PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
2527253-3	1989	Platelets that were incubated with DEA to inhibit G-6-PD activity augmented xanthine oxidase-induced lung edema and pulmonary hypertension at both doses of xanthine oxidase.	dea	35-38	glucose-6-phosphate dehydrogenase	Homo sapiens	50-56
34381466-10	2021	The increase in DEA under grazing exclusion suggests that the dependence of DEA on the availability of NO3 - produced is due to the combined activity of ammonia oxidizers and denitrifiers.	dea	16-19	NBL1, DAN family BMP antagonist	Homo sapiens	103-106
34381466-10	2021	The increase in DEA under grazing exclusion suggests that the dependence of DEA on the availability of NO3 - produced is due to the combined activity of ammonia oxidizers and denitrifiers.	dea	76-79	NBL1, DAN family BMP antagonist	Homo sapiens	103-106
27126574-4	2016	METHODS: Serum albumin (SA) was S-nitrosated by reacting with (i) NaNO2 in acidic medium; (ii) different low-molecular weight S-nitrosothiols (RSNO) (S-nitrosocysteine (CysNO), S-nitrosoglutathione (GSNO), and S,S"-dinitrosobucillamine (Buc(NO)2)); and (iii) diethylamine NONOate (DEA/NO).	dea	281-284	albumin	Homo sapiens	9-22
30087260-10	2018	IWP-051-potentiated DEA/NO-induced cGMP signals in the striatum of NO-GC2 knockout mice but was ineffective in the striatum of NO-GC1 knockout mice.	dea	20-23	guanylate cyclase 2f	Mus musculus	70-73
29924440-2	2018	Using a POEGMA as the macromolecular chain transfer agent, chain extension with BnMA and DEA is conducted in ethanol, where PBnMA acts as the core-forming block, and the PDEA block endows the solvophilicity and CO2 -responsiveness.	dea	89-92	phosphodiesterase 6A	Homo sapiens	170-174
32217410-5	2020	The predominant compounds of ATZs in tap water were ATZ and DEA, with a detection frequency of 99.5% and 98.0%, respectively, followed by ATZ-OH (87.3%), DACT (84.0%), and DIA (78.1%).	dea	60-63	nuclear RNA export factor 1	Homo sapiens	37-40
32429371-2	2020	Linear copolymer P(DEA-co-IAM) was introduced into a solution of DEA monomer to prepare pH-thermo dual responsive P(DEA-co-IAM)/PDEA semi-IPN hydrogels.	dea	19-22	phosphodiesterase 6A	Homo sapiens	128-132
24576258-6	2014	RESULTS: DEA/NO-induced VASP phosphorylation was significantly higher in PLTs from APCs on Days 2 and 5 compared to WB, conditioned by a stronger increase of cyclic guanosine monophosphate (cGMP), but not cyclic adenosine monophosphate (cAMP), in stored PLTs.	dea	9-12	vasodilator stimulated phosphoprotein	Homo sapiens	24-28
26254861-4	2015	ME (3 muM)-induced desensitization was enhanced by a NO donor (DEA/NO 100 muM), two soluble guanylate cyclase (sGC) activators (A 350619 30 muM and BAY 418543 1 muM) or a cGMP-dependent protein kinase (PKG) activator (8-pCPT-cGMP 30 muM).	dea	63-66	latexin	Homo sapiens	6-9
27084390-6	2016	Deletion of a single allele of E24 (shift to Mypt1 LZ+) enhanced vasorelaxation of first-order mesenteric arteries (MA1) to diethylamine-NONOate (DEA/NO) and to cGMP in permeabilized and calcium-clamped arteries and lowered blood pressure.	dea	146-149	protein phosphatase 1, regulatory subunit 12A	Mus musculus	45-50
27065874-5	2016	At the highest concentration tested, both RLX and DEA/NO promoted MMP-2 and MMP-9 levels by 25-33%, while inhibiting pSmad2 and alpha-SMA expression by up to 50% (all p < 0.05 vs. untreated and vehicle-treated cells).	dea	50-53	matrix metallopeptidase 2	Homo sapiens	66-71
27065874-5	2016	At the highest concentration tested, both RLX and DEA/NO promoted MMP-2 and MMP-9 levels by 25-33%, while inhibiting pSmad2 and alpha-SMA expression by up to 50% (all p < 0.05 vs. untreated and vehicle-treated cells).	dea	50-53	matrix metallopeptidase 9	Homo sapiens	76-81
27065874-8	2016	CONCLUSION: These findings confirmed that RLX mediates its TGF-beta1-inhibitory and gelatinase-promoting effects via a NO-sGC-cGMP-dependent pathway, which was additively augmented by co-administration of DEA/NO.	dea	205-208	transforming growth factor beta 1	Homo sapiens	59-68
26254861-5	2015	DEA/NO-induced enhancement was blocked by the sGC inhibitor NS 2028 (10 muM).	dea	0-3	guanylate cyclase 1 soluble subunit beta 2	Rattus norvegicus	46-49
26254861-5	2015	DEA/NO-induced enhancement was blocked by the sGC inhibitor NS 2028 (10 muM).	dea	0-3	latexin	Homo sapiens	72-75
24779061-2	2014	SA1 was synthesized through a simple structural modification of a recently reported receptor SA2 by the incorporation of the N,Ndiethylamino (DEA) group as a fine controllable unit.	dea	142-145	stromal antigen 1	Homo sapiens	0-3
24779061-4	2014	The presence of the DEA group in SA1 led to its dual channel emission due to the TICT state and at the same time its hydrophobic nature was also responsible for controlling the strong hydration of Al3+ ions in aqueous media which ultimately led to the high sensitivity of SA1 for Al3+.	dea	20-23	stromal antigen 1	Homo sapiens	33-36
24779061-4	2014	The presence of the DEA group in SA1 led to its dual channel emission due to the TICT state and at the same time its hydrophobic nature was also responsible for controlling the strong hydration of Al3+ ions in aqueous media which ultimately led to the high sensitivity of SA1 for Al3+.	dea	20-23	stromal antigen 1	Homo sapiens	272-275
22515961-3	2012	METHODS: ALP catalytic activity was measured in 50 serum samples and 16 commercial materials, including control materials from EQAS programs, using primary reference measurement procedure and two routine measurement procedures with AMP and DEA as buffers.	dea	240-243	ATHS	Homo sapiens	9-12
22653417-4	2012	DEA/NO-induced depression of the developed tension of the right atrium was inhibited by [erythro-9-(2-hydroxy-3-nonyl)adenine] (PDE2 inhibitor), augmented by milrinone (PDE3 inhibitor), and upturned by rolipram (PDE4 inhibitor).	dea	0-3	phosphodiesterase 2A	Rattus norvegicus	128-132
22653417-4	2012	DEA/NO-induced depression of the developed tension of the right atrium was inhibited by [erythro-9-(2-hydroxy-3-nonyl)adenine] (PDE2 inhibitor), augmented by milrinone (PDE3 inhibitor), and upturned by rolipram (PDE4 inhibitor).	dea	0-3	phosphodiesterase 4D, cAMP-specific-like 1	Rattus norvegicus	169-173
21332241-1	2011	The amino acid-based anionic surfactant, N-dodecanoylglutamic acid (designated as LAD), when neutralized with 2-aminoethanol (MEA), 2,2"-iminodiethanol (DEA), or 2,2",2""-nitrilotriethanol (TEA) forms globular type of micelles in aqueous system at 25  C, and the viscosity of each solution is very close to that of pure water.	dea	153-156	dihydrolipoamide dehydrogenase	Homo sapiens	82-85
22122932-7	2012	The explanation for so high ACFs can be found in the extremely efficient retention mechanisms that the DeA-based SUPRAS provides for CPAHs (i.e. formation of hydrogen bonds and hydrophobic interactions), and the high number of binding sites that it contains (i.e. the concentration of biosurfactant in the SUPRAS was 0.56 mg muL(-1)).	dea	103-106	mitochondrial E3 ubiquitin protein ligase 1	Homo sapiens	325-331
21311889-4	2012	The NO donor diethylamine NONOate (DEA/NO) (0.1-100 muM) depressed the resting and developed tensions, as well as the sinus rate, of the right atrium.	dea	35-38	latexin	Homo sapiens	52-55
21311889-5	2012	The effect of DEA/NO on contractions of the right atrium was blocked by the soluble guanylate cyclase (sGC) inhibitor, ODQ (1H-[1,2,4]oxadiazolo[4,3-alpha]quinoxalin-1-one) (10 muM).	dea	14-17	guanylate cyclase 1 soluble subunit beta 2	Rattus norvegicus	76-101
21311889-5	2012	The effect of DEA/NO on contractions of the right atrium was blocked by the soluble guanylate cyclase (sGC) inhibitor, ODQ (1H-[1,2,4]oxadiazolo[4,3-alpha]quinoxalin-1-one) (10 muM).	dea	14-17	guanylate cyclase 1 soluble subunit beta 2	Rattus norvegicus	103-106
21311889-5	2012	The effect of DEA/NO on contractions of the right atrium was blocked by the soluble guanylate cyclase (sGC) inhibitor, ODQ (1H-[1,2,4]oxadiazolo[4,3-alpha]quinoxalin-1-one) (10 muM).	dea	14-17	latexin	Homo sapiens	177-180
21311889-6	2012	The ATP-sensitive potassium channel (K(ATP)) blocker glyburide (3 muM) reversed DEA/NO-induced decreases in the resting tension.	dea	80-83	latexin	Homo sapiens	66-69
21414102-3	2011	Our aim was to determine the functional response of afferent and efferent fibres supplying the proximal jejunum to the CB(1) agonist docosatetraenylethanolamide (DEA) in fed and fasted animals.	dea	162-165	cannabinoid receptor 1	Rattus norvegicus	119-124
19958137-5	2010	Salicylhydroxamic acid (SHAM, an AOX inhibitor) pretreatment reduced the DEA/NO-induced cyanide-resistant respiration and partially compromised induced resistance to TMV.	dea	73-76	acyl-CoA oxidase 1	Homo sapiens	33-36
20493497-1	2010	UNLABELLED: The aim of this study was to determine the effects of desethyl-amiodarone (DEA), the major metabolite of the class III antiarrhythmic drug amiodarone, on human ether-a-go-go-related gene (hERG) encoded potassium channel current.	dea	87-90	ETS transcription factor ERG	Homo sapiens	200-204
20493497-6	2010	CONCLUSIONS: Because hERG underlies native cardiac "I(Kr)" channels, hERG/I(Kr) inhibition by DEA as well as amiodarone may contribute to the overall effects of amiodarone administration on cardiac repolarization.	dea	94-97	ETS transcription factor ERG	Homo sapiens	69-73
19056486-3	2009	Depletion of intracellular glutathione enhanced the inhibitory effect of the NO donor 1,1-diethyl-2-hydroxy-2-nitrosohydrazine (DEA/NO) on EGFR tyrosine kinase activity, supporting the notion that such inhibition was a consequence of an S-nitrosylation reaction.	dea	128-131	epidermal growth factor receptor	Mus musculus	139-143
19958137-3	2010	Application of exogenous potassium cyanide (KCN, a cytochrome pathway inhibitor) at nonlethal concentrations and NO donor diethylamine NONOate (DEA/NO) to the upper uninoculated leaves greatly induced accumulation of AOX transcript, reduced TMV viral RNA accumulation, and increased the leaf photochemical quantum yield at photosystem II.	dea	144-147	acyl-CoA oxidase 1	Homo sapiens	217-220
19056486-4	2009	Addition of DEA/NO to cell lysates resulted in the S-nitrosylation of a large number of proteins including the EGFR, as confirmed by the chemical detection of nitrosothiol groups in the immunoprecipitated receptor.	dea	12-15	epidermal growth factor receptor	Mus musculus	111-115
17827785-3	2007	It has been reported that AMD and N-monodesethylamiodarone (DEA), the active metabolite of AMD, inhibit the P-glycoprotein (P-gp/MDR1)-mediated digoxin transport.	dea	60-63	ATP binding cassette subfamily B member 1	Homo sapiens	108-122
17827785-3	2007	It has been reported that AMD and N-monodesethylamiodarone (DEA), the active metabolite of AMD, inhibit the P-glycoprotein (P-gp/MDR1)-mediated digoxin transport.	dea	60-63	phosphoglycolate phosphatase	Homo sapiens	124-128
17827785-3	2007	It has been reported that AMD and N-monodesethylamiodarone (DEA), the active metabolite of AMD, inhibit the P-glycoprotein (P-gp/MDR1)-mediated digoxin transport.	dea	60-63	ATP binding cassette subfamily B member 1	Homo sapiens	129-133
17827785-10	2007	These results suggest that an ATP-binding cassette (ABC) transporter, which is different from P-gp, MRPs and BCRP, mediates the efflux of DEA across the apical membrane in Caco-2 cells and that thyroid hormone inhibits this transporter.	dea	138-141	phosphoglycolate phosphatase	Homo sapiens	94-98
17827785-10	2007	These results suggest that an ATP-binding cassette (ABC) transporter, which is different from P-gp, MRPs and BCRP, mediates the efflux of DEA across the apical membrane in Caco-2 cells and that thyroid hormone inhibits this transporter.	dea	138-141	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	109-113
17138620-7	2007	Bath application of the soluble guanylate cyclase (sGC) inhibitor 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ) abolished NO(aq)- and DEA/NO-induced potentiation of evoked EPSPs, IPSPs and depolarization.	dea	138-141	guanylate cyclase 1 soluble subunit beta 2	Rattus norvegicus	24-49
17610578-3	2007	We have found that deletion of the alpha-synuclein gene blocks both the long-lasting enhancement of evoked and miniature transmitter release and the increase in the number of functional presynaptic boutons evoked through the NO donor, DEA/NO, and the cGMP analog, 8-Br-cGMP.	dea	235-238	synuclein alpha	Homo sapiens	35-50
17610578-4	2007	In agreement with these findings both DEA/NO and 8-Br-cGMP were capable of producing a long-lasting increase in number of clusters for alpha-synuclein through activation of soluble guanylyl cyclase, cGK and calcium/calmodulin-dependent protein kinase IIalpha.	dea	38-41	synuclein alpha	Homo sapiens	135-150
17610578-4	2007	In agreement with these findings both DEA/NO and 8-Br-cGMP were capable of producing a long-lasting increase in number of clusters for alpha-synuclein through activation of soluble guanylyl cyclase, cGK and calcium/calmodulin-dependent protein kinase IIalpha.	dea	38-41	protein kinase cGMP-dependent 1	Homo sapiens	199-202
17612739-5	2007	These low energy fragmentations become much stronger in the larger molecules and the strongest DEA process in the compounds with two hydroxyl groups, which thus represent an intermediate case between the behavior of small alcohols and the sugar ribose which was discovered to have strong DEA fragmentations near zero electron energy [S. Ptasinska, S. Denifl, P. Scheier and T. D. Mark, J. Chem.	dea	95-98	microtubule affinity regulating kinase 1	Homo sapiens	380-384
17612739-5	2007	These low energy fragmentations become much stronger in the larger molecules and the strongest DEA process in the compounds with two hydroxyl groups, which thus represent an intermediate case between the behavior of small alcohols and the sugar ribose which was discovered to have strong DEA fragmentations near zero electron energy [S. Ptasinska, S. Denifl, P. Scheier and T. D. Mark, J. Chem.	dea	288-291	microtubule affinity regulating kinase 1	Homo sapiens	380-384
17138620-7	2007	Bath application of the soluble guanylate cyclase (sGC) inhibitor 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ) abolished NO(aq)- and DEA/NO-induced potentiation of evoked EPSPs, IPSPs and depolarization.	dea	138-141	guanylate cyclase 1 soluble subunit beta 2	Rattus norvegicus	51-54
16033898-6	2005	We also found that Abeta blocks the increase in cGMP immunoreactivity occurring immediately after LTP and that DEA/NO counteracts the effect of Abeta.	dea	111-114	amyloid beta precursor protein	Homo sapiens	144-149
17177535-4	2006	Yields as high as 32% were obtained for the Mn(TFPP)Cl/PhIO system, which shows that these catalysts can mimic both the in vivo and the in vitro action of cytochrome P-450, with formation of the metabolites DEA and DIA.	dea	207-210	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	155-171
12500976-5	2003	Simultaneous treatment with LPS and the NO donor, diethylamine NONOate (DEA/NO), enhanced and prolonged JNK and p38 phosphorylation.	dea	72-75	mitogen-activated protein kinase 8	Homo sapiens	104-107
15363661-6	2004	Furthermore, NO donors (SNP, SNAP, and Sin-1), including the pure NO donor DEA/NO, directly suppressed in vitro FMO activity (N- or S-oxidation of ranitidine, trimethylamine, and thiobenzamide) in human liver microsomal proteins and recombinant human FMO3.	dea	75-78	flavin containing dimethylaniline monoxygenase 3	Homo sapiens	251-255
15246877-2	2004	We have found that Trx thiol groups are the targets for S-nitrosation by N2O3-like species generated in the system containing xanthine/xanthine oxidase (superoxide producing system) and DEA/NO-the *NO donating compound, however, they have shown low sensitivity to the *NO derived from DEA/NO.	dea	186-189	thioredoxin	Homo sapiens	19-22
15246877-2	2004	We have found that Trx thiol groups are the targets for S-nitrosation by N2O3-like species generated in the system containing xanthine/xanthine oxidase (superoxide producing system) and DEA/NO-the *NO donating compound, however, they have shown low sensitivity to the *NO derived from DEA/NO.	dea	285-288	thioredoxin	Homo sapiens	19-22
14697665-3	2003	The short-lived NO donor DEA/NO induces a transient activation of ERK-1/2 that totally disappears 2 h after NO administration.	dea	25-28	mitogen-activated protein kinase 3	Homo sapiens	66-73
15779890-5	2005	ICP-AES of samples treated with 10 microM DEA/NO showed a decrease in zinc content (0.23 +/- 0.01 to 0.09 +/- 0.01 mol of Zn/mol of iNOS dimer) with no loss of heme iron.	dea	42-45	nitric oxide synthase 2	Homo sapiens	132-136
15779890-6	2005	Gel filtration of wild-type iNOS treated similarly resulted in approximately 20% more monomeric iNOS compared to a DEA-treated sample.	dea	115-118	nitric oxide synthase 2	Homo sapiens	28-32
15779890-7	2005	Only wild-type iNOS had decreased activity (42 +/- 2%) after reaction with 50 microM DEA/NO compared to a control sample.	dea	85-88	nitric oxide synthase 2	Homo sapiens	15-19
15034673-5	2004	Using the specific agonist docosatetraenoylethanolamide (DEA), we have observed that the norepinephrine-induced migration of colon carcinoma cells is inhibited by the CB1-R.	dea	57-60	cannabinoid receptor 1	Homo sapiens	167-172
12500976-5	2003	Simultaneous treatment with LPS and the NO donor, diethylamine NONOate (DEA/NO), enhanced and prolonged JNK and p38 phosphorylation.	dea	72-75	mitogen-activated protein kinase 14	Homo sapiens	112-115
12500976-7	2003	Whereas DEA/NO alone was sufficient to induce JNK and p38 phosphorylation, it was not sufficient to cause IkappaB-alpha degradation.	dea	8-11	mitogen-activated protein kinase 8	Homo sapiens	46-49
12500976-7	2003	Whereas DEA/NO alone was sufficient to induce JNK and p38 phosphorylation, it was not sufficient to cause IkappaB-alpha degradation.	dea	8-11	mitogen-activated protein kinase 14	Homo sapiens	54-57
12500976-8	2003	The enhancement of IkappaB-alpha degradation by DEA/NO correlated with an increase in the nuclear levels of the p50 and p65 subunits and DNA-binding activity determined by electrophoretic mobility shift assay.	dea	48-51	NFKB inhibitor alpha	Homo sapiens	19-32
12500976-8	2003	The enhancement of IkappaB-alpha degradation by DEA/NO correlated with an increase in the nuclear levels of the p50 and p65 subunits and DNA-binding activity determined by electrophoretic mobility shift assay.	dea	48-51	nuclear factor kappa B subunit 1	Homo sapiens	112-115
12500976-8	2003	The enhancement of IkappaB-alpha degradation by DEA/NO correlated with an increase in the nuclear levels of the p50 and p65 subunits and DNA-binding activity determined by electrophoretic mobility shift assay.	dea	48-51	RELA proto-oncogene, NF-kB subunit	Homo sapiens	120-123
12500976-9	2003	DEA/NO and an additional NO donor, MAHMA/NO, are further demonstrated to enhance the transcriptional expression of the IFN-beta gene.	dea	0-3	interferon beta 1	Homo sapiens	119-127
11215662-8	2001	Significant stimulation of DEA (p = 0.027) by N03- -N amendments occurred only in the meander scar soils receiving low NO3- -N (<3.6 mg L(-1)) concentrations.	dea	27-30	NBL1, DAN family BMP antagonist	Homo sapiens	119-122
11996880-5	2002	The initial treatment of microsomal GST with either GSNO or DEA/NO was associated with an 85% loss of free sulfhydryl groups.	dea	60-63	hematopoietic prostaglandin D synthase	Rattus norvegicus	36-39
11160856-6	2001	The effect of YC-1 was further enhanced by addition of DEA/NO, resulting in a approximately 160-fold stimulation of cGMP accumulation.	dea	55-58	RNA binding motif single stranded interacting protein 1	Homo sapiens	14-18
12466224-10	2002	DEA/NO and PAPA/NO reduced [(3)H]-MPP(+) uptake, whereas the release of [(3)H]-MPP(+) was not modified, demonstrating that NO can inhibit uptake of DA transporter substrate without accelerating DA transporter-mediated reverse transport of substrate under the same conditions.	dea	0-3	M-phase phosphoprotein 6	Homo sapiens	34-37
11156580-6	2001	The constrictor response to 10 nM ET-1 was fully reversed by the NO-donor diethylamine NONOate (DEA/NO; EC(50) 2.0 microM, 95% CI: 0.8 - 4.8 microM; n=5).	dea	96-99	endothelin 1	Homo sapiens	34-38
11156580-9	2001	The increase in cyclic GMP by 30 microM DEA/NO was abolished in the presence of 100 microM ODQ (n=6).	dea	40-43	5'-nucleotidase, cytosolic II	Homo sapiens	23-26
10710123-5	2000	In vitro YC-1 increased both VASP phosphorylation and cyclic guanosine monophosphate (cGMP) levels as did the NO donors 2-(N,N-diethylamino)-diazenolate-2-oxide (DEA/NO) and sodium nitroprusside (SNP).	dea	162-165	glutathione S-transferase alpha 1	Rattus norvegicus	9-13
10771518-9	2000	NO releasers (SNAP, DEA/NO, SIN-1) also significantly enhanced Nb2 cell proliferation in the presence of a submaximal dose of PRL (0.125 ng/ml).	dea	20-23	prolactin	Rattus norvegicus	126-129
10771518-11	2000	L-arginine or the NO releaser DEA/NO alone significantly inhibited apoptosis in Nb2 cells deprived of PRL for 5 days.	dea	30-33	prolactin	Rattus norvegicus	102-105
11078363-5	2000	These data suggest that the NONOates DEA/NO and DETA/NO can physiologically antagonize the effects of ET-1 in human arteries and may prove to be useful therapeutic agents in the treatment of cardiovascular disease.	dea	37-40	endothelin 1	Homo sapiens	102-106
8118926-3	1994	This report shows the inhibition of the DNA repair protein, O6-methylguanine-DNA-methyltransferase, by Et2N[N(O)NO]Na (DEA/NO), a compound which decomposes with concurrent release of NO.	dea	119-122	O-6-methylguanine-DNA methyltransferase	Homo sapiens	60-98
9930922-11	1999	The synergistic stimulation of DEA/NO and YC-1 was attenuated by the sGC inhibitor 1H-(1,2,4)oxadiazole(4,3-a)quinoxalin-1-one (ODQ) (10 microM) by 94%.	dea	31-34	guanylate cyclase 1 soluble subunit beta 2	Rattus norvegicus	69-72
9452441-5	1998	The NO donor DEA/NO activated sGC in a GSH-independent manner.	dea	13-16	guanylate cyclase 1 soluble subunit beta 2	Rattus norvegicus	30-33
9701054-7	1997	In the CHO/HGPRT assay, DEA/NO was weakly mutagenic only at the highest concentration used, 20 mM, inducing a mutant frequency per survivor that was 2.5 x control, while SPER/NO was mutagenic at 0.5 mM with a mutant frequency of 2.5 x control.	dea	24-27	hypoxanthine-guanine phosphoribosyltransferase	Cricetulus griseus	11-16
9701054-8	1997	When the CHO cells were given 10 repetitive 20 mM DEA/NO exposures (3 min each), HGPRT mutant frequency was 4.1 x control.	dea	50-53	hypoxanthine-guanine phosphoribosyltransferase	Cricetulus griseus	81-86
8891878-12	1996	The interaction between amiodarone and lidocaine may be explained by the inhibition of CYP3A4 by amiodarone and/or by its main metabolite DEA.	dea	138-141	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	87-93
7554056-5	1995	The genotypic mutation assay, which has a sensitivity of 1 x 10(-6), showed that 4 mM ENU induces detectable numbers of G --> A transitions in codon 248 of p53 while 5-methylcytosine deamination was not detected in either iNOS-transfected cells or cells exposed to 4 mM DEA/NO.	dea	273-276	tumor protein p53	Homo sapiens	159-162
9756558-8	1998	NOHA inhibited urea production by Caco-2 cells and inhibited arginase catalytic activity (85% at 3 microM), whereas NO (DEA/NO and SNAP) inhibited ODC activity (>/=60% at 30 microM) without affecting arginase activity.	dea	120-123	ornithine decarboxylase 1	Homo sapiens	147-150
9719478-9	1998	In conclusion, SNP on the one hand and MAHMA/NO and DEA/NO on the other appeared to release different NOx species with different efficiency on ODC activity.	dea	52-55	ornithine decarboxylase 1	Homo sapiens	143-146
9396061-5	1997	Met-enkephalin decreased systemic arterial and hindquarters perfusion pressures and responses to the opioid receptor agonist were significantly reduced by naloxone, whereas decreases in systemic arterial pressure in response to the nitric oxide donor, DEA/NO, were not altered.	dea	252-255	proopiomelanocortin	Homo sapiens	0-14