PMID-sentid	Pub_year	Sent_text	comp_official_name	comp_offset	protein_name	organism	prot_offset
2458879-3	1988	Concomitant trimethoprim significantly increased the plasma AUC(0-12) of both procainamide and NAPA (63% and 52%, respectively), with concurrent decreases in their renal clearances (47% and 13%, respectively) and a 39% increase in the mean urinary recovery of NAPA (as percentage of procainamide and NAPA recovery).	Trimethoprim	12-24	NSF attachment protein alpha	Homo sapiens	95-99
2458879-3	1988	Concomitant trimethoprim significantly increased the plasma AUC(0-12) of both procainamide and NAPA (63% and 52%, respectively), with concurrent decreases in their renal clearances (47% and 13%, respectively) and a 39% increase in the mean urinary recovery of NAPA (as percentage of procainamide and NAPA recovery).	Trimethoprim	12-24	NSF attachment protein alpha	Homo sapiens	260-264
2458879-3	1988	Concomitant trimethoprim significantly increased the plasma AUC(0-12) of both procainamide and NAPA (63% and 52%, respectively), with concurrent decreases in their renal clearances (47% and 13%, respectively) and a 39% increase in the mean urinary recovery of NAPA (as percentage of procainamide and NAPA recovery).	Trimethoprim	12-24	NSF attachment protein alpha	Homo sapiens	260-264
2458879-5	1988	The change in procainamide and NAPA renal clearances after trimethoprim coadministration strongly correlated with their baseline renal clearances (r = 0.84 and r = 0.74, respectively, p less than 0.0001).	Trimethoprim	59-71	NSF attachment protein alpha	Homo sapiens	31-35
2458879-7	1988	We conclude that trimethoprim increases the plasma concentrations of procainamide and NAPA by decreasing their renal clearances and allowing more conversion of procainamide to NAPA.	Trimethoprim	17-29	NSF attachment protein alpha	Homo sapiens	86-90
2458879-7	1988	We conclude that trimethoprim increases the plasma concentrations of procainamide and NAPA by decreasing their renal clearances and allowing more conversion of procainamide to NAPA.	Trimethoprim	17-29	NSF attachment protein alpha	Homo sapiens	176-180
2458879-7	1988	We conclude that trimethoprim increases the plasma concentrations of procainamide and NAPA by decreasing their renal clearances and allowing more conversion of procainamide to NAPA.	Procainamide	160-172	NSF attachment protein alpha	Homo sapiens	86-90
2457560-3	1988	NAPA levels 1.2 mcg/ml or greater were present for 72 h and in four of the six subjects little further decline occurred at 96 h. PA total body clearance (TBC) averaged 143 ml/min; TBC for NAPA was 29.8 ml/min.	tbc	180-183	NSF attachment protein alpha	Homo sapiens	188-192
3368667-9	1988	The following results were obtained: 1) component Pa (or Na-Pa) of AEMLR has significant lateralization, 2) the generation site of Pa may be in the subcortical thalamic projection of the contralateral lobe, 3) component Po (or No-Po) is a true neurogenic response but is frequently enhanced by the post-auricular reflex, 4) the contralateral inferior colliculus is very important for the generation of Po, 5) the auditory system (hearing) may have contralateral AEMLR dominancy.	Protactinium	50-52	NSF attachment protein alpha	Homo sapiens	57-62
3368667-9	1988	The following results were obtained: 1) component Pa (or Na-Pa) of AEMLR has significant lateralization, 2) the generation site of Pa may be in the subcortical thalamic projection of the contralateral lobe, 3) component Po (or No-Po) is a true neurogenic response but is frequently enhanced by the post-auricular reflex, 4) the contralateral inferior colliculus is very important for the generation of Po, 5) the auditory system (hearing) may have contralateral AEMLR dominancy.	Polonium	220-222	NSF attachment protein alpha	Homo sapiens	57-62
2457345-1	1988	Although procainamide (PA) has been widely used to treat patients with both ventricular and supraventricular arrhythmias since 1951, more than twenty years elapsed before N-acetylprocainamide (NAPA) was identified as a major PA metabolite and shown in PA-treated patients to have plasma concentrations generally equaling or being 2 to 3 times greater than those of the parent drug.	Acecainide	171-191	NSF attachment protein alpha	Homo sapiens	193-197
2447406-8	1987	Thus, these data suggest that NAPA, especially when present at high levels, may markedly affect expected responses in patients being treated with procainamide.	Procainamide	146-158	NSF attachment protein alpha	Homo sapiens	30-34
2443639-1	1987	We report a reversed-phase high-performance liquid chromatography method for the determination of procainamide (PA) and three of its metabolites, n-acetylprocainamide (NAPA), deethylprocainamide (DEPA), and deethyl-n-acetylprocainamide (DENAPA), in serum and urine.	Procainamide	98-110	NSF attachment protein alpha	Homo sapiens	168-172
2439251-1	1987	We attempted to correlate clinical response with the effects of N-acetylprocainamide (NAPA) on the QT interval in five patients with stable chronic ventricular arrhythmias.	Acecainide	64-84	NSF attachment protein alpha	Homo sapiens	86-90
2436466-1	1987	N-acetylprocainamide (NAPA) is the active metabolite of procainamide currently undergoing evaluation for its antiarrhythmic properties.	Procainamide	8-20	NSF attachment protein alpha	Homo sapiens	22-26
2436466-5	1987	NAPA increased heart rate (3% at 10 minutes; p less than 0.01), decreased mean pulmonary arterial pressure (14%; p less than 0.05) and capillary wedge pressure (27%; p less than 0.01), decreased mean arterial pressure (12%; p less than 0.01), cardiac index (8%; p less than 0.01), LV dp/dtmax (9%; p less than 0.05), and stroke work index (17%; p less than 0.01).	dp	284-286	NSF attachment protein alpha	Homo sapiens	0-4
2436466-5	1987	NAPA increased heart rate (3% at 10 minutes; p less than 0.01), decreased mean pulmonary arterial pressure (14%; p less than 0.05) and capillary wedge pressure (27%; p less than 0.01), decreased mean arterial pressure (12%; p less than 0.01), cardiac index (8%; p less than 0.01), LV dp/dtmax (9%; p less than 0.05), and stroke work index (17%; p less than 0.01).	dtmax	287-292	NSF attachment protein alpha	Homo sapiens	0-4
2431875-2	1987	In patients with unilateral temporal lobe lesions, the amplitude of Pa and hence that of the Na-Pa complex was reduced over the involved hemisphere but remained intact over the contralateral hemisphere.	Protactinium	68-70	NSF attachment protein alpha	Homo sapiens	93-98
33649116-8	2021	The analysis revealed that neutrophil-activating protein (NapA; HP0243) promoted H2O2-induced biofilm formation and conferred multidrug resistance.	Hydrogen Peroxide	81-85	NSF attachment protein alpha	Homo sapiens	58-62
2433967-3	1986	The N-acetylation of procainamide leads to the pharmacologically active compound, N-acetylprocainamide (NAPA).	Procainamide	21-33	NSF attachment protein alpha	Homo sapiens	104-108
2433970-1	1986	Shortly after Dreyfus and his colleagues demonstrated that procainamide was metabolized by acetylation to N-acetylprocainamide (NAPA), Drayer, Reidenberg and Sevy reported that NAPA had antiarrhythmic activity in an animal model.	Procainamide	59-71	NSF attachment protein alpha	Homo sapiens	128-132
2433970-1	1986	Shortly after Dreyfus and his colleagues demonstrated that procainamide was metabolized by acetylation to N-acetylprocainamide (NAPA), Drayer, Reidenberg and Sevy reported that NAPA had antiarrhythmic activity in an animal model.	Procainamide	59-71	NSF attachment protein alpha	Homo sapiens	177-181
2433970-2	1986	We confirmed these findings and found that plasma levels of NAPA were high enough to warrant consideration in managing patients requiring procainamide therapy.	Procainamide	138-150	NSF attachment protein alpha	Homo sapiens	60-64
2433970-4	1986	In these studies, we showed that NAPA has an elimination-phase half-life that is more than twice as long as procainamide and suggested that patient compliance and arrhythmia suppression might be improved if NAPA were used to circumvent the inconvenience of the frequent dosing schedule that has been recommended for procainamide.	Procainamide	108-120	NSF attachment protein alpha	Homo sapiens	33-37
2433970-4	1986	In these studies, we showed that NAPA has an elimination-phase half-life that is more than twice as long as procainamide and suggested that patient compliance and arrhythmia suppression might be improved if NAPA were used to circumvent the inconvenience of the frequent dosing schedule that has been recommended for procainamide.	Procainamide	316-328	NSF attachment protein alpha	Homo sapiens	33-37
2433970-4	1986	In these studies, we showed that NAPA has an elimination-phase half-life that is more than twice as long as procainamide and suggested that patient compliance and arrhythmia suppression might be improved if NAPA were used to circumvent the inconvenience of the frequent dosing schedule that has been recommended for procainamide.	Procainamide	316-328	NSF attachment protein alpha	Homo sapiens	207-211
2433971-2	1986	Acetylation of procainamide results in the formation of N-acetylprocainamide (NAPA) the propensity of which to induce SLE and to increase antinuclear antibodies is negligible while its antiarrhythmic properties remain.	Procainamide	15-27	NSF attachment protein alpha	Homo sapiens	78-82
2433971-4	1986	This is also suggested by the remission of PA-induced SLE when PA is replaced with NAPA for the control of cardiac arrhythmias.	Procainamide	43-45	NSF attachment protein alpha	Homo sapiens	83-87
2424305-2	1986	This lead to severe PA and N-acetyl procainamide (NAPA) toxicity.	Acecainide	27-48	NSF attachment protein alpha	Homo sapiens	50-54
6201304-1	1984	We measured procainamide and its active metabolite, N-acetylprocainamide (NAPA), in 80 sera from 37 patients by a new fluorimmunoassay procedure and an established "high-performance" liquid-chromatographic method.	Procainamide	12-24	NSF attachment protein alpha	Homo sapiens	74-78
6189384-1	1983	To define electrophysiologic properties and antiarrhythmic mechanisms of N-acetylprocainamide (NAPA), we studied 16 patients with symptomatic ventricular dysrhythmias.	Acecainide	73-93	NSF attachment protein alpha	Homo sapiens	95-99
6189384-4	1983	Programmed atrial stimulation revealed that NAPA had no discernible effects on AV nodal conduction; however, it exerted depressive effects on the His-Purkinje system in 9 of 16 patients.	Histidine	146-149	NSF attachment protein alpha	Homo sapiens	44-48
6189384-6	1983	In 8 of 16 patients who had inducible repetitive ventricular response (RVR) because of reentry within the His-Purkinje system, NAPA narrowed or abolished the RVR zone in 3 patients and slowed the RVR rate with widening of the RVR zone in the remaining 5 patients.	Histidine	106-109	NSF attachment protein alpha	Homo sapiens	127-131
6188570-5	1983	NAPA therapy was associated with positive antibody titers in only one patient and seems less prone to cause drug-induced lupus erythematosus than procainamide, but NAPA shares the gastrointestinal and other side effects of procainamide.	Procainamide	223-235	NSF attachment protein alpha	Homo sapiens	164-168
6198178-5	1983	The unchanged PA fraction (PA/PA + NAPA) in the rapid acetylators was somewhat lower than in the slow acetylators.	Procainamide	14-16	NSF attachment protein alpha	Homo sapiens	35-39
6179685-1	1982	Kinetics of and clinical responses to N-acetylprocainamide (NAPA) were evaluated in 10 patients with chronic ventricular arrhythmias who had not responded to usual doses of currently available antiarrhythmic drugs.	Acecainide	38-58	NSF attachment protein alpha	Homo sapiens	60-64
91468-3	1979	Renal clearance of NAPA correlated well with ClCr.	clcr	45-49	NSF attachment protein alpha	Homo sapiens	19-23
91468-5	1979	Dialysis itself resulted in a 77% reduction in ClS that limited the total amount of NAPA removed by this procedure.	Chlorine	47-50	NSF attachment protein alpha	Homo sapiens	84-88
91468-6	1979	This reduction in ClS was sustained for at least 3 hr after dialysis and attenuated rebound in plasma NAPA concentrations.	Chlorine	18-21	NSF attachment protein alpha	Homo sapiens	102-106
872496-1	1977	N-Acetylprocainamide (NAPA) accumulated in the plasma of 6 cardiac patients with renal failure taking procainamide chronically for therapy (4 were undergoing hemodialysis) and contributed to the therapeutic and toxic effects of the procainamide.	Acecainide	0-20	NSF attachment protein alpha	Homo sapiens	22-26
872496-1	1977	N-Acetylprocainamide (NAPA) accumulated in the plasma of 6 cardiac patients with renal failure taking procainamide chronically for therapy (4 were undergoing hemodialysis) and contributed to the therapeutic and toxic effects of the procainamide.	Procainamide	8-20	NSF attachment protein alpha	Homo sapiens	22-26
872496-1	1977	N-Acetylprocainamide (NAPA) accumulated in the plasma of 6 cardiac patients with renal failure taking procainamide chronically for therapy (4 were undergoing hemodialysis) and contributed to the therapeutic and toxic effects of the procainamide.	Procainamide	102-114	NSF attachment protein alpha	Homo sapiens	22-26
872496-2	1977	NAPA plasma levels ranged from 14.0 to 28.0 microgram/ml 3 hr after a dose of procainamide which is well above the 3-hr NAPA plasma levels of nonazotemic cardiac patients (range 1.9 to 6.3 microgram/ml; p = 0.002) on larger doses of procainamide.	Procainamide	78-90	NSF attachment protein alpha	Homo sapiens	0-4
872496-2	1977	NAPA plasma levels ranged from 14.0 to 28.0 microgram/ml 3 hr after a dose of procainamide which is well above the 3-hr NAPA plasma levels of nonazotemic cardiac patients (range 1.9 to 6.3 microgram/ml; p = 0.002) on larger doses of procainamide.	Procainamide	233-245	NSF attachment protein alpha	Homo sapiens	0-4
872496-4	1977	In one of the patients with renal failure NAPA was still present 15 days (13.8 microgram/ml) and 38 days (0.9 microgram/ml) after procainamide was stopped, indicating a half-life of several days.	Procainamide	130-142	NSF attachment protein alpha	Homo sapiens	42-46
872496-6	1977	Since NAPA accumulates in patients with impaired renal function, the concentrations of both this active metabolite and procainamide should be determined in these patients if drug level monitoring is to be helpful.	Procainamide	119-131	NSF attachment protein alpha	Homo sapiens	6-10
322922-6	1977	The mean NAPA elimination half-life of 10.9 hr was longer than the 6.2 hr half-life reported for normal subjects, but its prolongation was predictably correlated with reductions in creatinine clearance.	Creatinine	181-191	NSF attachment protein alpha	Homo sapiens	9-13
975731-2	1976	Hemodialysis doubled the rate of procainamide elimination and increased fourfold the clearance of NAPA, the N-acetylated metabolite of procainamide.	Procainamide	135-147	NSF attachment protein alpha	Homo sapiens	98-102
975731-3	1976	Observations of procainamide and N-acetylprocainamide (NAPA) plasma levels during the patient"s recovery suggest that lethargy and profound hypotension can be expected when these levels total 60 mug/ml and that severe cardiac toxicity should be anticipated with levels totaling 42 mug/ml or more.	Acecainide	33-53	NSF attachment protein alpha	Homo sapiens	55-59
776488-1	1976	Oral administration of a 1.5-gm dose of N-acetylprocainamide (NAPA) to 9 patients with premature ventricular contractions (PVCs) confirmed previous indirect evidence that this metabolite of procainamide has antiarrhythmic efficacy and potency comparable to those of procainamide.	Procainamide	48-60	NSF attachment protein alpha	Homo sapiens	62-66
776488-1	1976	Oral administration of a 1.5-gm dose of N-acetylprocainamide (NAPA) to 9 patients with premature ventricular contractions (PVCs) confirmed previous indirect evidence that this metabolite of procainamide has antiarrhythmic efficacy and potency comparable to those of procainamide.	Procainamide	190-202	NSF attachment protein alpha	Homo sapiens	62-66
1263131-1	1976	N-acetylprocainamide (NAPA), a major metabolite of procainamide (PA) in man, has been reported recently to be biologically active.	Acecainide	0-20	NSF attachment protein alpha	Homo sapiens	22-26
1263131-1	1976	N-acetylprocainamide (NAPA), a major metabolite of procainamide (PA) in man, has been reported recently to be biologically active.	Procainamide	8-20	NSF attachment protein alpha	Homo sapiens	22-26
1122675-5	1975	Since patients on long-term procainamide therapy have plasma concentrations of NAPA that are usually comparable to, and occasionally greater than, their procainamide levels, dose regiments based on procainamide levels alone need revision to include consideration of the levels of this metabolite.	Procainamide	28-40	NSF attachment protein alpha	Homo sapiens	79-83
33562013-0	2021	Biochemical and Computational Studies of the Interaction between a Glucosamine Derivative, NAPA, and the IKKalpha Kinase.	Glucosamine	67-78	NSF attachment protein alpha	Homo sapiens	91-95
33562013-1	2021	The glucosamine derivative 2-(N-Acetyl)-L-phenylalanylamido-2-deoxy-beta-D-glucose (NAPA), was shown to inhibit the kinase activity of IKKalpha, one of the two catalytic subunits of IKK complex, decreasing the inflammatory status in osteoarthritis chondrocytes.	Glucosamine	4-15	NSF attachment protein alpha	Homo sapiens	84-88
33562013-1	2021	The glucosamine derivative 2-(N-Acetyl)-L-phenylalanylamido-2-deoxy-beta-D-glucose (NAPA), was shown to inhibit the kinase activity of IKKalpha, one of the two catalytic subunits of IKK complex, decreasing the inflammatory status in osteoarthritis chondrocytes.	Glucose	75-82	NSF attachment protein alpha	Homo sapiens	84-88
33562013-8	2021	This evidence, combined with computational results, consistently indicates that the inhibition is non-competitive, and that the NAPA binding site is different than that of ATP or IKKtide.	Adenosine Triphosphate	172-175	NSF attachment protein alpha	Homo sapiens	128-132
33562013-8	2021	This evidence, combined with computational results, consistently indicates that the inhibition is non-competitive, and that the NAPA binding site is different than that of ATP or IKKtide.	ikktide	179-186	NSF attachment protein alpha	Homo sapiens	128-132
2410877-1	1985	A 66-year-old female with chronic renal failure received five doses of procainamide and developed marked QT interval prolongation and recurrent episodes of torsades de pointes, which were temporally related to high serum n-acetylprocainamide (NAPA) levels and not to procainamide levels.	Procainamide	71-83	NSF attachment protein alpha	Homo sapiens	243-247
2410877-1	1985	A 66-year-old female with chronic renal failure received five doses of procainamide and developed marked QT interval prolongation and recurrent episodes of torsades de pointes, which were temporally related to high serum n-acetylprocainamide (NAPA) levels and not to procainamide levels.	Acecainide	221-241	NSF attachment protein alpha	Homo sapiens	243-247
2410877-3	1985	Torsades de pointes is a potential hazard of NAPA accumulation during procainamide administration to patients with renal insufficiency.	Procainamide	70-82	NSF attachment protein alpha	Homo sapiens	45-49
6206104-1	1984	N-Acetylprocainamide (NAPA), a class III antiarrhythmic drug, caused torsade de pointes in a 72 year old woman who had this arrhythmia on two previous occasions while being treated with quinidine and disopyramide.	Acecainide	0-20	NSF attachment protein alpha	Homo sapiens	22-26
6206104-1	1984	N-Acetylprocainamide (NAPA), a class III antiarrhythmic drug, caused torsade de pointes in a 72 year old woman who had this arrhythmia on two previous occasions while being treated with quinidine and disopyramide.	Quinidine	186-195	NSF attachment protein alpha	Homo sapiens	22-26
6206104-1	1984	N-Acetylprocainamide (NAPA), a class III antiarrhythmic drug, caused torsade de pointes in a 72 year old woman who had this arrhythmia on two previous occasions while being treated with quinidine and disopyramide.	Disopyramide	200-212	NSF attachment protein alpha	Homo sapiens	22-26
6204527-3	1984	The N-acetylprocainamide (NAPA) dialysis clearance was 5.3 mL/min.	Acecainide	4-24	NSF attachment protein alpha	Homo sapiens	26-30
6204527-4	1984	The CAPD clearance of procainamide and its active metabolite, NAPA, is much lower than that reported for hemodialysis.	Procainamide	22-34	NSF attachment protein alpha	Homo sapiens	62-66
6084435-4	1984	From 30 to 60% of a PA dose is excreted as the metabolite, N-acetylprocainamide (NAPA), and PA"s metabolism is determined genetically (fast or slow acetylation phenotype).	Acecainide	59-79	NSF attachment protein alpha	Homo sapiens	81-85
6261406-4	1981	N-acetylprocainamide (NAPA) should probably be prescribed in preference to procainamide.	Acecainide	0-20	NSF attachment protein alpha	Homo sapiens	22-26
6261406-4	1981	N-acetylprocainamide (NAPA) should probably be prescribed in preference to procainamide.	Procainamide	8-20	NSF attachment protein alpha	Homo sapiens	22-26
6160014-1	1980	The kinetics of N-acetylprocainamide (NAPA) deacetylation to procainamide (PA) were determined in a normal subject using NAPA-13C, labeled in the acetyl group.	Procainamide	24-36	NSF attachment protein alpha	Homo sapiens	38-42
6160014-5	1980	Despite reports that patients with the PA-induced systemic lupus erythematosus-like reaction have had symptomatic and immunologic remission when switched to NAPA, the demonstration that NAPA is deacetylated to PA indicates that the apparently greater immunologic safety of NAPA may be relative rather than absolute.	Procainamide	39-41	NSF attachment protein alpha	Homo sapiens	186-190
6160014-5	1980	Despite reports that patients with the PA-induced systemic lupus erythematosus-like reaction have had symptomatic and immunologic remission when switched to NAPA, the demonstration that NAPA is deacetylated to PA indicates that the apparently greater immunologic safety of NAPA may be relative rather than absolute.	Procainamide	39-41	NSF attachment protein alpha	Homo sapiens	186-190
6158263-1	1980	The antiarrhythmic efficacy and pharmacokinetics of N-acetylprocainamide (NAPA), the major metabolite of procainamide, were investigated in 23 patients with chronic, high frequency ventricular ectopic depolarizations.	Procainamide	60-72	NSF attachment protein alpha	Homo sapiens	74-78
6156049-1	1980	N-Acetylprocainamide (NAPA) disposition kinetics was studied in eight patients with coronary artery disease.	Acecainide	0-20	NSF attachment protein alpha	Homo sapiens	22-26
6161089-0	1980	Pharmacokinetic studies of procainamide (PA) and N-acetylprocainamide (NAPA) in healthy subjects.	Acecainide	49-69	NSF attachment protein alpha	Homo sapiens	71-75
33649116-9	2021	Furthermore, vitamin C exhibited anti-H. pylori biofilm activity and downregulated the expression of napA in vitro These findings provide novel insight into the clearance of H. pylori biofilms.	Ascorbic Acid	13-22	NSF attachment protein alpha	Homo sapiens	101-105
32824566-5	2020	Using this new platform, we designed primers for several functional genes in the nitrogen cycle, including napA and amoA.	Nitrogen	81-89	NSF attachment protein alpha	Homo sapiens	107-111
33249309-9	2021	Gene abundance and enzymatic activity tests confirmed that nitrate reductase gene napA functioned crucially in chemoautotrophic V(V) reduction by Fe(II) and S(-II) donating electron.	ammonium ferrous sulfate	146-152	NSF attachment protein alpha	Homo sapiens	82-86
31769510-0	2020	The Glucosamine-derivative NAPA Suppresses MAPK Activation and Restores Collagen Deposition in Human Diploid Fibroblasts Challenged with Environmental Levels of UVB.	Glucosamine	4-15	NSF attachment protein alpha	Homo sapiens	27-31
31769510-2	2020	In this study we investigated the effects of the glucosamine-derivative 2-(N-Acetyl)-L-phenylalanylamido-2-deoxy-beta-D-glucose (NAPA) on human primary fibroblasts (FBs) stimulated in vitro with environmental levels of UVB radiation.	Glucosamine	49-60	NSF attachment protein alpha	Homo sapiens	129-133
31769510-2	2020	In this study we investigated the effects of the glucosamine-derivative 2-(N-Acetyl)-L-phenylalanylamido-2-deoxy-beta-D-glucose (NAPA) on human primary fibroblasts (FBs) stimulated in vitro with environmental levels of UVB radiation.	Deoxyglucose	72-127	NSF attachment protein alpha	Homo sapiens	129-133
28891586-2	2017	This work presents for the first time the synthesis and development of novel poly-N-acryloyl l-phenylalanine methyl ester hollow core nanocapsules (NAPA-HPNs) of avg.	poly-n-acryloyl l-phenylalanine methyl ester	77-121	NSF attachment protein alpha	Homo sapiens	148-152
31537813-3	2019	The ability of the N-acetyl phenylalanine glucosamine derivative (NAPA) to increase anabolism and reduce catabolism via inhibition of IKKalpha kinase has been previously observed in vitro and in vivo.	n-acetyl phenylalanine glucosamine	19-53	NSF attachment protein alpha	Homo sapiens	66-70
28891586-5	2017	NAPA-HPNs are biocompatible and capable of encapsulating sodium nitroprusside (SNP) at a rate of ~1.3 muM per mg of capsules.	Nitroprusside	57-77	NSF attachment protein alpha	Homo sapiens	0-4
28891586-7	2017	These NAPA-HPNs also facilitate the prolonged release of a low level of nitric oxide (NO) and enhance the metabolic activities of pro-inflammatory macrophages, which are important for the action of various drugs in body fluids.	Nitric Oxide	72-84	NSF attachment protein alpha	Homo sapiens	6-10
26498108-5	2015	These techniques were also key in elucidating mechanistic details into how the SNARE complex is disassembled, including details of the energetics required for ATP-dependent alpha-SNAP/NSF-mediated SNARE complex disassembly, and the structural changes that accompany ATP hydrolysis by the disassembly machinery.	Adenosine Triphosphate	159-162	NSF attachment protein alpha	Homo sapiens	173-183
25219669-1	2015	OBJECTIVE: Aim of this study is to investigate the effects of Glucosamine (GlcN) and its peptidyl-derivative, 2-(N-Acetyl)-L-phenylalanylamido-2-deoxy-beta-D-glucose (NAPA), on extracellular matrix (ECM) synthesis in human primary chondrocytes (HPCs).	Glucosamine	62-73	NSF attachment protein alpha	Homo sapiens	167-171
26156199-4	2015	The expression of alphaSNAP was assessed in the temporal lobe from patients with TLE and pilocarpine-induced epileptic rats.	Pilocarpine	89-100	NSF attachment protein alpha	Homo sapiens	18-27
30546552-7	2015	Blood examination revealed that N-acetyl procainamide (NAPA), metabolite of procainamide, was significantly higher than the recommended threshold.	Procainamide	41-53	NSF attachment protein alpha	Homo sapiens	55-59
30546552-8	2015	NAPA was identified as the cause of prolonged QTc and procainamide was stopped.	Procainamide	54-66	NSF attachment protein alpha	Homo sapiens	0-4
25492864-2	2015	N-Ethylmaleimide sensitive factor recycles SNAREs after fusion by binding to the SNARE complex through an adaptor protein, alphaSNAP, and using the energy of ATP hydrolysis to disassemble the complex.	Ethylmaleimide	0-16	NSF attachment protein alpha	Homo sapiens	123-132
25492864-2	2015	N-Ethylmaleimide sensitive factor recycles SNAREs after fusion by binding to the SNARE complex through an adaptor protein, alphaSNAP, and using the energy of ATP hydrolysis to disassemble the complex.	Adenosine Triphosphate	158-161	NSF attachment protein alpha	Homo sapiens	123-132
25492864-5	2015	Using the trimerized alphaSNAP, we find that N-ethylmaleimide-sensitive factor hydrolyzes 10 ATP molecules on average to disassemble a single SNARE complex.	Adenosine Triphosphate	93-96	NSF attachment protein alpha	Homo sapiens	21-30
25902545-1	2015	Sec17 [soluble N-ethylmaleimide-sensitive factor (NSF) attachment protein; alpha-SNAP] and Sec18 (NSF) perform ATP-dependent disassembly of cis-SNARE complexes, liberating SNAREs for subsequent assembly of trans-complexes for fusion.	Adenosine Triphosphate	111-114	NSF attachment protein alpha	Homo sapiens	75-85
25219669-7	2015	Both molecules were able to induce Insulin Growth Factor-I (IGF-I) and to stimulate SOX-9, whereas NAPA and G + N were able to up-regulate both Hyaluronic Acid Synthase-2 and Hyaluronic acid.	Hyaluronic Acid	175-190	NSF attachment protein alpha	Homo sapiens	99-103
25219669-1	2015	OBJECTIVE: Aim of this study is to investigate the effects of Glucosamine (GlcN) and its peptidyl-derivative, 2-(N-Acetyl)-L-phenylalanylamido-2-deoxy-beta-D-glucose (NAPA), on extracellular matrix (ECM) synthesis in human primary chondrocytes (HPCs).	Glucosamine	75-79	NSF attachment protein alpha	Homo sapiens	167-171
25219669-1	2015	OBJECTIVE: Aim of this study is to investigate the effects of Glucosamine (GlcN) and its peptidyl-derivative, 2-(N-Acetyl)-L-phenylalanylamido-2-deoxy-beta-D-glucose (NAPA), on extracellular matrix (ECM) synthesis in human primary chondrocytes (HPCs).	2-(n-acetyl)-l-phenylalanylamido-2-deoxy-beta-d-glucose	110-165	NSF attachment protein alpha	Homo sapiens	167-171
25219669-2	2015	METHODS: Dose-dependent effect of GlcN and NAPA on Glycosaminoglycan (GAG), Collagen type II (Col2) and Small Leucine-Rich Proteoglycans (SLRPs) was examined by incubating HPCs, cultured in micromasses (3D), with various amounts of two molecules, administered as either GlcN alone or NAPA alone or GlcN plus NAPA (G + N).	Glucosamine	34-38	NSF attachment protein alpha	Homo sapiens	284-288
25219669-2	2015	METHODS: Dose-dependent effect of GlcN and NAPA on Glycosaminoglycan (GAG), Collagen type II (Col2) and Small Leucine-Rich Proteoglycans (SLRPs) was examined by incubating HPCs, cultured in micromasses (3D), with various amounts of two molecules, administered as either GlcN alone or NAPA alone or GlcN plus NAPA (G + N).	Glucosamine	34-38	NSF attachment protein alpha	Homo sapiens	284-288
25219669-2	2015	METHODS: Dose-dependent effect of GlcN and NAPA on Glycosaminoglycan (GAG), Collagen type II (Col2) and Small Leucine-Rich Proteoglycans (SLRPs) was examined by incubating HPCs, cultured in micromasses (3D), with various amounts of two molecules, administered as either GlcN alone or NAPA alone or GlcN plus NAPA (G + N).	Glucosamine	270-274	NSF attachment protein alpha	Homo sapiens	43-47
25219669-2	2015	METHODS: Dose-dependent effect of GlcN and NAPA on Glycosaminoglycan (GAG), Collagen type II (Col2) and Small Leucine-Rich Proteoglycans (SLRPs) was examined by incubating HPCs, cultured in micromasses (3D), with various amounts of two molecules, administered as either GlcN alone or NAPA alone or GlcN plus NAPA (G + N).	Glucosamine	270-274	NSF attachment protein alpha	Homo sapiens	43-47
23187805-7	2012	Loss of alphaSNAP caused fragmentation of the Golgi and downregulation of the Golgi-specific GTP exchange factors, GBF1, BIG1 and BIG2.	Guanosine Triphosphate	93-96	NSF attachment protein alpha	Homo sapiens	8-17
24081657-5	2014	Using siRNA in cultured human umbilical vein ECs and human pulmonary artery ECs, depletion of Galpha12 and soluble N-ethylmaleimide-sensitive-fusion factor attachment protein alpha (alpha-SNAP), but not Galpha13, inhibited both basal and thrombin-induced vWF secretion, whereas overexpression of activated Galpha12 promoted vWF secretion.	Ethylmaleimide	115-131	NSF attachment protein alpha	Homo sapiens	182-192
24430487-5	2014	As NapA has a high affinity for nitrate compared with the membrane-bound enzyme, its occurrence in vent Epsilonproteobacteria may represent an adaptation of these organisms to the low nitrate concentrations typically found in vent fluids.	Nitrates	32-39	NSF attachment protein alpha	Homo sapiens	3-7
24430487-5	2014	As NapA has a high affinity for nitrate compared with the membrane-bound enzyme, its occurrence in vent Epsilonproteobacteria may represent an adaptation of these organisms to the low nitrate concentrations typically found in vent fluids.	Nitrates	184-191	NSF attachment protein alpha	Homo sapiens	3-7
24778182-4	2014	Using chromaffin granules and liposomes we now show that alpha-SNAP on its own interferes with the zippering of membrane-anchored SNARE complexes midway through the zippering reaction, arresting SNAREs in a partially assembled trans-complex and preventing fusion.	chromaffin	6-16	NSF attachment protein alpha	Homo sapiens	57-67
23967680-4	2013	Frequency of neutrophil-activating protein A(Nap A), which encoded by nap A, with threonine at amino acid residue No.	Threonine	82-91	NSF attachment protein alpha	Homo sapiens	45-50
23967680-4	2013	Frequency of neutrophil-activating protein A(Nap A), which encoded by nap A, with threonine at amino acid residue No.	Threonine	82-91	NSF attachment protein alpha	Homo sapiens	70-75
23967680-6	2013	Strains with Thr70-type Nap A showed significantly higher levels of Fe3+ and Fe2+ uptake than strains with other type, Ser70-type Nap A, which is found in standard strains.	ferric sulfate	68-72	NSF attachment protein alpha	Homo sapiens	24-29
23967680-6	2013	Strains with Thr70-type Nap A showed significantly higher levels of Fe3+ and Fe2+ uptake than strains with other type, Ser70-type Nap A, which is found in standard strains.	ammonium ferrous sulfate	77-81	NSF attachment protein alpha	Homo sapiens	24-29
23878724-0	2013	An essential and NSF independent role for alpha-SNAP in store-operated calcium entry.	Calcium	71-78	NSF attachment protein alpha	Homo sapiens	42-52
20844569-5	2011	Expression levels of 82 genes diagnostic for transformations in the marine nitrogen, phosphorus and sulfur cycles ranged from below detection (<1 x 10(6) transcripts per liter) for 36 genes (for example, phosphonate metabolism gene phnH, dissimilatory nitrate reductase subunit napA) to >2.7 x 10(9) transcripts per liter (ammonia transporter amt and ammonia monooxygenase subunit amoC).	Nitrogen	75-83	NSF attachment protein alpha	Homo sapiens	281-285
20844569-5	2011	Expression levels of 82 genes diagnostic for transformations in the marine nitrogen, phosphorus and sulfur cycles ranged from below detection (<1 x 10(6) transcripts per liter) for 36 genes (for example, phosphonate metabolism gene phnH, dissimilatory nitrate reductase subunit napA) to >2.7 x 10(9) transcripts per liter (ammonia transporter amt and ammonia monooxygenase subunit amoC).	Sulfur	100-106	NSF attachment protein alpha	Homo sapiens	281-285
19880322-7	2009	In this study, we report an N-acylpolyamine (NAPA) scaffold that supports numerous sidechains in a compact atomic arrangement.	n-acylpolyamine	28-43	NSF attachment protein alpha	Homo sapiens	45-49
20653109-0	2010	Knockdown of NAPA using short-hairpin RNA sensitizes cancer cells to cisplatin: implications to overcome chemoresistance.	Cisplatin	69-78	NSF attachment protein alpha	Homo sapiens	13-17
20653109-2	2010	In the present study, we found that NAPA--a protein found in the endoplasmic reticulum (ER) and implicated in protein trafficking--protects cells against cisplatin.	Cisplatin	154-163	NSF attachment protein alpha	Homo sapiens	36-40
20653109-4	2010	A low dose of cisplatin also elicited a mild ER stress response associated with the accumulation of the protective proteins BiP and NAPA.	Cisplatin	14-23	NSF attachment protein alpha	Homo sapiens	132-136
20653109-5	2010	Remarkably, knockdown of NAPA induced apoptosis and enhanced cisplatin-induced cytotoxicity/apoptosis, thereby sensitizing cancer cells to cisplatin.	Cisplatin	61-70	NSF attachment protein alpha	Homo sapiens	25-29
20653109-5	2010	Remarkably, knockdown of NAPA induced apoptosis and enhanced cisplatin-induced cytotoxicity/apoptosis, thereby sensitizing cancer cells to cisplatin.	Cisplatin	139-148	NSF attachment protein alpha	Homo sapiens	25-29
20653109-6	2010	On the other hand, overexpression of NAPA increased resistance to cisplatin by reducing cisplatin-induced ER stress and apoptosis.	Cisplatin	66-75	NSF attachment protein alpha	Homo sapiens	37-41
20653109-6	2010	On the other hand, overexpression of NAPA increased resistance to cisplatin by reducing cisplatin-induced ER stress and apoptosis.	Cisplatin	88-97	NSF attachment protein alpha	Homo sapiens	37-41
20653109-8	2010	A partial reversal of cisplatin resistance was also observed in cisplatin-resistant HeLa cells following knockdown of NAPA.	Cisplatin	22-31	NSF attachment protein alpha	Homo sapiens	118-122
20653109-8	2010	A partial reversal of cisplatin resistance was also observed in cisplatin-resistant HeLa cells following knockdown of NAPA.	Cisplatin	64-73	NSF attachment protein alpha	Homo sapiens	118-122
20653109-11	2010	Taken together, these observations suggest that NAPA represents a target of cisplatin, and that knockdown of NAPA may improve cisplatin-based cancer therapy.	Cisplatin	76-85	NSF attachment protein alpha	Homo sapiens	48-52
20653109-11	2010	Taken together, these observations suggest that NAPA represents a target of cisplatin, and that knockdown of NAPA may improve cisplatin-based cancer therapy.	Cisplatin	126-135	NSF attachment protein alpha	Homo sapiens	109-113
20361941-4	2010	We identified nine genes (NAPA, CITED2, CABIN1, ADM, HIST1H1A, EHD1, MARK2, PTPN21, and MVD), which were consistently upregulated in two cisplatin-resistant HeLa cell lines.	Cisplatin	137-146	NSF attachment protein alpha	Homo sapiens	26-30
20361941-7	2010	Among the treatments performed, shRNA knockdown of NAPA was the most efficient treatment able to sensitize cells to cisplatin.	Cisplatin	116-125	NSF attachment protein alpha	Homo sapiens	51-55
17543321-3	2007	Particular attention was paid to the dissolution of calcite at equilibrium and as a function of sodium polyacrylate (NaPA) concentration.	carbopol 940	96-115	NSF attachment protein alpha	Homo sapiens	117-121
18507051-1	2008	BACKGROUND: Sodium phenylacetate (NaPa) inhibits breast cancer cell proliferation decreasing prenylation of small G proteins including Ras.	phenylacetic acid	12-32	NSF attachment protein alpha	Homo sapiens	34-38
17038314-8	2006	The tethering-defective vesicles generated in the presence of dominant-negative alpha-SNAP specifically lacked the Rab1 effectors p115 and GM130 but not other peripheral membrane proteins.	gm130	139-144	NSF attachment protein alpha	Homo sapiens	80-90
12941689-2	2003	We present the three-dimensional structure of the hydrolysis mutant E329Q of NSF complexed with an ATP-ADP mixture at 11 A resolution by electron cryomicroscopy and single-particle averaging of NSF.alpha-SNAP.SNARE complexes.	atp-adp	99-106	NSF attachment protein alpha	Homo sapiens	198-208
17030577-1	2006	Neutrophil-activating protein (NapA) has been well documented to play roles in human neutrophil recruitment and in stimulating host cell production of reactive oxygen intermediates (ROI).	reactive oxygen intermediates	151-180	NSF attachment protein alpha	Homo sapiens	31-35
15980433-3	2005	Glutathione S-transferase pull-down assays showed the selective interaction of alphaSNAP with G alpha12 in COS-7 as well as in human umbilical vein endothelial cells.	carbonyl sulfide	107-110	NSF attachment protein alpha	Homo sapiens	79-88
15793163-3	2005	During ciprofloxacin treatment, only procainamide and NAPA renal clearances decreased significantly.	Ciprofloxacin	7-20	NSF attachment protein alpha	Homo sapiens	54-58
15272311-4	2004	Notably, a highly conserved leucine residue in the BH3 domain of BNIP1 plays an important role not only in the induction of apoptosis but also in the binding of alpha-SNAP, an adaptor that serves as a link between the chaperone ATPase NSF and SNAREs.	Leucine	28-35	NSF attachment protein alpha	Homo sapiens	161-171
15272311-6	2004	Indeed, overexpression of alpha-SNAP markedly delayed staurosporine-induced apoptosis.	Staurosporine	54-67	NSF attachment protein alpha	Homo sapiens	26-36
12663329-6	2003	Membrane-associated alpha-SNAP was not released from the membrane fraction when the cells were lyzed in the presence of Ca2+ or Mg2+ATP.	magnesium ion	128-132	NSF attachment protein alpha	Homo sapiens	20-30
12663329-6	2003	Membrane-associated alpha-SNAP was not released from the membrane fraction when the cells were lyzed in the presence of Ca2+ or Mg2+ATP.	Adenosine Triphosphate	132-135	NSF attachment protein alpha	Homo sapiens	20-30
12663329-8	2003	Phase separation using Triton X-114 showed that alpha-SNAP partitioned into both aqueous and detergent phases.	Nonidet P-40	23-35	NSF attachment protein alpha	Homo sapiens	48-58
12663329-10	2003	Permeabilization of type II cells with beta-escin resulted in a partial loss of alpha-SNAP from the cells, but cellular NSF was relatively unchanged.	Escin	39-49	NSF attachment protein alpha	Homo sapiens	80-90
12663329-12	2003	An alpha-SNAP antisense oligonucleotide decreased its protein level and inhibited surfactant secretion.	Oligonucleotides	24-39	NSF attachment protein alpha	Homo sapiens	3-13
17149548-1	2006	Anionic polyacrylate chains (NaPA) form precipitates if alkaline earth cations are added in stoichiometric amounts.	carbopol 940	8-20	NSF attachment protein alpha	Homo sapiens	29-33
16407249-10	2006	cAMP-elicited exocytosis was sensitive to anti-alpha-SNAP, anti-NSF, and anti-Rab3A antibodies, to intra-acrosomal Ca2+ chelators, and to botulinum toxins but was resistant to cAMP-dependent protein kinase blockers.	Cyclic AMP	0-4	NSF attachment protein alpha	Homo sapiens	47-57
15972253-8	2005	We suggest that electrons might be transferred to NapA either from menaquinol via NapC, or from other electron donors such as formate or hydrogen via the small tetraheme cytochrome, NapM.	menaquinol	67-77	NSF attachment protein alpha	Homo sapiens	50-54
15972253-8	2005	We suggest that electrons might be transferred to NapA either from menaquinol via NapC, or from other electron donors such as formate or hydrogen via the small tetraheme cytochrome, NapM.	N-acetyl-S-(propionamide)cysteine	82-86	NSF attachment protein alpha	Homo sapiens	50-54
15972253-8	2005	We suggest that electrons might be transferred to NapA either from menaquinol via NapC, or from other electron donors such as formate or hydrogen via the small tetraheme cytochrome, NapM.	formic acid	126-133	NSF attachment protein alpha	Homo sapiens	50-54
15972253-8	2005	We suggest that electrons might be transferred to NapA either from menaquinol via NapC, or from other electron donors such as formate or hydrogen via the small tetraheme cytochrome, NapM.	Hydrogen	137-145	NSF attachment protein alpha	Homo sapiens	50-54
12730228-4	2003	Replacing basic residues on this surface with alanines reduced SNARE complex binding and disassembly, whereas replacing acidic residues with alanines enhanced alpha-SNAP efficacy in both assays.	Alanine	141-149	NSF attachment protein alpha	Homo sapiens	159-169
12553014-1	2002	Sodium phenylacetate (NaPa) and some bisphosphonates demonstrated antiproliferative and proapoptotic properties against cancer.	phenylacetic acid	0-20	NSF attachment protein alpha	Homo sapiens	22-26
12837618-6	2003	Palmitoylated and nonacylated SNAP-25 form SDS-resistant SNARE complexes which could then be disassembled by NSF and alpha-SNAP.	Sodium Dodecyl Sulfate	43-46	NSF attachment protein alpha	Homo sapiens	117-127
11259095-0	2001	Decrease of breast cancer cell invasiveness by sodium phenylacetate (NaPa) is associated with an increased expression of adhesive molecules.	phenylacetic acid	47-67	NSF attachment protein alpha	Homo sapiens	69-73
12070132-4	2002	NSF/alpha-SNAP catalyze the binding of GATE-16 to GOS-28, a Golgi v-SNARE, in a manner that requires ATP but not ATP hydrolysis.	Adenosine Triphosphate	101-104	NSF attachment protein alpha	Homo sapiens	4-14
12070132-4	2002	NSF/alpha-SNAP catalyze the binding of GATE-16 to GOS-28, a Golgi v-SNARE, in a manner that requires ATP but not ATP hydrolysis.	Adenosine Triphosphate	113-116	NSF attachment protein alpha	Homo sapiens	4-14
11762430-3	2001	Here, we show that the ionic-layer glutamine of syntaxin is required for efficient alpha-SNAP and NSF-mediated dissociation of the complex.	Glutamine	35-44	NSF attachment protein alpha	Homo sapiens	83-93
11762430-6	2001	We propose that alpha-SNAP and NSF drive conformational changes at the ionic layer through specific interactions with the syntaxin glutamine, resulting in the dissociation of the SNARE complex.	Glutamine	131-140	NSF attachment protein alpha	Homo sapiens	16-26
11423412-5	2001	Reconstituted t-SNAREs in supported bilayers bound soluble green fluorescent protein/vesicle-associated membrane protein (v-SNARE), and the SNARE complexes could be specifically dissociated by NSF/alpha-SNAP in the presence of ATP.	Adenosine Triphosphate	227-230	NSF attachment protein alpha	Homo sapiens	197-207
11259095-1	2001	Sodium phenylacetate (NaPa), a non-toxic phenylalanine metabolite, has been shown to induce in vivo and in vitro cytostatic and antiproliferative effects on various cell types.	phenylacetic acid	0-20	NSF attachment protein alpha	Homo sapiens	22-26
11259095-1	2001	Sodium phenylacetate (NaPa), a non-toxic phenylalanine metabolite, has been shown to induce in vivo and in vitro cytostatic and antiproliferative effects on various cell types.	Phenylalanine	41-54	NSF attachment protein alpha	Homo sapiens	22-26
11222293-7	2001	Experiments that involve inserting peptide fragments of soluble N-ethylmaleimide-sensitive fusion attachment protein (alpha-SNAP) into varicosities, a procedure that is known to block quantal release, left the slow component of release unaffected.	Ethylmaleimide	64-80	NSF attachment protein alpha	Homo sapiens	118-128
10648404-4	2000	This calcium-induced secretion relies on the SNARE proteins because it is stimulated by the addition of recombinant alpha-SNAP and inhibited by a dominant negative alpha-SNAP-L294A mutant or by anti-alpha-SNAP and anti-NSF antibodies.	Calcium	5-12	NSF attachment protein alpha	Homo sapiens	116-126
10662817-0	2000	Comparison of cysteine string protein (Csp) and mutant alpha-SNAP overexpression reveals a role for csp in late steps of membrane fusion in dense-core granule exocytosis in adrenal chromaffin cells.	chromaffin	181-191	NSF attachment protein alpha	Homo sapiens	55-65
10861786-5	2000	GCVs bound SNAREs but not NSF or alpha-SNAP; whereas in the rabphilin-supplied IGC, GCVs recruited both NSF and alpha-SNAP, to form the SNARE-NSF-SNAP complex.	Ganciclovir	84-88	NSF attachment protein alpha	Homo sapiens	112-122
10648404-4	2000	This calcium-induced secretion relies on the SNARE proteins because it is stimulated by the addition of recombinant alpha-SNAP and inhibited by a dominant negative alpha-SNAP-L294A mutant or by anti-alpha-SNAP and anti-NSF antibodies.	Calcium	5-12	NSF attachment protein alpha	Homo sapiens	164-174
10648404-4	2000	This calcium-induced secretion relies on the SNARE proteins because it is stimulated by the addition of recombinant alpha-SNAP and inhibited by a dominant negative alpha-SNAP-L294A mutant or by anti-alpha-SNAP and anti-NSF antibodies.	Calcium	5-12	NSF attachment protein alpha	Homo sapiens	164-174
10470159-0	1999	Sodium phenylacetate (NaPa) induces modifications of the proliferation, the adhesion and the cell cycle of tumoral epithelial breast cells.	phenylacetic acid	0-20	NSF attachment protein alpha	Homo sapiens	22-26
10470159-1	1999	Sodium phenylacetate (NaPa), a physiological product of phenylalanine metabolism, present in micromolar concentrations in human plasma, has been shown to induce in vivo and in vitro cytostatic antiproliferative effects at millimolar concentrations.	phenylacetic acid	0-20	NSF attachment protein alpha	Homo sapiens	22-26
10470159-1	1999	Sodium phenylacetate (NaPa), a physiological product of phenylalanine metabolism, present in micromolar concentrations in human plasma, has been shown to induce in vivo and in vitro cytostatic antiproliferative effects at millimolar concentrations.	Phenylalanine	56-69	NSF attachment protein alpha	Homo sapiens	22-26
9485559-3	1998	This paper describes the population pharmacokinetics of procainamide and N-acetylprocainamide (NAPA), the major metabolite, in healthy volunteers and patients with VPD by combining Cmax, tmax, Cmin, and AUC(0-12) values at steady state from six multiple-dose studies in which one 1000-mg or two 500-mg Procanbid tablets were administered.	Acecainide	73-93	NSF attachment protein alpha	Homo sapiens	95-99
9843441-0	1998	Characterization of vesicular membrane-bound alpha-SNAP and NSF in adrenal chromaffin cells.	chromaffin	75-85	NSF attachment protein alpha	Homo sapiens	45-55
9843441-7	1998	In the sucrose gradient 30% alpha-SNAP and 27% NSF were recovered with chromaffin vesicles.	Sucrose	7-14	NSF attachment protein alpha	Homo sapiens	28-38
9843441-7	1998	In the sucrose gradient 30% alpha-SNAP and 27% NSF were recovered with chromaffin vesicles.	chromaffin	71-81	NSF attachment protein alpha	Homo sapiens	28-38
9701561-0	1998	Alpha-SNAP but not gamma-SNAP is required for ER-Golgi transport after vesicle budding and the Rab1-requiring step but before the EGTA-sensitive step.	Egtazic Acid	130-134	NSF attachment protein alpha	Homo sapiens	0-10
9701561-10	1998	It has been shown previously that EGTA blocks ER-Golgi transport at a step after vesicle docking but before fusion and we show here that alpha-SNAP acts before the step that is blocked by EGTA.	Egtazic Acid	34-38	NSF attachment protein alpha	Homo sapiens	137-147
9701561-10	1998	It has been shown previously that EGTA blocks ER-Golgi transport at a step after vesicle docking but before fusion and we show here that alpha-SNAP acts before the step that is blocked by EGTA.	Egtazic Acid	188-192	NSF attachment protein alpha	Homo sapiens	137-147
9485559-3	1998	This paper describes the population pharmacokinetics of procainamide and N-acetylprocainamide (NAPA), the major metabolite, in healthy volunteers and patients with VPD by combining Cmax, tmax, Cmin, and AUC(0-12) values at steady state from six multiple-dose studies in which one 1000-mg or two 500-mg Procanbid tablets were administered.	Procainamide	302-311	NSF attachment protein alpha	Homo sapiens	95-99
9485559-5	1998	Procainamide and NAPA pharmacokinetic parameters observed after administration of Procanbid tablets were similar in blacks and whites, and in men and women.	Procainamide	82-91	NSF attachment protein alpha	Homo sapiens	17-21
9325254-2	1997	When Golgi extract is preincubated with soluble NSF attachment proteins (alpha-SNAP) and N-ethylmaleimide-sensitive factor (NSF) under conditions that allow ATP hydrolysis by NSF, GS28 and syntaxin 5 become dissociated.	Adenosine Triphosphate	157-160	NSF attachment protein alpha	Homo sapiens	73-83
9362506-6	1997	Sequence alignment of known SNAPs revealed only leucine 294 to be conserved in the final 10 amino acids of alpha-SNAP.	Leucine	48-55	NSF attachment protein alpha	Homo sapiens	107-117
9362506-11	1997	In the presence of MgATP, alpha-SNAP (1-285) and alpha-SNAP (L294A) were unable to fully disassemble the 20S complex and did not allow vesicle-associated membrane protein dissociation to any greater level than seen in control incubations.	Adenosine Triphosphate	19-24	NSF attachment protein alpha	Homo sapiens	26-36
9362506-11	1997	In the presence of MgATP, alpha-SNAP (1-285) and alpha-SNAP (L294A) were unable to fully disassemble the 20S complex and did not allow vesicle-associated membrane protein dissociation to any greater level than seen in control incubations.	Adenosine Triphosphate	19-24	NSF attachment protein alpha	Homo sapiens	49-59
9430666-6	1998	Our results indicate that NSF mutants in the first ATP binding domain completely abrogate alpha-SNAP release, whereas no inhibitory effect is observed with a mutant in the second ATP binding domain.	Adenosine Triphosphate	51-54	NSF attachment protein alpha	Homo sapiens	90-100
9443381-1	1998	An improved high-performance liquid chromatographic assay for the determination of procainamide and N-acetylprocainamide (NAPA) at concentrations observed up to 32 h after a single oral dose administration of procainamide to human subjects is reported.	Acecainide	100-120	NSF attachment protein alpha	Homo sapiens	122-126
9443381-1	1998	An improved high-performance liquid chromatographic assay for the determination of procainamide and N-acetylprocainamide (NAPA) at concentrations observed up to 32 h after a single oral dose administration of procainamide to human subjects is reported.	Procainamide	108-120	NSF attachment protein alpha	Homo sapiens	122-126
9334216-9	1997	Nucleotide concentration greatly affected the ability of NSF to interact with alpha-SNAP.SNARE (soluble NSF attachment protein-SNAP receptor) complex, suggesting that only when the D1 domain ATP-binding sites are occupied does NSF bind to the alpha-SNAP.SNARE complex.	Adenosine Triphosphate	191-194	NSF attachment protein alpha	Homo sapiens	78-88
9315716-3	1997	Analysis of NSF and alpha-SNAP distribution in fractionation of organelles from adrenal medulla indicated that a substantial amount of both proteins distributed with chromaffin granules.	chromaffin	166-176	NSF attachment protein alpha	Homo sapiens	20-30
9331092-1	1997	The aim of this study was to determine the antiproliferative activity of sodium phenylacetate (NaPa) against ovarian carcinoma cell lines.	phenylacetic acid	73-93	NSF attachment protein alpha	Homo sapiens	95-99
9331092-3	1997	Both cisplatin-sensitive and -resistant cell lines responded to NaPa, and growth-inhibitory activity was also detected against cells freshly isolated from malignant ascites of previously treated patients.	Cisplatin	5-14	NSF attachment protein alpha	Homo sapiens	64-68
9315716-5	1997	These results suggest that NSF and alpha-SNAP are associated with chromaffin granules and support the idea that they function prior to docking of the granules on the plasma membrane.	chromaffin	66-76	NSF attachment protein alpha	Homo sapiens	35-45
8477118-6	1993	Her N-acetylprocainamide (NAPA) concentration was elevated to 52 mg/L upon admission.	Acecainide	4-24	NSF attachment protein alpha	Homo sapiens	26-30
8671917-0	1996	Relative efficacy of haemoperfusion, haemodialysis and CAPD in the removal of procainamide and NAPA in a patient with severe procainamide toxicity.	Procainamide	125-137	NSF attachment protein alpha	Homo sapiens	95-99
8786250-1	1995	Procainamide administration often results in excessively high serum N-acetylprocainamide (NAPA) concentrations and subtherapeutic serum procainamide concentrations.	Procainamide	0-12	NSF attachment protein alpha	Homo sapiens	90-94
8786250-2	1995	Inhibition of N-acetylation of procainamide may prevent accumulation of excessive NAPA while maintaining therapeutic serum procainamide concentrations.	Nitrogen	14-15	NSF attachment protein alpha	Homo sapiens	82-86
8786250-2	1995	Inhibition of N-acetylation of procainamide may prevent accumulation of excessive NAPA while maintaining therapeutic serum procainamide concentrations.	Procainamide	31-43	NSF attachment protein alpha	Homo sapiens	82-86
8786250-10	1995	However, concomitant PABA administration with procainamide resulted in increases in NAPA AUC0-00 and t1/2 and reductions in NAPA Ke, procainamide acetylation (NAPA formation) clearance, and NAPA renal clearance.	4-Aminobenzoic Acid	21-25	NSF attachment protein alpha	Homo sapiens	84-88
8786250-10	1995	However, concomitant PABA administration with procainamide resulted in increases in NAPA AUC0-00 and t1/2 and reductions in NAPA Ke, procainamide acetylation (NAPA formation) clearance, and NAPA renal clearance.	4-Aminobenzoic Acid	21-25	NSF attachment protein alpha	Homo sapiens	124-128
8786250-10	1995	However, concomitant PABA administration with procainamide resulted in increases in NAPA AUC0-00 and t1/2 and reductions in NAPA Ke, procainamide acetylation (NAPA formation) clearance, and NAPA renal clearance.	4-Aminobenzoic Acid	21-25	NSF attachment protein alpha	Homo sapiens	124-128
8786250-10	1995	However, concomitant PABA administration with procainamide resulted in increases in NAPA AUC0-00 and t1/2 and reductions in NAPA Ke, procainamide acetylation (NAPA formation) clearance, and NAPA renal clearance.	4-Aminobenzoic Acid	21-25	NSF attachment protein alpha	Homo sapiens	124-128
8786250-10	1995	However, concomitant PABA administration with procainamide resulted in increases in NAPA AUC0-00 and t1/2 and reductions in NAPA Ke, procainamide acetylation (NAPA formation) clearance, and NAPA renal clearance.	Procainamide	46-58	NSF attachment protein alpha	Homo sapiens	84-88
8786250-10	1995	However, concomitant PABA administration with procainamide resulted in increases in NAPA AUC0-00 and t1/2 and reductions in NAPA Ke, procainamide acetylation (NAPA formation) clearance, and NAPA renal clearance.	Procainamide	46-58	NSF attachment protein alpha	Homo sapiens	124-128
8786250-10	1995	However, concomitant PABA administration with procainamide resulted in increases in NAPA AUC0-00 and t1/2 and reductions in NAPA Ke, procainamide acetylation (NAPA formation) clearance, and NAPA renal clearance.	Procainamide	46-58	NSF attachment protein alpha	Homo sapiens	124-128
8786250-10	1995	However, concomitant PABA administration with procainamide resulted in increases in NAPA AUC0-00 and t1/2 and reductions in NAPA Ke, procainamide acetylation (NAPA formation) clearance, and NAPA renal clearance.	Procainamide	46-58	NSF attachment protein alpha	Homo sapiens	124-128
8786250-11	1995	Although PABA inhibits metabolic conversion of procainamide to NAPA, it also impairs the renal clearance of NAPA (but not procainamide) in healthy subjects.	4-Aminobenzoic Acid	9-13	NSF attachment protein alpha	Homo sapiens	63-67
8786250-11	1995	Although PABA inhibits metabolic conversion of procainamide to NAPA, it also impairs the renal clearance of NAPA (but not procainamide) in healthy subjects.	4-Aminobenzoic Acid	9-13	NSF attachment protein alpha	Homo sapiens	108-112
7835334-7	1995	The effect of alpha-SNAP was Ca(2+)- and MgATP-dependent and was inhibited by N-ethylmaleimide and botulinum A neurotoxin, indicating a bona fide action on the exocytotic mechanism.	Adenosine Triphosphate	41-46	NSF attachment protein alpha	Homo sapiens	14-24
7835334-7	1995	The effect of alpha-SNAP was Ca(2+)- and MgATP-dependent and was inhibited by N-ethylmaleimide and botulinum A neurotoxin, indicating a bona fide action on the exocytotic mechanism.	Ethylmaleimide	78-94	NSF attachment protein alpha	Homo sapiens	14-24
7835334-8	1995	Furthermore, Ca2+ concentrations which trigger catecholamine secretion acted to prevent the leakage of NSF and alpha-SNAP from permeabilized cells.	Catecholamines	47-60	NSF attachment protein alpha	Homo sapiens	111-121
7525982-6	1994	As observed after PA administration, NAPA (an active metabolite) had a t1/2 longer than PA of 6.31 +/- 1.49 h. Peak NAPA concentrations (1.91 +/- 0.51 micrograms/ml) occurred at 5.2 h after the PA i.v.	Procainamide	18-20	NSF attachment protein alpha	Homo sapiens	37-41
7525982-6	1994	As observed after PA administration, NAPA (an active metabolite) had a t1/2 longer than PA of 6.31 +/- 1.49 h. Peak NAPA concentrations (1.91 +/- 0.51 micrograms/ml) occurred at 5.2 h after the PA i.v.	Procainamide	39-41	NSF attachment protein alpha	Homo sapiens	116-120
7525982-6	1994	As observed after PA administration, NAPA (an active metabolite) had a t1/2 longer than PA of 6.31 +/- 1.49 h. Peak NAPA concentrations (1.91 +/- 0.51 micrograms/ml) occurred at 5.2 h after the PA i.v.	Procainamide	39-41	NSF attachment protein alpha	Homo sapiens	116-120
8886991-0	1996	Patch-clamp capacitance analysis of the effects of alpha-SNAP on exocytosis in adrenal chromaffin cells.	chromaffin	87-97	NSF attachment protein alpha	Homo sapiens	51-61
8886991-1	1996	We have examined the effect of alpha-SNAP on exocytosis in adrenal chromaffin cells by direct assay of exocytosis using patch-clamp capacitance analysis.	chromaffin	67-77	NSF attachment protein alpha	Homo sapiens	31-41
8886991-7	1996	These results show directly that alpha-SNAP has a specific and marked stimulatory effect on exocytosis in chromaffin cells.	chromaffin	106-116	NSF attachment protein alpha	Homo sapiens	33-43
8844445-1	1996	A study was conducted to evaluate the pharmacokinetics of procainamide and its active metabolite, N-acetylprocainamide (NAPA), as a function of dose and formulation and to characterize the relationship between ventricular premature depolarization (VPD) rate and plasma concentrations of procainamide and NAPA.	Procainamide	58-70	NSF attachment protein alpha	Homo sapiens	120-124
8844445-1	1996	A study was conducted to evaluate the pharmacokinetics of procainamide and its active metabolite, N-acetylprocainamide (NAPA), as a function of dose and formulation and to characterize the relationship between ventricular premature depolarization (VPD) rate and plasma concentrations of procainamide and NAPA.	Acecainide	98-118	NSF attachment protein alpha	Homo sapiens	120-124
8844445-1	1996	A study was conducted to evaluate the pharmacokinetics of procainamide and its active metabolite, N-acetylprocainamide (NAPA), as a function of dose and formulation and to characterize the relationship between ventricular premature depolarization (VPD) rate and plasma concentrations of procainamide and NAPA.	Procainamide	106-118	NSF attachment protein alpha	Homo sapiens	120-124
8844445-4	1996	Maximum and steady-state average concentrations of procainamide and NAPA after administration of Procanbid tablets were equivalent to those after administration of an equivalent daily dose of Procan SR tablets.	Procainamide	97-106	NSF attachment protein alpha	Homo sapiens	68-72
8844445-4	1996	Maximum and steady-state average concentrations of procainamide and NAPA after administration of Procanbid tablets were equivalent to those after administration of an equivalent daily dose of Procan SR tablets.	Procainamide	97-103	NSF attachment protein alpha	Homo sapiens	68-72
8744944-3	1996	Functional evidence for a role of alpha-SNAP in exocytosis in adrenal chromaffin cells comes from the ability of this protein to stimulate Ca(2+)-dependent exocytosis in digitonin-permeabilized cells.	chromaffin	70-80	NSF attachment protein alpha	Homo sapiens	34-44
8744944-3	1996	Functional evidence for a role of alpha-SNAP in exocytosis in adrenal chromaffin cells comes from the ability of this protein to stimulate Ca(2+)-dependent exocytosis in digitonin-permeabilized cells.	Digitonin	170-179	NSF attachment protein alpha	Homo sapiens	34-44
8744944-9	1996	The involvement of the C-terminus of alpha-SNAP, which contains a predicted coiled-coil domain, in the binding of both syntaxin and NSF would place the latter two proteins in proximity in a ternary complex whereupon the energy derived from ATP hydrolysis by NSF could induce a conformational change in syntaxin required for exocytosis to proceed.	Adenosine Triphosphate	240-243	NSF attachment protein alpha	Homo sapiens	37-47
8604041-9	1996	The syntaxin domains required for synaptotagmin binding overlap with the domains for vesicle-associated membrane protein (or VAMP) and alpha-soluble N-ethyl-maleimide-sensitive fusion protein attachment protein (or alphaSNAP) interactions.	Ethylmaleimide	149-166	NSF attachment protein alpha	Homo sapiens	215-224
7501022-1	1995	Several proteins have been implicated in the rapid (millisecond) calcium-controlled release of transmitters at nerve endings, including soluble N-ethylmaleimide-sensitive fusion protein (NSF) and soluble NSF attachment protein (alpha-SNAP), the synaptic SNAP receptor (SNARE) and the calcium-binding protein synaptotagmin, which may function as a calcium sensor in exocytosis.	Calcium	65-72	NSF attachment protein alpha	Homo sapiens	228-238
7657692-7	1995	The data show that these three proteins have distinct stage-specific actions on exocytosis and indicate that alpha-SNAP acts in an early MgATP-requiring stage and not in the late Ca(2+)-triggered steps immediately prior to membrane fusion as previously suggested.	Adenosine Triphosphate	137-142	NSF attachment protein alpha	Homo sapiens	109-119
7622514-6	1995	NSF binds to syntaxin through alpha-SNAP and in the presence of ATP catalyzes a conformational rearrangement which abolishes binding of itself and alpha-SNAP.	Adenosine Triphosphate	64-67	NSF attachment protein alpha	Homo sapiens	147-157
8221884-5	1993	The alpha-SNAP-SNARE complex can bind NSF, and NSF-dependent hydrolysis of ATP dissociates the complex, separating syntaxin, SNAP-25, and VAMP.	Adenosine Triphosphate	75-78	NSF attachment protein alpha	Homo sapiens	4-14
8477118-7	1993	Procainamide was discontinued and her NAPA concentration returned to within normal limits in two days.	Procainamide	0-12	NSF attachment protein alpha	Homo sapiens	38-42
1384320-1	1992	Several extracorporeal techniques have been used to remove N-acetylprocainamide (NAPA), the major metabolite of procainamide, in patients intoxicated with this substance.	Acecainide	59-79	NSF attachment protein alpha	Homo sapiens	81-85
1384320-1	1992	Several extracorporeal techniques have been used to remove N-acetylprocainamide (NAPA), the major metabolite of procainamide, in patients intoxicated with this substance.	Procainamide	67-79	NSF attachment protein alpha	Homo sapiens	81-85
237647-6	1975	Reflecting the blood level differences, the NAPA/procainamide ratio in urine (collected 99 to 180 min after last dose) was found to be higher in rapid than in slow acetylators.	Procainamide	49-61	NSF attachment protein alpha	Homo sapiens	44-48
237647-8	1975	Since NAPA seems to have an antiarrhythmic potency similar to procainamide, NAPA probably contributes to the antiarrhythmic activity of procainamide therapy, especially in genetic rapid acetylators.	Procainamide	136-148	NSF attachment protein alpha	Homo sapiens	76-80
34209933-2	2021	The Napa soil of Tanah Datar district, West Sumatra, Indonesia is a natural material which contains SiO2 and Al2O3 as its major components.	Silicon Dioxide	100-104	NSF attachment protein alpha	Homo sapiens	4-8
34617854-3	2021	Pharmacokinetic analysis of procainamide and its metabolite, N-acetylprocainamide (NAPA), was performed using serum and urine specimens.	Procainamide	28-40	NSF attachment protein alpha	Homo sapiens	83-87
34617854-3	2021	Pharmacokinetic analysis of procainamide and its metabolite, N-acetylprocainamide (NAPA), was performed using serum and urine specimens.	Acecainide	61-81	NSF attachment protein alpha	Homo sapiens	83-87
34209933-2	2021	The Napa soil of Tanah Datar district, West Sumatra, Indonesia is a natural material which contains SiO2 and Al2O3 as its major components.	Aluminum Oxide	109-114	NSF attachment protein alpha	Homo sapiens	4-8
2467982-1	1989	Ranitidine, procainamide and its active N-acetyl metabolite (NAPA) are renally secreted bases which can compete for carrier-mediated transport processes.	Ranitidine	0-10	NSF attachment protein alpha	Homo sapiens	61-65
2474402-1	1989	N-Acetylprocainamide (NAPA) absorption and disposition were profiled in five patients with ventricular arrhythmias by the simultaneous intravenous administration of NAPA-13C and oral administration of a 500 mg NAPA hydrochloride tablet.	Acecainide	0-20	NSF attachment protein alpha	Homo sapiens	22-26
2474402-5	1989	The least-squares estimate of 1.67 for the NAPA renal clearance/creatinine clearance ratio was similar to the value of 1.68 previously reported for functionally anephric patients and showed the expected age-associated decrease.	Creatinine	64-74	NSF attachment protein alpha	Homo sapiens	43-47
2474402-7	1989	Because fast intercompartmental clearance partly reflects splanchnic blood flow, hemodynamic changes may affect NAPA bioavailability, as has been found for procainamide.	Procainamide	156-168	NSF attachment protein alpha	Homo sapiens	112-116
2467982-1	1989	Ranitidine, procainamide and its active N-acetyl metabolite (NAPA) are renally secreted bases which can compete for carrier-mediated transport processes.	Procainamide	12-24	NSF attachment protein alpha	Homo sapiens	61-65
2467982-2	1989	The effect of ranitidine on the disposition of procainamide and NAPA was evaluated in 13 healthy men.	Ranitidine	14-24	NSF attachment protein alpha	Homo sapiens	64-68