo sapiens	51-56
33876629-6	2021	Kinetic analysis of inhibition and docking studies reveal that the inhibitors bind to a complex of SirT1 and nicotinamide adenine dinucleotide, similar to selisistat.	NAD	109-142	sirtuin 1	Homo sapiens	99-104
33976173-3	2021	Here, we identify NAMPT, the rate limiting enzyme in NAD salvage synthesis, as a target of STAT1 during cellular activation by interferon gamma, an important driver of macrophage polarization and antitumor responses.	NAD	53-56	signal transducer and activator of transcription 1	Homo sapiens	91-96
33957971-0	2021	MiR-34a suppression targets Nampt to ameliorate bone marrow mesenchymal stem cell senescence by regulating NAD+-Sirt1 pathway.	NAD	107-111	sirtuin 1	Homo sapiens	112-117
33689977-5	2021	Inhibition of MDH2 by our compounds was expected to decrease the NADH level.	NAD	65-69	malate dehydrogenase 2	Homo sapiens	14-18
33981300-4	2021	Sirtuin-1 (SIRT1), an NAD+-dependent histone deacetylase, has been shown to be a pivotal regulator in various physiological processes, including cell differentiation, apoptosis, metabolism, aging, and immune responses, via modulation of different signaling pathways, such as the nuclear factor kappa-light-chain-enhancer of activated B cells and activator protein 1 pathways.	NAD	22-25	sirtuin 1	Homo sapiens	0-9
33981300-4	2021	Sirtuin-1 (SIRT1), an NAD+-dependent histone deacetylase, has been shown to be a pivotal regulator in various physiological processes, including cell differentiation, apoptosis, metabolism, aging, and immune responses, via modulation of different signaling pathways, such as the nuclear factor kappa-light-chain-enhancer of activated B cells and activator protein 1 pathways.	NAD	22-25	sirtuin 1	Homo sapiens	11-16
33902947-0	2022	Corrigendum to "Increasing ovarian NAD+ levels improve mitochondrial functions and reverse ovarian aging" [Free Rad.	NAD	35-39	RRAD, Ras related glycolysis inhibitor and calcium channel regulator	Homo sapiens	112-115
33871064-0	2021	Inhibition of CD38 and supplementation of nicotinamide riboside ameliorate lipopolysaccharide-induced microglial and astrocytic neuroinflammation by increasing NAD.	NAD	160-163	CD38 antigen	Mus musculus	14-18
33871064-4	2021	Our previous study demonstrated that deletion of CD38, which consumes NAD+ , suppressed cuprizone-induced demyelination, neuroinflammation and glial activation.	NAD	70-74	CD38 antigen	Mus musculus	49-53
33871064-5	2021	However, it is still unknown whether CD38 directly affects neuroinflammation through regulating brain NAD+ level.	NAD	102-106	CD38 antigen	Mus musculus	37-41
33871064-12	2021	These results suggest that CD38-mediated neuroinflammation is linked to NAD+ consumption and that boosting NAD+ by CD38 inhibition and NR supplementation directly suppress neuroinflammation in the brain.	NAD	72-76	CD38 antigen	Mus musculus	27-31
33871064-12	2021	These results suggest that CD38-mediated neuroinflammation is linked to NAD+ consumption and that boosting NAD+ by CD38 inhibition and NR supplementation directly suppress neuroinflammation in the brain.	NAD	107-111	CD38 antigen	Mus musculus	115-119
33784074-4	2021	When not present in protein complexes, NADH and its phosphorylated form NADPH degrade through intricate mechanisms.	NAD	39-43	2,4-dienoyl-CoA reductase 1	Homo sapiens	72-77
33838082-5	2021	To further understand this, we have discovered a heterobifunctional small molecule designed based on a catalytic inhibitor of PARP14 that binds in the enzyme"s NAD + -binding site and recruits the E3 ligase cereblon to ubiquitinate it and selectively target it for degradation.	NAD	160-165	poly(ADP-ribose) polymerase family member 14	Homo sapiens	126-132
33893948-3	2021	Photoactivation of astrocytes led to activation of neurogenesis and changes in the expression of molecules (Cx43 and CD38) that determine bioavailability of NAD+ to ensure proliferative activity of cells in the neurogenic niche.	NAD	157-161	CD38 antigen	Mus musculus	117-121
33609723-12	2021	Taken together, our results suggested that CS-induced senescence of AT2 cells was due to decreased autophagy mediated by SIRT1 inactivation, which was attributed to competitive consumption of NAD+ caused by DNA damage-induced PARP1 activation.	NAD	192-196	poly (ADP-ribose) polymerase family, member 1	Mus musculus	226-231
33738067-1	2021	SIRT1, a member of the sirtuin family, catalyzes the deacetylation of proteins with the transformation of NAD+ into nicotinamide and 2"-O-acetyl-ADP-ribose.	NAD	106-110	sirtuin 1	Homo sapiens	0-5
33388853-4	2021	This review focuses on SIRT1, an NAD+-dependent class III histone deacetylase which counterbalances the intrinsic histone acetyltransferase activity of one of the clock genes, CLOCK.	NAD	33-36	sirtuin 1	Homo sapiens	23-28
33326842-7	2021	Together, our results indicate that resveratrol improves ethanol-triggered beta-cell senescence and consequently recovers beta-cell mass loss by inhibiting p38MAPK/p16 pathway through an NAD+/SIRT1 dependent pathway.	NAD	187-191	cyclin-dependent kinase inhibitor 2A	Rattus norvegicus	164-167
33563078-5	2021	RNA-seq shows that NAMPT deletion leads to the increase of mRNA levels of enzymes in NAD metabolism, in particular PARP family of NAD+ consumption enzymes, as well as glycolytic genes Glut1, Hk2 and PFBFK3 before GAPDH.	NAD	85-88	poly (ADP-ribose) polymerase family, member 1	Mus musculus	115-119
33563078-5	2021	RNA-seq shows that NAMPT deletion leads to the increase of mRNA levels of enzymes in NAD metabolism, in particular PARP family of NAD+ consumption enzymes, as well as glycolytic genes Glut1, Hk2 and PFBFK3 before GAPDH.	NAD	130-134	poly (ADP-ribose) polymerase family, member 1	Mus musculus	115-119
32710757-5	2021	RESULTS: We found that SIRT1 activation led to marked augmentation of NAD+ depletion and accentuation of cytotoxicity, when combined with nicotinamide phosphoribosyltransferase inhibition (NAMPTi), consistent with the enzymatic activity of SIRT1 as a primary cellular NAD+ consumer in IDH-mutant cells.	NAD	70-74	sirtuin 1	Homo sapiens	23-28
32710757-5	2021	RESULTS: We found that SIRT1 activation led to marked augmentation of NAD+ depletion and accentuation of cytotoxicity, when combined with nicotinamide phosphoribosyltransferase inhibition (NAMPTi), consistent with the enzymatic activity of SIRT1 as a primary cellular NAD+ consumer in IDH-mutant cells.	NAD	268-272	sirtuin 1	Homo sapiens	23-28
33513091-0	2021	NAD+ enhances ribitol and ribose rescue of alpha-dystroglycan functional glycosylation in human FKRP-mutant myotubes.	NAD	0-4	fukutin related protein	Homo sapiens	96-100
33513091-7	2021	These findings provide the rationale for testing ribose/ribitol in combination with NAD+ to treat WWS and other diseases associated with FKRP mutations.	NAD	84-88	fukutin related protein	Homo sapiens	137-141
33577446-2	2021	Sirtuin 1 (SIRT1) is an NAD+-dependent deacetylase that is expressed in a variety of tissues.	NAD	24-27	sirtuin 1	Homo sapiens	0-9
33577446-2	2021	Sirtuin 1 (SIRT1) is an NAD+-dependent deacetylase that is expressed in a variety of tissues.	NAD	24-27	sirtuin 1	Homo sapiens	11-16
32977107-1	2021	Reduced nicotinamide adenine dinucleotide (NADH) and its phosphate ester (NADPH) participate in numerous metabolic processes in living cells as electron carriers.	NAD	8-41	2,4-dienoyl-CoA reductase 1	Homo sapiens	74-79
32977107-1	2021	Reduced nicotinamide adenine dinucleotide (NADH) and its phosphate ester (NADPH) participate in numerous metabolic processes in living cells as electron carriers.	NAD	43-47	2,4-dienoyl-CoA reductase 1	Homo sapiens	74-79
32977107-7	2021	This review is expected to inspire the generation of novel fluorescent probes for the detection of NADH and NADPH, and stimulate more attention in the development of fluorescent probes based on carbon dots and nanoparticles, as well as metal complex-based, time-gated luminescent probes for monitoring NADH and NADPH in both living cells and in vivo.	NAD	99-103	2,4-dienoyl-CoA reductase 1	Homo sapiens	311-316
32977107-7	2021	This review is expected to inspire the generation of novel fluorescent probes for the detection of NADH and NADPH, and stimulate more attention in the development of fluorescent probes based on carbon dots and nanoparticles, as well as metal complex-based, time-gated luminescent probes for monitoring NADH and NADPH in both living cells and in vivo.	NAD	302-306	2,4-dienoyl-CoA reductase 1	Homo sapiens	108-113
32977107-7	2021	This review is expected to inspire the generation of novel fluorescent probes for the detection of NADH and NADPH, and stimulate more attention in the development of fluorescent probes based on carbon dots and nanoparticles, as well as metal complex-based, time-gated luminescent probes for monitoring NADH and NADPH in both living cells and in vivo.	NAD	302-306	2,4-dienoyl-CoA reductase 1	Homo sapiens	311-316
33510840-2	2021	These functions might be modulated by its redox-linked structural transition that enables hAIF to act as a NAD(H/+) redox sensor.	NAD	107-112	apoptosis inducing factor mitochondria associated 1	Homo sapiens	90-94
33510840-3	2021	Upon reduction with NADH, hAIF undergoes a conformational reorganization in two specific insertions-the flexible regulatory C-loop and the 190-202 beta-harpin-promoting protein dimerization and the stabilization of a long-life charge transfer complex (CTC) that modulates its monomer-dimer equilibrium and its protein interaction network in healthy mitochondria.	NAD	20-24	apoptosis inducing factor mitochondria associated 1	Homo sapiens	26-30
33510840-6	2021	Kinetic studies complemented with computational simulations reveal that W196 and the beta-hairpin conformation modulate the low efficiency of hAIF as NADH oxidoreductase, contributing to configure its active site in a noncompetent geometry for hydride transfer and to stabilize the CTC state by enhancing the affinity for NAD+.	NAD	322-326	apoptosis inducing factor mitochondria associated 1	Homo sapiens	142-146
32403131-1	2021	CONTEXT: The sirtuins (SIRT1 to SIRT7) constitute a family of highly conserved nicotinamide adenine dinucleotide-dependent proteins.	NAD	79-112	sirtuin 1	Homo sapiens	23-28
32403131-1	2021	CONTEXT: The sirtuins (SIRT1 to SIRT7) constitute a family of highly conserved nicotinamide adenine dinucleotide-dependent proteins.	NAD	79-112	sirtuin 7	Homo sapiens	32-37
33010451-0	2021	CD38 downregulation modulates NAD+ and NADP(H) levels in thermogenic adipose tissues.	NAD	30-34	CD38 antigen	Mus musculus	0-4
33010451-2	2021	CD38 is a NAD+-dependent enzyme involved in the regulation of different cell functions.	NAD	10-13	CD38 antigen	Mus musculus	0-4
33010451-4	2021	In this study we aim to understand the functional relevance of CD38 for NAD+ and energy metabolism in BAT and WAT, also using a CD38-/- mouse model.	NAD	72-76	CD38 antigen	Mus musculus	63-67
33010451-8	2021	Increased NAD+ levels were observed in BAT/WAT from CD38-/- compared with wild type mice, in line with CD38 being a major NAD+-consumer in AT.	NAD	10-14	CD38 antigen	Mus musculus	52-56
33010451-8	2021	Increased NAD+ levels were observed in BAT/WAT from CD38-/- compared with wild type mice, in line with CD38 being a major NAD+-consumer in AT.	NAD	10-14	CD38 antigen	Mus musculus	103-107
33010451-8	2021	Increased NAD+ levels were observed in BAT/WAT from CD38-/- compared with wild type mice, in line with CD38 being a major NAD+-consumer in AT.	NAD	122-126	CD38 antigen	Mus musculus	103-107
32527186-7	2021	The activity-based assay uses an alpha-NAD+, anomer of beta-NAD+, which is accepted as a substrate by MacroD1, MacroD2, and ARH3 due to its resemblance to the protein-linked ADP-ribose.	NAD	55-64	mono-ADP ribosylhydrolase 2	Homo sapiens	111-118
33519472-6	2020	Further analysis revealed that these effects of acacetin rely on Sirt1 activation by increasing NAD+ followed by increasing Sirt3, pAMPK and PGC-1alpha.	NAD	96-100	sirtuin 1	Homo sapiens	65-70
33297334-6	2020	Moreover, the NADH-stabilized 26S PC is efficient in degrading intrinsically disordered protein (IDP) substrates that might not require ATP-dependent unfolding, such as p27, Tau, c-Fos and more.	NAD	14-18	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	179-184
33385109-4	2021	Boosting NAD+ via genetic or pharmacological CD38 targeting or NAD+ precursor supplementation protected mice from skin, lung, and peritoneal fibrosis.	NAD	9-13	CD38 antigen	Mus musculus	45-49
33385109-5	2021	In mechanistic experiments, CD38 was found to reduce NAD+ levels and sirtuin activity to augment cellular fibrotic responses, while inhibiting CD38 had the opposite effect.	NAD	53-57	CD38 antigen	Mus musculus	28-32
33385109-6	2021	Thus, we identify CD38 upregulation and resulting disrupted NAD+ homeostasis as a fundamental mechanism driving fibrosis in SSc, suggesting that CD38 might represent a novel therapeutic target.	NAD	60-64	CD38 antigen	Mus musculus	18-22
33385109-6	2021	Thus, we identify CD38 upregulation and resulting disrupted NAD+ homeostasis as a fundamental mechanism driving fibrosis in SSc, suggesting that CD38 might represent a novel therapeutic target.	NAD	60-64	CD38 antigen	Mus musculus	145-149
33038659-5	2020	SIRT1 that is an NAD+-dependent deacetylase positively regulates circadian clock and telomere homeostasis.	NAD	17-20	sirtuin 1	Homo sapiens	0-5
32963340-5	2020	The mechanism of signalling might be direct or indirect targeting of peroxisome proliferator-activated receptors by fatty acid ligands, by fatty acid-induced NAD+-stimulated activation of sirtuin 1 and/or fatty acid-mediated activation of AMP-activated protein kinase.	NAD	158-162	sirtuin 1	Homo sapiens	188-197
33203024-3	2020	Here, we present a patient with a severe phenotype of SSADHD caused by a novel genetic variant c.728T > C that leads to an exchange of leucine to proline at residue 243, located within the highly conserved nicotinamide adenine dinucleotide (NAD)+ binding domain of SSADH.	NAD	206-239	aldehyde dehydrogenase 5 family member A1	Homo sapiens	54-59
33203024-3	2020	Here, we present a patient with a severe phenotype of SSADHD caused by a novel genetic variant c.728T > C that leads to an exchange of leucine to proline at residue 243, located within the highly conserved nicotinamide adenine dinucleotide (NAD)+ binding domain of SSADH.	NAD	241-244	aldehyde dehydrogenase 5 family member A1	Homo sapiens	54-59
33153131-8	2020	Sirt-1 activator SRT2104 and NAD+ (Nicotinamide Adenine Dinucleotide) supplement may dose-dependently relieve the cerebrovascular endothelial damage memory.	NAD	35-68	sirtuin 1	Homo sapiens	0-6
33176238-6	2020	The combined treatment of EAE mice with atorvastatin plus NAD+ relieved the clinical signs and histologic changes, increased the proportion of Treg cells, attenuated IL-17 production, reduced proinflammatory cytokine secretion of Th17 cells, and increased cytokine secretion of Treg cells.	NAD	58-62	interleukin 17A	Mus musculus	166-171
32669363-4	2020	Using 1D and 2D nuclear magnetic resonance (NMR), we elucidated the multistep enzymatic mechanism of the oxidoreductase (RgNanOx) that leads to the reversible conversion of 2,7-anhydro-Neu5Ac to Neu5Ac through formation of a 4-keto-DANA intermediate and NAD+ regeneration.	NAD	254-258	oxidoreductase	Escherichia coli	105-119
32389809-1	2020	BACKGROUND & AIM: Abundantly expressed in the metabolically active cells including hepatocytes, N-nicotinamide methyltransferase (NNMT) catalyzes S-adenosylmethionine (SAM)-dependent methylation/degradation of nicotinamide, the predominant precursor for intracellular nicotinamide adenine dinucleotide (NAD+) regeneration via the salvage pathway.	NAD	268-301	nicotinamide N-methyltransferase	Mus musculus	96-128
32389809-1	2020	BACKGROUND & AIM: Abundantly expressed in the metabolically active cells including hepatocytes, N-nicotinamide methyltransferase (NNMT) catalyzes S-adenosylmethionine (SAM)-dependent methylation/degradation of nicotinamide, the predominant precursor for intracellular nicotinamide adenine dinucleotide (NAD+) regeneration via the salvage pathway.	NAD	268-301	nicotinamide N-methyltransferase	Mus musculus	130-134
32389809-1	2020	BACKGROUND & AIM: Abundantly expressed in the metabolically active cells including hepatocytes, N-nicotinamide methyltransferase (NNMT) catalyzes S-adenosylmethionine (SAM)-dependent methylation/degradation of nicotinamide, the predominant precursor for intracellular nicotinamide adenine dinucleotide (NAD+) regeneration via the salvage pathway.	NAD	303-307	nicotinamide N-methyltransferase	Mus musculus	96-128
32989246-1	2020	SIRT1 (Sir2) is an NAD+-dependent deacetylase that plays critical roles in a broad range of biological events, including metabolism, the immune response and ageing1-5.	NAD	19-22	sirtuin 1	Homo sapiens	0-5
32989246-1	2020	SIRT1 (Sir2) is an NAD+-dependent deacetylase that plays critical roles in a broad range of biological events, including metabolism, the immune response and ageing1-5.	NAD	19-22	sirtuin 1	Homo sapiens	7-11
32998280-8	2020	Quantification of free vs. bound nicotinamide adenine dinucleotide (NADH) and flavin adenine dinucleotide (FAD) revealed increased glucose utilization and TCA cycle flux in LPL-depleted neurons compared to controls.	NAD	33-66	lipoprotein lipase	Mus musculus	173-176
32998280-8	2020	Quantification of free vs. bound nicotinamide adenine dinucleotide (NADH) and flavin adenine dinucleotide (FAD) revealed increased glucose utilization and TCA cycle flux in LPL-depleted neurons compared to controls.	NAD	68-72	lipoprotein lipase	Mus musculus	173-176
32992843-0	2020	Sex and SP-A2 Dependent NAD(H) Redox Alterations in Mouse Alveolar Macrophages in Response to Ozone Exposure: Potential Implications for COVID-19.	NAD	24-30	sperm head anomaly 2	Mus musculus	8-13
32822587-2	2020	We found that NAD+-dependent ADP-ribosylation of histone H2B-Glu35 by small nucleolar RNA (snoRNA)-activated PARP-1 inhibits AMP kinase-mediated phosphorylation of adjacent H2B-Ser36, which is required for the proadipogenic gene expression program.	NAD	14-18	poly (ADP-ribose) polymerase family, member 1	Mus musculus	109-115
32822587-3	2020	The activity of PARP-1 on H2B requires NMNAT-1, a nuclear NAD+ synthase, which directs PARP-1 catalytic activity to Glu and Asp residues.	NAD	58-61	poly (ADP-ribose) polymerase family, member 1	Mus musculus	16-22
32822587-3	2020	The activity of PARP-1 on H2B requires NMNAT-1, a nuclear NAD+ synthase, which directs PARP-1 catalytic activity to Glu and Asp residues.	NAD	58-61	nicotinamide nucleotide adenylyltransferase 1	Mus musculus	39-46
32822587-3	2020	The activity of PARP-1 on H2B requires NMNAT-1, a nuclear NAD+ synthase, which directs PARP-1 catalytic activity to Glu and Asp residues.	NAD	58-61	poly (ADP-ribose) polymerase family, member 1	Mus musculus	87-93
32473481-6	2020	Moreover, the decreased NAD could downregulate NADPH and further suppress the innate antioxidant defense system by inhibiting reduction of GSSG.	NAD	24-27	2,4-dienoyl-CoA reductase 1	Homo sapiens	47-52
31494696-9	2020	This was accompanied by an increased protein content of NMNAT3, the rate-limiting enzyme for NAD + biosynthesis and mitochondrial proteins, including MTCO1 and ATP5a.	NAD	93-98	nicotinamide nucleotide adenylyltransferase 3	Mus musculus	56-62
32531731-0	2020	Evidence for NAD+-dependent histone dynamics and tunneling associated conformational transitions in circadian deacetylase SIRT1.	NAD	13-17	sirtuin 1	Homo sapiens	122-127
32531731-2	2020	Sirtuin 1 (SIRT1) is a 747 amino acid-long class III Nicotinamide adenine dinucleotide (NAD+)-dependent histone that acts as a circadian deacetylase.	NAD	53-86	sirtuin 1	Homo sapiens	0-9
32531731-2	2020	Sirtuin 1 (SIRT1) is a 747 amino acid-long class III Nicotinamide adenine dinucleotide (NAD+)-dependent histone that acts as a circadian deacetylase.	NAD	53-86	sirtuin 1	Homo sapiens	11-16
32531731-2	2020	Sirtuin 1 (SIRT1) is a 747 amino acid-long class III Nicotinamide adenine dinucleotide (NAD+)-dependent histone that acts as a circadian deacetylase.	NAD	88-92	sirtuin 1	Homo sapiens	0-9
32531731-2	2020	Sirtuin 1 (SIRT1) is a 747 amino acid-long class III Nicotinamide adenine dinucleotide (NAD+)-dependent histone that acts as a circadian deacetylase.	NAD	88-92	sirtuin 1	Homo sapiens	11-16
32531731-5	2020	Due to increased flexibility, SIRT1-specific SER275, SER442 and ARG466 residues involved in NAD+ association facilitated in the formation of a transient tunnel (17.77 A) that was further elongated to 19.25 A upon SIRT1NAD+/Zn+2 binding to H4KAC16.	NAD	92-96	sirtuin 1	Homo sapiens	30-35
32524997-6	2020	In contrast to ERalpha activity, the nuclear AIF is increased with an ERbeta agonist, DPN and blocked with an ERbeta antagonist, PHTPP.	NAD	86-89	apoptosis inducing factor mitochondria associated 1	Homo sapiens	45-48
32861997-1	2020	SIRT7 is a member of the mammalian sirtuins and functions as an NAD+-dependent deacylase.	NAD	64-67	sirtuin 7	Homo sapiens	0-5
32923413-2	2020	Sirtuin1 (Sirt1) is a deacetylase that depends on NAD+, which has an important role in antioxidant metabolism.	NAD	50-54	sirtuin 1	Homo sapiens	0-8
32923413-2	2020	Sirtuin1 (Sirt1) is a deacetylase that depends on NAD+, which has an important role in antioxidant metabolism.	NAD	50-54	sirtuin 1	Homo sapiens	10-15
31909898-8	2020	We found that the mitochondrially encoded NADH dehydrogenase 2 (MT-ND2) mRNA was differentially expressed in the serum of individuals with early-stage YDH syndrome.	NAD	42-46	mitochondrially encoded NADH dehydrogenase 2	Homo sapiens	64-70
32657204-2	2020	Sirtuin-1 (SIRT1), a NAD-dependent deacetylase, is involved in multiple biological functions.	NAD	21-24	sirtuin 1	Homo sapiens	0-9
32657204-2	2020	Sirtuin-1 (SIRT1), a NAD-dependent deacetylase, is involved in multiple biological functions.	NAD	21-24	sirtuin 1	Homo sapiens	11-16
32586688-1	2020	Sirtuin 7 (SIRT7) is a NAD+ (nicotinamide adenine dinucleotide) dependent deacetylase that is reported to contribute to tumour growth and invasion by selectively acting on histone H3K18.	NAD	23-26	sirtuin 7	Homo sapiens	0-9
32586688-1	2020	Sirtuin 7 (SIRT7) is a NAD+ (nicotinamide adenine dinucleotide) dependent deacetylase that is reported to contribute to tumour growth and invasion by selectively acting on histone H3K18.	NAD	23-26	sirtuin 7	Homo sapiens	11-16
32586688-1	2020	Sirtuin 7 (SIRT7) is a NAD+ (nicotinamide adenine dinucleotide) dependent deacetylase that is reported to contribute to tumour growth and invasion by selectively acting on histone H3K18.	NAD	29-62	sirtuin 7	Homo sapiens	0-9
32586688-1	2020	Sirtuin 7 (SIRT7) is a NAD+ (nicotinamide adenine dinucleotide) dependent deacetylase that is reported to contribute to tumour growth and invasion by selectively acting on histone H3K18.	NAD	29-62	sirtuin 7	Homo sapiens	11-16
32732457-6	2020	Because PARP1 consumes NAD+ while exerting its catalytic activity, we investigated whether PARP1 impedes autophagy mediated by sirtuin1 (SIRT1), which uses NAD+ as its cofactor.	NAD	156-160	sirtuin 1	Homo sapiens	137-142
32732457-7	2020	A NAD+ precursor restored autophagy and protected mitochondria in ARPE-19 cells by preserving SIRT1 activity upon H2O2.	NAD	2-6	sirtuin 1	Homo sapiens	94-99
32848753-15	2020	Moreover, our study found that TMZ upregulated Sirt1 expression by increasing the expression of nicotinamide phosphoribosyl transferase (Nampt), which is a rate limiting enzyme for nicotinamide adenine dinucleotide (NAD+) generation by salvage pathway.	NAD	181-214	nicotinamide phosphoribosyltransferase	Rattus norvegicus	96-135
32848753-15	2020	Moreover, our study found that TMZ upregulated Sirt1 expression by increasing the expression of nicotinamide phosphoribosyl transferase (Nampt), which is a rate limiting enzyme for nicotinamide adenine dinucleotide (NAD+) generation by salvage pathway.	NAD	181-214	nicotinamide phosphoribosyltransferase	Rattus norvegicus	137-142
32848753-15	2020	Moreover, our study found that TMZ upregulated Sirt1 expression by increasing the expression of nicotinamide phosphoribosyl transferase (Nampt), which is a rate limiting enzyme for nicotinamide adenine dinucleotide (NAD+) generation by salvage pathway.	NAD	216-220	nicotinamide phosphoribosyltransferase	Rattus norvegicus	96-135
32848753-15	2020	Moreover, our study found that TMZ upregulated Sirt1 expression by increasing the expression of nicotinamide phosphoribosyl transferase (Nampt), which is a rate limiting enzyme for nicotinamide adenine dinucleotide (NAD+) generation by salvage pathway.	NAD	216-220	nicotinamide phosphoribosyltransferase	Rattus norvegicus	137-142
32608971-7	2020	Whereas the iron oxidation kinetics were not affected by the presence of NCOA4, iron mobilization from ferritin by two different reducing agents (FMN/NADH and sodium dithionite) showed a strong inhibition effect that was dependent on the concentration of NCOA4 present in solution.	NAD	150-154	nuclear receptor coactivator 4	Homo sapiens	255-260
32665411-5	2020	Reducing mitochondrial Ca2+ inhibited alphaKGDH activity and increased NAD+, which induced SIRT1-dependent autophagy in both OXPHOS-competent and OXPHOS-defective cells.	NAD	71-75	sirtuin 1	Homo sapiens	91-96
32645959-12	2020	NQO1 and cytochrome b5 reductase can neutralize ROS in the plasma membrane and induce a high NAD+/NADH ratio, which then activates SIRT1 and mitochondrial bioenergetics.	NAD	93-97	sirtuin 1	Homo sapiens	131-136
32645959-12	2020	NQO1 and cytochrome b5 reductase can neutralize ROS in the plasma membrane and induce a high NAD+/NADH ratio, which then activates SIRT1 and mitochondrial bioenergetics.	NAD	98-102	sirtuin 1	Homo sapiens	131-136
32364937-4	2020	The nanofibres assembled into a three-dimensional network with a high specific surface area, which contributed to low charge transfer resistance and high transduction activity towards the co-enzyme NADH, delivering a wide linear range of 20-960 muM and a high sensitivity of 0.224 muA muM-1 cm-2 at the Nano-PEDOT-COOH50% interface.	NAD	198-202	PWWP domain containing 3A, DNA repair factor	Homo sapiens	285-290
32519817-4	2020	We further demonstrated that the NAD-dependent protein deacetylase, SIRT7, and the FOXO4 transcription factor acted as endogenous brakes for GLS1 expression, which are inhibited by TGF-beta.	NAD	33-36	sirtuin 7	Homo sapiens	68-73
32369735-0	2020	NAD+ Controls Circadian Reprogramming through PER2 Nuclear Translocation to Counter Aging.	NAD	0-4	period circadian regulator 2	Homo sapiens	46-50
32369735-2	2020	Here, we reveal that supplementation with the NAD+ precursor nicotinamide riboside (NR) markedly reprograms metabolic and stress-response pathways that decline with aging through inhibition of the clock repressor PER2.	NAD	46-50	period circadian regulator 2	Homo sapiens	213-217
32493904-3	2020	We also find that over-expressing BNA2, the first Biosynthesis of NAD+ (kynurenine) pathway gene, reduces LD accumulation during aging and extends lifespan.	NAD	66-70	dioxygenase BNA2	Saccharomyces cerevisiae S288C	34-38
32298659-3	2020	Nicotinamide (NAM) acts as a substrate of visfatin and Nicotinamide N-Methyltransferase (NNMT) leading to the generation of Nicotinamide Adenine Dinucleotide (NAD) and N1-Methylnicotinamide (MNAM), respectively.	NAD	124-157	nicotinamide phosphoribosyltransferase	Rattus norvegicus	42-50
32298659-3	2020	Nicotinamide (NAM) acts as a substrate of visfatin and Nicotinamide N-Methyltransferase (NNMT) leading to the generation of Nicotinamide Adenine Dinucleotide (NAD) and N1-Methylnicotinamide (MNAM), respectively.	NAD	159-162	nicotinamide phosphoribosyltransferase	Rattus norvegicus	42-50
32087266-6	2020	Meanwhile, NAD+ booster nicotinamide mononucleotide also counteracted the deleterious effects of ethanol by increasing SIRT1, suggesting the regulation of SIRT1-UCP2 axis may be associated with cellular NAD+/NADH ratio.	NAD	11-15	uncoupling protein 2	Rattus norvegicus	161-165
32087266-6	2020	Meanwhile, NAD+ booster nicotinamide mononucleotide also counteracted the deleterious effects of ethanol by increasing SIRT1, suggesting the regulation of SIRT1-UCP2 axis may be associated with cellular NAD+/NADH ratio.	NAD	203-207	uncoupling protein 2	Rattus norvegicus	161-165
32087266-6	2020	Meanwhile, NAD+ booster nicotinamide mononucleotide also counteracted the deleterious effects of ethanol by increasing SIRT1, suggesting the regulation of SIRT1-UCP2 axis may be associated with cellular NAD+/NADH ratio.	NAD	208-212	uncoupling protein 2	Rattus norvegicus	161-165
31652343-3	2020	Glu427 is invariant in the ALDH superfamily and forms ionic hydrogen bonds with the nicotinamide ribose of the NAD+ cofactor.	NAD	111-114	aldehyde dehydrogenase 7 family member A1	Homo sapiens	27-31
31652343-11	2020	We also show that these mutations reduce the amount of active tetrameric ALDH7A1 at the concentration of NAD+ tested.	NAD	105-108	aldehyde dehydrogenase 7 family member A1	Homo sapiens	73-80
32344695-1	2020	PolyADP-ribosylation is a post-translational modification of proteins, and poly(ADP-ribose) (PAR) polymerase (PARP) family proteins synthesize PAR using NAD as a substrate.	NAD	153-156	poly (ADP-ribose) polymerase family, member 1	Mus musculus	110-114
32363189-3	2020	Mechanistic studies demonstrated that overexpression of CD38 specifically downregulated the expression of Rab7 and its adaptor protein pleckstrin homology domain-containing protein family member 1 (PLEKHM1) through nicotinamide adenine dinucleotide (NAD)-dependent and non-NAD-dependent pathways, respectively.	NAD	273-276	CD38 antigen	Mus musculus	56-60
32363189-3	2020	Mechanistic studies demonstrated that overexpression of CD38 specifically downregulated the expression of Rab7 and its adaptor protein pleckstrin homology domain-containing protein family member 1 (PLEKHM1) through nicotinamide adenine dinucleotide (NAD)-dependent and non-NAD-dependent pathways, respectively.	NAD	273-276	pleckstrin homology domain containing, family M (with RUN domain) member 1	Mus musculus	198-205
32128683-1	2020	Betaine aldehyde dehydrogenase (BADH) catalyzes the oxidation of betaine aldehyde to glycine betaine using NAD+ as a coenzyme.	NAD	107-111	aldehyde dehydrogenase 7 family member A1	Homo sapiens	0-30
32128683-1	2020	Betaine aldehyde dehydrogenase (BADH) catalyzes the oxidation of betaine aldehyde to glycine betaine using NAD+ as a coenzyme.	NAD	107-111	aldehyde dehydrogenase 7 family member A1	Homo sapiens	32-36
32180563-4	2020	METHODS: Here we report that the oxidoreductase cytochrome b5 reductase 3 (Cyb5r3) links FoxO1 signaling to beta-cell stimulus/secretion coupling by regulating mitochondrial function, reactive oxygen species generation, and nicotinamide actin dysfunction (NAD)/reduced nicotinamide actin dysfunction (NADH) ratios.	NAD	301-305	cytochrome b5 reductase 3	Mus musculus	48-73
32180563-4	2020	METHODS: Here we report that the oxidoreductase cytochrome b5 reductase 3 (Cyb5r3) links FoxO1 signaling to beta-cell stimulus/secretion coupling by regulating mitochondrial function, reactive oxygen species generation, and nicotinamide actin dysfunction (NAD)/reduced nicotinamide actin dysfunction (NADH) ratios.	NAD	301-305	cytochrome b5 reductase 3	Mus musculus	75-81
32270032-3	2020	Here, we showed that NAD+-dependent class III HDAC sirtuin 1 (Sirt1) is highly expressed in resting B cells and down-regulated by stimuli inducing AID.	NAD	21-25	sirtuin 1	Homo sapiens	51-60
32270032-3	2020	Here, we showed that NAD+-dependent class III HDAC sirtuin 1 (Sirt1) is highly expressed in resting B cells and down-regulated by stimuli inducing AID.	NAD	21-25	sirtuin 1	Homo sapiens	62-67
31945382-1	2020	Silent Information Regulator 1 (SIRT1), an NAD+-dependent deacetylase, contributes to the neuroprotective effect.	NAD	43-46	sirtuin 1	Homo sapiens	0-30
31945382-1	2020	Silent Information Regulator 1 (SIRT1), an NAD+-dependent deacetylase, contributes to the neuroprotective effect.	NAD	43-46	sirtuin 1	Homo sapiens	32-37
31932306-5	2020	Here, we show that HAS2 expression can be modulated by sirtuin 1 (SIRT1), the master metabolic sensor of the cell, belonging to the class of NAD+-dependent deacetylases.	NAD	141-144	sirtuin 1	Homo sapiens	55-64
31932306-5	2020	Here, we show that HAS2 expression can be modulated by sirtuin 1 (SIRT1), the master metabolic sensor of the cell, belonging to the class of NAD+-dependent deacetylases.	NAD	141-144	sirtuin 1	Homo sapiens	66-71
31988240-0	2020	A nicotinamide phosphoribosyltransferase-GAPDH interaction sustains the stress-induced NMN/NAD+ salvage pathway in the nucleus.	NAD	91-94	glyceraldehyde-3-phosphate dehydrogenase	Mus musculus	41-46
32168855-7	2020	Enhancing intracellular antioxidant capacity in addition to activating NAD-dependent deacetylase sirtuin-1 (SIRT1) and AMP-activated protein kinase (AMPK) are the prime mechanisms involved in the therapeutic effects of these compounds.	NAD	71-74	sirtuin 1	Homo sapiens	108-113
32168855-7	2020	Enhancing intracellular antioxidant capacity in addition to activating NAD-dependent deacetylase sirtuin-1 (SIRT1) and AMP-activated protein kinase (AMPK) are the prime mechanisms involved in the therapeutic effects of these compounds.	NAD	71-74	protein kinase AMP-activated non-catalytic subunit beta 1	Homo sapiens	149-153
32021996-1	2020	Encapsulation of two enzymes, alcohol dehydrogenase (ADH) and glucose oxidase (GOx), within peroxidase-like tourmaline microparticle (TM)-based colloidosomes was used to construct a functionalized microsystem capable of sustainable cascade cycling of nicotinamide cofactor (NAD+/NADH) via chemical signaling between spatially confined dual-enzyme and active membranes.	NAD	274-277	aldo-keto reductase family 1 member A1	Homo sapiens	30-51
32021996-1	2020	Encapsulation of two enzymes, alcohol dehydrogenase (ADH) and glucose oxidase (GOx), within peroxidase-like tourmaline microparticle (TM)-based colloidosomes was used to construct a functionalized microsystem capable of sustainable cascade cycling of nicotinamide cofactor (NAD+/NADH) via chemical signaling between spatially confined dual-enzyme and active membranes.	NAD	274-277	hydroxyacid oxidase 1	Homo sapiens	62-77
32021996-1	2020	Encapsulation of two enzymes, alcohol dehydrogenase (ADH) and glucose oxidase (GOx), within peroxidase-like tourmaline microparticle (TM)-based colloidosomes was used to construct a functionalized microsystem capable of sustainable cascade cycling of nicotinamide cofactor (NAD+/NADH) via chemical signaling between spatially confined dual-enzyme and active membranes.	NAD	274-277	hydroxyacid oxidase 1	Homo sapiens	79-82
32021996-1	2020	Encapsulation of two enzymes, alcohol dehydrogenase (ADH) and glucose oxidase (GOx), within peroxidase-like tourmaline microparticle (TM)-based colloidosomes was used to construct a functionalized microsystem capable of sustainable cascade cycling of nicotinamide cofactor (NAD+/NADH) via chemical signaling between spatially confined dual-enzyme and active membranes.	NAD	279-283	aldo-keto reductase family 1 member A1	Homo sapiens	30-51
32021996-1	2020	Encapsulation of two enzymes, alcohol dehydrogenase (ADH) and glucose oxidase (GOx), within peroxidase-like tourmaline microparticle (TM)-based colloidosomes was used to construct a functionalized microsystem capable of sustainable cascade cycling of nicotinamide cofactor (NAD+/NADH) via chemical signaling between spatially confined dual-enzyme and active membranes.	NAD	279-283	hydroxyacid oxidase 1	Homo sapiens	62-77
32021996-1	2020	Encapsulation of two enzymes, alcohol dehydrogenase (ADH) and glucose oxidase (GOx), within peroxidase-like tourmaline microparticle (TM)-based colloidosomes was used to construct a functionalized microsystem capable of sustainable cascade cycling of nicotinamide cofactor (NAD+/NADH) via chemical signaling between spatially confined dual-enzyme and active membranes.	NAD	279-283	hydroxyacid oxidase 1	Homo sapiens	79-82
31838391-6	2020	Moreover, our results showed that NAD+ insufficiency is responsible for BDE-47-mediated mitophagy defect and mitochondrial dysfunction in mouse livers, which was associated with suppression of Sirt3/FoxO3a/PINK1 signaling.	NAD	34-37	forkhead box O3	Mus musculus	199-205
32061543-2	2020	Recently, Katsuyama et al., demonstrated that the CD38/NAD/Sirtuin1/EZH2 axis reduces cytolytic CD8+ T cell function and might be targeted to overcome incidence of infections.	NAD	55-58	sirtuin 1	Homo sapiens	59-67
32061543-2	2020	Recently, Katsuyama et al., demonstrated that the CD38/NAD/Sirtuin1/EZH2 axis reduces cytolytic CD8+ T cell function and might be targeted to overcome incidence of infections.	NAD	55-58	CD8a molecule	Homo sapiens	96-99
32093281-9	2020	This led to the upregulation of Sirtuin1 (SIRT1), a NAD-dependent protein deacetylase, to deacetylate p53 and attenuated its transcriptional activation on PISD.	NAD	52-55	sirtuin 1	Homo sapiens	32-40
32093281-9	2020	This led to the upregulation of Sirtuin1 (SIRT1), a NAD-dependent protein deacetylase, to deacetylate p53 and attenuated its transcriptional activation on PISD.	NAD	52-55	sirtuin 1	Homo sapiens	42-47
32054506-10	2020	In addition, DPN treatment upregulated the LC3II/I expression level and downregulated P62 and mTOR (mRNA level) and p-mTOR (protein level) expression levels.	NAD	13-16	sequestosome 1	Homo sapiens	86-89
32042007-2	2020	Despite its role in DNA repair, AAG-initiated BER promotes cytotoxicity in a process dependent on poly (ADP-ribose) polymerase-1 (PARP-1); a NAD+-consuming enzyme activated by strand break intermediates of the AAG-initiated repair process.	NAD	141-144	N-methylpurine DNA glycosylase	Homo sapiens	32-35
32042007-7	2020	Accordingly, Aag-/- cells are protected from MMS-induced NAD+ depletion and glycolysis inhibition.	NAD	57-60	N-methylpurine DNA glycosylase	Homo sapiens	13-16
32042007-10	2020	Thus, AAG plays an important role in the metabolic response to alkylation that could be exploited in the treatment of conditions associated with NAD+ dysregulation.	NAD	145-148	N-methylpurine DNA glycosylase	Homo sapiens	6-9
32046300-2	2020	PARP inhibitors, which inhibit PARylation through competitively binding to NAD+ binding site of PARP1 and PARP2, have improved clinical benefits for BRCA mutated tumors, leading to their accelerated clinical application.	NAD	75-78	BRCA1 DNA repair associated	Homo sapiens	149-153
31936501-5	2020	The activation of GPD1-mediated NAD+ regeneration in peroxisomes by GPD1 over-expression or activation of the malate-oxaloacetate NADH peroxisomal shuttle, by increasing flux in this NADH shuttle and over-expression of MDH3, resulted in lifespan extension of agc1Delta yeasts.	NAD	32-35	glycerol-3-phosphate dehydrogenase (NAD(+)) GPD1	Saccharomyces cerevisiae S288C	18-22
31936501-5	2020	The activation of GPD1-mediated NAD+ regeneration in peroxisomes by GPD1 over-expression or activation of the malate-oxaloacetate NADH peroxisomal shuttle, by increasing flux in this NADH shuttle and over-expression of MDH3, resulted in lifespan extension of agc1Delta yeasts.	NAD	32-35	glycerol-3-phosphate dehydrogenase (NAD(+)) GPD1	Saccharomyces cerevisiae S288C	68-72
31936501-5	2020	The activation of GPD1-mediated NAD+ regeneration in peroxisomes by GPD1 over-expression or activation of the malate-oxaloacetate NADH peroxisomal shuttle, by increasing flux in this NADH shuttle and over-expression of MDH3, resulted in lifespan extension of agc1Delta yeasts.	NAD	110-134	glycerol-3-phosphate dehydrogenase (NAD(+)) GPD1	Saccharomyces cerevisiae S288C	18-22
31936501-5	2020	The activation of GPD1-mediated NAD+ regeneration in peroxisomes by GPD1 over-expression or activation of the malate-oxaloacetate NADH peroxisomal shuttle, by increasing flux in this NADH shuttle and over-expression of MDH3, resulted in lifespan extension of agc1Delta yeasts.	NAD	130-134	glycerol-3-phosphate dehydrogenase (NAD(+)) GPD1	Saccharomyces cerevisiae S288C	18-22
31936501-7	2020	The effect of PEX34-mediated longevity required the presence of the GPD1-mediated NADH peroxisomal shuttle, which was independent of the presence of the peroxisomal malate-oxaloacetate NADH shuttle and PEX34-induced peroxisome proliferation.	NAD	82-86	glycerol-3-phosphate dehydrogenase (NAD(+)) GPD1	Saccharomyces cerevisiae S288C	68-72
31942817-1	2020	SIRT1, a NAD+-dependent deacetylase, is the most well-studied member of class III histone deacetylases.	NAD	9-12	sirtuin 1	Homo sapiens	0-5
31407410-1	2020	The NAD-dependent deacetylase Sirtuin 1 (SIRT1) plays a vital role in leukemogenesis.	NAD	4-7	sirtuin 1	Homo sapiens	41-46
31658992-7	2020	Unexpectedly, we found that NAD+- and NADH-capped RNAs associate with IFIT5 with kinetic parameters comparable to pppG-RNA.	NAD	28-31	interferon induced protein with tetratricopeptide repeats 5	Homo sapiens	70-75
31658992-7	2020	Unexpectedly, we found that NAD+- and NADH-capped RNAs associate with IFIT5 with kinetic parameters comparable to pppG-RNA.	NAD	38-42	interferon induced protein with tetratricopeptide repeats 5	Homo sapiens	70-75
31875550-0	2019	Decapping Enzyme NUDT12 Partners with BLMH for Cytoplasmic Surveillance of NAD-Capped RNAs.	NAD	75-78	bleomycin hydrolase	Homo sapiens	38-42
31878234-1	2019	Calorie restriction can extend lifespan by increasing intracellular nicotinamide adenine dinucleotide (NAD+), thereby upregulating the activity of sirtuins (Caenorhabditis elegans Sir-2.1; human SIRT1).	NAD	68-101	sirtuin 1	Homo sapiens	195-200
31878234-7	2019	Additionally, the saturating concentration of NAD+ required by SIRT1 was approximately 200 muM; however, the steady-state concentration of NAD+ in Hs68 cells reached up to 460 muM.	NAD	46-49	sirtuin 1	Homo sapiens	63-68
31863054-1	2019	Potential inhibitors of a target biomolecule, NAD-dependent deacetylase Sirtuin 1, were identified by a contest-based approach, in which participants were asked to propose a prioritized list of 400 compounds from a designated compound library containing 2.5 million compounds using in silico methods and scoring.	NAD	46-49	sirtuin 1	Homo sapiens	72-81
31849941-3	2019	The functions of these enzymes highly depend on the availability of key products of cellular metabolism pathways such as acetyl-CoA, NAD (Nicotinamide adenine dinucleotide) and SEM (S-adenosylmethionine), suggesting that there is a close crosstalk between the metabolic and the epigenetic regulation of CD8+ T cells.	NAD	133-136	CD8a molecule	Homo sapiens	303-306
31849941-3	2019	The functions of these enzymes highly depend on the availability of key products of cellular metabolism pathways such as acetyl-CoA, NAD (Nicotinamide adenine dinucleotide) and SEM (S-adenosylmethionine), suggesting that there is a close crosstalk between the metabolic and the epigenetic regulation of CD8+ T cells.	NAD	138-171	CD8a molecule	Homo sapiens	303-306
31665043-4	2019	In contrast to ScNDI1, which is permanently active in yeast naturally devoid of CI, plant alternative NADH dehydrogenases (NDH-2) support the oxidation of NADH only when the CI is metabolically inactive and conceivably when the concentration of matrix NADH exceeds a certain threshold.	NAD	102-106	NADH-ubiquinone reductase (H(+)-translocating) NDE2	Saccharomyces cerevisiae S288C	123-128
31665043-4	2019	In contrast to ScNDI1, which is permanently active in yeast naturally devoid of CI, plant alternative NADH dehydrogenases (NDH-2) support the oxidation of NADH only when the CI is metabolically inactive and conceivably when the concentration of matrix NADH exceeds a certain threshold.	NAD	155-159	NADH-ubiquinone reductase (H(+)-translocating) NDE2	Saccharomyces cerevisiae S288C	123-128
31665043-4	2019	In contrast to ScNDI1, which is permanently active in yeast naturally devoid of CI, plant alternative NADH dehydrogenases (NDH-2) support the oxidation of NADH only when the CI is metabolically inactive and conceivably when the concentration of matrix NADH exceeds a certain threshold.	NAD	155-159	NADH-ubiquinone reductase (H(+)-translocating) NDE2	Saccharomyces cerevisiae S288C	123-128
31590397-0	2019	Ginsenoside Rb1 Attenuates High Glucose-Induced Oxidative Injury via the NAD-PARP-SIRT Axis in Rat Retinal Capillary Endothelial Cells.	NAD	73-76	RB transcriptional corepressor 1	Rattus norvegicus	12-15
31679124-0	2019	Treatment with the poly(ADP-ribose) polymerase inhibitor PJ-34 improves cerebromicrovascular endothelial function, neurovascular coupling responses and cognitive performance in aged mice, supporting the NAD+ depletion hypothesis of neurovascular aging.	NAD	203-207	poly (ADP-ribose) polymerase family, member 1	Mus musculus	19-46
31679124-4	2019	The mechanisms underlying the age-related decline in [NAD+] in cells of the neurovascular unit are likely multifaceted and may include increased utilization of NAD+ by activated poly (ADP-ribose) polymerase (PARP-1).	NAD	54-58	poly (ADP-ribose) polymerase family, member 1	Mus musculus	178-206
31571997-11	2019	In contrast, the expression of sirtuin 1 (SIRT1), known as NAD-dependent deacetylase, was downregulated in RB samples and cell lines.	NAD	59-62	sirtuin 1	Homo sapiens	31-40
31571997-11	2019	In contrast, the expression of sirtuin 1 (SIRT1), known as NAD-dependent deacetylase, was downregulated in RB samples and cell lines.	NAD	59-62	sirtuin 1	Homo sapiens	42-47
31341018-5	2019	We observed that recombinant MtpB methylates Co(I)-MtqC in the presence of proline betaine and that other quaternary amines are much less preferred substrates.	NAD	45-50	hydroxyacyl-CoA dehydrogenase trifunctional multienzyme complex subunit beta	Homo sapiens	29-33
31341018-7	2019	To our knowledge, MtpB methylation of Co(I)-MtqC for the subsequent methylation of tetrahydrofolate represents the first described anoxic mechanism of proline betaine demethylation.	NAD	38-43	hydroxyacyl-CoA dehydrogenase trifunctional multienzyme complex subunit beta	Homo sapiens	18-22
31511627-2	2019	Additionally, NAD serves as a substrate for poly(ADP-ribose) polymerase (PARP), sirtuin, and NAD glycohydrolase, and it regulates DNA repair, gene expression, energy metabolism, and stress responses.	NAD	14-17	poly (ADP-ribose) polymerase family, member 1	Mus musculus	44-71
31511627-2	2019	Additionally, NAD serves as a substrate for poly(ADP-ribose) polymerase (PARP), sirtuin, and NAD glycohydrolase, and it regulates DNA repair, gene expression, energy metabolism, and stress responses.	NAD	14-17	poly (ADP-ribose) polymerase family, member 1	Mus musculus	73-77
31511627-4	2019	Previously, we demonstrated that nicotinamide guanine dinucleotide (NGD) and nicotinamide hypoxanthine dinucleotide (NHD), which are analogs of NAD, are significantly increased in Nmnat3-overexpressing mice.	NAD	144-147	nicotinamide nucleotide adenylyltransferase 3	Mus musculus	180-186
31492851-2	2019	Here, we find that the reductive consequence of ALDH7A1 activity, which generates NADH (nicotinamide adenine dinucleotide, reduced form) from NAD, underlies how ALDH7A1 coordinates a broad inhibition of the intracellular transport pathways.	NAD	82-86	aldehyde dehydrogenase 7 family member A1	Homo sapiens	48-55
31492851-2	2019	Here, we find that the reductive consequence of ALDH7A1 activity, which generates NADH (nicotinamide adenine dinucleotide, reduced form) from NAD, underlies how ALDH7A1 coordinates a broad inhibition of the intracellular transport pathways.	NAD	82-86	aldehyde dehydrogenase 7 family member A1	Homo sapiens	161-168
31492851-2	2019	Here, we find that the reductive consequence of ALDH7A1 activity, which generates NADH (nicotinamide adenine dinucleotide, reduced form) from NAD, underlies how ALDH7A1 coordinates a broad inhibition of the intracellular transport pathways.	NAD	88-121	aldehyde dehydrogenase 7 family member A1	Homo sapiens	48-55
31492851-2	2019	Here, we find that the reductive consequence of ALDH7A1 activity, which generates NADH (nicotinamide adenine dinucleotide, reduced form) from NAD, underlies how ALDH7A1 coordinates a broad inhibition of the intracellular transport pathways.	NAD	88-121	aldehyde dehydrogenase 7 family member A1	Homo sapiens	161-168
31492851-2	2019	Here, we find that the reductive consequence of ALDH7A1 activity, which generates NADH (nicotinamide adenine dinucleotide, reduced form) from NAD, underlies how ALDH7A1 coordinates a broad inhibition of the intracellular transport pathways.	NAD	82-85	aldehyde dehydrogenase 7 family member A1	Homo sapiens	48-55
31492851-2	2019	Here, we find that the reductive consequence of ALDH7A1 activity, which generates NADH (nicotinamide adenine dinucleotide, reduced form) from NAD, underlies how ALDH7A1 coordinates a broad inhibition of the intracellular transport pathways.	NAD	82-85	aldehyde dehydrogenase 7 family member A1	Homo sapiens	161-168
31492851-3	2019	Studying vesicle formation by the Coat Protein I (COPI) complex, we elucidate that NADH generated by ALDH7A1 targets Brefeldin-A ADP-Ribosylated Substrate (BARS) to inhibit COPI vesicle fission.	NAD	83-87	aldehyde dehydrogenase 7 family member A1	Homo sapiens	101-108
31551807-11	2019	The expression of SOD2 was increased and the NOX4 expression was decreased in H9c2 cells after NAD+ supplementation.	NAD	95-98	superoxide dismutase 2	Rattus norvegicus	18-22
31551807-11	2019	The expression of SOD2 was increased and the NOX4 expression was decreased in H9c2 cells after NAD+ supplementation.	NAD	95-98	NADPH oxidase 4	Rattus norvegicus	45-49
31439867-3	2019	Specifically, we show that mutant PPM1D drives hypermethylation of CpG islands throughout the genome and promotes epigenetic silencing of nicotinic acid phosphoribosyltransferase (NAPRT), a key gene involved in NAD biosynthesis.	NAD	211-214	protein phosphatase, Mg2+/Mn2+ dependent 1D	Homo sapiens	34-39
31439867-3	2019	Specifically, we show that mutant PPM1D drives hypermethylation of CpG islands throughout the genome and promotes epigenetic silencing of nicotinic acid phosphoribosyltransferase (NAPRT), a key gene involved in NAD biosynthesis.	NAD	211-214	nicotinate phosphoribosyltransferase	Homo sapiens	138-178
31439867-3	2019	Specifically, we show that mutant PPM1D drives hypermethylation of CpG islands throughout the genome and promotes epigenetic silencing of nicotinic acid phosphoribosyltransferase (NAPRT), a key gene involved in NAD biosynthesis.	NAD	211-214	nicotinate phosphoribosyltransferase	Homo sapiens	180-185
31439867-5	2019	Overall, our results reveal a promising approach for the targeting of PPM1D mutant tumors, and define a critical link between oncogenic driver mutations and NAD metabolism, which can be exploited for tumor-specific cell killing.	NAD	157-160	protein phosphatase, Mg2+/Mn2+ dependent 1D	Homo sapiens	70-75
31448236-0	2019	NAMPT and NAPRT, Key Enzymes in NAD Salvage Synthesis Pathway, Are of Negative Prognostic Value in Colorectal Cancer.	NAD	32-35	nicotinate phosphoribosyltransferase	Homo sapiens	10-15
31448236-2	2019	Nicotinamide phosphoribosyltransferase (NAMPT) and nicotinate phosphoribosyltransferase (NAPRT) are key enzymes for NAD salvage biosynthesis pathway, which reciprocally synthesize NAD to supply the main source of NAD biosythesis.	NAD	116-119	nicotinate phosphoribosyltransferase	Homo sapiens	51-87
31448236-2	2019	Nicotinamide phosphoribosyltransferase (NAMPT) and nicotinate phosphoribosyltransferase (NAPRT) are key enzymes for NAD salvage biosynthesis pathway, which reciprocally synthesize NAD to supply the main source of NAD biosythesis.	NAD	116-119	nicotinate phosphoribosyltransferase	Homo sapiens	89-94
31448236-2	2019	Nicotinamide phosphoribosyltransferase (NAMPT) and nicotinate phosphoribosyltransferase (NAPRT) are key enzymes for NAD salvage biosynthesis pathway, which reciprocally synthesize NAD to supply the main source of NAD biosythesis.	NAD	180-183	nicotinate phosphoribosyltransferase	Homo sapiens	51-87
31448236-2	2019	Nicotinamide phosphoribosyltransferase (NAMPT) and nicotinate phosphoribosyltransferase (NAPRT) are key enzymes for NAD salvage biosynthesis pathway, which reciprocally synthesize NAD to supply the main source of NAD biosythesis.	NAD	180-183	nicotinate phosphoribosyltransferase	Homo sapiens	89-94
31448236-2	2019	Nicotinamide phosphoribosyltransferase (NAMPT) and nicotinate phosphoribosyltransferase (NAPRT) are key enzymes for NAD salvage biosynthesis pathway, which reciprocally synthesize NAD to supply the main source of NAD biosythesis.	NAD	180-183	nicotinate phosphoribosyltransferase	Homo sapiens	51-87
31448236-2	2019	Nicotinamide phosphoribosyltransferase (NAMPT) and nicotinate phosphoribosyltransferase (NAPRT) are key enzymes for NAD salvage biosynthesis pathway, which reciprocally synthesize NAD to supply the main source of NAD biosythesis.	NAD	180-183	nicotinate phosphoribosyltransferase	Homo sapiens	89-94
30453040-3	2019	As a family of NAD+ dependent protein modifying enzymes, sirtuins (SIRT1-SIRT7) have multiple catalytic functions such as deacetylase, desuccinylase, demalonylase, demyristoylase, depalmitoylase, and/or mono-ADP-ribosyltransferase.	NAD	15-18	sirtuin 1	Homo sapiens	67-72
30453040-3	2019	As a family of NAD+ dependent protein modifying enzymes, sirtuins (SIRT1-SIRT7) have multiple catalytic functions such as deacetylase, desuccinylase, demalonylase, demyristoylase, depalmitoylase, and/or mono-ADP-ribosyltransferase.	NAD	15-18	sirtuin 7	Homo sapiens	73-78
33365629-3	2019	Excluding tRNA sequences, sequence divergence rate was lowest in rRNA genes and highest in genes encoding NADH (specifically ND1, ND2, ND3) and the control region.	NAD	106-110	mitochondrially encoded NADH dehydrogenase 2	Homo sapiens	130-133
31185608-2	2019	Interleukin-1beta (IL-1beta) has been shown to induce the upregulation of MMP-9 through nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX)-reactive oxygen species (ROS)-dependent signaling pathways.	NAD	88-121	matrix metallopeptidase 9	Rattus norvegicus	74-79
31206100-7	2019	H2AQ104 methylation and chromatin dynamics are regulated by fibrillarin (FBL) and the NAD+-dependent nucleolar deacetylase sirtuin 7 (SIRT7).	NAD	86-90	sirtuin 7	Homo sapiens	123-132
31206100-7	2019	H2AQ104 methylation and chromatin dynamics are regulated by fibrillarin (FBL) and the NAD+-dependent nucleolar deacetylase sirtuin 7 (SIRT7).	NAD	86-90	sirtuin 7	Homo sapiens	134-139
30996115-3	2019	Sirtuin 1 (SIRT 1), a longevity gene related to many diseases associated with aging, is a nicotinamide adenine dinucleotide (NAD+)-dependent protein deacetylase and master metabolic regulator.	NAD	90-123	sirtuin 1	Homo sapiens	0-9
30996115-3	2019	Sirtuin 1 (SIRT 1), a longevity gene related to many diseases associated with aging, is a nicotinamide adenine dinucleotide (NAD+)-dependent protein deacetylase and master metabolic regulator.	NAD	90-123	sirtuin 1	Homo sapiens	11-17
30996115-3	2019	Sirtuin 1 (SIRT 1), a longevity gene related to many diseases associated with aging, is a nicotinamide adenine dinucleotide (NAD+)-dependent protein deacetylase and master metabolic regulator.	NAD	125-129	sirtuin 1	Homo sapiens	0-9
30996115-3	2019	Sirtuin 1 (SIRT 1), a longevity gene related to many diseases associated with aging, is a nicotinamide adenine dinucleotide (NAD+)-dependent protein deacetylase and master metabolic regulator.	NAD	125-129	sirtuin 1	Homo sapiens	11-17
30885568-3	2019	In this paper, we developed inhibitors of nicotinamide adenine dinucleotide-dependent deacetylase isoform 2 of Sirtuin protein (SIRT2), based on HPH-1Trt/HPH-2Trt, and aimed to generate new anti-cancer drugs.	NAD	42-75	polyhomeotic homolog 2	Homo sapiens	154-159
30915433-4	2019	However, the external NADH dehydrogenases (Nde1/2) and the L-glycerol 3-phosphate shuttle (composed of Gpd1/2 and Gut2), both coupled to the respiratory chain, are known to contribute to cytosolic NAD+ regeneration during growth on non-fermentable carbon sources.	NAD	197-201	NADH-ubiquinone reductase (H(+)-translocating) NDE1	Saccharomyces cerevisiae S288C	43-49
30915433-4	2019	However, the external NADH dehydrogenases (Nde1/2) and the L-glycerol 3-phosphate shuttle (composed of Gpd1/2 and Gut2), both coupled to the respiratory chain, are known to contribute to cytosolic NAD+ regeneration during growth on non-fermentable carbon sources.	NAD	197-201	glycerol-3-phosphate dehydrogenase (NAD(+)) GPD1	Saccharomyces cerevisiae S288C	103-109
30954031-5	2019	Especially, ER-FPP and GDH-FPP enable the continuous conversion of 4-(4-Methoxyphenyl)-3-buten-2-one with NAD+ recycling.	NAD	106-110	glucose-6-phosphate dehydrogenase	Homo sapiens	23-26
30995985-1	2019	Deficiency of the Nox2 (gp91phox) catalytic subunit of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase is a genetic cause of X-linked chronic granulomatous disease, a condition in which patients are prone to infection resulting from the loss of oxidant production by neutrophils.	NAD	55-88	cytochrome b-245 beta chain	Homo sapiens	18-22
30995985-1	2019	Deficiency of the Nox2 (gp91phox) catalytic subunit of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase is a genetic cause of X-linked chronic granulomatous disease, a condition in which patients are prone to infection resulting from the loss of oxidant production by neutrophils.	NAD	55-88	cytochrome b-245 beta chain	Homo sapiens	24-32
30794798-2	2019	3alpha-HSD/CR uses remote binding interactions to accelerate the reaction of androsterone with NAD+.	NAD	95-99	aldo-keto reductase family 1 member C4	Homo sapiens	0-10
30794798-3	2019	Here, we examine the enthalpic and entropic components of the remote binding energy in the 3alpha-HSD/CR-catalyzed reaction of NAD+ with androsterone versus the substrate analogs, 2-decalol and cyclohexanol, by analyzing the temperature-dependent kinetic parameters through steady-state kinetics.	NAD	127-131	aldo-keto reductase family 1 member C4	Homo sapiens	91-101
30909652-10	2019	This decreased the NAD+-dependent activity of Sirtuin 1 (SIRT1) deacetylase.	NAD	19-23	sirtuin 1	Homo sapiens	46-55
30909652-10	2019	This decreased the NAD+-dependent activity of Sirtuin 1 (SIRT1) deacetylase.	NAD	19-23	sirtuin 1	Homo sapiens	57-62
30886180-7	2019	Chemical inhibition of ATM in rat cardiomyoblast cells (H9c2) significantly decreased the excited-state autofluorescence lifetime of enzyme-bound reduced NADH and its phosphorylated form, NADPH (NAD(P)H; 2.77 +- 0.26 ns compared to 2.57 +- 0.14 ns in KU60019-treated cells).	NAD	154-158	ATM serine/threonine kinase	Rattus norvegicus	23-26
30537158-1	2019	Human sirtuin 1 (hSIRT1) is a NAD+ -dependent deacetylase that regulates several cellular processes.	NAD	30-33	sirtuin 1	Homo sapiens	6-15
30537158-1	2019	Human sirtuin 1 (hSIRT1) is a NAD+ -dependent deacetylase that regulates several cellular processes.	NAD	30-33	sirtuin 1	Homo sapiens	17-23
31208524-5	2019	One of the key pathways that is impaired in diabetic peripheral neuropathy (DPN) is the energy sensing pathway comprising the nicotinamide-adenine dinucleotide (NAD+)-dependent Sirtuin 1 (SIRT1)/peroxisome proliferator-activated receptor-gamma coactivator alpha (PGC-1alpha)/Mt transcription factor A (TFAM or mtTFA) signaling pathway.	NAD	161-165	sirtuin 1	Homo sapiens	177-186
31208524-5	2019	One of the key pathways that is impaired in diabetic peripheral neuropathy (DPN) is the energy sensing pathway comprising the nicotinamide-adenine dinucleotide (NAD+)-dependent Sirtuin 1 (SIRT1)/peroxisome proliferator-activated receptor-gamma coactivator alpha (PGC-1alpha)/Mt transcription factor A (TFAM or mtTFA) signaling pathway.	NAD	161-165	sirtuin 1	Homo sapiens	188-193
31208524-8	2019	Furthermore, administration of nicotinamide riboside (NR), a precursor of NAD+, prevents and reverses DPN, in part by increasing NAD+ levels and SIRT1 activity.	NAD	74-78	sirtuin 1	Homo sapiens	145-150
30093629-1	2019	SIRT7 is an NAD+-dependent histone/non-histone deacetylase, which is highly expressed in different types of cancer including thyroid cancer; however, its biological function in thyroid cancer is still undiscovered.	NAD	12-16	sirtuin 7	Mus musculus	0-5
30427660-3	2018	Here, a nano therapeutic agent is realized by directly associating the clinical formulation of tPA to the porous structure of soft discoidal polymeric nanoconstructs (tPA-DPNs).	NAD	171-175	chromosome 20 open reading frame 181	Homo sapiens	95-98
30427660-3	2018	Here, a nano therapeutic agent is realized by directly associating the clinical formulation of tPA to the porous structure of soft discoidal polymeric nanoconstructs (tPA-DPNs).	NAD	171-175	chromosome 20 open reading frame 181	Homo sapiens	167-170
30427660-4	2018	The porous matrix of DPNs protects tPA from rapid degradation, allowing tPA-DPNs to preserve over 70% of the tPA original activity after 3 h of exposure to serum proteins.	NAD	21-25	chromosome 20 open reading frame 181	Homo sapiens	35-38
30427660-4	2018	The porous matrix of DPNs protects tPA from rapid degradation, allowing tPA-DPNs to preserve over 70% of the tPA original activity after 3 h of exposure to serum proteins.	NAD	21-25	chromosome 20 open reading frame 181	Homo sapiens	72-75
30427660-4	2018	The porous matrix of DPNs protects tPA from rapid degradation, allowing tPA-DPNs to preserve over 70% of the tPA original activity after 3 h of exposure to serum proteins.	NAD	21-25	chromosome 20 open reading frame 181	Homo sapiens	72-75
30427660-5	2018	Under dynamic conditions, tPA-DPNs dissolve clots more efficiently than free tPA, as demonstrated in a microfluidic chip where clots are formed mimicking in vivo conditions.	NAD	30-34	chromosome 20 open reading frame 181	Homo sapiens	26-29
30427660-6	2018	At 60 min post-treatment initiation, the clot area reduces by half (57 +- 8%) with tPA-DPNs, whereas a similar result (56 +- 21%) is obtained only after 90 min for free tPA.	NAD	87-91	chromosome 20 open reading frame 181	Homo sapiens	83-86
30576653-2	2018	(2018) describe a mechanism by which insulin signaling represses the NAD+-dependent SIRT1 deacetylase by promoting PACS-2 binding and provide structural clues to understanding how SIRT1 activating compounds (STACs) work.	NAD	69-73	sirtuin 1	Homo sapiens	84-89
30576653-2	2018	(2018) describe a mechanism by which insulin signaling represses the NAD+-dependent SIRT1 deacetylase by promoting PACS-2 binding and provide structural clues to understanding how SIRT1 activating compounds (STACs) work.	NAD	69-73	sirtuin 1	Homo sapiens	180-185
30395713-1	2018	Protein lysine deacylases comprise three zinc-dependent families and the NAD+-dependent sirtuins Sirt1-7, which contribute to aging-related diseases.	NAD	73-77	sirtuin 1	Homo sapiens	97-104
30242091-4	2018	NAMPT is a component of a salvage biosynthetic pathway for NAD, and inhibition of this enzyme results in disruption of primary cellular metabolism leading to cell death.	NAD	59-62	nicotinamide phosphoribosyltransferase	Rattus norvegicus	0-5
30348778-3	2018	Recent studies found the NAD+-dependent histone deacetylase, SIRT1, directly regulates acetylation status of clock components and influences circadian amplitude in cells.	NAD	25-29	sirtuin 1	Homo sapiens	61-66
30585266-5	2018	The lower NADH level in atrophic nonunion tissues disrupted CtBP2 dimerization and enhanced the blockage of the accessibility of the p300-Runx2 complex to the promoters of a series of bone-related target genes, such as OSC, ALPL, COL1A1, IBSP, SPP1 and MMP13.	NAD	10-14	collagen type I alpha 1 chain	Homo sapiens	230-236
30356218-3	2018	Here we show that alpha-amino-beta-carboxymuconate-epsilon-semialdehyde decarboxylase (ACMSD), the enzyme that limits spontaneous cyclization of alpha-amino-beta-carboxymuconate-epsilon-semialdehyde in the de novo NAD+ synthesis pathway, controls cellular NAD+ levels via an evolutionarily conserved mechanism in Caenorhabditis elegans and mouse.	NAD	214-218	amino carboxymuconate semialdehyde decarboxylase	Mus musculus	87-92
30356218-3	2018	Here we show that alpha-amino-beta-carboxymuconate-epsilon-semialdehyde decarboxylase (ACMSD), the enzyme that limits spontaneous cyclization of alpha-amino-beta-carboxymuconate-epsilon-semialdehyde in the de novo NAD+ synthesis pathway, controls cellular NAD+ levels via an evolutionarily conserved mechanism in Caenorhabditis elegans and mouse.	NAD	256-260	amino carboxymuconate semialdehyde decarboxylase	Mus musculus	87-92
30356218-4	2018	Genetic and pharmacological inhibition of ACMSD boosts de novo NAD+ synthesis and sirtuin 1 activity, ultimately enhancing mitochondrial function.	NAD	63-67	amino carboxymuconate semialdehyde decarboxylase	Mus musculus	42-47
30356218-7	2018	In summary, we identify ACMSD as a key modulator of cellular NAD+ levels, sirtuin activity and mitochondrial homeostasis in kidney and liver.	NAD	61-65	amino carboxymuconate semialdehyde decarboxylase	Mus musculus	24-29
30322911-3	2018	nsP3 has a highly conserved macrodomain (MD) that binds ADP-ribose (ADPr), which can be conjugated to protein as a posttranslational modification involving transfer of ADPr from NAD+ by poly ADPr polymerases (PARPs).	NAD	178-182	SH2 domain containing 3C	Homo sapiens	0-4
30416425-1	2018	Silent information regulator 1 (SIRT1) is a mammalian homolog of the nicotinamide adenine dinucleotide (NAD)-dependent deacetylase sirtuin family.	NAD	69-102	sirtuin 1	Homo sapiens	0-30
30416425-1	2018	Silent information regulator 1 (SIRT1) is a mammalian homolog of the nicotinamide adenine dinucleotide (NAD)-dependent deacetylase sirtuin family.	NAD	69-102	sirtuin 1	Homo sapiens	32-37
30416425-1	2018	Silent information regulator 1 (SIRT1) is a mammalian homolog of the nicotinamide adenine dinucleotide (NAD)-dependent deacetylase sirtuin family.	NAD	104-107	sirtuin 1	Homo sapiens	0-30
30416425-1	2018	Silent information regulator 1 (SIRT1) is a mammalian homolog of the nicotinamide adenine dinucleotide (NAD)-dependent deacetylase sirtuin family.	NAD	104-107	sirtuin 1	Homo sapiens	32-37
30366365-7	2018	Second, AMPK activates histone deacetylases (HDACs) sirtuins by increasing the cellular concentration of NAD+, a cofactor of sirtuins.	NAD	105-109	protein kinase AMP-activated non-catalytic subunit beta 1	Homo sapiens	8-12
30259779-2	2018	Agents that increase NAD+ levels, which are diminished with age, may be senopreventive through restoration of SIRT1 and normal mitochondrial activity.	NAD	21-25	sirtuin 1	Homo sapiens	110-115
30158377-6	2018	The results showed that the expression of the NAMPT/NAD+/Sirt1 signaling pathway was up-regulated in the peripheral blood of patients with ACS.	NAD	52-56	sirtuin 1	Homo sapiens	57-62
30158377-9	2018	The addition of NAD+ in the cell culture supernatant had no significant effect on the polarization of M1 but increased the M2 polarization and the expression levels of IL-10 and IL-1ra.	NAD	16-20	interleukin 10	Homo sapiens	168-173
30158377-10	2018	Our findings suggested that NAMPT is involved in the pathogenesis of atherosclerosis; the increased expression of eNAMPT in ACS patients may play a protective role by the up regulation of the NAMPT/NAD+/Sirt1 signaling pathway.	NAD	198-202	sirtuin 1	Homo sapiens	203-208
29807115-1	2018	SIRT1, an NAD+-dependent histone/protein deacetylase, has diverse physiological actions.	NAD	10-13	sirtuin 1	Homo sapiens	0-5
30096284-3	2018	We found that ERalpha and/or ERbeta activation using their agonists (0.5 mg/kg E2, PPT or DPN) ameliorate memory impairment in the Morris water maze (MWM) and Y-maze tests and suppress apoptosis as evidenced by decreased caspase-3 activity and increased ratio of Bcl-2/Bax.	NAD	90-93	caspase 3	Mus musculus	221-230
30096284-3	2018	We found that ERalpha and/or ERbeta activation using their agonists (0.5 mg/kg E2, PPT or DPN) ameliorate memory impairment in the Morris water maze (MWM) and Y-maze tests and suppress apoptosis as evidenced by decreased caspase-3 activity and increased ratio of Bcl-2/Bax.	NAD	90-93	BCL2-associated X protein	Mus musculus	269-272
29976663-5	2018	PARP1, or poly(ADP-ribose) polymerase 1, catalyzes the transfer of a poly(ADP-ribose) (PAR) moiety from NAD+ onto acceptor proteins, including itself, histone proteins, and CTCF.	NAD	104-108	CCCTC-binding factor	Homo sapiens	173-177
30139380-2	2018	Poly (ADP-ribose) polymerase 1 (PARP1) and sirtuin 1 (SIRT1) affect cellular NAD+ levels and play essential roles in regulating metabolism.	NAD	77-81	sirtuin 1	Homo sapiens	43-52
30139380-2	2018	Poly (ADP-ribose) polymerase 1 (PARP1) and sirtuin 1 (SIRT1) affect cellular NAD+ levels and play essential roles in regulating metabolism.	NAD	77-81	sirtuin 1	Homo sapiens	54-59
29901258-0	2018	Overexpression of Nmnat3 efficiently increases NAD and NGD levels and ameliorates age-associated insulin resistance.	NAD	47-50	nicotinamide nucleotide adenylyltransferase 3	Mus musculus	18-24
29901258-2	2018	As a coenzyme, NAD controls mitochondrial respiration through enzymes of the tricarboxylic acid (TCA) cycle, beta-oxidation, and oxidative phosphorylation and also serves as a substrate for posttranslational protein modifications, such as deacetylation and ADP-ribosylation by sirtuins and poly(ADP-ribose) polymerase (PARP), respectively.	NAD	15-18	poly (ADP-ribose) polymerase family, member 1	Mus musculus	290-317
29901258-2	2018	As a coenzyme, NAD controls mitochondrial respiration through enzymes of the tricarboxylic acid (TCA) cycle, beta-oxidation, and oxidative phosphorylation and also serves as a substrate for posttranslational protein modifications, such as deacetylation and ADP-ribosylation by sirtuins and poly(ADP-ribose) polymerase (PARP), respectively.	NAD	15-18	poly (ADP-ribose) polymerase family, member 1	Mus musculus	319-323
29901258-7	2018	In this study, Nmnat3 overexpression in mice efficiently increased NAD levels in various tissues and prevented aging-related declines in NAD levels.	NAD	67-70	nicotinamide nucleotide adenylyltransferase 3	Mus musculus	15-21
29901258-7	2018	In this study, Nmnat3 overexpression in mice efficiently increased NAD levels in various tissues and prevented aging-related declines in NAD levels.	NAD	137-140	nicotinamide nucleotide adenylyltransferase 3	Mus musculus	15-21
29901258-11	2018	Interestingly, we also found that concentrations of the NAD analog nicotinamide guanine dinucleotide (NGD) were dramatically increased in Nmnat3 Tg mice.	NAD	56-59	nicotinamide nucleotide adenylyltransferase 3	Mus musculus	138-144
29674119-1	2018	NMNAT1 (nicotinamide mononucleotide adenylyltransferase 1) encodes a rate-limiting enzyme that catalyzes the biosynthesis of NAD+ and plays a role in neuroprotection.	NAD	125-129	nicotinamide nucleotide adenylyltransferase 1	Mus musculus	0-6
29674119-1	2018	NMNAT1 (nicotinamide mononucleotide adenylyltransferase 1) encodes a rate-limiting enzyme that catalyzes the biosynthesis of NAD+ and plays a role in neuroprotection.	NAD	125-129	nicotinamide nucleotide adenylyltransferase 1	Mus musculus	8-57
29958828-1	2018	Stimulation of the cytosolic NAD+ dependent deacetylase SIRT1 is cardioprotective against ischemia-reperfusion (IR) injury.	NAD	29-33	sirtuin 1	Homo sapiens	56-61
29958828-2	2018	NAD+ precursors including nicotinamide mononucleotide (NMN) are thought to induce cardioprotection via SIRT1.	NAD	0-4	sirtuin 1	Homo sapiens	103-108
29901193-7	2018	The expression levels of the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase subunits, NADPH oxidase 2 (Nox2) and p67phox, were upregulated by Hcy, with a peak in levels following treatment with a concentration of 200 microM.	NAD	29-62	cytochrome b-245 beta chain	Homo sapiens	99-114
29901193-7	2018	The expression levels of the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase subunits, NADPH oxidase 2 (Nox2) and p67phox, were upregulated by Hcy, with a peak in levels following treatment with a concentration of 200 microM.	NAD	29-62	cytochrome b-245 beta chain	Homo sapiens	116-120
29991742-1	2018	Sirtuin-1 (SIRT1), the mammalian ortholog of yeast Sir2p, is well known to be a highly conserved NAD+-dependent protein deacetylase that has been emerging as a key cancer target.	NAD	97-100	sirtuin 1	Homo sapiens	0-9
29991742-1	2018	Sirtuin-1 (SIRT1), the mammalian ortholog of yeast Sir2p, is well known to be a highly conserved NAD+-dependent protein deacetylase that has been emerging as a key cancer target.	NAD	97-100	sirtuin 1	Homo sapiens	11-16
29427626-2	2018	SIRT1 is an NAD+-dependent histone/protein deacetylase speculated to function as an oncogene.	NAD	12-16	sirtuin 1	Homo sapiens	0-5
30271963-1	2018	Previous genomic studies in humans indicate that SIRT1, a nicotinamide adenine dinucleotide (NAD+)-dependent protein deacetylase, is involved in anxiety and depression, but the mechanisms are unclear.	NAD	58-91	sirtuin 1	Homo sapiens	49-54
30271963-1	2018	Previous genomic studies in humans indicate that SIRT1, a nicotinamide adenine dinucleotide (NAD+)-dependent protein deacetylase, is involved in anxiety and depression, but the mechanisms are unclear.	NAD	93-96	sirtuin 1	Homo sapiens	49-54
29997610-9	2018	Moreover, overexpression of HAP4 might extend the life span of cells under caloric restriction by lowering the NADH level.	NAD	111-115	transcription factor HAP4	Saccharomyces cerevisiae S288C	28-32
29874586-5	2018	Furthermore, we identify SIRT6, a NAD+-dependent histone deacetylase, as a corepressor of ATF4 transcriptional activity.	NAD	34-37	activating transcription factor 4	Homo sapiens	90-94
29872122-8	2018	These data indicate that NNMT links the NAD+ and methionine metabolic pathways and promotes liver steatosis and fibrosis.	NAD	40-44	nicotinamide N-methyltransferase	Mus musculus	25-29
29194618-4	2018	It is reported that Sirtuin1 (SIRT1), a NAD+ dependent class III histone deacetylase is associated with tumor metastasis through positive regulation of EMT in several types of cancers.	NAD	40-43	sirtuin 1	Homo sapiens	20-28
29194618-4	2018	It is reported that Sirtuin1 (SIRT1), a NAD+ dependent class III histone deacetylase is associated with tumor metastasis through positive regulation of EMT in several types of cancers.	NAD	40-43	sirtuin 1	Homo sapiens	30-35
29653431-6	2018	Etoposide decreased protein abundance of NAD-dependent deacetylases SIRTUIN1.	NAD	41-44	sirtuin 1	Homo sapiens	68-76
29476819-2	2018	SIRT1 deacetylates p53 in a NAD+-dependent manner to inhibit transcription activity of p53, in turn modulate pathways that are implicated in regulation of tissue homoeostasis and many disease states.	NAD	28-32	sirtuin 1	Homo sapiens	0-5
28750181-1	2018	SIRT1 is a NAD-dependent protein deacetylase that participates in cellular regulation.	NAD	11-14	sirtuin 1	Homo sapiens	0-5
29436637-1	2018	Nicotinamide phosphoribosyltransferase (Nampt), also termed visfatin, catalyses the rate-limiting step in the nicotinamide adenine dinucleotide (NAD) salvage pathway.	NAD	110-143	nicotinamide phosphoribosyltransferase	Rattus norvegicus	0-38
29436637-1	2018	Nicotinamide phosphoribosyltransferase (Nampt), also termed visfatin, catalyses the rate-limiting step in the nicotinamide adenine dinucleotide (NAD) salvage pathway.	NAD	110-143	nicotinamide phosphoribosyltransferase	Rattus norvegicus	40-45
29436637-1	2018	Nicotinamide phosphoribosyltransferase (Nampt), also termed visfatin, catalyses the rate-limiting step in the nicotinamide adenine dinucleotide (NAD) salvage pathway.	NAD	110-143	nicotinamide phosphoribosyltransferase	Rattus norvegicus	60-68
29436637-1	2018	Nicotinamide phosphoribosyltransferase (Nampt), also termed visfatin, catalyses the rate-limiting step in the nicotinamide adenine dinucleotide (NAD) salvage pathway.	NAD	145-148	nicotinamide phosphoribosyltransferase	Rattus norvegicus	0-38
29436637-1	2018	Nicotinamide phosphoribosyltransferase (Nampt), also termed visfatin, catalyses the rate-limiting step in the nicotinamide adenine dinucleotide (NAD) salvage pathway.	NAD	145-148	nicotinamide phosphoribosyltransferase	Rattus norvegicus	40-45
29436637-1	2018	Nicotinamide phosphoribosyltransferase (Nampt), also termed visfatin, catalyses the rate-limiting step in the nicotinamide adenine dinucleotide (NAD) salvage pathway.	NAD	145-148	nicotinamide phosphoribosyltransferase	Rattus norvegicus	60-68
29715067-1	2018	SIRT1 is an NAD+-dependent deacetylase that acts as a nutrient sensitive regulator of longevity.	NAD	12-15	sirtuin 1	Homo sapiens	0-5
29584709-3	2018	In previous studies of the related NADH: ubiquinone oxidoreductase crystal structure from Saccharomyces cerevisiae, two ubiquinone-binding sites (UQI and UQII) were identified and shown to play an important role in the NDH-2-catalyzed oxidoreduction reaction.	NAD	35-39	NADH-ubiquinone reductase (H(+)-translocating) NDE2	Saccharomyces cerevisiae S288C	219-224
29240402-3	2018	However, only a small number of ALDH1A2 inhibitors have been reported, and information on the structure of ALDH1A2 was limited to the NAD-liganded enzyme void of substrate or inhibitors.	NAD	134-137	aldehyde dehydrogenase 1 family member A2	Homo sapiens	107-114
29511198-0	2018	Author Correction: Rev1 contributes to proper mitochondrial function via the PARP-NAD+-SIRT1-PGC1alpha axis.	NAD	82-86	sirtuin 1	Homo sapiens	87-92
29175372-0	2018	NAD-biosynthetic enzyme NMNAT1 reduces early behavioral impairment in the htau mouse model of tauopathy.	NAD	0-3	nicotinamide nucleotide adenylyltransferase 1	Mus musculus	24-30
29643977-3	2018	Silent information regulator 1 (Sirt1) is a deacetylase at the consumption of NAD+ and is involved in gene silencing, cell cycle, fat and glucose metabolism, cellular oxidative stress, and senescence.	NAD	78-82	sirtuin 1	Homo sapiens	0-30
29643977-3	2018	Silent information regulator 1 (Sirt1) is a deacetylase at the consumption of NAD+ and is involved in gene silencing, cell cycle, fat and glucose metabolism, cellular oxidative stress, and senescence.	NAD	78-82	sirtuin 1	Homo sapiens	32-37
28473297-0	2018	NADH reduction of nitroaromatics as a probe for residual ferric form high-spin in a cytochrome P450.	NAD	0-4	spindlin 1	Homo sapiens	74-78
30509041-6	2018	Moreover, the effect of ceramide and SEW 2871 (agonist for S1P receptor-1) on Sirt1 (NAD+-dependent nuclear enzyme responsible for stress response) gene expression under A  toxicity was analyzed.	NAD	85-89	sphingosine-1-phosphate receptor 1	Homo sapiens	59-73
30518708-1	2018	SIRT1, an NAD+-dependent deacetylase, causes deacetylation and down-regulation of its target p53.	NAD	10-13	sirtuin 1	Homo sapiens	0-5
29807573-2	2018	Indeed, upon genotoxic stress, CCAR2, phosphorylated by the apical DDR kinases ATM and ATR, increases its binding to the NAD+-dependent histone deacetylase SIRT1 and inhibits SIRT1 activity.	NAD	121-125	sirtuin 1	Homo sapiens	156-161
29807573-2	2018	Indeed, upon genotoxic stress, CCAR2, phosphorylated by the apical DDR kinases ATM and ATR, increases its binding to the NAD+-dependent histone deacetylase SIRT1 and inhibits SIRT1 activity.	NAD	121-125	sirtuin 1	Homo sapiens	175-180
29239724-4	2017	Sirtuin 2 (SIRT2), one of the mammalian nicotinamide adenine dinucleotide (NAD)-dependent lysine deacylases, catalyzes the removal of fatty acylation from K-Ras4a.	NAD	40-73	KRAS proto-oncogene, GTPase	Homo sapiens	155-162
29239724-4	2017	Sirtuin 2 (SIRT2), one of the mammalian nicotinamide adenine dinucleotide (NAD)-dependent lysine deacylases, catalyzes the removal of fatty acylation from K-Ras4a.	NAD	75-78	KRAS proto-oncogene, GTPase	Homo sapiens	155-162
28625351-2	2017	The tolerance mechanisms involved in the strain might have existed through the upregulation of genes involved in NAD(H)/NADP(H) cofactors generations (ALD6, ZWF1, GND1), membrane robustness for efflux pump (YOR1, PDR5, TPO3) and cation/polyamine transport (TPO3).	NAD	113-119	phosphogluconate dehydrogenase (decarboxylating) GND1	Saccharomyces cerevisiae S288C	163-167
28625351-2	2017	The tolerance mechanisms involved in the strain might have existed through the upregulation of genes involved in NAD(H)/NADP(H) cofactors generations (ALD6, ZWF1, GND1), membrane robustness for efflux pump (YOR1, PDR5, TPO3) and cation/polyamine transport (TPO3).	NAD	113-119	ATP-binding cassette multidrug transporter PDR5	Saccharomyces cerevisiae S288C	213-217
29039590-0	2017	MicroRNA-218 promotes prostaglandin E2 to inhibit osteogenic differentiation in synovial mesenchymal stem cells by targeting 15-hydroxyprostaglandin dehydrogenase [NAD(+)].	NAD	164-170	carbonyl reductase 1	Homo sapiens	125-162
29039590-7	2017	Western blotting and reverse transcription-quantitative polymerase chain reaction analysis of gene expression demonstrated the upregulation of 15-hydroxyprostaglandin dehydrogenase [NAD(+)] (15-HPGD), prostaglandin E2 (PGE2) and rate limiting enzymes responsible for the synthesis of PGE2 precursors throughout chondrogenesis.	NAD	182-188	carbonyl reductase 1	Homo sapiens	143-180
29187201-6	2017	METHODS: A two-hybrid chimera interacting system allowed to identify Sirt1, a NAD+ dependent type III histone deacetylase, as a novel Smad2 interactor.	NAD	78-81	sirtuin 1	Homo sapiens	69-74
29120608-2	2017	Secondary alcohol dehydrogenase (S-ADH) can reduce acetone and oxidize nicotinamide adenine dinucleotide (NADH to NAD+) in a weak acid environment.	NAD	71-104	aldo-keto reductase family 1 member A1	Homo sapiens	10-31
29120608-2	2017	Secondary alcohol dehydrogenase (S-ADH) can reduce acetone and oxidize nicotinamide adenine dinucleotide (NADH to NAD+) in a weak acid environment.	NAD	106-110	aldo-keto reductase family 1 member A1	Homo sapiens	10-31
29120608-2	2017	Secondary alcohol dehydrogenase (S-ADH) can reduce acetone and oxidize nicotinamide adenine dinucleotide (NADH to NAD+) in a weak acid environment.	NAD	114-118	aldo-keto reductase family 1 member A1	Homo sapiens	10-31
29329924-2	2017	Polyphenols could reduce oxidative stress and restore endothelial function by inhibiting the nicotinamide-adenine-dinucleotide-phosphate (NADPH) oxidase isoform Nox2.	NAD	93-126	cytochrome b-245 beta chain	Homo sapiens	161-165
29045138-1	2017	Aldehyde dehydrogenase 7A1 (ALDH7A1) catalyzes the terminal step of lysine catabolism, the NAD+-dependent oxidation of alpha-aminoadipate semialdehyde to alpha-aminoadipate.	NAD	91-95	aldehyde dehydrogenase 7 family member A1	Homo sapiens	0-26
29045138-1	2017	Aldehyde dehydrogenase 7A1 (ALDH7A1) catalyzes the terminal step of lysine catabolism, the NAD+-dependent oxidation of alpha-aminoadipate semialdehyde to alpha-aminoadipate.	NAD	91-95	aldehyde dehydrogenase 7 family member A1	Homo sapiens	28-35
28137513-1	2017	3alpha-Hydroxysteroid dehydrogenase/carbonyl reductase (3alpha-HSD/CR) catalyzes the oxidation of androsterone with NAD+ to form androstanedione and NADH with the rate limiting step being the release of NADH.	NAD	116-120	aldo-keto reductase family 1 member C4	Homo sapiens	56-66
28137513-1	2017	3alpha-Hydroxysteroid dehydrogenase/carbonyl reductase (3alpha-HSD/CR) catalyzes the oxidation of androsterone with NAD+ to form androstanedione and NADH with the rate limiting step being the release of NADH.	NAD	149-153	aldo-keto reductase family 1 member C4	Homo sapiens	56-66
28137513-1	2017	3alpha-Hydroxysteroid dehydrogenase/carbonyl reductase (3alpha-HSD/CR) catalyzes the oxidation of androsterone with NAD+ to form androstanedione and NADH with the rate limiting step being the release of NADH.	NAD	203-207	aldo-keto reductase family 1 member C4	Homo sapiens	56-66
28137513-5	2017	The rate limiting step is hydride transfer for 3alpha-HSD/CR catalyzing the reaction of cyclohexanol with NAD+ based on the observed rapid equilibrium ordered mechanism and equal deuterium isotope effects of 3.9 on V and V/K for cyclohexanol.	NAD	106-110	aldo-keto reductase family 1 member C4	Homo sapiens	47-57
28803211-0	2017	Melatonin protects chondrocytes from impairment induced by glucocorticoids via NAD+-dependent SIRT1.	NAD	79-83	sirtuin 1	Homo sapiens	94-99
28803211-9	2017	The enhancement of NAD+-dependent SIRT1 activity contributes to the chondroprotecfive effects of melatonin, which has a great benefit to prevent dexamethasone-induced chondrocytes impairment.	NAD	19-23	sirtuin 1	Homo sapiens	34-39
29100430-5	2017	Niacin can rescue NAD+ biosynthesis through a parallel pathway that depends on nicotinic acid phosphoribosyltransferase (NAPRT) expression.	NAD	18-22	nicotinate phosphoribosyltransferase	Homo sapiens	79-119
29100430-5	2017	Niacin can rescue NAD+ biosynthesis through a parallel pathway that depends on nicotinic acid phosphoribosyltransferase (NAPRT) expression.	NAD	18-22	nicotinate phosphoribosyltransferase	Homo sapiens	121-126
28543772-5	2017	Both cell lines showed an increase in NAD+ levels following PARP inhibitor treatment in comparison with temozolomide treatment.	NAD	38-42	poly (ADP-ribose) polymerase family, member 1	Mus musculus	60-64
28543772-6	2017	Liver extracts from PARP1 WT mice showed a significant increase in NAD+ levels after rucaparib treatment compared with untreated mouse liver, and a significant decrease in NAD+ levels in the temozolomide-treated group.	NAD	67-71	poly (ADP-ribose) polymerase family, member 1	Mus musculus	20-25
28543772-6	2017	Liver extracts from PARP1 WT mice showed a significant increase in NAD+ levels after rucaparib treatment compared with untreated mouse liver, and a significant decrease in NAD+ levels in the temozolomide-treated group.	NAD	172-176	poly (ADP-ribose) polymerase family, member 1	Mus musculus	20-25
28543772-8	2017	The 1 H-MRS results show that NAD+ levels can be used as a biomarker of PARP inhibitor and methylating agent treatments, and suggest that in vivo measurement of NAD+ would be valuable.	NAD	30-34	poly (ADP-ribose) polymerase family, member 1	Mus musculus	72-76
29137352-6	2017	The mitochondrial dysfunction-associated senescence in pups was accompanied by a drop in NAD+/NADH ratio and alteration in the NAD+-dependent enzymes PARP1 and SIRT1.	NAD	127-131	poly (ADP-ribose) polymerase family, member 1	Mus musculus	150-155
29029387-0	2017	The beta-NAD+ salvage pathway and PKC-mediated signaling influence localized PARP-1 activity and CTCF Poly(ADP)ribosylation.	NAD	4-13	CCCTC-binding factor	Homo sapiens	97-101
29029387-4	2017	These enzymes are downregulated in cells that exhibit reduced CTCF PARylation, resulting in a decreased concentration of nuclear beta-NAD+.	NAD	129-138	CCCTC-binding factor	Homo sapiens	62-66
29029387-9	2017	Our findings suggest that CTCF PARylation is underpinned by a cellular metabolic context engendered by regulation of the beta-NAD+ salvage pathway in which NMNAT-1 acts as a rheostat to control localized beta-NAD+ synthesis at CTCF/PARP-1 complexes.	NAD	121-130	CCCTC-binding factor	Homo sapiens	26-30
29029387-9	2017	Our findings suggest that CTCF PARylation is underpinned by a cellular metabolic context engendered by regulation of the beta-NAD+ salvage pathway in which NMNAT-1 acts as a rheostat to control localized beta-NAD+ synthesis at CTCF/PARP-1 complexes.	NAD	121-130	CCCTC-binding factor	Homo sapiens	227-231
29029387-9	2017	Our findings suggest that CTCF PARylation is underpinned by a cellular metabolic context engendered by regulation of the beta-NAD+ salvage pathway in which NMNAT-1 acts as a rheostat to control localized beta-NAD+ synthesis at CTCF/PARP-1 complexes.	NAD	204-213	CCCTC-binding factor	Homo sapiens	26-30
29029387-9	2017	Our findings suggest that CTCF PARylation is underpinned by a cellular metabolic context engendered by regulation of the beta-NAD+ salvage pathway in which NMNAT-1 acts as a rheostat to control localized beta-NAD+ synthesis at CTCF/PARP-1 complexes.	NAD	204-213	CCCTC-binding factor	Homo sapiens	227-231
28824383-1	2017	Poly (ADP-ribose) polymerases (PARPs) are enzymes that catalyze ADP-ribose units transfer from NAD to their substrate proteins.	NAD	95-98	poly (ADP-ribose) polymerase family, member 1	Mus musculus	31-36
28724806-5	2017	At baseline, the FXN-KO heart has mitochondrial protein hyperacetylation, reduced Sirt3 mRNA expression, and evidence of increased NAD+ salvage.	NAD	131-135	frataxin	Mus musculus	17-20
28724915-7	2017	Activation of QPRT with clofibrate (CLO) or addition of QPRT catabolite NAD both inhibited HCV replication in cells, probably through NAD+-dependent Sirt1 inhibition of cellular lipogenesis.	NAD	72-75	sirtuin 1	Homo sapiens	149-154
28724915-7	2017	Activation of QPRT with clofibrate (CLO) or addition of QPRT catabolite NAD both inhibited HCV replication in cells, probably through NAD+-dependent Sirt1 inhibition of cellular lipogenesis.	NAD	134-138	sirtuin 1	Homo sapiens	149-154
28507103-3	2017	Here, we show the gene encoding nicotinic acid phosphoribosyltransferase (NAPRT), a second NAD+-producing enzyme, is amplified and overexpressed in a subset of common types of cancer, including ovarian cancer, where NAPRT expression correlates with a BRCAness gene expression signature.	NAD	91-95	nicotinate phosphoribosyltransferase	Homo sapiens	32-72
28507103-3	2017	Here, we show the gene encoding nicotinic acid phosphoribosyltransferase (NAPRT), a second NAD+-producing enzyme, is amplified and overexpressed in a subset of common types of cancer, including ovarian cancer, where NAPRT expression correlates with a BRCAness gene expression signature.	NAD	91-95	nicotinate phosphoribosyltransferase	Homo sapiens	74-79
28507103-3	2017	Here, we show the gene encoding nicotinic acid phosphoribosyltransferase (NAPRT), a second NAD+-producing enzyme, is amplified and overexpressed in a subset of common types of cancer, including ovarian cancer, where NAPRT expression correlates with a BRCAness gene expression signature.	NAD	91-95	nicotinate phosphoribosyltransferase	Homo sapiens	216-221
28507103-4	2017	Both NAPRT and NAMPT increased intracellular NAD+ levels.	NAD	45-49	nicotinate phosphoribosyltransferase	Homo sapiens	5-10
28507103-8	2017	In conclusion, NAPRT-dependent NAD+ biosynthesis contributes to cell metabolism and to the DNA repair process in a subset of tumors.	NAD	31-35	nicotinate phosphoribosyltransferase	Homo sapiens	15-20
28597012-5	2017	Our electrochemical measurements have shown that the entrapped ADH exhibits high ability to exchange electrons in the presence of the NAD+/NADH cofactor and that the SWCNT-rGO nanohybrid significantly enhances the biocatalytic activity of the immobilized ADH and the electrochemical oxidation of NADH in comparison with either SWCNTs or rGO.	NAD	134-138	aldo-keto reductase family 1 member A1	Homo sapiens	63-66
28582846-1	2017	BACKGROUND: Members of the SIRT family are a highly conserved family of NAD+-dependent enzymes, many of which (SIRT1-7) play an important role in tumor formation.	NAD	72-76	sirtuin 1	Homo sapiens	111-116
28978059-5	2017	Further, inhibition of 6PGD activity reduced NADH levels and enzymatic activity of the oxidized NADH-dependent sirtuin-1.	NAD	96-100	sirtuin 1	Homo sapiens	111-120
28592850-5	2017	We demonstrated for the first time that the activities and expression of SIRT1 were suppressed by reduction of intracellular NAD+ levels and the p53-microRNA-34a pathway in caerulein-induced AP.	NAD	125-129	sirtuin 1	Homo sapiens	73-78
28915567-6	2017	Melatonin reduced the IL-1beta-increased nicotinamide phosphoribosyltransferase (NAMPT) expression and the NAD+ level in chondrocytes in a Sirt1-dependent manner.	NAD	107-111	sirtuin 1	Homo sapiens	139-144
28537485-0	2017	The NAD+/PARP1/SIRT1 Axis in Aging.	NAD	4-8	poly (ADP-ribose) polymerase family, member 1	Mus musculus	9-14
28537485-4	2017	Decreased NAD+ levels cause NAD+-binding protein DBC1 to form a complex with PARP1, inhibiting poly(adenosine diphosphate-ribose) polymerase (PARP) catalytic activity.	NAD	10-14	poly (ADP-ribose) polymerase family, member 1	Mus musculus	77-82
28537485-4	2017	Decreased NAD+ levels cause NAD+-binding protein DBC1 to form a complex with PARP1, inhibiting poly(adenosine diphosphate-ribose) polymerase (PARP) catalytic activity.	NAD	10-14	poly (ADP-ribose) polymerase family, member 1	Mus musculus	95-140
28537485-4	2017	Decreased NAD+ levels cause NAD+-binding protein DBC1 to form a complex with PARP1, inhibiting poly(adenosine diphosphate-ribose) polymerase (PARP) catalytic activity.	NAD	10-14	poly (ADP-ribose) polymerase family, member 1	Mus musculus	77-81
28537485-4	2017	Decreased NAD+ levels cause NAD+-binding protein DBC1 to form a complex with PARP1, inhibiting poly(adenosine diphosphate-ribose) polymerase (PARP) catalytic activity.	NAD	28-32	poly (ADP-ribose) polymerase family, member 1	Mus musculus	77-82
28537485-4	2017	Decreased NAD+ levels cause NAD+-binding protein DBC1 to form a complex with PARP1, inhibiting poly(adenosine diphosphate-ribose) polymerase (PARP) catalytic activity.	NAD	28-32	poly (ADP-ribose) polymerase family, member 1	Mus musculus	95-140
28537485-4	2017	Decreased NAD+ levels cause NAD+-binding protein DBC1 to form a complex with PARP1, inhibiting poly(adenosine diphosphate-ribose) polymerase (PARP) catalytic activity.	NAD	28-32	poly (ADP-ribose) polymerase family, member 1	Mus musculus	77-81
28620281-9	2017	Silencing GC1 in primary astrocytes resulted in a reduced nicotinamide adenine dinucleotide (Phosphate) (NAD(P)H) formation upon glutamate stimulation.	NAD	58-91	solute carrier family 25 member 22	Rattus norvegicus	10-13
28536482-7	2017	Strikingly, treatment in vivo with the NAD+ repleting agent nicotinamide, a form of vitamin B3, prevented thymus atrophy and hepatosteatosis by dioxin and increased sirtuin activity, providing a therapeutic approach for preventing dioxin toxicities in vivo.	NAD	39-43	sirtuin 3	Gallus gallus	165-172
28490746-4	2017	We found that p62 deficiency is associated with inhibited complex I mitochondrial respiration due to lack of NADH for the electron transport chain.	NAD	109-113	sequestosome 1	Homo sapiens	14-17
28315326-4	2017	In this study, we purified the macrodomain-containing PARP14 enzyme and established an assay for detecting the auto-ribosylation activity of PARP14 using RapidFire high-throughput mass spectrometry and immunoradiometric assay using [3H]NAD+.	NAD	236-240	poly(ADP-ribose) polymerase family member 14	Homo sapiens	54-60
28315326-4	2017	In this study, we purified the macrodomain-containing PARP14 enzyme and established an assay for detecting the auto-ribosylation activity of PARP14 using RapidFire high-throughput mass spectrometry and immunoradiometric assay using [3H]NAD+.	NAD	236-240	poly(ADP-ribose) polymerase family member 14	Homo sapiens	141-147
28315326-6	2017	Co-crystal structures of PARP14 with certain hit compounds revealed that the inhibitors bind to the NAD+-binding site.	NAD	100-104	poly(ADP-ribose) polymerase family member 14	Homo sapiens	25-31
28246678-6	2017	Among the rejection groups, statistically significant differences for CXCL10 levels were found between ACR vs. NAD (p &lt; 0.001), ACR vs. BLR (p = 0.019) and AVR vs. NAD (p = 0.009).	NAD	111-114	C-X-C motif chemokine ligand 10	Homo sapiens	70-76
28443115-2	2017	The recombinant wheat NAD-GAPDH was phosphorylated in vitro at Ser205 by a SNF1-Related protein kinase 1 (SnRK1) from wheat heterotrophic (but not from photosynthetic) tissues.	NAD	22-25	snRK1	Triticum aestivum	75-104
28443115-2	2017	The recombinant wheat NAD-GAPDH was phosphorylated in vitro at Ser205 by a SNF1-Related protein kinase 1 (SnRK1) from wheat heterotrophic (but not from photosynthetic) tissues.	NAD	22-25	snRK1	Triticum aestivum	106-111
28443244-3	2017	Intramitochondrial Ca2+ controls energy metabolism by enhancing the rate of NADH production via modulating critical enzymes in the tricarboxylic acid cycle and fatty acid oxidation.	NAD	76-80	carbonic anhydrase 2	Homo sapiens	19-22
27821631-6	2017	Analysis of global gene expression profiles in nondiseased primary proximal tubule cells from black patients revealed that the nicotinate phosphoribosyltransferase gene, responsible for NAD biosynthesis, was among the top downregulated transcripts in cells with two APOL1 renal-risk variants compared with those without renal-risk variants; nicotinate phosphoribosyltransferase also displayed gene expression patterns linked to mitochondrial dysfunction in HEK293 Tet-on APOL1 cell pathway analyses.	NAD	186-189	nicotinate phosphoribosyltransferase	Homo sapiens	127-163
27821631-6	2017	Analysis of global gene expression profiles in nondiseased primary proximal tubule cells from black patients revealed that the nicotinate phosphoribosyltransferase gene, responsible for NAD biosynthesis, was among the top downregulated transcripts in cells with two APOL1 renal-risk variants compared with those without renal-risk variants; nicotinate phosphoribosyltransferase also displayed gene expression patterns linked to mitochondrial dysfunction in HEK293 Tet-on APOL1 cell pathway analyses.	NAD	186-189	nicotinate phosphoribosyltransferase	Homo sapiens	341-377
28469468-5	2017	TDO is regulated by glucocorticoid induction, substrate activation and stabilization by Trp, cofactor activation by heme, and end-product inhibition by reduced nicotinamide adenine dinucleotide (phosphate).	NAD	160-193	tryptophan 2,3-dioxygenase	Homo sapiens	0-3
28382184-5	2017	Herein, we compare the substrate scope and applicability of different NAD+ analogues for the investigation of the polymer-synthesising enzymes ARTD1, ARTD2, ARTD5 and ARTD6.	NAD	70-74	tankyrase 2	Homo sapiens	167-172
28252007-7	2017	Here we show that the natural activators ARs increased the Vmax of recombinant SIRT1 for NAD+ and peptide substrate, and that ARs decreased acetylated histone in human monocyte cells by stimulating SIRT1-dependent deacetylation of substrates.	NAD	89-93	sirtuin 1	Homo sapiens	79-84
27986658-6	2017	These data reveal that Kvbeta1.1 is required in the mediated inactivation of Kv4.2 currents, when NADH (lactate) levels are increased.	NAD	98-102	potassium voltage-gated channel, Shal-related family, member 2	Mus musculus	77-82
27913299-7	2017	beta-L treatment of RANKL-induced osteoclastogenesis significantly increased the cellular NAD+/NADH ratio and resulted in the activation of 5" AMP-activated protein kinase (AMPK), a negative regulator of osteoclast differentiation.	NAD	90-94	TNF superfamily member 11	Homo sapiens	20-25
27913299-7	2017	beta-L treatment of RANKL-induced osteoclastogenesis significantly increased the cellular NAD+/NADH ratio and resulted in the activation of 5" AMP-activated protein kinase (AMPK), a negative regulator of osteoclast differentiation.	NAD	95-99	TNF superfamily member 11	Homo sapiens	20-25
33133786-5	2017	Replacing AOx with the enzyme alcohol dehydrogenase (ADH), which requires the diffusional nicotinamide adenine dinucleotide cofactor (NAD+/NADH), resulted in only 0.2% BuOH conversion due to NAD+ dimerization at the photoanode.	NAD	90-123	acyl-CoA oxidase 1	Homo sapiens	10-13
33133786-5	2017	Replacing AOx with the enzyme alcohol dehydrogenase (ADH), which requires the diffusional nicotinamide adenine dinucleotide cofactor (NAD+/NADH), resulted in only 0.2% BuOH conversion due to NAD+ dimerization at the photoanode.	NAD	134-138	acyl-CoA oxidase 1	Homo sapiens	10-13
33133786-5	2017	Replacing AOx with the enzyme alcohol dehydrogenase (ADH), which requires the diffusional nicotinamide adenine dinucleotide cofactor (NAD+/NADH), resulted in only 0.2% BuOH conversion due to NAD+ dimerization at the photoanode.	NAD	139-143	acyl-CoA oxidase 1	Homo sapiens	10-13
33133786-5	2017	Replacing AOx with the enzyme alcohol dehydrogenase (ADH), which requires the diffusional nicotinamide adenine dinucleotide cofactor (NAD+/NADH), resulted in only 0.2% BuOH conversion due to NAD+ dimerization at the photoanode.	NAD	191-195	acyl-CoA oxidase 1	Homo sapiens	10-13
27663419-3	2017	METHODS: As poly ADP-ribosylation (PARylation) of proteins by PARPs consumes nicotinamide adenine dinucleotide (NAD+), we hypothesized that overactivation of PARPs drives NAD+ depletion in NAFLD.	NAD	77-110	poly (ADP-ribose) polymerase family, member 1	Mus musculus	62-67
27663419-3	2017	METHODS: As poly ADP-ribosylation (PARylation) of proteins by PARPs consumes nicotinamide adenine dinucleotide (NAD+), we hypothesized that overactivation of PARPs drives NAD+ depletion in NAFLD.	NAD	77-110	poly (ADP-ribose) polymerase family, member 1	Mus musculus	158-163
27663419-3	2017	METHODS: As poly ADP-ribosylation (PARylation) of proteins by PARPs consumes nicotinamide adenine dinucleotide (NAD+), we hypothesized that overactivation of PARPs drives NAD+ depletion in NAFLD.	NAD	112-116	poly (ADP-ribose) polymerase family, member 1	Mus musculus	62-67
27663419-3	2017	METHODS: As poly ADP-ribosylation (PARylation) of proteins by PARPs consumes nicotinamide adenine dinucleotide (NAD+), we hypothesized that overactivation of PARPs drives NAD+ depletion in NAFLD.	NAD	112-116	poly (ADP-ribose) polymerase family, member 1	Mus musculus	158-163
27663419-3	2017	METHODS: As poly ADP-ribosylation (PARylation) of proteins by PARPs consumes nicotinamide adenine dinucleotide (NAD+), we hypothesized that overactivation of PARPs drives NAD+ depletion in NAFLD.	NAD	171-175	poly (ADP-ribose) polymerase family, member 1	Mus musculus	62-67
27663419-3	2017	METHODS: As poly ADP-ribosylation (PARylation) of proteins by PARPs consumes nicotinamide adenine dinucleotide (NAD+), we hypothesized that overactivation of PARPs drives NAD+ depletion in NAFLD.	NAD	171-175	poly (ADP-ribose) polymerase family, member 1	Mus musculus	158-163
27663419-4	2017	Therefore, we assessed the effectiveness of PARP inhibition to replenish NAD+ and activate NAD+-dependent sirtuins, hence improving hepatic fatty acid oxidation.	NAD	73-77	poly (ADP-ribose) polymerase family, member 1	Mus musculus	44-48
27663419-4	2017	Therefore, we assessed the effectiveness of PARP inhibition to replenish NAD+ and activate NAD+-dependent sirtuins, hence improving hepatic fatty acid oxidation.	NAD	91-95	poly (ADP-ribose) polymerase family, member 1	Mus musculus	44-48
28904318-1	2017	SIRT1 is a NAD-dependent histone deacetylase that is important in a wide variety of physiological and pathophysiological processes.	NAD	11-14	sirtuin 1	Homo sapiens	0-5
27422263-2	2017	1.4.1.3) is a mitochondrial enzyme that catalyzes the reversible oxidative deamination of glutamate to alpha-ketoglutarate and ammonia while reducing NAD+ and/or NADP+ to NADH and/or NADPH.	NAD	150-154	2,4-dienoyl-CoA reductase 1	Homo sapiens	183-188
27422263-2	2017	1.4.1.3) is a mitochondrial enzyme that catalyzes the reversible oxidative deamination of glutamate to alpha-ketoglutarate and ammonia while reducing NAD+ and/or NADP+ to NADH and/or NADPH.	NAD	171-175	2,4-dienoyl-CoA reductase 1	Homo sapiens	183-188
28546854-4	2017	The longevity regulator Sirt1 is a NAD+-dependent deacetylase that has a potential antioxidative stress activity in vascular ECs.	NAD	35-38	sirtuin 1	Homo sapiens	24-29
27789183-3	2017	The purpose of this study was to investigate the expression of nicotinamide adenine dinucleotide (NADH) dehydrogenase (ubiquinone) 1 alpha subcomplex, 13 (NDUFA13) in the spermatozoa of men with asthenozoospermia and its possible pathogenesis.	NAD	63-96	NADH:ubiquinone oxidoreductase subunit A13	Homo sapiens	155-162
27789183-3	2017	The purpose of this study was to investigate the expression of nicotinamide adenine dinucleotide (NADH) dehydrogenase (ubiquinone) 1 alpha subcomplex, 13 (NDUFA13) in the spermatozoa of men with asthenozoospermia and its possible pathogenesis.	NAD	98-102	NADH:ubiquinone oxidoreductase subunit A13	Homo sapiens	155-162
27793057-2	2016	HIC1 is a transcriptional repressor that directly binds to the promoter region of NAD-dependent deacetylase sirtuin-1 (SIRT1).	NAD	82-85	sirtuin 1	Homo sapiens	119-124
27998274-10	2016	Furthermore, Peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1alpha), a regulator of mitochondrial biogenesis and function was repressed, and lower expression levels of NAD-dependent deacetylase sirtuin1 (SIRT1) were found in AMD RPE-iPSC-RPE and AMD Skin-iPSC-RPE as compared to normal RPE-iPSC-RPE.	NAD	195-198	sirtuin 1	Homo sapiens	221-229
27998274-10	2016	Furthermore, Peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1alpha), a regulator of mitochondrial biogenesis and function was repressed, and lower expression levels of NAD-dependent deacetylase sirtuin1 (SIRT1) were found in AMD RPE-iPSC-RPE and AMD Skin-iPSC-RPE as compared to normal RPE-iPSC-RPE.	NAD	195-198	sirtuin 1	Homo sapiens	231-236
27818101-0	2016	Defining NADH-Driven Allostery Regulating Apoptosis-Inducing Factor.	NAD	9-13	apoptosis inducing factor mitochondria associated 1	Homo sapiens	42-67
27818101-1	2016	Apoptosis-inducing factor (AIF) is critical for mitochondrial respiratory complex biogenesis and for mediating necroptotic parthanatos; these functions are seemingly regulated by enigmatic allosteric switching driven by NADH charge-transfer complex (CTC) formation.	NAD	220-224	apoptosis inducing factor mitochondria associated 1	Homo sapiens	0-25
27818101-1	2016	Apoptosis-inducing factor (AIF) is critical for mitochondrial respiratory complex biogenesis and for mediating necroptotic parthanatos; these functions are seemingly regulated by enigmatic allosteric switching driven by NADH charge-transfer complex (CTC) formation.	NAD	220-224	apoptosis inducing factor mitochondria associated 1	Homo sapiens	27-30
27756843-0	2016	Mechanism of Sirt1 NAD+-dependent Protein Deacetylase Inhibition by Cysteine S-Nitrosation.	NAD	19-23	sirtuin 1	Homo sapiens	13-18
27791113-3	2016	Fluctuations in intracellular NAD+ levels regulate SIRT1 activity, but how SIRT1 enzymatic activity impacts on NAD+ levels and its intracellular distribution remains unclear.	NAD	111-115	sirtuin 1	Homo sapiens	75-80
27791113-4	2016	Here, we show that SIRT1 determines the nuclear organization of protein-bound NADH.	NAD	78-82	sirtuin 1	Homo sapiens	19-24
27791113-5	2016	Using multiphoton microscopy in live cells, we show that free and bound NADH are compartmentalized inside of the nucleus, and its subnuclear distribution depends on SIRT1.	NAD	72-76	sirtuin 1	Homo sapiens	165-170
27791113-7	2016	In addition, using fluorescence fluctuation spectroscopy in single living cells, we reveal that NAD+ metabolism in the nucleus is linked to subnuclear dynamics of active SIRT1.	NAD	96-100	sirtuin 1	Homo sapiens	170-175
27791113-8	2016	These results reveal a connection between NAD+ metabolism, NADH distribution, and SIRT1 activity in the nucleus of live cells and pave the way to decipher links between nuclear organization and metabolism.	NAD	42-46	sirtuin 1	Homo sapiens	82-87
27819261-4	2016	In this study, we provide evidence that the NAD+-dependent class III protein deacetylase SIRT1 deacetylates Nkx2.5 in cardiomyocytes and represses the transcriptional activity of Nkx2.5.	NAD	44-48	sirtuin 1	Homo sapiens	89-94
27552971-1	2016	The sirtuins (SIRT1-7) are a family of nicotinamide adenine dinucleotide (NAD+)-dependent deacylases with remarkable abilities to prevent diseases and even reverse aspects of ageing.	NAD	39-72	sirtuin 1	Homo sapiens	14-21
27552971-1	2016	The sirtuins (SIRT1-7) are a family of nicotinamide adenine dinucleotide (NAD+)-dependent deacylases with remarkable abilities to prevent diseases and even reverse aspects of ageing.	NAD	74-77	sirtuin 1	Homo sapiens	14-21
27595158-5	2016	Using phenol as a substrate and NADH as reducing agent, which showed negligible background due to low electroactivity of phenol and high oxidation overpotential of NADH, the oxygenation activity of tyrosinase could convert poorly electroactive phenol to highly electroactive catechol to trigger an NADH-related nonenzymatic electrochemical-chemical (EC) catalysis.	NAD	32-36	tyrosinase	Homo sapiens	198-208
27595158-5	2016	Using phenol as a substrate and NADH as reducing agent, which showed negligible background due to low electroactivity of phenol and high oxidation overpotential of NADH, the oxygenation activity of tyrosinase could convert poorly electroactive phenol to highly electroactive catechol to trigger an NADH-related nonenzymatic electrochemical-chemical (EC) catalysis.	NAD	164-168	tyrosinase	Homo sapiens	198-208
27595158-5	2016	Using phenol as a substrate and NADH as reducing agent, which showed negligible background due to low electroactivity of phenol and high oxidation overpotential of NADH, the oxygenation activity of tyrosinase could convert poorly electroactive phenol to highly electroactive catechol to trigger an NADH-related nonenzymatic electrochemical-chemical (EC) catalysis.	NAD	164-168	tyrosinase	Homo sapiens	198-208
28164517-1	2016	BACKGROUND: SIRT1 is the homologue of sir2 in mammals, which is a nicotinamide adenine dinucleotide (NAD+) dependent histone deacetylase.	NAD	66-99	sirtuin 1	Homo sapiens	12-17
28164517-1	2016	BACKGROUND: SIRT1 is the homologue of sir2 in mammals, which is a nicotinamide adenine dinucleotide (NAD+) dependent histone deacetylase.	NAD	66-99	sirtuin 1	Homo sapiens	38-42
28164517-1	2016	BACKGROUND: SIRT1 is the homologue of sir2 in mammals, which is a nicotinamide adenine dinucleotide (NAD+) dependent histone deacetylase.	NAD	101-105	sirtuin 1	Homo sapiens	12-17
28164517-1	2016	BACKGROUND: SIRT1 is the homologue of sir2 in mammals, which is a nicotinamide adenine dinucleotide (NAD+) dependent histone deacetylase.	NAD	101-105	sirtuin 1	Homo sapiens	38-42
27542221-8	2016	In addition, we demonstrate that NAD-dependent histone deacetylase SIRT1 physically binds to and deacetylates FOXM1 in vivo.	NAD	33-36	sirtuin 1	Homo sapiens	67-72
27542221-8	2016	In addition, we demonstrate that NAD-dependent histone deacetylase SIRT1 physically binds to and deacetylates FOXM1 in vivo.	NAD	33-36	forkhead box M1	Homo sapiens	110-115
26804254-8	2016	RONS may activate LKB1 through Sestrin2 and SIRT1 (NAD(+)/NADH.H(+)-dependent deacetylase).	NAD	51-57	sirtuin 1	Homo sapiens	44-49
26804254-8	2016	RONS may activate LKB1 through Sestrin2 and SIRT1 (NAD(+)/NADH.H(+)-dependent deacetylase).	NAD	58-62	sirtuin 1	Homo sapiens	44-49
26359921-5	2016	Cyt b gene is terminated with AGA as stop codon, ND1 and ND2 genes are terminated with TAG as stop codon, COII, COIII, ND3, and ND4 end with T, while ATP6, ATP8, COI, ND4L, ND5, and ND6 end with TAA.	NAD	106-109	cytochrome b	Sus scrofa	0-5
28725474-6	2016	The mammalian NAD+-dependent protein deacetylase SIRT1 and the key NAD+ biosynthetic enzyme NAMPT mediate these inter-tissue communications.	NAD	14-18	sirtuin 1	Homo sapiens	49-54
28725474-6	2016	The mammalian NAD+-dependent protein deacetylase SIRT1 and the key NAD+ biosynthetic enzyme NAMPT mediate these inter-tissue communications.	NAD	67-71	sirtuin 1	Homo sapiens	49-54
27404282-10	2016	They suggest that NADH-dependent CBR can replace NADPH-dependent POR in the P450 1A1-catalyzed metabolism of BaP.	NAD	18-22	carbonyl reductase 1	Homo sapiens	33-36
27567805-3	2016	PARP-1 catalyzes the poly(ADP-ribosylation), a post-translational modification of proteins, cleaving the substrate NAD+ and transferring the ADP-ribose moieties to the enzyme itself or to an acceptor protein to form branched polymers of ADP-ribose.	NAD	115-119	poly (ADP-ribose) polymerase family, member 1	Mus musculus	0-6
27163581-5	2016	The NAD(+)-binding site contains a hydrophobic cavity which accommodates the 2-aryl group; in TNKS-2, this has a tunnel to the exterior but the cavity is closed in PARP-1.	NAD	4-10	tankyrase 2	Homo sapiens	94-100
27608947-1	2016	Nicotinamide phosphoribosyltransferase (NAMPT) catalyzes the first rate-limiting step in converting nicotinamide to NAD(+), essential for a number of enzymes and regulatory proteins involved in a variety of cellular processes, including deacetylation enzyme SIRT1 which modulates several tumor suppressors such as p53 and FOXO.	NAD	116-122	sirtuin 1	Homo sapiens	258-263
26928132-6	2016	Incubation of purified Ogdh in 2.5mM GSH led to significant increase in O2( -)/H2O2 formation which also lowered NADH production.	NAD	113-117	oxoglutarate (alpha-ketoglutarate) dehydrogenase (lipoamide)	Mus musculus	23-27
26928132-8	2016	Similarly pre-incubation of permeabilized liver mitochondria from mouse depleted of GSH showed an approximately ~3.5-fold increase in Ogdh-mediated O2( -)/H2O2 production that was matched by a significant decrease in NADH formation which could be reversed by Grx2.	NAD	217-221	oxoglutarate (alpha-ketoglutarate) dehydrogenase (lipoamide)	Mus musculus	134-138
27499729-3	2016	As these beta-NAD(+) metabolites activate warm-sensitive TRPM2 cation channels, when the incubation temperature is increased, the [Ca(2+)]i in hypothalamic neurons is elevated.	NAD	9-20	transient receptor potential cation channel, subfamily M, member 2	Mus musculus	57-62
27264719-0	2016	SIRT2 mediates NADH-induced increases in Nrf2, GCL, and glutathione by modulating Akt phosphorylation in PC12 cells.	NAD	15-19	sirtuin 2	Rattus norvegicus	0-5
27264719-3	2016	By studying NADH-treated differentiated PC12 cells, we found that NADH induced a significant increase in the nuclear Nrf2, which was prevented by both SIRT2 siRNA and SIRT2 inhibitor, AGK2.	NAD	12-16	sirtuin 2	Rattus norvegicus	151-156
27264719-3	2016	By studying NADH-treated differentiated PC12 cells, we found that NADH induced a significant increase in the nuclear Nrf2, which was prevented by both SIRT2 siRNA and SIRT2 inhibitor, AGK2.	NAD	12-16	sirtuin 2	Rattus norvegicus	167-172
27264719-3	2016	By studying NADH-treated differentiated PC12 cells, we found that NADH induced a significant increase in the nuclear Nrf2, which was prevented by both SIRT2 siRNA and SIRT2 inhibitor, AGK2.	NAD	66-70	sirtuin 2	Rattus norvegicus	151-156
27264719-3	2016	By studying NADH-treated differentiated PC12 cells, we found that NADH induced a significant increase in the nuclear Nrf2, which was prevented by both SIRT2 siRNA and SIRT2 inhibitor, AGK2.	NAD	66-70	sirtuin 2	Rattus norvegicus	167-172
27264719-4	2016	SIRT2 siRNA also blocked the NADH-induced increases in glutamate cysteine ligase (GCL) and glutathione.	NAD	29-33	sirtuin 2	Rattus norvegicus	0-5
27264719-5	2016	Moreover, SIRT2 siRNA and AGK2 blocked NADH-induced Akt phosphorylation, and inhibition of Akt phosphorylation prevented NADH-induced increases in the nuclear Nrf2 and glutathione.	NAD	39-43	sirtuin 2	Rattus norvegicus	10-15
27181414-1	2016	Recent research in nutritional control of aging suggests that cytosolic increases in the reduced form of nicotinamide adenine dinucleotide and decreasing nicotinamide adenine dinucleotide metabolism plays a central role in controlling the longevity gene products sirtuin 1 (SIRT1), adenosine monophosphate-activated protein kinase (AMPK) and forkhead box O3 (FOXO3).	NAD	105-138	sirtuin 1	Homo sapiens	263-272
27181414-1	2016	Recent research in nutritional control of aging suggests that cytosolic increases in the reduced form of nicotinamide adenine dinucleotide and decreasing nicotinamide adenine dinucleotide metabolism plays a central role in controlling the longevity gene products sirtuin 1 (SIRT1), adenosine monophosphate-activated protein kinase (AMPK) and forkhead box O3 (FOXO3).	NAD	105-138	sirtuin 1	Homo sapiens	274-279
27181414-1	2016	Recent research in nutritional control of aging suggests that cytosolic increases in the reduced form of nicotinamide adenine dinucleotide and decreasing nicotinamide adenine dinucleotide metabolism plays a central role in controlling the longevity gene products sirtuin 1 (SIRT1), adenosine monophosphate-activated protein kinase (AMPK) and forkhead box O3 (FOXO3).	NAD	154-187	sirtuin 1	Homo sapiens	263-272
27181414-1	2016	Recent research in nutritional control of aging suggests that cytosolic increases in the reduced form of nicotinamide adenine dinucleotide and decreasing nicotinamide adenine dinucleotide metabolism plays a central role in controlling the longevity gene products sirtuin 1 (SIRT1), adenosine monophosphate-activated protein kinase (AMPK) and forkhead box O3 (FOXO3).	NAD	154-187	sirtuin 1	Homo sapiens	274-279
27181414-4	2016	My research and others" suggest that the SIRT1-liver kinase B1-AMPK cascade creates positive feedback through nicotinamide adenine dinucleotide synthesis to help cells cope with metabolic stress.	NAD	110-143	sirtuin 1	Homo sapiens	41-46
27081083-1	2016	SIRT1 is a multifaceted NAD+-dependent protein deacetylase known to act as a tumor promoter or suppressor in different cancers.	NAD	24-28	sirtuin 1	Homo sapiens	0-5
26926998-6	2016	maculicola ES4326, and transgenic expression of the coding region of ELO3/AtELP3 in elo3/Atelp3 restores NAD(+) responsiveness to the mutant plants, demonstrating that ELO3/AtELP3 is required for exogenous NAD(+)-induced defense responses.	NAD	206-212	radical SAM domain-containing protein / GCN5-related N-acetyltransferase (GNAT) family protein	Arabidopsis thaliana	84-88
26986234-1	2016	Several members of the sirtuin family (SIRT1-7), which are a highly conserved family of NAD+-dependent enzymes, play an important role in tumor formation.	NAD	88-92	sirtuin 1	Homo sapiens	39-44
26912654-1	2016	Poly(ADP-ribose) polymerases (PARPs) synthesize and bind branched polymers of ADP-ribose to acceptor proteins using NAD as a substrate and participate in the control of gene transcription and DNA repair.	NAD	116-119	poly (ADP-ribose) polymerase family, member 1	Mus musculus	30-35
27098689-1	2016	UNLABELLED: ARALAR/AGC1/Slc25a12, the aspartate-glutamate carrier from brain mitochondria, is the regulatory step in the malate-aspartate NADH shuttle, MAS.	NAD	138-142	solute carrier family 25 (mitochondrial carrier, Aralar), member 12	Mus musculus	24-32
26896648-10	2016	Alcohol dehydrogenase is present in every visceral organ in the body so that there is a systemic reduction of NAD(+) levels in all of these organs during binge drinking.	NAD	110-116	aldo-keto reductase family 1 member A1	Homo sapiens	0-21
26943589-4	2016	The metabolic facet of BRCA1 one-hit might involve tissue-specific alterations in acetyl-CoA, alpha-ketoglutarate, NAD+, FAD, or S-adenosylmethionine, critical factors for de/methylation or de/acetylation dynamics in the nuclear epigenome.	NAD	115-119	BRCA1 DNA repair associated	Homo sapiens	23-28
26882000-0	2016	Correction to The 2.5 A Crystal Structure of the SIRT1 Catalytic Domain Bound to Nicotinamide Adenine Dinucleotide (NAD(+)) and an Indole (EX527 Analogue) Reveals a Novel Mechanism of Histone Deacetylase Inhibition.	NAD	81-114	sirtuin 1	Homo sapiens	49-54
26882000-0	2016	Correction to The 2.5 A Crystal Structure of the SIRT1 Catalytic Domain Bound to Nicotinamide Adenine Dinucleotide (NAD(+)) and an Indole (EX527 Analogue) Reveals a Novel Mechanism of Histone Deacetylase Inhibition.	NAD	116-122	sirtuin 1	Homo sapiens	49-54
26341473-5	2016	Here, we demonstrate that the levels and activities of sirtuin-1 (SIRT1) are suppressed by the reduction of intracellular NAD(+) levels in cisplatin-mediated ototoxicity.	NAD	122-128	sirtuin 1	Homo sapiens	55-64
26341473-5	2016	Here, we demonstrate that the levels and activities of sirtuin-1 (SIRT1) are suppressed by the reduction of intracellular NAD(+) levels in cisplatin-mediated ototoxicity.	NAD	122-128	sirtuin 1	Homo sapiens	66-71
26341473-7	2016	Furthermore, we show that the induction of cellular NAD(+) levels using dunnione, which targets intracellular NQO1, prevents the toxic effects of cisplatin through the regulation of PARP-1 and SIRT1 activity.	NAD	52-58	sirtuin 1	Homo sapiens	193-198
26899247-4	2016	At later time points, Akt delivered the NAD(+)-dependent protein deacetylase Sirtuin 2 (Sirt 2) to the vicinity of phosphorylated H2A in response to irreversible DNA damage, thereby inducing H2A deacetylation and subsequently leading to apoptotic death.	NAD	40-46	sirtuin 2	Rattus norvegicus	77-86
26899247-4	2016	At later time points, Akt delivered the NAD(+)-dependent protein deacetylase Sirtuin 2 (Sirt 2) to the vicinity of phosphorylated H2A in response to irreversible DNA damage, thereby inducing H2A deacetylation and subsequently leading to apoptotic death.	NAD	40-46	sirtuin 2	Rattus norvegicus	88-94
26344168-4	2016	In this context, Sirtuin 1 (SIRT1), a NAD+-dependent deacetylase enzyme, has been proposed to act as a key mediator of the adaptations to nutrient deprivation in eukaryotes, and SIRT1 activating compounds have been often referred to as "dietary restriction mimetic" molecules.	NAD	38-41	sirtuin 1	Homo sapiens	17-26
26344168-4	2016	In this context, Sirtuin 1 (SIRT1), a NAD+-dependent deacetylase enzyme, has been proposed to act as a key mediator of the adaptations to nutrient deprivation in eukaryotes, and SIRT1 activating compounds have been often referred to as "dietary restriction mimetic" molecules.	NAD	38-41	sirtuin 1	Homo sapiens	28-33
26344168-4	2016	In this context, Sirtuin 1 (SIRT1), a NAD+-dependent deacetylase enzyme, has been proposed to act as a key mediator of the adaptations to nutrient deprivation in eukaryotes, and SIRT1 activating compounds have been often referred to as "dietary restriction mimetic" molecules.	NAD	38-41	sirtuin 1	Homo sapiens	178-183
26655722-3	2016	The NAD(+)-dependent protein deacetylase sirtuin 1 (SIRT1), a key regulator of mammalian metabolism, maintains proper metabolic functions in many tissues, counteracting obesity.	NAD	4-10	sirtuin 1	Homo sapiens	41-50
26655722-3	2016	The NAD(+)-dependent protein deacetylase sirtuin 1 (SIRT1), a key regulator of mammalian metabolism, maintains proper metabolic functions in many tissues, counteracting obesity.	NAD	4-10	sirtuin 1	Homo sapiens	52-57
26675378-2	2016	As cancer cells have increased NAD requirements, the main NAD salvage enzymes in humans, nicotinamide phosphoribosyltransferase (NAMPT) and nicotinate phosphoribosyltransferase (NAPRT), are involved in the development of novel anti-cancer therapies.	NAD	31-34	nicotinate phosphoribosyltransferase	Homo sapiens	140-176
26675378-2	2016	As cancer cells have increased NAD requirements, the main NAD salvage enzymes in humans, nicotinamide phosphoribosyltransferase (NAMPT) and nicotinate phosphoribosyltransferase (NAPRT), are involved in the development of novel anti-cancer therapies.	NAD	31-34	nicotinate phosphoribosyltransferase	Homo sapiens	178-183
26675378-2	2016	As cancer cells have increased NAD requirements, the main NAD salvage enzymes in humans, nicotinamide phosphoribosyltransferase (NAMPT) and nicotinate phosphoribosyltransferase (NAPRT), are involved in the development of novel anti-cancer therapies.	NAD	58-61	nicotinate phosphoribosyltransferase	Homo sapiens	140-176
26675378-2	2016	As cancer cells have increased NAD requirements, the main NAD salvage enzymes in humans, nicotinamide phosphoribosyltransferase (NAMPT) and nicotinate phosphoribosyltransferase (NAPRT), are involved in the development of novel anti-cancer therapies.	NAD	58-61	nicotinate phosphoribosyltransferase	Homo sapiens	178-183
26507856-1	2016	NBDB database describes protein motifs, elementary functional loops (EFLs) that are involved in binding of nucleotide-containing ligands and other biologically relevant cofactors/coenzymes, including ATP, AMP, ATP, GMP, GDP, GTP, CTP, PAP, PPS, FMN, FAD(H), NAD(H), NADP, cAMP, cGMP, c-di-AMP and c-di-GMP, ThPP, THD, F-420, ACO, CoA, PLP and SAM.	NAD	258-264	proteolipid protein 1	Homo sapiens	335-338
25185954-4	2016	ATP6, ATP8, COI, COII, COIII, Cyt b, ND1, ND2, ND3, ND4L and ND5 genes are terminated with TAA as stop codon, ND6 ends with TAG, and ND4 ends with T.	NAD	12-15	ND6	Argiope amoena	110-113
27547294-4	2016	Here, we showed that the hearts of CD38 deficient mice or wild type mice supplied with exogenous NAD were significantly protected from ischemia/reperfusion injury, seen as reduction of the myocardial infarct sizes when the mice were subjected to 30 min ischemia followed by 24 hours of reperfusion.	NAD	97-100	CD38 antigen	Mus musculus	35-39
26112889-1	2015	Sirtuins (Sirt1-Sirt7) comprise a family of nicotinamide adenine dinucleotide (NAD(+))-dependent enzymes.	NAD	44-77	sirtuin 1	Homo sapiens	10-15
26112889-1	2015	Sirtuins (Sirt1-Sirt7) comprise a family of nicotinamide adenine dinucleotide (NAD(+))-dependent enzymes.	NAD	44-77	sirtuin 7	Homo sapiens	16-21
26112889-1	2015	Sirtuins (Sirt1-Sirt7) comprise a family of nicotinamide adenine dinucleotide (NAD(+))-dependent enzymes.	NAD	79-85	sirtuin 1	Homo sapiens	10-15
26112889-1	2015	Sirtuins (Sirt1-Sirt7) comprise a family of nicotinamide adenine dinucleotide (NAD(+))-dependent enzymes.	NAD	79-85	sirtuin 7	Homo sapiens	16-21
26112889-12	2015	Given the availability of specific Sirt1 activators or pan-sirtuin activators that boost levels of the sirtuin cofactor NAD+, we anticipate that this field will move quickly from bench to bedside.	NAD	120-124	sirtuin 1	Homo sapiens	35-40
26265307-2	2015	D-Lactate dehydrogenase (D-LDH) was utilized to catalyze D-lactate and NAD(+) to pyruvate and NADH, respectively.	NAD	71-77	lactate dehydrogenase D	Homo sapiens	0-23
26265307-2	2015	D-Lactate dehydrogenase (D-LDH) was utilized to catalyze D-lactate and NAD(+) to pyruvate and NADH, respectively.	NAD	71-77	lactate dehydrogenase D	Homo sapiens	25-30
26330291-0	2015	A Nampt inhibitor FK866 mimics vitamin B3 deficiency by causing senescence of human fibroblastic Hs68 cells via attenuation of NAD(+)-SIRT1 signaling.	NAD	127-133	sirtuin 1	Homo sapiens	134-139
26330291-6	2015	We hypothesized that FK866 induced the senescence of Hs68 cells via an attenuation of NAD(+)-silent information regulator T1 (SIRT1) signaling.	NAD	86-92	sirtuin 1	Homo sapiens	126-131
26330291-10	2015	These results suggest that FK866 induces cell senescence via attenuation of NAD(+)-SIRT1 signaling.	NAD	76-82	sirtuin 1	Homo sapiens	83-88
26535916-0	2015	Key Role of the Adenylate Moiety and Integrity of the Adenylate-Binding Site for the NAD(+)/H Binding to Mitochondrial Apoptosis-Inducing Factor.	NAD	85-91	apoptosis inducing factor mitochondria associated 1	Homo sapiens	119-144
26535916-4	2015	A unique feature of AIF is the ability to form a tight, air-stable charge-transfer (CT) complex upon reaction with NADH and to undergo a conformational switch leading to dimerization, proposed to be important for its vital and lethal functions.	NAD	115-119	apoptosis inducing factor mitochondria associated 1	Homo sapiens	20-23
26535916-5	2015	Although some aspects of interaction of AIF with NAD(+)/H have been analyzed, its precise mechanism is not fully understood.	NAD	49-55	apoptosis inducing factor mitochondria associated 1	Homo sapiens	40-43
26535916-6	2015	We investigated how the oxidized and photoreduced wild-type and G307A and -E variants of murine AIF associate with NAD(+)/H and nicotinamide mononucleotide (NMN(+)/H) to determine the role of the adenylate moiety in the binding process.	NAD	115-121	apoptosis-inducing factor, mitochondrion-associated 1	Mus musculus	96-99
26620281-7	2015	Deacetylation of GKRP is effected by the NAD(+)-dependent, class III histone deacetylase SIRT2, which is inhibited by nicotinamide.	NAD	41-47	glucokinase regulatory protein	Mus musculus	17-21
26401995-1	2015	The brain aspartate-glutamate carrier (AGC1) is specifically expressed in neurons, where it transports aspartate from the mitochondria to the cytosol, and plays a role in transfer of nicotinamide adenine dinucleotide (NADH)-reducing equivalents into the mitochondria as a part of the malate-aspartate shuttle.	NAD	183-216	aggrecan	Homo sapiens	39-43
26401995-1	2015	The brain aspartate-glutamate carrier (AGC1) is specifically expressed in neurons, where it transports aspartate from the mitochondria to the cytosol, and plays a role in transfer of nicotinamide adenine dinucleotide (NADH)-reducing equivalents into the mitochondria as a part of the malate-aspartate shuttle.	NAD	218-222	aggrecan	Homo sapiens	39-43
25850461-2	2015	Along with a role in bioenergetics, NAMPT regulates the activity of proteins such as SIRT-1 that utilize NAD as a cofactor.	NAD	105-108	sirtuin 1	Homo sapiens	85-91
26089537-4	2015	The contribution of the ADO-generating ectoenzymes in the regulatory response was shown by: 1) selective inhibition of the enzymatic activities of CD39, CD73, and CD38; 2) the ability of suppressor T cells to convert exogenously added ATP and NAD(+) to ADO; and 3) a positive correlation between ectoenzyme expression, ADO levels, and suppression abilities.	NAD	243-249	ectonucleoside triphosphate diphosphohydrolase 1	Mus musculus	147-151
26089537-4	2015	The contribution of the ADO-generating ectoenzymes in the regulatory response was shown by: 1) selective inhibition of the enzymatic activities of CD39, CD73, and CD38; 2) the ability of suppressor T cells to convert exogenously added ATP and NAD(+) to ADO; and 3) a positive correlation between ectoenzyme expression, ADO levels, and suppression abilities.	NAD	243-249	CD38 antigen	Mus musculus	163-167
26405459-4	2015	RESULTS: In this study, we demonstrate that PLZF is deacetylated by both histone deacetylase 3 and the NAD+ dependent deacetylase silent mating type information regulation 2 homolog 1 (SIRT1).	NAD	103-106	zinc finger and BTB domain containing 16	Homo sapiens	44-48
26405459-4	2015	RESULTS: In this study, we demonstrate that PLZF is deacetylated by both histone deacetylase 3 and the NAD+ dependent deacetylase silent mating type information regulation 2 homolog 1 (SIRT1).	NAD	103-106	sirtuin 1	Homo sapiens	185-190
26211444-8	2015	Also, reduction of NAD-dependent deacetylase sirtuin-3 (SIRT-3)/proline hydroxylase-2 (PHD-2) signaling pathway was evaluated.	NAD	19-22	egl-9 family hypoxia-inducible factor 1	Rattus norvegicus	87-92
26292147-4	2015	We further integrate the nanoplasmonic response of catalytic growth of Au NPs with NADH-mediated reduction of 1,3,5-trinitro-1,3,5-triazinane (RDX) for the quantitative analysis of RDX explosive residues in latent fingerprints.	NAD	83-87	radixin	Homo sapiens	143-146
26292147-4	2015	We further integrate the nanoplasmonic response of catalytic growth of Au NPs with NADH-mediated reduction of 1,3,5-trinitro-1,3,5-triazinane (RDX) for the quantitative analysis of RDX explosive residues in latent fingerprints.	NAD	83-87	radixin	Homo sapiens	181-184
26267483-3	2015	Two of these CD38 inhibitors, 1ah and 1ai, were shown to elevate NAD tissue levels in liver and muscle in a diet-induced obese (DIO) C57BL/6 mouse model.	NAD	65-68	CD38 antigen	Mus musculus	13-17
26275361-1	2015	Sirtuin (Sirt) 1 and Sirt 3 are nicotinamide adenine dinucleotide ((+))-dependent protein deacetylases that are important to a number of mitochondrial-related functions; thus, identification of sirtuin activators is important.	NAD	32-65	sirtuin 1	Homo sapiens	0-16
26152715-0	2015	Metformin Inhibits the Production of Reactive Oxygen Species from NADH:Ubiquinone Oxidoreductase to Limit Induction of Interleukin-1beta (IL-1beta) and Boosts Interleukin-10 (IL-10) in Lipopolysaccharide (LPS)-activated Macrophages.	NAD	66-70	interleukin 10	Homo sapiens	159-173
26152715-0	2015	Metformin Inhibits the Production of Reactive Oxygen Species from NADH:Ubiquinone Oxidoreductase to Limit Induction of Interleukin-1beta (IL-1beta) and Boosts Interleukin-10 (IL-10) in Lipopolysaccharide (LPS)-activated Macrophages.	NAD	66-70	interleukin 10	Homo sapiens	175-180
26284089-4	2015	The terminal step of both pathways, the conversion of delta(1)-pyrroline-5-carboxylate (P5C) to L-proline, is catalyzed by P5C reductase (P5CR) using NADH or NADPH as a cofactor.	NAD	150-154	pyrroline-5-carboxylate reductase 1	Homo sapiens	54-86
26284089-4	2015	The terminal step of both pathways, the conversion of delta(1)-pyrroline-5-carboxylate (P5C) to L-proline, is catalyzed by P5C reductase (P5CR) using NADH or NADPH as a cofactor.	NAD	150-154	pyrroline-5-carboxylate reductase 1	Homo sapiens	88-91
26284089-4	2015	The terminal step of both pathways, the conversion of delta(1)-pyrroline-5-carboxylate (P5C) to L-proline, is catalyzed by P5C reductase (P5CR) using NADH or NADPH as a cofactor.	NAD	150-154	pyrroline-5-carboxylate reductase 1	Homo sapiens	123-136
26284089-4	2015	The terminal step of both pathways, the conversion of delta(1)-pyrroline-5-carboxylate (P5C) to L-proline, is catalyzed by P5C reductase (P5CR) using NADH or NADPH as a cofactor.	NAD	150-154	pyrroline-5-carboxylate reductase 1	Homo sapiens	138-142
26218895-2	2015	Activation of PARP-1 in response to oxidative stress catalyzes the covalent attachment of the poly (ADP-ribose) (PAR) groups on itself and other acceptor proteins, utilizing NAD+ as a substrate.	NAD	174-178	poly (ADP-ribose) polymerase family, member 1	Mus musculus	14-20
26218895-3	2015	Overactivation of PARP-1 depletes intracellular NAD+ influencing mitochondrial electron transport, cellular ATP generation and, if persistent, can result in necrotic cell death.	NAD	48-52	poly (ADP-ribose) polymerase family, member 1	Mus musculus	18-24
26134520-1	2015	SIRT1, the founding member of the mammalian family of seven NAD(+)-dependent sirtuins, is composed of 747 amino acids forming a catalytic domain and extended N- and C-terminal regions.	NAD	60-66	sirtuin 1	Homo sapiens	0-5
25709099-3	2015	Alternatively, cells can convert NA to NAD through the NAPRT1-dependent salvage pathway.	NAD	39-42	nicotinate phosphoribosyltransferase	Homo sapiens	55-61
26098102-3	2015	The deletion of erg5 led to redox imbalance with higher ratio of cytosolic free NADH/NAD+ and more glycerol and ethanol accumulation.	NAD	80-84	C-22 sterol desaturase	Saccharomyces cerevisiae S288C	16-20
26098102-3	2015	The deletion of erg5 led to redox imbalance with higher ratio of cytosolic free NADH/NAD+ and more glycerol and ethanol accumulation.	NAD	85-89	C-22 sterol desaturase	Saccharomyces cerevisiae S288C	16-20
25839883-1	2015	Class I sirtuin genes including SIRT1, SIRT2 and SIRT3, are members of the nicotinamide adenine dinucleotide (NAD)-dependent family of histone deacetylases, and play essential roles in senescence, metabolism, and apoptosis.	NAD	75-108	sirtuin 1	Bos taurus	32-37
25839883-1	2015	Class I sirtuin genes including SIRT1, SIRT2 and SIRT3, are members of the nicotinamide adenine dinucleotide (NAD)-dependent family of histone deacetylases, and play essential roles in senescence, metabolism, and apoptosis.	NAD	110-113	sirtuin 1	Bos taurus	32-37
26020938-5	2015	The proposed model involves two DNA damage response proteins, SIRT1 and PARP1, that are each consumers of nicotinamide adenine dinucleotide (NAD), a metabolite involved in oxidation-reduction reactions and in ATP synthesis.	NAD	106-139	sirtuin 1	Homo sapiens	62-67
26020938-5	2015	The proposed model involves two DNA damage response proteins, SIRT1 and PARP1, that are each consumers of nicotinamide adenine dinucleotide (NAD), a metabolite involved in oxidation-reduction reactions and in ATP synthesis.	NAD	141-144	sirtuin 1	Homo sapiens	62-67
26020938-6	2015	This model builds on two key findings: 1) that SIRT1 (a protein deacetylase) is involved in both the positive (i.e. transcriptional activation) and negative (i.e. transcriptional repression) arms of the circadian regulation and 2) that PARP1 is a major consumer of NAD during the DNA damage response.	NAD	265-268	sirtuin 1	Homo sapiens	47-52
26020938-7	2015	In our simulations, we observe that increased PARP1 activity may be able to trigger SIRT1-induced circadian phase advancements by decreasing SIRT1 activity through competition for NAD supplies.	NAD	180-183	sirtuin 1	Homo sapiens	84-89
26020938-7	2015	In our simulations, we observe that increased PARP1 activity may be able to trigger SIRT1-induced circadian phase advancements by decreasing SIRT1 activity through competition for NAD supplies.	NAD	180-183	sirtuin 1	Homo sapiens	141-146
25934505-8	2015	The increase in spermidine was accompanied by reduced levels of nicotinamide N-methyltransferase, which promotes polyamine synthesis, enables nicotinamide salvage to regenerate NAD(+), and is associated with obesity resistance.	NAD	177-183	nicotinamide N-methyltransferase	Mus musculus	64-96
25765152-0	2015	A structural model for FOXRED1, an FAD-dependent oxidoreductase necessary for NADH: Ubiquinone oxidoreductase (complex I) assembly.	NAD	78-82	thioredoxin reductase 1	Homo sapiens	49-63
25765152-0	2015	A structural model for FOXRED1, an FAD-dependent oxidoreductase necessary for NADH: Ubiquinone oxidoreductase (complex I) assembly.	NAD	78-82	thioredoxin reductase 1	Homo sapiens	95-109
25643703-5	2015	The H2O2 produced, however, is effectively masked by a continuously cycling redox circuit that links, via glutathione/thioredoxin, to NNT, which catalyses the regeneration of NADPH from NADH at the expense of DeltaPsim.	NAD	186-190	thioredoxin 1	Mus musculus	118-129
25635049-6	2015	The crystal structure of the PARP homology domain of PARP13 shows obstruction of the canonical active site, precluding NAD(+) binding.	NAD	119-125	zinc finger CCCH-type containing, antiviral 1	Homo sapiens	53-59
25606689-3	2015	Two isoenzymes of malate dehydrogenase (MDH) operate as components of the malate-aspartate shuttle, in which a reducing equivalent is transported via malate, which when oxidized to oxaloacetate, transfers an electron pair to reduce NAD to NADH.	NAD	232-235	malic enzyme 1	Homo sapiens	18-38
25606689-3	2015	Two isoenzymes of malate dehydrogenase (MDH) operate as components of the malate-aspartate shuttle, in which a reducing equivalent is transported via malate, which when oxidized to oxaloacetate, transfers an electron pair to reduce NAD to NADH.	NAD	232-235	malate dehydrogenase 2, NAD (mitochondrial)	Mus musculus	40-43
25606689-3	2015	Two isoenzymes of malate dehydrogenase (MDH) operate as components of the malate-aspartate shuttle, in which a reducing equivalent is transported via malate, which when oxidized to oxaloacetate, transfers an electron pair to reduce NAD to NADH.	NAD	239-243	malic enzyme 1	Homo sapiens	18-38
25606689-3	2015	Two isoenzymes of malate dehydrogenase (MDH) operate as components of the malate-aspartate shuttle, in which a reducing equivalent is transported via malate, which when oxidized to oxaloacetate, transfers an electron pair to reduce NAD to NADH.	NAD	239-243	malate dehydrogenase 2, NAD (mitochondrial)	Mus musculus	40-43
25628599-4	2014	The elevated survival rate and alteration of NADH/NAD(+) ratio in the mutant cells is reversed by introduction of the wild-type Per2 gene.	NAD	45-49	period circadian regulator 2	Homo sapiens	128-132
25628599-4	2014	The elevated survival rate and alteration of NADH/NAD(+) ratio in the mutant cells is reversed by introduction of the wild-type Per2 gene.	NAD	50-56	period circadian regulator 2	Homo sapiens	128-132
25304127-5	2015	In the lungs, SIRT1 inhibits autophagy, cellular senescence, fibrosis, and inflammation by deacetylation of target proteins using NAD(+) as co-substrate and is therefore linked to the redox state.	NAD	130-136	sirtuin 1	Homo sapiens	14-19
25325377-7	2015	The knockdown of CIP2A decreased the expression of LDH-A as well as the enzymatic activity, accompanying with a decreased lactate production, an increased NADH/NAD+ ratio and ROS production.	NAD	155-159	cellular inhibitor of PP2A	Homo sapiens	17-22
25325377-7	2015	The knockdown of CIP2A decreased the expression of LDH-A as well as the enzymatic activity, accompanying with a decreased lactate production, an increased NADH/NAD+ ratio and ROS production.	NAD	160-164	cellular inhibitor of PP2A	Homo sapiens	17-22
25404345-4	2014	Under lean conditions, CREB acetylation was low due to an association with the energy-sensing NAD(+)-dependent deacetylase SirT1; amounts of acetylated CREB were increased in obesity, when SirT1 undergoes proteolytic degradation.	NAD	94-100	cAMP responsive element binding protein 1	Homo sapiens	23-27
25404345-4	2014	Under lean conditions, CREB acetylation was low due to an association with the energy-sensing NAD(+)-dependent deacetylase SirT1; amounts of acetylated CREB were increased in obesity, when SirT1 undergoes proteolytic degradation.	NAD	94-100	sirtuin 1	Homo sapiens	123-128
25404345-4	2014	Under lean conditions, CREB acetylation was low due to an association with the energy-sensing NAD(+)-dependent deacetylase SirT1; amounts of acetylated CREB were increased in obesity, when SirT1 undergoes proteolytic degradation.	NAD	94-100	sirtuin 1	Homo sapiens	189-194
25429139-6	2014	Hypoxia produced PARP1-dependent depletion of nicotinamide adenine dinucleotide (NAD(+)) and inhibition of the NAD(+)-dependent class III histone deactelyase (HDAC) sirtuin-1 (SIRT1).	NAD	46-79	poly (ADP-ribose) polymerase family, member 1	Mus musculus	17-22
25429139-6	2014	Hypoxia produced PARP1-dependent depletion of nicotinamide adenine dinucleotide (NAD(+)) and inhibition of the NAD(+)-dependent class III histone deactelyase (HDAC) sirtuin-1 (SIRT1).	NAD	81-87	poly (ADP-ribose) polymerase family, member 1	Mus musculus	17-22
25429139-9	2014	Together, these data illustrate a direct PARP1-mediated hypoxic signaling pathway involving NAD(+) depletion, SIRT1 inhibition, FoxO3a-driven Bnip3 generation, and mitochondrial AIF release.	NAD	92-98	poly (ADP-ribose) polymerase family, member 1	Mus musculus	41-46
25450376-2	2014	Here, we describe a nuclear isoform of lactate dehydrogenase (nLDH) and its ability to orchestrate histone deacetylation by controlling the availability of nicotinamide adenine dinucleotide (NAD(+)), a key ingredient of the sirtuin-1 (SIRT1) deacetylase system.	NAD	156-189	sirtuin 1	Homo sapiens	224-233
25450376-2	2014	Here, we describe a nuclear isoform of lactate dehydrogenase (nLDH) and its ability to orchestrate histone deacetylation by controlling the availability of nicotinamide adenine dinucleotide (NAD(+)), a key ingredient of the sirtuin-1 (SIRT1) deacetylase system.	NAD	156-189	sirtuin 1	Homo sapiens	235-240
25440059-5	2014	Notably, beta-hydroxybutyrate levels are increased by the high-fat diet, and beta-hydroxybutyrate, PARP inhibition, or NAD(+) supplementation can activate SIRT1 and rescue CS-associated phenotypes.	NAD	119-125	sirtuin 1	Homo sapiens	155-160
25440059-7	2014	This study connects two emerging longevity metabolites, beta-hydroxybutyrate and NAD(+), through the deacetylase SIRT1 and suggests possible interventions for CS.	NAD	81-87	sirtuin 1	Homo sapiens	113-118
25223558-3	2014	Distinct metabolic routes, starting from various precursors, are known to support NAD(+) biosynthesis with tissue/cell-specific efficiencies, probably reflecting differential expression of the corresponding rate-limiting enzymes, i.e. nicotinamide phosphoribosyltransferase, quinolinate phosphoribosyltransferase, nicotinate phosphoribosyltransferase and nicotinamide riboside kinase.	NAD	82-88	nicotinate phosphoribosyltransferase	Homo sapiens	314-350
25001863-4	2014	We reported in a sepsis cell model and human sepsis blood leukocytes that nuclear NAD+ sensor SIRT1 deacetylase remodels chromatin at specific gene sets to switch the acute-phase proinflammatory response to hypoinflammatory.	NAD	82-86	sirtuin 1	Homo sapiens	94-99
25223978-6	2014	The GAD and GABA-T enzyme activities were determined by measuring GABA and NADH production, respectively.	NAD	75-79	4-aminobutyrate aminotransferase	Mus musculus	12-18
25176140-0	2014	High-resolution crystal structures of the photoreceptor glyceraldehyde 3-phosphate dehydrogenase (GAPDH) with three and four-bound NAD molecules.	NAD	131-134	LOC786101	Bos taurus	56-96
25176140-0	2014	High-resolution crystal structures of the photoreceptor glyceraldehyde 3-phosphate dehydrogenase (GAPDH) with three and four-bound NAD molecules.	NAD	131-134	LOC786101	Bos taurus	98-103
25176140-1	2014	Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) catalyzes the oxidative phosphorylation of d-glyceraldehyde 3-phosphate (G3P) into 1,3-diphosphoglycerate (BGP) in the presence of the NAD cofactor.	NAD	184-187	LOC786101	Bos taurus	0-40
25176140-1	2014	Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) catalyzes the oxidative phosphorylation of d-glyceraldehyde 3-phosphate (G3P) into 1,3-diphosphoglycerate (BGP) in the presence of the NAD cofactor.	NAD	184-187	LOC786101	Bos taurus	42-47
25176140-4	2014	Here, we report two structures for native bovine photoreceptor GAPDH as a homotetramer with differing occupancy by NAD, bGAPDH(NAD)4 , and bGAPDH(NAD)3 .	NAD	115-118	LOC786101	Bos taurus	63-68
25190802-4	2014	Several studies have shown that SREBPs are regulated by the NAD(+)-dependent histone deacetylase SIRT1, which forms a complex with the lysine-specific histone demethylase LSD1.	NAD	60-66	sirtuin 1	Homo sapiens	97-102
25190802-4	2014	Several studies have shown that SREBPs are regulated by the NAD(+)-dependent histone deacetylase SIRT1, which forms a complex with the lysine-specific histone demethylase LSD1.	NAD	60-66	lysine demethylase 1A	Homo sapiens	171-175
25323003-5	2014	Interestingly, although BRCA1 inactivation events inhibited SIRT1 expression, they led to a substantial increase in NAD levels that enhanced NAD-related SIRT1 activity.	NAD	116-119	BRCA1 DNA repair associated	Homo sapiens	24-29
25323003-5	2014	Interestingly, although BRCA1 inactivation events inhibited SIRT1 expression, they led to a substantial increase in NAD levels that enhanced NAD-related SIRT1 activity.	NAD	116-119	sirtuin 1	Homo sapiens	153-158
25323003-5	2014	Interestingly, although BRCA1 inactivation events inhibited SIRT1 expression, they led to a substantial increase in NAD levels that enhanced NAD-related SIRT1 activity.	NAD	141-144	BRCA1 DNA repair associated	Homo sapiens	24-29
25323003-5	2014	Interestingly, although BRCA1 inactivation events inhibited SIRT1 expression, they led to a substantial increase in NAD levels that enhanced NAD-related SIRT1 activity.	NAD	141-144	sirtuin 1	Homo sapiens	153-158
25118045-4	2014	Formation of the Co(i) species of the B12 complex in the copolymer was confirmed by the UV-vis spectral change in [C4mim][NTf2] containing a sacrificial reductant (triethanolamine) under irradiation with visible light.	NAD	17-22	nuclear transport factor 2	Homo sapiens	122-126
25280219-3	2014	Here, we show that the NAD-dependent SIRT1 deacetylase is selectively overexpressed in primary human FLT3-ITD AML LSCs.	NAD	23-26	sirtuin 1	Homo sapiens	37-42
25201160-1	2014	Nicotinamide phosphoribosyltransferase (NAMPT) and nicotinate phosphoribosyltransferase domain containing 1 (NAPRT1) are the main human NAD salvage enzymes.	NAD	136-139	nicotinate phosphoribosyltransferase	Homo sapiens	51-107
25201160-1	2014	Nicotinamide phosphoribosyltransferase (NAMPT) and nicotinate phosphoribosyltransferase domain containing 1 (NAPRT1) are the main human NAD salvage enzymes.	NAD	136-139	nicotinate phosphoribosyltransferase	Homo sapiens	109-115
25026599-0	2014	Troxerutin improves hepatic lipid homeostasis by restoring NAD(+)-depletion-mediated dysfunction of lipin 1 signaling in high-fat diet-treated mice.	NAD	59-65	lipin 1	Mus musculus	100-107
25026599-9	2014	In conclusion, troxerutin displayed beneficial effects on hepatic lipid homeostasis in HFD-induced NAFLD by blocking oxidative stress to restore NAD(+)-depletion-mediated dysfunction of lipin 1 signaling.	NAD	145-151	lipin 1	Mus musculus	186-193
24953559-5	2014	Erythropoietin increased cellular nicotinamide adenine dinucleotide via increased AMP-activated protein kinase activity, possibly leading to Sirtuin1 activation.	NAD	34-67	sirtuin 1	Homo sapiens	141-149
24916412-3	2014	Because PARP inhibitors are substrate (NAD(+)) competitors, there is a need for a deeper understanding of their cross-reactivity.	NAD	39-46	poly (ADP-ribose) polymerase family, member 1	Mus musculus	8-12
24875419-2	2014	Sirtuin 1 (SIRT1), a highly conserved NAD-dependent class III deacetylase, has been implicated in human diseases.	NAD	38-41	sirtuin 1	Homo sapiens	0-9
24875419-2	2014	Sirtuin 1 (SIRT1), a highly conserved NAD-dependent class III deacetylase, has been implicated in human diseases.	NAD	38-41	sirtuin 1	Homo sapiens	11-16
25054226-6	2014	A key factor for the production of 2-butanol was the availability of NADH, which was achieved by growing cells lacking the GPD1 and GPD2 isogenes under anaerobic conditions.	NAD	69-73	glycerol-3-phosphate dehydrogenase (NAD(+)) GPD1	Saccharomyces cerevisiae S288C	123-127
25023514-2	2014	We show that ATP synthase beta is deacetylated by a human nicotinamide adenine dinucleotide (NAD(+))-dependent protein deacetylase, sirtuin 3, and its Drosophila melanogaster homologue, dSirt2.	NAD	58-91	ATP synthase, subunit B	Drosophila melanogaster	13-30
25023514-2	2014	We show that ATP synthase beta is deacetylated by a human nicotinamide adenine dinucleotide (NAD(+))-dependent protein deacetylase, sirtuin 3, and its Drosophila melanogaster homologue, dSirt2.	NAD	93-99	ATP synthase, subunit B	Drosophila melanogaster	13-30
24880902-6	2014	We propose that binding of the inhibitors repels the entering of the nicotinamide moiety of NAD(+) to the C pocket, prevents its transformation to the productive conformation and therefore inhibits the deacetylation catalyzed by SIRT1.	NAD	92-98	sirtuin 1	Homo sapiens	229-234
24967705-6	2014	High levels of CD38 reduced intracellular nicotinamide adenine dinucleotide (NAD+) levels and blocked acquired resistance by inhibiting the activity of the NAD+-dependent SIRT1 deacetylase that we have previously shown to promote resistance in CML cells by facilitating error-prone DNA damage repair.	NAD	42-75	sirtuin 1	Homo sapiens	171-176
24967705-6	2014	High levels of CD38 reduced intracellular nicotinamide adenine dinucleotide (NAD+) levels and blocked acquired resistance by inhibiting the activity of the NAD+-dependent SIRT1 deacetylase that we have previously shown to promote resistance in CML cells by facilitating error-prone DNA damage repair.	NAD	77-81	sirtuin 1	Homo sapiens	171-176
24967705-6	2014	High levels of CD38 reduced intracellular nicotinamide adenine dinucleotide (NAD+) levels and blocked acquired resistance by inhibiting the activity of the NAD+-dependent SIRT1 deacetylase that we have previously shown to promote resistance in CML cells by facilitating error-prone DNA damage repair.	NAD	156-160	sirtuin 1	Homo sapiens	171-176
24922076-7	2014	Moreover, we show that the induction of cellular NAD(+) levels using beta-lapachone (beta-Lap), whose intracellular target is NQO1, prevents the toxic effects of cisplatin through the regulation of PARP-1 and SIRT1 activity.	NAD	49-55	sirtuin 1	Homo sapiens	209-214
24657895-3	2014	The NAD World hypothesis - postulated as a systemic regulatory network for the metabolism and ageing, linked with mammalian, NAD+ dependent Sirtuin 1 - conceptually involves two critical elements.	NAD	4-7	sirtuin 1	Homo sapiens	140-149
24657895-3	2014	The NAD World hypothesis - postulated as a systemic regulatory network for the metabolism and ageing, linked with mammalian, NAD+ dependent Sirtuin 1 - conceptually involves two critical elements.	NAD	125-129	sirtuin 1	Homo sapiens	140-149
24657895-4	2014	One is the systemic, Nampt-controlled NAD+ (nicotinamide phosphoribosyltransferase) biosynthesis, where Nampt (nicotinamide phosphoribosyltransferase) acts as "propulsion" for metabolism and the other is NAD+ dependent deacetylase (SIRT1) - a regulator responsible for various biological effects, depending on its localisation in organism.	NAD	38-42	sirtuin 1	Homo sapiens	232-237
24657895-4	2014	One is the systemic, Nampt-controlled NAD+ (nicotinamide phosphoribosyltransferase) biosynthesis, where Nampt (nicotinamide phosphoribosyltransferase) acts as "propulsion" for metabolism and the other is NAD+ dependent deacetylase (SIRT1) - a regulator responsible for various biological effects, depending on its localisation in organism.	NAD	38-41	sirtuin 1	Homo sapiens	232-237
24667915-1	2014	Preserving mitochondrial pools of nicotinamide adenine dinucleotide (NAD) or nicotinamide phosphoribosyltransferase (Nampt), an enzyme involved in NAD production, maintains mitochondrial function and confers neuroprotection after ischemic stress.	NAD	147-150	nicotinamide phosphoribosyltransferase	Rattus norvegicus	77-115
24667915-1	2014	Preserving mitochondrial pools of nicotinamide adenine dinucleotide (NAD) or nicotinamide phosphoribosyltransferase (Nampt), an enzyme involved in NAD production, maintains mitochondrial function and confers neuroprotection after ischemic stress.	NAD	147-150	nicotinamide phosphoribosyltransferase	Rattus norvegicus	117-122
24824795-1	2014	Functional morphodynamic behavior of differentiated macrophages is strongly controlled by actin cytoskeleton rearrangements, a process in which also metabolic cofactors ATP and NAD(H) (i.e. NAD+ and NADH) and NADP(H) (i.e. NADP+ and NADPH) play an essential role.	NAD	177-183	2,4-dienoyl-CoA reductase 1	Homo sapiens	223-238
24824795-1	2014	Functional morphodynamic behavior of differentiated macrophages is strongly controlled by actin cytoskeleton rearrangements, a process in which also metabolic cofactors ATP and NAD(H) (i.e. NAD+ and NADH) and NADP(H) (i.e. NADP+ and NADPH) play an essential role.	NAD	190-194	2,4-dienoyl-CoA reductase 1	Homo sapiens	223-238
24824795-1	2014	Functional morphodynamic behavior of differentiated macrophages is strongly controlled by actin cytoskeleton rearrangements, a process in which also metabolic cofactors ATP and NAD(H) (i.e. NAD+ and NADH) and NADP(H) (i.e. NADP+ and NADPH) play an essential role.	NAD	199-203	2,4-dienoyl-CoA reductase 1	Homo sapiens	223-238
24819061-8	2014	This effect was specific for p53(+/+) cancer cells and correlated with (i) reduced activity of NAD(+)-dependent deacetylase sirtuin 1 (SIRT1) and (ii) an increase in acetylated p53, a known target of SIRT1 deacetylation activity.	NAD	95-101	sirtuin 1	Homo sapiens	135-140
24819061-8	2014	This effect was specific for p53(+/+) cancer cells and correlated with (i) reduced activity of NAD(+)-dependent deacetylase sirtuin 1 (SIRT1) and (ii) an increase in acetylated p53, a known target of SIRT1 deacetylation activity.	NAD	95-101	sirtuin 1	Homo sapiens	200-205
30736167-6	2014	(iii) Treatment with E2, DPN (ER agonist), but not PPT (ER agonist) increased VDR.	NAD	25-28	vitamin D receptor	Homo sapiens	78-81
24362075-9	2014	Chronic administration of rCT-1 caused downregulation of lipogenic genes and genes involved in FA import to hepatocytes together with amelioration of ER stress, elevation of NAD(+)/NADH ratio, phosphorylation of LKB1 and AMPK, increased expression and activity of sirtuin1 (SIRT1) and upregulation of genes mediating FA oxidation.	NAD	174-180	cardiotrophin 1	Rattus norvegicus	26-31
24362075-9	2014	Chronic administration of rCT-1 caused downregulation of lipogenic genes and genes involved in FA import to hepatocytes together with amelioration of ER stress, elevation of NAD(+)/NADH ratio, phosphorylation of LKB1 and AMPK, increased expression and activity of sirtuin1 (SIRT1) and upregulation of genes mediating FA oxidation.	NAD	181-185	cardiotrophin 1	Rattus norvegicus	26-31
24504697-10	2014	Based on these observations, we conclude NADH pyrophosphohydrolase activity conferred by AtNUDT7 is important for NAD:NADH homeostasis in seeds.	NAD	41-44	MutT/nudix family protein	Arabidopsis thaliana	89-96
24504697-10	2014	Based on these observations, we conclude NADH pyrophosphohydrolase activity conferred by AtNUDT7 is important for NAD:NADH homeostasis in seeds.	NAD	41-45	MutT/nudix family protein	Arabidopsis thaliana	89-96
24760190-2	2014	Hydroxyprostaglandin dehydrogenase 15-(nicotinamide adenine dinucleotide) (15-PGDH, HPGD) is down-regulated in colorectal cancers and functions as a metabolic antagonist of PTGS2.	NAD	39-72	carbonyl reductase 1	Homo sapiens	84-88
24719103-0	2014	ArfGAP3 is a component of the photoreceptor synaptic ribbon complex and forms an NAD(H)-regulated, redox-sensitive complex with RIBEYE that is important for endocytosis.	NAD	81-87	C-terminal binding protein 2	Mus musculus	128-134
24719103-9	2014	ArfGAP3 binds to RIBEYE(B)-domain in an NAD(H)-dependent manner.	NAD	40-46	C-terminal binding protein 2	Mus musculus	17-23
24719103-10	2014	The interaction is redox sensitive because NADH is more efficient than the oxidized NAD(+) in promoting ArfGAP3-RIBEYE interaction.	NAD	43-47	C-terminal binding protein 2	Mus musculus	112-118
24719103-10	2014	The interaction is redox sensitive because NADH is more efficient than the oxidized NAD(+) in promoting ArfGAP3-RIBEYE interaction.	NAD	84-90	C-terminal binding protein 2	Mus musculus	112-118
24147777-5	2014	The NAD+-dependent deacetylase SIRT1 (silent information regulator T1) was found to be up-regulated after AICAR treatment but, conversely, was down-regulated after IL-1beta treatment.	NAD	4-8	sirtuin 1	Homo sapiens	31-36
24627100-3	2014	Visfatin, also known as nicotinamide phosphoribosyltransferase (NAMPT), modulates sirtuin1 (SIRT1) through the regulation of nicotinamide adenine dinucleotide (NAD).	NAD	125-158	sirtuin 1	Homo sapiens	92-97
24025646-9	2014	Thus, intracellular regulation of NAD(+) levels through NQO1 activation might be a promising therapeutic target for the protection of cisplatin-induced acute kidney injury.	NAD	34-40	NAD(P)H dehydrogenase, quinone 1	Mus musculus	56-60
24444429-6	2014	Comparison of bacterial NDH-2 with the yeast NADH dehydrogenase (Ndi1) structure revealed non-overlapping binding sites for quinone and NADH in the bacterial enzyme.	NAD	45-49	NADH-ubiquinone reductase (H(+)-translocating) NDE2	Saccharomyces cerevisiae S288C	24-29
24120939-6	2014	The apo form adopts a distinct open conformation, in which the smaller subdomain of SIRT1 undergoes a rotation with respect to the larger NAD(+)-binding subdomain.	NAD	138-144	sirtuin 1	Homo sapiens	84-89
23715855-8	2014	Due to its wide pH optimum, promising thermostability, and high organic solvent tolerance, O. parapolymorpha FDH may be a good NADH regeneration catalyst candidate.	NAD	127-131	HPODL_03145	Ogataea parapolymorpha DL-1	109-112
24022598-2	2014	Recently, increasing studies have indicated that sirtuin1 (SIRT1), a NAD+-dependent deacetylase, has potential anti-inflammatory effect in endothelial cells.	NAD	69-72	sirtuin 1	Homo sapiens	49-57
24022598-2	2014	Recently, increasing studies have indicated that sirtuin1 (SIRT1), a NAD+-dependent deacetylase, has potential anti-inflammatory effect in endothelial cells.	NAD	69-72	sirtuin 1	Homo sapiens	59-64
23798335-9	2014	Glu-AGE or Glycer-AGE reduced the expression of the malate dehydrogenase (Mdh1/2) gene, which plays a critical role in the nicotinamide adenine dinucleotide (NADH) shuttle.	NAD	123-156	malate dehydrogenase 1	Rattus norvegicus	74-80
23798335-9	2014	Glu-AGE or Glycer-AGE reduced the expression of the malate dehydrogenase (Mdh1/2) gene, which plays a critical role in the nicotinamide adenine dinucleotide (NADH) shuttle.	NAD	158-162	malate dehydrogenase 1	Rattus norvegicus	74-80
24293653-4	2014	We discovered that poly(ADP-ribose) synthesis catalysed by PARP1 at the sites of unrepaired SBs activates ARF transcription through a protein signalling cascade, including the NAD(+)-dependent deacetylase SIRT1 and the transcription factor E2F1.	NAD	176-182	sirtuin 1	Homo sapiens	205-210
24293653-5	2014	Our data suggest that poly(ADP-ribose) synthesis at the sites of SBs initiates DNA damage signal transduction by reducing the cellular concentration of NAD(+), thus down-regulating SIRT1 activity and consequently activating E2F1-dependent ARF transcription.	NAD	152-158	sirtuin 1	Homo sapiens	181-186
24498241-12	2014	The results obtained herein are consistent with a scenario where lactate, taken up by germ cells, becomes oxidized to pyruvate with the resultant increase in NADH, which is a substrate for NOX4.	NAD	158-162	NADPH oxidase 4	Rattus norvegicus	189-193
25932355-6	2014	The activation of PGC-1alpha by FGF21 occurred via the NAD(+)-dependent deacetylase Sirtuin-1 (SIRT1) subsequent to an increase in the enzyme, nicotinamide phosphoribosyltransferase (Nampt).	NAD	55-61	sirtuin 1	Homo sapiens	84-93
25932355-6	2014	The activation of PGC-1alpha by FGF21 occurred via the NAD(+)-dependent deacetylase Sirtuin-1 (SIRT1) subsequent to an increase in the enzyme, nicotinamide phosphoribosyltransferase (Nampt).	NAD	55-61	sirtuin 1	Homo sapiens	95-100
25485588-5	2014	Interestingly, the high efficiency of PARP1 triggered by BRCA1 inactivation may further inhibit BRCA1 transcription by NAD depletion.	NAD	119-122	BRCA1 DNA repair associated	Homo sapiens	57-62
25485588-5	2014	Interestingly, the high efficiency of PARP1 triggered by BRCA1 inactivation may further inhibit BRCA1 transcription by NAD depletion.	NAD	119-122	BRCA1 DNA repair associated	Homo sapiens	96-101
25486197-0	2014	BRCA1 as a nicotinamide adenine dinucleotide (NAD)-dependent metabolic switch in ovarian cancer.	NAD	11-44	BRCA1 DNA repair associated	Homo sapiens	0-5
25486197-0	2014	BRCA1 as a nicotinamide adenine dinucleotide (NAD)-dependent metabolic switch in ovarian cancer.	NAD	46-49	BRCA1 DNA repair associated	Homo sapiens	0-5
25486197-3	2014	Here, we showed that: (i) BRCA1 inactivation events (mutation and promoter methylation) were accompanied by elevated levels of NAD; (ii) the knockdown or overexpression of BRCA1 was an effective way to induce an increase or decrease of nicotinamide phosphoribosyltransferase (Nampt)-related NAD synthesis, respectively; and (iii) BRCA1 expression patterns were inversely correlated with NAD levels in human ovarian cancer specimens.	NAD	127-130	BRCA1 DNA repair associated	Homo sapiens	26-31
25486197-3	2014	Here, we showed that: (i) BRCA1 inactivation events (mutation and promoter methylation) were accompanied by elevated levels of NAD; (ii) the knockdown or overexpression of BRCA1 was an effective way to induce an increase or decrease of nicotinamide phosphoribosyltransferase (Nampt)-related NAD synthesis, respectively; and (iii) BRCA1 expression patterns were inversely correlated with NAD levels in human ovarian cancer specimens.	NAD	127-130	BRCA1 DNA repair associated	Homo sapiens	172-177
25486197-3	2014	Here, we showed that: (i) BRCA1 inactivation events (mutation and promoter methylation) were accompanied by elevated levels of NAD; (ii) the knockdown or overexpression of BRCA1 was an effective way to induce an increase or decrease of nicotinamide phosphoribosyltransferase (Nampt)-related NAD synthesis, respectively; and (iii) BRCA1 expression patterns were inversely correlated with NAD levels in human ovarian cancer specimens.	NAD	127-130	BRCA1 DNA repair associated	Homo sapiens	172-177
25486197-3	2014	Here, we showed that: (i) BRCA1 inactivation events (mutation and promoter methylation) were accompanied by elevated levels of NAD; (ii) the knockdown or overexpression of BRCA1 was an effective way to induce an increase or decrease of nicotinamide phosphoribosyltransferase (Nampt)-related NAD synthesis, respectively; and (iii) BRCA1 expression patterns were inversely correlated with NAD levels in human ovarian cancer specimens.	NAD	291-294	BRCA1 DNA repair associated	Homo sapiens	26-31
25486197-3	2014	Here, we showed that: (i) BRCA1 inactivation events (mutation and promoter methylation) were accompanied by elevated levels of NAD; (ii) the knockdown or overexpression of BRCA1 was an effective way to induce an increase or decrease of nicotinamide phosphoribosyltransferase (Nampt)-related NAD synthesis, respectively; and (iii) BRCA1 expression patterns were inversely correlated with NAD levels in human ovarian cancer specimens.	NAD	291-294	BRCA1 DNA repair associated	Homo sapiens	172-177
23859614-1	2014	Sirtuin 1 (SIRT1) is an NAD+-dependent histone deacetylase which regulates many normal physiological and pathological processes.	NAD	24-27	sirtuin 1	Homo sapiens	0-9
23859614-1	2014	Sirtuin 1 (SIRT1) is an NAD+-dependent histone deacetylase which regulates many normal physiological and pathological processes.	NAD	24-27	sirtuin 1	Homo sapiens	11-16
25289390-0	2014	Regulation of rat hepatic alpha-amino-beta-carboxymuconate-epsilon-semialdehyde decarboxylase, a key enzyme in the tryptophan- NAD pathway, by dietary cholesterol and sterol regulatory element-binding protein-2.	NAD	127-130	sterol regulatory element binding transcription factor 2	Rattus norvegicus	167-210
24126171-4	2014	NCF1, one of the variably deleted Williams genes, is a component of the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase complex and is involved in the generation of oxidative stress, making it an interesting candidate modifier for vascular stiffness.	NAD	72-105	neutrophil cytosolic factor 1	Homo sapiens	0-4
24097869-9	2013	CONCLUSIONS: Tumor-specific promoter hypermethylation of NAPRT1 inactivates one of two NAD salvage pathways, resulting in synthetic lethality with the coadministration of a NAMPT inhibitor.	NAD	87-90	nicotinate phosphoribosyltransferase	Homo sapiens	57-63
23480676-7	2013	RESULTS: In replicon cells, the level of ROS and MDA increased, SOD activity and the value of NAD(+) /NADH decreased, then the activity and expression level of mRNA and protein of SIRT1 reduced.	NAD	94-100	sirtuin 1	Homo sapiens	180-185
23480676-7	2013	RESULTS: In replicon cells, the level of ROS and MDA increased, SOD activity and the value of NAD(+) /NADH decreased, then the activity and expression level of mRNA and protein of SIRT1 reduced.	NAD	102-106	sirtuin 1	Homo sapiens	180-185
23480676-11	2013	CONCLUSION: HCV replication decreasing NAD(+) /NADH ratio may downregulate the activity and the expression of SIRT1, then change the expression profile of lipid metabolism-related genes, thereby cause lipid metabolism disorders of hepatocytes and promote HCV replication.	NAD	39-45	sirtuin 1	Homo sapiens	110-115
23480676-11	2013	CONCLUSION: HCV replication decreasing NAD(+) /NADH ratio may downregulate the activity and the expression of SIRT1, then change the expression profile of lipid metabolism-related genes, thereby cause lipid metabolism disorders of hepatocytes and promote HCV replication.	NAD	47-51	sirtuin 1	Homo sapiens	110-115
24126058-1	2013	The NAD(+)-dependent deacetylase SirT1 regulates gene silencing and genomic stability in response to nutrient deprivation and DNA damage.	NAD	4-10	sirtuin 1	Homo sapiens	33-38
23855981-1	2013	Silent information regulator 1 (SIRT1) is a type of histone deacetylase whose activity is dependent on nicotinamide adenine dinucleotide.	NAD	103-136	sirtuin 1	Homo sapiens	0-30
23855981-1	2013	Silent information regulator 1 (SIRT1) is a type of histone deacetylase whose activity is dependent on nicotinamide adenine dinucleotide.	NAD	103-136	sirtuin 1	Homo sapiens	32-37
24403854-2	2013	Alternatively, nicotinic acid (NA) is metabolized to NAD through the nicotinic acid phosphoribosyltransferase domain containing 1 (NAPRT1)-dependent salvage pathway.	NAD	53-56	nicotinate phosphoribosyltransferase	Homo sapiens	131-137
24403854-8	2013	Furthermore, NAM co-administration with GNE-617 led to increased tumor NAD levels and rescued in vivo efficacy as well.	NAD	71-74	glucosamine (UDP-N-acetyl)-2-epimerase/N-acetylmannosamine kinase	Homo sapiens	40-43
24437277-0	2013	[Importance of NAMPT-mediated NAD-biosynthesis and NAD-dependent deacetylase SIRT1 in the crosstalk between circadian rhythm and metabolism].	NAD	51-54	sirtuin 1	Homo sapiens	77-82
24437277-3	2013	We recently found that the key NAD biosynthetic enzyme, nicotinamide phosphoribosyltransferase (NAMPT), and NAD-dependent deacetylase SIRT1 play a critical role in such crosstalk, by creating a novel feedback loop in which NAD functions as a "metabolic oscillator".	NAD	31-34	sirtuin 1	Homo sapiens	134-139
24437277-3	2013	We recently found that the key NAD biosynthetic enzyme, nicotinamide phosphoribosyltransferase (NAMPT), and NAD-dependent deacetylase SIRT1 play a critical role in such crosstalk, by creating a novel feedback loop in which NAD functions as a "metabolic oscillator".	NAD	108-111	sirtuin 1	Homo sapiens	134-139
24437277-3	2013	We recently found that the key NAD biosynthetic enzyme, nicotinamide phosphoribosyltransferase (NAMPT), and NAD-dependent deacetylase SIRT1 play a critical role in such crosstalk, by creating a novel feedback loop in which NAD functions as a "metabolic oscillator".	NAD	108-111	sirtuin 1	Homo sapiens	134-139
24258275-1	2013	The NAD(+)-dependent deacetylase SIRT1 is involved in diverse cellular processes, and has also been linked with multiple disease states.	NAD	4-10	sirtuin 1	Homo sapiens	33-38
24210820-3	2013	Here, we show that SIRT7, an NAD(+)-dependent H3K18Ac deacetylase, functions at chromatin to suppress ER stress and prevent the development of fatty liver disease.	NAD	29-35	sirtuin 7	Mus musculus	19-24
23648587-1	2013	Sirtuins (Sirt1-7) are nicotinamide adenine dinucleotide (NAD)-dependent protein deacetylases/ADP-ribosyltransferases that modulate many metabolic responses affecting aging.	NAD	23-56	sirtuin 1	Homo sapiens	10-15
23648587-1	2013	Sirtuins (Sirt1-7) are nicotinamide adenine dinucleotide (NAD)-dependent protein deacetylases/ADP-ribosyltransferases that modulate many metabolic responses affecting aging.	NAD	58-61	sirtuin 1	Homo sapiens	10-15
24331693-11	2013	CONCLUSION: HCV may decrease the NAD+/NADH ratio in hepatocytes, leading to a down-regulation of SIRT1 activity and expression and perturbing the downstream expression profile of lipid metabolism-related factors, ultimately causing lipid metabolism disorders and establishing a permissive intracellular environment for HCV replication.	NAD	33-37	sirtuin 1	Homo sapiens	97-102
23916946-2	2013	To realize its synthetic biological application for coenzyme recycling use, computational design and site-directed mutagenesis have been used to engineer Gox2181 to utilize not only NADH but also NADPH as the electron donor.	NAD	182-186	hydroxyacid oxidase 1	Homo sapiens	154-157
23916946-6	2013	Steady-state turnover measurement results indicated that Gox2181-D43Q could use both NADH and NADPH as its coenzyme, and so could Gox2181-Q20R&amp;D43Q.	NAD	85-89	hydroxyacid oxidase 1	Homo sapiens	57-60
23838793-2	2013	Overexpression of both the 6-phosphofructokinase (pfkA) and pyruvate kinase (pykA) genes increased intracellular concentrations of ATP and NADH and also resistance to butanol toxicity.	NAD	139-143	pykA	Clostridium acetobutylicum ATCC 824	60-75
23838793-2	2013	Overexpression of both the 6-phosphofructokinase (pfkA) and pyruvate kinase (pykA) genes increased intracellular concentrations of ATP and NADH and also resistance to butanol toxicity.	NAD	139-143	pykA	Clostridium acetobutylicum ATCC 824	77-81
23542362-3	2013	SIRT1 is regulated by a NAD(+)-dependent DNA repair enzyme, poly(ADP-ribose) polymerase-1 (PARP1), and subsequent NAD(+) depletion by oxidative stress may have consequent effects on inflammatory and stress responses as well as cellular senescence.	NAD	24-30	sirtuin 1	Homo sapiens	0-5
23542362-3	2013	SIRT1 is regulated by a NAD(+)-dependent DNA repair enzyme, poly(ADP-ribose) polymerase-1 (PARP1), and subsequent NAD(+) depletion by oxidative stress may have consequent effects on inflammatory and stress responses as well as cellular senescence.	NAD	114-120	sirtuin 1	Homo sapiens	0-5
23639754-4	2013	The AaALDH3 is structurally and functionally a NAD(+)-dependent class 3 ALDH showing tissue- and developmental-stage-specific splice variants.	NAD	47-53	aldehyde dehydrogenase 3 family member A2	Homo sapiens	6-10
24137378-1	2013	Silent mating-type information regulation 2, homolog 1 (SIRT1) represents an NAD+-dependent deacetylase that regulates the processes of stress response and cell survival.	NAD	77-80	sirtuin 1	Homo sapiens	56-61
23737528-3	2013	NMNAT1 binds to nucleomethylin and is recruited into a ternary complex containing the NAD(+)-dependent deacetylase SirT1.	NAD	86-92	sirtuin 1	Homo sapiens	115-120
23870485-1	2013	BACKGROUND: The NAD-dependent protein deacetylase SIRT1 has a wide range of different targets, which may be regulated either directly through deacetylation and thus potentially altering their activity or localization or indirectly by deacetylation of histones, which in turn alters their transcription rate and availability.	NAD	16-19	sirtuin 1	Homo sapiens	50-55
23786618-3	2013	In one of the adult fibroblast strains evaluated, these changes in procollagen-1 and NAD(+)/NADH in response to the complex of bioactives were in parallel with increased expression of mRNA biomarkers related primarily to dermal matrix and basement membrane structure, including COL1A1, COL3A1, COL5A1, COL14A1, ELN and LOXL2, in addition to SOD2, NAMPT and TGFBR3; MMP1 was decreased in expression.	NAD	85-91	collagen type I alpha 1 chain	Homo sapiens	278-284
23786618-3	2013	In one of the adult fibroblast strains evaluated, these changes in procollagen-1 and NAD(+)/NADH in response to the complex of bioactives were in parallel with increased expression of mRNA biomarkers related primarily to dermal matrix and basement membrane structure, including COL1A1, COL3A1, COL5A1, COL14A1, ELN and LOXL2, in addition to SOD2, NAMPT and TGFBR3; MMP1 was decreased in expression.	NAD	85-91	elastin	Homo sapiens	311-314
23786618-3	2013	In one of the adult fibroblast strains evaluated, these changes in procollagen-1 and NAD(+)/NADH in response to the complex of bioactives were in parallel with increased expression of mRNA biomarkers related primarily to dermal matrix and basement membrane structure, including COL1A1, COL3A1, COL5A1, COL14A1, ELN and LOXL2, in addition to SOD2, NAMPT and TGFBR3; MMP1 was decreased in expression.	NAD	85-91	transforming growth factor beta receptor 3	Homo sapiens	357-363
23786618-3	2013	In one of the adult fibroblast strains evaluated, these changes in procollagen-1 and NAD(+)/NADH in response to the complex of bioactives were in parallel with increased expression of mRNA biomarkers related primarily to dermal matrix and basement membrane structure, including COL1A1, COL3A1, COL5A1, COL14A1, ELN and LOXL2, in addition to SOD2, NAMPT and TGFBR3; MMP1 was decreased in expression.	NAD	92-96	collagen type I alpha 1 chain	Homo sapiens	278-284
23786618-3	2013	In one of the adult fibroblast strains evaluated, these changes in procollagen-1 and NAD(+)/NADH in response to the complex of bioactives were in parallel with increased expression of mRNA biomarkers related primarily to dermal matrix and basement membrane structure, including COL1A1, COL3A1, COL5A1, COL14A1, ELN and LOXL2, in addition to SOD2, NAMPT and TGFBR3; MMP1 was decreased in expression.	NAD	92-96	elastin	Homo sapiens	311-314
23786618-3	2013	In one of the adult fibroblast strains evaluated, these changes in procollagen-1 and NAD(+)/NADH in response to the complex of bioactives were in parallel with increased expression of mRNA biomarkers related primarily to dermal matrix and basement membrane structure, including COL1A1, COL3A1, COL5A1, COL14A1, ELN and LOXL2, in addition to SOD2, NAMPT and TGFBR3; MMP1 was decreased in expression.	NAD	92-96	transforming growth factor beta receptor 3	Homo sapiens	357-363
23680022-1	2013	Sirtuins belong to a class of NAD-dependent deacetylases, and include seven distinct isoforms, of which SIRT7 is the least studied member.	NAD	30-33	sirtuin 7	Homo sapiens	104-109
23510538-10	2013	CONCLUSIONS: HCV core protein induces alterations in cellular redox state (decrease in the NAD(+)/NADH ratio), which could influence the activity of SIRT1 and secondarily AMPK, then change the expression profile of glucose and lipid metabolism-related genes, thereby causing metabolism disorders of hepatocytes.	NAD	91-97	sirtuin 1	Homo sapiens	149-154
23510538-10	2013	CONCLUSIONS: HCV core protein induces alterations in cellular redox state (decrease in the NAD(+)/NADH ratio), which could influence the activity of SIRT1 and secondarily AMPK, then change the expression profile of glucose and lipid metabolism-related genes, thereby causing metabolism disorders of hepatocytes.	NAD	98-102	sirtuin 1	Homo sapiens	149-154
23825667-8	2013	Moreover, concomitant suppression of NAD-dependent deacetylase SIRT1 and AMPK is observed in atherosclerotic pigs, which leads to the proteolytic activation of SREBP-1 by diminishing the deacetylation and Ser-372 phosphorylation of SREBP-1.	NAD	37-40	sirtuin 1	Sus scrofa	63-68
23497876-1	2013	An electrochemical method was developed to measure the enzymatic activity of alcohol dehydrogenase (ADH) by monitoring the amount of reduced nicotinamide adenine dinucleotide (NADH) generated in the catalysed oxidation of ethanol by ADH.	NAD	141-174	aldo-keto reductase family 1 member A1	Homo sapiens	77-98
23497876-1	2013	An electrochemical method was developed to measure the enzymatic activity of alcohol dehydrogenase (ADH) by monitoring the amount of reduced nicotinamide adenine dinucleotide (NADH) generated in the catalysed oxidation of ethanol by ADH.	NAD	141-174	aldo-keto reductase family 1 member A1	Homo sapiens	100-103
23497876-1	2013	An electrochemical method was developed to measure the enzymatic activity of alcohol dehydrogenase (ADH) by monitoring the amount of reduced nicotinamide adenine dinucleotide (NADH) generated in the catalysed oxidation of ethanol by ADH.	NAD	141-174	aldo-keto reductase family 1 member A1	Homo sapiens	177-180
23497876-1	2013	An electrochemical method was developed to measure the enzymatic activity of alcohol dehydrogenase (ADH) by monitoring the amount of reduced nicotinamide adenine dinucleotide (NADH) generated in the catalysed oxidation of ethanol by ADH.	NAD	176-180	aldo-keto reductase family 1 member A1	Homo sapiens	77-98
23497876-1	2013	An electrochemical method was developed to measure the enzymatic activity of alcohol dehydrogenase (ADH) by monitoring the amount of reduced nicotinamide adenine dinucleotide (NADH) generated in the catalysed oxidation of ethanol by ADH.	NAD	176-180	aldo-keto reductase family 1 member A1	Homo sapiens	100-103
23641059-4	2013	Superoxide production by a model bacterium within the ubiquitous Roseobacter clade involves an extracellular oxidoreductase that is stimulated by the reduced form of nicotinamide adenine dinucleotide (NADH), suggesting a surprising homology with eukaryotic organisms.	NAD	201-205	thioredoxin reductase 1	Homo sapiens	109-123
23762469-4	2013	Both types of wine increased rat Schwann cell- (rSC) expression of the NAD+-dependent deacetylase sirtuin-two-homolog 2 (Sirt2), a protein known to be involved in myelination.	NAD	71-74	sirtuin 2	Rattus norvegicus	98-119
23762469-4	2013	Both types of wine increased rat Schwann cell- (rSC) expression of the NAD+-dependent deacetylase sirtuin-two-homolog 2 (Sirt2), a protein known to be involved in myelination.	NAD	71-74	sirtuin 2	Rattus norvegicus	121-126
23435312-9	2013	PBEF1 activity and NAD(+) content were reduced in MM cells by APO866, resulting in lower activity of PARP-1 and SIRT-1.	NAD	19-25	sirtuin 1	Homo sapiens	112-118
23710766-7	2013	Repression of these target genes during the diauxic shift is specifically dependent on Sir2/Hst1/Sum1 binding to the ORF and sufficiently high intracellular NAD+ concentrations.	NAD	157-161	Sum1p	Saccharomyces cerevisiae S288C	97-101
23457190-4	2013	We provide evidence that extracellular quinolinic acid enters the cell via Tna1, a high-affinity nicotinic acid permease, and thereby helps to increase the intracellular concentration of NAD(+).	NAD	187-193	Tna1p	Saccharomyces cerevisiae S288C	75-79
23457190-5	2013	Transcription of genes involved in the kynurenine pathway and Tna1 was increased, responding to a low intracellular NAD(+) concentration, in cells bearing mutations of these genes; this transcriptional induction was suppressed by supplementation with quinolinic acid or nicotinic acid.	NAD	116-122	Tna1p	Saccharomyces cerevisiae S288C	62-66
23403179-4	2013	PURPOSE: This study examined stroke-induced changes in NAD+, a key energy molecule involved in PARP-1 activation in both sexes.	NAD	55-59	poly (ADP-ribose) polymerase family, member 1	Mus musculus	95-101
23403179-11	2013	PARP-1 deletion prevented the stroke-induced loss in NAD+ in males, but worsened NAD+ loss in PARP-1 deficient females.	NAD	53-57	poly (ADP-ribose) polymerase family, member 1	Mus musculus	0-6
23403179-11	2013	PARP-1 deletion prevented the stroke-induced loss in NAD+ in males, but worsened NAD+ loss in PARP-1 deficient females.	NAD	81-85	poly (ADP-ribose) polymerase family, member 1	Mus musculus	0-6
23403179-12	2013	Preventing NAD+ loss with nicotinamide reduced infarct in wild-type males and PARP-1 knockout mice of both sexes, with no effect in WT females.	NAD	11-15	poly (ADP-ribose) polymerase family, member 1	Mus musculus	78-84
23552949-1	2013	The Sir2 family of enzymes or sirtuins are known as nicotinamide adenine dinucleotide (NAD)-dependent deacetylases and have been implicated in the regulation of transcription, genome stability, metabolism and lifespan.	NAD	52-85	sirtuin 1	Homo sapiens	4-8
23172919-0	2013	Flavonoid apigenin is an inhibitor of the NAD+ ase CD38: implications for cellular NAD+ metabolism, protein acetylation, and treatment of metabolic syndrome.	NAD	42-46	CD38 antigen	Mus musculus	51-55
23172919-6	2013	Moreover, CD38 knockout mice have higher NAD(+) levels and are protected against obesity and metabolic syndrome.	NAD	41-47	CD38 antigen	Mus musculus	10-14
23172919-7	2013	Here, we show that CD38 regulates global protein acetylation through changes in NAD(+) levels and sirtuin activity.	NAD	80-86	CD38 antigen	Mus musculus	19-23
23172919-9	2013	We show that pharmacological inhibition of CD38 results in higher intracellular NAD(+) levels and that treatment of cell cultures with apigenin decreases global acetylation as well as the acetylation of p53 and RelA-p65.	NAD	80-86	CD38 antigen	Mus musculus	43-47
23172919-11	2013	Our results show that CD38 is a novel pharmacological target to treat metabolic diseases via NAD(+)-dependent pathways.	NAD	93-99	CD38 antigen	Mus musculus	22-26
23339189-1	2013	Sirtuins (SIRT1-7) are a highly conserved family of NAD(+)-dependent enzymes that control the activity of histone and nonhistone regulatory proteins.	NAD	52-58	sirtuin 1	Homo sapiens	10-15
23274584-8	2013	Similarly, ZnT3-KO and RPE65-KO mice showed less Zn(2+) staining, NAD(+) loss, and RPE or photoreceptor death than C57/BI6/J control mice.	NAD	66-72	solute carrier family 30 (zinc transporter), member 3	Mus musculus	11-15
24020005-1	2013	NAD(+)-dependent deacetylase SIRT1 is a master regulator of nucleosome positioning and chromatin structure, thereby reprogramming gene expression.	NAD	0-6	sirtuin 1	Homo sapiens	29-34
24020005-3	2013	This sequence depends on shifts in NAD(+) availability for SIRT1 activation and deacetylation of signaling proteins, which support orderly gene reprogramming during acute inflammation by switching between euchromatin and heterochromatin.	NAD	35-41	sirtuin 1	Homo sapiens	59-64
22975787-1	2013	TRPM2 (transient receptor potential melastatin 2) is the unique fusion of a Ca(2+)-permeable pore with an enzymatic domain that binds the NAD(+)-metabolite ADP-ribose (ADPR), resulting in channel opening.	NAD	138-144	transient receptor potential cation channel, subfamily M, member 2	Mus musculus	0-5
22975787-1	2013	TRPM2 (transient receptor potential melastatin 2) is the unique fusion of a Ca(2+)-permeable pore with an enzymatic domain that binds the NAD(+)-metabolite ADP-ribose (ADPR), resulting in channel opening.	NAD	138-144	transient receptor potential cation channel, subfamily M, member 2	Mus musculus	7-48
23442768-8	2013	There were increased levels of 15-PGDH protein in the centre of CRCLM associated with reduced 15-PGDH activity and low NAD+/NADH levels.	NAD	119-123	carbonyl reductase 1	Homo sapiens	31-38
23442768-8	2013	There were increased levels of 15-PGDH protein in the centre of CRCLM associated with reduced 15-PGDH activity and low NAD+/NADH levels.	NAD	124-128	carbonyl reductase 1	Homo sapiens	31-38
23442768-10	2013	NAD+ availability controlled 15-PGDH activity in human CRC cells in vitro.	NAD	0-4	carbonyl reductase 1	Homo sapiens	29-36
23341587-3	2013	In addition, SIRT1 activity is regulated in a cyclic manner in virtue of the circadian oscillation of the coenzyme NAD(+).	NAD	115-121	sirtuin 1	Homo sapiens	13-18
23169992-2	2013	Sirtuin 1 (SIRT1) is a NAD+-dependent class III histone deacetylase that has been linked to gene silencing, control of the cell cycle, apoptosis, and energy homeostasis.	NAD	23-27	sirtuin 1	Homo sapiens	0-9
23169992-2	2013	Sirtuin 1 (SIRT1) is a NAD+-dependent class III histone deacetylase that has been linked to gene silencing, control of the cell cycle, apoptosis, and energy homeostasis.	NAD	23-27	sirtuin 1	Homo sapiens	11-16
23361587-4	2013	Sirt1 functions as an intracellular energy sensor to detect the concentration of NAD(+), and controls in vivo metabolic changes under caloric restriction and starvation through its deacetylase activity to many targets including histones, nuclear transcriptional factors, and enzymes.	NAD	81-87	sirtuin 1	Homo sapiens	0-5
23103769-9	2013	Ethanol and CCK activated MPTP through different mechanisms-ethanol by reducing the ratio of oxidized nicotinamide adenine dinucleotide to reduced nicotinamide adenine dinucleotide, as a result of oxidative metabolism, and CCK by increasing cytosolic Ca(2+).	NAD	102-135	cholecystokinin	Mus musculus	12-15
23103769-9	2013	Ethanol and CCK activated MPTP through different mechanisms-ethanol by reducing the ratio of oxidized nicotinamide adenine dinucleotide to reduced nicotinamide adenine dinucleotide, as a result of oxidative metabolism, and CCK by increasing cytosolic Ca(2+).	NAD	147-180	cholecystokinin	Mus musculus	12-15
23153509-7	2013	MiR-182 was involved in Tat-induced NAD(+) depletion, down-regulation of SIRT1 protein expression and activity, increased acetylation of p65.	NAD	36-42	microRNA 182	Homo sapiens	0-7
23301673-10	2013	SIRT1 has a role in the modulation of AKT activation and PARP1 has been described to be a gatekeeper for SIRT1 activity by limiting NAD+ availability.	NAD	132-136	sirtuin 1	Homo sapiens	0-5
23301673-10	2013	SIRT1 has a role in the modulation of AKT activation and PARP1 has been described to be a gatekeeper for SIRT1 activity by limiting NAD+ availability.	NAD	132-136	sirtuin 1	Homo sapiens	105-110
25379308-1	2013	Chronic granulomatous disease (CGD) is a rare inherited immunodeficiency syndrome that results from abnormal nicotinamide adenine dinucleotide phosphate (NADPH) oxidase function.	NAD	109-142	cytochrome b-245 beta chain	Homo sapiens	31-34
23451094-9	2013	Because alcohol dehydrogenase regenerates NAD(+) in glycolytic cells that lack TCA cycle function, this result raises the possibility that lactate dehydrogenase, which plays the equivalent role in human cells, might be a target of interest for PGL therapy.	NAD	42-48	aldo-keto reductase family 1 member A1	Homo sapiens	8-29
23086949-1	2012	Sir2 proteins, or sirtuins, are a family of enzymes that catalyze NAD(+)-dependent deacetylation reactions and can also process ribosyltransferase, demalonylase, and desuccinylase activities.	NAD	66-72	sirtuin 1	Homo sapiens	0-4
23201684-4	2012	Here, we show that the NAD-dependent deacetylase SIRT2 binds constitutively to RIP3 and that deletion or knockdown of SIRT2 prevents formation of the RIP1-RIP3 complex in mice.	NAD	23-26	receptor-interacting serine-threonine kinase 3	Mus musculus	79-83
23201684-4	2012	Here, we show that the NAD-dependent deacetylase SIRT2 binds constitutively to RIP3 and that deletion or knockdown of SIRT2 prevents formation of the RIP1-RIP3 complex in mice.	NAD	23-26	receptor-interacting serine-threonine kinase 3	Mus musculus	155-159
23160044-6	2012	BCL6 triggered exclusion of the co-activator Mastermind-like 1 and recruitment of the NAD(+)-dependent deacetylase Sirt1, which was required for BCL6-dependent neurogenesis.	NAD	86-92	B cell leukemia/lymphoma 6	Mus musculus	0-4
23160044-6	2012	BCL6 triggered exclusion of the co-activator Mastermind-like 1 and recruitment of the NAD(+)-dependent deacetylase Sirt1, which was required for BCL6-dependent neurogenesis.	NAD	86-92	B cell leukemia/lymphoma 6	Mus musculus	145-149
22366648-0	2012	Social memory, amnesia, and autism: brain oxytocin secretion is regulated by NAD+ metabolites and single nucleotide polymorphisms of CD38.	NAD	77-81	oxytocin	Mus musculus	42-50
23070521-2	2012	At least part of the beneficial effect of resveratrol on human health stems from its capacity to promote autophagy by activating the NAD-dependent deacetylase sirtuin 1.	NAD	133-136	sirtuin 1	Homo sapiens	159-168
22893703-3	2012	Zymosan produced the location of sirtuin 1 (SIRT1) to the nucleus, enhanced its association with the il12a promoter, increased the nuclear concentration of the SIRT1 co-substrate NAD(+), and decreased chromatin accessibility in the nucleosome-1 of il12a, which contains a kappaB-site.	NAD	179-185	sirtuin 1	Homo sapiens	160-165
22949654-2	2012	In various organisms, complex I can be replaced by the alternative NADH-quinone oxidoreductase (NDH-2), which catalyzes the transfer of an electron from NADH via FAD to quinone, without proton pumping.	NAD	67-71	NADH-ubiquinone reductase (H(+)-translocating) NDE2	Saccharomyces cerevisiae S288C	96-101
22648686-2	2012	ALD6 encoding an aldehyde dehydrogenases of the indigenous yeast was replaced by a GPD1 and CUP1 gene cassette, which are responsible for NAD-dependent glycerol-3-phosphatase dehydrogenase and copper resistance, respectively.	NAD	138-141	glycerol-3-phosphate dehydrogenase (NAD(+)) GPD1	Saccharomyces cerevisiae S288C	83-87
22571857-4	2012	The fuel switch to fatty acid oxidation depends on the sensing of AMP and NAD(+) by AMPK and the SirT family of deacetylases (e.g., SirT1, -6, and -3), respectively, which couple inflammation and metabolism by chromatin and protein reprogramming.	NAD	74-80	sirtuin 1	Homo sapiens	132-149
22904041-8	2012	We then describe the role of NAD(+) and NADH as signal transducers through NAD(+)-dependent enzymes such as PARP-1 and Sirt1.	NAD	29-35	sirtuin 1	Homo sapiens	119-124
22904041-8	2012	We then describe the role of NAD(+) and NADH as signal transducers through NAD(+)-dependent enzymes such as PARP-1 and Sirt1.	NAD	40-44	sirtuin 1	Homo sapiens	119-124
22904041-8	2012	We then describe the role of NAD(+) and NADH as signal transducers through NAD(+)-dependent enzymes such as PARP-1 and Sirt1.	NAD	75-81	sirtuin 1	Homo sapiens	119-124
22904041-9	2012	PARP-1 is activated by damaged DNA in order to repair the DNA, which attenuates energy production through NAD(+) consumption; Sirt1 is activated by an increased NAD(+)/NADH ratio to facilitate signal transduction for metabolic adaption as well as stress responses.	NAD	106-112	sirtuin 1	Homo sapiens	126-131
22904041-9	2012	PARP-1 is activated by damaged DNA in order to repair the DNA, which attenuates energy production through NAD(+) consumption; Sirt1 is activated by an increased NAD(+)/NADH ratio to facilitate signal transduction for metabolic adaption as well as stress responses.	NAD	161-167	sirtuin 1	Homo sapiens	126-131
22904041-9	2012	PARP-1 is activated by damaged DNA in order to repair the DNA, which attenuates energy production through NAD(+) consumption; Sirt1 is activated by an increased NAD(+)/NADH ratio to facilitate signal transduction for metabolic adaption as well as stress responses.	NAD	168-172	sirtuin 1	Homo sapiens	126-131
22863012-3	2012	Here we report that gain of function of the NAD-dependent deacetylase SirT1 or loss of function of its endogenous inhibitor Deleted in breast cancer-1 (Dbc1) promote "browning" of WAT by deacetylating peroxisome proliferator-activated receptor (Ppar)-gamma on Lys268 and Lys293.	NAD	44-47	sirtuin 1	Homo sapiens	70-75
22554968-1	2012	BACKGROUND: The class III histone deacetylase SIRT1 is a nicotinamide adenine dinucleotide (NAD(+))-dependent deacetylase, and has been reported to serve diverse roles in various biological processes, such as caloric restriction, apoptosis, neuronal protection, cell growth, differentiation and tumourigenesis.	NAD	57-90	sirtuin 1	Homo sapiens	46-51
22554968-1	2012	BACKGROUND: The class III histone deacetylase SIRT1 is a nicotinamide adenine dinucleotide (NAD(+))-dependent deacetylase, and has been reported to serve diverse roles in various biological processes, such as caloric restriction, apoptosis, neuronal protection, cell growth, differentiation and tumourigenesis.	NAD	92-97	sirtuin 1	Homo sapiens	46-51
22700727-4	2012	CD38 is a multifunctional ectoenzyme that uses nicotinamide adenine dinucleotide as a substrate to generate second messengers.	NAD	47-80	CD38 antigen	Mus musculus	0-4
22700961-0	2012	NAD+-dependent sirtuin 1 and 6 proteins coordinate a switch from glucose to fatty acid oxidation during the acute inflammatory response.	NAD	0-4	sirtuin 1	Homo sapiens	15-24
22700961-2	2012	We reported previously that switching from the early to the late acute inflammatory response following TLR4 stimulation depends on NAD(+) activation of deacetylase sirtuin 1 (SirT1).	NAD	131-137	sirtuin 1	Homo sapiens	164-173
22700961-2	2012	We reported previously that switching from the early to the late acute inflammatory response following TLR4 stimulation depends on NAD(+) activation of deacetylase sirtuin 1 (SirT1).	NAD	131-137	sirtuin 1	Homo sapiens	175-180
22535743-1	2012	Poly(ADP)-ribose polymerase (PARP) is an abundant nuclear protein that is activated by DNA damage; once active, it modifies nuclear proteins through attachment of poly(ADP)-ribose units derived from beta-nicotinamide adenine dinucleotide (NAD(+)).	NAD	199-237	poly (ADP-ribose) polymerase family, member 1	Mus musculus	0-27
22535743-1	2012	Poly(ADP)-ribose polymerase (PARP) is an abundant nuclear protein that is activated by DNA damage; once active, it modifies nuclear proteins through attachment of poly(ADP)-ribose units derived from beta-nicotinamide adenine dinucleotide (NAD(+)).	NAD	199-237	poly (ADP-ribose) polymerase family, member 1	Mus musculus	29-33
22535743-1	2012	Poly(ADP)-ribose polymerase (PARP) is an abundant nuclear protein that is activated by DNA damage; once active, it modifies nuclear proteins through attachment of poly(ADP)-ribose units derived from beta-nicotinamide adenine dinucleotide (NAD(+)).	NAD	239-245	poly (ADP-ribose) polymerase family, member 1	Mus musculus	0-27
22535743-1	2012	Poly(ADP)-ribose polymerase (PARP) is an abundant nuclear protein that is activated by DNA damage; once active, it modifies nuclear proteins through attachment of poly(ADP)-ribose units derived from beta-nicotinamide adenine dinucleotide (NAD(+)).	NAD	239-245	poly (ADP-ribose) polymerase family, member 1	Mus musculus	29-33
23355957-5	2012	We found that NAM induced nuclear translocation of NAD-dependent histone deacetylase SIRT1 and global chromatin silencing, while RA induced silencing of pluripotence-associated hsa-miR-302 family and drastic up-regulation of neuroectodermal Hox miRNA hsa-miR-10 family to high levels.	NAD	51-54	sirtuin 1	Homo sapiens	85-90
22553202-1	2012	The NAD(+)-dependent deacetylase SIRT1 is a key regulator of several aspects of metabolism and aging.	NAD	4-10	sirtuin 1	Homo sapiens	33-38
22677942-4	2012	SIRT1, the mammalian homologue of Sir2 in yeast, is a nicotinamide-adenine dinucleotide (NAD(+))-dependent histone deacetylase that belongs to the family of HDAC class III sirtuins.	NAD	54-87	sirtuin 1	Homo sapiens	0-5
22677942-4	2012	SIRT1, the mammalian homologue of Sir2 in yeast, is a nicotinamide-adenine dinucleotide (NAD(+))-dependent histone deacetylase that belongs to the family of HDAC class III sirtuins.	NAD	54-87	sirtuin 1	Homo sapiens	34-38
22677942-4	2012	SIRT1, the mammalian homologue of Sir2 in yeast, is a nicotinamide-adenine dinucleotide (NAD(+))-dependent histone deacetylase that belongs to the family of HDAC class III sirtuins.	NAD	89-95	sirtuin 1	Homo sapiens	0-5
22677942-4	2012	SIRT1, the mammalian homologue of Sir2 in yeast, is a nicotinamide-adenine dinucleotide (NAD(+))-dependent histone deacetylase that belongs to the family of HDAC class III sirtuins.	NAD	89-95	sirtuin 1	Homo sapiens	34-38
22586264-1	2012	SIRT1 is a NAD(+)-dependent histone H4K16 deacetylase that controls several different normal physiologic and disease processes.	NAD	11-17	sirtuin 1	Homo sapiens	0-5
22844791-4	2012	Recently, a deacetylating protein SIRT1 mediated metabolic pathway is discovered to be interlocked with core oscillatory loop via Nampt expression, a late-limiting enzyme in NAD+ salvage pathway.	NAD	174-178	sirtuin 1	Homo sapiens	34-39
22844811-8	2012	SIRT1, the NAD-dependent deacetylase, attenuates telomere shortening, while PGC-1alpha, a master modulator of gene expression, is phosphorylated by AMP kinase and deacetylated by SIRT1.	NAD	11-14	sirtuin 1	Homo sapiens	0-5
22547068-0	2012	NAD+ levels control Ca2+ store replenishment and mitogen-induced increase of cytosolic Ca2+ by Cyclic ADP-ribose-dependent TRPM2 channel gating in human T lymphocytes.	NAD	0-4	transient receptor potential cation channel subfamily M member 2	Homo sapiens	123-128
22200675-3	2012	The amplitude and time course of the increase of superoxide anion observed early during apoptosis correlated with the increase of the content of soluble cytochrome b(5), a substrate of the NADH-dependent oxidase activity of the cytochrome b(5) reductase associated with lipid rafts in CGN.	NAD	189-193	mitochondrially encoded cytochrome b	Homo sapiens	153-165
22200675-3	2012	The amplitude and time course of the increase of superoxide anion observed early during apoptosis correlated with the increase of the content of soluble cytochrome b(5), a substrate of the NADH-dependent oxidase activity of the cytochrome b(5) reductase associated with lipid rafts in CGN.	NAD	189-193	mitochondrially encoded cytochrome b	Homo sapiens	228-240
22401932-4	2012	The nicotinamide adenine dinucleotide (NAD)-dependent deacetylase SIRT1 has been involved in the protection against metabolic disorders, against cancers and in the enhancement of life span.	NAD	4-37	sirtuin 1	Homo sapiens	66-71
22401932-4	2012	The nicotinamide adenine dinucleotide (NAD)-dependent deacetylase SIRT1 has been involved in the protection against metabolic disorders, against cancers and in the enhancement of life span.	NAD	39-42	sirtuin 1	Homo sapiens	66-71
22493485-8	2012	Together, our results indicate that a metabolic state resulting in an elevated [NAD(+)]/[NADH] ratio can modulate mitochondrial quantity and quality via pathways that may include SIRT1-mediated mitochondrial autophagy.	NAD	80-86	sirtuin 1	Homo sapiens	179-184
22493485-8	2012	Together, our results indicate that a metabolic state resulting in an elevated [NAD(+)]/[NADH] ratio can modulate mitochondrial quantity and quality via pathways that may include SIRT1-mediated mitochondrial autophagy.	NAD	89-93	sirtuin 1	Homo sapiens	179-184
22345574-5	2012	Surprisingly, at a pH of ~7, N-PCN was more reactive than PCN with respect to NADH oxidation but resulted in a similar magnitude of superoxide production as detected by electron paramagnetic resonance and spin trapping experiments.	NAD	78-82	cytochrome P450, family 3, subfamily a, polypeptide 11	Mus musculus	31-34
22352983-6	2012	The intranasal administration of NAD+ (20 mg/kg) immediately after TBI protected neurons in CA1, CA3, and dentate gyrus of the hippocampus, but not in the cortex.	NAD	33-37	carbonic anhydrase 3	Rattus norvegicus	97-100
22425157-3	2012	Targeting the NAD(+) biosynthetic enzyme Nmnat to mitochondria was sufficient to fully phenocopy Wld(S), and Wld(S) was specifically localized to mitochondria in synaptic preparations from mouse brain.	NAD	14-20	nicotinamide nucleotide adenylyltransferase 1	Mus musculus	41-46
22198152-5	2012	NAM is a known potent inhibitor of several classes of ribosylase enzymes that require NAD for their activity, as well as sirtuin (SIRT1), class III NAD(+)-dependent-histone-deacetylase.	NAD	148-154	sirtuin 1	Homo sapiens	130-135
22038097-3	2012	In this study, we found that NAD-dependent protein deacetylase SIRT1 is differentially expressed in both human bone marrow-derived MSCs (B-MSCs) and adipose tissue-derived MSCs after increasing passages of cell culture.	NAD	29-32	sirtuin 1	Homo sapiens	63-68
22528139-4	2012	The enzyme kinetics of UMPK showed K(m) of 2.80 +- 0.1 muM and Vmax 51.38 +- 1.39 muM of NADH/min/mg.	NAD	89-93	cytidine/uridine monophosphate kinase 1	Homo sapiens	23-27
22499122-6	2012	Moreover, we have newly identified the two genes that are down-regulated in ESCC: monoamine oxidase A, an enzyme that catalyzes monoamines oxidation and 15-hydroxyprostaglandin dehydrogenase [NAD+], a prostaglandin-synthesizing enzyme that physiologically antagonizes COX-2.	NAD	192-196	carbonyl reductase 1	Homo sapiens	153-190
22293203-1	2012	CD38 is a multifunctional enzyme that can not only generate cyclic adenosine diphosphate-ribose (cADPR) - a key Ca(2+) -mobilizing second messenger - by consuming NAD(+), but also hydrolyze extracellular NAD(+).	NAD	163-169	CD38 antigen	Mus musculus	0-4
22293203-1	2012	CD38 is a multifunctional enzyme that can not only generate cyclic adenosine diphosphate-ribose (cADPR) - a key Ca(2+) -mobilizing second messenger - by consuming NAD(+), but also hydrolyze extracellular NAD(+).	NAD	204-210	CD38 antigen	Mus musculus	0-4
22204778-6	2012	The addition of the ALP substrate and the co-reactant NADH results in the formation of a redox cycle between the enzymatic product and the electrochemically oxidized species and the signal is thus significantly amplified.	NAD	54-58	ATHS	Homo sapiens	20-23
21796450-2	2012	O-acetyl-ADP-ribose (AAR) is a small metabolic molecule that is generated during NAD-dependent deacetylation by Sir2.	NAD	81-84	sirtuin 1	Homo sapiens	112-116
22226147-1	2012	The transient receptor potential M2 channel (TRPM2) is the Ca(2+)-permeable cation channel controlled by cellular redox status via beta-NAD(+) and ADP-ribose (ADPR).	NAD	131-142	transient receptor potential cation channel subfamily M member 2	Homo sapiens	4-43
22226147-1	2012	The transient receptor potential M2 channel (TRPM2) is the Ca(2+)-permeable cation channel controlled by cellular redox status via beta-NAD(+) and ADP-ribose (ADPR).	NAD	131-142	transient receptor potential cation channel subfamily M member 2	Homo sapiens	45-50
22204321-5	2012	For examples, the key NAD(+)-dependent enzymes SIRT1 and SIRT2 have been indicated to strongly affect the pathological changes of PD and AD; PARP-1 inhibition can profoundly reduce the brain injury in the animal models of multiple neurological diseases; and administration of either NAD(+) or nicotinamide can also decrease ischemic brain damage.	NAD	283-289	sirtuin 1	Homo sapiens	47-52
22276961-4	2012	The high-K(+) -evoked overflow of beta-NAD(+)  is attenuated by cleavage of SNAP-25 with botulinum neurotoxin A, by inhibition of N-type voltage-dependent Ca(2+)  channels with omega-conotoxin GVIA, and by inhibition of the proton gradient of synaptic vesicles with bafilomycin A1, suggesting that beta-NAD(+)  is likely released via vesicle exocytosis.	NAD	34-45	synaptosome associated protein 25	Rattus norvegicus	76-83
22276961-4	2012	The high-K(+) -evoked overflow of beta-NAD(+)  is attenuated by cleavage of SNAP-25 with botulinum neurotoxin A, by inhibition of N-type voltage-dependent Ca(2+)  channels with omega-conotoxin GVIA, and by inhibition of the proton gradient of synaptic vesicles with bafilomycin A1, suggesting that beta-NAD(+)  is likely released via vesicle exocytosis.	NAD	298-309	synaptosome associated protein 25	Rattus norvegicus	76-83
22319497-2	2012	The activity of the sirtuin (SirT) family - made up of seven members (SirT1-7) - is NAD(+) dependent.	NAD	84-90	sirtuin 1	Homo sapiens	70-75
22190494-6	2012	NAMPT is the rate-limiting enzyme of the NAD(+) salvage pathway and enhances SIRT1 activity by increasing the amount of NAD(+).	NAD	120-126	sirtuin 1	Homo sapiens	77-82
21979946-11	2012	This loss of p53 was regulated by MDM2-independent NADH quinone oxidoreductase 1-mediated protein degradation, likely due to the imbalance of flavin adenine dinucleotide/nicotinamide adenine dinucleotide in SDH(var+) cells.	NAD	170-203	MDM2 proto-oncogene	Homo sapiens	34-38
22244328-0	2012	SIRT1 regulation-it ain"t all NAD.	NAD	30-33	sirtuin 1	Homo sapiens	0-5
21909679-3	2012	In this study, S. cerevisiae was engineered to investigate the effects of the sole and double disruption of NADH-dependent glycerol-3-phosphate dehydrogenase 1 (GPD1) and NADPH-requiring glutamate dehydrogenase 1 (GDH1) on the production of glycerol and ethanol from glucose.	NAD	108-112	glycerol-3-phosphate dehydrogenase (NAD(+)) GPD1	Saccharomyces cerevisiae S288C	123-159
21909679-3	2012	In this study, S. cerevisiae was engineered to investigate the effects of the sole and double disruption of NADH-dependent glycerol-3-phosphate dehydrogenase 1 (GPD1) and NADPH-requiring glutamate dehydrogenase 1 (GDH1) on the production of glycerol and ethanol from glucose.	NAD	108-112	glycerol-3-phosphate dehydrogenase (NAD(+)) GPD1	Saccharomyces cerevisiae S288C	161-165
22186411-5	2012	The case of nicotinamide adenine dinucleotide, which modulates the circadian activity of the deacetylase sirtuin 1, constitutes a paradigmatic example of the link between cyclic cellular metabolism and chromatin remodeling.	NAD	12-45	sirtuin 1	Homo sapiens	105-114
23213344-2	2012	The enzymatic activity of CD38 generates cyclic ADP-ribose from beta-NAD.	NAD	64-72	CD38 antigen	Mus musculus	26-30
22302044-2	2012	SirT1, a nicotinamide adenine dinucleotide (NAD(+))-dependent histone/protein deacetylase, has been linked to the decrease of radiation-induced DNA damage and seems to be critical for cancer therapy.	NAD	9-42	sirtuin 1	Homo sapiens	0-5
22302044-2	2012	SirT1, a nicotinamide adenine dinucleotide (NAD(+))-dependent histone/protein deacetylase, has been linked to the decrease of radiation-induced DNA damage and seems to be critical for cancer therapy.	NAD	44-51	sirtuin 1	Homo sapiens	0-5
23226106-4	2012	This new phenotype is mediated by a new downstream target of Hiw: the NAD+ biosynthetic enzyme nicotinamide mononucleotide adenyltransferase (Nmnat), which acts in parallel to a previously known target of Hiw, the Wallenda dileucine zipper kinase (Wnd/DLK) MAPKKK.	NAD	70-74	nicotinamide nucleotide adenylyltransferase 1	Mus musculus	95-140
23226106-4	2012	This new phenotype is mediated by a new downstream target of Hiw: the NAD+ biosynthetic enzyme nicotinamide mononucleotide adenyltransferase (Nmnat), which acts in parallel to a previously known target of Hiw, the Wallenda dileucine zipper kinase (Wnd/DLK) MAPKKK.	NAD	70-74	nicotinamide nucleotide adenylyltransferase 1	Mus musculus	142-147
23226106-4	2012	This new phenotype is mediated by a new downstream target of Hiw: the NAD+ biosynthetic enzyme nicotinamide mononucleotide adenyltransferase (Nmnat), which acts in parallel to a previously known target of Hiw, the Wallenda dileucine zipper kinase (Wnd/DLK) MAPKKK.	NAD	70-74	ATPase, Cu++ transporting, beta polypeptide	Mus musculus	248-251
23300904-3	2012	The present method has been optimized for NMNAT isozymes derived from Mus musculus, a species often used as a model for NAD-biosynthesis-related physiology and disorders, such as peripheral neuropathies.	NAD	120-123	nicotinamide nucleotide adenylyltransferase 1	Mus musculus	42-47
22363646-6	2012	In this study we also showed that the NAD(+)-dependent histone deacetylase SIRT1 was required for ATF4-induced MDR effect in gastric cancer cells.	NAD	38-44	sirtuin 1	Homo sapiens	75-80
22363646-6	2012	In this study we also showed that the NAD(+)-dependent histone deacetylase SIRT1 was required for ATF4-induced MDR effect in gastric cancer cells.	NAD	38-44	activating transcription factor 4	Homo sapiens	98-102
22033928-1	2011	The ADP-ribosyl cyclase CD38 whose catalytic domain resides in outside of the cell surface produces the second messenger cyclic ADP-ribose (cADPR) from NAD(+).	NAD	152-158	CD38 antigen	Mus musculus	24-28
22033928-3	2011	It has been known that intracellular NAD(+) approaches ecto-CD38 via its export by connexin (Cx43) hemichannels, a component of gap junctions.	NAD	37-43	CD38 antigen	Mus musculus	60-64
22139171-1	2011	The Saccharomyces cerevisiae NAD(+)-dependent deacetylase HST1 belongs to the class III HDAC family; it acts as a transcriptional corepressor for the specific middle sporulation and de novo NAD(+)-biosynthesis genes and also takes part in the SET3C and SUM1-RFM1-HST1 complexes.	NAD	29-33	Sum1p	Saccharomyces cerevisiae S288C	253-257
22139171-1	2011	The Saccharomyces cerevisiae NAD(+)-dependent deacetylase HST1 belongs to the class III HDAC family; it acts as a transcriptional corepressor for the specific middle sporulation and de novo NAD(+)-biosynthesis genes and also takes part in the SET3C and SUM1-RFM1-HST1 complexes.	NAD	29-35	Sum1p	Saccharomyces cerevisiae S288C	253-257
22058226-3	2011	Increased expression of the NAD synthesizing enzyme nicotinamide mononucleotide adenylyl transferase 1 (Nmnat1) has been shown to be neuroprotective against axonal injury in the peripheral nervous system.	NAD	28-31	nicotinamide nucleotide adenylyltransferase 1	Mus musculus	52-102
22058226-3	2011	Increased expression of the NAD synthesizing enzyme nicotinamide mononucleotide adenylyl transferase 1 (Nmnat1) has been shown to be neuroprotective against axonal injury in the peripheral nervous system.	NAD	28-31	nicotinamide nucleotide adenylyltransferase 1	Mus musculus	104-110
22313312-1	2011	Nicotinamide adenine dinucleotide (NAD+) is synthesized by the action of nicotinamide mononucleotide adenylyltransferase (NMNAT) from NMN and ATP.	NAD	0-33	nicotinamide nucleotide adenylyltransferase 1	Mus musculus	73-120
22313312-1	2011	Nicotinamide adenine dinucleotide (NAD+) is synthesized by the action of nicotinamide mononucleotide adenylyltransferase (NMNAT) from NMN and ATP.	NAD	0-33	nicotinamide nucleotide adenylyltransferase 1	Mus musculus	122-127
22313312-1	2011	Nicotinamide adenine dinucleotide (NAD+) is synthesized by the action of nicotinamide mononucleotide adenylyltransferase (NMNAT) from NMN and ATP.	NAD	35-39	nicotinamide nucleotide adenylyltransferase 1	Mus musculus	73-120
22313312-1	2011	Nicotinamide adenine dinucleotide (NAD+) is synthesized by the action of nicotinamide mononucleotide adenylyltransferase (NMNAT) from NMN and ATP.	NAD	35-39	nicotinamide nucleotide adenylyltransferase 1	Mus musculus	122-127
21453200-7	2011	INNOVATION: Treating Abcd1(-) mice with the antioxidants N-acetylcysteine and alpha-lipoic acid (LA) prevents protein oxidation; preserves NADH, NADPH, ATP, and GSH levels; and normalizes pyruvate kinase activity, which implies that oxidative stress provoked by VLCFA results in bioenergetic dysfunction, at a presymptomatic stage.	NAD	139-143	ATP-binding cassette, sub-family D (ALD), member 1	Mus musculus	21-26
21775503-11	2011	Binding of Hsp70 to GAPDH was nicotinamide adenine dinucleotide-dependent suggesting another type of association.	NAD	30-63	heat shock protein family A (Hsp70) member 4	Homo sapiens	11-16
21861471-8	2011	In the context of the structure of the enzyme, these results suggest that an observed asymmetry between heterotetramers in the holoenzyme contributes to interactions between IDH2 Cys-150 residues and to half-site binding of isocitrate, but that a form of negative cooperativity may limit access to apparently equivalent NAD(+) binding sites.	NAD	320-326	isocitrate dehydrogenase (NAD(+)) IDH2	Saccharomyces cerevisiae S288C	174-178
21596782-5	2011	DBC1 was recently shown to function as a negative regulator of the NAD-dependent protein deacetylase SIRT1.	NAD	67-70	sirtuin 1	Homo sapiens	101-106
21664341-2	2011	The apoptogenic action of AIF is redox controlled as the NADH-reduced AIF dimer has lower affinity for DNA than the oxidized monomer.	NAD	57-61	apoptosis inducing factor mitochondria associated 1	Homo sapiens	26-29
21664341-2	2011	The apoptogenic action of AIF is redox controlled as the NADH-reduced AIF dimer has lower affinity for DNA than the oxidized monomer.	NAD	57-61	apoptosis inducing factor mitochondria associated 1	Homo sapiens	70-73
21664341-4	2011	Our data indicate that the NADH:quinone oxidoreduction catalyzed by AIF follows a "ping-pong" scheme, with the reductive half-reaction being rate-limiting and the FADH(-)-NAD(+) charge-transfer complex serving as an electron donor.	NAD	27-31	apoptosis inducing factor mitochondria associated 1	Homo sapiens	68-71
21664341-8	2011	However, high-potential quinones, e.g. a toxic natural compound naphthazarin, maintain AIF in the oxidized state when a significant excess of NADH is present.	NAD	142-146	apoptosis inducing factor mitochondria associated 1	Homo sapiens	87-90
21636977-1	2011	SIRT1 is a NAD-dependent deacetylase that participates in cellular controls of gene expression, metabolism, genomic stability and anti-aging.	NAD	11-14	sirtuin 1	Homo sapiens	0-5
21667995-3	2011	NADH/NAD(+) is the cofactor responsible for the oxidation of l-malate by malate dehydrogenase (MDH), in the Krebs" cycle.	NAD	0-4	malic enzyme 1	Homo sapiens	73-93
21667995-3	2011	NADH/NAD(+) is the cofactor responsible for the oxidation of l-malate by malate dehydrogenase (MDH), in the Krebs" cycle.	NAD	0-4	malic enzyme 1	Homo sapiens	95-98
21667995-3	2011	NADH/NAD(+) is the cofactor responsible for the oxidation of l-malate by malate dehydrogenase (MDH), in the Krebs" cycle.	NAD	5-11	malic enzyme 1	Homo sapiens	73-93
21667995-3	2011	NADH/NAD(+) is the cofactor responsible for the oxidation of l-malate by malate dehydrogenase (MDH), in the Krebs" cycle.	NAD	5-11	malic enzyme 1	Homo sapiens	95-98
21550345-0	2011	Dissecting systemic control of metabolism and aging in the NAD World: the importance of SIRT1 and NAMPT-mediated NAD biosynthesis.	NAD	59-62	sirtuin 1	Homo sapiens	88-93
21550345-3	2011	Our studies on the mammalian NAD-dependent deacetylase SIRT1 and nicotinamide phosphoribosyltransferase (NAMPT)-mediated systemic NAD biosynthesis led us to propose a comprehensive model for the systemic regulatory network connecting metabolism and aging, termed the "NAD World".	NAD	29-32	sirtuin 1	Homo sapiens	55-60
21550345-3	2011	Our studies on the mammalian NAD-dependent deacetylase SIRT1 and nicotinamide phosphoribosyltransferase (NAMPT)-mediated systemic NAD biosynthesis led us to propose a comprehensive model for the systemic regulatory network connecting metabolism and aging, termed the "NAD World".	NAD	130-133	sirtuin 1	Homo sapiens	55-60
21550345-3	2011	Our studies on the mammalian NAD-dependent deacetylase SIRT1 and nicotinamide phosphoribosyltransferase (NAMPT)-mediated systemic NAD biosynthesis led us to propose a comprehensive model for the systemic regulatory network connecting metabolism and aging, termed the "NAD World".	NAD	130-133	sirtuin 1	Homo sapiens	55-60
21550345-4	2011	In this article, I will discuss the importance of SIRT1 and NAMPT-mediated NAD biosynthesis in the NAD World and the system dynamics of this hierarchical network for the connection between metabolism and aging.	NAD	99-102	sirtuin 1	Homo sapiens	50-55
21616968-7	2011	Poly(ADP-ribose) polymerase is activated by oxidative stress and consumes nicotinamide adenine dinucleotide, decreasing substrate availability.	NAD	74-107	poly (ADP-ribose) polymerase family, member 1	Mus musculus	0-27
21616968-10	2011	Exposure of co-cultures to beta-amyloid for >8 h decreased nicotinamide adenine dinucleotide and mitochondrial membrane potential and increased cell death in neurons, all of which were prevented by poly(ADP-ribose) polymerase inhibitors.	NAD	59-92	poly (ADP-ribose) polymerase family, member 1	Mus musculus	198-225
21459330-3	2011	Here we show that the deletion of the poly(ADP-ribose) polymerase-1 (PARP-1) gene, encoding a major NAD(+)-consuming enzyme, increases NAD(+) content and SIRT1 activity in brown adipose tissue and muscle.	NAD	100-106	poly (ADP-ribose) polymerase family, member 1	Mus musculus	38-67
21459330-3	2011	Here we show that the deletion of the poly(ADP-ribose) polymerase-1 (PARP-1) gene, encoding a major NAD(+)-consuming enzyme, increases NAD(+) content and SIRT1 activity in brown adipose tissue and muscle.	NAD	100-106	poly (ADP-ribose) polymerase family, member 1	Mus musculus	69-75
21459330-3	2011	Here we show that the deletion of the poly(ADP-ribose) polymerase-1 (PARP-1) gene, encoding a major NAD(+)-consuming enzyme, increases NAD(+) content and SIRT1 activity in brown adipose tissue and muscle.	NAD	135-141	poly (ADP-ribose) polymerase family, member 1	Mus musculus	38-67
21459330-3	2011	Here we show that the deletion of the poly(ADP-ribose) polymerase-1 (PARP-1) gene, encoding a major NAD(+)-consuming enzyme, increases NAD(+) content and SIRT1 activity in brown adipose tissue and muscle.	NAD	135-141	poly (ADP-ribose) polymerase family, member 1	Mus musculus	69-75
21459330-5	2011	Also, the pharmacologic inhibition of PARP in vitro and in vivo increased NAD(+) content and SIRT1 activity and enhanced oxidative metabolism.	NAD	74-80	poly (ADP-ribose) polymerase family, member 1	Mus musculus	38-42
21165789-3	2011	Here, we show the regulation of an adenoviral genome by the nicotinamide adenine dinucleotide (NAD(+))-dependent histone deacetylator Sirt1 in dorsal root ganglion neurons.	NAD	60-93	sirtuin 1	Homo sapiens	134-139
21165789-3	2011	Here, we show the regulation of an adenoviral genome by the nicotinamide adenine dinucleotide (NAD(+))-dependent histone deacetylator Sirt1 in dorsal root ganglion neurons.	NAD	95-101	sirtuin 1	Homo sapiens	134-139
21205922-6	2011	Pretreatment with compound C or 1,2-dihydro-3H-naphtho[2,1-b]pyran-3-one (splitomicin), an inhibitor of the NAD(+) activated deacetylase SIRT1, only partially blocked activation of CYP4F2 expression by resveratrol, suggesting that a SIRT1/AMPK-independent pathway also contributes to increased CYP4F2 expression.	NAD	108-114	sirtuin 1	Homo sapiens	137-142
21168501-5	2011	Nmnat1 enzyme generates nicotinamide adenine dinucleotide (NAD) from nicotinamide mononucleotide.	NAD	24-57	nicotinamide nucleotide adenylyltransferase 1	Rattus norvegicus	0-6
21168501-5	2011	Nmnat1 enzyme generates nicotinamide adenine dinucleotide (NAD) from nicotinamide mononucleotide.	NAD	59-62	nicotinamide nucleotide adenylyltransferase 1	Rattus norvegicus	0-6
21193400-2	2011	The present study describes a redox cycling pathway that involves the enzymatic reduction of CFZ by NDH-2, the primary respiratory chain NADH:quinone oxidoreductase of mycobacteria and nonenzymatic oxidation of reduced CFZ by O(2) yielding CFZ and reactive oxygen species (ROS).	NAD	137-141	NADH-ubiquinone reductase (H(+)-translocating) NDE2	Saccharomyces cerevisiae S288C	100-105
21735612-0	2010	Potent and selective inhibitors of NAD(+)-dependent 15-hydroxyprostaglandin dehydrogenase (HPGD) 15-hydroxyprostaglandin dehydrogenase (15-PGDH; HPGD) is the key enzyme for the inactivation of prostaglandins, and thus regulates processes such as inflammation or proliferation.	NAD	35-41	carbonyl reductase 1	Homo sapiens	52-89
21735612-0	2010	Potent and selective inhibitors of NAD(+)-dependent 15-hydroxyprostaglandin dehydrogenase (HPGD) 15-hydroxyprostaglandin dehydrogenase (15-PGDH; HPGD) is the key enzyme for the inactivation of prostaglandins, and thus regulates processes such as inflammation or proliferation.	NAD	35-41	carbonyl reductase 1	Homo sapiens	97-134
21735612-0	2010	Potent and selective inhibitors of NAD(+)-dependent 15-hydroxyprostaglandin dehydrogenase (HPGD) 15-hydroxyprostaglandin dehydrogenase (15-PGDH; HPGD) is the key enzyme for the inactivation of prostaglandins, and thus regulates processes such as inflammation or proliferation.	NAD	35-41	carbonyl reductase 1	Homo sapiens	136-143
21175596-4	2011	In addition, the expression of p47-phox was up-regulated by SAA (P &lt; 0 001) and diphenyliodonium (DPI), a nicotinamide adenine dinucleotide phosphate (NADPH) oxidase inhibitor, reduced the release of O(2) (-) by 50%.	NAD	109-142	neutrophil cytosolic factor 1	Homo sapiens	31-39
20956937-2	2011	NAMPT has crucial roles for many cellular functions by regulating NAD(+)-dependent SIRT1 deacetylase.	NAD	66-72	sirtuin 1	Homo sapiens	83-88
21345219-2	2011	The activation of PARP-1 and subsequent depletion of nicotinamide adenine dinucleotide (NAD+) and adenosine triphosphate (ATP) contributes to significant cytotoxicity in inflammation of various etiologies.	NAD	53-86	poly (ADP-ribose) polymerase family, member 1	Mus musculus	18-24
21345219-2	2011	The activation of PARP-1 and subsequent depletion of nicotinamide adenine dinucleotide (NAD+) and adenosine triphosphate (ATP) contributes to significant cytotoxicity in inflammation of various etiologies.	NAD	88-92	poly (ADP-ribose) polymerase family, member 1	Mus musculus	18-24
21293192-1	2011	SIRT1 is a NAD (+) -dependent class III histone deacetylase (HDAC) that mediates the effects of caloric restriction on lifespan and metabolic pathways in various organisms.	NAD	11-18	sirtuin 1	Homo sapiens	0-5
21183487-4	2011	We show that (i) gamma oscillation power, oxygen consumption and expression of complex I (nicotinamide adenine dinucleotide:ubiquinone oxidoreductase) subunits are higher in hippocampal subfield CA3 than in CA1 and dentate gyrus; (ii) the amount of oxygen consumption of gamma oscillations reaches that of seizure-like events; (iii) gamma oscillations are exquisitely sensitive to pharmacological complex I inhibition; and (iv) gamma oscillations utilize mitochondrial oxidative capacity near limit.	NAD	90-123	carbonic anhydrase 3	Rattus norvegicus	195-198
21133413-1	2011	Yeast NAD(+)-specific isocitrate dehydrogenase (IDH) is an octameric enzyme composed of four heterodimers of regulatory IDH1 and catalytic IDH2 subunits.	NAD	6-12	isocitrate dehydrogenase (NAD(+)) IDH2	Saccharomyces cerevisiae S288C	139-143
20844277-1	2011	Human sirtuin (SIRT) 1 and SIRT2, which possess nicotinamide adenosine dinucleotide (NAD(+))-dependent deacetylase activity, exhibit anti-inflammatory actions.	NAD	85-91	sirtuin 1	Homo sapiens	6-22
21126600-3	2011	In the present study, the GPD1 gene, encoding NAD+-dependent glycerol-3-phosphate dehydrogenase in an industrial ethanol producing strain of S. cerevisiae, was deleted.	NAD	46-49	glycerol-3-phosphate dehydrogenase (NAD(+)) GPD1	Saccharomyces cerevisiae S288C	26-30
21980421-4	2011	Kinetic data demonstrated that the S346K/K347Y/K362Q c-NADP-ME was transformed into a debilitated NAD+-utilizing enzyme, as shown by a severe decrease in catalytic efficiency using NADP+ as the cofactor without a significant increase in catalysis using NAD+ as the cofactor.	NAD	98-102	malic enzyme 1	Homo sapiens	55-62
21980421-4	2011	Kinetic data demonstrated that the S346K/K347Y/K362Q c-NADP-ME was transformed into a debilitated NAD+-utilizing enzyme, as shown by a severe decrease in catalytic efficiency using NADP+ as the cofactor without a significant increase in catalysis using NAD+ as the cofactor.	NAD	253-257	malic enzyme 1	Homo sapiens	55-62
21980421-11	2011	Here, we demonstrate that a series of E314A-containing c-NADP-ME quadruple mutants have been changed to NAD+-utilizing enzymes by abrogating NADP+ binding and increasing NAD+ binding.	NAD	104-108	malic enzyme 1	Homo sapiens	57-64
21980421-11	2011	Here, we demonstrate that a series of E314A-containing c-NADP-ME quadruple mutants have been changed to NAD+-utilizing enzymes by abrogating NADP+ binding and increasing NAD+ binding.	NAD	170-174	malic enzyme 1	Homo sapiens	57-64
21637345-4	2011	Here, using tandem affinity purification (TAP) screening, we have identified an NAD-dependent deacetylase in mycobacteria which is a homologue of the eukaryotic Sir2 protein and interacts directly with Ku.	NAD	80-83	sirtuin 1	Homo sapiens	161-165
22163924-1	2011	The effects of different aluminum species on malate dehydrogenase (MDH) activity were investigated by monitoring amperometric i-t curves for the oxidation of NADH at low overpotential using a functionalized multi-wall nanotube (MWNT) modified glass carbon electrode (GCE).	NAD	158-162	malic enzyme 1	Homo sapiens	45-65
22163924-1	2011	The effects of different aluminum species on malate dehydrogenase (MDH) activity were investigated by monitoring amperometric i-t curves for the oxidation of NADH at low overpotential using a functionalized multi-wall nanotube (MWNT) modified glass carbon electrode (GCE).	NAD	158-162	malic enzyme 1	Homo sapiens	67-70
20818429-0	2010	Redox-dependent Brca1 transcriptional regulation by an NADH-sensor CtBP1.	NAD	55-59	BRCA1 DNA repair associated	Homo sapiens	16-21
20818429-4	2010	Additionally, the recruitment of CtBP1 to the Brca1 promoter is redox-dependent, that is, increased at high NADH levels in hypoxic conditions.	NAD	108-112	BRCA1 DNA repair associated	Homo sapiens	46-51
20818429-6	2010	Pharmacological disruption of CtBP1 binding to Brca1 promoter by the antioxidant Tempol, which reduces NADH levels, relieved CtBP1-mediated repression of Brca1, leading to increased DNA repair in HNSCC cells.	NAD	103-107	BRCA1 DNA repair associated	Homo sapiens	47-52
20818429-6	2010	Pharmacological disruption of CtBP1 binding to Brca1 promoter by the antioxidant Tempol, which reduces NADH levels, relieved CtBP1-mediated repression of Brca1, leading to increased DNA repair in HNSCC cells.	NAD	103-107	BRCA1 DNA repair associated	Homo sapiens	154-159
20818429-7	2010	As tumor cells are generally hypoxic with increased NADH levels, the dynamic control of Brca1 by a "metabolic switch" found in this study not only provides an important link between tumor metabolism and tumor suppressor expression but also suggests a potential chemo preventative or therapeutic strategy for HNSCC by blocking NADH-dependent CtBP1 activity at early stages of HNSCC carcinogenesis.	NAD	52-56	BRCA1 DNA repair associated	Homo sapiens	88-93
20818429-7	2010	As tumor cells are generally hypoxic with increased NADH levels, the dynamic control of Brca1 by a "metabolic switch" found in this study not only provides an important link between tumor metabolism and tumor suppressor expression but also suggests a potential chemo preventative or therapeutic strategy for HNSCC by blocking NADH-dependent CtBP1 activity at early stages of HNSCC carcinogenesis.	NAD	326-330	BRCA1 DNA repair associated	Homo sapiens	88-93
21106760-2	2010	Nicotinamide adenine dinucleotide (NAD)-dependent proteins such as poly(ADP ribose) polymerases (PARPs) and sirtuin deacetylases play important roles in this regulation, thus NAD provides a crucial link between metabolism and these cellular signaling processes.	NAD	0-33	poly (ADP-ribose) polymerase family, member 1	Mus musculus	97-102
21106760-2	2010	Nicotinamide adenine dinucleotide (NAD)-dependent proteins such as poly(ADP ribose) polymerases (PARPs) and sirtuin deacetylases play important roles in this regulation, thus NAD provides a crucial link between metabolism and these cellular signaling processes.	NAD	35-38	poly (ADP-ribose) polymerase family, member 1	Mus musculus	97-102
21106760-2	2010	Nicotinamide adenine dinucleotide (NAD)-dependent proteins such as poly(ADP ribose) polymerases (PARPs) and sirtuin deacetylases play important roles in this regulation, thus NAD provides a crucial link between metabolism and these cellular signaling processes.	NAD	175-178	poly (ADP-ribose) polymerase family, member 1	Mus musculus	97-102
20149622-1	2010	Mitochondrial malate dehydrogenase (mMDH) from the intestine is the NAD-linked oxidoreductase of the tricarboxylic acid cycle with the highest activity and response to vitamin D treatment in vitamin D-deficient chicks (-D).	NAD	68-71	malate dehydrogenase 2, NAD (mitochondrial)	Mus musculus	36-40
20975043-4	2010	Moreover, lower T reg cell numbers are found in mice deficient for the NAD-hydrolase CD38 than in wild-type, P2X7-deficient, or ART2-deficient mice, indicating a role for extracellular NAD(+) in T reg cell homeostasis.	NAD	185-191	CD38 antigen	Mus musculus	85-89
20645413-2	2010	Extracellularly applied NAD(+) prevents astrocyte death caused by excessive activation of poly(ADP-ribose) polymerase-1, of which the molecular mechanism has not been fully elucidated.	NAD	24-30	poly (ADP-ribose) polymerase family, member 1	Mus musculus	90-119
20975832-1	2010	BACKGROUND: The NAD-dependent deacetylase SIRT1 is a nutrient-sensitive coordinator of stress-tolerance, multiple homeostatic processes and healthspan, while p53 is a stress-responsive transcription factor and our paramount tumour suppressor.	NAD	16-19	sirtuin 1	Homo sapiens	42-47
20699658-2	2010	Recently, 15-hydroxyprostaglandin dehydrogenase [NAD+] (15-PGDH), the key enzyme in prostaglandin degradation, was found to be down-regulated in human gastric cancer tissues, but little is known about its role in gastric tumorigenesis.	NAD	49-53	carbonyl reductase 1	Homo sapiens	10-47
20601277-3	2010	In this regard, one area of major interest concerns the effects of RESV on the activity of sirtuin 1 (SIRT1), an NAD(+)-dependent histone deacetylase that has been implicated in aging.	NAD	113-119	sirtuin 1	Homo sapiens	91-100
20601277-3	2010	In this regard, one area of major interest concerns the effects of RESV on the activity of sirtuin 1 (SIRT1), an NAD(+)-dependent histone deacetylase that has been implicated in aging.	NAD	113-119	sirtuin 1	Homo sapiens	102-107
20943487-1	2010	SIRT1 is an NAD+-dependent deacetylase in mammalian cells and plays important roles in senescence, cell death and tumorigenesis.	NAD	12-15	sirtuin 1	Homo sapiens	0-5
20561255-4	2010	Prolonged ABA treatment increased the expression of the cox2 gene in complex IV and nad genes in complex I to a higher level than no ABA treatment in the wild type, but only to a moderate level in abo5, probably because abo5 already expressed high levels of mitochondrial-encoded cox2 and nad genes under no ABA treatment.	NAD	289-292	ABA Overly-Sensitive 5	Arabidopsis thaliana	220-224
20631301-1	2010	The longevity-promoting NAD+-dependent class III histone deacetylase Sirtuin 1 (SIRT1) is involved in stem cell function by controlling cell fate decision and/or by regulating the p53-dependent expression of NANOG.	NAD	24-28	sirtuin 1	Homo sapiens	69-78
20631301-1	2010	The longevity-promoting NAD+-dependent class III histone deacetylase Sirtuin 1 (SIRT1) is involved in stem cell function by controlling cell fate decision and/or by regulating the p53-dependent expression of NANOG.	NAD	24-28	sirtuin 1	Homo sapiens	80-85
20631301-1	2010	The longevity-promoting NAD+-dependent class III histone deacetylase Sirtuin 1 (SIRT1) is involved in stem cell function by controlling cell fate decision and/or by regulating the p53-dependent expression of NANOG.	NAD	24-28	Nanog homeobox	Homo sapiens	208-213
20413424-2	2010	Furthermore, because sirtuins require NAD for their deacetylase activity, nicotinamide phosphoribosyltransferase (Nampt), which is a rate-limiting enzyme in the intracellular NAD biosynthetic pathway, influences their activity.	NAD	38-41	nicotinamide phosphoribosyltransferase	Rattus norvegicus	74-112
20413424-2	2010	Furthermore, because sirtuins require NAD for their deacetylase activity, nicotinamide phosphoribosyltransferase (Nampt), which is a rate-limiting enzyme in the intracellular NAD biosynthetic pathway, influences their activity.	NAD	38-41	nicotinamide phosphoribosyltransferase	Rattus norvegicus	114-119
20660252-2	2010	The mammalian nicotinamide-adenine dinucleotide-dependent deacetylase SIRT1 impacts different processes potentially involved in the maintenance of brain integrity, such as chromatin remodeling, DNA repair, cell survival, and neurogenesis.	NAD	14-47	sirtuin 1	Homo sapiens	70-75
20335317-9	2010	The pcDNA3.1-RSOR/MIOX transfectants had an increased NADH/NAD(+) ratio, PKC and TGF-beta activity, Raf1:Ras association, and p-ERK phosphorylation.	NAD	54-58	myo-inositol oxygenase	Mus musculus	13-17
20335317-9	2010	The pcDNA3.1-RSOR/MIOX transfectants had an increased NADH/NAD(+) ratio, PKC and TGF-beta activity, Raf1:Ras association, and p-ERK phosphorylation.	NAD	54-58	myo-inositol oxygenase	Mus musculus	18-22
20335317-9	2010	The pcDNA3.1-RSOR/MIOX transfectants had an increased NADH/NAD(+) ratio, PKC and TGF-beta activity, Raf1:Ras association, and p-ERK phosphorylation.	NAD	59-65	myo-inositol oxygenase	Mus musculus	13-17
20335317-9	2010	The pcDNA3.1-RSOR/MIOX transfectants had an increased NADH/NAD(+) ratio, PKC and TGF-beta activity, Raf1:Ras association, and p-ERK phosphorylation.	NAD	59-65	myo-inositol oxygenase	Mus musculus	18-22
20445064-7	2010	More specifically, the mouse Wld(S) (Wallerian degeneration slow) protein, which is mainly composed of the full-length sequence of the NAD(+) biosynthetic Nmnat1 enzyme, can suppress dendritic pruning in C4da (class IV dendritic arborization) sensory neurons in parallel to the fly effector caspases.	NAD	135-141	nicotinamide nucleotide adenylyltransferase 1	Mus musculus	155-161
19908284-1	2010	The mitochondrial aspartate-glutamate carriers (AGC) aralar (SLC25A12) and citrin (SLC25A13) are components of the malate aspartate shuttle (MAS), a major intracellular pathway to transfer reducing equivalents from NADH to the mitochondrial matrix.	NAD	215-219	solute carrier family 25 (mitochondrial carrier, Aralar), member 12	Mus musculus	61-69
20375713-1	2010	The DNA-damaging agent N-methyl-N"-nitro-N-nitrosoguanidine (MNNG) causes cardiomyocyte death as a result of energy loss from excessive activation of poly-(ADP) ribose polymerase-1 (PARP-1) resulting in depletion of its substrates nicotinamide adenine dinucleotide (NAD) and ATP.	NAD	231-264	poly (ADP-ribose) polymerase family, member 1	Mus musculus	150-180
20375713-1	2010	The DNA-damaging agent N-methyl-N"-nitro-N-nitrosoguanidine (MNNG) causes cardiomyocyte death as a result of energy loss from excessive activation of poly-(ADP) ribose polymerase-1 (PARP-1) resulting in depletion of its substrates nicotinamide adenine dinucleotide (NAD) and ATP.	NAD	231-264	poly (ADP-ribose) polymerase family, member 1	Mus musculus	182-188
20375713-1	2010	The DNA-damaging agent N-methyl-N"-nitro-N-nitrosoguanidine (MNNG) causes cardiomyocyte death as a result of energy loss from excessive activation of poly-(ADP) ribose polymerase-1 (PARP-1) resulting in depletion of its substrates nicotinamide adenine dinucleotide (NAD) and ATP.	NAD	266-269	poly (ADP-ribose) polymerase family, member 1	Mus musculus	150-180
20375713-1	2010	The DNA-damaging agent N-methyl-N"-nitro-N-nitrosoguanidine (MNNG) causes cardiomyocyte death as a result of energy loss from excessive activation of poly-(ADP) ribose polymerase-1 (PARP-1) resulting in depletion of its substrates nicotinamide adenine dinucleotide (NAD) and ATP.	NAD	266-269	poly (ADP-ribose) polymerase family, member 1	Mus musculus	182-188
20174634-6	2010	CONCLUSIONS/SIGNIFICANCE: Our structural data suggest that a deletion of three amino acids in E. coli SSADH permits this enzyme to use NADP+, whereas in contrast the human enzyme utilises NAD+.	NAD	188-192	aldehyde dehydrogenase 5 family member A1	Homo sapiens	102-107
19928762-8	2010	Moreover, we also found that AMPK activity mediated by resveratrol in cancer cells was due to inducing the expression of Sirtuin type 1 (SIRT1) via elevation in the cellular NAD(+)/NADH in ER-positive cells.	NAD	174-180	sirtuin 1	Homo sapiens	121-135
19928762-8	2010	Moreover, we also found that AMPK activity mediated by resveratrol in cancer cells was due to inducing the expression of Sirtuin type 1 (SIRT1) via elevation in the cellular NAD(+)/NADH in ER-positive cells.	NAD	174-180	sirtuin 1	Homo sapiens	137-142
19928762-8	2010	Moreover, we also found that AMPK activity mediated by resveratrol in cancer cells was due to inducing the expression of Sirtuin type 1 (SIRT1) via elevation in the cellular NAD(+)/NADH in ER-positive cells.	NAD	181-185	sirtuin 1	Homo sapiens	121-135
19928762-8	2010	Moreover, we also found that AMPK activity mediated by resveratrol in cancer cells was due to inducing the expression of Sirtuin type 1 (SIRT1) via elevation in the cellular NAD(+)/NADH in ER-positive cells.	NAD	181-185	sirtuin 1	Homo sapiens	137-142
20014444-9	2010	This possibility was assessed using an NAD(+) binding assay, which showed that nitrated GAPDH was incapable of binding NAD(+).	NAD	39-45	glyceraldehyde-3-phosphate dehydrogenase	Oryctolagus cuniculus	88-93
19727706-8	2010	Glycerol is produced to dispose excess cytosolic reduced nicotinamide adenine dinucleotide (NADH), and the regulating step in the pathway is mediated by glycerol 3-phosphate dehydrogenase (encoded by GPD1 and GPD2 genes).	NAD	57-90	glycerol-3-phosphate dehydrogenase (NAD(+)) GPD1	Saccharomyces cerevisiae S288C	200-204
19727706-8	2010	Glycerol is produced to dispose excess cytosolic reduced nicotinamide adenine dinucleotide (NADH), and the regulating step in the pathway is mediated by glycerol 3-phosphate dehydrogenase (encoded by GPD1 and GPD2 genes).	NAD	92-96	glycerol-3-phosphate dehydrogenase (NAD(+)) GPD1	Saccharomyces cerevisiae S288C	200-204
20834177-1	2010	The effect of NADH on melanogenesis under aerobic conditions involves three types of reaction: (a) acting as tyrosinase substrate (a competitive substrate of L-tyrosine and L-DOPA), (b) irreversible inactivation acting as a suicide substrate of tyrosinase, and (c) non-enzymatic reduction of o-dopaquinone by NADH.	NAD	14-18	tyrosinase	Homo sapiens	109-119
20834177-1	2010	The effect of NADH on melanogenesis under aerobic conditions involves three types of reaction: (a) acting as tyrosinase substrate (a competitive substrate of L-tyrosine and L-DOPA), (b) irreversible inactivation acting as a suicide substrate of tyrosinase, and (c) non-enzymatic reduction of o-dopaquinone by NADH.	NAD	14-18	tyrosinase	Homo sapiens	245-255
20834177-2	2010	Under anaerobic conditions, NADH irreversibly inhibits the enzymatic forms met-tyrosinase and deoxy-tyrosinase.	NAD	28-32	tyrosinase	Homo sapiens	79-89
20834177-2	2010	Under anaerobic conditions, NADH irreversibly inhibits the enzymatic forms met-tyrosinase and deoxy-tyrosinase.	NAD	28-32	tyrosinase	Homo sapiens	100-110
20160399-1	2010	NAD-dependent deacetylase SIRT1 is known to be activated by caloric restriction and is related to longevity.	NAD	0-3	sirtuin 1	Homo sapiens	26-31
19929131-2	2010	Recently, it was found that visfatin is identical with the Nampt (nicotinamide phosphoribosyltransferase) gene that codes for an intra- and extracellular NAD biosynthetic enzyme and is predominantly expressed outside the adipose tissue.	NAD	154-157	nicotinamide phosphoribosyltransferase	Rattus norvegicus	28-36
19929131-2	2010	Recently, it was found that visfatin is identical with the Nampt (nicotinamide phosphoribosyltransferase) gene that codes for an intra- and extracellular NAD biosynthetic enzyme and is predominantly expressed outside the adipose tissue.	NAD	154-157	nicotinamide phosphoribosyltransferase	Rattus norvegicus	59-64
19929131-2	2010	Recently, it was found that visfatin is identical with the Nampt (nicotinamide phosphoribosyltransferase) gene that codes for an intra- and extracellular NAD biosynthetic enzyme and is predominantly expressed outside the adipose tissue.	NAD	154-157	nicotinamide phosphoribosyltransferase	Rattus norvegicus	66-104
19929131-6	2010	RNAi-mediated downregulation of visfatin expression in Fao cells was associated with significantly reduced NAD biosynthesis (0.3+/-0.01 vs. 0.5+/-0.01 mmol/h/g, P&lt;0.05) and with significantly decreased incremental glucose uptake after stimulation with insulin when compared to controls with normal expression of visfatin (0.6+/-0.2 vs. 2.2+/-0.5 nnmol/g/2 h, P=0.02).	NAD	107-110	nicotinamide phosphoribosyltransferase	Rattus norvegicus	32-40
19929131-7	2010	These results provide evidence that visfatin exhibits important autocrine effects on sensitivity of liver cells to insulin action possibly through its effects on NAD biosynthesis.	NAD	162-165	nicotinamide phosphoribosyltransferase	Rattus norvegicus	36-44
19895790-1	2009	Sirt1 appear to be NAD(+)-dependent deacetylase that deacetylates histones and several non-histone proteins.	NAD	19-25	sirtuin 1	Homo sapiens	0-5
19729610-6	2009	Mice treated with the ERbeta-specific agonist, DPN had no effect on uterine weight but a 28% decrease in aortic lesion area in HSP27(o/e)apoE(-/-) compared to apoE(-/-) mice.	NAD	47-50	heat shock protein 1	Mus musculus	127-132
19729610-7	2009	HSP27 serum levels showed a similar gradual increase with E2 and DPN replacement treatment but did not change in untreated mice.	NAD	65-68	heat shock protein 1	Mus musculus	0-5
19745168-2	2009	GPD1-L has &gt;80% amino acid homology with glycerol-3-phosphate dehydrogenase, which is involved in NAD-dependent energy metabolism.	NAD	101-104	glycerol-3-phosphate dehydrogenase 1-like	Mus musculus	0-6
19745168-6	2009	A280V GPD1-L caused a 2.48+/-0.17-fold increase in intracellular NADH level (P&lt;0.001).	NAD	65-69	glycerol-3-phosphate dehydrogenase 1-like	Mus musculus	6-12
19745168-7	2009	NADH application or cotransfection with A280V GPD1-L resulted in decreased I(Na) (0.48+/-0.09 or 0.19+/-0.04 of control group, respectively; P&lt;0.01), which was reversed by NAD+, chelerythrine, or superoxide dismutase.	NAD	175-179	glycerol-3-phosphate dehydrogenase 1-like	Mus musculus	46-52
19745168-8	2009	NAD+ antagonism of the Na+ channel downregulation by A280V GPD1-L or NADH was prevented by a protein kinase (PK)A inhibitor, PKAI(6-22).	NAD	0-4	glycerol-3-phosphate dehydrogenase 1-like	Mus musculus	59-65
19745168-11	2009	Extracellular application of NAD+ to SCN5A(+/-) mouse hearts ameliorated the risk of ventricular tachycardia.	NAD	29-33	sodium channel, voltage-gated, type V, alpha	Mus musculus	37-42
19745168-15	2009	Mutations of GPD1-L may downregulate Na(v)1.5 by altering the oxidized to reduced NAD(H) balance.	NAD	82-88	glycerol-3-phosphate dehydrogenase 1-like	Mus musculus	13-19
19745168-15	2009	Mutations of GPD1-L may downregulate Na(v)1.5 by altering the oxidized to reduced NAD(H) balance.	NAD	82-88	sodium channel, voltage-gated, type V, alpha	Mus musculus	37-45
19502564-7	2009	We also found that HDAC inhibitors decreased cellular PMET activity and that a selective inhibition of PMET activity with extracellular NADH induced a robust Hsp70 surface expression.	NAD	136-140	heat shock protein family A (Hsp70) member 4	Homo sapiens	158-163
19656905-2	2009	Levels of NADH and ADP-Rib were decreased in the Pro(35S):AtNUDX7 plants but increased in the KO-nudx7 plants under normal conditions and oxidative stress compared with the control plants, indicating that AtNUDX7 hydrolyzes both ADP-Rib and NADH as physiological substrates.	NAD	10-14	MutT/nudix family protein	Arabidopsis thaliana	58-65
19656905-2	2009	Levels of NADH and ADP-Rib were decreased in the Pro(35S):AtNUDX7 plants but increased in the KO-nudx7 plants under normal conditions and oxidative stress compared with the control plants, indicating that AtNUDX7 hydrolyzes both ADP-Rib and NADH as physiological substrates.	NAD	10-14	MutT/nudix family protein	Arabidopsis thaliana	97-102
19656905-5	2009	Depletion of NAD(+) and ATP resulting from the activation of the PAR reaction under oxidative stress was completely suppressed in the Pro(35S):AtNUDX7 plants.	NAD	13-19	MutT/nudix family protein	Arabidopsis thaliana	143-150
19656905-6	2009	Accumulation of NAD(+) and ATP was observed in the KO-nudx7- and 3-aminobenzamide-treated plants, in which the PAR reaction was suppressed.	NAD	16-22	MutT/nudix family protein	Arabidopsis thaliana	54-59
19656905-8	2009	These findings suggest that AtNUDX7 controls the balance between NADH and NAD(+) by NADH turnover under normal conditions.	NAD	65-69	MutT/nudix family protein	Arabidopsis thaliana	28-35
19656905-8	2009	These findings suggest that AtNUDX7 controls the balance between NADH and NAD(+) by NADH turnover under normal conditions.	NAD	74-80	MutT/nudix family protein	Arabidopsis thaliana	28-35
19656905-8	2009	These findings suggest that AtNUDX7 controls the balance between NADH and NAD(+) by NADH turnover under normal conditions.	NAD	84-88	MutT/nudix family protein	Arabidopsis thaliana	28-35
19656905-9	2009	Under oxidative stress, AtNUDX7 serves to maintain NAD(+) levels by supplying ATP via nucleotide recycling from free ADP-Rib molecules and thus regulates the defense mechanisms against oxidative DNA damage via modulation of the PAR reaction.	NAD	51-57	MutT/nudix family protein	Arabidopsis thaliana	24-31
19439501-3	2009	SIRT1, a nicotinamide adenine dinucleotide (NAD(+))-dependent sirtuin, has been shown to promote cell survival by inhibiting apoptosis or cellular senescence in mammalian cells.	NAD	9-42	sirtuin 1	Homo sapiens	0-5
19439501-3	2009	SIRT1, a nicotinamide adenine dinucleotide (NAD(+))-dependent sirtuin, has been shown to promote cell survival by inhibiting apoptosis or cellular senescence in mammalian cells.	NAD	44-51	sirtuin 1	Homo sapiens	0-5
18681908-1	2009	SIRT1 is a member of a highly conserved gene family (sirtuins) encoding nicotinamide adenine dinucleotide (NAD)(+)-dependent deacetylases, originally found to deacetylate histones leading to increased DNA stability and prolonged survival in yeast and higher organisms, including mammals.	NAD	72-105	sirtuin 1	Homo sapiens	0-5
18681908-1	2009	SIRT1 is a member of a highly conserved gene family (sirtuins) encoding nicotinamide adenine dinucleotide (NAD)(+)-dependent deacetylases, originally found to deacetylate histones leading to increased DNA stability and prolonged survival in yeast and higher organisms, including mammals.	NAD	107-110	sirtuin 1	Homo sapiens	0-5
19703305-9	2009	Notably, CRP* expression in the presence of glucose results in an elevated intracellular NADPH concentration and reduced NADH concentration relative to wild-type CRP.	NAD	121-125	catabolite gene activator protein	Escherichia coli	9-13
19703305-9	2009	Notably, CRP* expression in the presence of glucose results in an elevated intracellular NADPH concentration and reduced NADH concentration relative to wild-type CRP.	NAD	121-125	catabolite gene activator protein	Escherichia coli	9-12
19474721-1	2009	PURPOSE OF REVIEW: This review aims to summarize the importance of the mammalian nicotinamide adenine dinucleotide (NAD)-dependent deacetylase SIRT1 as a critical mediator that coordinates metabolic responses to caloric restriction and the recent progress in the development of SIRT1-targeted caloric restriction mimetics.	NAD	81-114	sirtuin 1	Homo sapiens	143-148
19474721-1	2009	PURPOSE OF REVIEW: This review aims to summarize the importance of the mammalian nicotinamide adenine dinucleotide (NAD)-dependent deacetylase SIRT1 as a critical mediator that coordinates metabolic responses to caloric restriction and the recent progress in the development of SIRT1-targeted caloric restriction mimetics.	NAD	81-114	sirtuin 1	Homo sapiens	278-283
19474721-1	2009	PURPOSE OF REVIEW: This review aims to summarize the importance of the mammalian nicotinamide adenine dinucleotide (NAD)-dependent deacetylase SIRT1 as a critical mediator that coordinates metabolic responses to caloric restriction and the recent progress in the development of SIRT1-targeted caloric restriction mimetics.	NAD	116-119	sirtuin 1	Homo sapiens	143-148
19474721-1	2009	PURPOSE OF REVIEW: This review aims to summarize the importance of the mammalian nicotinamide adenine dinucleotide (NAD)-dependent deacetylase SIRT1 as a critical mediator that coordinates metabolic responses to caloric restriction and the recent progress in the development of SIRT1-targeted caloric restriction mimetics.	NAD	116-119	sirtuin 1	Homo sapiens	278-283
19408950-0	2009	SAR studies for a new class of antibacterial NAD biosynthesis inhibitors.	NAD	45-48	sarcosine dehydrogenase	Homo sapiens	0-3
19351806-2	2009	Visfatin, a NAD biosynthetic enzyme, regulates the activity of the cellular survival factor, Sirt1.	NAD	12-15	sirtuin 1	Homo sapiens	93-98
19484146-7	2009	In cells, the decrease in FDG uptake was shown to correlate with changes in plasma membrane expression of the facilitative glucose transporters, whereas the decrease in pyruvate to lactate flux could be explained by an increase in poly(ADP-ribose) polymerase activity and subsequent depletion of the NAD(H) pool.	NAD	300-306	poly (ADP-ribose) polymerase family, member 1	Mus musculus	231-258
19217932-4	2009	Increased NAD(P)H fluorescence in CA1 neurons during hypoxia and demonstration that NADH manipulation increases [Ca2+](i) in an IP3R-dependent manner revealed a primary role of cellular redox state in liberation of Ca2+ from the ER.	NAD	84-88	inositol 1,4,5-trisphosphate receptor, type 1	Rattus norvegicus	128-132
19441923-1	2009	BACKGROUND: Sirtuin 1-7 (SIRT1-7) are deacetylases that are dependent on NAD(+) for their activity.	NAD	73-79	sirtuin 1	Homo sapiens	12-23
19441923-1	2009	BACKGROUND: Sirtuin 1-7 (SIRT1-7) are deacetylases that are dependent on NAD(+) for their activity.	NAD	73-79	sirtuin 1	Homo sapiens	25-32
18351441-6	2009	Furthermore, we found that the recombinant protein GST-LDHAL6A can catalyze the pyruvate convert into the lactate with NADH as its coenzyme.	NAD	119-123	lactate dehydrogenase A like 6A	Homo sapiens	55-62
19188449-1	2009	The NAD(+)-dependent histone deacetylase hSirT1 regulates cell survival and stress responses by inhibiting p53-, NF-kappaB-, and E2F1-dependent transcription.	NAD	4-10	sirtuin 1	Homo sapiens	41-47
19188449-6	2009	In cells exposed to apoptotic DNA damage, nuclear NAD(+) levels decrease and inactivate hSirT1 without altering the hSirT1 interaction with PCAF and hSirT1 binding to the P1p73 promoter.	NAD	50-56	sirtuin 1	Homo sapiens	88-94
19188449-7	2009	The reactivation of hSirT1 by pyruvate that increases the [NAD(+)]/[NADH] ratio completely abolished the DNA damage-induced activation of TAp73 expression, thus linking the modulation of chromatin-bound hSirT1 deacetylase activity by the intracellular redox state with P1p73 promoter activity.	NAD	59-65	sirtuin 1	Homo sapiens	20-26
19188449-7	2009	The reactivation of hSirT1 by pyruvate that increases the [NAD(+)]/[NADH] ratio completely abolished the DNA damage-induced activation of TAp73 expression, thus linking the modulation of chromatin-bound hSirT1 deacetylase activity by the intracellular redox state with P1p73 promoter activity.	NAD	68-72	sirtuin 1	Homo sapiens	20-26
19441904-1	2009	BACKGROUND: The sirtuin family of deacetylase enzymes comprises seven proteins (SIRT1-7) that are dependent on NAD(+) for their activity.	NAD	111-117	sirtuin 1	Homo sapiens	80-87
19103747-1	2009	SIRT1 is a prominent member of a family of NAD(+)-dependent enzymes and affects a variety of cellular functions ranging from gene silencing, regulation of the cell cycle and apoptosis, to energy homeostasis.	NAD	43-49	sirtuin 1	Homo sapiens	0-5
19217406-7	2009	Additionally, a byproduct of Sir2-mediated NAD hydrolysis, O-acetyl-ADP-ribose, increases the efficiency with which Sir3 and Sir2-3-4 bind nucleosomes.	NAD	43-46	chromatin-silencing protein SIR3	Saccharomyces cerevisiae S288C	116-120
19217406-7	2009	Additionally, a byproduct of Sir2-mediated NAD hydrolysis, O-acetyl-ADP-ribose, increases the efficiency with which Sir3 and Sir2-3-4 bind nucleosomes.	NAD	43-46	chromatin-silencing protein SIR3	Saccharomyces cerevisiae S288C	125-131
19060927-1	2009	Sirtuin 1 (Sirt1) and Sirtuin 2 (Sirt2) belong to the family of NAD+ (nicotinamide adenine dinucleotide-positive)-dependent class III histone deacetylases and are involved in regulating lifespan.	NAD	64-68	sirtuin 1	Homo sapiens	0-9
19060927-1	2009	Sirtuin 1 (Sirt1) and Sirtuin 2 (Sirt2) belong to the family of NAD+ (nicotinamide adenine dinucleotide-positive)-dependent class III histone deacetylases and are involved in regulating lifespan.	NAD	64-68	sirtuin 1	Homo sapiens	11-16
19060927-1	2009	Sirtuin 1 (Sirt1) and Sirtuin 2 (Sirt2) belong to the family of NAD+ (nicotinamide adenine dinucleotide-positive)-dependent class III histone deacetylases and are involved in regulating lifespan.	NAD	70-103	sirtuin 1	Homo sapiens	0-9
19060927-1	2009	Sirtuin 1 (Sirt1) and Sirtuin 2 (Sirt2) belong to the family of NAD+ (nicotinamide adenine dinucleotide-positive)-dependent class III histone deacetylases and are involved in regulating lifespan.	NAD	70-103	sirtuin 1	Homo sapiens	11-16
19164523-0	2009	The conserved NAD(H)-dependent corepressor CTBP-1 regulates Caenorhabditis elegans life span.	NAD	14-20	C-terminal-binding protein 1	Caenorhabditis elegans	43-49
19164523-3	2009	Here, we report that genetic inactivation of the Caenorhabditis elegans homolog, ctbp-1, results in life span extension, which is suppressed by reintroduction of the ctbp-1 genomic DNA encoding wild-type but not NAD(H)-binding defective CTBP-1 protein.	NAD	212-218	C-terminal-binding protein 1	Caenorhabditis elegans	81-87
19164523-3	2009	Here, we report that genetic inactivation of the Caenorhabditis elegans homolog, ctbp-1, results in life span extension, which is suppressed by reintroduction of the ctbp-1 genomic DNA encoding wild-type but not NAD(H)-binding defective CTBP-1 protein.	NAD	212-218	C-terminal-binding protein 1	Caenorhabditis elegans	166-172
19018525-1	2009	The two homologous genes GPD1 and GPD2, encoding two isoenzymes of NAD(+)-dependent glycerol-3-phosphate dehydrogenase in industrial yeast Saccharomyces cerevisiae CICIMY0086, had been deleted.	NAD	67-73	glycerol-3-phosphate dehydrogenase (NAD(+)) GPD1	Saccharomyces cerevisiae S288C	25-29
19182797-0	2009	NAMPT is essential for the G-CSF-induced myeloid differentiation via a NAD(+)-sirtuin-1-dependent pathway.	NAD	71-77	sirtuin 1	Homo sapiens	78-87
19182797-5	2009	The molecular events triggered by NAMPT include NAD(+)-dependent sirtuin-1 activation, subsequent induction of CCAAT/enhancer binding protein-alpha and CCAAT/enhancer binding protein-beta, and, ultimately, upregulation of G-CSF synthesis and G-CSF receptor expression.	NAD	48-54	sirtuin 1	Homo sapiens	65-74
19113843-1	2009	The logic network composed of three enzymes (alcohol dehydrogenase, glucose dehydrogenase, and glucose oxidase) operating in concert as four concatenated logic gates (AND/OR), was designed to process four different chemical input signals (NADH, acetaldehyde, glucose, and oxygen).	NAD	239-243	aldo-keto reductase family 1 member A1	Homo sapiens	45-66
19035664-3	2009	The decrease in oxaloacetic acid was coupled to NADH formation by malate dehydrogenase, which allowed the rates of both initial carbinolamine formation (as part of the imination step) and decarboxylation to be determined.	NAD	48-52	malic enzyme 1	Homo sapiens	66-86
19117466-5	2009	The new composite electrode showed good activity toward hydrogen peroxide and NADH, with the possibility of fabricating a sensitive biosensor for glucose and alcohol using glucose oxidase and alcohol dehydrogenase, respectively, by simply incorporating the specific enzyme within the composite matrix.	NAD	78-82	aldo-keto reductase family 1 member A1	Homo sapiens	192-213
19273250-2	2009	For the past several years, studies on the mammalian NAD-dependent protein deacetylase SIRT1 and systemic NAD biosynthesis mediated by nicotinamide phosphoribosyltransferase (NAMPT) have demonstrated that these two regulatory components together play a critical role in the regulation of glucose homeostasis, particularly in the regulation of glucose-stimulated insulin secretion in pancreatic beta cells.	NAD	53-56	sirtuin 1	Homo sapiens	87-92
19053786-0	2009	NAD(+)/NADH-sensitive quantum dots: applications to probe NAD(+)-dependent enzymes and to sense the RDX explosive.	NAD	0-6	radixin	Homo sapiens	100-103
19053786-0	2009	NAD(+)/NADH-sensitive quantum dots: applications to probe NAD(+)-dependent enzymes and to sense the RDX explosive.	NAD	7-11	radixin	Homo sapiens	100-103
19053786-5	2009	The NADH-functionalized QDs were used for the optical analysis of the 1,3,5-trinitrotriazine, RDX explosive, with a detection limit that corresponded to 1 x 10(-10) M. We demonstrate cooperative optical and catalytic functions of the core-shell components of the QDs in the analysis of RDX.	NAD	4-8	radixin	Homo sapiens	94-97
19053786-5	2009	The NADH-functionalized QDs were used for the optical analysis of the 1,3,5-trinitrotriazine, RDX explosive, with a detection limit that corresponded to 1 x 10(-10) M. We demonstrate cooperative optical and catalytic functions of the core-shell components of the QDs in the analysis of RDX.	NAD	4-8	radixin	Homo sapiens	286-289
19017485-3	2008	SIRT1 (the mammalian Sir2), which has NAD(+)-dependent class III histone deacetylase activity, may be a key gene linking the modulation of cancer and aging.	NAD	38-44	sirtuin 1	Homo sapiens	0-5
19017485-3	2008	SIRT1 (the mammalian Sir2), which has NAD(+)-dependent class III histone deacetylase activity, may be a key gene linking the modulation of cancer and aging.	NAD	38-44	sirtuin 1	Homo sapiens	21-25
18706836-7	2008	These results suggest that the rapid recovery in the level of glutathione and the formation of metHb by BHP require NADPH and NADH consumption.	NAD	126-130	hemoglobin subunit gamma 2	Homo sapiens	95-100
18706836-10	2008	Methemoglobin reductase requires NADH as a co-factor, and oxidized form (NHADP(+)) is reduced via the glycolytic reaction catalyzed by glyceraldehyde 3-phosphate dehydrogenase.	NAD	33-37	hemoglobin subunit gamma 2	Homo sapiens	0-13
19008647-1	2008	SIRT1 is one of seven mammalian orthologs of yeast silent information regulator 2 (Sir2), and it functions as a nicotinamide adenine dinucleotide (NAD)-dependent deacetylase.	NAD	112-145	sirtuin 1	Homo sapiens	0-5
19008647-1	2008	SIRT1 is one of seven mammalian orthologs of yeast silent information regulator 2 (Sir2), and it functions as a nicotinamide adenine dinucleotide (NAD)-dependent deacetylase.	NAD	112-145	sirtuin 1	Homo sapiens	83-87
19008647-1	2008	SIRT1 is one of seven mammalian orthologs of yeast silent information regulator 2 (Sir2), and it functions as a nicotinamide adenine dinucleotide (NAD)-dependent deacetylase.	NAD	147-150	sirtuin 1	Homo sapiens	0-5
19008647-1	2008	SIRT1 is one of seven mammalian orthologs of yeast silent information regulator 2 (Sir2), and it functions as a nicotinamide adenine dinucleotide (NAD)-dependent deacetylase.	NAD	147-150	sirtuin 1	Homo sapiens	83-87
19806227-1	2008	BACKGROUND: Sirt-1 is a NAD+-dependent nuclear deacetylase of 747 residues that in mammals is involved in various important metabolic pathways, such as glucose metabolism and insulin secretion, and often works on many different metabolic substrates as a multifunctional protein.	NAD	24-28	sirtuin 1	Homo sapiens	12-18
18828915-0	2008	A genome wide analysis of the response to uncapped telomeres in budding yeast reveals a novel role for the NAD+ biosynthetic gene BNA2 in chromosome end protection.	NAD	107-111	dioxygenase BNA2	Saccharomyces cerevisiae S288C	130-134
18828915-7	2008	BNA2, required for the biosynthesis of NAD+, is highly and significantly up-regulated upon telomere uncapping in cdc13-1 strains.	NAD	39-43	dioxygenase BNA2	Saccharomyces cerevisiae S288C	0-4
18828915-8	2008	We find that deletion of BNA2 and NPT1, which is also involved in NAD+ synthesis, suppresses the temperature sensitivity of cdc13-1 strains, indicating that NAD+ metabolism may be linked to telomere end protection.	NAD	66-70	dioxygenase BNA2	Saccharomyces cerevisiae S288C	25-29
18828915-8	2008	We find that deletion of BNA2 and NPT1, which is also involved in NAD+ synthesis, suppresses the temperature sensitivity of cdc13-1 strains, indicating that NAD+ metabolism may be linked to telomere end protection.	NAD	157-161	dioxygenase BNA2	Saccharomyces cerevisiae S288C	25-29
18982432-3	2008	The NADH oxidation domain harbouring the FMN cofactor is connected via a chain of iron-sulfur clusters to the ubiquinone reduction site that is located in a large pocket formed by the PSST- and 49-kDa subunits of complex I.	NAD	4-8	NADH:ubiquinone oxidoreductase core subunit S7	Homo sapiens	184-188
18619469-2	2008	Next, Sir2/3/4 proteins propagate across these loci as histones are deacetylated by the NAD(+)-dependent histone deacetylase Sir2p, ultimately resulting in the cessation of transcription and in the loss of SET1- and DOT1-dependent methylation of histone H3 within silent chromatin.	NAD	88-94	chromatin-silencing protein SIR3	Saccharomyces cerevisiae S288C	6-12
18752667-5	2008	Given that increased levels of nicotinamide adenine dinucleotide (NAD) via deletion of CD38 have been shown to prevent high fat diet induced obesity in mice in a SIRT-1 dependent fashion we explored the possibility of directly applying NAD to zebrafish.	NAD	31-64	CD38 antigen	Mus musculus	87-91
18752667-5	2008	Given that increased levels of nicotinamide adenine dinucleotide (NAD) via deletion of CD38 have been shown to prevent high fat diet induced obesity in mice in a SIRT-1 dependent fashion we explored the possibility of directly applying NAD to zebrafish.	NAD	66-69	CD38 antigen	Mus musculus	87-91
18662537-4	2008	(2008) now demonstrate that the NAD(+)-dependent enzyme SIRT1 functions as a histone deacetylase that counteracts the activity of CLOCK.	NAD	32-38	sirtuin 1	Homo sapiens	56-61
18662546-6	2008	Given the NAD(+) dependence of SIRT1 deacetylase activity, it is likely that SIRT1 connects cellular metabolism to the circadian core clockwork circuitry.	NAD	10-16	sirtuin 1	Homo sapiens	31-36
18662546-6	2008	Given the NAD(+) dependence of SIRT1 deacetylase activity, it is likely that SIRT1 connects cellular metabolism to the circadian core clockwork circuitry.	NAD	10-16	sirtuin 1	Homo sapiens	77-82
18485895-1	2008	NAD(+)-dependent protein deacetylase Sirt1 regulates cellular apoptosis.	NAD	0-6	sirtuin 1	Homo sapiens	37-42
18485866-4	2008	They show that an altered NAD(+)/NADH ratio in response to glucose starvation regulates the silencing activity of eNoSC, a complex consisting of the NAD(+)-dependent histone deacetylase SIRT1, the histone methyltransferase SUV39H1, and a new protein called nucleomethylin (NML).	NAD	26-32	sirtuin 1	Homo sapiens	186-191
18485866-4	2008	They show that an altered NAD(+)/NADH ratio in response to glucose starvation regulates the silencing activity of eNoSC, a complex consisting of the NAD(+)-dependent histone deacetylase SIRT1, the histone methyltransferase SUV39H1, and a new protein called nucleomethylin (NML).	NAD	33-37	sirtuin 1	Homo sapiens	186-191
18485866-4	2008	They show that an altered NAD(+)/NADH ratio in response to glucose starvation regulates the silencing activity of eNoSC, a complex consisting of the NAD(+)-dependent histone deacetylase SIRT1, the histone methyltransferase SUV39H1, and a new protein called nucleomethylin (NML).	NAD	149-155	sirtuin 1	Homo sapiens	186-191
18485871-6	2008	Both SIRT1 and SUV39H1 are required for energy-dependent transcriptional repression, suggesting that a change in the NAD(+)/NADH ratio induced by reduction of energy status could activate SIRT1, leading to deacetylation of histone H3 and dimethylation at Lys9 by SUV39H1, thus establishing silent chromatin in the rDNA locus.	NAD	117-123	sirtuin 1	Homo sapiens	5-10
18485871-6	2008	Both SIRT1 and SUV39H1 are required for energy-dependent transcriptional repression, suggesting that a change in the NAD(+)/NADH ratio induced by reduction of energy status could activate SIRT1, leading to deacetylation of histone H3 and dimethylation at Lys9 by SUV39H1, thus establishing silent chromatin in the rDNA locus.	NAD	117-123	sirtuin 1	Homo sapiens	188-193
18485871-6	2008	Both SIRT1 and SUV39H1 are required for energy-dependent transcriptional repression, suggesting that a change in the NAD(+)/NADH ratio induced by reduction of energy status could activate SIRT1, leading to deacetylation of histone H3 and dimethylation at Lys9 by SUV39H1, thus establishing silent chromatin in the rDNA locus.	NAD	124-128	sirtuin 1	Homo sapiens	5-10
18485871-6	2008	Both SIRT1 and SUV39H1 are required for energy-dependent transcriptional repression, suggesting that a change in the NAD(+)/NADH ratio induced by reduction of energy status could activate SIRT1, leading to deacetylation of histone H3 and dimethylation at Lys9 by SUV39H1, thus establishing silent chromatin in the rDNA locus.	NAD	124-128	sirtuin 1	Homo sapiens	188-193
18402469-6	2008	P450 and AKR enzymes equally competed for (+/-)-B[ a]P-7,8-diol substrate at an NADPH/NAD (+) ratio equal to 0.001.	NAD	86-93	aldo-keto reductase family 1 member A1	Homo sapiens	9-12
18203716-3	2008	Sir2, an NAD-dependent histone deacetylase, has been proven to extend life span in yeast and Caenorhabditis elegans.	NAD	9-12	sirtuin 1	Homo sapiens	0-4
18322014-8	2008	In the absence of Txnip, oxidative inactivation of PTEN and subsequent activation of Akt attenuated mitochondrial respiration, resulting in the accumulation of NADH, a competitive inhibitor of thioredoxin NADPH-reductive activation of PTEN.	NAD	160-164	thioredoxin 1	Mus musculus	193-204
18298901-5	2008	Caspase-3 and the expressions of Akt, p-Akt, a nicotinamide adenine dinucleotide (NAD+)-dependent histone deacetylase (SIRT1), p53, and p-p53 were detected by Western blot analysis.	NAD	82-86	sirtuin 1	Homo sapiens	119-124
19704728-6	2008	Based on in vitro enzymatic characterization, it was speculated that ADP-ribose (ADPR) and/or NADH may be biologically significant substrates of AtNUDT7.	NAD	94-98	MutT/nudix family protein	Arabidopsis thaliana	145-152
18230186-5	2008	Overexpression of p49/STRAP altered the intracellular level of NAD, and reduced the NAD/NADH ratio.	NAD	63-66	serum response factor binding protein 1	Homo sapiens	18-21
18230186-5	2008	Overexpression of p49/STRAP altered the intracellular level of NAD, and reduced the NAD/NADH ratio.	NAD	84-87	serum response factor binding protein 1	Homo sapiens	18-21
18230186-5	2008	Overexpression of p49/STRAP altered the intracellular level of NAD, and reduced the NAD/NADH ratio.	NAD	88-92	serum response factor binding protein 1	Homo sapiens	18-21
18537630-6	2008	Resveratrol directly increases sirtuin 1 (SIRT1) activity, a NAD(+) (oxidized form of nicotinamide adenine dinucleotide)-dependent histone deacetylase related to increased lifespan in various species similar to calorie restriction.	NAD	61-67	sirtuin 1	Homo sapiens	31-40
18537630-6	2008	Resveratrol directly increases sirtuin 1 (SIRT1) activity, a NAD(+) (oxidized form of nicotinamide adenine dinucleotide)-dependent histone deacetylase related to increased lifespan in various species similar to calorie restriction.	NAD	61-67	sirtuin 1	Homo sapiens	42-47
18537630-6	2008	Resveratrol directly increases sirtuin 1 (SIRT1) activity, a NAD(+) (oxidized form of nicotinamide adenine dinucleotide)-dependent histone deacetylase related to increased lifespan in various species similar to calorie restriction.	NAD	86-119	sirtuin 1	Homo sapiens	31-40
18537630-6	2008	Resveratrol directly increases sirtuin 1 (SIRT1) activity, a NAD(+) (oxidized form of nicotinamide adenine dinucleotide)-dependent histone deacetylase related to increased lifespan in various species similar to calorie restriction.	NAD	86-119	sirtuin 1	Homo sapiens	42-47
18039331-6	2008	Similar to the microsomal RDHs, RDH11, RDH12 and RDH14, RDH13 exhibits a much lower Km value for NADPH than for NADH and has a greater catalytic efficiency in the reductive than in the oxidative direction.	NAD	112-116	short chain dehydrogenase/reductase family 9C member 7	Homo sapiens	26-30
19325715-2	2008	In the current study, we have experimentally demonstrated that, the potent inhibition we obtained previously for one of these enzymes (i.e. sirtuin type 1 (SIRT1)) by simply replacing N(epsilon)-thioacetyl-lysine for N(epsilon)-acetyl-lysine in its peptide substrate, represented a general and efficient strategy to develop potent and selective inhibitors of human NAD(+)-dependent protein deacetylase enzymes.	NAD	365-371	sirtuin 1	Homo sapiens	140-154
19325715-2	2008	In the current study, we have experimentally demonstrated that, the potent inhibition we obtained previously for one of these enzymes (i.e. sirtuin type 1 (SIRT1)) by simply replacing N(epsilon)-thioacetyl-lysine for N(epsilon)-acetyl-lysine in its peptide substrate, represented a general and efficient strategy to develop potent and selective inhibitors of human NAD(+)-dependent protein deacetylase enzymes.	NAD	365-371	sirtuin 1	Homo sapiens	156-161
18158899-2	2007	The formation of these domains involves the recruitment of the SIR complex, composed of Sir2, Sir3, and Sir4, followed by iterative cycles of NAD-dependent histone deacetylation and spreading of SIR complexes over adjacent chromatin domains.	NAD	142-145	chromatin-silencing protein SIR3	Saccharomyces cerevisiae S288C	94-98
17680780-1	2007	Sirt1 is an NAD+-dependent deacetylase that plays a role in cellular processes such as transcriptional regulation, stress response, longevity and apoptosis.	NAD	12-15	sirtuin 1	Homo sapiens	0-5
17620057-7	2007	The ability of SIRT1 to catalyse the deacetylation of Rb was dependent on NAD and was inhibited by the SIRT1 inhibitor nicotinamide.	NAD	74-77	sirtuin 1	Homo sapiens	15-20
17604275-1	2007	NAD plays critical roles in various biological processes through the function of SIRT1.	NAD	0-3	sirtuin 1	Homo sapiens	81-86
17604275-3	2007	We here identified NA phosphoribosyltransferase (NAPRT) in humans and provided direct evidence of tight link between NAPRT and the increase in cellular NAD levels.	NAD	152-155	nicotinate phosphoribosyltransferase	Homo sapiens	19-47
17604275-3	2007	We here identified NA phosphoribosyltransferase (NAPRT) in humans and provided direct evidence of tight link between NAPRT and the increase in cellular NAD levels.	NAD	152-155	nicotinate phosphoribosyltransferase	Homo sapiens	49-54
17604275-3	2007	We here identified NA phosphoribosyltransferase (NAPRT) in humans and provided direct evidence of tight link between NAPRT and the increase in cellular NAD levels.	NAD	152-155	nicotinate phosphoribosyltransferase	Homo sapiens	117-122
17604275-5	2007	In cells expressing endogenous NAPRT, the addition of NA but not Nam almost doubled cellular NAD contents and decreased cytotoxicity by H(2)O(2).	NAD	93-96	nicotinate phosphoribosyltransferase	Homo sapiens	31-36
17604275-7	2007	These results indicate that NAPRT is essential for NA to increase cellular NAD levels and, thus, to prevent oxidative stress of the cells.	NAD	75-78	nicotinate phosphoribosyltransferase	Homo sapiens	28-33
17604275-9	2007	Together, we conclude that NA elevates cellular NAD levels through NAPRT function and, thus, protects the cells against stress, partly due to lack of feedback inhibition of NAPRT but not NamPRT by NAD.	NAD	48-51	nicotinate phosphoribosyltransferase	Homo sapiens	67-72
17640816-1	2007	Poly(ADP-ribose) polymerases (PARPs) are members of a family of enzymes that utilize nicotinamide adenine dinucleotide (NAD(+)) as substrate to form large ADP-ribose polymers (PAR) in the nucleus.	NAD	85-118	poly (ADP-ribose) polymerase family, member 1	Mus musculus	30-35
17640816-1	2007	Poly(ADP-ribose) polymerases (PARPs) are members of a family of enzymes that utilize nicotinamide adenine dinucleotide (NAD(+)) as substrate to form large ADP-ribose polymers (PAR) in the nucleus.	NAD	120-126	poly (ADP-ribose) polymerase family, member 1	Mus musculus	30-35
17508915-8	2007	For example, through CtBP, the high NADH to NAD(+) ratio decreases an expression of SirT1, the protein inducing longevity and anti-apoptosis.	NAD	36-40	sirtuin 1	Homo sapiens	84-89
17508915-8	2007	For example, through CtBP, the high NADH to NAD(+) ratio decreases an expression of SirT1, the protein inducing longevity and anti-apoptosis.	NAD	44-50	sirtuin 1	Homo sapiens	84-89
17555402-6	2007	In combination with the hypoxia-induced expression of LDHA (lactate dehydrogenase A), which converts pyruvate into lactate, PDK1 reduces the delivery of acetyl-CoA to the tricarboxylic acid cycle, thus reducing the levels of NADH and FADH2 delivered to the electron-transport chain.	NAD	225-229	pyruvate dehydrogenase kinase 1	Homo sapiens	124-128
17579037-6	2007	Intravenous injection of NAD(+) used to exacerbate NICD in vivo results in fast and dramatic ART2- and P2X7-dependent depletion of CD4+ and CD8+ T lymphocytes, which can affect up to 80% of peripheral T cells in CD38(-/-) mice.	NAD	25-31	CD38 antigen	Mus musculus	212-216
17579037-8	2007	Consistently, treatment with NAD(+) abolishes primary Ab response to a T-dependent Ag in NICD-susceptible CD38(-/-) mice but has no effect on the secondary response when given several days after priming.	NAD	29-35	CD38 antigen	Mus musculus	106-110
17336418-5	2007	PPT or DPN increased hepatic heat shock protein 32 (Hsp32) mRNA/protein expressions above levels observed after trauma-hemorrhage.	NAD	7-10	heme oxygenase 1	Rattus norvegicus	29-50
17336418-5	2007	PPT or DPN increased hepatic heat shock protein 32 (Hsp32) mRNA/protein expressions above levels observed after trauma-hemorrhage.	NAD	7-10	heme oxygenase 1	Rattus norvegicus	52-57
17395143-3	2007	In this system, NAADP is first converted into nicotinic acid adenine dinucleotide (NAAD) by alkaline phosphatase, after which the NAAD is converted to NAD, AMP, and PPi by NAD synthetase (NADS) in the presence of ATP and ammonia.	NAD	151-154	NAD synthetase 1	Homo sapiens	172-186
17439123-0	2007	Sir2 deacetylases exhibit nucleophilic participation of acetyl-lysine in NAD+ cleavage.	NAD	73-77	sirtuin 1	Homo sapiens	0-4
17679296-4	2007	Intestinal adaptation is the process by which, throughout 1-2 years, intestinal absorption is reestablished to the situation prior to intestinal resection, and is a key factor determining whether a patient with SBS will progress to intestinal failure and depend on DPN.	NAD	265-268	CYLD lysine 63 deubiquitinase	Homo sapiens	211-214
17323922-0	2007	Structures of the dI2dIII1 complex of proton-translocating transhydrogenase with bound, inactive analogues of NADH and NADPH reveal active site geometries.	NAD	110-114	Inhibitor-2	Drosophila melanogaster	18-26
17186476-2	2007	In this paper, we present a comparison of the calculated absorption and emission spectra of NADH in liver alcohol dehydrogenase (LADH), using quantum mechanical/molecular mechanical methods, in which we vary the QM component.	NAD	92-96	aldo-keto reductase family 1 member A1	Homo sapiens	106-127
17213307-2	2007	A unique feature of these enzymes is their utilization of NAD(+) as a cosubstrate, which has led to the suggestion that Sir2 activity reflects the cellular energy state.	NAD	58-64	sirtuin 1	Homo sapiens	120-124
17157196-1	2007	Poly(ADP-ribose) is synthesized from nicotinamide adenine dinucleotide (NAD) by poly(ADP-ribose) polymerase 1 (PARP-1) and degraded by poly(ADP-ribose) glycohydrolase (PARG).	NAD	37-70	poly (ADP-ribose) polymerase family, member 1	Mus musculus	80-109
17157196-1	2007	Poly(ADP-ribose) is synthesized from nicotinamide adenine dinucleotide (NAD) by poly(ADP-ribose) polymerase 1 (PARP-1) and degraded by poly(ADP-ribose) glycohydrolase (PARG).	NAD	37-70	poly (ADP-ribose) polymerase family, member 1	Mus musculus	111-117
17157196-1	2007	Poly(ADP-ribose) is synthesized from nicotinamide adenine dinucleotide (NAD) by poly(ADP-ribose) polymerase 1 (PARP-1) and degraded by poly(ADP-ribose) glycohydrolase (PARG).	NAD	37-70	poly (ADP-ribose) glycohydrolase	Mus musculus	135-166
17157196-1	2007	Poly(ADP-ribose) is synthesized from nicotinamide adenine dinucleotide (NAD) by poly(ADP-ribose) polymerase 1 (PARP-1) and degraded by poly(ADP-ribose) glycohydrolase (PARG).	NAD	37-70	poly (ADP-ribose) glycohydrolase	Mus musculus	168-172
17157196-1	2007	Poly(ADP-ribose) is synthesized from nicotinamide adenine dinucleotide (NAD) by poly(ADP-ribose) polymerase 1 (PARP-1) and degraded by poly(ADP-ribose) glycohydrolase (PARG).	NAD	72-75	poly (ADP-ribose) polymerase family, member 1	Mus musculus	80-109
17157196-1	2007	Poly(ADP-ribose) is synthesized from nicotinamide adenine dinucleotide (NAD) by poly(ADP-ribose) polymerase 1 (PARP-1) and degraded by poly(ADP-ribose) glycohydrolase (PARG).	NAD	72-75	poly (ADP-ribose) polymerase family, member 1	Mus musculus	111-117
17157196-1	2007	Poly(ADP-ribose) is synthesized from nicotinamide adenine dinucleotide (NAD) by poly(ADP-ribose) polymerase 1 (PARP-1) and degraded by poly(ADP-ribose) glycohydrolase (PARG).	NAD	72-75	poly (ADP-ribose) glycohydrolase	Mus musculus	135-166
17157196-1	2007	Poly(ADP-ribose) is synthesized from nicotinamide adenine dinucleotide (NAD) by poly(ADP-ribose) polymerase 1 (PARP-1) and degraded by poly(ADP-ribose) glycohydrolase (PARG).	NAD	72-75	poly (ADP-ribose) glycohydrolase	Mus musculus	168-172
17347859-3	2007	Theories to explain this "fructose effect" are based on the assumption that NAD+, the coenzyme for alcohol dehydrogenase, is regenerated faster in the presence of fructose.	NAD	76-80	aldo-keto reductase family 1 member A1	Homo sapiens	99-120
17099246-1	2006	The nicotinamide adenine dinucleotide (NAD(+))-dependent protein deacetylase SIRT1 has been linked to fatty acid metabolism via suppression of peroxysome proliferator-activated receptor gamma (PPAR-gamma) and to inflammatory processes by deacetylating the transcription factor NF-kappaB.	NAD	39-46	sirtuin 1	Homo sapiens	77-82
17046555-0	2006	Activation of nicotinamide adenine dinucleotide phosphate (reduced form) oxidase by advanced glycation end products links oxidative stress to altered retinal vascular endothelial growth factor expression.	NAD	14-47	vascular endothelial growth factor A	Bos taurus	158-192
17380200-8	2006	Finally, crosstalk between CD38 and other NAD(+) utilizing enzymes such as ART2, SIRT1, and PARP-1 impacts NAD(+) homeostasis, inflammation, and immunity.	NAD	42-48	CD38 antigen	Mus musculus	27-31
17380200-8	2006	Finally, crosstalk between CD38 and other NAD(+) utilizing enzymes such as ART2, SIRT1, and PARP-1 impacts NAD(+) homeostasis, inflammation, and immunity.	NAD	42-48	poly (ADP-ribose) polymerase family, member 1	Mus musculus	92-98
17380200-8	2006	Finally, crosstalk between CD38 and other NAD(+) utilizing enzymes such as ART2, SIRT1, and PARP-1 impacts NAD(+) homeostasis, inflammation, and immunity.	NAD	107-113	CD38 antigen	Mus musculus	27-31
17380200-8	2006	Finally, crosstalk between CD38 and other NAD(+) utilizing enzymes such as ART2, SIRT1, and PARP-1 impacts NAD(+) homeostasis, inflammation, and immunity.	NAD	107-113	poly (ADP-ribose) polymerase family, member 1	Mus musculus	92-98
17041593-4	2006	This reduced expression is mediated by the transcription factor NRSF, which recruits the NADH-binding co-repressor CtBP to generate a repressive chromatin environment around the BDNF promoter.	NAD	89-93	brain-derived neurotrophic factor	Rattus norvegicus	178-182
16939484-1	2006	Sir2 is an NAD+-dependent deacetylase that regulates lifespan in yeast, worms and flies.	NAD	11-14	sirtuin 1	Homo sapiens	0-4
17127736-5	2006	The LD inhibition by the patient"s IgA1 was blocked by reduction and alkylation and by NADH.	NAD	87-91	immunoglobulin heavy constant alpha 1	Homo sapiens	35-39
17127736-7	2006	Moreover, the possibility exists that part of the patient"s IgA1 molecule fits into a pocket of LD in instead of NADH.	NAD	113-117	immunoglobulin heavy constant alpha 1	Homo sapiens	60-64
16930323-3	2006	Here, we show a novel strategy in which a sorbitol cycle was engineered by introducing apple cDNA encoding NAD-dependent sorbitol dehydrogenase (SDH) in addition to sorbitol-6-phosphate dehydrogenase (S6PDH).	NAD	107-110	NADP-dependent D-sorbitol-6-phosphate dehydrogenase	Malus domestica	201-206
16720381-4	2006	Of particular interest, NAD+-dependent generation of ADP-ribose, cyclic ADP-ribose and O-acetyl-ADP-ribose can mediate calcium homeostasis by affecting TRPM2 receptors and ryanodine receptors; and sirtuins and PARPs appear to play key roles in aging, cell death and a variety of cellular functions.	NAD	24-28	transient receptor potential cation channel subfamily M member 2	Homo sapiens	152-157
16844764-1	2006	We have previously established a model of cytosolic phospholipase A(2) (cPLA(2))-deficient PLB-985 cells and demonstrated that cPLA(2)-generated arachidonic acid (AA) is essential for reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activation and NADPH-dependent diaphorase activity.	NAD	192-225	phospholipase A2 group IVA	Homo sapiens	72-79
16687393-3	2006	During attempts to understand the mode of regulation of H2A.z, we found that overexpression of silent information regulator 2alpha (Sir2alpha) specifically induced down-regulation of H2A.z via NAD-dependent activity.	NAD	193-196	sirtuin 1	Homo sapiens	132-141
16730329-0	2006	Regulation of intracellular levels of NAD: a novel role for CD38.	NAD	38-41	CD38 antigen	Mus musculus	60-64
16730329-8	2006	However, its major enzymatic activity is the hydrolysis of NAD, in fact, CD38 will generate one molecule of cADPR for every 100 molecules of NAD hydrolyzed.	NAD	59-62	CD38 antigen	Mus musculus	73-77
16730329-8	2006	However, its major enzymatic activity is the hydrolysis of NAD, in fact, CD38 will generate one molecule of cADPR for every 100 molecules of NAD hydrolyzed.	NAD	141-144	CD38 antigen	Mus musculus	73-77
16730329-9	2006	To date, the role of CD38 as a modulator of levels of NAD has not been explored.	NAD	54-57	CD38 antigen	Mus musculus	21-25
16730329-12	2006	In accordance with our hypothesis, we found that tissue levels of NAD in CD38 deficient mice are 10- to 20-fold higher than in wild-type animals.	NAD	66-69	CD38 antigen	Mus musculus	73-77
16730329-14	2006	These data support the novel concept that CD38 is a major regulator of cellular NAD levels.	NAD	80-83	CD38 antigen	Mus musculus	42-46
16772165-2	2006	The Wlds protein is a fusion of nicotinamide mononucleotide adenyltransferase-1 (Nmnat1), an essential enzyme in the biosynthesis pathway of nicotinamide adenine dinucleotide (NAD), with the N-terminal 70 amino acids of the Ube4b ubiquitination assembly factor.	NAD	141-174	nicotinamide nucleotide adenylyltransferase 1	Mus musculus	32-79
16772165-2	2006	The Wlds protein is a fusion of nicotinamide mononucleotide adenyltransferase-1 (Nmnat1), an essential enzyme in the biosynthesis pathway of nicotinamide adenine dinucleotide (NAD), with the N-terminal 70 amino acids of the Ube4b ubiquitination assembly factor.	NAD	141-174	nicotinamide nucleotide adenylyltransferase 1	Mus musculus	81-87
16772165-2	2006	The Wlds protein is a fusion of nicotinamide mononucleotide adenyltransferase-1 (Nmnat1), an essential enzyme in the biosynthesis pathway of nicotinamide adenine dinucleotide (NAD), with the N-terminal 70 amino acids of the Ube4b ubiquitination assembly factor.	NAD	176-179	nicotinamide nucleotide adenylyltransferase 1	Mus musculus	32-79
16772165-2	2006	The Wlds protein is a fusion of nicotinamide mononucleotide adenyltransferase-1 (Nmnat1), an essential enzyme in the biosynthesis pathway of nicotinamide adenine dinucleotide (NAD), with the N-terminal 70 amino acids of the Ube4b ubiquitination assembly factor.	NAD	176-179	nicotinamide nucleotide adenylyltransferase 1	Mus musculus	81-87
16788056-4	2006	The recombinant TBER1 efficiently oxidized 17beta-hydroxysteroids and xenobiotic alicyclic alcohols using NAD+ as the preferred coenzyme at pH 7.4, and showed low activity towards 20alpha- and 3alpha-hydroxysteroids, and 9-hydroxyprostaglandins.	NAD	106-110	aldo-keto reductase family 1, member C12	Rattus norvegicus	16-21
16328543-5	2006	T-DNA knock out plants of GFG1 gene, gfg1-1, exhibit pleiotropic phenotypes such as reduced size, increased levels of reactive oxygen species and NADH, microscopic cell death, constitutive expression of pathogenesis-related genes and enhanced resistance to bacterial pathogens.	NAD	146-150	MutT/nudix family protein	Arabidopsis thaliana	26-30
16328543-5	2006	T-DNA knock out plants of GFG1 gene, gfg1-1, exhibit pleiotropic phenotypes such as reduced size, increased levels of reactive oxygen species and NADH, microscopic cell death, constitutive expression of pathogenesis-related genes and enhanced resistance to bacterial pathogens.	NAD	146-150	MutT/nudix family protein	Arabidopsis thaliana	37-43
16585549-1	2006	Ubiquitously expressed CD38 and T cell-expressed ADP-ribosyltransferase 2 (ART2) are ectoenzymes competing for NAD substrate.	NAD	111-114	CD38 antigen	Mus musculus	23-27
16291748-12	2006	The delta ndt1 delta ndt2 double mutant exhibited lower mitochondrial NAD+ and NADH levels than the single deletants and a more pronounced delay in growth on nonfermentable carbon sources.	NAD	70-74	NAD+ transporter	Saccharomyces cerevisiae S288C	21-25
16291748-12	2006	The delta ndt1 delta ndt2 double mutant exhibited lower mitochondrial NAD+ and NADH levels than the single deletants and a more pronounced delay in growth on nonfermentable carbon sources.	NAD	79-83	NAD+ transporter	Saccharomyces cerevisiae S288C	21-25
16291748-13	2006	The main role of Ndt1p and Ndt2p is to import NAD+ into mitochondria by unidirectional transport or by exchange with intramitochondrially generated (d)AMP and (d)GMP.	NAD	46-50	NAD+ transporter	Saccharomyces cerevisiae S288C	27-32
16390171-2	2006	The spectrophotometric determination is based on the enzymatic reaction catalyzed by alcohol dehydrogenase in the presence of NAD+.	NAD	126-130	aldo-keto reductase family 1 member A1	Homo sapiens	85-106
16276532-4	2006	About 82% yield of dTDP-L-rhamnose was obtained based on initial dTMP concentration at 20 mM dTMP, 1 mM ATP, 10 mM NADH, 60 mM acetyl phosphate, and 80 mM glucose-1-phosphate.	NAD	115-119	TAR DNA-binding protein-43 homolog	Drosophila melanogaster	19-23
16278810-4	2005	Compared to controls (n = 8), doxorubicin-exposed hearts (n = 6) showed low absolute enzyme activity of mtDNA-encoded nicotinamide adenine dinucleotide hydrogen dehydrogenase (NADH DH, 79% residual activity, p = 0.03) and cytochrome c oxidase (COX, 59% residual activity, p &lt; 0.001), but not of succinate dehydrogenase (SDH), which is encoded exclusively by nuclear DNA.	NAD	176-180	succinate dehydrogenase complex iron sulfur subunit B	Homo sapiens	298-321
16278810-4	2005	Compared to controls (n = 8), doxorubicin-exposed hearts (n = 6) showed low absolute enzyme activity of mtDNA-encoded nicotinamide adenine dinucleotide hydrogen dehydrogenase (NADH DH, 79% residual activity, p = 0.03) and cytochrome c oxidase (COX, 59% residual activity, p &lt; 0.001), but not of succinate dehydrogenase (SDH), which is encoded exclusively by nuclear DNA.	NAD	176-180	succinate dehydrogenase complex iron sulfur subunit B	Homo sapiens	323-326
16216070-1	2005	Cytochrome b5 reductase (cb5r), a member of the ferredoxin:NADP+ reductase family of flavoprotein transhydrogenases, catalyzes the NADH-dependent reduction of cytochrome b5.	NAD	131-135	cytochrome b5 type A	Rattus norvegicus	0-13
16216070-1	2005	Cytochrome b5 reductase (cb5r), a member of the ferredoxin:NADP+ reductase family of flavoprotein transhydrogenases, catalyzes the NADH-dependent reduction of cytochrome b5.	NAD	131-135	cytochrome b5 type A	Rattus norvegicus	159-172
15952035-4	2005	Other stimuli of TRPM2 include NAD and H(2)O(2) and cyclic ADPR, which may act synergistically with ADPR.	NAD	31-34	transient receptor potential cation channel subfamily M member 2	Homo sapiens	17-22
16154098-2	2005	We show that the forkhead protein FoxO1 protects beta cells against oxidative stress by forming a complex with the promyelocytic leukemia protein Pml and the NAD-dependent deacetylase Sirt1 to activate expression of NeuroD and MafA, two Insulin2 (Ins2) gene transcription factors.	NAD	158-161	sirtuin 1	Homo sapiens	184-189
16115062-6	2005	The deduced amino acid sequence of Rat1 shows significant sequence homology to the conserved NAD+-binding domain of poly(ADP-ribose) polymerases of eukaryotic organisms.	NAD	93-97	uncharacterized protein	Chlamydomonas reinhardtii	35-39
16012755-7	2005	In contrast, mammalian SIRT1 was found to bind to FOXO4, catalyze its deacetylation in an NAD-dependent manner, and thereby increase its transactivation activity.	NAD	90-93	sirtuin 1	Homo sapiens	23-28
16012755-11	2005	These results indicate that mammalian SIRT1 plays a pivotal role for FOXO function via NAD-dependent deacetylation in response to oxidative stress, and thereby may contribute to cellular stress resistance and longevity.	NAD	87-90	sirtuin 1	Homo sapiens	38-43
16043516-2	2005	Important insight into the mechanisms of axon degeneration arose from findings that the degeneration of transected axons is delayed in Wallerian degeneration slow (Wlds) mice with the overexpression of a fusion protein with the nicotinamide adenine dinucleotide (NAD) synthetic enzyme, nicotinamide mononucleotide adenylyltransferase (Nmnat1).	NAD	228-261	nicotinamide nucleotide adenylyltransferase 1	Mus musculus	335-341
16043516-6	2005	Furthermore, we provide evidence that such Nmnat1/NAD-mediated protection is primarily mediated by their effects on local bioenergetics.	NAD	50-53	nicotinamide nucleotide adenylyltransferase 1	Mus musculus	43-49
16132700-1	2005	Poly(ADP-ribose) polymerases or PARPs are a family of NAD(+)-dependent enzymes that modify themselves and other substrate proteins with ADP-ribose polymers.	NAD	54-60	poly(ADP-ribose) polymerase 1	Canis lupus familiaris	32-37
16132700-3	2005	Excessive PARP 1 activation following genotoxin treatment causes NAD(+) depletion and cell death, whereas pharmacological PARP 1 inhibition protects cells from genotoxicity.	NAD	65-71	poly(ADP-ribose) polymerase 1	Canis lupus familiaris	10-16
16132700-4	2005	This study investigates whether cellular viability and NAD(+) metabolism are regulated by tankyrase-1, a PARP member localized predominantly in the cytosol.	NAD	55-61	tankyrase	Canis lupus familiaris	90-101
16132700-5	2005	Using a tetracycline-sensitive promoter to regulate tankyrase-1 expression in Madin-Darby canine kidney (MDCK) cells, we found that a 40-fold induction of tankyrase-1 (from 1,500 to 60,000 copies per cell) lowers steady-state NAD(+) levels but does not affect basal cellular viability.	NAD	226-232	tankyrase	Canis lupus familiaris	155-166
16132700-8	2005	Instead, tankyrase-1 appears to protect cells by preventing genotoxins from activating PARP 1-mediated reactions such as PARP 1 automodification and NAD(+) consumption.	NAD	149-155	tankyrase	Canis lupus familiaris	9-20
16132700-8	2005	Instead, tankyrase-1 appears to protect cells by preventing genotoxins from activating PARP 1-mediated reactions such as PARP 1 automodification and NAD(+) consumption.	NAD	149-155	poly(ADP-ribose) polymerase 1	Canis lupus familiaris	87-93
16132700-9	2005	Our findings therefore indicate a cytoprotective function of tankyrase-1 mediated through altered NAD(+) homeostasis and inhibition of PARP 1 function.	NAD	98-104	tankyrase	Canis lupus familiaris	61-72
15788720-11	2005	This enzymatic activity requires GSH, NAD, and glycolytic substrates, and purportedly involves one or both of the two functionally linked glycolytic enzymes, glyceraldehyde-3-phosphate dehydrogenase and phosphoglycerate kinase.	NAD	38-41	glyceraldehyde-3-phosphate dehydrogenase	Rattus norvegicus	158-198
15893190-1	2005	OBJECTIVES: We investigated the role of SH2-domain containing phosphatase-1 (SHP-1) in endothelial reduced nicotinamide adenine dinucleotide (phosphate) (NAD[P]H)-oxidase-dependent oxidant production.	NAD	107-140	protein tyrosine phosphatase non-receptor type 6	Homo sapiens	40-75
15893190-1	2005	OBJECTIVES: We investigated the role of SH2-domain containing phosphatase-1 (SHP-1) in endothelial reduced nicotinamide adenine dinucleotide (phosphate) (NAD[P]H)-oxidase-dependent oxidant production.	NAD	107-140	protein tyrosine phosphatase non-receptor type 6	Homo sapiens	77-82
15752608-6	2005	The combined effect is a much higher catalytic efficiency for NAD(+)/H, with a minor decrease of that for NADP(+)/H.	NAD	62-68	2,4-dienoyl-CoA reductase 1	Homo sapiens	106-115
15780941-0	2005	Mechanism of sirtuin inhibition by nicotinamide: altering the NAD(+) cosubstrate specificity of a Sir2 enzyme.	NAD	62-68	sirtuin 1	Homo sapiens	98-102
15677308-3	2005	Continuous or excessive activation of poly(ADP-ribose) polymerase-1 produces extended chains of ADP-ribose on nuclear proteins and results in a substantial depletion of intracellular NAD(+) and subsequently, ATP, leading to cellular dysfunction and, ultimately, cell death.	NAD	183-189	poly (ADP-ribose) polymerase family, member 1	Mus musculus	38-67
15557339-1	2005	In the yeast Saccharomyces cerevisiae, the most important systems for conveying excess cytosolic NADH to the mitochondrial respiratory chain are the external NADH dehydrogenases (Nde1p and Nde2p) and the glycerol-3-phosphate dehydrogenase shuttle.	NAD	97-101	NADH-ubiquinone reductase (H(+)-translocating) NDE1	Saccharomyces cerevisiae S288C	179-184
15557339-1	2005	In the yeast Saccharomyces cerevisiae, the most important systems for conveying excess cytosolic NADH to the mitochondrial respiratory chain are the external NADH dehydrogenases (Nde1p and Nde2p) and the glycerol-3-phosphate dehydrogenase shuttle.	NAD	97-101	NADH-ubiquinone reductase (H(+)-translocating) NDE2	Saccharomyces cerevisiae S288C	189-194
15557339-2	2005	In the latter system, NADH is oxidized to NAD+ and dihydroxyacetone phosphate is reduced to glycerol 3-phosphate by the cytosolic Gpd1p.	NAD	22-26	glycerol-3-phosphate dehydrogenase (NAD(+)) GPD1	Saccharomyces cerevisiae S288C	130-135
15581601-0	2005	Key NAD+-binding residues in human 15-hydroxyprostaglandin dehydrogenase.	NAD	4-8	carbonyl reductase 1	Homo sapiens	35-72
15581601-4	2005	In this report, we propose that three more residues in 15-PGDH, Ile-17, Asn-91, and Val-186, are also involved in the interaction with NAD(+).	NAD	135-141	carbonyl reductase 1	Homo sapiens	55-62
15581601-14	2005	These results suggest that Ile-17, Asn-91, and Val-186 are involved in the interaction with NAD(+) and contribute to the full catalytic activity of 15-PGDH.	NAD	92-98	carbonyl reductase 1	Homo sapiens	148-155
15506920-0	2004	Structure and chemistry of the Sir2 family of NAD+-dependent histone/protein deactylases.	NAD	46-50	sirtuin 1	Homo sapiens	31-35
15506920-1	2004	The yeast Sir2 (silent information regulator-2) protein functions as an NAD(+)-dependent histone deacetylase to silence gene expression from the mating-type locus, tolomeres and rDNA and also promotes longevity and genome stability in response to calorie restriction.	NAD	72-78	sirtuin 1	Homo sapiens	10-14
15506920-3	2004	We have determined the X-ray crystal structure of a Sir2 homologue from yeast Hst2 (yHst2), in various liganded forms, including the yHst2/acetyl-Lys-16 histone H4/NAD(+) ternary complex; we have also performed related biochemical studies to address the conserved mode of catalysis by these enzymes as well as the distinguishing features that allow different members of the family to target their respective cognate substrates.	NAD	164-170	sirtuin 1	Homo sapiens	52-56
15383625-12	2004	Using NAD+, the 3-hydroxymetabolites were efficiently oxidized by homogeneous recombinant AKR1C2 and AKR1C4.	NAD	6-10	aldo-keto reductase family 1 member C4	Homo sapiens	101-107
15531787-6	2004	In another experiment, HPLS was coupled to ADH in the presence of NADH.	NAD	66-70	aldo-keto reductase family 1 member A1	Homo sapiens	43-46
15564879-5	2004	Ethanol-oxidizing activities of recombinant ADH1B1, ADH1B2, ADH1B3, ADH1C1, ADH1C2 and ADH2 were determined at pH 7.5 in the presence of 0.5 mm NAD with 2-50 mm ethanol.	NAD	144-147	alcohol dehydrogenase 1B (class I), beta polypeptide	Homo sapiens	87-91
15461452-2	2004	PDR is responsible for transferring electrons from NADH to the Rieske center of PDO, and the Rieske center supplies electrons to the mononuclear center for the oxygenation of substrate.	NAD	51-55	PDR	Homo sapiens	0-3
15501022-4	2004	In addition, the NAD(+)-dependent histone deacetylase SIRT1, the mammalian ortholog of the yeast SIR2 (silence information regulator 2) and a member of the Sirtuin family, was hypothesized to decrease in satellite cell nuclei of old rats.	NAD	17-23	sirtuin 1	Homo sapiens	54-59
15210723-0	2004	Distinct intracellular localization of Gpd1p and Gpd2p, the two yeast isoforms of NAD+-dependent glycerol-3-phosphate dehydrogenase, explains their different contributions to redox-driven glycerol production.	NAD	82-85	glycerol-3-phosphate dehydrogenase (NAD(+)) GPD1	Saccharomyces cerevisiae S288C	39-44
15226302-3	2004	Capillary electrophoresis was used to examine substrate conversion by WbpA, and the data revealed that WbpA is a UDP-N-acetyl-D-glucosamine 6-dehydrogenase (EC 1.1.1.136), which uses NAD(+) as a coenzyme.	NAD	183-189	UDP-N-acetyl-d-glucosamine 6-dehydrogenase	Pseudomonas aeruginosa PAO1	103-107
15226302-8	2004	In addition, WbpA has a K(0.5) for NAD(+) of 220 microM, a k(cat) of 86 min(-1), and a Hill coefficient of 1.1.	NAD	35-41	UDP-N-acetyl-d-glucosamine 6-dehydrogenase	Pseudomonas aeruginosa PAO1	13-17
15150415-0	2004	Structural basis for nicotinamide cleavage and ADP-ribose transfer by NAD(+)-dependent Sir2 histone/protein deacetylases.	NAD	70-76	sirtuin 1	Homo sapiens	87-91
15150415-3	2004	To provide structural insights into the chemistry catalyzed by Sir2 proteins we report the high-resolution ternary structure of yeast Hst2 (homologue of Sir two 2) with an acetyllysine histone H4 peptide and a nonhydrolyzable NAD(+) analogue, carba-NAD(+), as well as an analogous ternary complex with a reaction intermediate analog formed immediately after nicotinamide hydrolysis, ADP-ribose.	NAD	226-232	sirtuin 1	Homo sapiens	63-67
15187521-1	2004	OBJECTIVE: Poly(ADP-ribose) is synthesized from nicotinamide adenine dinucleotide by poly(ADP-ribose) polymerase (PARP) and degraded by poly(ADP-ribose) glycohydrolase (PARG).	NAD	48-81	poly (ADP-ribose) polymerase family, member 1	Mus musculus	85-112
15187521-1	2004	OBJECTIVE: Poly(ADP-ribose) is synthesized from nicotinamide adenine dinucleotide by poly(ADP-ribose) polymerase (PARP) and degraded by poly(ADP-ribose) glycohydrolase (PARG).	NAD	48-81	poly (ADP-ribose) polymerase family, member 1	Mus musculus	114-118
15187521-1	2004	OBJECTIVE: Poly(ADP-ribose) is synthesized from nicotinamide adenine dinucleotide by poly(ADP-ribose) polymerase (PARP) and degraded by poly(ADP-ribose) glycohydrolase (PARG).	NAD	48-81	poly (ADP-ribose) glycohydrolase	Mus musculus	136-167
15187521-1	2004	OBJECTIVE: Poly(ADP-ribose) is synthesized from nicotinamide adenine dinucleotide by poly(ADP-ribose) polymerase (PARP) and degraded by poly(ADP-ribose) glycohydrolase (PARG).	NAD	48-81	poly (ADP-ribose) glycohydrolase	Mus musculus	169-173
15146068-9	2004	Furthermore, growth improvement by the SFKs on high NaCl plus FK506 was shown to require GPD1, which encodes an NADH-dependent glycerol-3-phosphate dehydrogenase that is important for the production of glycerol in response to osmotic stress.	NAD	112-116	glycerol-3-phosphate dehydrogenase (NAD(+)) GPD1	Saccharomyces cerevisiae S288C	89-93
14749354-0	2004	Synergistic induction of the nicotinamide adenine dinucleotide-linked 15-hydroxyprostaglandin dehydrogenase by an androgen and interleukin-6 or forskolin in human prostate cancer cells.	NAD	29-62	carbonyl reductase 1	Homo sapiens	70-107
14749354-1	2004	The nicotinamide adenine dinucleotide-dependent 15-hydroxyprostaglandin dehydrogenase (15-PGDH) catalyzes the oxidation of 15 (S)-hydroxyl group of prostaglandins and lipoxins and participates along with cyclooxygenases and lipoxygenases in controlling the cellular levels of prostaglandins and lipoxins.	NAD	4-37	carbonyl reductase 1	Homo sapiens	48-85
14749354-1	2004	The nicotinamide adenine dinucleotide-dependent 15-hydroxyprostaglandin dehydrogenase (15-PGDH) catalyzes the oxidation of 15 (S)-hydroxyl group of prostaglandins and lipoxins and participates along with cyclooxygenases and lipoxygenases in controlling the cellular levels of prostaglandins and lipoxins.	NAD	4-37	carbonyl reductase 1	Homo sapiens	87-94
15082529-0	2004	The NAD(+)-dependent Sir2p histone deacetylase is a negative regulator of chromosomal DNA replication.	NAD	4-10	histone deacetylase	Saccharomyces cerevisiae S288C	27-46
15023335-2	2004	Although structures of Sir2 enzymes in the presence and absence of peptide substrate or NAD(+) have been determined, the role of the enzyme in the mechanism of deacetylation and NAD(+) cleavage is still unclear.	NAD	88-94	sirtuin 1	Homo sapiens	23-27
15009646-5	2004	We also measured levels of NAD+, a cofactor for dopamine biosynthesis and substrate of the DNA damage surveillance enzyme, poly(ADP-ribose) polymerase (PARP).	NAD	27-31	poly (ADP-ribose) polymerase family, member 1	Mus musculus	123-150
15009646-5	2004	We also measured levels of NAD+, a cofactor for dopamine biosynthesis and substrate of the DNA damage surveillance enzyme, poly(ADP-ribose) polymerase (PARP).	NAD	27-31	poly (ADP-ribose) polymerase family, member 1	Mus musculus	152-156
15009646-6	2004	Constitutive activation of PARP has been posited to cause NAD+ depletion.	NAD	58-62	poly (ADP-ribose) polymerase family, member 1	Mus musculus	27-31
14762203-2	2004	The intrinsic mechanism of PARP-1-mediated endothelial cell dysfunction could be related to PARP-1 overactivation, NAD(+) consumption and ATP depletion.	NAD	115-121	poly (ADP-ribose) polymerase family, member 1	Mus musculus	27-33
14709821-1	2003	CD38 is an ectoenzyme with ADP-ribosyl cyclase and hydrolase activities, which synthesizes cyclic ADP-ribose from NAD and hydrolyzes cyclic ADP-ribose to ADP-ribose.	NAD	114-117	CD38 antigen	Mus musculus	0-4
12871940-5	2003	Pi oxidized cytochrome b (cyto-b) and reduced cytochrome c (cyto-c), potentially improving the coupling between the NADH free energy and the proton motive force.	NAD	116-120	mitochondrially encoded cytochrome b	Homo sapiens	12-24
12871940-5	2003	Pi oxidized cytochrome b (cyto-b) and reduced cytochrome c (cyto-c), potentially improving the coupling between the NADH free energy and the proton motive force.	NAD	116-120	mitochondrially encoded cytochrome b	Homo sapiens	26-32
12972620-8	2003	The known Hst1p binding partner, Sum1p, is present at promoters of highly inducible NAD(+) biosynthesis genes.	NAD	84-90	Sum1p	Saccharomyces cerevisiae S288C	33-38
12972620-10	2003	Transcript array analysis shows that reduction in cellular NAD(+) levels preferentially affects Hst1p-regulated genes in comparison to genes regulated with other NAD(+)-dependent deacetylases (Sir2p, Hst2p, Hst3p, and Hst4p).	NAD	59-65	NAD-dependent histone deacetylase HST4	Saccharomyces cerevisiae S288C	218-223
14503867-6	2003	Wild-type cytochrome b(5) reductase only formed a stable charge-transfer complex with NADH while D239T formed complexes with both NADH and NADPH.	NAD	86-90	cytochrome b5 type A	Rattus norvegicus	10-25
14503867-6	2003	Wild-type cytochrome b(5) reductase only formed a stable charge-transfer complex with NADH while D239T formed complexes with both NADH and NADPH.	NAD	130-134	cytochrome b5 type A	Rattus norvegicus	10-25
14511320-1	2003	We have previously suggested that zinc-induced neuronal death may be mediated in part by inhibition of the glycolytic enzyme glyceraldehyde-3-phosphate dehydrogenase (GAPDH), secondary to depletion of the essential cosubstrate NAD+.	NAD	227-231	glyceraldehyde-3-phosphate dehydrogenase	Mus musculus	167-172
14511320-2	2003	Given convergent evidence implicating the NAD+-catabolizing enzyme, poly ADP ribosyl polymerase (PARP) in mediating ATP depletion and neuronal death after excitotoxic and ischemic insults, we tested the specific hypothesis that the neuronal death induced by exposure to toxic levels of extracellular zinc might be partly mediated by PARP.	NAD	42-46	poly (ADP-ribose) polymerase family, member 1	Mus musculus	68-95
14511320-2	2003	Given convergent evidence implicating the NAD+-catabolizing enzyme, poly ADP ribosyl polymerase (PARP) in mediating ATP depletion and neuronal death after excitotoxic and ischemic insults, we tested the specific hypothesis that the neuronal death induced by exposure to toxic levels of extracellular zinc might be partly mediated by PARP.	NAD	42-46	poly (ADP-ribose) polymerase family, member 1	Mus musculus	97-101
14511320-2	2003	Given convergent evidence implicating the NAD+-catabolizing enzyme, poly ADP ribosyl polymerase (PARP) in mediating ATP depletion and neuronal death after excitotoxic and ischemic insults, we tested the specific hypothesis that the neuronal death induced by exposure to toxic levels of extracellular zinc might be partly mediated by PARP.	NAD	42-46	poly (ADP-ribose) polymerase family, member 1	Mus musculus	333-337
12924878-7	2003	Reaction of 4 with excess CO resulted in the monovalent, dicarbonyl product [PhBP(iPr)(3)]Co(I)(CO)(2) (9).	NAD	90-95	hyaluronan binding protein 2	Homo sapiens	77-88
12879452-3	2003	The decline of NAD(+) and the rise of nicotinamide may downregulate the activity of Sir2, the NAD(+)-dependent deacetylases, because deacetylation by Sir2 is dependent on high concentration of NAD(+) and inhibited by physiologic level of nicotinamide.	NAD	15-21	sirtuin 1	Homo sapiens	84-88
12879452-3	2003	The decline of NAD(+) and the rise of nicotinamide may downregulate the activity of Sir2, the NAD(+)-dependent deacetylases, because deacetylation by Sir2 is dependent on high concentration of NAD(+) and inhibited by physiologic level of nicotinamide.	NAD	15-21	sirtuin 1	Homo sapiens	150-154
12879452-3	2003	The decline of NAD(+) and the rise of nicotinamide may downregulate the activity of Sir2, the NAD(+)-dependent deacetylases, because deacetylation by Sir2 is dependent on high concentration of NAD(+) and inhibited by physiologic level of nicotinamide.	NAD	94-100	sirtuin 1	Homo sapiens	84-88
12879452-3	2003	The decline of NAD(+) and the rise of nicotinamide may downregulate the activity of Sir2, the NAD(+)-dependent deacetylases, because deacetylation by Sir2 is dependent on high concentration of NAD(+) and inhibited by physiologic level of nicotinamide.	NAD	94-100	sirtuin 1	Homo sapiens	150-154
12879452-5	2003	It is conceivable that poly(ADP-ribosyl)ation by PARP-1, which is induced by DNA damage, could modulate protein deacetylation by Sir2 via the NAD(+)/nicotinamide connection.	NAD	142-148	sirtuin 1	Homo sapiens	129-133
12867036-8	2003	Our findings suggest that the NAD(+)-dependent deacetylase Sir2 plays an important and conserved role in heterochromatin assembly in eukaryotes.	NAD	30-36	sirtuin 1	Homo sapiens	59-63
12676948-9	2003	These microarray data show that ADR1 coordinates the biochemical pathways that generate acetyl-CoA and NADH from non-fermentable substrates.	NAD	103-107	DNA-binding transcription factor ADR1	Saccharomyces cerevisiae S288C	32-36
12962302-4	2003	This novel GapCp is closely related to cytosolic GapC and displays glycolytic NAD+ cosubstrate specificity.	NAD	78-82	glyceraldehyde-3-phosphate dehydrogenase GAPCP1, chloroplastic	Capsicum annuum	11-16
12962302-4	2003	This novel GapCp is closely related to cytosolic GapC and displays glycolytic NAD+ cosubstrate specificity.	NAD	78-82	glyceraldehyde-3-phosphate dehydrogenase GAPCP1, chloroplastic	Capsicum annuum	11-15
12887892-7	2003	Cells with reduced Sir2 levels are less sensitive to the inhibition imposed by an elevated [NAD(+)]/[NADH] ratio.	NAD	92-98	sirtuin 1	Homo sapiens	19-23
12887892-7	2003	Cells with reduced Sir2 levels are less sensitive to the inhibition imposed by an elevated [NAD(+)]/[NADH] ratio.	NAD	101-105	sirtuin 1	Homo sapiens	19-23
12821320-2	2003	All 25 currently identified type I and type II methemoglobinemia mutants have been expressed in Escherichia coli using a novel six histidine-tagged rat cytochrome b5/cytochrome b5 reductase fusion protein designated NADH:cytochrome c reductase (H6NCR).	NAD	216-220	cytochrome b5 type A	Rattus norvegicus	152-165
12821320-2	2003	All 25 currently identified type I and type II methemoglobinemia mutants have been expressed in Escherichia coli using a novel six histidine-tagged rat cytochrome b5/cytochrome b5 reductase fusion protein designated NADH:cytochrome c reductase (H6NCR).	NAD	216-220	cytochrome b5 type A	Rattus norvegicus	166-179
12663656-1	2003	Escherichia coli flavohemoglobin (HMP) is shown to be capable of catalyzing the reduction of several alkylhydroperoxide substrates into their corresponding alcohols using NADH as an electron donor.	NAD	171-175	inner membrane mitochondrial protein	Homo sapiens	34-37
12832719-5	2003	Pretreatment with adenosine deaminase (adenosine degrading enzyme, 2 U/min/kg) or theophylline (P1-receptors antagonist, 0.2 mmol/min/kg) ceased responses to NAD, whereas Ap4A-induced changes were not affected.	NAD	158-161	adenosine deaminase	Rattus norvegicus	18-37
12750003-4	2003	PARP activation depletes NAD and ATP pools, ultimately resulting in necrotic cell death by loss of energy stores.	NAD	25-28	poly (ADP-ribose) polymerase family, member 1	Mus musculus	0-4
12694396-1	2003	Poly(ADP-ribose) polymerase-1 (PARP-1) is a homeostatic enzyme that paradoxically contributes to disturbances in spatial memory acquisition after traumatic brain injury (TBI) in transgenic mice, thought to be related to depletion of its substrate nicotinamide adenine dinucleotide (NAD+).	NAD	247-280	poly (ADP-ribose) polymerase family, member 1	Mus musculus	0-29
12694396-1	2003	Poly(ADP-ribose) polymerase-1 (PARP-1) is a homeostatic enzyme that paradoxically contributes to disturbances in spatial memory acquisition after traumatic brain injury (TBI) in transgenic mice, thought to be related to depletion of its substrate nicotinamide adenine dinucleotide (NAD+).	NAD	247-280	poly (ADP-ribose) polymerase family, member 1	Mus musculus	31-37
12694396-1	2003	Poly(ADP-ribose) polymerase-1 (PARP-1) is a homeostatic enzyme that paradoxically contributes to disturbances in spatial memory acquisition after traumatic brain injury (TBI) in transgenic mice, thought to be related to depletion of its substrate nicotinamide adenine dinucleotide (NAD+).	NAD	282-286	poly (ADP-ribose) polymerase family, member 1	Mus musculus	0-29
12694396-1	2003	Poly(ADP-ribose) polymerase-1 (PARP-1) is a homeostatic enzyme that paradoxically contributes to disturbances in spatial memory acquisition after traumatic brain injury (TBI) in transgenic mice, thought to be related to depletion of its substrate nicotinamide adenine dinucleotide (NAD+).	NAD	282-286	poly (ADP-ribose) polymerase family, member 1	Mus musculus	31-37
12694396-2	2003	In this study, systemic administration of the PARP-1 inhibitor 5-iodo-6-amino-1,2-benzopyrone (INH2BP) after TBI preserved brain NAD+ levels and dose-dependently reduced poly-ADP-ribosylation 24 h after injury.	NAD	129-133	poly (ADP-ribose) polymerase family, member 1	Mus musculus	46-52
12547821-5	2003	Consistent with the domain structures, biochemical assays indicated (i) that both NADsyn1 and NADsyn2 have NAD synthetase activity, (ii) that NADsyn1 uses glutamine as well as ammonia as an amide donor, whereas NADsyn2 catalyzes only ammonia-dependent NAD synthesis, and (iii) that mutant NADsyn1 in which Cys-175 corresponding to the catalytic cysteine residue in nitrilases was replaced with Ser does not use glutamine.	NAD	82-85	NAD synthetase 1	Homo sapiens	107-121
12547821-5	2003	Consistent with the domain structures, biochemical assays indicated (i) that both NADsyn1 and NADsyn2 have NAD synthetase activity, (ii) that NADsyn1 uses glutamine as well as ammonia as an amide donor, whereas NADsyn2 catalyzes only ammonia-dependent NAD synthesis, and (iii) that mutant NADsyn1 in which Cys-175 corresponding to the catalytic cysteine residue in nitrilases was replaced with Ser does not use glutamine.	NAD	82-85	NAD synthetase 1	Homo sapiens	142-149
12547821-5	2003	Consistent with the domain structures, biochemical assays indicated (i) that both NADsyn1 and NADsyn2 have NAD synthetase activity, (ii) that NADsyn1 uses glutamine as well as ammonia as an amide donor, whereas NADsyn2 catalyzes only ammonia-dependent NAD synthesis, and (iii) that mutant NADsyn1 in which Cys-175 corresponding to the catalytic cysteine residue in nitrilases was replaced with Ser does not use glutamine.	NAD	82-85	NAD synthetase 1	Homo sapiens	142-149
12631263-10	2003	It is suggested that this side-effect of the 2-oxo acid oxidation at low NAD+in vivo would be overcome by cooperation of mitochondrial thioredoxin and the thioredoxin-dependent peroxidase, SP-22.	NAD	73-77	peroxiredoxin 3	Homo sapiens	189-194
12459552-11	2003	On the basis of these data, we present a new kinetic scheme to explain the mechanism of electron transfer from NADH to one-electron acceptors including cytochrome b(5).	NAD	111-115	mitochondrially encoded cytochrome b	Homo sapiens	152-164
12585477-5	2003	The ISFET devices functionalized with the NADH and NADPH membranes are employed in the analysis of the biocatalyzed oxidation of lactic acid and ethanol in the presence of lactate dehydrogenase and alcohol dehydrogenase, respectively.	NAD	42-46	aldo-keto reductase family 1 member A1	Homo sapiens	198-219
12534287-9	2003	Labeling of the ND5 subunit was stimulated by NADH/NADPH but was prevented by various complex I inhibitors.	NAD	46-50	NADH dehydrogenase subunit 5	Bos taurus	16-19
12517343-5	2003	Peroxisomal diseases that arise because of point mutations in the dehydrogenase-coding region of the MFE-2 gene can be mapped to changes in amino acids involved in NAD(+) binding and protein dimerization.	NAD	164-170	hydroxysteroid (17-beta) dehydrogenase 4	Rattus norvegicus	101-106
12475791-1	2002	Twenty years ago, we first proposed our hypothesis on beta-cell damage and its prevention (the Okamoto model), according to which poly(ADP-ribose) synthetase/polymerase (PARP) activation is critically involved in the consumption of NAD(+), leading to energy depletion and cell death by necrosis.	NAD	232-238	poly (ADP-ribose) polymerase family, member 1	Mus musculus	130-168
12475791-1	2002	Twenty years ago, we first proposed our hypothesis on beta-cell damage and its prevention (the Okamoto model), according to which poly(ADP-ribose) synthetase/polymerase (PARP) activation is critically involved in the consumption of NAD(+), leading to energy depletion and cell death by necrosis.	NAD	232-238	poly (ADP-ribose) polymerase family, member 1	Mus musculus	170-174
12475791-6	2002	Because PARP is involved in Reg gene transcription to induce beta-cell regeneration, and the PARP activation reduces the cellular NAD(+) to decrease the formation of cADPR (a second messenger for insulin secretion) and further to cause necrotic beta-cell death, PARP and its inhibitors have key roles in the induction of beta-cell regeneration, the maintenance of insulin secretion, and the prevention of beta-cell death.	NAD	130-136	poly (ADP-ribose) polymerase family, member 1	Mus musculus	93-97
12475791-6	2002	Because PARP is involved in Reg gene transcription to induce beta-cell regeneration, and the PARP activation reduces the cellular NAD(+) to decrease the formation of cADPR (a second messenger for insulin secretion) and further to cause necrotic beta-cell death, PARP and its inhibitors have key roles in the induction of beta-cell regeneration, the maintenance of insulin secretion, and the prevention of beta-cell death.	NAD	130-136	poly (ADP-ribose) polymerase family, member 1	Mus musculus	93-97
12457869-7	2002	DNA damage caused by H(2)O(2) was shown to activate polyADP-ribosyl polymerase (PARP), leading to depletion of NAD and ATP.	NAD	111-114	poly (ADP-ribose) polymerase family, member 1	Mus musculus	52-78
12457869-7	2002	DNA damage caused by H(2)O(2) was shown to activate polyADP-ribosyl polymerase (PARP), leading to depletion of NAD and ATP.	NAD	111-114	poly (ADP-ribose) polymerase family, member 1	Mus musculus	80-84
12142562-2	2002	The cell death resulting from PARP1 activation is linked to NAD+ depletion and energy failure, but the intervening steps are not well understood.	NAD	60-64	poly (ADP-ribose) polymerase family, member 1	Mus musculus	30-35
11978644-1	2002	Poly(ADP-ribose) polymerase-1 (PARP-1) is a nuclear enzyme that consumes NAD in response to DNA strand breaks.	NAD	73-76	poly (ADP-ribose) polymerase family, member 1	Mus musculus	0-29
11978644-1	2002	Poly(ADP-ribose) polymerase-1 (PARP-1) is a nuclear enzyme that consumes NAD in response to DNA strand breaks.	NAD	73-76	poly (ADP-ribose) polymerase family, member 1	Mus musculus	31-37
11939620-11	2002	CONCLUSION: We conclude that insulin increases cGMP production in VSMC with iNOS by raising the cell NADH/NAD+ redox state, which may increase the availability of iNOS-derived NO.	NAD	106-110	insulin	Canis lupus familiaris	29-36
11874980-0	2002	A novel mechanism for coupling cellular intermediary metabolism to cytosolic Ca2+ signaling via CD38/ADP-ribosyl cyclase, a putative intracellular NAD+ sensor.	NAD	147-151	CD38 antigen	Mus musculus	96-100
11874980-1	2002	CD38 is an ectocyclase that converts NAD+ to the Ca2+-releasing second messenger cyclic ADP-ribose (cADPr).	NAD	37-41	CD38 antigen	Mus musculus	0-4
11874980-2	2002	Here we report that in addition to CD38 ecto-catalysis, intracellularly expressed CD38 may catalyze NAD+--&gt;cADPr conversion to cause cytosolic Ca2+ release.	NAD	100-106	CD38 antigen	Mus musculus	82-86
11874980-8	2002	The Delta(-49)-CD38-EGFP mutant with a deleted amino-terminal tail and transmembrane domain appeared mainly in the mitochondria with an expected loss of its membrane localization, but the NAD+-induced cytosolic Ca2+ signal was preserved.	NAD	188-192	CD38 antigen	Mus musculus	15-19
11874980-11	2002	We conclude that intracellularly expressed CD38 might link cellular NAD+ production to cytosolic Ca2+ signaling.	NAD	68-72	CD38 antigen	Mus musculus	43-47
11901108-6	2002	Deletion of a gene in the de novo NAD(+) synthesis pathway BNA1 resulted in a significant rDNA silencing defect only on medium deficient in nicotinic acid, an NAD(+) precursor.	NAD	34-40	3-hydroxyanthranilate 3,4-dioxygenase	Saccharomyces cerevisiae S288C	59-63
11901108-6	2002	Deletion of a gene in the de novo NAD(+) synthesis pathway BNA1 resulted in a significant rDNA silencing defect only on medium deficient in nicotinic acid, an NAD(+) precursor.	NAD	159-165	3-hydroxyanthranilate 3,4-dioxygenase	Saccharomyces cerevisiae S288C	59-63
11748298-0	2002	Detection of poly(ADP-ribose) polymerase activation in oxidatively stressed cells and tissues using biotinylated NAD substrate.	NAD	113-116	poly (ADP-ribose) polymerase family, member 1	Mus musculus	13-40
11748298-2	2002	Activated PARP cleaves NAD(+) into nicotinamide and (ADP-ribose) and polymerizes the latter on nuclear acceptor proteins.	NAD	23-29	poly (ADP-ribose) polymerase family, member 1	Mus musculus	10-14
11748298-9	2002	Hydrogen peroxide-induced PARP activation and its inhibition by pharmacological PARP inhibitors could be detected in J774 cells with the ELISA assay that showed good correlation with the traditional [(3)H]-NAD incorporation method.	NAD	206-209	poly (ADP-ribose) polymerase family, member 1	Mus musculus	26-30
11748298-9	2002	Hydrogen peroxide-induced PARP activation and its inhibition by pharmacological PARP inhibitors could be detected in J774 cells with the ELISA assay that showed good correlation with the traditional [(3)H]-NAD incorporation method.	NAD	206-209	poly (ADP-ribose) polymerase family, member 1	Mus musculus	80-84
11748298-10	2002	The bio-NAD(+) assays represent sensitive, specific, and non-radioactive alternatives for detection of PARP activation.	NAD	8-14	poly (ADP-ribose) polymerase family, member 1	Mus musculus	103-107
11602597-0	2001	A self-restricted CD38-connexin 43 cross-talk affects NAD+ and cyclic ADP-ribose metabolism and regulates intracellular calcium in 3T3 fibroblasts.	NAD	54-58	CD38 antigen	Mus musculus	18-22
11602597-1	2001	Connexin 43 (Cx43) hexameric hemichannels, recently demonstrated to mediate NAD(+) transport, functionally interact in the plasma membrane of several cells with the ectoenzyme CD38 that converts NAD(+) to the universal calcium mobilizer cyclic ADP-ribose (cADPR).	NAD	76-82	CD38 antigen	Mus musculus	176-180
11602597-1	2001	Connexin 43 (Cx43) hexameric hemichannels, recently demonstrated to mediate NAD(+) transport, functionally interact in the plasma membrane of several cells with the ectoenzyme CD38 that converts NAD(+) to the universal calcium mobilizer cyclic ADP-ribose (cADPR).	NAD	195-201	CD38 antigen	Mus musculus	176-180
11602597-2	2001	Here we demonstrate that functional uncoupling between CD38 and Cx43 in CD38-transfected 3T3 murine fibroblasts is paralleled by decreased [Ca(2+)](i) levels as a result of reduced intracellular conversion of NAD(+) to cADPR.	NAD	209-215	CD38 antigen	Mus musculus	55-59
11602597-2	2001	Here we demonstrate that functional uncoupling between CD38 and Cx43 in CD38-transfected 3T3 murine fibroblasts is paralleled by decreased [Ca(2+)](i) levels as a result of reduced intracellular conversion of NAD(+) to cADPR.	NAD	209-215	CD38 antigen	Mus musculus	72-76
11602597-3	2001	A sharp inverse correlation emerged between [Ca(2+)](i) levels and NAD(+) transport (measured as influx into cells and as efflux therefrom), both in the CD38(+) cells (high [Ca(2+)](i), low transport) and in the CD38(-) fibroblasts (low [Ca(2+)](i), high transport).	NAD	67-73	CD38 antigen	Mus musculus	153-157
11602597-3	2001	A sharp inverse correlation emerged between [Ca(2+)](i) levels and NAD(+) transport (measured as influx into cells and as efflux therefrom), both in the CD38(+) cells (high [Ca(2+)](i), low transport) and in the CD38(-) fibroblasts (low [Ca(2+)](i), high transport).	NAD	67-73	CD38 antigen	Mus musculus	212-216
11722568-5	2001	rNOX1 catalyzes the oxidation of NADH, producing both H(2)O(2) and H(2)O as reduction products of O(2) (O(2) + 1-2NADH + 1-2H(+) --&gt; 1-2NAD(+) + H(2)O(2) or 2H(2)O).	NAD	33-37	NADPH oxidase 1	Rattus norvegicus	0-5
11672522-3	2001	Nicotinamide (Vitamin B3) inhibits an NAD-dependent p53 deacetylation induced by Sir2alpha, and also enhances the p53 acetylation levels in vivo.	NAD	38-41	sirtuin 1	Homo sapiens	81-90
11672523-0	2001	hSIR2(SIRT1) functions as an NAD-dependent p53 deacetylase.	NAD	29-32	sirtuin 1	Homo sapiens	0-5
11672523-0	2001	hSIR2(SIRT1) functions as an NAD-dependent p53 deacetylase.	NAD	29-32	sirtuin 1	Homo sapiens	6-11
11461900-7	2001	The TNF-induced activation of poly(ADP-ribose) polymerase (PARP), which requires PARP binding to DNA strand breaks, and the consequent depletion of the PARP substrate NAD were markedly delayed in DFF45(-/-) cells, suggesting a role for DFF in PARP activation.	NAD	167-170	poly (ADP-ribose) polymerase family, member 1	Mus musculus	59-63
11461900-7	2001	The TNF-induced activation of poly(ADP-ribose) polymerase (PARP), which requires PARP binding to DNA strand breaks, and the consequent depletion of the PARP substrate NAD were markedly delayed in DFF45(-/-) cells, suggesting a role for DFF in PARP activation.	NAD	167-170	DNA fragmentation factor, alpha subunit	Mus musculus	196-201
11707529-11	2001	Taken together, these experiments indicate that the apoptotic DBD of PARP-1 acts cooperatively with the proteolytic inactivation of the enzyme to trans-inhibit NAD hydrolysis and to maintain the energy levels of the cell.	NAD	160-163	poly (ADP-ribose) polymerase family, member 1	Mus musculus	69-75
11665837-7	2001	Taken together, it is suggested that NADH/NADPH oxidase-derived superoxide is implicated in periarterial blood-induced vasospasm via increased expression of ICAM-1 with subsequent mobilization of granulocyte/macrophage.	NAD	37-41	intercellular adhesion molecule 1	Rattus norvegicus	157-163
11418099-5	2001	However, there were striking exceptions where an apparent interaction was found between the PSST and ND1 subunits: preincubation with NADH increases PSST labeling and decreases ND1 labeling; the very weak complex I inhibitor 1-methyl-4-phenylpyridinium ion (MPP(+)) and the semiquinone analogue stigmatellin show the opposite effect with increased labeling at ND1 coupled to decreased labeling at PSST in a concentration- and time-dependent manner.	NAD	134-138	NADH:ubiquinone oxidoreductase core subunit S7	Homo sapiens	92-96
11418099-5	2001	However, there were striking exceptions where an apparent interaction was found between the PSST and ND1 subunits: preincubation with NADH increases PSST labeling and decreases ND1 labeling; the very weak complex I inhibitor 1-methyl-4-phenylpyridinium ion (MPP(+)) and the semiquinone analogue stigmatellin show the opposite effect with increased labeling at ND1 coupled to decreased labeling at PSST in a concentration- and time-dependent manner.	NAD	134-138	NADH:ubiquinone oxidoreductase core subunit S7	Homo sapiens	149-153
11418099-5	2001	However, there were striking exceptions where an apparent interaction was found between the PSST and ND1 subunits: preincubation with NADH increases PSST labeling and decreases ND1 labeling; the very weak complex I inhibitor 1-methyl-4-phenylpyridinium ion (MPP(+)) and the semiquinone analogue stigmatellin show the opposite effect with increased labeling at ND1 coupled to decreased labeling at PSST in a concentration- and time-dependent manner.	NAD	134-138	NADH:ubiquinone oxidoreductase core subunit S7	Homo sapiens	149-153
11508269-4	2001	METHODS: ART2.2 and CD38, another NAD-utilizing enzyme, were measured by flow cytometry.	NAD	34-37	CD38 antigen	Mus musculus	20-24
11376692-1	2001	Poly(ADP-ribose) polymerase (Parp) monitors DNA strand breaks and poly(ADP-ribosyl)ates nuclear proteins using NAD as a substrate.	NAD	111-114	poly (ADP-ribose) polymerase family, member 1	Mus musculus	0-27
11376692-1	2001	Poly(ADP-ribose) polymerase (Parp) monitors DNA strand breaks and poly(ADP-ribosyl)ates nuclear proteins using NAD as a substrate.	NAD	111-114	poly (ADP-ribose) polymerase family, member 1	Mus musculus	29-33
11410738-6	2001	RESULTS: Class I, III, and IV ADH activities were 17.5 +/- 8.4, 4.2 +/- 2.5, and 8.9 +/- 3.9 nmol of nicotinamide adenine dinucleotide oxidation per minute per milligram of protein, respectively, for the entire population.	NAD	101-134	aldo-keto reductase family 1 member A1	Homo sapiens	30-33
11371181-8	2001	In the NADH-menadione oxidoreductase reaction, the reduction of the flavin by NADH is rate limiting as is the reduction of flavin by CH(3)-H(4)folate in the CH(3)-H(4)folate-menadione oxidoreductase reaction.	NAD	7-11	oxidoreductase	Escherichia coli	22-36
11371181-8	2001	In the NADH-menadione oxidoreductase reaction, the reduction of the flavin by NADH is rate limiting as is the reduction of flavin by CH(3)-H(4)folate in the CH(3)-H(4)folate-menadione oxidoreductase reaction.	NAD	7-11	oxidoreductase	Escherichia coli	184-198
11443349-11	2001	Probably these lyases descend from an SDR, which has lost the capability to bind NAD+, but the enzyme reaction mechanisms may still be similar.	NAD	81-85	Secreted decoy of InR	Drosophila melanogaster	38-41
11141304-7	2001	The electrocatalytic oxidation of NADH and the subsequent ADH-catalyzed formation of NADH are monitored electrochemically.	NAD	85-89	aldo-keto reductase family 1 member A1	Homo sapiens	35-38
11153263-1	2001	The nicotinamide adenine dinucleotides (NAD, NADH, NADP, and NADPH) are essential cofactors in all living systems and function as hydride acceptors (NAD, NADP) and hydride donors (NADH, NADPH) in biochemical redox reactions.	NAD	4-38	2,4-dienoyl-CoA reductase 1	Homo sapiens	61-66
11153263-1	2001	The nicotinamide adenine dinucleotides (NAD, NADH, NADP, and NADPH) are essential cofactors in all living systems and function as hydride acceptors (NAD, NADP) and hydride donors (NADH, NADPH) in biochemical redox reactions.	NAD	4-38	2,4-dienoyl-CoA reductase 1	Homo sapiens	186-191
11153263-1	2001	The nicotinamide adenine dinucleotides (NAD, NADH, NADP, and NADPH) are essential cofactors in all living systems and function as hydride acceptors (NAD, NADP) and hydride donors (NADH, NADPH) in biochemical redox reactions.	NAD	40-43	2,4-dienoyl-CoA reductase 1	Homo sapiens	186-191
11153263-1	2001	The nicotinamide adenine dinucleotides (NAD, NADH, NADP, and NADPH) are essential cofactors in all living systems and function as hydride acceptors (NAD, NADP) and hydride donors (NADH, NADPH) in biochemical redox reactions.	NAD	45-49	2,4-dienoyl-CoA reductase 1	Homo sapiens	186-191
11153263-1	2001	The nicotinamide adenine dinucleotides (NAD, NADH, NADP, and NADPH) are essential cofactors in all living systems and function as hydride acceptors (NAD, NADP) and hydride donors (NADH, NADPH) in biochemical redox reactions.	NAD	45-48	2,4-dienoyl-CoA reductase 1	Homo sapiens	186-191
11153263-1	2001	The nicotinamide adenine dinucleotides (NAD, NADH, NADP, and NADPH) are essential cofactors in all living systems and function as hydride acceptors (NAD, NADP) and hydride donors (NADH, NADPH) in biochemical redox reactions.	NAD	180-184	2,4-dienoyl-CoA reductase 1	Homo sapiens	61-66
11095743-5	2000	Two genes appear to participate in feedback loops that modulate HDAC activity: ZRT1 encodes a zinc transporter and is repressed by RPD3 (Rpd3p is zinc-dependent); BNA1 encodes a nicotinamide adenine dinucleotide (NAD)-biosynthesis enzyme and is repressed by SIR2 (Sir2p is NAD-dependent).	NAD	178-211	histone deacetylase	Saccharomyces cerevisiae S288C	64-68
11095743-5	2000	Two genes appear to participate in feedback loops that modulate HDAC activity: ZRT1 encodes a zinc transporter and is repressed by RPD3 (Rpd3p is zinc-dependent); BNA1 encodes a nicotinamide adenine dinucleotide (NAD)-biosynthesis enzyme and is repressed by SIR2 (Sir2p is NAD-dependent).	NAD	213-216	histone deacetylase	Saccharomyces cerevisiae S288C	64-68
11095743-5	2000	Two genes appear to participate in feedback loops that modulate HDAC activity: ZRT1 encodes a zinc transporter and is repressed by RPD3 (Rpd3p is zinc-dependent); BNA1 encodes a nicotinamide adenine dinucleotide (NAD)-biosynthesis enzyme and is repressed by SIR2 (Sir2p is NAD-dependent).	NAD	273-276	histone deacetylase	Saccharomyces cerevisiae S288C	64-68
11080311-5	2000	The basic biochemical properties of the monofunctional SDH, including its pH optimum as well as the apparent Michaelis constant (K(m)) values for its substrates saccharopine and nicotinamide adenine dinucleotide at neutral and basic pH values, were similar to those of its SDH counterpart that is linked to LKR.	NAD	178-211	lysine-ketoglutarate reductase/saccharopine dehydrogenase bifunctional enzyme	Arabidopsis thaliana	55-58
10733557-10	2000	ADH gammagamma isozyme was identified as the iso bile acid 3beta-HSD present in human liver cytosol, with NAD(+) as a cofactor.	NAD	106-112	aldo-keto reductase family 1 member A1	Homo sapiens	0-3
10733557-10	2000	ADH gammagamma isozyme was identified as the iso bile acid 3beta-HSD present in human liver cytosol, with NAD(+) as a cofactor.	NAD	106-112	hydroxy-delta-5-steroid dehydrogenase, 3 beta- and steroid delta-isomerase 1	Homo sapiens	59-68
10774743-8	2000	This result indicates that GDH saturated with NADH or 2-oxoglutarate is still open to attack by phenylglyoxal.	NAD	46-50	Glu/Leu/Phe/Val dehydrogenase	Saccharolobus solfataricus	27-30
10625631-7	2000	A detergent-containing system was reconstructed with thylakoid Ndh complex and peroxidase which oxidized NADH with H(2)O(2) in a plastoquinone-dependent process.	NAD	105-109	prx7	Hordeum vulgare	79-89
10562410-5	1999	This cytokine-mediated increase in NAD concentration was markedly enhanced by the inhibition of poly(ADP-ribose) polymerase or nitric oxide synthase or following treatment with the synthetic glucocorticoid dexamethasone.	NAD	35-38	poly (ADP-ribose) polymerase family, member 1	Mus musculus	96-123
10492239-1	1999	PURPOSE: Biliverdin reductase is an oxidoreductase unique among all enzymes characterized to date in having dual pH/dual cofactor requirement - NADH and NADPH at 6.7 and 8.7, respectively.	NAD	144-148	thioredoxin reductase 1	Homo sapiens	36-50
10462438-0	1999	Prediction of the active-site structure and NAD(+) binding in SQD1, a protein essential for sulfolipid biosynthesis in Arabidopsis.	NAD	44-50	sulfoquinovosyldiacylglycerol 1	Arabidopsis thaliana	62-66
10423528-4	1999	The expressed GST-4ABH fusion protein (recombinant 4ABH) in the soluble fraction exhibits decarboxylative hydroxylation and additional NADH oxidation activities.We investigated a new ultraviolet spectrometric method for determining serum gamma-glutamyltransferase (gamma-GT) using recombinant 4ABH as a coupling enzyme.	NAD	135-139	alkB homolog 1, histone H2A dioxygenase	Homo sapiens	19-22
10381390-4	1999	We have identified YLNDH2 as the only gene encoding an alternative NADH:ubiquinone oxidoreductase (NDH2) in the obligate aerobic yeast Yarrowia lipolytica.	NAD	67-71	NADH-ubiquinone reductase (H(+)-translocating) NDE2	Saccharomyces cerevisiae S288C	21-25
10318960-3	1999	We show that mice lacking the gene for poly(ADP-ribose) polymerase (PARP), which catalyzes the attachment of ADP ribose units from NAD to nuclear proteins after DNA damage, are dramatically spared from MPTP neurotoxicity.	NAD	131-134	poly (ADP-ribose) polymerase family, member 1	Mus musculus	39-66
10318960-3	1999	We show that mice lacking the gene for poly(ADP-ribose) polymerase (PARP), which catalyzes the attachment of ADP ribose units from NAD to nuclear proteins after DNA damage, are dramatically spared from MPTP neurotoxicity.	NAD	131-134	poly (ADP-ribose) polymerase family, member 1	Mus musculus	68-72
10224250-4	1999	We have previously reported a novel phenotype associated with mutants defective in the IDH2 gene encoding the Idh2p subunit of the NAD+-dependent isocitrate dehydrogenase (NAD-IDH).	NAD	131-135	isocitrate dehydrogenase (NAD(+)) IDH2	Saccharomyces cerevisiae S288C	87-91
10224250-4	1999	We have previously reported a novel phenotype associated with mutants defective in the IDH2 gene encoding the Idh2p subunit of the NAD+-dependent isocitrate dehydrogenase (NAD-IDH).	NAD	131-135	isocitrate dehydrogenase (NAD(+)) IDH2	Saccharomyces cerevisiae S288C	110-115
10077636-2	1999	Poly(ADP-ribose) polymerase (PARP) is a nuclear enzyme whose overactivation by DNA strand breaks depletes its substrate NAD+ and then ATP, leading to cellular death from energy depletion.	NAD	120-124	poly (ADP-ribose) polymerase family, member 1	Mus musculus	0-27
10077636-2	1999	Poly(ADP-ribose) polymerase (PARP) is a nuclear enzyme whose overactivation by DNA strand breaks depletes its substrate NAD+ and then ATP, leading to cellular death from energy depletion.	NAD	120-124	poly (ADP-ribose) polymerase family, member 1	Mus musculus	29-33
10068448-1	1999	CD38 is a 46-kDa type II transmembrane glycoprotein that catalyses the synthesis of cyclic ADP-ribose (cADPR) from NAD+.	NAD	115-119	ADP-ribosyl cyclase/cyclic ADP-ribose hydrolase 1	Cricetulus griseus	0-4
10086388-5	1999	Cultivated PARP-/- islet cells resisted streptozocin-induced lysis and maintained intracellular NAD+ levels.	NAD	96-100	poly (ADP-ribose) polymerase family, member 1	Mus musculus	11-15
10086388-6	1999	Our results identify NAD+ depletion caused by PARP activation as the dominant metabolic event in islet-cell destruction, and provide information for the development of strategies to prevent the progression or manifestation of the disease in individuals at risk of developing type 1 diabetes.	NAD	21-25	poly (ADP-ribose) polymerase family, member 1	Mus musculus	46-50
9872926-6	1999	Sorbitol dehydrogenase, the second enzyme in the polyol pathway that converts sorbitol to fructose, also contributes to oxidative stress, most likely because depletion of its cofactor NAD+ leads to more glucose being channeled through the polyol pathway.	NAD	184-188	sorbitol dehydrogenase	Mus musculus	0-22
9733747-0	1998	The Saccharomyces cerevisiae NDE1 and NDE2 genes encode separate mitochondrial NADH dehydrogenases catalyzing the oxidation of cytosolic NADH.	NAD	79-83	NADH-ubiquinone reductase (H(+)-translocating) NDE1	Saccharomyces cerevisiae S288C	29-33
9733747-0	1998	The Saccharomyces cerevisiae NDE1 and NDE2 genes encode separate mitochondrial NADH dehydrogenases catalyzing the oxidation of cytosolic NADH.	NAD	79-83	NADH-ubiquinone reductase (H(+)-translocating) NDE2	Saccharomyces cerevisiae S288C	38-42
9733747-3	1998	To investigate whether open reading frames YMR145c/NDE1 and YDL 085w/NDE2, which exhibit sequence similarity with NDI1, encode the latter enzyme, NADH-dependent mitochondrial respiration was assayed in wild-type S. cerevisiae and nde deletion mutants.	NAD	146-150	NADH-ubiquinone reductase (H(+)-translocating) NDE1	Saccharomyces cerevisiae S288C	51-55
9733747-3	1998	To investigate whether open reading frames YMR145c/NDE1 and YDL 085w/NDE2, which exhibit sequence similarity with NDI1, encode the latter enzyme, NADH-dependent mitochondrial respiration was assayed in wild-type S. cerevisiae and nde deletion mutants.	NAD	146-150	NADH-ubiquinone reductase (H(+)-translocating) NDE2	Saccharomyces cerevisiae S288C	69-73
9733747-11	1998	Apparently, under these conditions alternative systems for reoxidation of cytosolic NADH could replace the role of Nde1p and Nde2p in S. cerevisiae.	NAD	84-88	NADH-ubiquinone reductase (H(+)-translocating) NDE1	Saccharomyces cerevisiae S288C	115-120
9733747-11	1998	Apparently, under these conditions alternative systems for reoxidation of cytosolic NADH could replace the role of Nde1p and Nde2p in S. cerevisiae.	NAD	84-88	NADH-ubiquinone reductase (H(+)-translocating) NDE2	Saccharomyces cerevisiae S288C	125-130
9707645-10	1998	Nonsymbiotic hemoglobins are likely ancestors of an early form of hemoglobin that sequestered oxygen in low oxygen environments, providing a source of oxygen to oxidize NADH to provide ATP for cell growth and development.	NAD	169-173	non-symbiotic hemoglobin	Zea mays	13-23
9694721-2	1998	The extracellular domain of CD38 can mediate the catalysis of NAD+ to cyclic adenosine diphosphoribose (cADPR), a Ca2+-mobilizing second messenger, adenosine diphosphoribose (ADPR), and nicotinamide.	NAD	62-66	CD38 antigen	Mus musculus	28-32
9888536-7	1998	Furthermore, the coenzyme-activation profiles support our proposed two-step enzyme mechanism in which NADH produced by the 3beta-HSD activity induces the enzyme to assume the isomerase conformation.	NAD	102-106	hydroxy-delta-5-steroid dehydrogenase, 3 beta- and steroid delta-isomerase 1	Homo sapiens	123-132
9696750-5	1998	Disruption of the gene designated NDH1 results in a threefold reduction in total mitochondrial NADH dehydrogenase activity in cells cultivated with glucose and in a fourfold reduction in the respiration of isolated mitochondria with NADH as the substrate.	NAD	95-99	NADH-ubiquinone reductase (H(+)-translocating) NDE1	Saccharomyces cerevisiae S288C	34-38
9696750-6	1998	Thus, Ndh1p appears to be a mitochondrial dehydrogenase capable of using exogenous NADH.	NAD	83-87	NADH-ubiquinone reductase (H(+)-translocating) NDE1	Saccharomyces cerevisiae S288C	6-11
9696750-9	1998	Codisruption of NDH1 and genes encoding malate dehydrogenases essentially eliminates growth on nonfermentable carbon sources, suggesting that the external mitochondrial NADH dehydrogenase and the malate-aspartate shuttle may both contribute to reoxidation of cytosolic NADH under these growth conditions.	NAD	169-173	NADH-ubiquinone reductase (H(+)-translocating) NDE1	Saccharomyces cerevisiae S288C	16-20
9616178-0	1998	Lymphocyte-specific protein 1 expression in eukaryotic cells reproduces the morphologic and motile abnormality of NAD 47/89 neutrophils.	NAD	114-117	lymphocyte specific protein 1	Homo sapiens	0-29
9616178-4	1998	We now show that overexpression of LSP1 produces F-actin bundles that are likely responsible for the morphologic and motile abnormalities characteristic of the NAD 47/89 phenotype.	NAD	160-163	lymphocyte specific protein 1	Homo sapiens	35-39
9616178-8	1998	Therefore, these studies show that overexpression of LSP1 alone can recreate the morphologic and motile defects seen in NAD 47/89 and suggest that LSP1 is distinct from other known actin binding proteins in its effect on F-actin network structure.	NAD	120-123	lymphocyte specific protein 1	Homo sapiens	53-57
9625705-0	1998	The NAD(P)H dehydrogenase in barley thylakoids is photoactivatable and uses NADPH as well as NADH An improved light-dependent assay was used to characterize the NAD(P)H dehydrogenase (NDH) in thylakoids of barley (Hordeum vulgare L.).	NAD	93-97	PorB	Hordeum vulgare	4-25
9625705-0	1998	The NAD(P)H dehydrogenase in barley thylakoids is photoactivatable and uses NADPH as well as NADH An improved light-dependent assay was used to characterize the NAD(P)H dehydrogenase (NDH) in thylakoids of barley (Hordeum vulgare L.).	NAD	93-97	PorB	Hordeum vulgare	5-26
9625705-0	1998	The NAD(P)H dehydrogenase in barley thylakoids is photoactivatable and uses NADPH as well as NADH An improved light-dependent assay was used to characterize the NAD(P)H dehydrogenase (NDH) in thylakoids of barley (Hordeum vulgare L.).	NAD	93-97	PorB	Hordeum vulgare	185-188
9586947-8	1998	Upon reconstitution, human liver b5 plus NADH:b5 reductase and CYP2C9 plus NADPH:P450 reductase were both effective catalysts of AZT reduction, which was also supported when CYP2A6 or CYP2E1 was substituted for CYP2C9.	NAD	41-45	cytochrome P450 family 2 subfamily A member 6	Homo sapiens	174-180
9559543-10	1998	Our results also demonstrated that of the two isoforms of NAD-dependent glycerol 3-phosphate dehydrogenase, only the enzyme encoded by GPD1 appeared important for the shuttle, since the enhanced glycerol production that occurs in a gut2 delta strain proved dependent on GPD1 but not on GPD2.	NAD	58-61	glycerol-3-phosphate dehydrogenase (NAD(+)) GPD1	Saccharomyces cerevisiae S288C	135-139
9559543-10	1998	Our results also demonstrated that of the two isoforms of NAD-dependent glycerol 3-phosphate dehydrogenase, only the enzyme encoded by GPD1 appeared important for the shuttle, since the enhanced glycerol production that occurs in a gut2 delta strain proved dependent on GPD1 but not on GPD2.	NAD	58-61	glycerol-3-phosphate dehydrogenase (NAD(+)) GPD1	Saccharomyces cerevisiae S288C	270-274
9293375-2	1997	When the purified LD mixed with NADH was eluted through the CNBr-Sepharose 4B coupled to Suzuki-BJP or Miki-IgG, the affinity with these adsorbents was not demonstrated.	NAD	32-36	HEPACAM family member 2	Homo sapiens	103-107
9166744-3	1997	NO is known to increase the amount of radioisotopic labeled glyceraldehyde-3-phosphate dehydrogenase (GAPDH) in the presence of [32P]NAD and to inhibit the enzyme activity.	NAD	133-136	glyceraldehyde-3-phosphate dehydrogenase	Mus musculus	60-100
9166744-3	1997	NO is known to increase the amount of radioisotopic labeled glyceraldehyde-3-phosphate dehydrogenase (GAPDH) in the presence of [32P]NAD and to inhibit the enzyme activity.	NAD	133-136	glyceraldehyde-3-phosphate dehydrogenase	Mus musculus	102-107
9148900-2	1997	An additional enzymatic activity of CD38 shared by monofunctional ADP-ribosyl cyclase from Aplysia californica is the exchange of the base group of NAD+ (nicotinamide) with various nucleophiles.	NAD	148-152	ADP-ribosyl cyclase/cyclic ADP-ribose hydrolase	Aplysia californica	66-85
9195888-6	1997	RESULTS: The X-ray structure of bovine ALDH2 has been solved to 2.65 A in its free form and to 2.75 A in a complex with NAD+.	NAD	120-124	aldehyde dehydrogenase 2 family member	Bos taurus	39-44
9195888-9	1997	The active site of ALDH2 is divided into two halves by the nicotinamide ring of NAD+.	NAD	80-84	aldehyde dehydrogenase 2 family member	Bos taurus	19-24
9195888-11	1997	CONCLUSIONS: Although there is a recognizable Rossmann-type fold, the coenzyme-binding region of ALDH2 binds NAD+ in a manner not seen in other NAD+-binding enzymes.	NAD	109-113	aldehyde dehydrogenase 2 family member	Bos taurus	97-102
9195888-11	1997	CONCLUSIONS: Although there is a recognizable Rossmann-type fold, the coenzyme-binding region of ALDH2 binds NAD+ in a manner not seen in other NAD+-binding enzymes.	NAD	144-148	aldehyde dehydrogenase 2 family member	Bos taurus	97-102
9171333-0	1997	The two isoenzymes for yeast NAD+-dependent glycerol 3-phosphate dehydrogenase encoded by GPD1 and GPD2 have distinct roles in osmoadaptation and redox regulation.	NAD	29-33	glycerol-3-phosphate dehydrogenase (NAD(+)) GPD1	Saccharomyces cerevisiae S288C	90-94
9171333-1	1997	The two homologous genes GPD1 and GPD2 encode the isoenzymes of NAD-dependent glycerol 3-phosphate dehydrogenase in the yeast Saccharomyces cerevisiae.	NAD	64-67	glycerol-3-phosphate dehydrogenase (NAD(+)) GPD1	Saccharomyces cerevisiae S288C	25-29
9168606-0	1997	Escherichia coli flavohaemoglobin (Hmp) reduces cytochrome c and Fe(III)-hydroxamate K by electron transfer from NADH via FAD: sensitivity of oxidoreductase activity to haem-bound dioxygen.	NAD	113-117	oxidoreductase	Escherichia coli	142-156
9113998-4	1997	In view of the strict stereospecificity of catalysis by LDH and the conformational averaging of bound NAD+ that we infer from solution-state NMR, we suggest that LDH binds the cofactor in both syn and anti conformations, but that binding interactions in the syn conformation are not catalytically productive.	NAD	102-106	synemin	Homo sapiens	193-196
9113998-4	1997	In view of the strict stereospecificity of catalysis by LDH and the conformational averaging of bound NAD+ that we infer from solution-state NMR, we suggest that LDH binds the cofactor in both syn and anti conformations, but that binding interactions in the syn conformation are not catalytically productive.	NAD	102-106	synemin	Homo sapiens	258-261
9125501-2	1997	A reaction mechanism for proton and hydride transfers associated with MDH and cofactor nicotinamide adenine dinucleotide (NAD) is deduced from the topology of the calculated energy surface.	NAD	87-120	malic enzyme 1	Homo sapiens	70-73
9125501-2	1997	A reaction mechanism for proton and hydride transfers associated with MDH and cofactor nicotinamide adenine dinucleotide (NAD) is deduced from the topology of the calculated energy surface.	NAD	122-125	malic enzyme 1	Homo sapiens	70-73
9133646-4	1997	The enzyme had an apparent subunit molecular weight of 54000, required NAD+ as cofactor, had optimal activity at pH 9.8, and was thermolabile at 47 degrees C. Fatty aldehyde dehydrogenase had high activity towards saturated and unsaturated aliphatic aldehydes ranging from 6 to 24 carbons in length, as well as dihydrophytal, a 20-carbon branched chain aldehyde.	NAD	71-75	aldehyde dehydrogenase 3 family member A2	Homo sapiens	159-187
9079661-3	1997	The oxidative half-reaction of XDH with molecular oxygen has been studied in detail, at 25 degrees C, pH 7.5, to determine the basis of the preference of XDH for NAD over oxygen as oxidizing substrate.	NAD	162-165	xanthine dehydrogenase	Bos taurus	31-34
9079661-3	1997	The oxidative half-reaction of XDH with molecular oxygen has been studied in detail, at 25 degrees C, pH 7.5, to determine the basis of the preference of XDH for NAD over oxygen as oxidizing substrate.	NAD	162-165	xanthine dehydrogenase	Bos taurus	154-157