PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
25331892-0	2014	VEGF-induced neoangiogenesis is mediated by NAADP and two-pore channel-2-dependent Ca2+ signaling.	NAADP	44-49	vascular endothelial growth factor A	Mus musculus	0-4
25331892-4	2014	Targeting this intracellular pathway pharmacologically using the NAADP antagonist Ned-19 or genetically using Tpcn2(-/-) mice was found to inhibit angiogenic responses to VEGF in vitro and in vivo.	NAADP	65-70	vascular endothelial growth factor A	Mus musculus	171-175
25331892-8	2014	These results demonstrate that a VEGFR2/NAADP/TPC2/Ca(2+) signaling pathway is critical for VEGF-induced angiogenesis in vitro and in vivo.	NAADP	40-45	kinase insert domain protein receptor	Mus musculus	33-39
25331892-8	2014	These results demonstrate that a VEGFR2/NAADP/TPC2/Ca(2+) signaling pathway is critical for VEGF-induced angiogenesis in vitro and in vivo.	NAADP	40-45	vascular endothelial growth factor A	Mus musculus	33-37
25157141-7	2014	Nicotinic acid adenine dinucleotide phosphate (NAADP)-evoked Ca(2+) release was also impaired using either a Rab binding-defective TPC2 mutant or a Rab inhibitor.	NAADP	0-45	two pore segment channel 2	Homo sapiens	131-135
25275102-1	2014	In addition to mobilizing Ca2+, NAADP plays a role in modulating the luminal pH (pHL) of acidic stores of the endolysosomal system.	NAADP	32-37	BCR activator of RhoGEF and GTPase	Homo sapiens	81-84
25275102-2	2014	The effects of NAADP on pHL have been most extensively studied in the sea urchin egg, both in the intact egg and in egg homogenates.	NAADP	15-20	BCR activator of RhoGEF and GTPase	Homo sapiens	24-27
25275102-4	2014	Although the connection between Ca2+ mobilization and increase in pHL is not understood, pHL can be a useful parameter to measure when studying NAADP-mediated signaling.	NAADP	144-149	BCR activator of RhoGEF and GTPase	Homo sapiens	89-92
25157141-7	2014	Nicotinic acid adenine dinucleotide phosphate (NAADP)-evoked Ca(2+) release was also impaired using either a Rab binding-defective TPC2 mutant or a Rab inhibitor.	NAADP	47-52	two pore segment channel 2	Homo sapiens	131-135
24451262-2	2014	Hence, the second messenger NAADP, promoting efflux of calcium from lysosome-like compartments and one of its potential molecular targets, the two-pore channel 1 (TPC1), were analyzed for its involvement in triggering the acrosome reaction using a TPCN1 gene-deficient mouse strain.	NAADP	28-33	two pore channel 1	Mus musculus	163-167
25126414-2	2014	In pulmonary artery smooth muscle cells (PASMCs) it has been proposed that nicotinic acid adenine dinucleotide phosphate (NAADP) triggers increases in cytoplasmic Ca (2+) via L-SR junctions, in a manner that requires initial Ca (2+) release from lysosomes and subsequent Ca (2+)-induced Ca (2+) release (CICR) via ryanodine receptor (RyR) subtype 3 on the SR membrane proximal to lysosomes.	NAADP	75-120	ryanodine receptor 1	Homo sapiens	314-332
25126414-2	2014	In pulmonary artery smooth muscle cells (PASMCs) it has been proposed that nicotinic acid adenine dinucleotide phosphate (NAADP) triggers increases in cytoplasmic Ca (2+) via L-SR junctions, in a manner that requires initial Ca (2+) release from lysosomes and subsequent Ca (2+)-induced Ca (2+) release (CICR) via ryanodine receptor (RyR) subtype 3 on the SR membrane proximal to lysosomes.	NAADP	75-120	ryanodine receptor 1	Homo sapiens	334-337
25126414-2	2014	In pulmonary artery smooth muscle cells (PASMCs) it has been proposed that nicotinic acid adenine dinucleotide phosphate (NAADP) triggers increases in cytoplasmic Ca (2+) via L-SR junctions, in a manner that requires initial Ca (2+) release from lysosomes and subsequent Ca (2+)-induced Ca (2+) release (CICR) via ryanodine receptor (RyR) subtype 3 on the SR membrane proximal to lysosomes.	NAADP	122-127	ryanodine receptor 1	Homo sapiens	314-332
25126414-2	2014	In pulmonary artery smooth muscle cells (PASMCs) it has been proposed that nicotinic acid adenine dinucleotide phosphate (NAADP) triggers increases in cytoplasmic Ca (2+) via L-SR junctions, in a manner that requires initial Ca (2+) release from lysosomes and subsequent Ca (2+)-induced Ca (2+) release (CICR) via ryanodine receptor (RyR) subtype 3 on the SR membrane proximal to lysosomes.	NAADP	122-127	ryanodine receptor 1	Homo sapiens	334-337
25126414-7	2014	Simulations of NAADP-dependent junctional Ca (2+) transients demonstrate that the magnitude of these signals can breach the threshold for CICR via RyR3.	NAADP	15-20	ryanodine receptor 3	Homo sapiens	147-151
24972488-10	2014	Exposure of RyR1 channels to cyclic ADP ribose (cADPr), nicotinic acid adenine dinucleotide phosphate (NAADP) or dantrolene did not alter the single channel activity stimulated by Ca(2+), and thus, it is unlikely these molecules directly modulate RyR1 channel activity.	NAADP	56-101	ryanodine receptor 1	Homo sapiens	12-16
24847115-0	2014	Reconstituted human TPC1 is a proton-permeable ion channel and is activated by NAADP or Ca2+.	NAADP	79-84	two pore segment channel 1	Homo sapiens	20-24
24847115-5	2014	NAADP or Ca2+ activated TPC1, and the presence of one of these ligands was required for channel activation.	NAADP	0-5	two pore segment channel 1	Homo sapiens	24-28
24847115-7	2014	Furthermore, our data showed that, although both TPC1 and TPC2 are stimulated by NAADP, these channels differ in ion selectivity and modulation by Ca2+ and pH.	NAADP	81-86	two pore segment channel 1	Homo sapiens	49-53
24847115-7	2014	Furthermore, our data showed that, although both TPC1 and TPC2 are stimulated by NAADP, these channels differ in ion selectivity and modulation by Ca2+ and pH.	NAADP	81-86	two pore segment channel 2	Homo sapiens	58-62
24847115-8	2014	We propose that NAADP triggers H+ release from lysosomes and endolysomes through activation of TPC1, but that the Ca2+ -releasing ability of TPC1 will depend on the ionic composition of the acidic stores and may be influenced by other regulators that affect TPC1 ion permeation.	NAADP	16-21	two pore segment channel 1	Homo sapiens	95-99
24445604-3	2014	Here, we revealed a previously undefined role of CD38, an enzyme that metabolizes NADP(+) into NAADP, in the regulation of autophagic flux in coronary arterial myocytes (CAMs).	NAADP	95-100	CD38 antigen	Mus musculus	49-53
24502975-6	2014	Under controlled Mg(2+), TPC2 is readily activated by NAADP with channel properties identical to those in response to PI(3,5)P2.	NAADP	54-59	two pore segment channel 2	Homo sapiens	25-29
24502975-8	2014	Notably, NAADP-mediated Ca(2+) release in intact cells is regulated by Mg(2+), PI(3,5)P2, and P38/JNK kinases, thus paralleling regulation of TPC2 currents.	NAADP	9-14	mitogen-activated protein kinase 14	Homo sapiens	94-97
24502975-8	2014	Notably, NAADP-mediated Ca(2+) release in intact cells is regulated by Mg(2+), PI(3,5)P2, and P38/JNK kinases, thus paralleling regulation of TPC2 currents.	NAADP	9-14	mitogen-activated protein kinase 8	Homo sapiens	98-101
24502975-8	2014	Notably, NAADP-mediated Ca(2+) release in intact cells is regulated by Mg(2+), PI(3,5)P2, and P38/JNK kinases, thus paralleling regulation of TPC2 currents.	NAADP	9-14	two pore segment channel 2	Homo sapiens	142-146
24502975-9	2014	Our data affirm a key role for TPC2 in NAADP-mediated Ca(2+) signaling and link this pathway to Mg(2+) homeostasis and MAP kinases, pointing to roles for lysosomal Ca(2+) in cell growth, inflammation and cancer.	NAADP	39-44	two pore segment channel 2	Homo sapiens	31-35
24451262-3	2014	The present study documents that TPC1 and NAADP-binding sites showed a colocalization at the acrosomal region and that treatment of spermatozoa with NAADP resulted in a loss of the acrosomal vesicle that showed typical properties described for TPCs: Registered responses were not detectable for its chemical analogue NADP and were blocked by the NAADP antagonist trans-Ned-19.	NAADP	149-154	two pore segment channel 1	Homo sapiens	33-37
24451262-3	2014	The present study documents that TPC1 and NAADP-binding sites showed a colocalization at the acrosomal region and that treatment of spermatozoa with NAADP resulted in a loss of the acrosomal vesicle that showed typical properties described for TPCs: Registered responses were not detectable for its chemical analogue NADP and were blocked by the NAADP antagonist trans-Ned-19.	NAADP	149-154	two pore segment channel 1	Homo sapiens	33-37
24451262-4	2014	In addition, two narrow bell-shaped dose-response curves were identified with maxima in either the nanomolar or low micromolar NAADP concentration range, where TPC1 was found to be responsible for activating the low affinity pathway.	NAADP	127-132	two pore segment channel 1	Homo sapiens	160-164
23836916-2	2013	Nicotinic acid adenine dinucleotide phosphate (NAADP), one of the most potent Ca(2+) mobilizing messengers, elicits Ca(2+) release from lysosomes via the two pore channel 2 (TPC2) in many cell types.	NAADP	0-45	two pore segment channel 2	Homo sapiens	154-172
23836916-2	2013	Nicotinic acid adenine dinucleotide phosphate (NAADP), one of the most potent Ca(2+) mobilizing messengers, elicits Ca(2+) release from lysosomes via the two pore channel 2 (TPC2) in many cell types.	NAADP	0-45	two pore segment channel 2	Homo sapiens	174-178
23836916-2	2013	Nicotinic acid adenine dinucleotide phosphate (NAADP), one of the most potent Ca(2+) mobilizing messengers, elicits Ca(2+) release from lysosomes via the two pore channel 2 (TPC2) in many cell types.	NAADP	47-52	two pore segment channel 2	Homo sapiens	154-172
23836916-2	2013	Nicotinic acid adenine dinucleotide phosphate (NAADP), one of the most potent Ca(2+) mobilizing messengers, elicits Ca(2+) release from lysosomes via the two pore channel 2 (TPC2) in many cell types.	NAADP	47-52	two pore segment channel 2	Homo sapiens	174-178
23836916-4	2013	Treatment of TPC2 expressing cells with a cell permeant-NAADP agonist, NAADP-AM, further induced autophagosome accumulation.	NAADP	56-61	two pore segment channel 2	Homo sapiens	13-17
23836916-5	2013	On the other hand, TPC2 knockdown or treatment of cells with Ned-19, a NAADP antagonist, markedly decreased the accumulation of autophagosomes.	NAADP	71-76	two pore segment channel 2	Homo sapiens	19-23
23836916-10	2013	Taken together, our data demonstrate that TPC2/NAADP/Ca(2+) signaling alkalinizes lysosomal pH to specifically inhibit the later stage of basal autophagy progression.	NAADP	47-52	two pore segment channel 2	Homo sapiens	42-46
23814062-8	2013	Conversely, activation of GPR55 at the membrane of intracellular organelles promotes Ca(2+) release from acidic-like Ca(2+) stores via the endolysosomal NAADP-sensitive two-pore channels.	NAADP	153-158	G protein-coupled receptor 55	Homo sapiens	26-31
23634879-3	2013	The introduction of fluorophores at the N-terminus of TPC1 does not affect its subcellular location, but does reversibly abolish NAADP sensitivity.	NAADP	129-134	two pore segment channel 1	Homo sapiens	54-58
24749015-4	2013	For example, some new models are emerging for the agonist receptor coupling of CD38 or ADP-ribosylcyclase and for the formation of an acidic microenvironment to facilitate the production of NAADP in vascular cells.	NAADP	190-195	CD38 molecule	Homo sapiens	79-83
23763317-3	2013	In their paper "The N-terminal region of two-pore channel 1 regulates trafficking and activation by NAADP" published in this issue of the Biochemical Journal Patel and colleagues describe that the N-terminus of one of the NAADP receptor protein/Ca2+ channel candidates, TPC1 (two-pore channel 1), is crucial for protein targeting and for sensitivity to NAADP.	NAADP	100-105	two pore segment channel 1	Homo sapiens	41-59
23763317-3	2013	In their paper "The N-terminal region of two-pore channel 1 regulates trafficking and activation by NAADP" published in this issue of the Biochemical Journal Patel and colleagues describe that the N-terminus of one of the NAADP receptor protein/Ca2+ channel candidates, TPC1 (two-pore channel 1), is crucial for protein targeting and for sensitivity to NAADP.	NAADP	100-105	two pore segment channel 1	Homo sapiens	270-274
23763317-3	2013	In their paper "The N-terminal region of two-pore channel 1 regulates trafficking and activation by NAADP" published in this issue of the Biochemical Journal Patel and colleagues describe that the N-terminus of one of the NAADP receptor protein/Ca2+ channel candidates, TPC1 (two-pore channel 1), is crucial for protein targeting and for sensitivity to NAADP.	NAADP	100-105	two pore segment channel 1	Homo sapiens	276-294
23763317-3	2013	In their paper "The N-terminal region of two-pore channel 1 regulates trafficking and activation by NAADP" published in this issue of the Biochemical Journal Patel and colleagues describe that the N-terminus of one of the NAADP receptor protein/Ca2+ channel candidates, TPC1 (two-pore channel 1), is crucial for protein targeting and for sensitivity to NAADP.	NAADP	222-227	two pore segment channel 1	Homo sapiens	41-59
23763317-3	2013	In their paper "The N-terminal region of two-pore channel 1 regulates trafficking and activation by NAADP" published in this issue of the Biochemical Journal Patel and colleagues describe that the N-terminus of one of the NAADP receptor protein/Ca2+ channel candidates, TPC1 (two-pore channel 1), is crucial for protein targeting and for sensitivity to NAADP.	NAADP	222-227	two pore segment channel 1	Homo sapiens	270-274
23763317-3	2013	In their paper "The N-terminal region of two-pore channel 1 regulates trafficking and activation by NAADP" published in this issue of the Biochemical Journal Patel and colleagues describe that the N-terminus of one of the NAADP receptor protein/Ca2+ channel candidates, TPC1 (two-pore channel 1), is crucial for protein targeting and for sensitivity to NAADP.	NAADP	222-227	two pore segment channel 1	Homo sapiens	276-294
23726915-0	2013	Intracellular NAADP increase induced by extracellular NAADP via the P2Y11-like receptor.	NAADP	14-19	purinergic receptor P2Y11	Homo sapiens	68-73
23726915-0	2013	Intracellular NAADP increase induced by extracellular NAADP via the P2Y11-like receptor.	NAADP	54-59	purinergic receptor P2Y11	Homo sapiens	68-73
23726915-1	2013	The aim of the study was to identify a signalling pathway allowing NAADP-induced intracellular NAADP increase and involving the P2Y11-like receptor.	NAADP	67-72	purinergic receptor P2Y11	Homo sapiens	128-133
23726915-1	2013	The aim of the study was to identify a signalling pathway allowing NAADP-induced intracellular NAADP increase and involving the P2Y11-like receptor.	NAADP	95-100	purinergic receptor P2Y11	Homo sapiens	128-133
23726915-4	2013	Using a Langendorff model we report a positive inotropic response induced by extracellular NAADP via P2Y11-like receptor stimulation.	NAADP	91-96	purinergic receptor P2Y11	Homo sapiens	101-106
23726915-5	2013	In cardiomyocyte cultures, P2Y11-like receptor stimulation by extracellular NAADP ([NAADP]e) increased intracellular cADP-ribose and NAADP concentration as evidenced by direct measurements.	NAADP	76-81	purinergic receptor P2Y11	Homo sapiens	27-32
23726915-5	2013	In cardiomyocyte cultures, P2Y11-like receptor stimulation by extracellular NAADP ([NAADP]e) increased intracellular cADP-ribose and NAADP concentration as evidenced by direct measurements.	NAADP	84-89	purinergic receptor P2Y11	Homo sapiens	27-32
23726915-5	2013	In cardiomyocyte cultures, P2Y11-like receptor stimulation by extracellular NAADP ([NAADP]e) increased intracellular cADP-ribose and NAADP concentration as evidenced by direct measurements.	NAADP	84-89	purinergic receptor P2Y11	Homo sapiens	27-32
23726915-6	2013	NF546, a new selective P2Y11 receptor agonist, increased intracellular cAMP, cADP-ribose and NAADP concentration confirming the involvement of the P2Y11-like receptor in this signalling pathway.	NAADP	93-98	purinergic receptor P2Y11	Homo sapiens	23-28
23726915-7	2013	NF157, a P2Y11 receptor antagonist, suppressed the increase in intracellular cADPr, NAADP and NAAD induced by either [NAADP]e or NF546.	NAADP	84-89	purinergic receptor P2Y11	Homo sapiens	9-14
23726915-7	2013	NF157, a P2Y11 receptor antagonist, suppressed the increase in intracellular cADPr, NAADP and NAAD induced by either [NAADP]e or NF546.	NAADP	118-123	purinergic receptor P2Y11	Homo sapiens	9-14
23726915-8	2013	The response profile for intracellular cADP-ribose and NAADP concentration following P2Y11-like stimulation with NF546 was similar to reported data relating beta-adrenergic stimulation with isoprenaline.	NAADP	55-60	purinergic receptor P2Y11	Homo sapiens	85-90
23726915-10	2013	Moreover, this study provides a signalling pathway: intracellular NAADP increase induced by extracellular NAADP via metabotropic activity of P2Y11-like receptor.	NAADP	66-71	purinergic receptor P2Y11	Homo sapiens	141-146
23726915-10	2013	Moreover, this study provides a signalling pathway: intracellular NAADP increase induced by extracellular NAADP via metabotropic activity of P2Y11-like receptor.	NAADP	106-111	purinergic receptor P2Y11	Homo sapiens	141-146
23726915-11	2013	This pathway implying P2Y11-like could take part in the intracellular calcium rise reported for extracellular NAADP.	NAADP	110-115	purinergic receptor P2Y11	Homo sapiens	22-27
23177620-0	2012	NAADP mediates insulin-stimulated glucose uptake and insulin sensitization by PPARgamma in adipocytes.	NAADP	0-5	peroxisome proliferator activated receptor gamma	Mus musculus	78-87
23394946-4	2013	The channel is a complex formed by two-pore channels (TPC1 and TPC2), ion channels previously thought to be gated by nicotinic acid adenine dinucleotide phosphate (NAADP), and the mammalian target of rapamycin (mTOR).	NAADP	117-162	two pore segment channel 1	Homo sapiens	54-58
23394946-4	2013	The channel is a complex formed by two-pore channels (TPC1 and TPC2), ion channels previously thought to be gated by nicotinic acid adenine dinucleotide phosphate (NAADP), and the mammalian target of rapamycin (mTOR).	NAADP	117-162	two pore segment channel 2	Homo sapiens	63-67
23394946-4	2013	The channel is a complex formed by two-pore channels (TPC1 and TPC2), ion channels previously thought to be gated by nicotinic acid adenine dinucleotide phosphate (NAADP), and the mammalian target of rapamycin (mTOR).	NAADP	164-169	two pore segment channel 1	Homo sapiens	54-58
23394946-4	2013	The channel is a complex formed by two-pore channels (TPC1 and TPC2), ion channels previously thought to be gated by nicotinic acid adenine dinucleotide phosphate (NAADP), and the mammalian target of rapamycin (mTOR).	NAADP	164-169	two pore segment channel 2	Homo sapiens	63-67
23394946-4	2013	The channel is a complex formed by two-pore channels (TPC1 and TPC2), ion channels previously thought to be gated by nicotinic acid adenine dinucleotide phosphate (NAADP), and the mammalian target of rapamycin (mTOR).	NAADP	164-169	mechanistic target of rapamycin kinase	Homo sapiens	211-215
23583195-10	2013	In cardiomyocyte cultures, NF157 suppressed cAMP and inositol phosphate accumulation induced by [NAADP]e. [NAADP]e induced phosphorylation of ERK 1/2, AKT and its downstream target GSK-3beta (p<0.05).	NAADP	107-112	mitogen activated protein kinase 3	Rattus norvegicus	142-149
23583195-10	2013	In cardiomyocyte cultures, NF157 suppressed cAMP and inositol phosphate accumulation induced by [NAADP]e. [NAADP]e induced phosphorylation of ERK 1/2, AKT and its downstream target GSK-3beta (p<0.05).	NAADP	107-112	AKT serine/threonine kinase 1	Rattus norvegicus	151-154
23583195-10	2013	In cardiomyocyte cultures, NF157 suppressed cAMP and inositol phosphate accumulation induced by [NAADP]e. [NAADP]e induced phosphorylation of ERK 1/2, AKT and its downstream target GSK-3beta (p<0.05).	NAADP	107-112	glycogen synthase kinase 3 beta	Rattus norvegicus	181-190
23177620-4	2012	We also demonstrate that PPARgamma mediates insulin sensitization by enhancing NAADP production through upregulation of CD38, the only enzyme identified for NAADP synthesis.	NAADP	79-84	peroxisome proliferator activated receptor gamma	Mus musculus	25-34
23177620-4	2012	We also demonstrate that PPARgamma mediates insulin sensitization by enhancing NAADP production through upregulation of CD38, the only enzyme identified for NAADP synthesis.	NAADP	79-84	CD38 antigen	Mus musculus	120-124
23177620-4	2012	We also demonstrate that PPARgamma mediates insulin sensitization by enhancing NAADP production through upregulation of CD38, the only enzyme identified for NAADP synthesis.	NAADP	157-162	peroxisome proliferator activated receptor gamma	Mus musculus	25-34
23177620-3	2012	Here, we demonstrate that insulin stimulates GLUT4 and GLUT1 translocation, and glucose uptake, by activating the signaling pathway involving nicotinic acid adenine dinucleotide phosphate (NAADP), a calcium mobilizer, in adipocytes.	NAADP	142-187	solute carrier family 2 (facilitated glucose transporter), member 4	Mus musculus	45-50
23177620-4	2012	We also demonstrate that PPARgamma mediates insulin sensitization by enhancing NAADP production through upregulation of CD38, the only enzyme identified for NAADP synthesis.	NAADP	157-162	CD38 antigen	Mus musculus	120-124
23177620-5	2012	Insulin produced NAADP by both CD38-dependent and -independent pathways, whereas PPARgamma produced NAADP by CD38-dependent pathway.	NAADP	100-105	peroxisome proliferator activated receptor gamma	Mus musculus	81-90
23177620-5	2012	Insulin produced NAADP by both CD38-dependent and -independent pathways, whereas PPARgamma produced NAADP by CD38-dependent pathway.	NAADP	100-105	CD38 antigen	Mus musculus	109-113
23177620-6	2012	Blocking the NAADP signaling pathway abrogated both insulin-stimulated and PPARgamma-induced GLUT4 and GLUT1 translocation, thereby inhibiting glucose uptake.	NAADP	13-18	peroxisome proliferator activated receptor gamma	Mus musculus	75-84
23177620-3	2012	Here, we demonstrate that insulin stimulates GLUT4 and GLUT1 translocation, and glucose uptake, by activating the signaling pathway involving nicotinic acid adenine dinucleotide phosphate (NAADP), a calcium mobilizer, in adipocytes.	NAADP	142-187	solute carrier family 2 (facilitated glucose transporter), member 1	Mus musculus	55-60
23177620-6	2012	Blocking the NAADP signaling pathway abrogated both insulin-stimulated and PPARgamma-induced GLUT4 and GLUT1 translocation, thereby inhibiting glucose uptake.	NAADP	13-18	solute carrier family 2 (facilitated glucose transporter), member 4	Mus musculus	93-98
23177620-3	2012	Here, we demonstrate that insulin stimulates GLUT4 and GLUT1 translocation, and glucose uptake, by activating the signaling pathway involving nicotinic acid adenine dinucleotide phosphate (NAADP), a calcium mobilizer, in adipocytes.	NAADP	189-194	solute carrier family 2 (facilitated glucose transporter), member 4	Mus musculus	45-50
23177620-6	2012	Blocking the NAADP signaling pathway abrogated both insulin-stimulated and PPARgamma-induced GLUT4 and GLUT1 translocation, thereby inhibiting glucose uptake.	NAADP	13-18	solute carrier family 2 (facilitated glucose transporter), member 1	Mus musculus	103-108
23177620-3	2012	Here, we demonstrate that insulin stimulates GLUT4 and GLUT1 translocation, and glucose uptake, by activating the signaling pathway involving nicotinic acid adenine dinucleotide phosphate (NAADP), a calcium mobilizer, in adipocytes.	NAADP	189-194	solute carrier family 2 (facilitated glucose transporter), member 1	Mus musculus	55-60
23177620-9	2012	These results demonstrated that the NAADP signaling pathway is a critical molecular target for PPARgamma-mediated insulin sensitization.	NAADP	36-41	peroxisome proliferator activated receptor gamma	Mus musculus	95-104
22500018-1	2012	Nicotinic acid adenine dinucleotide phosphate (NAADP) is a potent second messenger that mobilizes Ca(2+) from the acidic endolysosomes by activation of the two-pore channels TPC1 and TPC2.	NAADP	0-45	two pore segment channel 1	Homo sapiens	174-178
23063126-1	2012	Mammalian two-pore channel proteins (TPC1, TPC2; TPCN1, TPCN2) encode ion channels in intracellular endosomes and lysosomes and were proposed to mediate endolysosomal calcium release triggered by the second messenger, nicotinic acid adenine dinucleotide phosphate (NAADP).	NAADP	218-263	two pore segment channel 1	Homo sapiens	37-41
23063126-1	2012	Mammalian two-pore channel proteins (TPC1, TPC2; TPCN1, TPCN2) encode ion channels in intracellular endosomes and lysosomes and were proposed to mediate endolysosomal calcium release triggered by the second messenger, nicotinic acid adenine dinucleotide phosphate (NAADP).	NAADP	218-263	two pore segment channel 2	Homo sapiens	43-47
23063126-1	2012	Mammalian two-pore channel proteins (TPC1, TPC2; TPCN1, TPCN2) encode ion channels in intracellular endosomes and lysosomes and were proposed to mediate endolysosomal calcium release triggered by the second messenger, nicotinic acid adenine dinucleotide phosphate (NAADP).	NAADP	218-263	two pore segment channel 1	Homo sapiens	49-54
23063126-1	2012	Mammalian two-pore channel proteins (TPC1, TPC2; TPCN1, TPCN2) encode ion channels in intracellular endosomes and lysosomes and were proposed to mediate endolysosomal calcium release triggered by the second messenger, nicotinic acid adenine dinucleotide phosphate (NAADP).	NAADP	218-263	two pore segment channel 2	Homo sapiens	56-61
23063126-1	2012	Mammalian two-pore channel proteins (TPC1, TPC2; TPCN1, TPCN2) encode ion channels in intracellular endosomes and lysosomes and were proposed to mediate endolysosomal calcium release triggered by the second messenger, nicotinic acid adenine dinucleotide phosphate (NAADP).	NAADP	265-270	two pore segment channel 1	Homo sapiens	37-41
23063126-1	2012	Mammalian two-pore channel proteins (TPC1, TPC2; TPCN1, TPCN2) encode ion channels in intracellular endosomes and lysosomes and were proposed to mediate endolysosomal calcium release triggered by the second messenger, nicotinic acid adenine dinucleotide phosphate (NAADP).	NAADP	265-270	two pore segment channel 2	Homo sapiens	43-47
23063126-1	2012	Mammalian two-pore channel proteins (TPC1, TPC2; TPCN1, TPCN2) encode ion channels in intracellular endosomes and lysosomes and were proposed to mediate endolysosomal calcium release triggered by the second messenger, nicotinic acid adenine dinucleotide phosphate (NAADP).	NAADP	265-270	two pore segment channel 1	Homo sapiens	49-54
23063126-1	2012	Mammalian two-pore channel proteins (TPC1, TPC2; TPCN1, TPCN2) encode ion channels in intracellular endosomes and lysosomes and were proposed to mediate endolysosomal calcium release triggered by the second messenger, nicotinic acid adenine dinucleotide phosphate (NAADP).	NAADP	265-270	two pore segment channel 2	Homo sapiens	56-61
22988879-0	2012	A link between LRRK2, autophagy and NAADP-mediated endolysosomal calcium signalling.	NAADP	36-41	leucine rich repeat kinase 2	Homo sapiens	15-20
22988879-6	2012	In the present paper, we review our current knowledge of the link between LRRK2 and autophagic-lysosomal clearance, including regulation of Ca2+-dependent events involving NAADP.	NAADP	172-177	leucine rich repeat kinase 2	Homo sapiens	74-79
22851169-4	2012	CD38, a promiscuous enzyme described to be involved in NAADP metabolism, was not detectable in HeLa cells.	NAADP	55-60	CD38 molecule	Homo sapiens	0-4
22500018-0	2012	Membrane potential regulates nicotinic acid adenine dinucleotide phosphate (NAADP) dependence of the pH- and Ca2+-sensitive organellar two-pore channel TPC1.	NAADP	29-74	two pore segment channel 1	Homo sapiens	152-156
22500018-0	2012	Membrane potential regulates nicotinic acid adenine dinucleotide phosphate (NAADP) dependence of the pH- and Ca2+-sensitive organellar two-pore channel TPC1.	NAADP	76-81	two pore segment channel 1	Homo sapiens	152-156
22500018-1	2012	Nicotinic acid adenine dinucleotide phosphate (NAADP) is a potent second messenger that mobilizes Ca(2+) from the acidic endolysosomes by activation of the two-pore channels TPC1 and TPC2.	NAADP	0-45	two pore segment channel 2	Homo sapiens	183-187
22500018-1	2012	Nicotinic acid adenine dinucleotide phosphate (NAADP) is a potent second messenger that mobilizes Ca(2+) from the acidic endolysosomes by activation of the two-pore channels TPC1 and TPC2.	NAADP	47-52	two pore segment channel 1	Homo sapiens	174-178
22500018-1	2012	Nicotinic acid adenine dinucleotide phosphate (NAADP) is a potent second messenger that mobilizes Ca(2+) from the acidic endolysosomes by activation of the two-pore channels TPC1 and TPC2.	NAADP	47-52	two pore segment channel 2	Homo sapiens	183-187
22500018-4	2012	The native and recombinant TPC1 channels are activated by NAADP.	NAADP	58-63	two pore segment channel 1	Homo sapiens	27-31
22500018-10	2012	Intriguingly, the apparent affinity for activation of TPC1 by its ligand NAADP is not constant.	NAADP	73-78	two pore segment channel 1	Homo sapiens	54-58
22500018-11	2012	Rather, hyperpolarization increases the apparent affinity of TPC1 for NAADP by 10 nm/mV.	NAADP	70-75	two pore segment channel 1	Homo sapiens	61-65
22500018-12	2012	The concerted regulation of TPC1 activity by luminal Ca(2+) and by membrane potential thus provides a potential mechanism to explain NAADP-induced Ca(2+) oscillations.	NAADP	133-138	two pore segment channel 1	Homo sapiens	28-32
21610076-5	2011	We also show that NAADP increases acidic vesicular organelle formation and levels of the autophagic markers, LC3II and beclin-1.	NAADP	18-23	beclin 1	Rattus norvegicus	119-127
22534131-1	2012	Nicotinic acid adenine dinucleotide phosphate (NAADP) is a potent Ca(2+)-releasing second messenger that might regulate different ion channels, including the ryanodine receptor, two-pore channels, and TRP-ML1 (transient receptor potential channel, subtype mucolipin 1), a Ca(2+) channel localized to lysosomes.	NAADP	0-45	mucolipin TRP cation channel 1	Homo sapiens	201-208
22534131-1	2012	Nicotinic acid adenine dinucleotide phosphate (NAADP) is a potent Ca(2+)-releasing second messenger that might regulate different ion channels, including the ryanodine receptor, two-pore channels, and TRP-ML1 (transient receptor potential channel, subtype mucolipin 1), a Ca(2+) channel localized to lysosomes.	NAADP	47-52	mucolipin TRP cation channel 1	Homo sapiens	201-208
22012985-0	2012	Leucine-rich repeat kinase 2 regulates autophagy through a calcium-dependent pathway involving NAADP.	NAADP	95-100	leucine rich repeat kinase 2	Homo sapiens	0-28
22117075-7	2012	Furthermore, labeling of high affinity NAADP binding sites was preserved in pancreatic samples from TPC1 and TPC2 knock-out mice.	NAADP	39-44	two pore channel 1	Mus musculus	100-104
22142305-1	2012	CD38 is a signaling enzyme responsible for catalyzing the synthesis of cyclic ADP ribose (cADPR) and nicotinic acid adenine dinucleotide phosphate; both are universal Ca(2+) messenger molecules.	NAADP	101-146	CD38 molecule	Homo sapiens	0-4
22627736-2	2012	We and others previously demonstrated that glucose activates CD38/ADP-ribosyl cyclase (ADPR-cyclase) to produce two Ca(2+) second messengers, cyclic ADP-ribose (cADPR) and nicotinic acid adenine dinucleotide phosphate (NAADP).	NAADP	172-217	CD38 molecule	Homo sapiens	61-65
22627736-2	2012	We and others previously demonstrated that glucose activates CD38/ADP-ribosyl cyclase (ADPR-cyclase) to produce two Ca(2+) second messengers, cyclic ADP-ribose (cADPR) and nicotinic acid adenine dinucleotide phosphate (NAADP).	NAADP	219-224	CD38 molecule	Homo sapiens	61-65
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.	NAADP	157-202	CD38 antigen	Mus musculus	10-14
21967541-4	2012	In human platelets, NAADP has been shown to release Ca2+ in permeabilized human platelets and contribute to thrombin-mediated platelet activation.	NAADP	20-25	coagulation factor II, thrombin	Homo sapiens	108-116
21967541-5	2012	In the present study, we have further characterized NAADP-mediated Ca2+ release in human platelets in response to both thrombin and the GPVI (glycoprotein VI)-specific agonist CRP (collagen-related peptide).	NAADP	52-57	coagulation factor II, thrombin	Homo sapiens	119-127
21967541-5	2012	In the present study, we have further characterized NAADP-mediated Ca2+ release in human platelets in response to both thrombin and the GPVI (glycoprotein VI)-specific agonist CRP (collagen-related peptide).	NAADP	52-57	glycoprotein VI platelet	Homo sapiens	136-140
21967541-5	2012	In the present study, we have further characterized NAADP-mediated Ca2+ release in human platelets in response to both thrombin and the GPVI (glycoprotein VI)-specific agonist CRP (collagen-related peptide).	NAADP	52-57	glycoprotein VI platelet	Homo sapiens	142-157
21967541-8	2012	Ned-19, a novel cell-permeant NAADP receptor antagonist, competes for the NAADP-binding site in platelets and can inhibit both thrombin- and CRP-induced Ca2+ release in human platelets.	NAADP	30-35	coagulation factor II, thrombin	Homo sapiens	127-135
22020217-0	2011	CD38: a NAADP degrading enzyme.	NAADP	8-13	CD38 molecule	Homo sapiens	0-4
22020217-1	2011	The role of the multifunctional enzyme CD38 in formation of the Ca(2+)-mobilizing second messenger nicotinic acid adenine dinucleotide phosphate (NAADP) was investigated.	NAADP	99-144	CD38 molecule	Homo sapiens	39-43
22020217-1	2011	The role of the multifunctional enzyme CD38 in formation of the Ca(2+)-mobilizing second messenger nicotinic acid adenine dinucleotide phosphate (NAADP) was investigated.	NAADP	146-151	CD38 molecule	Homo sapiens	39-43
22020217-4	2011	Thus in vivo CD38 appears to be a NAADP degrading rather than a NAADP forming enzyme, perhaps avoiding desensitizing NAADP levels in intact cells.	NAADP	34-39	CD38 molecule	Homo sapiens	13-17
22020217-4	2011	Thus in vivo CD38 appears to be a NAADP degrading rather than a NAADP forming enzyme, perhaps avoiding desensitizing NAADP levels in intact cells.	NAADP	64-69	CD38 molecule	Homo sapiens	13-17
22020217-4	2011	Thus in vivo CD38 appears to be a NAADP degrading rather than a NAADP forming enzyme, perhaps avoiding desensitizing NAADP levels in intact cells.	NAADP	64-69	CD38 molecule	Homo sapiens	13-17
21724254-3	2011	We recently reported that Niemann-Pick type C (NPC) is the first human disease to be associated with defective lysosomal Ca(2+) uptake and defective NAADP-mediated lysosomal Ca(2+) release.	NAADP	149-154	NPC intracellular cholesterol transporter 1	Homo sapiens	26-45
21613607-2	2011	Given that lysosomal nicotinic acid adenine dinucleotide phosphate (NAADP)-Ca(2+) release channel activity is associated with TRP-ML1, the present study was designed to test the hypothesis that NAADP regulates lysosome function via activation of TRP-ML1 channel activity.	NAADP	21-66	mucolipin TRP cation channel 1	Homo sapiens	126-133
21613607-2	2011	Given that lysosomal nicotinic acid adenine dinucleotide phosphate (NAADP)-Ca(2+) release channel activity is associated with TRP-ML1, the present study was designed to test the hypothesis that NAADP regulates lysosome function via activation of TRP-ML1 channel activity.	NAADP	21-66	mucolipin TRP cation channel 1	Homo sapiens	246-253
21613607-2	2011	Given that lysosomal nicotinic acid adenine dinucleotide phosphate (NAADP)-Ca(2+) release channel activity is associated with TRP-ML1, the present study was designed to test the hypothesis that NAADP regulates lysosome function via activation of TRP-ML1 channel activity.	NAADP	68-73	mucolipin TRP cation channel 1	Homo sapiens	126-133
21613607-2	2011	Given that lysosomal nicotinic acid adenine dinucleotide phosphate (NAADP)-Ca(2+) release channel activity is associated with TRP-ML1, the present study was designed to test the hypothesis that NAADP regulates lysosome function via activation of TRP-ML1 channel activity.	NAADP	194-199	mucolipin TRP cation channel 1	Homo sapiens	126-133
21613607-2	2011	Given that lysosomal nicotinic acid adenine dinucleotide phosphate (NAADP)-Ca(2+) release channel activity is associated with TRP-ML1, the present study was designed to test the hypothesis that NAADP regulates lysosome function via activation of TRP-ML1 channel activity.	NAADP	194-199	mucolipin TRP cation channel 1	Homo sapiens	246-253
21613607-3	2011	Using lysosomal preparations from wild-type (TRP-ML1(+/+)) human fibroblasts, channel reconstitution experiments demonstrated that NAADP (0.01-1.0 muM) produced a concentration-dependent increase in TRP-ML1 channel activity.	NAADP	131-136	mucolipin TRP cation channel 1	Homo sapiens	45-52
21613607-3	2011	Using lysosomal preparations from wild-type (TRP-ML1(+/+)) human fibroblasts, channel reconstitution experiments demonstrated that NAADP (0.01-1.0 muM) produced a concentration-dependent increase in TRP-ML1 channel activity.	NAADP	131-136	mucolipin TRP cation channel 1	Homo sapiens	199-206
21613607-4	2011	This NAADP-induced activation of TRP-ML1 channels could not be observed in lysosomes from TRP-ML1(-/-) cells, but was restored by introducing a TRP-ML1 transgene into these cells.	NAADP	5-10	mucolipin TRP cation channel 1	Homo sapiens	33-40
21613607-4	2011	This NAADP-induced activation of TRP-ML1 channels could not be observed in lysosomes from TRP-ML1(-/-) cells, but was restored by introducing a TRP-ML1 transgene into these cells.	NAADP	5-10	mucolipin TRP cation channel 1	Homo sapiens	90-97
21613607-4	2011	This NAADP-induced activation of TRP-ML1 channels could not be observed in lysosomes from TRP-ML1(-/-) cells, but was restored by introducing a TRP-ML1 transgene into these cells.	NAADP	5-10	mucolipin TRP cation channel 1	Homo sapiens	90-97
21613607-5	2011	Microscopic Ca(2+) fluorescence imaging showed that NAADP significantly increased intracellular Ca(2+) concentration to 302.4 +- 74.28 nM (vs. 180 +- 44.13 nM of the basal) in TRP-ML1(+/+) cells, but it had no effect in TRP-ML1(-/-) cells.	NAADP	52-57	mucolipin TRP cation channel 1	Homo sapiens	176-183
21613607-5	2011	Microscopic Ca(2+) fluorescence imaging showed that NAADP significantly increased intracellular Ca(2+) concentration to 302.4 +- 74.28 nM (vs. 180 +- 44.13 nM of the basal) in TRP-ML1(+/+) cells, but it had no effect in TRP-ML1(-/-) cells.	NAADP	52-57	mucolipin TRP cation channel 1	Homo sapiens	220-227
21613607-6	2011	If a TRP-ML1 gene was transfected into TRP-ML1(-/-) cells, the Ca(2+) response to NAADP was restored to the level comparable to TRP-ML1(+/+) cells.	NAADP	82-87	mucolipin TRP cation channel 1	Homo sapiens	5-12
21613607-6	2011	If a TRP-ML1 gene was transfected into TRP-ML1(-/-) cells, the Ca(2+) response to NAADP was restored to the level comparable to TRP-ML1(+/+) cells.	NAADP	82-87	mucolipin TRP cation channel 1	Homo sapiens	39-46
21613607-6	2011	If a TRP-ML1 gene was transfected into TRP-ML1(-/-) cells, the Ca(2+) response to NAADP was restored to the level comparable to TRP-ML1(+/+) cells.	NAADP	82-87	mucolipin TRP cation channel 1	Homo sapiens	39-46
21613607-7	2011	Functionally, confocal microscopy revealed that NAADP significantly enhanced the dynamic interaction of endosomes and lysosomes and the lipid delivery to lysosomes in TRP-ML1(+/+) cells.	NAADP	48-53	mucolipin TRP cation channel 1	Homo sapiens	167-174
21613607-8	2011	This functional action of NAADP was abolished in TRP-ML1(-/-) cells, but restored after TRP-ML1 gene was rescued in these cells.	NAADP	26-31	mucolipin TRP cation channel 1	Homo sapiens	49-56
21613607-8	2011	This functional action of NAADP was abolished in TRP-ML1(-/-) cells, but restored after TRP-ML1 gene was rescued in these cells.	NAADP	26-31	mucolipin TRP cation channel 1	Homo sapiens	88-95
21613607-9	2011	Our results suggest that NAADP increases lysosomal TRP-ML1 channel activity to release Ca(2+), which promotes the interaction of endosomes and lysosomes and thereby regulates lipid transport to lysosomes.	NAADP	25-30	mucolipin TRP cation channel 1	Homo sapiens	51-58
21601596-6	2011	NAADP releases Ca(2+) from acidic lysosomal-like Ca(2+) stores in MEG01 cells probably mediated by the activation of TPC1 and TPC2 as demonstrated by TPC1 and TPC2 expression silencing and overexpression.	NAADP	0-5	two pore segment channel 1	Homo sapiens	117-121
21601596-6	2011	NAADP releases Ca(2+) from acidic lysosomal-like Ca(2+) stores in MEG01 cells probably mediated by the activation of TPC1 and TPC2 as demonstrated by TPC1 and TPC2 expression silencing and overexpression.	NAADP	0-5	two pore segment channel 2	Homo sapiens	126-130
21601596-6	2011	NAADP releases Ca(2+) from acidic lysosomal-like Ca(2+) stores in MEG01 cells probably mediated by the activation of TPC1 and TPC2 as demonstrated by TPC1 and TPC2 expression silencing and overexpression.	NAADP	0-5	two pore segment channel 1	Homo sapiens	150-154
21601596-6	2011	NAADP releases Ca(2+) from acidic lysosomal-like Ca(2+) stores in MEG01 cells probably mediated by the activation of TPC1 and TPC2 as demonstrated by TPC1 and TPC2 expression silencing and overexpression.	NAADP	0-5	two pore segment channel 2	Homo sapiens	159-163
21601596-8	2011	CONCLUSION: Our results show for the first time NAADP-evoked Ca(2+) release from acidic compartments through the activation of TPC1 and TPC2, and CICR, in a megakaryoblastic cell line.	NAADP	48-53	two pore segment channel 1	Homo sapiens	127-131
21601596-8	2011	CONCLUSION: Our results show for the first time NAADP-evoked Ca(2+) release from acidic compartments through the activation of TPC1 and TPC2, and CICR, in a megakaryoblastic cell line.	NAADP	48-53	two pore segment channel 2	Homo sapiens	136-140
21724254-3	2011	We recently reported that Niemann-Pick type C (NPC) is the first human disease to be associated with defective lysosomal Ca(2+) uptake and defective NAADP-mediated lysosomal Ca(2+) release.	NAADP	149-154	NPC intracellular cholesterol transporter 1	Homo sapiens	47-50
21786193-9	2011	This article gives a historical account of the cADPR/NAADP/CD38-signaling pathway and describes current efforts in elucidating the structure and function of its components.	NAADP	53-58	CD38 antigen	Mus musculus	59-63
21540176-14	2011	We conclude that although TRPML1 and TPCs are present in the same complex, they function as two independent organellar ion channels and that TPCs, not TRPMLs, are the targets for NAADP.	NAADP	179-184	mucolipin TRP cation channel 1	Homo sapiens	26-32
21641214-2	2011	It is involved in the conversion of NAD(P)(+) into cyclic ADP-ribose, NAADP(+) and ADP-ribose and the role of these metabolites in multiple Ca(2+) signaling pathways makes CD38 a novel potential pharmacological target.	NAADP	70-75	CD38 molecule	Homo sapiens	172-176
21664355-4	2011	Pharmacological disruption of either NAADP or lysosomal signalling reduced Ca(2+) responses induced by ATP and endothelin-1, but not by bradykinin.	NAADP	37-42	endothelin 1	Homo sapiens	111-123
20870729-4	2010	In pancreatic acinar cells, the hormone cholecystokinin (CCK) stimulates NAADP production evoking Ca(2+) signals by discharging acidic Ca(2+) stores and leading to digestive enzyme secretion.	NAADP	73-78	cholecystokinin	Rattus norvegicus	57-60
21339289-1	2011	CD38, a multifunctional enzyme that catalyzes the synthesis of intracellular Ca(2+) messengers, cyclic ADP-ribose (cADPR) and nicotinic acid adenine dinucleotide phosphate (NAADP), is known to be expressed on platelets.	NAADP	126-171	CD38 antigen	Mus musculus	0-4
21339289-1	2011	CD38, a multifunctional enzyme that catalyzes the synthesis of intracellular Ca(2+) messengers, cyclic ADP-ribose (cADPR) and nicotinic acid adenine dinucleotide phosphate (NAADP), is known to be expressed on platelets.	NAADP	173-178	CD38 antigen	Mus musculus	0-4
21173144-9	2011	Mutation of all three glycosylation sites in TPC1 enhances NAADP-evoked cytosolic Ca(2+) signals.	NAADP	59-64	two pore segment channel 1	Homo sapiens	45-49
21134381-1	2011	The extracellular domain of human CD38 is a multifunctional enzyme involved in the metabolism of two Ca(2+) messengers: cyclic ADP-ribose and nicotinic acid adenine dinucleotide phosphate.	NAADP	142-187	CD38 molecule	Homo sapiens	34-38
21364192-0	2011	NAADP links histamine H1 receptors to secretion of von Willebrand factor in human endothelial cells.	NAADP	0-5	von Willebrand factor	Homo sapiens	51-72
21364192-2	2011	In search of new intracellular mechanisms modulating endothelial effector functions, we identified nicotinic acid adenine dinucleotide phosphate (NAADP) as a crucial second messenger in histamine-induced Ca(2+) release via H1 receptors (H1R).	NAADP	99-144	histamine receptor H1	Homo sapiens	223-241
21364192-2	2011	In search of new intracellular mechanisms modulating endothelial effector functions, we identified nicotinic acid adenine dinucleotide phosphate (NAADP) as a crucial second messenger in histamine-induced Ca(2+) release via H1 receptors (H1R).	NAADP	146-151	histamine receptor H1	Homo sapiens	223-241
21364192-4	2011	Using the human EA.hy926 endothelial cell line and primary human umbilical vein endothelial cells, we show that selective H1R activation increases intracellular NAADP levels and that H1R-induced calcium release involves both acidic organelles and the endoplasmic reticulum.	NAADP	161-166	histamine receptor H1	Homo sapiens	122-125
21364192-5	2011	To assess that NAADP links H1R to Ca(2+)-signaling we used both microinjection of self-inactivating concentrations of NAADP and the specific NAADP receptor antagonist, Ned-19, both of which completely abolished H1R-induced but not thrombin-induced Ca(2+) mobilization.	NAADP	15-20	histamine receptor H1	Homo sapiens	27-30
21364192-5	2011	To assess that NAADP links H1R to Ca(2+)-signaling we used both microinjection of self-inactivating concentrations of NAADP and the specific NAADP receptor antagonist, Ned-19, both of which completely abolished H1R-induced but not thrombin-induced Ca(2+) mobilization.	NAADP	15-20	histamine receptor H1	Homo sapiens	211-214
21364192-5	2011	To assess that NAADP links H1R to Ca(2+)-signaling we used both microinjection of self-inactivating concentrations of NAADP and the specific NAADP receptor antagonist, Ned-19, both of which completely abolished H1R-induced but not thrombin-induced Ca(2+) mobilization.	NAADP	118-123	histamine receptor H1	Homo sapiens	27-30
21364192-7	2011	These findings demonstrate a novel and specific Ca(2+)-signaling mechanism activated through H1R in human endothelial cells, which reveals an obligatory role of NAADP in the control of VWF secretion.	NAADP	161-166	histamine receptor H1	Homo sapiens	93-96
21339289-3	2011	Our present results show that treatment of platelets with thrombin results in a rapid and sustained Ca(2+) signal, resulting from a coordinated interplay of Ca(2+)-mobilizing messengers, inositol 1,4,5-trisphosphate, cADPR, and NAADP.	NAADP	228-233	coagulation factor II	Mus musculus	58-66
21339289-4	2011	By dissecting the signaling pathway using various agents, we delineated that cADPR and NAADP are sequentially produced through CD38 internalization by protein kinase C via myosin heavy chain IIA following phospholipase C activation in thrombin-induced platelets.	NAADP	87-92	CD38 antigen	Mus musculus	127-131
21339289-4	2011	By dissecting the signaling pathway using various agents, we delineated that cADPR and NAADP are sequentially produced through CD38 internalization by protein kinase C via myosin heavy chain IIA following phospholipase C activation in thrombin-induced platelets.	NAADP	87-92	coagulation factor II	Mus musculus	235-243
21339289-5	2011	An inositol 1,4,5-trisphosphate receptor antagonist blocked the thrombin-induced formation of cADPR and NAADP as well as Ca(2+) signals.	NAADP	104-109	coagulation factor II	Mus musculus	64-72
21339289-10	2011	These results demonstrate that CD38 plays an essential role in thrombin-induced procoagulant activity of platelets and hemostasis via Ca(2+) signaling mediated by its products, cADPR and NAADP.	NAADP	187-192	CD38 antigen	Mus musculus	31-35
21339289-10	2011	These results demonstrate that CD38 plays an essential role in thrombin-induced procoagulant activity of platelets and hemostasis via Ca(2+) signaling mediated by its products, cADPR and NAADP.	NAADP	187-192	coagulation factor II	Mus musculus	63-71
20870729-5	2010	From cells derived from CD38(-/-) mice, we provide the first physiological evidence that CD38 is required for endogenous NAADP generation in response to CCK stimulation.	NAADP	121-126	CD38 antigen	Mus musculus	24-28
20870729-5	2010	From cells derived from CD38(-/-) mice, we provide the first physiological evidence that CD38 is required for endogenous NAADP generation in response to CCK stimulation.	NAADP	121-126	CD38 antigen	Mus musculus	89-93
20870729-5	2010	From cells derived from CD38(-/-) mice, we provide the first physiological evidence that CD38 is required for endogenous NAADP generation in response to CCK stimulation.	NAADP	121-126	cholecystokinin	Mus musculus	153-156
20870729-9	2010	We propose that CD38 is an NAADP synthase required for coupling receptor activation to NAADP-mediated Ca(2+) release from lysosomal stores in pancreatic acinar cells.	NAADP	27-32	CD38 molecule	Rattus norvegicus	16-20
20880839-3	2010	Here, we redirect TPC2 from lysosomes to the plasma membrane and show that NAADP evokes Ca(2+) influx independent of ryanodine receptors and that it activates a Ca(2+)-permeable channel whose conductance is reduced by mutation of a residue within a putative pore.	NAADP	75-80	two pore segment channel 2	Homo sapiens	18-22
21118107-3	2010	The recent findings that dysfunctional NAADP release leads to defective endocytic function which in turn results in secondary lipid accumulation in the lysosomal storage disease Niemann-Pick type C, is the first evidence of a direct connection between a human disease and defective lysosomal calcium release.	NAADP	39-44	protein interacting with PRKCA 1	Homo sapiens	186-190
20650899-3	2010	Superfusion of TRPM2-expressing cells with H(2)O(2) or intracellular dialysis of cyclic ADPR (cADPR) or nicotinic acid adenine dinucleotide phosphate (NAADP) activates, whereas dialysis of AMP inhibits, TRPM2 whole-cell currents.	NAADP	104-149	transient receptor potential cation channel subfamily M member 2	Homo sapiens	15-20
20720007-5	2010	NAADP opens TPC2 channels in a concentration-dependent manner, binding to high affinity activation and low affinity inhibition sites.	NAADP	0-5	two pore segment channel 2	Homo sapiens	12-16
20720007-7	2010	The sensitivity of TPC2 to NAADP is steeply dependent on the luminal [Ca(2+)] allowing extremely low levels of NAADP to open the channel.	NAADP	27-32	two pore segment channel 2	Homo sapiens	19-23
20720007-7	2010	The sensitivity of TPC2 to NAADP is steeply dependent on the luminal [Ca(2+)] allowing extremely low levels of NAADP to open the channel.	NAADP	111-116	two pore segment channel 2	Homo sapiens	19-23
20720007-8	2010	In parallel, luminal pH controls NAADP affinity for TPC2 by switching from reversible activation of TPC2 at low pH to irreversible activation at neutral pH.	NAADP	33-38	two pore segment channel 2	Homo sapiens	52-56
20720007-8	2010	In parallel, luminal pH controls NAADP affinity for TPC2 by switching from reversible activation of TPC2 at low pH to irreversible activation at neutral pH.	NAADP	33-38	two pore segment channel 2	Homo sapiens	100-104
20720007-10	2010	Ned-19 antagonizes NAADP-activation of TPC2 in a non-competitive manner at 1 muM but potentiates NAADP activation at nanomolar concentrations.	NAADP	19-24	two pore segment channel 2	Homo sapiens	39-43
20650899-3	2010	Superfusion of TRPM2-expressing cells with H(2)O(2) or intracellular dialysis of cyclic ADPR (cADPR) or nicotinic acid adenine dinucleotide phosphate (NAADP) activates, whereas dialysis of AMP inhibits, TRPM2 whole-cell currents.	NAADP	151-156	transient receptor potential cation channel subfamily M member 2	Homo sapiens	15-20
20650899-3	2010	Superfusion of TRPM2-expressing cells with H(2)O(2) or intracellular dialysis of cyclic ADPR (cADPR) or nicotinic acid adenine dinucleotide phosphate (NAADP) activates, whereas dialysis of AMP inhibits, TRPM2 whole-cell currents.	NAADP	151-156	transient receptor potential cation channel subfamily M member 2	Homo sapiens	203-208
20442403-2	2010	In this study we examined the possibility that IL-8 activates CD38 to produce another messenger, nicotinic acid adenine dinucleotide phosphate (NAADP), in LAK cells, and we showed that IL-8 induced NAADP formation after cADPR production.	NAADP	144-149	chemokine (C-X-C motif) ligand 15	Mus musculus	47-51
20495006-2	2010	Here, we employ a glass chip-based method to record for the first time nicotinic acid adenine dinucleotide phosphate -dependent currents through a two-pore channel (TPCN2) from intact lysosomes.	NAADP	71-116	two pore segment channel 2	Homo sapiens	165-170
21099331-2	2010	These studies have highlighted a role for NAADP-induced Ca(2+) mobilization not only in mediating the effects of the incretin, GLP-1 and the autocrine proliferative effects of insulin, but also possibly a fundamental role in glucose-mediated insulin secretion in the pancreatic beta-cell.	NAADP	42-47	glucagon like peptide 1 receptor	Homo sapiens	127-132
21099331-2	2010	These studies have highlighted a role for NAADP-induced Ca(2+) mobilization not only in mediating the effects of the incretin, GLP-1 and the autocrine proliferative effects of insulin, but also possibly a fundamental role in glucose-mediated insulin secretion in the pancreatic beta-cell.	NAADP	42-47	insulin	Homo sapiens	176-183
20442403-0	2010	Generation of cyclic ADP-ribose and nicotinic acid adenine dinucleotide phosphate by CD38 for Ca2+ signaling in interleukin-8-treated lymphokine-activated killer cells.	NAADP	36-81	CD38 antigen	Mus musculus	85-89
20442403-0	2010	Generation of cyclic ADP-ribose and nicotinic acid adenine dinucleotide phosphate by CD38 for Ca2+ signaling in interleukin-8-treated lymphokine-activated killer cells.	NAADP	36-81	chemokine (C-X-C motif) ligand 15	Mus musculus	112-125
20442403-2	2010	In this study we examined the possibility that IL-8 activates CD38 to produce another messenger, nicotinic acid adenine dinucleotide phosphate (NAADP), in LAK cells, and we showed that IL-8 induced NAADP formation after cADPR production.	NAADP	144-149	CD38 antigen	Mus musculus	62-66
20442403-2	2010	In this study we examined the possibility that IL-8 activates CD38 to produce another messenger, nicotinic acid adenine dinucleotide phosphate (NAADP), in LAK cells, and we showed that IL-8 induced NAADP formation after cADPR production.	NAADP	97-142	chemokine (C-X-C motif) ligand 15	Mus musculus	47-51
20442403-2	2010	In this study we examined the possibility that IL-8 activates CD38 to produce another messenger, nicotinic acid adenine dinucleotide phosphate (NAADP), in LAK cells, and we showed that IL-8 induced NAADP formation after cADPR production.	NAADP	144-149	chemokine (C-X-C motif) ligand 15	Mus musculus	185-189
20442403-2	2010	In this study we examined the possibility that IL-8 activates CD38 to produce another messenger, nicotinic acid adenine dinucleotide phosphate (NAADP), in LAK cells, and we showed that IL-8 induced NAADP formation after cADPR production.	NAADP	97-142	CD38 antigen	Mus musculus	62-66
20442403-2	2010	In this study we examined the possibility that IL-8 activates CD38 to produce another messenger, nicotinic acid adenine dinucleotide phosphate (NAADP), in LAK cells, and we showed that IL-8 induced NAADP formation after cADPR production.	NAADP	97-142	chemokine (C-X-C motif) ligand 15	Mus musculus	185-189
20442403-2	2010	In this study we examined the possibility that IL-8 activates CD38 to produce another messenger, nicotinic acid adenine dinucleotide phosphate (NAADP), in LAK cells, and we showed that IL-8 induced NAADP formation after cADPR production.	NAADP	198-203	chemokine (C-X-C motif) ligand 15	Mus musculus	47-51
20442403-2	2010	In this study we examined the possibility that IL-8 activates CD38 to produce another messenger, nicotinic acid adenine dinucleotide phosphate (NAADP), in LAK cells, and we showed that IL-8 induced NAADP formation after cADPR production.	NAADP	198-203	CD38 antigen	Mus musculus	62-66
20442403-2	2010	In this study we examined the possibility that IL-8 activates CD38 to produce another messenger, nicotinic acid adenine dinucleotide phosphate (NAADP), in LAK cells, and we showed that IL-8 induced NAADP formation after cADPR production.	NAADP	198-203	chemokine (C-X-C motif) ligand 15	Mus musculus	185-189
20442403-3	2010	These calcium signaling messengers were not produced when LAK cells prepared from CD38 knock-out mice were treated with IL-8, indicating that the synthesis of both NAADP and cADPR is catalyzed by CD38 in LAK cells.	NAADP	164-169	chemokine (C-X-C motif) ligand 15	Mus musculus	120-124
20442403-3	2010	These calcium signaling messengers were not produced when LAK cells prepared from CD38 knock-out mice were treated with IL-8, indicating that the synthesis of both NAADP and cADPR is catalyzed by CD38 in LAK cells.	NAADP	164-169	CD38 antigen	Mus musculus	196-200
20442403-8	2010	Furthermore, activation of Rap1, a downstream molecule of Epac, was required for IL-8-induced NAADP formation in LAK cells.	NAADP	94-99	RAS-related protein 1a	Mus musculus	27-31
20442403-8	2010	Furthermore, activation of Rap1, a downstream molecule of Epac, was required for IL-8-induced NAADP formation in LAK cells.	NAADP	94-99	chemokine (C-X-C motif) ligand 15	Mus musculus	81-85
20442403-9	2010	Taken together, our data suggest that IL-8-induced NAADP production is mediated by CD38 activation through the actions of cAMP/Epac/protein kinase A/Rap1 in LAK cells and that NAADP plays a key role in Ca(2+) signaling of IL-8-induced LAK cell migration.	NAADP	51-56	chemokine (C-X-C motif) ligand 15	Mus musculus	38-42
20442403-9	2010	Taken together, our data suggest that IL-8-induced NAADP production is mediated by CD38 activation through the actions of cAMP/Epac/protein kinase A/Rap1 in LAK cells and that NAADP plays a key role in Ca(2+) signaling of IL-8-induced LAK cell migration.	NAADP	51-56	CD38 antigen	Mus musculus	83-87
20442403-9	2010	Taken together, our data suggest that IL-8-induced NAADP production is mediated by CD38 activation through the actions of cAMP/Epac/protein kinase A/Rap1 in LAK cells and that NAADP plays a key role in Ca(2+) signaling of IL-8-induced LAK cell migration.	NAADP	51-56	RAS-related protein 1a	Mus musculus	149-153
20442403-9	2010	Taken together, our data suggest that IL-8-induced NAADP production is mediated by CD38 activation through the actions of cAMP/Epac/protein kinase A/Rap1 in LAK cells and that NAADP plays a key role in Ca(2+) signaling of IL-8-induced LAK cell migration.	NAADP	51-56	chemokine (C-X-C motif) ligand 15	Mus musculus	222-226
20442403-9	2010	Taken together, our data suggest that IL-8-induced NAADP production is mediated by CD38 activation through the actions of cAMP/Epac/protein kinase A/Rap1 in LAK cells and that NAADP plays a key role in Ca(2+) signaling of IL-8-induced LAK cell migration.	NAADP	176-181	chemokine (C-X-C motif) ligand 15	Mus musculus	38-42
20442403-9	2010	Taken together, our data suggest that IL-8-induced NAADP production is mediated by CD38 activation through the actions of cAMP/Epac/protein kinase A/Rap1 in LAK cells and that NAADP plays a key role in Ca(2+) signaling of IL-8-induced LAK cell migration.	NAADP	176-181	chemokine (C-X-C motif) ligand 15	Mus musculus	222-226
20200208-3	2010	The hypothesis being tested is that CD38 signaling pathway mediates FasL-induced intracellular Ca(2+) release through nicotinic acid adenine dinucleotide phosphate (NAADP) in mouse coronary arterial myocytes (CAMs) and thereby produces vasoconstriction in coronary arteries.	NAADP	118-163	CD38 antigen	Mus musculus	36-40
20200208-3	2010	The hypothesis being tested is that CD38 signaling pathway mediates FasL-induced intracellular Ca(2+) release through nicotinic acid adenine dinucleotide phosphate (NAADP) in mouse coronary arterial myocytes (CAMs) and thereby produces vasoconstriction in coronary arteries.	NAADP	118-163	Fas ligand (TNF superfamily, member 6)	Mus musculus	68-72
20200208-3	2010	The hypothesis being tested is that CD38 signaling pathway mediates FasL-induced intracellular Ca(2+) release through nicotinic acid adenine dinucleotide phosphate (NAADP) in mouse coronary arterial myocytes (CAMs) and thereby produces vasoconstriction in coronary arteries.	NAADP	165-170	CD38 antigen	Mus musculus	36-40
20200208-3	2010	The hypothesis being tested is that CD38 signaling pathway mediates FasL-induced intracellular Ca(2+) release through nicotinic acid adenine dinucleotide phosphate (NAADP) in mouse coronary arterial myocytes (CAMs) and thereby produces vasoconstriction in coronary arteries.	NAADP	165-170	Fas ligand (TNF superfamily, member 6)	Mus musculus	68-72
20200208-4	2010	HPLC analysis demonstrated that FasL markedly increased NAADP production in CAMs from wild-type mice (CD38(+/+)) but not in cells from CD38 knockout (CD38(-/-)) mice.	NAADP	56-61	Fas ligand (TNF superfamily, member 6)	Mus musculus	32-36
20200208-6	2010	However, direct delivery of NAADP, the CD38 metabolite, into CD38(-/-) CAMs still markedly increased Ca(2+) release, which could be significantly attenuated by a lysosomal function inhibitor, bafilomycin A1 (Baf), or a NAADP antagonist, pyridoxalphosphate-6-azophenyl-2-disulfonic acid.	NAADP	28-33	CD38 antigen	Mus musculus	39-43
20200208-6	2010	However, direct delivery of NAADP, the CD38 metabolite, into CD38(-/-) CAMs still markedly increased Ca(2+) release, which could be significantly attenuated by a lysosomal function inhibitor, bafilomycin A1 (Baf), or a NAADP antagonist, pyridoxalphosphate-6-azophenyl-2-disulfonic acid.	NAADP	28-33	CD38 antigen	Mus musculus	61-65
20200208-6	2010	However, direct delivery of NAADP, the CD38 metabolite, into CD38(-/-) CAMs still markedly increased Ca(2+) release, which could be significantly attenuated by a lysosomal function inhibitor, bafilomycin A1 (Baf), or a NAADP antagonist, pyridoxalphosphate-6-azophenyl-2-disulfonic acid.	NAADP	219-224	CD38 antigen	Mus musculus	39-43
20200208-9	2010	These results strongly indicate that the early response of CAMs to FasL is to increase intracellular Ca(2+) levels and enhance the vascular reactivity through stimulation of NAADP production and lysosome-associated two-phase Ca(2+) release in coronary arteries.	NAADP	174-179	Fas ligand (TNF superfamily, member 6)	Mus musculus	67-71
20346675-3	2010	Recently, we showed that heterologous expression of two-pore channel (TPC) proteins enhances NAADP-induced Ca(2+) release, whereas the NAADP response was abolished in pancreatic beta cells from Tpcn2 gene knockout mice [2].	NAADP	135-140	two pore segment channel 2	Mus musculus	194-199
20346675-7	2010	Thus, TPC1 and TPC2 both mediate NAADP-induced Ca(2+) release, but the subsequent amplification of this trigger Ca(2+) by IP(3)Rs is more tightly coupled for TPC2.	NAADP	33-38	two pore channel 1	Mus musculus	6-10
21099275-0	2009	Insulin receptor signaling for the proliferation of pancreatic beta-cells: involvement of Ca2+ second messengers, IP3, NAADP and cADPR.	NAADP	119-124	insulin receptor	Homo sapiens	0-16
20018950-3	2010	That TPCs act as NAADP-gated calcium release channels is clear, given that NAADP binds to high- and low-affinity sites associated with TPC2 and thereby induces calcium release and homologous desensitization, as observed in the case of endogenous NAADP receptors.	NAADP	75-80	two pore segment channel 2	Homo sapiens	135-139
20018950-4	2010	Moreover, NAADP-evoked calcium signals via TPC2 are ablated by short hairpin RNA knockdown of TPC2 and by depletion of acidic calcium stores with bafilomycin.	NAADP	10-15	two pore segment channel 2	Homo sapiens	43-47
20018950-4	2010	Moreover, NAADP-evoked calcium signals via TPC2 are ablated by short hairpin RNA knockdown of TPC2 and by depletion of acidic calcium stores with bafilomycin.	NAADP	10-15	two pore segment channel 2	Homo sapiens	94-98
20018950-5	2010	Importantly, however, NAADP-evoked calcium signals were biphasic in nature, with an initial phase of calcium release from lysosomes via TPC2, being subsequently amplified by calcium-induced calcium release (CICR) from the endoplasmic reticulum (ER).	NAADP	22-27	two pore segment channel 2	Homo sapiens	136-140
19910464-4	2010	In this study, we showed that angiotensin II (Ang II) evoked long lasting Ca(2+) rises and induced NAADP or cADPR productions via CD38 in HSCs.	NAADP	99-104	angiotensinogen (serpin peptidase inhibitor, clade A, member 8)	Mus musculus	30-44
19910464-4	2010	In this study, we showed that angiotensin II (Ang II) evoked long lasting Ca(2+) rises and induced NAADP or cADPR productions via CD38 in HSCs.	NAADP	99-104	angiotensinogen (serpin peptidase inhibitor, clade A, member 8)	Mus musculus	46-52
19910464-4	2010	In this study, we showed that angiotensin II (Ang II) evoked long lasting Ca(2+) rises and induced NAADP or cADPR productions via CD38 in HSCs.	NAADP	99-104	CD38 antigen	Mus musculus	130-134
19910464-5	2010	Inositol 1,4,5-trisphosphate as well as NAADP-induced initial Ca(2+) transients were prerequisite for the production of cADPR, which was responsible for later sustained Ca(2+) rises in the Ang II-treated HSCs.	NAADP	40-45	angiogenin, ribonuclease, RNase A family, 5	Mus musculus	189-192
19910464-6	2010	Ang II-mediated inositol 1,4,5-trisphosphate- and NAADP-stimulated Ca(2+) signals cross-talked in a dependent manner with each other.	NAADP	50-55	angiotensinogen (serpin peptidase inhibitor, clade A, member 8)	Mus musculus	0-6
20056832-11	2010	Activation of Raf-1 leads to both an ERK-dependent pathway that involves nicotinic acid adenine dinucleotide phosphate-sensitive Ca(2+) stores and Ca(2+)-dependent phosphorylation events, and an ERK-independent pathway that involves Bad inactivation at the mitochondria.	NAADP	73-118	v-raf-leukemia viral oncogene 1	Mus musculus	14-19
20056832-11	2010	Activation of Raf-1 leads to both an ERK-dependent pathway that involves nicotinic acid adenine dinucleotide phosphate-sensitive Ca(2+) stores and Ca(2+)-dependent phosphorylation events, and an ERK-independent pathway that involves Bad inactivation at the mitochondria.	NAADP	73-118	mitogen-activated protein kinase 1	Mus musculus	37-40
19910464-1	2010	CD38 is a type II glycoprotein that is responsible for the synthesis and hydrolysis of cyclic ADP-ribose (cADPR) and nicotinic acid adenine dinucleotide phosphate (NAADP), Ca(2+)-mobilizing second messengers.	NAADP	117-162	CD38 antigen	Mus musculus	0-4
19910464-1	2010	CD38 is a type II glycoprotein that is responsible for the synthesis and hydrolysis of cyclic ADP-ribose (cADPR) and nicotinic acid adenine dinucleotide phosphate (NAADP), Ca(2+)-mobilizing second messengers.	NAADP	164-169	CD38 antigen	Mus musculus	0-4
21099275-2	2009	Herein, we show the insulin receptor signaling pathway underlying CD38/ADPR-cyclase activation for NAADP/cADPR formation to induce Ca2+ rise, ultimately resulting in beta-cell proliferation.	NAADP	99-104	insulin receptor	Homo sapiens	20-36
21099275-2	2009	Herein, we show the insulin receptor signaling pathway underlying CD38/ADPR-cyclase activation for NAADP/cADPR formation to induce Ca2+ rise, ultimately resulting in beta-cell proliferation.	NAADP	99-104	CD38 molecule	Homo sapiens	66-70
21099275-4	2009	Activation of PLC generates IP3 and DAG; the former induces Ca (2+) release, resulting in activation of CD38/ADPR-cyclase for cADPR production via cGMP-dependent mechanism and the latter activates PKC, resulting in activation of ADPR-cyclase for NAADP synthesis.	NAADP	246-251	heparan sulfate proteoglycan 2	Homo sapiens	14-17
21099275-4	2009	Activation of PLC generates IP3 and DAG; the former induces Ca (2+) release, resulting in activation of CD38/ADPR-cyclase for cADPR production via cGMP-dependent mechanism and the latter activates PKC, resulting in activation of ADPR-cyclase for NAADP synthesis.	NAADP	246-251	CD38 molecule	Homo sapiens	104-108
21099275-7	2009	However, evidence indicates that a hitherto-unidentified ADPR cyclase in addition to CD38 participates in insulin-induced signaling through cADPR and NAADP synthesis.	NAADP	150-155	CD38 molecule	Homo sapiens	85-89
21099275-7	2009	However, evidence indicates that a hitherto-unidentified ADPR cyclase in addition to CD38 participates in insulin-induced signaling through cADPR and NAADP synthesis.	NAADP	150-155	insulin	Homo sapiens	106-113
21099275-8	2009	In conclusion, insulin receptor signaling in beta-cells employs three Ca (2+) signaling messengers, IP3, NAADP, and cADPR through a complex but concerted action of signaling molecules for Ca2+ signaling, which is involved in the proliferation of the islets.	NAADP	105-110	insulin receptor	Homo sapiens	15-31
18754814-2	2009	The present study tested the hypothesis that NAADP induces Ca(2+) release from the lysosomal store via a TRP-ML1 (transient receptor potential-mucolipin 1)-mediated Ca(2+) release channel in coronary arterial myocytes (CAMs).	NAADP	45-50	mucolipin TRP cation channel 1	Homo sapiens	105-112
19763610-10	2009	Conversely, significant upregulation of TRPML2sv transcripts was observed when primary mouse lymphoid cells were treated with nicotinic acid adenine dinucleotide phosphate, or N-(2-[p-bromocinnamylamino]ethyl)-5-isoquinoline sulfonamide, both known activators of TRPML1.	NAADP	126-171	mucolipin 2	Mus musculus	40-46
19763610-10	2009	Conversely, significant upregulation of TRPML2sv transcripts was observed when primary mouse lymphoid cells were treated with nicotinic acid adenine dinucleotide phosphate, or N-(2-[p-bromocinnamylamino]ethyl)-5-isoquinoline sulfonamide, both known activators of TRPML1.	NAADP	126-171	mucolipin 1	Mus musculus	263-269
18754814-2	2009	The present study tested the hypothesis that NAADP induces Ca(2+) release from the lysosomal store via a TRP-ML1 (transient receptor potential-mucolipin 1)-mediated Ca(2+) release channel in coronary arterial myocytes (CAMs).	NAADP	45-50	mucolipin TRP cation channel 1	Homo sapiens	114-154
18754814-8	2009	Immunoprecipitation or blockade of TRP-ML1 by anti-TRP-ML1 antibodies almost abolished NAADP-induced activation of lysosomal Ca(2+) channels (to 14.0 +/- 4.4% of control).	NAADP	87-92	mucolipin TRP cation channel 1	Homo sapiens	35-42
18754814-8	2009	Immunoprecipitation or blockade of TRP-ML1 by anti-TRP-ML1 antibodies almost abolished NAADP-induced activation of lysosomal Ca(2+) channels (to 14.0 +/- 4.4% of control).	NAADP	87-92	mucolipin TRP cation channel 1	Homo sapiens	51-58
18288637-5	2008	These data demonstrate a primary role of NAADP in ETB-mediated Ca(2+) signaling and strongly suggest a novel role of lipid rafts/caveolae in triggering ET-induced NAADP signaling.	NAADP	41-46	endothelin receptor type B	Rattus norvegicus	50-53
19557428-0	2009	The two-pore channel TPCN2 mediates NAADP-dependent Ca(2+)-release from lysosomal stores.	NAADP	36-41	two pore segment channel 2	Homo sapiens	21-26
19557428-6	2009	TPCN2 mediates intracellular Ca(2+)-release after activation with low-nanomolar concentrations of NAADP while it is desensitized by micromolar concentrations of this second messenger and is insensitive to the NAADP analog nicotinamide adenine dinucleotide phosphate (NADP).	NAADP	98-103	two pore segment channel 2	Homo sapiens	0-5
19541638-6	2009	Downstream events of Ca(2+) mobilization, such as nuclear translocation of "nuclear factor of activated T cells" (NFAT), T cell receptor-driven interleukin-2 production, and proliferation in antigen-experienced CD4(+) effector T cells, were attenuated by the NAADP antagonist.	NAADP	259-264	CD4 molecule	Homo sapiens	211-214
19387438-5	2009	Membranes enriched with TPC2 show high affinity NAADP binding, and TPC2 underpins NAADP-induced Ca(2+) release from lysosome-related stores that is subsequently amplified by Ca(2+)-induced Ca(2+) release by InsP(3)Rs.	NAADP	48-53	two pore segment channel 2	Homo sapiens	24-28
19387438-5	2009	Membranes enriched with TPC2 show high affinity NAADP binding, and TPC2 underpins NAADP-induced Ca(2+) release from lysosome-related stores that is subsequently amplified by Ca(2+)-induced Ca(2+) release by InsP(3)Rs.	NAADP	82-87	two pore segment channel 2	Homo sapiens	24-28
19387438-5	2009	Membranes enriched with TPC2 show high affinity NAADP binding, and TPC2 underpins NAADP-induced Ca(2+) release from lysosome-related stores that is subsequently amplified by Ca(2+)-induced Ca(2+) release by InsP(3)Rs.	NAADP	82-87	two pore segment channel 2	Homo sapiens	67-71
19387438-6	2009	Responses to NAADP were abolished by disrupting the lysosomal proton gradient and by ablating TPC2 expression, but were only attenuated by depleting endoplasmic reticulum Ca(2+) stores or by blocking InsP(3)Rs.	NAADP	13-18	two pore segment channel 2	Homo sapiens	94-98
18984909-6	2008	The enzyme CD38 can catalyze both the synthesis and hydrolysis of NAADP, making it ideal for effecting the rapid metabolism of NAADP.	NAADP	66-71	CD38 molecule	Homo sapiens	11-15
18984909-6	2008	The enzyme CD38 can catalyze both the synthesis and hydrolysis of NAADP, making it ideal for effecting the rapid metabolism of NAADP.	NAADP	127-132	CD38 molecule	Homo sapiens	11-15
18516691-9	2009	In vitro mass spectrometry analysis showed that BA formed adducts with the CD38 products and Ca2+ channel agonists cyclic adenosine diphosphate ribose (cADPR) and nicotinic acid adenine dinucleotide phosphate (NAADP).	NAADP	163-208	CD38 molecule	Homo sapiens	75-79
18516691-9	2009	In vitro mass spectrometry analysis showed that BA formed adducts with the CD38 products and Ca2+ channel agonists cyclic adenosine diphosphate ribose (cADPR) and nicotinic acid adenine dinucleotide phosphate (NAADP).	NAADP	210-215	CD38 molecule	Homo sapiens	75-79
19620632-0	2009	Essential requirement for two-pore channel 1 in NAADP-mediated calcium signaling.	NAADP	48-53	two pore segment channel 1	Homo sapiens	26-44
19620632-3	2009	In this study, we show that the previously uncharacterized human two-pore channels (TPC1 and TPC2) are endolysosomal proteins, that NAADP-mediated calcium signals are enhanced by overexpression of TPC1 and attenuated after knockdown of TPC1, and that mutation of a single highly conserved residue within a putative pore region abrogated calcium release by NAADP.	NAADP	132-137	two pore segment channel 1	Homo sapiens	84-88
19620632-3	2009	In this study, we show that the previously uncharacterized human two-pore channels (TPC1 and TPC2) are endolysosomal proteins, that NAADP-mediated calcium signals are enhanced by overexpression of TPC1 and attenuated after knockdown of TPC1, and that mutation of a single highly conserved residue within a putative pore region abrogated calcium release by NAADP.	NAADP	132-137	two pore segment channel 2	Homo sapiens	93-97
19620632-3	2009	In this study, we show that the previously uncharacterized human two-pore channels (TPC1 and TPC2) are endolysosomal proteins, that NAADP-mediated calcium signals are enhanced by overexpression of TPC1 and attenuated after knockdown of TPC1, and that mutation of a single highly conserved residue within a putative pore region abrogated calcium release by NAADP.	NAADP	132-137	two pore segment channel 1	Homo sapiens	197-201
19620632-3	2009	In this study, we show that the previously uncharacterized human two-pore channels (TPC1 and TPC2) are endolysosomal proteins, that NAADP-mediated calcium signals are enhanced by overexpression of TPC1 and attenuated after knockdown of TPC1, and that mutation of a single highly conserved residue within a putative pore region abrogated calcium release by NAADP.	NAADP	132-137	two pore segment channel 1	Homo sapiens	197-201
19620632-3	2009	In this study, we show that the previously uncharacterized human two-pore channels (TPC1 and TPC2) are endolysosomal proteins, that NAADP-mediated calcium signals are enhanced by overexpression of TPC1 and attenuated after knockdown of TPC1, and that mutation of a single highly conserved residue within a putative pore region abrogated calcium release by NAADP.	NAADP	356-361	two pore segment channel 1	Homo sapiens	84-88
19620632-3	2009	In this study, we show that the previously uncharacterized human two-pore channels (TPC1 and TPC2) are endolysosomal proteins, that NAADP-mediated calcium signals are enhanced by overexpression of TPC1 and attenuated after knockdown of TPC1, and that mutation of a single highly conserved residue within a putative pore region abrogated calcium release by NAADP.	NAADP	356-361	two pore segment channel 2	Homo sapiens	93-97
19620632-4	2009	Thus, TPC1 is critical for NAADP action and is likely the long sought after target channel for NAADP.	NAADP	27-32	two pore segment channel 1	Homo sapiens	6-10
19620632-4	2009	Thus, TPC1 is critical for NAADP action and is likely the long sought after target channel for NAADP.	NAADP	95-100	two pore segment channel 1	Homo sapiens	6-10
18572241-2	2008	Other TRPM2 regulators include cADPR, NAADP and H(2)O(2), which synergize with ADPR to potentiate TRPM2 activation.	NAADP	38-43	transient receptor potential cation channel subfamily M member 2	Homo sapiens	6-11
18572241-2	2008	Other TRPM2 regulators include cADPR, NAADP and H(2)O(2), which synergize with ADPR to potentiate TRPM2 activation.	NAADP	38-43	transient receptor potential cation channel subfamily M member 2	Homo sapiens	98-103
18581239-1	2008	CD38 is a 45-kD ectoenzyme involved in the synthesis of potent calcium (Ca(2+))-mobilizing agents, cyclic adenosine diphosphate-ribose (cADPR), and nicotinic acid adenine dinucleotide phosphate (NAADP+).	NAADP	148-193	CD38 molecule	Homo sapiens	0-4
18581239-1	2008	CD38 is a 45-kD ectoenzyme involved in the synthesis of potent calcium (Ca(2+))-mobilizing agents, cyclic adenosine diphosphate-ribose (cADPR), and nicotinic acid adenine dinucleotide phosphate (NAADP+).	NAADP	195-200	CD38 molecule	Homo sapiens	0-4
18191199-5	2008	We conclude that a subpopulation of lysosomes cluster in the perinuclear region of the cell and form junctions with SR containing a high density of RyR3 to comprise a trigger zone for Ca(2+) signalling by NAADP.	NAADP	205-210	ryanodine receptor 3	Rattus norvegicus	148-152
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.	NAADP	131-136	CD38 molecule	Homo sapiens	48-52
18288637-1	2008	We have investigated the role of NAADP-mediated Ca(2+) mobilization in endothelin (ET) signaling via endothelin receptor subtype A (ETA) and endothelin receptor subtype B (ETB) in rat peritubular smooth muscle cells.	NAADP	33-38	endothelin receptor type A	Rattus norvegicus	132-135
18288637-3	2008	Ca(2+) release in response to selective ETB stimulation was abolished by inhibition of NAADP signaling through the same strategies, while these treatments only partially impaired ETA-dependent Ca(2+) signaling, showing that transduction of the ETB signal is dependent on NAADP.	NAADP	87-92	endothelin receptor type B	Rattus norvegicus	40-43
18288637-3	2008	Ca(2+) release in response to selective ETB stimulation was abolished by inhibition of NAADP signaling through the same strategies, while these treatments only partially impaired ETA-dependent Ca(2+) signaling, showing that transduction of the ETB signal is dependent on NAADP.	NAADP	87-92	endothelin receptor type B	Rattus norvegicus	244-247
18288637-3	2008	Ca(2+) release in response to selective ETB stimulation was abolished by inhibition of NAADP signaling through the same strategies, while these treatments only partially impaired ETA-dependent Ca(2+) signaling, showing that transduction of the ETB signal is dependent on NAADP.	NAADP	271-276	endothelin receptor type B	Rattus norvegicus	40-43
18288637-3	2008	Ca(2+) release in response to selective ETB stimulation was abolished by inhibition of NAADP signaling through the same strategies, while these treatments only partially impaired ETA-dependent Ca(2+) signaling, showing that transduction of the ETB signal is dependent on NAADP.	NAADP	271-276	endothelin receptor type B	Rattus norvegicus	244-247
18288637-4	2008	In addition, we show that lipid rafts/caveolae contain ETA, ETB, and NAADP/cADPR generating enzyme CD38 and that stimulation of ETB receptors results in increased CD38 activity; interestingly, ETB- (but not ETA-) mediated Ca(2+) responses were antagonized by disruption of lipid rafts/caveolae with methyl-beta-cyclodextrin.	NAADP	69-74	CD38 molecule	Rattus norvegicus	99-103
17707504-8	2008	In human granulocytes, endogenous P2Y(11) proved to be responsible for the NAADP+-induced cell activation (as demonstrated by the use of NF157, a selective and potent inhibitor of P2Y(11)), unveiling a role of NAADP+ as a pro-inflammatory cytokine.	NAADP	75-80	purinergic receptor P2Y11	Homo sapiens	34-41
17707504-8	2008	In human granulocytes, endogenous P2Y(11) proved to be responsible for the NAADP+-induced cell activation (as demonstrated by the use of NF157, a selective and potent inhibitor of P2Y(11)), unveiling a role of NAADP+ as a pro-inflammatory cytokine.	NAADP	210-215	purinergic receptor P2Y11	Homo sapiens	34-41
17786980-1	2008	CD38 is a type II transmembrane glycoprotein found mainly on the plasma membrane involved in the metabolism of cADPR and NAADP, two nucleotides with calcium mobilizing activity independent of inositol trisphosphate.	NAADP	121-126	CD38 molecule	Homo sapiens	0-4
18184929-7	2008	GLP-1 sequentially stimulated production of NAADP and cyclic ADPR in the organelles through protein kinase A and cAMP-regulated guanine nucleotide exchange factor II.	NAADP	44-49	glucagon	Mus musculus	0-5
18184929-8	2008	Furthermore, the results showed that NAADP production from acidic organelles governed overall Ca(2+) signals, including insulin secretion by GLP-1, and that in addition to CD38, enzymes capable of synthesizing NAADP and/or cyclic ADPR were present in beta-cells.	NAADP	37-42	glucagon	Mus musculus	141-146
18184929-9	2008	These observations were supported by the study with Cd38(-/-) beta-cells, demonstrating production of NAADP, cyclic ADPR, and Ca(2+) signal with normal insulin secretion stimulated by GLP-1.	NAADP	102-107	CD38 antigen	Mus musculus	52-56
18184929-10	2008	CONCLUSIONS: Our findings demonstrate that the GLP-1-mediated Ca(2+) signal for insulin secretion in pancreatic beta-cells is a cooperative action of NAADP and cyclic ADPR spatiotemporally formed by multiple enzymes.	NAADP	150-155	glucagon	Mus musculus	47-52
18184929-0	2008	Generation of nicotinic acid adenine dinucleotide phosphate and cyclic ADP-ribose by glucagon-like peptide-1 evokes Ca2+ signal that is essential for insulin secretion in mouse pancreatic islets.	NAADP	14-59	glucagon	Mus musculus	85-108
18184929-6	2008	RESULTS: A GLP-1-induced [Ca(2+)](i) increase showed a cooperative Ca(2+) signal, i.e., an initial [Ca(2+)](i) rise mediated by the action of NAADP that was produced in acidic organelles and a subsequent long-lasting increase of [Ca(2+)](i) by the action of cyclic ADPR that was produced in plasma membranes and secretory granules.	NAADP	142-147	glucagon	Mus musculus	11-16
17233614-5	2007	The intracellular Ca(2+) channel triggered by cADPR is the RyR (ryanodine receptor); in the case of NAADP, both activation of RyR and a novel Ca(2+) channel have been proposed.	NAADP	100-105	ryanodine receptor 2	Homo sapiens	59-62
17395143-0	2007	An enzymatic cycling assay for nicotinic acid adenine dinucleotide phosphate using NAD synthetase.	NAADP	31-76	NAD synthetase 1	Homo sapiens	83-97
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.	NAADP	16-21	NAD synthetase 1	Homo sapiens	172-186
18308196-2	2008	Recent work has reported that Ca2+ release from the DTS is mediated by the generation of inositol 1,4,5-trisphosphate, whereas Ca2+ efflux from the acidic stores is mostly linked to nicotinic acid adenine dinucleotide phosphate.	NAADP	182-227	carbonic anhydrase 2	Homo sapiens	127-130
17233614-5	2007	The intracellular Ca(2+) channel triggered by cADPR is the RyR (ryanodine receptor); in the case of NAADP, both activation of RyR and a novel Ca(2+) channel have been proposed.	NAADP	100-105	ryanodine receptor 2	Homo sapiens	64-82
17233614-5	2007	The intracellular Ca(2+) channel triggered by cADPR is the RyR (ryanodine receptor); in the case of NAADP, both activation of RyR and a novel Ca(2+) channel have been proposed.	NAADP	100-105	ryanodine receptor 2	Homo sapiens	126-129
16875665-5	2006	Here we show that microinjection of the functionally active cofilin alters the Ca(2+) signalling mediated by the three major second messengers, InsP(3), NAADP, and cADPr.	NAADP	153-158	cofilin 1	Homo sapiens	60-67
16935261-3	2006	The enzyme CD38 is a multifunctional enzyme capable of synthesis of the second messenger, cADPR, NAADP, and ADPR.	NAADP	97-102	CD38 antigen	Mus musculus	11-15
17003338-1	2006	CD38 is a multifunctional enzyme capable of generating metabolites that release Ca2+ from intracellular stores, including nicotinic acid adenine dinucleotide phosphate (NAADP).	NAADP	122-167	CD38 antigen	Mus musculus	0-4
17003338-1	2006	CD38 is a multifunctional enzyme capable of generating metabolites that release Ca2+ from intracellular stores, including nicotinic acid adenine dinucleotide phosphate (NAADP).	NAADP	169-174	CD38 antigen	Mus musculus	0-4
17003338-3	2006	It has recently been shown that NAADP mediates Ca2+ mobilization by insulin in human pancreatic beta-cells.	NAADP	32-37	insulin	Homo sapiens	68-75
16790499-8	2007	The enzyme CD38 has been shown to catalyze the synthesis of NAADP in vitro by the base-exchange reaction.	NAADP	60-65	CD38 molecule	Homo sapiens	11-15
16790499-10	2007	Using CD38 knockout mice, we observed that both the basal and histamine stimulated levels of NAADP are independent of CD38 and the base-exchange reaction.	NAADP	93-98	CD38 antigen	Mus musculus	6-10
16790499-12	2007	Furthermore, the NAADP mediated mechanism in mammalian cells can be independent of RyRs and CD38.	NAADP	17-22	CD38 molecule	Homo sapiens	92-96
17074764-8	2006	RyR activation depends on receptors for nicotinic acid adenine dinucleotide phosphate (NAADP), because inactivation by a high NAADP concentration inhibited release from both stores, whereas a cyclic ADPR-ribose antagonist had no effect.	NAADP	40-85	ryanodine receptor 2	Homo sapiens	0-3
17074764-8	2006	RyR activation depends on receptors for nicotinic acid adenine dinucleotide phosphate (NAADP), because inactivation by a high NAADP concentration inhibited release from both stores, whereas a cyclic ADPR-ribose antagonist had no effect.	NAADP	87-92	ryanodine receptor 2	Homo sapiens	0-3
17074764-8	2006	RyR activation depends on receptors for nicotinic acid adenine dinucleotide phosphate (NAADP), because inactivation by a high NAADP concentration inhibited release from both stores, whereas a cyclic ADPR-ribose antagonist had no effect.	NAADP	126-131	ryanodine receptor 2	Homo sapiens	0-3
17027490-5	2006	CCK and ACh recruit Ca(2+) from lysosomes and from zymogen granules through different mechanisms; CCK uses NAADP and cADPR, respectively, and ACh uses Ca(2+) and IP(3), respectively.	NAADP	107-112	cholecystokinin	Homo sapiens	0-3
17027490-5	2006	CCK and ACh recruit Ca(2+) from lysosomes and from zymogen granules through different mechanisms; CCK uses NAADP and cADPR, respectively, and ACh uses Ca(2+) and IP(3), respectively.	NAADP	107-112	cholecystokinin	Homo sapiens	98-101
16861223-0	2006	Acidic residues at the active sites of CD38 and ADP-ribosyl cyclase determine nicotinic acid adenine dinucleotide phosphate (NAADP) synthesis and hydrolysis activities.	NAADP	78-123	CD38 molecule	Homo sapiens	39-43
16861223-0	2006	Acidic residues at the active sites of CD38 and ADP-ribosyl cyclase determine nicotinic acid adenine dinucleotide phosphate (NAADP) synthesis and hydrolysis activities.	NAADP	125-130	CD38 molecule	Homo sapiens	39-43
16861223-4	2006	Here we show that CD38 can, in fact, hydrolyze NAADP to ADP-ribose 2"-phosphate.	NAADP	47-52	CD38 molecule	Homo sapiens	18-22
16861223-12	2006	Synthesis of NAADP catalyzed by CD38 is known to have strong preference for acidic pH, suggesting that Glu(146) and Asp(155) are also critical determinants.	NAADP	13-18	CD38 molecule	Homo sapiens	32-36
16861223-14	2006	Likewise, using similar approaches, Glu(98) of the cyclase, which is equivalent to Glu(146) in CD38, was found to be responsible for controlling the pH dependence of NAADP synthesis by the cyclase.	NAADP	166-171	CD38 molecule	Homo sapiens	95-99
16875665-6	2006	Cofilin intensifies the Ca(2+) signals induced by InsP(3) and NAADP, and delays those induced by cADPr.	NAADP	62-67	cofilin 1	Homo sapiens	0-7
16627475-6	2006	In contrast, the NAADP concentration was elevated neither upon activation of the ADP-ribose/TRPM2 channel Ca2+ signaling system nor by an increase of the intracellular Ca2+ concentration upon thapsigargin stimulation.	NAADP	17-22	transient receptor potential cation channel subfamily M member 2	Homo sapiens	92-97
16690024-3	2006	Here we demonstrate that ADPRCs from both lower and higher Metazoa (including human CD38) can also synthesize NAADP+ starting from 2"-phospho-cyclic ADP-ribose (cADPRP) and NA.	NAADP	110-116	CD38 molecule	Homo sapiens	84-88
16473958-1	2006	The present study was designed to determine the production of nicotinic acid adenine dinucleotide phosphate (NAADP) and its role associated with lysosomes in mediating endothelin-1 (ET-1)-induced vasoconstriction in coronary arteries.	NAADP	62-107	endothelin 1	Homo sapiens	168-180
16473958-1	2006	The present study was designed to determine the production of nicotinic acid adenine dinucleotide phosphate (NAADP) and its role associated with lysosomes in mediating endothelin-1 (ET-1)-induced vasoconstriction in coronary arteries.	NAADP	62-107	endothelin 1	Homo sapiens	182-186
16473958-1	2006	The present study was designed to determine the production of nicotinic acid adenine dinucleotide phosphate (NAADP) and its role associated with lysosomes in mediating endothelin-1 (ET-1)-induced vasoconstriction in coronary arteries.	NAADP	109-114	endothelin 1	Homo sapiens	168-180
16473958-1	2006	The present study was designed to determine the production of nicotinic acid adenine dinucleotide phosphate (NAADP) and its role associated with lysosomes in mediating endothelin-1 (ET-1)-induced vasoconstriction in coronary arteries.	NAADP	109-114	endothelin 1	Homo sapiens	182-186
16473958-6	2006	Moreover, ET-1 significantly increased NAADP formation in CASMCs and resulted in the rise of [Ca2+]i in these cells with a large increase in global Ca2+ level of 1,815 +/- 84 nM.	NAADP	39-44	endothelin 1	Homo sapiens	10-14
16473958-10	2006	Our results suggest that a lysosome-mediated Ca2+ regulatory mechanism via NAADP contributes to ET-1-induced Ca2+ mobilization in CASMCs and consequent vasoconstriction of coronary arteries.	NAADP	75-80	endothelin 1	Homo sapiens	96-100
16405964-2	2006	Wild-type F(1)-ATPase was inhibited potently, albeit slowly, when incubated with MgCl(2), NaF, and NaADP.	NAADP	99-104	ATPase	Escherichia coli	15-21
16585058-0	2006	Nicotinic acid adenine dinucleotide phosphate and cyclic ADP-ribose regulate TRPM2 channels in T lymphocytes.	NAADP	0-45	transient receptor potential cation channel subfamily M member 2	Homo sapiens	77-82
16585058-3	2006	Here, we show that the two Ca2+-mobilizing second messengers cyclic ADP-ribose (cADPR) and nicotinic acid adenine dinucleotide phosphate (NAADP) strongly activate natively expressed TRPM2 channels in Jurkat T cells.	NAADP	91-136	transient receptor potential cation channel subfamily M member 2	Homo sapiens	182-187
16585058-3	2006	Here, we show that the two Ca2+-mobilizing second messengers cyclic ADP-ribose (cADPR) and nicotinic acid adenine dinucleotide phosphate (NAADP) strongly activate natively expressed TRPM2 channels in Jurkat T cells.	NAADP	138-143	transient receptor potential cation channel subfamily M member 2	Homo sapiens	182-187
16585058-4	2006	TRPM2 activation by both agonists can be partially suppressed by the ADPR antagonist adenosine monophosphate (AMP), which suggests that cADPR and NAADP lead to mobilization of endogenous ADPR presumably via metabolic conversion.	NAADP	146-151	transient receptor potential cation channel subfamily M member 2	Homo sapiens	0-5
16585058-5	2006	The remaining channel activity is due to direct gating of TRPM2 by the two agonists and can be completely suppressed by 8-Br-cADPR, which suggests that cADPR and NAADP share a common binding site on TRPM2 that can regulate TRPM2 activity in synergy with ADPR.	NAADP	162-167	transient receptor potential cation channel subfamily M member 2	Homo sapiens	58-63
16585058-5	2006	The remaining channel activity is due to direct gating of TRPM2 by the two agonists and can be completely suppressed by 8-Br-cADPR, which suggests that cADPR and NAADP share a common binding site on TRPM2 that can regulate TRPM2 activity in synergy with ADPR.	NAADP	162-167	transient receptor potential cation channel subfamily M member 2	Homo sapiens	199-204
16585058-5	2006	The remaining channel activity is due to direct gating of TRPM2 by the two agonists and can be completely suppressed by 8-Br-cADPR, which suggests that cADPR and NAADP share a common binding site on TRPM2 that can regulate TRPM2 activity in synergy with ADPR.	NAADP	162-167	transient receptor potential cation channel subfamily M member 2	Homo sapiens	199-204
16585058-6	2006	We conclude that cADPR and NAADP, in combination with ADPR, represent physiological co-activators of TRPM2 that contribute to Ca2+ influx in T lymphocytes and presumably other cell types that express this channel.	NAADP	27-32	transient receptor potential cation channel subfamily M member 2	Homo sapiens	101-106
16095882-9	2006	We suggest that thrombin evokes Ca2+ release from TBHQ-sensitive and insensitive stores, which requires both NAADP and IP3, respectively, while ADP and AVP exert an IP3-dependent release of Ca2+ from the TBHQ-insensitive compartment in human platelets.	NAADP	109-114	coagulation factor II, thrombin	Homo sapiens	16-24
15650244-1	2004	CD38, a multifunctional enzyme, generates two potent Ca2+-releasing signal metabolites, cyclic ADP-ribose (cADPR) and NAADP+, thereby upmodulating many important Ca2+-mediated cell functions.	NAADP	118-123	CD38 molecule	Homo sapiens	0-4
16061474-2	2005	Here we report that murine cortical astrocytes in culture and in acute slices respond with transient intracellular Ca2+ increases to extracellularly applied NAADP+ and express the NAADP+-producing enzyme CD38.	NAADP	157-162	CD38 antigen	Mus musculus	204-208
16061474-2	2005	Here we report that murine cortical astrocytes in culture and in acute slices respond with transient intracellular Ca2+ increases to extracellularly applied NAADP+ and express the NAADP+-producing enzyme CD38.	NAADP	180-185	CD38 antigen	Mus musculus	204-208
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.	NAADP	106-111	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.	NAADP	106-111	transient receptor potential cation channel, subfamily M, member 2	Mus musculus	208-213
12573222-4	2003	Here we show that glucose also increases [Ca(2+)](i) via the novel Ca(2+)-mobilizing agent nicotinic acid adenine dinucleotide phosphate (NAADP) in the insulin-secreting beta-cell line MIN6.	NAADP	91-136	insulin	Homo sapiens	152-159
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.	NAADP	94-100	CD38 molecule	Homo sapiens	6-10
12717813-3	2003	Recent studies by Johnson and Misler,1 Masgrau et al.2 and Mitchell et al.3 provide strong evidence (1) for the existence of intracellular Ca(2+) stores sensitive to NAADP, a potent Ca(2+)-mobilizing messenger, and (2) that these Ca(2+) stores are involved in both glucose- and insulin-mediated signal transduction.	NAADP	166-171	insulin	Homo sapiens	278-285
12717813-4	2003	NAADP may therefore play an important role in controlling secretion of insulin from pancreatic beta cells.	NAADP	0-5	insulin	Homo sapiens	71-78
12538591-9	2003	Because dantrolene strongly inhibited glucose-stimulated insulin secretion (from 3.07 +/- 0.51-fold stimulation to no significant glucose effect; n = 3, p < 0.01), we conclude that RyR I-mediated Ca(2+)-induced Ca(2+) release from secretory vesicles, possibly potentiated by NAADP, is essential for the activation of insulin secretion.	NAADP	278-283	ryanodine receptor 1, skeletal muscle	Mus musculus	184-187
12573222-4	2003	Here we show that glucose also increases [Ca(2+)](i) via the novel Ca(2+)-mobilizing agent nicotinic acid adenine dinucleotide phosphate (NAADP) in the insulin-secreting beta-cell line MIN6.	NAADP	138-143	insulin	Homo sapiens	152-159
12381785-0	2002	Nicotinic acid-adenine dinucleotide phosphate-sensitive calcium stores initiate insulin signaling in human beta cells.	NAADP	0-45	insulin	Homo sapiens	80-87
11181950-6	2001	ACh uses IP3 and Ca2+, whereas CCK uses cADPr and NAADP.	NAADP	50-55	cholecystokinin	Homo sapiens	31-34
12381785-10	2002	Injection of the CD38-derived Ca(2+) mobilizing metabolite, nicotinic acid-adenine dinucleotide phosphate (NAADP), at nanomolar concentrations, evoked oscillatory Ca(2+) signals that could be initiated in the presence of ryanodine, xestospongin C, and Ca(2+)-free solutions.	NAADP	60-105	CD38 molecule	Homo sapiens	17-21
12381785-10	2002	Injection of the CD38-derived Ca(2+) mobilizing metabolite, nicotinic acid-adenine dinucleotide phosphate (NAADP), at nanomolar concentrations, evoked oscillatory Ca(2+) signals that could be initiated in the presence of ryanodine, xestospongin C, and Ca(2+)-free solutions.	NAADP	107-112	CD38 molecule	Homo sapiens	17-21
12381785-11	2002	Desensitizing concentrations of NAADP abolished insulin-stimulated Ca(2+) signals.	NAADP	32-37	insulin	Homo sapiens	48-55
12102654-0	2002	Nicotinic acid-adenine dinucleotide phosphate activates the skeletal muscle ryanodine receptor.	NAADP	0-45	ryanodine receptor 1	Homo sapiens	60-94
11829748-0	2002	CD38 is the major enzyme responsible for synthesis of nicotinic acid-adenine dinucleotide phosphate in mammalian tissues.	NAADP	54-99	CD38 molecule	Homo sapiens	0-4
11829748-1	2002	In the present study, we have determined the role of the enzyme CD38 upon the synthesis of the Ca(2+)-releasing nucleotide nicotinic acid-adenine dinucleotide phosphate (NAADP).	NAADP	123-168	CD38 molecule	Homo sapiens	64-68
11829748-1	2002	In the present study, we have determined the role of the enzyme CD38 upon the synthesis of the Ca(2+)-releasing nucleotide nicotinic acid-adenine dinucleotide phosphate (NAADP).	NAADP	170-175	CD38 molecule	Homo sapiens	64-68
11829748-2	2002	In rat tissues, we observed that the capacity for NAADP synthesis could be co-immunoprecipitated with CD38 using an anti-CD38 antibody.	NAADP	50-55	CD38 molecule	Rattus norvegicus	102-106
11829748-2	2002	In rat tissues, we observed that the capacity for NAADP synthesis could be co-immunoprecipitated with CD38 using an anti-CD38 antibody.	NAADP	50-55	CD38 molecule	Rattus norvegicus	121-125
11829748-5	2002	These observations lead to the conclusion that CD38 is the major enzyme responsible for the synthesis of NAADP and cyclic ADP-ribose, and raises the possibility of a new signalling pathway where two different Ca(2+)-releasing nucleotides are synthesized by the same enzyme.	NAADP	105-110	CD38 molecule	Homo sapiens	47-51
11294249-3	2001	We report here that NAADP (3-10 microM) induces Ca2+ release from rat heart microsomes and that NAADP (1-10 microM) activates single ryanodine receptor/calcium release channels (RyR2) from dog heart incorporated into bilayer lipid membranes.	NAADP	96-101	ryanodine receptor 2	Rattus norvegicus	178-182
11294249-4	2001	The results indicate that NAADP may play a role in cardiac excitation-contraction coupling by acting on RyR2 channels.	NAADP	26-31	ryanodine receptor 2	Homo sapiens	104-108
11264460-2	2001	Although NAADP is a linear molecule, structurally distinct from the cyclic cADPR, it is synthesized by similar enzymes, ADP-ribosyl cyclase and its homolog, CD38.	NAADP	9-14	CD38 molecule	Homo sapiens	157-161
10781610-1	2000	CD38 is a ubiquitous protein originally identified as a lymphocyte antigen and recently also found to be a multifunctional enzyme participating in the synthesis and metabolism of two Ca(2+) messengers, cyclic ADP-ribose (cADPR) and nicotinic acid adenine dinucleotide phosphate.	NAADP	232-277	CD38 molecule	Homo sapiens	0-4
10985387-2	2000	It was reported recently that nicotinic acid adenine dinucleotide phosphate (NAADP) releases Ca2+ from mammalian brain microsomes [5] and triggers Ca2+ signals in pancreatic acinar cells, where it is proposed to mediate CCK-evoked Ca2+ signals [6].	NAADP	30-75	carbonic anhydrase 2	Homo sapiens	93-96
10985387-2	2000	It was reported recently that nicotinic acid adenine dinucleotide phosphate (NAADP) releases Ca2+ from mammalian brain microsomes [5] and triggers Ca2+ signals in pancreatic acinar cells, where it is proposed to mediate CCK-evoked Ca2+ signals [6].	NAADP	30-75	carbonic anhydrase 2	Homo sapiens	147-150
10985387-2	2000	It was reported recently that nicotinic acid adenine dinucleotide phosphate (NAADP) releases Ca2+ from mammalian brain microsomes [5] and triggers Ca2+ signals in pancreatic acinar cells, where it is proposed to mediate CCK-evoked Ca2+ signals [6].	NAADP	30-75	cholecystokinin	Homo sapiens	220-223
10985387-2	2000	It was reported recently that nicotinic acid adenine dinucleotide phosphate (NAADP) releases Ca2+ from mammalian brain microsomes [5] and triggers Ca2+ signals in pancreatic acinar cells, where it is proposed to mediate CCK-evoked Ca2+ signals [6].	NAADP	30-75	carbonic anhydrase 2	Homo sapiens	147-150
10985387-2	2000	It was reported recently that nicotinic acid adenine dinucleotide phosphate (NAADP) releases Ca2+ from mammalian brain microsomes [5] and triggers Ca2+ signals in pancreatic acinar cells, where it is proposed to mediate CCK-evoked Ca2+ signals [6].	NAADP	77-82	carbonic anhydrase 2	Homo sapiens	93-96
10985387-2	2000	It was reported recently that nicotinic acid adenine dinucleotide phosphate (NAADP) releases Ca2+ from mammalian brain microsomes [5] and triggers Ca2+ signals in pancreatic acinar cells, where it is proposed to mediate CCK-evoked Ca2+ signals [6].	NAADP	77-82	carbonic anhydrase 2	Homo sapiens	147-150
10985387-2	2000	It was reported recently that nicotinic acid adenine dinucleotide phosphate (NAADP) releases Ca2+ from mammalian brain microsomes [5] and triggers Ca2+ signals in pancreatic acinar cells, where it is proposed to mediate CCK-evoked Ca2+ signals [6].	NAADP	77-82	cholecystokinin	Homo sapiens	220-223
10985387-2	2000	It was reported recently that nicotinic acid adenine dinucleotide phosphate (NAADP) releases Ca2+ from mammalian brain microsomes [5] and triggers Ca2+ signals in pancreatic acinar cells, where it is proposed to mediate CCK-evoked Ca2+ signals [6].	NAADP	77-82	carbonic anhydrase 2	Homo sapiens	147-150
10985387-4	2000	Picomolar concentrations of bombesin and CCK evoked similar patterns of cytosolic Ca2+ oscillations, but high, desensitising, NAADP concentrations selectively inhibited CCK, but not bombesin-evoked signals.	NAADP	126-131	cholecystokinin	Homo sapiens	169-172
10985387-6	2000	We further tested whether NAADP is involved in Ca2+ signals triggered by activation of the low-affinity CCK receptor sites.	NAADP	26-31	carbonic anhydrase 2	Homo sapiens	47-50
10985387-6	2000	We further tested whether NAADP is involved in Ca2+ signals triggered by activation of the low-affinity CCK receptor sites.	NAADP	26-31	cholecystokinin	Homo sapiens	104-107
10985387-8	2000	Our results suggest that Ca2+-release channels gated by the novel Ca2+-mobilising molecule NAADP are only essential in specific Ca2+-mobilising pathways, whereas the IP3 receptors are generally required for Ca2+ signals.	NAADP	91-96	carbonic anhydrase 2	Homo sapiens	25-28
10985387-8	2000	Our results suggest that Ca2+-release channels gated by the novel Ca2+-mobilising molecule NAADP are only essential in specific Ca2+-mobilising pathways, whereas the IP3 receptors are generally required for Ca2+ signals.	NAADP	91-96	carbonic anhydrase 2	Homo sapiens	66-69
10985387-8	2000	Our results suggest that Ca2+-release channels gated by the novel Ca2+-mobilising molecule NAADP are only essential in specific Ca2+-mobilising pathways, whereas the IP3 receptors are generally required for Ca2+ signals.	NAADP	91-96	carbonic anhydrase 2	Homo sapiens	66-69
10985387-8	2000	Our results suggest that Ca2+-release channels gated by the novel Ca2+-mobilising molecule NAADP are only essential in specific Ca2+-mobilising pathways, whereas the IP3 receptors are generally required for Ca2+ signals.	NAADP	91-96	carbonic anhydrase 2	Homo sapiens	66-69
9193683-4	1997	Although the structures of cADPR and NAADP are totally distinct, both nucleotides can be synthesized by ADP-ribosyl cyclase or CD38, a lymphocyte antigen.	NAADP	37-42	CD38 molecule	Homo sapiens	127-131
10078532-5	1999	Cells were significantly more sensitive to NAADP than to either cADPR or InsP3, whereas higher concentrations of NAADP selectively inactivated CCK-evoked Ca2+ signals in pancreatic acinar cells, indicating that NAADP may function as an intracellular messenger in mammalian cells.	NAADP	113-118	cholecystokinin	Homo sapiens	143-146
10078532-5	1999	Cells were significantly more sensitive to NAADP than to either cADPR or InsP3, whereas higher concentrations of NAADP selectively inactivated CCK-evoked Ca2+ signals in pancreatic acinar cells, indicating that NAADP may function as an intracellular messenger in mammalian cells.	NAADP	113-118	cholecystokinin	Homo sapiens	143-146
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.	NAADP	144-189	CD38 molecule	Homo sapiens	0-4
33818279-6	2022	The NOX/PHOX (NADPH oxidase)-dependent oxidative burst was required for nuclear translocation of TFEB during phagocytosis of Gram-positive or -negative bacteria, and reactive oxygen species (ROS) were sufficient to trigger TFEB activation in a CD38- and NAADP (nicotinic acid adenine dinucleotide phosphate)-dependent manner.	NAADP	254-259	transcription factor EB	Homo sapiens	97-101
33818279-6	2022	The NOX/PHOX (NADPH oxidase)-dependent oxidative burst was required for nuclear translocation of TFEB during phagocytosis of Gram-positive or -negative bacteria, and reactive oxygen species (ROS) were sufficient to trigger TFEB activation in a CD38- and NAADP (nicotinic acid adenine dinucleotide phosphate)-dependent manner.	NAADP	261-306	transcription factor EB	Homo sapiens	97-101
33818279-7	2022	Consistent with the Ca2+-releasing activity of NAADP, intracellular Ca2+ chelation and PPP3/calcineurin inhibition prevented TFEB activation by phagocytosis and ROS (reactive oxygen species), impairing the induction of pro-inflammatory cytokines such as IL6 and TNF/TNFalpha.	NAADP	47-52	transcription factor EB	Homo sapiens	125-129
33818279-7	2022	Consistent with the Ca2+-releasing activity of NAADP, intracellular Ca2+ chelation and PPP3/calcineurin inhibition prevented TFEB activation by phagocytosis and ROS (reactive oxygen species), impairing the induction of pro-inflammatory cytokines such as IL6 and TNF/TNFalpha.	NAADP	47-52	interleukin 6	Homo sapiens	254-257
33818279-7	2022	Consistent with the Ca2+-releasing activity of NAADP, intracellular Ca2+ chelation and PPP3/calcineurin inhibition prevented TFEB activation by phagocytosis and ROS (reactive oxygen species), impairing the induction of pro-inflammatory cytokines such as IL6 and TNF/TNFalpha.	NAADP	47-52	tumor necrosis factor	Homo sapiens	262-265
33818279-7	2022	Consistent with the Ca2+-releasing activity of NAADP, intracellular Ca2+ chelation and PPP3/calcineurin inhibition prevented TFEB activation by phagocytosis and ROS (reactive oxygen species), impairing the induction of pro-inflammatory cytokines such as IL6 and TNF/TNFalpha.	NAADP	47-52	tumor necrosis factor	Homo sapiens	266-274
34971841-2	2022	This is in contrast to the hitherto prevailing view that CD38 is critical for NAADP formation.	NAADP	78-83	CD38 molecule	Homo sapiens	57-61
8701086-16	1996	Both ADP-ribosyl cyclase and CD38 can catalyze the exchange of the nicotinamide group in NADP+ with nicotinic acid, leading to the formation of another Ca+2 mobilizing metabolite, nicotinic acid dinucleotide phosphate (NAADP).	NAADP	219-224	CD38 molecule	Homo sapiens	29-33
8530456-11	1995	That two different products of ADP-ribosyl cyclase and CD38, cADPR and NAADP+, are both involved in Ca2+ mobilization suggests a crucial role of these enzymes in Ca2+ signaling.	NAADP	71-76	CD38 molecule	Homo sapiens	55-59
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.	NAADP	191-196	CD38 molecule	Homo sapiens	0-4
34896700-7	2022	Endocytosis can deliver surface type II CD38 to endo-lysosomes, which acidic environment favors the production of NAADP.	NAADP	114-119	CD38 molecule	Homo sapiens	40-44
34944620-15	2021	In cancer samples, NAADP reduced the activity of Na+/K+ ATPase by 9-times (p < 0.01) and the activity of Ca2+ ATPase EPR about 2-times (p < 0.05).	NAADP	19-24	carbonic anhydrase 2	Homo sapiens	105-116
34944620-16	2021	NAADP caused a tendency to decrease the activity of Ca2+ ATPase of PM, but increased basal ATPase activity by 2-fold vs. the mean of this index in cancer samples without the addition of NAADP.	NAADP	0-5	carbonic anhydrase 2	Homo sapiens	52-63
34944620-17	2021	In control samples NAADP caused only a tendency to decrease the activities of Na+/K+ ATPase and Ca2+ ATPase EPR, but statistically decreased the activity of Ca2+ ATPase of PM (p < 0.05).	NAADP	19-24	carbonic anhydrase 2	Homo sapiens	96-107
34944620-17	2021	In control samples NAADP caused only a tendency to decrease the activities of Na+/K+ ATPase and Ca2+ ATPase EPR, but statistically decreased the activity of Ca2+ ATPase of PM (p < 0.05).	NAADP	19-24	carbonic anhydrase 2	Homo sapiens	157-168
34944620-20	2021	NAADP caused a decrease in the activities of Na+/K+ ATPase and Ca2+ ATPase EPR in cancer samples and increased basal ATPase activity.	NAADP	0-5	carbonic anhydrase 2	Homo sapiens	63-74
34944620-21	2021	In control samples, NAADP decreased Ca2+ ATPase of PM and increased basal ATPase activity.	NAADP	20-25	carbonic anhydrase 2	Homo sapiens	36-47
34784249-0	2021	Dual NADPH oxidases DUOX1 and DUOX2 synthesize NAADP and are necessary for Ca2+ signaling during T cell activation.	NAADP	47-52	dual oxidase 1	Homo sapiens	20-25
34784249-0	2021	Dual NADPH oxidases DUOX1 and DUOX2 synthesize NAADP and are necessary for Ca2+ signaling during T cell activation.	NAADP	47-52	dual oxidase 2	Homo sapiens	30-35
34557192-4	2021	Our recent studies have identified HN1L/JPT2 as a high affinity NAADP binding protein that is essential for the modulation of Ca2+ channels.	NAADP	64-69	Jupiter microtubule associated homolog 2	Homo sapiens	35-39
34831261-4	2021	Partial blockade of NAADP signaling in naive CD4+ T cells in vitro promoted the differentiation of Th17 cells.	NAADP	20-25	CD4 antigen	Mus musculus	45-48
34831261-6	2021	Moreover, using an IL-17A fate mapping mouse model, we showed that NAADP inhibition promotes conversion of Th17 cells into regulatory T cells in vitro and in vivo.	NAADP	67-72	interleukin 17A	Mus musculus	19-25
34831261-8	2021	Thus, these results reveal a novel function of NAADP in controlling the differentiation and plasticity of CD4+ T cells.	NAADP	47-52	CD4 antigen	Mus musculus	106-109
34288391-5	2021	TRPV4-mediated Ca2+ entry, in turn, promoted the concerted interplay between inositol-1,4,5-trisphosphate- and nicotinic acid adenine dinucleotide phosphate-induced endogenous Ca2+ release and store-operated Ca2+ entry (SOCE).	NAADP	111-156	transient receptor potential cation channel subfamily V member 4	Homo sapiens	0-5
34362892-3	2021	Given the necessity of the endolysosomal two-pore channel (TPC1 or TPC2) in NAADP signaling, we performed affinity purification and quantitative proteomic analysis of the interacting proteins of NAADP and TPCs.	NAADP	76-81	two pore segment channel 1	Homo sapiens	59-63
34362892-3	2021	Given the necessity of the endolysosomal two-pore channel (TPC1 or TPC2) in NAADP signaling, we performed affinity purification and quantitative proteomic analysis of the interacting proteins of NAADP and TPCs.	NAADP	76-81	two pore segment channel 2	Homo sapiens	67-71
34362892-5	2021	Lsm12 directly binds to NAADP via its Lsm domain, colocalizes with TPC2, and mediates the apparent association of NAADP to isolated TPC2 or TPC2-containing membranes.	NAADP	24-29	LSM12 homolog	Homo sapiens	0-5
34362892-5	2021	Lsm12 directly binds to NAADP via its Lsm domain, colocalizes with TPC2, and mediates the apparent association of NAADP to isolated TPC2 or TPC2-containing membranes.	NAADP	114-119	LSM12 homolog	Homo sapiens	0-5
34362892-5	2021	Lsm12 directly binds to NAADP via its Lsm domain, colocalizes with TPC2, and mediates the apparent association of NAADP to isolated TPC2 or TPC2-containing membranes.	NAADP	114-119	two pore segment channel 2	Homo sapiens	132-136
34362892-6	2021	Lsm12 is essential and immediately participates in NAADP-evoked TPC activation and Ca2+ mobilization from acidic stores.	NAADP	51-56	LSM12 homolog	Homo sapiens	0-5
34313548-0	2022	LRRK2 is required for CD38-mediated NAADP-Ca2+ signaling and the downstream activation of TFEB (transcription factor EB) in immune cells.	NAADP	36-41	leucine rich repeat kinase 2	Homo sapiens	0-5
34313548-0	2022	LRRK2 is required for CD38-mediated NAADP-Ca2+ signaling and the downstream activation of TFEB (transcription factor EB) in immune cells.	NAADP	36-41	CD38 molecule	Homo sapiens	22-26
34313548-8	2022	This generates an NAADP-dependent calcium signal, which requires LRRK2 kinase activity, and results in the downstream activation of TFEB.	NAADP	18-23	leucine rich repeat kinase 2	Homo sapiens	65-70
34313548-8	2022	This generates an NAADP-dependent calcium signal, which requires LRRK2 kinase activity, and results in the downstream activation of TFEB.	NAADP	18-23	transcription factor EB	Homo sapiens	132-136
35563771-10	2022	Conversely, stimulation of TPC channel activity by one of its endogenous ligands, namely nicotinic adenine dinucleotide phosphate (NAADP) or phosphatidylinositol 3,5-bisphosphate (PI(3,5)P2), were found to trigger the release of Ca2+ from the endolysosomes; thereby improving the effect of TPC1 on regulated mast cell degranulation.	NAADP	131-136	two pore segment channel 1	Homo sapiens	290-294
35561646-5	2022	The recent identification of Lsm12 and JPT2 as NAADP-binding proteins provides a new molecular basis for understanding NAADP-evoked Ca2+ signaling.	NAADP	119-124	LSM12 homolog	Homo sapiens	29-34
35561646-6	2022	In this review, we summarize basic structural and functional aspects of TPCs and highlight the most recent studies on the newly discovered TPC in a parasitic protozoan and the NAADP-binding proteins LSM12 and JPT2 as new key players in NAADP signaling.	NAADP	236-241	LSM12 homolog	Homo sapiens	199-204
35511727-11	2022	The CGs-decreased GLUT1 expression was significantly inhibited by a Ca2+ chelator, a Ca2+ -ATPase inhibitor, and a NAADP antagonist.	NAADP	115-120	solute carrier family 2 member 1	Homo sapiens	18-23
33321420-4	2021	We have employed recombinant human NAD kinase expressed in E. coli as an enzymatic reagent to convert readily available synthetic NAD derivatives to NADP analogs, which were subsequently transformed into NAADP derivatives using enzyme catalyzed pyridine base exchange.	NAADP	204-209	NAD kinase	Homo sapiens	35-45
35392169-1	2022	Nicotinic acid adenine dinucleotide phosphate (NAADP) is a newly discovered second messenger that gates two pore channels 1 (TPC1) and 2 (TPC2) to elicit endo-lysosomal (EL) Ca2+ release.	NAADP	0-45	two pore segment channel 1	Homo sapiens	125-129
35392169-1	2022	Nicotinic acid adenine dinucleotide phosphate (NAADP) is a newly discovered second messenger that gates two pore channels 1 (TPC1) and 2 (TPC2) to elicit endo-lysosomal (EL) Ca2+ release.	NAADP	0-45	two pore segment channel 2	Homo sapiens	138-142
35392169-1	2022	Nicotinic acid adenine dinucleotide phosphate (NAADP) is a newly discovered second messenger that gates two pore channels 1 (TPC1) and 2 (TPC2) to elicit endo-lysosomal (EL) Ca2+ release.	NAADP	47-52	two pore segment channel 1	Homo sapiens	125-129
35392169-1	2022	Nicotinic acid adenine dinucleotide phosphate (NAADP) is a newly discovered second messenger that gates two pore channels 1 (TPC1) and 2 (TPC2) to elicit endo-lysosomal (EL) Ca2+ release.	NAADP	47-52	two pore segment channel 2	Homo sapiens	138-142
35392169-8	2022	Furthermore, NAADP-evoked Ca2+ release was required to mediate FBS-induced extracellular signal-regulated kinase (ERK), but not Akt, phosphorylation in C-MSCs.	NAADP	13-18	mitogen-activated protein kinase 1	Homo sapiens	75-112
35392169-8	2022	Furthermore, NAADP-evoked Ca2+ release was required to mediate FBS-induced extracellular signal-regulated kinase (ERK), but not Akt, phosphorylation in C-MSCs.	NAADP	13-18	mitogen-activated protein kinase 1	Homo sapiens	114-117
33873071-1	2021	NAADP (nicotinic acid adenine dinucleotide phosphate) is a potent second messenger releasing Ca2+ from endolysosomes through two-pore channels (TPCs) and from the endoplasmic reticulum (ER) through type 1 ryanodine receptors (RyR1).	NAADP	0-5	ryanodine receptor 1	Homo sapiens	226-230
33873071-1	2021	NAADP (nicotinic acid adenine dinucleotide phosphate) is a potent second messenger releasing Ca2+ from endolysosomes through two-pore channels (TPCs) and from the endoplasmic reticulum (ER) through type 1 ryanodine receptors (RyR1).	NAADP	7-52	ryanodine receptor 1	Homo sapiens	226-230
33758062-0	2021	HN1L/JPT2: A signaling protein that connects NAADP generation to Ca2+ microdomain formation.	NAADP	45-50	Jupiter microtubule associated homolog 2	Homo sapiens	0-4
33758062-1	2021	NAADP-evoked Ca2+ release through type 1 ryanodine receptors (RYR1) is a major mechanism underlying the earliest signals in T cell activation, which are the formation of Ca2+ microdomains.	NAADP	0-5	ryanodine receptor 1	Homo sapiens	62-66
33758062-2	2021	In our characterization of the molecular machinery underlying NAADP action, we identified an NAADP-binding protein, called hematological and neurological expressed 1-like protein (HN1L) [also known as Jupiter microtubule-associated homolog 2 (JPT2)].	NAADP	62-67	Jupiter microtubule associated homolog 2	Homo sapiens	123-178
33758062-2	2021	In our characterization of the molecular machinery underlying NAADP action, we identified an NAADP-binding protein, called hematological and neurological expressed 1-like protein (HN1L) [also known as Jupiter microtubule-associated homolog 2 (JPT2)].	NAADP	62-67	Jupiter microtubule associated homolog 2	Homo sapiens	180-184
33758062-4	2021	Photoaffinity labeling demonstrated direct binding of NAADP to recombinant HN1L/JPT2.	NAADP	54-59	Jupiter microtubule associated homolog 2	Homo sapiens	75-79
33758062-5	2021	T cell receptor/CD3-dependent coprecipitation of HN1L/JPT2 with RYRs and colocalization of these proteins suggest that HN1L/JPT2 connects NAADP formation with the activation of RYR channels within the first seconds of T cell activation.	NAADP	138-143	Jupiter microtubule associated homolog 2	Homo sapiens	49-53
33758062-5	2021	T cell receptor/CD3-dependent coprecipitation of HN1L/JPT2 with RYRs and colocalization of these proteins suggest that HN1L/JPT2 connects NAADP formation with the activation of RYR channels within the first seconds of T cell activation.	NAADP	138-143	Jupiter microtubule associated homolog 2	Homo sapiens	119-123
33758062-5	2021	T cell receptor/CD3-dependent coprecipitation of HN1L/JPT2 with RYRs and colocalization of these proteins suggest that HN1L/JPT2 connects NAADP formation with the activation of RYR channels within the first seconds of T cell activation.	NAADP	138-143	ryanodine receptor 1	Homo sapiens	64-67
33758062-6	2021	Thus, HN1L/JPT2 enables NAADP to activate Ca2+ release from the endoplasmic reticulum through RYR.	NAADP	24-29	Jupiter microtubule associated homolog 2	Homo sapiens	6-10
33758062-6	2021	Thus, HN1L/JPT2 enables NAADP to activate Ca2+ release from the endoplasmic reticulum through RYR.	NAADP	24-29	ryanodine receptor 1	Homo sapiens	94-97
33602742-8	2021	GPN blocked Ca2+ responses evoked by the novel NAADP-like agonist, TPC2-A1-N. GPN-evoked Ca2+ signals were thus better correlated with associated pH changes in the lysosome compared to the cytosol and coupled to lysosomal Ca2+ release.	NAADP	47-52	two pore segment channel 2	Homo sapiens	67-71
35198877-6	2022	SARM1 base exchange occurs also in DRG neurons and is thus a very likely physiological source of calcium-mobilizing agent NaADP.	NAADP	122-127	sterile alpha and TIR motif containing 1	Homo sapiens	0-5
32478984-10	2020	The latter resulted in two structurally distinct high affinity agonists, which are able to selectively activate TPC2 in either an NAADP- or PI(3,5)P2 -like manner.	NAADP	130-135	two pore segment channel 2	Homo sapiens	112-116
32583526-0	2021	Nicotinic acid adenine dinucleotide phosphate activates two-pore channel TPC1 to mediate lysosomal Ca2+ release in endothelial colony-forming cells.	NAADP	0-45	two pore segment channel 1	Homo sapiens	73-77
32583526-1	2021	Nicotinic acid adenine dinucleotide phosphate (NAADP) is the most recently discovered Ca2+ -releasing messenger that increases the intracellular Ca2+ concentration by mobilizing the lysosomal Ca2+ store through two-pore channels 1 (TPC1) and 2 (TPC2).	NAADP	0-45	two pore segment channel 1	Homo sapiens	232-236
32583526-1	2021	Nicotinic acid adenine dinucleotide phosphate (NAADP) is the most recently discovered Ca2+ -releasing messenger that increases the intracellular Ca2+ concentration by mobilizing the lysosomal Ca2+ store through two-pore channels 1 (TPC1) and 2 (TPC2).	NAADP	0-45	two pore segment channel 2	Homo sapiens	245-249
32583526-1	2021	Nicotinic acid adenine dinucleotide phosphate (NAADP) is the most recently discovered Ca2+ -releasing messenger that increases the intracellular Ca2+ concentration by mobilizing the lysosomal Ca2+ store through two-pore channels 1 (TPC1) and 2 (TPC2).	NAADP	47-52	two pore segment channel 1	Homo sapiens	232-236
32583526-1	2021	Nicotinic acid adenine dinucleotide phosphate (NAADP) is the most recently discovered Ca2+ -releasing messenger that increases the intracellular Ca2+ concentration by mobilizing the lysosomal Ca2+ store through two-pore channels 1 (TPC1) and 2 (TPC2).	NAADP	47-52	two pore segment channel 2	Homo sapiens	245-249
32583526-7	2021	Liposomal delivery of NAADP induced a transient Ca2+ signal that was abolished by disrupting the lysosomal Ca2+ store and by pharmacological and genetic blockade of TPC1.	NAADP	22-27	two pore segment channel 1	Homo sapiens	165-169
32583526-9	2021	Finally, NAADP-induced lysosomal Ca2+ release was found to trigger vascular endothelial growth factor-induced intracellular Ca2+ oscillations and proliferation, while it did not contribute to adenosine-5"-trisphosphate-induced Ca2+ signaling.	NAADP	9-14	vascular endothelial growth factor A	Homo sapiens	67-101
32583526-10	2021	These findings demonstrated that NAADP-induced TPC1-mediated Ca2+ release can selectively be recruited to induce the Ca2+ response to specific cues in circulating ECFCs.	NAADP	33-38	two pore segment channel 1	Homo sapiens	47-51
33027744-2	2020	The mammalian two-pore channels TPC1 and TPC2 are patho-physiologically relevant endo-lysosomal cation channels regulated by the Ca2+ mobilising messenger NAADP and the phosphoinositide PI(3,5)P2.	NAADP	155-160	two pore segment channel 1	Homo sapiens	32-36
33027744-2	2020	The mammalian two-pore channels TPC1 and TPC2 are patho-physiologically relevant endo-lysosomal cation channels regulated by the Ca2+ mobilising messenger NAADP and the phosphoinositide PI(3,5)P2.	NAADP	155-160	two pore segment channel 2	Homo sapiens	41-45
32588751-6	2020	Methods and Results: Using platelets from wild-type or SERCA3-deficient mice, we demonstrated that an early (within 5 to 10 seconds following stimulation) secretion of ADP specifically dependent on SERCA3 stored Ca2+ is exclusively mobilized by nicotinic acid adenosine dinucleotide phosphate (NAADP): both Ca2+ mobilization from SERCA3-dependent stores and primary ADP secretion are blocked by the NAADP receptor antagonist Ned-19, and reciprocally both are stimulated by permeant NAADP.	NAADP	399-404	ATPase, Ca++ transporting, ubiquitous	Mus musculus	198-204
32588751-6	2020	Methods and Results: Using platelets from wild-type or SERCA3-deficient mice, we demonstrated that an early (within 5 to 10 seconds following stimulation) secretion of ADP specifically dependent on SERCA3 stored Ca2+ is exclusively mobilized by nicotinic acid adenosine dinucleotide phosphate (NAADP): both Ca2+ mobilization from SERCA3-dependent stores and primary ADP secretion are blocked by the NAADP receptor antagonist Ned-19, and reciprocally both are stimulated by permeant NAADP.	NAADP	294-299	ATPase, Ca++ transporting, ubiquitous	Mus musculus	198-204
32588751-6	2020	Methods and Results: Using platelets from wild-type or SERCA3-deficient mice, we demonstrated that an early (within 5 to 10 seconds following stimulation) secretion of ADP specifically dependent on SERCA3 stored Ca2+ is exclusively mobilized by nicotinic acid adenosine dinucleotide phosphate (NAADP): both Ca2+ mobilization from SERCA3-dependent stores and primary ADP secretion are blocked by the NAADP receptor antagonist Ned-19, and reciprocally both are stimulated by permeant NAADP.	NAADP	294-299	ATPase, Ca++ transporting, ubiquitous	Mus musculus	198-204
32588751-6	2020	Methods and Results: Using platelets from wild-type or SERCA3-deficient mice, we demonstrated that an early (within 5 to 10 seconds following stimulation) secretion of ADP specifically dependent on SERCA3 stored Ca2+ is exclusively mobilized by nicotinic acid adenosine dinucleotide phosphate (NAADP): both Ca2+ mobilization from SERCA3-dependent stores and primary ADP secretion are blocked by the NAADP receptor antagonist Ned-19, and reciprocally both are stimulated by permeant NAADP.	NAADP	399-404	ATPase, Ca++ transporting, ubiquitous	Mus musculus	198-204
32588751-6	2020	Methods and Results: Using platelets from wild-type or SERCA3-deficient mice, we demonstrated that an early (within 5 to 10 seconds following stimulation) secretion of ADP specifically dependent on SERCA3 stored Ca2+ is exclusively mobilized by nicotinic acid adenosine dinucleotide phosphate (NAADP): both Ca2+ mobilization from SERCA3-dependent stores and primary ADP secretion are blocked by the NAADP receptor antagonist Ned-19, and reciprocally both are stimulated by permeant NAADP.	NAADP	399-404	ATPase, Ca++ transporting, ubiquitous	Mus musculus	198-204
32588751-6	2020	Methods and Results: Using platelets from wild-type or SERCA3-deficient mice, we demonstrated that an early (within 5 to 10 seconds following stimulation) secretion of ADP specifically dependent on SERCA3 stored Ca2+ is exclusively mobilized by nicotinic acid adenosine dinucleotide phosphate (NAADP): both Ca2+ mobilization from SERCA3-dependent stores and primary ADP secretion are blocked by the NAADP receptor antagonist Ned-19, and reciprocally both are stimulated by permeant NAADP.	NAADP	399-404	ATPase, Ca++ transporting, ubiquitous	Mus musculus	198-204
32676502-1	2020	Nicotinic acid adenine dinucleotide phosphate (NAADP) is a second messenger that evokes calcium release from intracellular organelles by the engagement of calcium release channels, including members of the Transient Receptor Potential (TRP) family, such as TRPML1, the (structurally) related Two Pore Channel type 1 (TPC1) and TPC2 channels as well as Ryanodine Receptors type 1 (RYR1; Guse, 2012).	NAADP	0-45	mucolipin 1	Mus musculus	257-263
32442744-1	2020	TPC2-A1-N and TPC2-A1-P, two novel small molecules, differentially activate two-pore channel 2 (TPC2) and mimic the activation of TPC2 with NAADP and PIP2, resulting in distinct ion channel selectivities.	NAADP	140-145	two pore segment channel 2	Homo sapiens	0-4
32442744-1	2020	TPC2-A1-N and TPC2-A1-P, two novel small molecules, differentially activate two-pore channel 2 (TPC2) and mimic the activation of TPC2 with NAADP and PIP2, resulting in distinct ion channel selectivities.	NAADP	140-145	two pore segment channel 2	Homo sapiens	14-18
32442744-1	2020	TPC2-A1-N and TPC2-A1-P, two novel small molecules, differentially activate two-pore channel 2 (TPC2) and mimic the activation of TPC2 with NAADP and PIP2, resulting in distinct ion channel selectivities.	NAADP	140-145	two pore segment channel 2	Homo sapiens	14-18
32442744-1	2020	TPC2-A1-N and TPC2-A1-P, two novel small molecules, differentially activate two-pore channel 2 (TPC2) and mimic the activation of TPC2 with NAADP and PIP2, resulting in distinct ion channel selectivities.	NAADP	140-145	two pore segment channel 2	Homo sapiens	14-18
32717131-0	2020	Interleukin-8 drives CD38 to form NAADP from NADP+ and NAAD in the endolysosomes to mobilize Ca2+ and effect cell migration.	NAADP	34-39	C-X-C motif chemokine ligand 8	Homo sapiens	0-13
32717131-0	2020	Interleukin-8 drives CD38 to form NAADP from NADP+ and NAAD in the endolysosomes to mobilize Ca2+ and effect cell migration.	NAADP	34-39	CD38 molecule	Homo sapiens	21-25
32717131-2	2020	In vitro, CD38-mediated NAADP synthesis requires an acidic pH and a nonphysiological concentration of nicotinic acid (NA).	NAADP	24-29	CD38 molecule	Homo sapiens	10-14
32717131-3	2020	We discovered that CD38 catalyzes synthesis of NAADP by exchanging the nicotinamide moiety of nicotinamide adenine dinucleotide phosphate (NADP+ ) for the NA group of nicotinic acid adenine dinucleotide (NAAD) inside endolysosomes of interleukin 8 (IL8)-treated lymphokine-activated killer (LAK) cells.	NAADP	47-52	CD38 molecule	Homo sapiens	19-23
32717131-3	2020	We discovered that CD38 catalyzes synthesis of NAADP by exchanging the nicotinamide moiety of nicotinamide adenine dinucleotide phosphate (NADP+ ) for the NA group of nicotinic acid adenine dinucleotide (NAAD) inside endolysosomes of interleukin 8 (IL8)-treated lymphokine-activated killer (LAK) cells.	NAADP	47-52	C-X-C motif chemokine ligand 8	Homo sapiens	234-247
32717131-3	2020	We discovered that CD38 catalyzes synthesis of NAADP by exchanging the nicotinamide moiety of nicotinamide adenine dinucleotide phosphate (NADP+ ) for the NA group of nicotinic acid adenine dinucleotide (NAAD) inside endolysosomes of interleukin 8 (IL8)-treated lymphokine-activated killer (LAK) cells.	NAADP	47-52	C-X-C motif chemokine ligand 8	Homo sapiens	249-252
32676502-1	2020	Nicotinic acid adenine dinucleotide phosphate (NAADP) is a second messenger that evokes calcium release from intracellular organelles by the engagement of calcium release channels, including members of the Transient Receptor Potential (TRP) family, such as TRPML1, the (structurally) related Two Pore Channel type 1 (TPC1) and TPC2 channels as well as Ryanodine Receptors type 1 (RYR1; Guse, 2012).	NAADP	0-45	two pore channel 1	Mus musculus	317-321
32676502-1	2020	Nicotinic acid adenine dinucleotide phosphate (NAADP) is a second messenger that evokes calcium release from intracellular organelles by the engagement of calcium release channels, including members of the Transient Receptor Potential (TRP) family, such as TRPML1, the (structurally) related Two Pore Channel type 1 (TPC1) and TPC2 channels as well as Ryanodine Receptors type 1 (RYR1; Guse, 2012).	NAADP	0-45	ryanodine receptor 1, skeletal muscle	Mus musculus	352-378
32676502-1	2020	Nicotinic acid adenine dinucleotide phosphate (NAADP) is a second messenger that evokes calcium release from intracellular organelles by the engagement of calcium release channels, including members of the Transient Receptor Potential (TRP) family, such as TRPML1, the (structurally) related Two Pore Channel type 1 (TPC1) and TPC2 channels as well as Ryanodine Receptors type 1 (RYR1; Guse, 2012).	NAADP	0-45	ryanodine receptor 1, skeletal muscle	Mus musculus	380-384
32676502-1	2020	Nicotinic acid adenine dinucleotide phosphate (NAADP) is a second messenger that evokes calcium release from intracellular organelles by the engagement of calcium release channels, including members of the Transient Receptor Potential (TRP) family, such as TRPML1, the (structurally) related Two Pore Channel type 1 (TPC1) and TPC2 channels as well as Ryanodine Receptors type 1 (RYR1; Guse, 2012).	NAADP	47-52	mucolipin 1	Mus musculus	257-263
32676502-1	2020	Nicotinic acid adenine dinucleotide phosphate (NAADP) is a second messenger that evokes calcium release from intracellular organelles by the engagement of calcium release channels, including members of the Transient Receptor Potential (TRP) family, such as TRPML1, the (structurally) related Two Pore Channel type 1 (TPC1) and TPC2 channels as well as Ryanodine Receptors type 1 (RYR1; Guse, 2012).	NAADP	47-52	two pore channel 1	Mus musculus	317-321
32676502-1	2020	Nicotinic acid adenine dinucleotide phosphate (NAADP) is a second messenger that evokes calcium release from intracellular organelles by the engagement of calcium release channels, including members of the Transient Receptor Potential (TRP) family, such as TRPML1, the (structurally) related Two Pore Channel type 1 (TPC1) and TPC2 channels as well as Ryanodine Receptors type 1 (RYR1; Guse, 2012).	NAADP	47-52	ryanodine receptor 1, skeletal muscle	Mus musculus	352-378
32676502-1	2020	Nicotinic acid adenine dinucleotide phosphate (NAADP) is a second messenger that evokes calcium release from intracellular organelles by the engagement of calcium release channels, including members of the Transient Receptor Potential (TRP) family, such as TRPML1, the (structurally) related Two Pore Channel type 1 (TPC1) and TPC2 channels as well as Ryanodine Receptors type 1 (RYR1; Guse, 2012).	NAADP	47-52	ryanodine receptor 1, skeletal muscle	Mus musculus	380-384
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)+.	NAADP	123-168	CD38 molecule	Homo sapiens	40-44
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)+.	NAADP	170-175	CD38 molecule	Homo sapiens	40-44
31995750-4	2020	To initiate the onset of resolution, TTP expression is increased by the second messengers, NAADP and cADPR, which downregulate CD38 expression.	NAADP	91-96	ZFP36 ring finger protein	Homo sapiens	37-40
31995750-4	2020	To initiate the onset of resolution, TTP expression is increased by the second messengers, NAADP and cADPR, which downregulate CD38 expression.	NAADP	91-96	CD38 molecule	Homo sapiens	127-131
30578820-4	2019	UVB induced H2O2 production through NADPH oxidase 4 activation, which is downstream to inositol 1,4,5-trisphosphate and nicotinic acid adenine dinucleotide phosphate.	NAADP	120-165	NADPH oxidase 4	Mus musculus	36-51
30408544-10	2019	These compounds inhibited endogenous NAADP-evoked Ca2+ release from sea urchin egg homogenates, NAADP-mediated channel activity of TPC2 re-routed to the plasma membrane, and PI(3,5)P2-mediated channel activity of TPC2 expressed in enlarged lysosomes.	NAADP	96-101	two pore segment channel 2	Homo sapiens	131-135
30408544-10	2019	These compounds inhibited endogenous NAADP-evoked Ca2+ release from sea urchin egg homogenates, NAADP-mediated channel activity of TPC2 re-routed to the plasma membrane, and PI(3,5)P2-mediated channel activity of TPC2 expressed in enlarged lysosomes.	NAADP	96-101	two pore segment channel 2	Homo sapiens	213-217
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.	NAADP	133-178	NAD kinase	Homo sapiens	68-72
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.	NAADP	133-178	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.	NAADP	133-178	calmodulin 1	Homo sapiens	329-332
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.	NAADP	133-178	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.	NAADP	180-185	calmodulin 1	Homo sapiens	329-332
31672920-8	2019	The surprising finding of another enzyme that produces cADPR and NAADP, sterile alpha and TIR motif containing1 (SARM1), is described.	NAADP	65-70	sterile alpha and TIR motif containing 1	Homo sapiens	113-118
31672920-10	2019	The intriguing finding that SARM1 is activated by nicotinamide mononucleotide to produce cADPR and NAADP suggests that it may function as a regulated Ca2+-signaling enzyme like CD38.	NAADP	99-104	sterile alpha and TIR motif containing 1	Homo sapiens	28-33
31672920-10	2019	The intriguing finding that SARM1 is activated by nicotinamide mononucleotide to produce cADPR and NAADP suggests that it may function as a regulated Ca2+-signaling enzyme like CD38.	NAADP	99-104	CD38 molecule	Homo sapiens	177-181
31836674-0	2019	Correction: CD38 produces nicotinic acid adenine dinucleotide phosphate in the lysosome.	NAADP	26-71	CD38 molecule	Homo sapiens	12-16
30091405-9	2018	Finally, arachidonic acid (AA) and nicotinic acid adenine dinucleotide phosphate (NAADP) stimulate ECFC proliferation by stimulating two-pore channel 1 (TPC1), thereby promoting Ca2+ release from the endolysosomal Ca2+ compartment.	NAADP	35-80	two pore segment channel 1	Homo sapiens	133-151
30991693-0	2019	Nicotinic Acid Adenine Dinucleotide Phosphate (NAADP) Induces Intracellular Ca2+ Release through the Two-Pore Channel TPC1 in Metastatic Colorectal Cancer Cells.	NAADP	0-45	two pore segment channel 1	Homo sapiens	118-122
30991693-0	2019	Nicotinic Acid Adenine Dinucleotide Phosphate (NAADP) Induces Intracellular Ca2+ Release through the Two-Pore Channel TPC1 in Metastatic Colorectal Cancer Cells.	NAADP	47-52	two pore segment channel 1	Homo sapiens	118-122
30991693-1	2019	Nicotinic acid adenine dinucleotide phosphate (NAADP) gates two-pore channels 1 and 2 (TPC1 and TPC2) to elicit endo-lysosomal (EL) Ca2+ release.	NAADP	0-45	two pore segment channel 1	Homo sapiens	87-91
30991693-1	2019	Nicotinic acid adenine dinucleotide phosphate (NAADP) gates two-pore channels 1 and 2 (TPC1 and TPC2) to elicit endo-lysosomal (EL) Ca2+ release.	NAADP	0-45	two pore segment channel 2	Homo sapiens	96-100
30991693-1	2019	Nicotinic acid adenine dinucleotide phosphate (NAADP) gates two-pore channels 1 and 2 (TPC1 and TPC2) to elicit endo-lysosomal (EL) Ca2+ release.	NAADP	47-52	two pore segment channel 1	Homo sapiens	87-91
30991693-1	2019	Nicotinic acid adenine dinucleotide phosphate (NAADP) gates two-pore channels 1 and 2 (TPC1 and TPC2) to elicit endo-lysosomal (EL) Ca2+ release.	NAADP	47-52	two pore segment channel 2	Homo sapiens	96-100
30991693-6	2019	Pharmacological and genetic manipulations revealed that the Ca2+ response to NAADP was triggered by TPC1, the most expressed TPC isoform in mCRC cells, and required ER-embedded InsP3 receptors.	NAADP	77-82	two pore segment channel 1	Homo sapiens	100-104
30563862-8	2018	Upon TCR activation, NAADP-evoked Ca2+ release through RYR1, in coordination with Ca2+ entry through ORAI1 and STIM, rapidly increases the number of Ca2+ microdomains, thereby initiating spread of Ca2+ signals deeper into the cytoplasm to promote full T cell activation.	NAADP	21-26	ryanodine receptor 1	Homo sapiens	55-59
30563862-8	2018	Upon TCR activation, NAADP-evoked Ca2+ release through RYR1, in coordination with Ca2+ entry through ORAI1 and STIM, rapidly increases the number of Ca2+ microdomains, thereby initiating spread of Ca2+ signals deeper into the cytoplasm to promote full T cell activation.	NAADP	21-26	ORAI calcium release-activated calcium modulator 1	Homo sapiens	101-106
29970392-3	2018	CD38 produces nicotinic acid adenine dinucleotide phosphate and adenosine 5"-diphosphate-ribose, both of which can act to increase intracellular Ca2+ levels.	NAADP	14-59	CD38 molecule	Homo sapiens	0-4
29632067-3	2018	CD38 is the only enzyme known to catalyze NAADP synthesis from NADP and nicotinic acid.	NAADP	42-47	CD38 molecule	Homo sapiens	0-4
29632067-4	2018	CD38-mediated catalysis requires an acidic pH, suggesting that NAADP may be produced in acidic endolysosomes, but this hypothesis is untested.	NAADP	63-68	CD38 molecule	Homo sapiens	0-4
29632067-7	2018	We also found that CD38 internalization occurred via a clathrin-dependent pathway, delivered CD38 to the endolysosome, and elevated intracellular NAADP levels.	NAADP	146-151	CD38 molecule	Homo sapiens	19-23
29632067-8	2018	We also created a CD38 variant for lysosome-specific expression, which not only withstood the degradative environment in the lysosome, but was also much more active than WT CD38 in elevating cellular NAADP levels.	NAADP	200-205	CD38 molecule	Homo sapiens	18-22
29632067-8	2018	We also created a CD38 variant for lysosome-specific expression, which not only withstood the degradative environment in the lysosome, but was also much more active than WT CD38 in elevating cellular NAADP levels.	NAADP	200-205	CD38 molecule	Homo sapiens	173-177
29632067-9	2018	Supplementing CD38-expressing cells with nicotinic acid substantially increased cellular NAADP levels.	NAADP	89-94	CD38 molecule	Homo sapiens	14-18
29632067-10	2018	These results demonstrate that endolysosomal CD38 can produce NAADP in human cells.	NAADP	62-67	CD38 molecule	Homo sapiens	45-49
29632067-11	2018	They further suggest that CD38"s compartmentalization to the lysosome may allow for its regulation via substrate access, rather than enzyme activation, thereby providing a reliable mechanism for regulating cellular NAADP production.	NAADP	215-220	CD38 molecule	Homo sapiens	26-30
29636391-7	2018	In HEK293 cells stably overexpressing human TPC2, shRNA-mediated knockdown of mTOR blocked rapamycin- and NAADP-evoked Ca2+ signals.	NAADP	106-111	two pore segment channel 2	Homo sapiens	44-48
29636391-7	2018	In HEK293 cells stably overexpressing human TPC2, shRNA-mediated knockdown of mTOR blocked rapamycin- and NAADP-evoked Ca2+ signals.	NAADP	106-111	mechanistic target of rapamycin kinase	Homo sapiens	78-82
30991693-8	2019	These data demonstrate that NAADP-gated TPC1 could be regarded as a novel target for alternative therapies to treat mCRC.	NAADP	28-33	two pore segment channel 1	Homo sapiens	40-44
29486595-1	2019	AIMS: Glucagon-like peptide-1 (GLP-1) increases intracellular Ca2+ concentrations, resulting in insulin secretion from pancreatic beta-cells through the sequential production of Ca2+ mobilizing messengers nicotinic acid adenine dinucleotide phosphate (NAADP) and cyclic ADP-ribose (cADPR).	NAADP	205-250	glucagon	Mus musculus	6-29
29486595-1	2019	AIMS: Glucagon-like peptide-1 (GLP-1) increases intracellular Ca2+ concentrations, resulting in insulin secretion from pancreatic beta-cells through the sequential production of Ca2+ mobilizing messengers nicotinic acid adenine dinucleotide phosphate (NAADP) and cyclic ADP-ribose (cADPR).	NAADP	205-250	glucagon	Mus musculus	31-36
29486595-1	2019	AIMS: Glucagon-like peptide-1 (GLP-1) increases intracellular Ca2+ concentrations, resulting in insulin secretion from pancreatic beta-cells through the sequential production of Ca2+ mobilizing messengers nicotinic acid adenine dinucleotide phosphate (NAADP) and cyclic ADP-ribose (cADPR).	NAADP	252-257	glucagon	Mus musculus	6-29
29486595-1	2019	AIMS: Glucagon-like peptide-1 (GLP-1) increases intracellular Ca2+ concentrations, resulting in insulin secretion from pancreatic beta-cells through the sequential production of Ca2+ mobilizing messengers nicotinic acid adenine dinucleotide phosphate (NAADP) and cyclic ADP-ribose (cADPR).	NAADP	252-257	glucagon	Mus musculus	31-36
29486595-2	2019	We previously found that NAADP activates the neuronal type of nitric oxide (NO) synthase (nNOS), the product of which, NO, activates guanylyl cyclase to produce cyclic guanosine monophosphate (cGMP), which, in turn, induces cADPR formation.	NAADP	25-30	nitric oxide synthase 1, neuronal	Mus musculus	90-94
29486595-4	2019	RESULTS: We show that NAADP-induced cGMP production by nNOS activation is dependent on carbon monoxide (CO) formation by heme oxygenase-2 (HO-2).	NAADP	22-27	nitric oxide synthase 1, neuronal	Mus musculus	55-59
29486595-4	2019	RESULTS: We show that NAADP-induced cGMP production by nNOS activation is dependent on carbon monoxide (CO) formation by heme oxygenase-2 (HO-2).	NAADP	22-27	heme oxygenase 2	Mus musculus	121-137
29486595-4	2019	RESULTS: We show that NAADP-induced cGMP production by nNOS activation is dependent on carbon monoxide (CO) formation by heme oxygenase-2 (HO-2).	NAADP	22-27	heme oxygenase 2	Mus musculus	139-143
30482851-0	2018	Hippocampal mGluR1-dependent long-term potentiation requires NAADP-mediated acidic store Ca2+ signaling.	NAADP	61-66	glutamate receptor, metabotropic 1	Mus musculus	12-18
30482851-4	2018	We found that metabotropic glutamate receptor 1 (mGluR1) was coupled to NAADP signaling that elicited Ca2+ release from acidic stores.	NAADP	72-77	glutamate receptor, metabotropic 1	Mus musculus	14-47
30482851-4	2018	We found that metabotropic glutamate receptor 1 (mGluR1) was coupled to NAADP signaling that elicited Ca2+ release from acidic stores.	NAADP	72-77	glutamate receptor, metabotropic 1	Mus musculus	49-55
30481925-18	2018	Compared with those in hypoxia 9 h group, expression of P62 in hypoxia 9 h+ NAADP group was significantly decreased (P&lt;0.01), while expression of microtubule-associated protein 1 light chain 3-II did not change significantly (P&gt;0.05).	NAADP	76-81	KH RNA binding domain containing, signal transduction associated 1	Rattus norvegicus	56-59
30481925-20	2018	Compared with those of cells in hypoxia 9 h+ NAADP group, expression of P62 of cells in hypoxia 9 h+ trans-Ned-19+ NAADP group was obviously increased (P&lt;0.01), while expression of microtubule-associated protein 1 light chain 3-II did not change significantly (P&gt;0.05).	NAADP	45-50	KH RNA binding domain containing, signal transduction associated 1	Rattus norvegicus	72-75
30481925-20	2018	Compared with those of cells in hypoxia 9 h+ NAADP group, expression of P62 of cells in hypoxia 9 h+ trans-Ned-19+ NAADP group was obviously increased (P&lt;0.01), while expression of microtubule-associated protein 1 light chain 3-II did not change significantly (P&gt;0.05).	NAADP	115-120	KH RNA binding domain containing, signal transduction associated 1	Rattus norvegicus	72-75
29636391-3	2018	We show that TPC2 is required for intracellular Ca2+ signaling in response to NAADP or to mTOR inhibition by rapamycin.	NAADP	78-83	two pore segment channel 2	Homo sapiens	13-17
30091405-9	2018	Finally, arachidonic acid (AA) and nicotinic acid adenine dinucleotide phosphate (NAADP) stimulate ECFC proliferation by stimulating two-pore channel 1 (TPC1), thereby promoting Ca2+ release from the endolysosomal Ca2+ compartment.	NAADP	35-80	two pore segment channel 1	Homo sapiens	153-157
30091405-9	2018	Finally, arachidonic acid (AA) and nicotinic acid adenine dinucleotide phosphate (NAADP) stimulate ECFC proliferation by stimulating two-pore channel 1 (TPC1), thereby promoting Ca2+ release from the endolysosomal Ca2+ compartment.	NAADP	82-87	two pore segment channel 1	Homo sapiens	133-151
30091405-9	2018	Finally, arachidonic acid (AA) and nicotinic acid adenine dinucleotide phosphate (NAADP) stimulate ECFC proliferation by stimulating two-pore channel 1 (TPC1), thereby promoting Ca2+ release from the endolysosomal Ca2+ compartment.	NAADP	82-87	two pore segment channel 1	Homo sapiens	153-157
28539361-4	2017	Membrane permeabilization of cardiac myocytes with saponin and/or Triton X-100 increased NAADP synthesis, indicating that intracellular CD38 contributes to NAADP production.	NAADP	156-161	CD38 antigen	Mus musculus	136-140
28539361-0	2017	Synthesis of the Ca2+-mobilizing messengers NAADP and cADPR by intracellular CD38 enzyme in the mouse heart: Role in beta-adrenoceptor signaling.	NAADP	44-49	CD38 antigen	Mus musculus	77-81
29129203-0	2017	NAADP-evoked Ca2+ signals through two-pore channel-1 require arginine residues in the first S4-S5 linker.	NAADP	0-5	two pore segment channel 1	Homo sapiens	34-52
29129203-5	2017	Accordingly, mutation of residues in TPC1 but not the analogous region in the second domain prevents Ca2+ release by NAADP in intact cells.	NAADP	117-122	two pore segment channel 1	Homo sapiens	37-41
28539361-11	2017	These observations support generation of NAADP and cADPR by intracellular CD38, which contributes to effects of beta-adrenoreceptor stimulation to increase both Ca2+ transients and the tendency to disturb heart rhythm.	NAADP	41-46	CD38 antigen	Mus musculus	74-78
28539361-2	2017	CD38, which belongs to the ADP-ribosyl cyclase family, catalyzes synthesis of both NAADP and cADPR in vitro However, it remains unclear whether this is the main enzyme for their production under physiological conditions.	NAADP	83-88	CD38 antigen	Mus musculus	0-4
28539361-4	2017	Membrane permeabilization of cardiac myocytes with saponin and/or Triton X-100 increased NAADP synthesis, indicating that intracellular CD38 contributes to NAADP production.	NAADP	89-94	CD38 antigen	Mus musculus	136-140
28340569-8	2017	CD157 has little or no base exchange activity, but some ADP-ribosyl cyclase activity, indicating that CD157 formed cyclic ADP-ribose but much less nicotinic acid adenine dinucleotide phosphate, with both mobilizing Ca2+ from intracellular Ca2+ pools.	NAADP	147-192	bone marrow stromal cell antigen 1	Mus musculus	0-5
28386045-8	2017	Ned19 also inhibited the NAADP-stimulated induction of gene expression by inhibiting the LPS-induced nuclear translocation of transcription factor EB (TFEB).	NAADP	25-30	transcription factor EB	Mus musculus	126-149
28386045-8	2017	Ned19 also inhibited the NAADP-stimulated induction of gene expression by inhibiting the LPS-induced nuclear translocation of transcription factor EB (TFEB).	NAADP	25-30	transcription factor EB	Mus musculus	151-155
28386045-9	2017	Hepatocyte autophagy protects against LPS-induced liver injury via the CD38/NAADP/Ca2+/TFEB pathway.	NAADP	76-81	CD38 antigen	Mus musculus	71-75
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).	NAADP	198-243	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).	NAADP	245-250	CD38 antigen	Mus musculus	0-4
28340569-11	2017	The functional features of CD157 can be explained in part through the production of cyclic ADP-ribose rather than nicotinic acid adenine dinucleotide phosphate.	NAADP	114-159	bone marrow stromal cell antigen 1	Mus musculus	27-32
28199837-3	2017	Antagonizing action of the Ca2+-mobilizing messenger NAADP, inhibiting its target endo-lysosomal ion channel, TPC1, and buffering local Ca2+ fluxes all clustered and enlarged late endosomes/lysosomes.	NAADP	53-58	two pore segment channel 1	Homo sapiens	110-114
28055974-1	2017	NAADP (nicotinic acid adenine dinucleotide phosphate) has been proposed as a second messenger for glutamate in neuronal and glial cells via the activation of the lysosomal Ca2+ channels TPC1 and TPC2.	NAADP	0-5	two pore segment channel 1	Homo sapiens	186-190
28055974-1	2017	NAADP (nicotinic acid adenine dinucleotide phosphate) has been proposed as a second messenger for glutamate in neuronal and glial cells via the activation of the lysosomal Ca2+ channels TPC1 and TPC2.	NAADP	0-5	two pore segment channel 2	Homo sapiens	195-199
28055974-1	2017	NAADP (nicotinic acid adenine dinucleotide phosphate) has been proposed as a second messenger for glutamate in neuronal and glial cells via the activation of the lysosomal Ca2+ channels TPC1 and TPC2.	NAADP	7-52	two pore segment channel 1	Homo sapiens	186-190
28055974-1	2017	NAADP (nicotinic acid adenine dinucleotide phosphate) has been proposed as a second messenger for glutamate in neuronal and glial cells via the activation of the lysosomal Ca2+ channels TPC1 and TPC2.	NAADP	7-52	two pore segment channel 2	Homo sapiens	195-199
28055974-5	2017	By contrast, the NAADP antagonist NED-19 or SiRNA-mediated inhibition of TPC1/2 decreases autophagy induced by glutamate, confirming a role for NAADP in this pathway.	NAADP	17-22	two pore segment channel 1	Homo sapiens	73-77
28055974-5	2017	By contrast, the NAADP antagonist NED-19 or SiRNA-mediated inhibition of TPC1/2 decreases autophagy induced by glutamate, confirming a role for NAADP in this pathway.	NAADP	144-149	two pore segment channel 1	Homo sapiens	73-77
28199837-5	2017	Reducing NAADP-dependent contacts delayed EGF receptor de-phosphorylation consistent with close apposition of endocytosed receptors with the ER-localized phosphatase PTP1B.	NAADP	9-14	protein tyrosine phosphatase non-receptor type 1	Homo sapiens	166-171
28192519-3	2017	Our results suggest that AA acts by interacting with a fatty acid G protein coupled receptor, initiating a G protein signalling cascade that may involve PLA2 and ERK activation, which in turn opens intracellular ryanodine-sensitive channels as well as NAADP-sensitive channels in acidic intracellular Ca2+ stores.	NAADP	252-257	Eph receptor B1	Rattus norvegicus	162-165
27862060-6	2016	At the same time, bafilomycin A1 (1 muM) completely prevented all effects of NAADP (1 muM) on activities of PMCA, SERCA, and basal Mg2+ -ATPase, confirming that these effects are dependent on acidic stores.	NAADP	77-82	ATPase, Ca++ transporting, ubiquitous	Mus musculus	114-119
26872338-2	2016	It is widely accepted that two types of two-pore channels, termed TPC1 and TPC2, are responsible for the NAADP-mediated Ca(2+) release but the underlying mechanisms regulating their gating appear to be different.	NAADP	105-110	two pore segment channel 1	Homo sapiens	66-70
27862060-3	2016	The increase the activity of plasma membrane Ca2+ ATPase (PMCA) under NAADP application (1 and 7 muM) was observed.	NAADP	70-75	dynein, axonemal, heavy chain 8	Mus musculus	29-56
27862060-4	2016	However, NAADP (1 muM) decreased activities of sarcoendoplasmic reticulum Ca2+ -ATPase (SERCA) and basal Mg2+ -ATPase.	NAADP	9-14	ATPase, Ca++ transporting, ubiquitous	Mus musculus	47-86
27862060-4	2016	However, NAADP (1 muM) decreased activities of sarcoendoplasmic reticulum Ca2+ -ATPase (SERCA) and basal Mg2+ -ATPase.	NAADP	9-14	ATPase, Ca++ transporting, ubiquitous	Mus musculus	88-93
27605449-4	2016	Moreover, we provide evidence that indicates a role for the intracellular messenger NAADP in the release of Ca2+ from acidic organelles following elevation of cAMP.	NAADP	84-89	cathelicidin antimicrobial peptide	Homo sapiens	159-163
26872338-2	2016	It is widely accepted that two types of two-pore channels, termed TPC1 and TPC2, are responsible for the NAADP-mediated Ca(2+) release but the underlying mechanisms regulating their gating appear to be different.	NAADP	105-110	two pore segment channel 2	Homo sapiens	75-79
26872338-3	2016	For example, although both TPC1 and TPC2 are activated by NAADP, TPC1 appears to be additionally regulated by cytosolic Ca(2+) .	NAADP	58-63	two pore segment channel 1	Homo sapiens	27-31
26872338-3	2016	For example, although both TPC1 and TPC2 are activated by NAADP, TPC1 appears to be additionally regulated by cytosolic Ca(2+) .	NAADP	58-63	two pore segment channel 2	Homo sapiens	36-40
28529829-5	2016	In particular, I highlight defects in lysosomal Ca2+ content and signalling through NAADP-regulated two-pore channels in patient fibroblasts harbouring mutations in the PD-linked genes, GBA1 and LRRK2.	NAADP	84-89	glucosylceramidase beta	Homo sapiens	186-190
26818887-2	2016	Our recent studies demonstrated that lysosomal Ca(2+) messenger of nicotinic acid adenine dinucleotide phosphate (NAADP), an enzymatic product of CD38 ADP-ribosylcyclase (CD38), promoted lipid endocytic trafficking in human fibroblast cells.	NAADP	67-112	CD38 molecule	Homo sapiens	146-150
26818887-2	2016	Our recent studies demonstrated that lysosomal Ca(2+) messenger of nicotinic acid adenine dinucleotide phosphate (NAADP), an enzymatic product of CD38 ADP-ribosylcyclase (CD38), promoted lipid endocytic trafficking in human fibroblast cells.	NAADP	67-112	CD38 molecule	Homo sapiens	171-175
26818887-2	2016	Our recent studies demonstrated that lysosomal Ca(2+) messenger of nicotinic acid adenine dinucleotide phosphate (NAADP), an enzymatic product of CD38 ADP-ribosylcyclase (CD38), promoted lipid endocytic trafficking in human fibroblast cells.	NAADP	114-119	CD38 molecule	Homo sapiens	146-150
26818887-2	2016	Our recent studies demonstrated that lysosomal Ca(2+) messenger of nicotinic acid adenine dinucleotide phosphate (NAADP), an enzymatic product of CD38 ADP-ribosylcyclase (CD38), promoted lipid endocytic trafficking in human fibroblast cells.	NAADP	114-119	CD38 molecule	Homo sapiens	171-175
27391070-5	2016	The expression of CD38 and ALP, upstream NAAD+ regulatory enzymes, was oppositely regulated between P- and S-231; high CD38 strongly correlated with NAADP in P-231 while high ALP with NAAD+ levels in S-231.	NAADP	149-154	CD38 molecule	Homo sapiens	18-22
27391070-5	2016	The expression of CD38 and ALP, upstream NAAD+ regulatory enzymes, was oppositely regulated between P- and S-231; high CD38 strongly correlated with NAADP in P-231 while high ALP with NAAD+ levels in S-231.	NAADP	149-154	ATHS	Homo sapiens	27-30
27391070-5	2016	The expression of CD38 and ALP, upstream NAAD+ regulatory enzymes, was oppositely regulated between P- and S-231; high CD38 strongly correlated with NAADP in P-231 while high ALP with NAAD+ levels in S-231.	NAADP	149-154	CD38 molecule	Homo sapiens	119-123
26818887-5	2016	Bodipy 493/503 fluorescence staining found that the deposited lipid in macrophages was mainly enclosed in lysosomal organelles and largely enhanced with the blockade of CD38/NAADP pathway.	NAADP	174-179	CD38 antigen	Mus musculus	169-173
26818887-9	2016	These data provide the first experimental evidence that the proper function of CD38/NAADP pathway plays an essential role in promoting free cholesterol efflux from lysosomes and that a defection of this signalling leads to lysosomal cholesterol accumulation in macrophages and results in coronary atherosclerosis in CD38(-/-) mice.	NAADP	84-89	CD38 antigen	Mus musculus	79-83
26818887-9	2016	These data provide the first experimental evidence that the proper function of CD38/NAADP pathway plays an essential role in promoting free cholesterol efflux from lysosomes and that a defection of this signalling leads to lysosomal cholesterol accumulation in macrophages and results in coronary atherosclerosis in CD38(-/-) mice.	NAADP	84-89	CD38 antigen	Mus musculus	316-320
28529829-5	2016	In particular, I highlight defects in lysosomal Ca2+ content and signalling through NAADP-regulated two-pore channels in patient fibroblasts harbouring mutations in the PD-linked genes, GBA1 and LRRK2.	NAADP	84-89	leucine rich repeat kinase 2	Homo sapiens	195-200
26744456-0	2016	SIDT2 is involved in the NAADP-mediated release of calcium from insulin secretory granules.	NAADP	25-30	SID1 transmembrane family, member 2	Mus musculus	0-5
26744456-9	2016	Bath-mediated application of 50nM nicotinic acid adenine dinucleotide phosphate (NAADP) normalized the [Ca(2+)]i response of Sidt2(-/-) beta-cells.	NAADP	34-79	SID1 transmembrane family, member 2	Mus musculus	125-130
26744456-11	2016	We conclude that Sidt2 is involved in NAADP-mediated release of calcium from insulin secretory granules and thus regulates insulin secretion.	NAADP	38-43	SID1 transmembrane family, member 2	Mus musculus	17-22
26744456-9	2016	Bath-mediated application of 50nM nicotinic acid adenine dinucleotide phosphate (NAADP) normalized the [Ca(2+)]i response of Sidt2(-/-) beta-cells.	NAADP	81-86	SID1 transmembrane family, member 2	Mus musculus	125-130
26838264-6	2016	Intracellular dialysis of NAADP into Fura-2-loaded DT40TKO-hTPC2 cells elicited cytosolic Ca(2+) transients, suggesting that hTPC2 was functionally active.	NAADP	26-31	two pore segment channel 2	Homo sapiens	59-64
26959359-8	2016	Thus, our findings indicate that beta-adrenergic stimulation contributes to the development of maladaptive cardiac hypertrophy via Ca2+ signaling mediated by NAADP-synthesizing enzyme and CD38 that produce NAADP and cADPR, respectively.	NAADP	206-211	CD38 antigen	Mus musculus	188-192
26728458-6	2016	NAADP was shown to evoke functionally relevant Ca(2+) signals in both naive CD4 and naive CD8 T cells.	NAADP	0-5	CD4 antigen	Mus musculus	76-79
26838264-6	2016	Intracellular dialysis of NAADP into Fura-2-loaded DT40TKO-hTPC2 cells elicited cytosolic Ca(2+) transients, suggesting that hTPC2 was functionally active.	NAADP	26-31	two pore segment channel 2	Homo sapiens	125-130
26769314-3	2016	Nicotinic acid adenine dinucleotide phosphate (NAADP), generated in beta-cells in response to high glucose, is a potent mobiliser of these stores, and has been proposed to act through two pore channels (TPC1 and TPC2, murine gene names Tpcn1 and Tpcn2).	NAADP	0-45	two pore channel 1	Mus musculus	203-207
26733361-1	2016	A novel transduction pathway for the powerful angiogenic factor VEGF has been recently shown in endothelial cells to operate through NAADP-controlled intracellular release of Ca(2+).	NAADP	133-138	vascular endothelial growth factor A	Mus musculus	64-68
26733361-2	2016	In the present report the possible involvement of NAADP-controlled Ca(2+) signaling in tumor vascularization, growth and metastatic dissemination was investigated in a murine model of VEGF-secreting melanoma.	NAADP	50-55	vascular endothelial growth factor A	Mus musculus	184-188
26733361-6	2016	To this regard, Ca(2+) imaging experiments showed that the response of B16 cells to VEGF stimulation is NAADP-dependent.	NAADP	104-109	vascular endothelial growth factor A	Mus musculus	84-88
26856703-1	2016	CD38 is an enzyme that catalyzes the formation of cyclic ADP ribose and nicotinic acid adenine dinucleotide phosphate, both of which are involved in the mobilization of Ca(2+) from intracellular stores.	NAADP	72-117	CD38 antigen	Mus musculus	0-4
26769314-3	2016	Nicotinic acid adenine dinucleotide phosphate (NAADP), generated in beta-cells in response to high glucose, is a potent mobiliser of these stores, and has been proposed to act through two pore channels (TPC1 and TPC2, murine gene names Tpcn1 and Tpcn2).	NAADP	0-45	two pore channel 1	Mus musculus	236-241
26769314-3	2016	Nicotinic acid adenine dinucleotide phosphate (NAADP), generated in beta-cells in response to high glucose, is a potent mobiliser of these stores, and has been proposed to act through two pore channels (TPC1 and TPC2, murine gene names Tpcn1 and Tpcn2).	NAADP	0-45	two pore segment channel 2	Mus musculus	246-251
26769314-3	2016	Nicotinic acid adenine dinucleotide phosphate (NAADP), generated in beta-cells in response to high glucose, is a potent mobiliser of these stores, and has been proposed to act through two pore channels (TPC1 and TPC2, murine gene names Tpcn1 and Tpcn2).	NAADP	47-52	two pore channel 1	Mus musculus	203-207
26769314-3	2016	Nicotinic acid adenine dinucleotide phosphate (NAADP), generated in beta-cells in response to high glucose, is a potent mobiliser of these stores, and has been proposed to act through two pore channels (TPC1 and TPC2, murine gene names Tpcn1 and Tpcn2).	NAADP	47-52	two pore channel 1	Mus musculus	236-241
26769314-3	2016	Nicotinic acid adenine dinucleotide phosphate (NAADP), generated in beta-cells in response to high glucose, is a potent mobiliser of these stores, and has been proposed to act through two pore channels (TPC1 and TPC2, murine gene names Tpcn1 and Tpcn2).	NAADP	47-52	two pore segment channel 2	Mus musculus	246-251
26100948-6	2015	In RyR3-KO, NAADP-evoked Ca(2+) release reduced by ~50% but, when combined with antibodies against RyR1, responses were 90% inhibited.	NAADP	12-17	ryanodine receptor 3	Homo sapiens	3-7
26395965-3	2015	Here, we investigated the role of the second messenger nicotinic acid adenine dinucleotide phosphate (NAADP), which is known in several cell types to induce Ca(2+) oscillations that initiate from acidic stores such as lysosomes, likely via two-pore channels (TPCs, TPC1 and 2).	NAADP	55-100	two pore channel 1	Mus musculus	265-275
26395965-3	2015	Here, we investigated the role of the second messenger nicotinic acid adenine dinucleotide phosphate (NAADP), which is known in several cell types to induce Ca(2+) oscillations that initiate from acidic stores such as lysosomes, likely via two-pore channels (TPCs, TPC1 and 2).	NAADP	102-107	two pore channel 1	Mus musculus	265-275
26462735-7	2015	Local Ca(2+) signals observed within 20 ms upon microinjection of Jurkat cells with NAADP were also sensitive to RyR knockdown.	NAADP	84-89	ryanodine receptor 1	Homo sapiens	113-116
26462735-8	2015	In contrast, TRPM2 (transient receptor potential channel, subtype melastatin 2), a potential NAADP target channel, was not required for the formation of initial Ca(2+) signals in primary T cells.	NAADP	93-98	transient receptor potential cation channel subfamily M member 2	Homo sapiens	13-18
26100948-8	2015	Antibodies to RyR1 inhibited NAADP-induced Ca(2+) liberation by 81%, but only reduced cADPR responses by 30%.	NAADP	29-34	ryanodine receptor 1	Homo sapiens	14-18
26100948-10	2015	The sequence of relative importance for NAADP-elicited Ca(2+) release from the all stores is RyR1&gt;TPC2&gt;RyR3&gt;TPC1&gt;&gt;RyR2.	NAADP	40-45	ryanodine receptor 1	Homo sapiens	93-97
25872774-5	2015	In Tpcn1/2(-/-) cells, NAADP sensitivity was restored by re-expressing wild-type TPCs, but not by mutant versions with impaired Ca(2+)-permeability, nor by TRPML1.	NAADP	23-28	two pore channel 1	Mus musculus	3-8
26100948-10	2015	The sequence of relative importance for NAADP-elicited Ca(2+) release from the all stores is RyR1&gt;TPC2&gt;RyR3&gt;TPC1&gt;&gt;RyR2.	NAADP	40-45	two pore segment channel 2	Homo sapiens	101-105
26100948-10	2015	The sequence of relative importance for NAADP-elicited Ca(2+) release from the all stores is RyR1&gt;TPC2&gt;RyR3&gt;TPC1&gt;&gt;RyR2.	NAADP	40-45	ryanodine receptor 3	Homo sapiens	109-113
26100948-10	2015	The sequence of relative importance for NAADP-elicited Ca(2+) release from the all stores is RyR1&gt;TPC2&gt;RyR3&gt;TPC1&gt;&gt;RyR2.	NAADP	40-45	two pore segment channel 1	Homo sapiens	117-121
26100948-10	2015	The sequence of relative importance for NAADP-elicited Ca(2+) release from the all stores is RyR1&gt;TPC2&gt;RyR3&gt;TPC1&gt;&gt;RyR2.	NAADP	40-45	ryanodine receptor 2	Homo sapiens	129-133
26100948-11	2015	However, when assessing NAADP-induced Ca(2+) release solely from the acidic stores (granules/endosomes/lysosomes), antibodies against TPC2 and TPC1 virtually abolished the Ca(2+) liberation as did antibodies against RyR1 and RyR3.	NAADP	24-29	two pore segment channel 2	Homo sapiens	134-138
26100948-11	2015	However, when assessing NAADP-induced Ca(2+) release solely from the acidic stores (granules/endosomes/lysosomes), antibodies against TPC2 and TPC1 virtually abolished the Ca(2+) liberation as did antibodies against RyR1 and RyR3.	NAADP	24-29	two pore segment channel 1	Homo sapiens	143-147
26100948-12	2015	Our results indicate that the primary, but very small, NAADP-elicited Ca(2+) release via TPCs from endosomes/lysosomes triggers the detectable Ca(2+)-induced Ca(2+) release via RyR1 and RyR3 occurring from the granules and the ER.	NAADP	55-60	ryanodine receptor 1	Homo sapiens	177-181
26100948-12	2015	Our results indicate that the primary, but very small, NAADP-elicited Ca(2+) release via TPCs from endosomes/lysosomes triggers the detectable Ca(2+)-induced Ca(2+) release via RyR1 and RyR3 occurring from the granules and the ER.	NAADP	55-60	ryanodine receptor 3	Homo sapiens	186-190
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.	NAADP	122-167	CD38 molecule	Homo sapiens	0-4
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.	NAADP	169-174	CD38 molecule	Homo sapiens	0-4
26247205-0	2015	Arginine Thiazolidine Carboxylate Stimulates Insulin Secretion through Production of Ca2+-Mobilizing Second Messengers NAADP and cADPR in Pancreatic Islets.	NAADP	119-124	insulin	Homo sapiens	45-52
25872774-7	2015	High-affinity [(32)P]NAADP binding still occurs in Tpcn1/2(-/-) tissue, suggesting that NAADP regulation is conferred by an accessory protein.	NAADP	21-26	two pore channel 1	Mus musculus	51-56
25872774-7	2015	High-affinity [(32)P]NAADP binding still occurs in Tpcn1/2(-/-) tissue, suggesting that NAADP regulation is conferred by an accessory protein.	NAADP	88-93	two pore channel 1	Mus musculus	51-56
25451935-4	2015	Intracellular dialysis of NAADP evoked a Ca(2+) transient in HEK293 cells that stably overexpressed hTPC1, hTPC2, and rTPC3, but not in cells that stably expressed cTPC3.	NAADP	26-31	two pore segment channel 1	Homo sapiens	100-105
25409702-4	2015	Here we show that in skeletal muscle, distinct Ca(2+) second messengers regulate GLUT4 translocation by contraction and insulin treatment; d-myo-inositol 1,4,5-trisphosphate/nicotinic acid adenine dinucleotide phosphate (NAADP) and cyclic ADP-ribose/NAADP are main players for insulin- and contraction-induced glucose uptake, respectively.	NAADP	174-219	solute carrier family 2 (facilitated glucose transporter), member 4	Mus musculus	81-86
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.	NAADP	45-50	transient receptor potential cation channel subfamily M member 2	Homo sapiens	76-81
25409702-4	2015	Here we show that in skeletal muscle, distinct Ca(2+) second messengers regulate GLUT4 translocation by contraction and insulin treatment; d-myo-inositol 1,4,5-trisphosphate/nicotinic acid adenine dinucleotide phosphate (NAADP) and cyclic ADP-ribose/NAADP are main players for insulin- and contraction-induced glucose uptake, respectively.	NAADP	221-226	solute carrier family 2 (facilitated glucose transporter), member 4	Mus musculus	81-86
25409702-4	2015	Here we show that in skeletal muscle, distinct Ca(2+) second messengers regulate GLUT4 translocation by contraction and insulin treatment; d-myo-inositol 1,4,5-trisphosphate/nicotinic acid adenine dinucleotide phosphate (NAADP) and cyclic ADP-ribose/NAADP are main players for insulin- and contraction-induced glucose uptake, respectively.	NAADP	250-255	solute carrier family 2 (facilitated glucose transporter), member 4	Mus musculus	81-86
25078456-1	2015	CD38 is a multifunctional enzyme that catalyzes the formation of the endogenous Ca(2+)-mobilizing messengers cyclic ADP-ribose (cADPR) and nicotinic acid adenosine dinucleotide phosphate (NAADP) for the activation of ryanodine receptors (RyRs) of sarcoplasmic reticulum and NAADP-sensitive Ca(2+) release channels in endolysosomes, respectively.	NAADP	188-193	CD38 molecule	Rattus norvegicus	0-4
25078456-1	2015	CD38 is a multifunctional enzyme that catalyzes the formation of the endogenous Ca(2+)-mobilizing messengers cyclic ADP-ribose (cADPR) and nicotinic acid adenosine dinucleotide phosphate (NAADP) for the activation of ryanodine receptors (RyRs) of sarcoplasmic reticulum and NAADP-sensitive Ca(2+) release channels in endolysosomes, respectively.	NAADP	274-279	CD38 molecule	Rattus norvegicus	0-4
25451935-4	2015	Intracellular dialysis of NAADP evoked a Ca(2+) transient in HEK293 cells that stably overexpressed hTPC1, hTPC2, and rTPC3, but not in cells that stably expressed cTPC3.	NAADP	26-31	two pore segment channel 2	Homo sapiens	107-112
25451935-7	2015	NAADP induced marked Ca(2+) transients in HEK293 cells that stably coexpressed hTPC2 with hTPC1 or cTPC3, but failed to evoke any such response in cells that coexpressed interacting hTPC2 and rTPC3 subunits.	NAADP	0-5	two pore segment channel 2	Homo sapiens	79-84
25451935-7	2015	NAADP induced marked Ca(2+) transients in HEK293 cells that stably coexpressed hTPC2 with hTPC1 or cTPC3, but failed to evoke any such response in cells that coexpressed interacting hTPC2 and rTPC3 subunits.	NAADP	0-5	two pore segment channel 1	Homo sapiens	90-95
25451935-7	2015	NAADP induced marked Ca(2+) transients in HEK293 cells that stably coexpressed hTPC2 with hTPC1 or cTPC3, but failed to evoke any such response in cells that coexpressed interacting hTPC2 and rTPC3 subunits.	NAADP	0-5	two pore segment channel 2	Homo sapiens	182-187
25406377-3	2014	CaV or NaV antagonists blocked NAADP (nicotinic acid adenine dinucleotide phosphate)-evoked Ca(2+) signals in sea urchin egg preparations and in intact cells that overexpressed TPC1.	NAADP	31-36	caveolin 1, caveolae protein	Mus musculus	0-3
26315049-13	2015	production was inhibited by 8-Br-cADPR, an antagonist of cADPR or NED-19, an antagonist of NAADP as product of CD38 ADP-ribosylcyclase, which significantly inhibited the level of cytosolic Ca2+ and the activation of Nrf2 under 7-Ket.	NAADP	91-96	CD38 antigen	Mus musculus	111-115
26315049-13	2015	production was inhibited by 8-Br-cADPR, an antagonist of cADPR or NED-19, an antagonist of NAADP as product of CD38 ADP-ribosylcyclase, which significantly inhibited the level of cytosolic Ca2+ and the activation of Nrf2 under 7-Ket.	NAADP	91-96	nuclear factor, erythroid derived 2, like 2	Mus musculus	216-220
25406377-3	2014	CaV or NaV antagonists blocked NAADP (nicotinic acid adenine dinucleotide phosphate)-evoked Ca(2+) signals in sea urchin egg preparations and in intact cells that overexpressed TPC1.	NAADP	31-36	two pore channel 1	Mus musculus	177-181
25406377-3	2014	CaV or NaV antagonists blocked NAADP (nicotinic acid adenine dinucleotide phosphate)-evoked Ca(2+) signals in sea urchin egg preparations and in intact cells that overexpressed TPC1.	NAADP	38-83	caveolin 1, caveolae protein	Mus musculus	0-3
25406377-3	2014	CaV or NaV antagonists blocked NAADP (nicotinic acid adenine dinucleotide phosphate)-evoked Ca(2+) signals in sea urchin egg preparations and in intact cells that overexpressed TPC1.	NAADP	38-83	two pore channel 1	Mus musculus	177-181