PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
24418856-9	2014	Three TTF-1-positive cases were also NapA positive.	Acecainide	37-41	NK2 homeobox 1	Homo sapiens	6-11
17924112-4	2008	Comparative in vitro study performed on rabbit primary chondrocytes revealed that GlcN and NAPA were also able to counteract the IL-1beta-upregulation of genes coding for metalloproteases and inflammatory cytokines.	Acecainide	91-95	interleukin-1 beta	Oryctolagus cuniculus	129-137
21945668-5	2011	In the present study, we found that LMP1 inhibits the expression of NAPA, an endoplasmic reticulum SNARE protein that possesses anti-apoptotic properties against the DNA-damaging drug cisplatin.	Acecainide	68-72	PDZ and LIM domain 7	Homo sapiens	36-40
21945668-8	2011	Similarly, overexpression of NAPA reduced the effect of LMP1 and induced resistance to cisplatin.	Acecainide	29-33	PDZ and LIM domain 7	Homo sapiens	56-60
21945668-10	2011	These findings suggest that the viral protein LMP1 may sensitize cancer cells to cisplatin chemotherapy by downregulating NAPA and by enhancing the formation of p50 homodimers which in turn inhibit the expression of NF-kappaB regulated anti-apoptotic genes.	Acecainide	122-126	PDZ and LIM domain 7	Homo sapiens	46-50
21903092-0	2011	Silencing of the SNARE protein NAPA sensitizes cancer cells to cisplatin by inducing ERK1/2 signaling, synoviolin ubiquitination and p53 accumulation.	Acecainide	31-35	small NF90 (ILF3) associated RNA E	Homo sapiens	17-22
21903092-0	2011	Silencing of the SNARE protein NAPA sensitizes cancer cells to cisplatin by inducing ERK1/2 signaling, synoviolin ubiquitination and p53 accumulation.	Acecainide	31-35	mitogen-activated protein kinase 3	Homo sapiens	85-91
21903092-0	2011	Silencing of the SNARE protein NAPA sensitizes cancer cells to cisplatin by inducing ERK1/2 signaling, synoviolin ubiquitination and p53 accumulation.	Acecainide	31-35	tumor protein p53	Homo sapiens	133-136
21903092-1	2011	We found earlier that NAPA represents an anti-apoptotic protein that promotes resistance to cisplatin in cancer cells by inducing the degradation of the tumor suppressor p53.	Acecainide	22-26	tumor protein p53	Homo sapiens	170-173
21903092-2	2011	In the present study, we investigated the cellular mechanism underlying the degradation of p53 by NAPA.	Acecainide	98-102	tumor protein p53	Homo sapiens	91-94
21903092-3	2011	Knockdown of NAPA using short-hairpin RNA was shown to induce p53 accumulation and to sensitize HEK293 cells to cisplatin.	Acecainide	13-17	tumor protein p53	Homo sapiens	62-65
21903092-5	2011	Expression of exogenous p53 in H1299 cells was increased following knockdown of NAPA and these cells showed increased sensitivity to cisplatin-induced apoptosis.	Acecainide	80-84	tumor protein p53	Homo sapiens	24-27
21903092-6	2011	Notably, knockdown of NAPA induced the ubiquitination and degradation of the E3 ubiquitin ligase synoviolin and the accumulation of p53 in unstressed HEK293 cells.	Acecainide	22-26	tumor protein p53	Homo sapiens	132-135
21903092-7	2011	Conversely, NAPA overexpression decreased the ubiquitination and degradation of synoviolin, and reduced p53 protein level.	Acecainide	12-16	tumor protein p53	Homo sapiens	104-107
21903092-8	2011	Knockdown of NAPA disrupted the interaction between synoviolin and proteins that form the endoplasmic reticulum-associated degradation (ERAD) complex and in turn decreased the ability of this complex to ubiquitinate p53.	Acecainide	13-17	tumor protein p53	Homo sapiens	216-219
21903092-9	2011	In addition, knockdown of NAPA induced the activation of the MAPK kinases ERK, JNK and p38, but only inhibition of ERK reduced synoviolin ubiquitination and p53 accumulation.	Acecainide	26-30	mitogen-activated protein kinase 3	Homo sapiens	61-65
21903092-9	2011	In addition, knockdown of NAPA induced the activation of the MAPK kinases ERK, JNK and p38, but only inhibition of ERK reduced synoviolin ubiquitination and p53 accumulation.	Acecainide	26-30	mitogen-activated protein kinase 1	Homo sapiens	74-77
21903092-9	2011	In addition, knockdown of NAPA induced the activation of the MAPK kinases ERK, JNK and p38, but only inhibition of ERK reduced synoviolin ubiquitination and p53 accumulation.	Acecainide	26-30	mitogen-activated protein kinase 8	Homo sapiens	79-82
21903092-9	2011	In addition, knockdown of NAPA induced the activation of the MAPK kinases ERK, JNK and p38, but only inhibition of ERK reduced synoviolin ubiquitination and p53 accumulation.	Acecainide	26-30	mitogen-activated protein kinase 1	Homo sapiens	87-90
21903092-9	2011	In addition, knockdown of NAPA induced the activation of the MAPK kinases ERK, JNK and p38, but only inhibition of ERK reduced synoviolin ubiquitination and p53 accumulation.	Acecainide	26-30	tumor protein p53	Homo sapiens	157-160
21903092-10	2011	These results indicate that NAPA promotes resistance to cisplatin through synoviolin and the ERAD complex which together induce the degradation of p53 and thus prevent apoptosis.	Acecainide	28-32	tumor protein p53	Homo sapiens	147-150
21903092-11	2011	Based on these findings, we propose that the combination of cisplatin and knockdown of NAPA represents a novel and attractive strategy to eradicate p53-sensitive cancer cells.	Acecainide	87-91	tumor protein p53	Homo sapiens	148-151
29147265-3	2011	Methods: The HBA-71 monoclonal antibody directed to the CD99/MIC2 antigen was used to stain a human osteoblast cell line as well as the two EFT cell lines KAL and EW-2 after pretreatment of the cells with the differentiation inducers calcitriol and the histone deacetylase (HDAC) inhibitors sodium butyrate (NaB), sodium phenylacetate (NaPA) as well as N, N"-hexamethylen-bis-acetamide (HMBA).	Acecainide	336-340	CD99 molecule (Xg blood group)	Homo sapiens	13-19
18953652-3	2009	To clarify the molecular mechanism of these effects, we examined the expression of Ras/MAPK signaling pathway-related molecules in human and canine breast cancer cell lines, and found that the level of c-Raf-1 protein was reduced by 5, 10 and 20 mM of NaPA treatments, though Ras activation was maintained.	Acecainide	252-256	mitogen-activated protein kinase 1	Canis lupus familiaris	87-91
18953652-3	2009	To clarify the molecular mechanism of these effects, we examined the expression of Ras/MAPK signaling pathway-related molecules in human and canine breast cancer cell lines, and found that the level of c-Raf-1 protein was reduced by 5, 10 and 20 mM of NaPA treatments, though Ras activation was maintained.	Acecainide	252-256	TNF receptor associated factor 3	Homo sapiens	202-209
18953652-4	2009	Dephosphorylation of c-Raf-1 at Serine (Ser) 259, Ser 338, and Ser 621 were also seen in NaPA-treated cells.	Acecainide	89-93	TNF receptor associated factor 3	Homo sapiens	21-28
18953652-7	2009	Furthermore, expression of an epithelial marker, E-cadherin, was increased by NaPA treatment.	Acecainide	78-82	cadherin 1	Canis lupus familiaris	49-59
18953652-8	2009	These results suggest that one of the molecular targets of NaPA treatment was the reduction of c-Raf-1 protein, and that its reduction results in the decrease of malignant characteristics of tumor cells through blockage of the Ras/MAPK signaling pathway.	Acecainide	59-63	TNF receptor associated factor 3	Homo sapiens	95-102
18953652-8	2009	These results suggest that one of the molecular targets of NaPA treatment was the reduction of c-Raf-1 protein, and that its reduction results in the decrease of malignant characteristics of tumor cells through blockage of the Ras/MAPK signaling pathway.	Acecainide	59-63	mitogen-activated protein kinase 1	Canis lupus familiaris	231-235
20113495-4	2010	METHODS: The human chondrosarcoma cell line HTB-94 and human primary chondrocytes were stimulated with tumor necrosis factor (TNF)alpha after pre-treatment with GlcN or NAPA.	Acecainide	169-173	tumor necrosis factor	Homo sapiens	103-124
20113495-8	2010	RESULTS: After TNFalpha stimulation, the mRNA expression level of some of the genes under NF-kappaB control, such as interleukin (IL)-6 and IL-8, increased, while treatment with GlcN and NAPA reverted the effect.	Acecainide	187-191	tumor necrosis factor	Homo sapiens	15-23
20113495-8	2010	RESULTS: After TNFalpha stimulation, the mRNA expression level of some of the genes under NF-kappaB control, such as interleukin (IL)-6 and IL-8, increased, while treatment with GlcN and NAPA reverted the effect.	Acecainide	187-191	C-X-C motif chemokine ligand 8	Homo sapiens	140-144
20113495-9	2010	We investigated the possibility that GlcN and NAPA inhibit IKK kinase activity and found that NAPA inhibits the IKKalpha kinase activity, whereas GlcN does not.	Acecainide	46-50	component of inhibitor of nuclear factor kappa B kinase complex	Homo sapiens	59-62
20113495-9	2010	We investigated the possibility that GlcN and NAPA inhibit IKK kinase activity and found that NAPA inhibits the IKKalpha kinase activity, whereas GlcN does not.	Acecainide	94-98	component of inhibitor of nuclear factor kappa B kinase complex	Homo sapiens	59-62
20113495-9	2010	We investigated the possibility that GlcN and NAPA inhibit IKK kinase activity and found that NAPA inhibits the IKKalpha kinase activity, whereas GlcN does not.	Acecainide	94-98	component of inhibitor of nuclear factor kappa B kinase complex	Homo sapiens	112-120
20113495-10	2010	Interestingly, both GlcN and NAPA inhibit IKKalpha nuclear re-localization.	Acecainide	29-33	component of inhibitor of nuclear factor kappa B kinase complex	Homo sapiens	42-50
20113495-13	2010	While NAPA can both specifically inhibit the IKKalpha kinase activity and IKKalpha nuclear re-localization, GlcN only acts on IKKalpha nuclear re-localization.	Acecainide	6-10	component of inhibitor of nuclear factor kappa B kinase complex	Homo sapiens	45-53
20113495-13	2010	While NAPA can both specifically inhibit the IKKalpha kinase activity and IKKalpha nuclear re-localization, GlcN only acts on IKKalpha nuclear re-localization.	Acecainide	6-10	component of inhibitor of nuclear factor kappa B kinase complex	Homo sapiens	74-82
20113495-13	2010	While NAPA can both specifically inhibit the IKKalpha kinase activity and IKKalpha nuclear re-localization, GlcN only acts on IKKalpha nuclear re-localization.	Acecainide	6-10	component of inhibitor of nuclear factor kappa B kinase complex	Homo sapiens	74-82
19414384-3	2009	In MDA-MB-231 cells, NaPa also induced (i) an autophagic process evidenced by the appearance of autophagic vacuoles and an increased phosphatase acid activity, (ii) the formation of pseudopodia and (iii) an increase in MMP-1 and MMP-9 secretion without affecting MT1-MMP.	Acecainide	21-25	matrix metallopeptidase 1	Homo sapiens	219-224
19414384-3	2009	In MDA-MB-231 cells, NaPa also induced (i) an autophagic process evidenced by the appearance of autophagic vacuoles and an increased phosphatase acid activity, (ii) the formation of pseudopodia and (iii) an increase in MMP-1 and MMP-9 secretion without affecting MT1-MMP.	Acecainide	21-25	matrix metallopeptidase 9	Homo sapiens	229-234
19414384-3	2009	In MDA-MB-231 cells, NaPa also induced (i) an autophagic process evidenced by the appearance of autophagic vacuoles and an increased phosphatase acid activity, (ii) the formation of pseudopodia and (iii) an increase in MMP-1 and MMP-9 secretion without affecting MT1-MMP.	Acecainide	21-25	matrix metallopeptidase 14	Homo sapiens	263-270
18173918-2	2007	We analyzed the influence of GlcN and its N-acetyl-phenylalanine derivative (NAPA) on mRNA transcription level of TNF-alpha-stimulated genes in cell culture.	Acecainide	77-81	tumor necrosis factor	Homo sapiens	114-123
19127062-6	2008	Furthermore, X-ALD lymphoblasts produced higher levels of nitric oxide (NO) and cytokines (tumor necrosis factor-alpha and interleukin 1 beta), and treatment with NaPA or lovastatin decreased the synthesis of NO.	Acecainide	163-167	tumor necrosis factor	Homo sapiens	91-118
19127062-6	2008	Furthermore, X-ALD lymphoblasts produced higher levels of nitric oxide (NO) and cytokines (tumor necrosis factor-alpha and interleukin 1 beta), and treatment with NaPA or lovastatin decreased the synthesis of NO.	Acecainide	163-167	interleukin 1 beta	Homo sapiens	123-141
18173918-5	2007	RESULTS: Several genes, whose mRNA level was increased by TNF-alpha treatment and significantly reduced by GlcN and NAPA in lbpva55 cells, were identified.	Acecainide	116-120	tumor necrosis factor	Homo sapiens	58-67
16581519-7	2006	Furthermore, several aspects of the napA phenotype are more severe than those evoked by the absence of SCAR alone.	Acecainide	36-40	ribosomal protein S4 X-linked	Homo sapiens	103-107
17161819-3	2007	In this study, three types of short chain fatty acids (sodium butyrate (NaB), sodium phenylbutyrate (NaPB), sodium phenylacetate (NaPA)) were found to have anti-inflammatory effects in IFN-gamma-stimulated RAW 264.7 cells.	Acecainide	130-134	interferon gamma	Mus musculus	185-194
17161819-5	2007	Their potency as anti-inflammatory agents was in the order of NaB>NaPB>NaPA.	Acecainide	77-81	N-ethylmaleimide sensitive fusion protein attachment protein beta	Mus musculus	69-73
17161819-8	2007	The potency of NF-kappaB and ERK inhibition was also in the order of NaB>NaPB>NaPA.	Acecainide	84-88	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	15-24
17161819-8	2007	The potency of NF-kappaB and ERK inhibition was also in the order of NaB>NaPB>NaPA.	Acecainide	84-88	mitogen-activated protein kinase 1	Mus musculus	29-32
17074894-4	2006	A bacterial two-hybrid protein-protein interaction system was used to demonstrate that NapF interacted in the cytoplasm with the terminal oxidoreductase NapA, but that it did not self-associate or interact with other electron-transport components of the Nap system, NapC, NapG or NapH, or with another cytoplasmic component, NapD.	Acecainide	153-157	oxidoreductase	Escherichia coli	138-152
16839052-4	2005	Evidence comes from matching experimental and theoretical data for all three constituent N-H stretches of NAPA, with a Delta(Experimental-Theoretical) = approximately 1-3 cm(-1), approximately 0-5 cm(-1), and approximately 1-6 cm(-1), at the L/61fp and B/6+ levels, respectively.	Acecainide	106-110	immunoglobulin kappa variable 3-11	Homo sapiens	242-256
11939777-2	2002	The NapB protein is essential in transferring electrons to the large catalytic subunit NapA, which subsequently reduces nitrate to nitrite.	Acecainide	87-91	NSF attachment protein beta	Homo sapiens	4-8
12646656-4	2003	However, pretreatment of MBP-primed T cells with NaPA markedly inhibited its ability to induce microglial expression of iNOS and activation of NF-kappaB.	Acecainide	49-53	myelin basic protein	Mus musculus	25-28
12646656-4	2003	However, pretreatment of MBP-primed T cells with NaPA markedly inhibited its ability to induce microglial expression of iNOS and activation of NF-kappaB.	Acecainide	49-53	nitric oxide synthase 2, inducible	Mus musculus	120-124
12646656-6	2003	Furthermore, MBP-primed T cells isolated from NaPA-treated donor mice were also less efficient than MBP-primed T cells isolated from normal donor mice in inducing iNOS in microglial cells and transferring EAE to recipient mice.	Acecainide	46-50	myelin basic protein	Homo sapiens	13-16
12646656-6	2003	Furthermore, MBP-primed T cells isolated from NaPA-treated donor mice were also less efficient than MBP-primed T cells isolated from normal donor mice in inducing iNOS in microglial cells and transferring EAE to recipient mice.	Acecainide	46-50	nitric oxide synthase 2, inducible	Mus musculus	163-167
12646656-9	2003	Histological and immunocytochemical analysis showed that NaPA inhibited EAE-induced spinal cord mononuclear cell invasion and normalized iNOS, nitrotyrosine, and p65 (the RelA subunit of NF-kappaB) expression within the spinal cord.	Acecainide	57-61	nitric oxide synthase 2, inducible	Mus musculus	137-141
12646656-9	2003	Histological and immunocytochemical analysis showed that NaPA inhibited EAE-induced spinal cord mononuclear cell invasion and normalized iNOS, nitrotyrosine, and p65 (the RelA subunit of NF-kappaB) expression within the spinal cord.	Acecainide	57-61	v-rel reticuloendotheliosis viral oncogene homolog A (avian)	Mus musculus	162-165
12089365-10	2002	The uptake of TEA mediated by hOCT2-A but not by hOCT2 was inhibited significantly by organic cations such as procainamide, N-acetylprocainamide, and levofloxacin, indicating that hOCT2-A differs from hOCT2 in its affinity for several compounds.	Acecainide	124-144	POU class 2 homeobox 2	Homo sapiens	30-35
11939777-8	2002	We propose a hypothetical but plausible model of the NapAB complex in which the four redox centers are positioned in a virtually linear configuration which spans a distance of nearly 40 A, suggesting an efficient pathway for the transfer of electrons from NapC, the physiological electron donor of NapB, to a nitrate molecule at the catalytic site of NapA.	Acecainide	53-57	NSF attachment protein beta	Homo sapiens	298-302
9703924-10	1998	Among growth factors secreted by MCF-7 and MCF-7ras, TGF beta synthesis is inhibited and stimulated in MCF-7 and MCF-7ras cells respectively after NaPa treatment.	Acecainide	147-151	transforming growth factor beta 1	Homo sapiens	53-61
11029704-5	2000	Deletion of the conserved B2 and B3 domains of ABI3 abolished transactivation of napA by ABI3.	Acecainide	81-85	B3 domain-containing transcription factor ABI3-like	Brassica napus	47-51
11029704-5	2000	Deletion of the conserved B2 and B3 domains of ABI3 abolished transactivation of napA by ABI3.	Acecainide	81-85	B3 domain-containing transcription factor ABI3-like	Brassica napus	89-93
9511735-2	1998	Our studies indicated that NaPA can impact on the RA differentiation program by upregulating nuclear retinoic acid receptor-beta (RAR beta) expression.	Acecainide	27-31	retinoic acid receptor beta	Homo sapiens	101-128
9673780-10	1998	In addition, there was a significant reduction in the amount of N-acetylprocainamide formed after 8 weeks of exercise (AUCNAPA = 739 ng mL-1 min-1).	Acecainide	64-84	L1 cell adhesion molecule	Mus musculus	136-146
10076540-3	1998	Monomorphic (NAT1) and polymorphic (NAT2) activities were determined using N-acetylprocainamide and N-acetamidobenzoic acid formation, respectively.	Acecainide	75-95	N-acetyltransferase 2	Rattus norvegicus	36-40
9511735-2	1998	Our studies indicated that NaPA can impact on the RA differentiation program by upregulating nuclear retinoic acid receptor-beta (RAR beta) expression.	Acecainide	27-31	retinoic acid receptor beta	Homo sapiens	130-138
9511735-4	1998	In contrast, NaPA was able to specifically activate a reporter gene construct (delta SV beta RE-CAT) which contains a retinoic acid response element (RARE beta) that is located in the RAR beta promoter.	Acecainide	13-17	retinoic acid receptor beta	Homo sapiens	184-192
9511735-6	1998	Taken together, our findings suggest that induction of RAR beta by NaPA is regulated at the level of transcription and mediated through the retinoic acid response element, RARE beta.	Acecainide	67-71	retinoic acid receptor beta	Homo sapiens	55-63
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
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
9389730-5	1997	Inhibition of LPS-mediated activation of NF-kbeta by lovastatin, NaPA, and FPT inhibitor II in astrocytes indicates that the observed inhibition of iNOS expression is mediated via inhibition of NF-kbeta activation.	Acecainide	65-69	nitric oxide synthase 2	Rattus norvegicus	148-152
9389730-6	1997	In addition to iNOS, lovastatin and NaPA also inhibited LPS-induced expression of TNF-alpha, IL-1beta, and IL-6 in rat primary astrocytes, microglia, and macrophages.	Acecainide	36-40	tumor necrosis factor	Rattus norvegicus	82-91
9389730-6	1997	In addition to iNOS, lovastatin and NaPA also inhibited LPS-induced expression of TNF-alpha, IL-1beta, and IL-6 in rat primary astrocytes, microglia, and macrophages.	Acecainide	36-40	interleukin 1 beta	Rattus norvegicus	93-101
9389730-6	1997	In addition to iNOS, lovastatin and NaPA also inhibited LPS-induced expression of TNF-alpha, IL-1beta, and IL-6 in rat primary astrocytes, microglia, and macrophages.	Acecainide	36-40	interleukin 6	Rattus norvegicus	107-111
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
9389730-2	1997	Lovastatin and sodium phenylacetate (NaPA) were found to inhibit LPS- and cytokine-mediated production of NO and expression of iNOS in rat primary astrocytes; this inhibition was not due to depletion of end products of mevalonate pathway (e.g., cholesterol and ubiquinone).	Acecainide	37-41	nitric oxide synthase 2	Rattus norvegicus	127-131
9389730-3	1997	Reversal of the inhibitory effect of lovastatin on LPS-induced iNOS expression by mevalonate and farnesyl pyrophosphate and reversal of the inhibitory effect of NaPA on LPS-induced iNOS expression by farnesyl pyrophosphate, however, suggests a role of farnesylation in the LPS-mediated induction of iNOS.	Acecainide	161-165	nitric oxide synthase 2	Rattus norvegicus	181-185
9389730-3	1997	Reversal of the inhibitory effect of lovastatin on LPS-induced iNOS expression by mevalonate and farnesyl pyrophosphate and reversal of the inhibitory effect of NaPA on LPS-induced iNOS expression by farnesyl pyrophosphate, however, suggests a role of farnesylation in the LPS-mediated induction of iNOS.	Acecainide	161-165	nitric oxide synthase 2	Rattus norvegicus	181-185
9164413-6	1997	The N-acetylprocainamide/procainamide ratio in urinary excretion was 0.60 +/- 0.17 (mean +/- SD) for those with NAT2*4/*4, 0.37 +/- 0.06 for NAT2*4/*6A, 0.40 +/- 0.03 for NAT2*4/*7B, and 0.17 for NAT2*6A/*7B.	Acecainide	4-24	N-acetyltransferase 2	Homo sapiens	112-116
9067263-7	1997	Furthermore, in vitro administration of 4-OH-tamoxifen induced a Bcl-2 up-regulation in MCF-7ras cells, which was completely abolished by NaPA pretreatment.	Acecainide	138-142	BCL2 apoptosis regulator	Homo sapiens	65-70
7585564-3	1995	Western blot analysis showed a Bcl-2 down-regulation after 48 h treatment with 5 mM NaPA, together with apparition of apoptotic nuclei by DAPI staining.	Acecainide	84-88	BCL2 apoptosis regulator	Homo sapiens	31-36
7691251-3	1993	We show here that sodium phenylacetate (NaPA) and its precursor, sodium 4-phenylbutyrate (NaPB), can enhance HbF production in cultured erythroid progenitor derived from normal donors and patients with SS anemia or beta-thal, when used at pharmacologic concentrations.	Acecainide	40-44	NSF attachment protein beta	Homo sapiens	90-94
7829265-3	1995	Using the LA-N-5 cell line, we have determined that NaPA can stimulate the differentiation of neuroblastoma cells, as evidenced by dose-dependent inhibition of cell proliferation, neurite outgrowth, increased acetylcholinesterase activity and reduction of N-myc expression.	Acecainide	52-56	MYCN proto-oncogene, bHLH transcription factor	Homo sapiens	256-261
7829265-5	1995	We have determined that NaPA can markedly enhance mRNA levels of the nuclear RA receptor-beta (RAR beta) in LA-N-5 cells prior to morphologic or other phenotypic changes induced by this compound.	Acecainide	24-28	retinoic acid receptor beta	Homo sapiens	95-103
7829265-7	1995	Thus among its varied effects on LA-N-5 cells, NaPA appears to interact with the RA pathway at the nuclear level by up-regulating RAR beta expression.	Acecainide	47-51	retinoic acid receptor beta	Homo sapiens	130-138
8180967-4	1994	The proportion of differentiated myosin-positive cells which was around 0.8-1.7% in control cultures 12 days after seeding was increased by NaPA treatment up to 47%.	Acecainide	140-144	myosin heavy chain 14	Homo sapiens	33-39
8202632-4	1994	Livers were removed 24 hr after the last dose and NAT activity was determined by measuring the formation of N-acetylprocainamide in cytosolic incubations in the presence of 0.42 mM acetyl CoA.	Acecainide	108-128	N-acetyltransferase 1	Rattus norvegicus	50-53
8486788-3	1993	NaPA treatment of androgen-independent PC3 and DU145 prostate cell lines, like that of hormone-responsive LNCaP cultures, resulted in dose-dependent inhibition of cell proliferation.	Acecainide	0-4	chromobox 8	Homo sapiens	39-42
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
34363898-17	2021	In addition, a novel negative correlation between FOXP3 mRNA levels and napA was shown in patients with gastritis and ulcer (r=-0.59).	Acecainide	72-76	forkhead box P3	Homo sapiens	50-55
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
2187866-7	1990	When cells were photolabeled with 125I-B2(2-nitro-4-azidophenylacetyl)-des-PheB1 (NAPA)-insulin, the proreceptor incorporated 10% as much label as the 130-kDa alpha subunit in spite of a 5-fold molar excess.	Acecainide	82-86	insulin	Homo sapiens	88-95
2187866-9	1990	Immunoprecipitation of NAPA-insulin-stimulated cells with anti-phosphotyrosine antibodies revealed that 62% of the processed labeled receptors, but very little proreceptor, contained phosphotyrosine.	Acecainide	23-27	insulin	Homo sapiens	28-35
34452094-7	2021	A physiological model for the pharmacokinetics of PA and NAPA in rats was useful for linking changes in the transcriptional and translational expressions of rOCTs and rMATE1 transporters to the altered pharmacokinetics of the drugs.	Acecainide	57-61	solute carrier family 47 member 1	Rattus norvegicus	167-173
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
2431636-5	1986	In 2 dogs (previously used in part II), N-acetylprocainamide (NAPA) was administered IV at a dose of 10 mg/kg.	Acecainide	40-60	NSF attachment protein alpha	Canis lupus familiaris	62-66
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
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
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
2479226-4	1989	Procainamide (PA) and N-acetylprocainamide (Acekainide, NAPA) display many undesired side effects, too.	Acecainide	22-42	alpha-soluble NSF attachment protein	Oryctolagus cuniculus	56-60
2483600-4	1989	Its active metabolite, N-acetylprocainamide (NAPA; Acecainide) is known to affect less noxiously the ventriculo-atrial conduction and the intraventricular++ conduction, and it does not impair contractility of the heart muscle.	Acecainide	51-61	alpha-soluble NSF attachment protein	Oryctolagus cuniculus	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
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
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
2416904-1	1985	The aim of this study was to investigate the possible influence of the time of administration on procainamide and N-acetylprocainamide (NAPA) kinetics in the rat.	Acecainide	114-134	NSF attachment protein alpha	Rattus norvegicus	136-140
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
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
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
310748-4	1979	Mean PEP/LVET, measured while the patients received placebo, was elevated at the beginning of the study but was normal after one year of NAPA therapy.	Acecainide	137-141	progestagen associated endometrial protein	Homo sapiens	5-8
6167356-1	1981	The major metabolite of procainamide (PA) is N-acetylprocainamide (NAPA).	Acecainide	45-65	NSF attachment protein alpha	Canis lupus familiaris	67-71
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
6175815-1	1982	The hypotensive effects of N-acetylprocainamide (NAPA) were studied in anesthetized dogs and in a normal subject.	Acecainide	27-47	NSF attachment protein alpha	Canis lupus familiaris	49-53
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
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
310748-5	1979	Comparison of NAPA and placebo period observations indicated a reduction in PEP/LVET when NAPA therapy was begun.	Acecainide	14-18	progestagen associated endometrial protein	Homo sapiens	76-79
310748-5	1979	Comparison of NAPA and placebo period observations indicated a reduction in PEP/LVET when NAPA therapy was begun.	Acecainide	90-94	progestagen associated endometrial protein	Homo sapiens	76-79
310748-7	1979	The apparent dependence of this effect on underlying status of left ventricular function suggests that the initial reduction in PEP/LVET represents an an indirect effect of NAPA rather than a direct inotropic action.	Acecainide	173-177	progestagen associated endometrial protein	Homo sapiens	128-131
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
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
618730-1	1978	The antiarrhythmic potency of procainamide (PA) and N-acetylprocainamide (NAPA) has been investigated in rabbits using isolated atrial preparations and ouabain-induced ventricular fibrillation in vivo.	Acecainide	52-72	alpha-soluble NSF attachment protein	Oryctolagus cuniculus	74-78
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
17895-8	1977	Mean ClR and mean ClB values were smaller with NAPA while both compounds showed similar dependence upon renal and non-renal clearance mechanisms.	Acecainide	47-51	citramalyl-CoA lyase	Homo sapiens	18-21
31461854-5	2019	Both NapA group and NapA+LtB group had elevated splenocyte production of IL-8, IL-10, IL-12, IL-17, IL-23 and INF-gamma.	Acecainide	20-24	lymphotoxin beta	Homo sapiens	25-28
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
29965477-5	2018	The analysis of the nitrogen conversion characteristics in two regions showed that the AOB had been in a dominant position in the aerobic zone, and the NOB was inhibited by DO and the matrix, NPRa increased from 0.22 kg (m3 d)-1 to 0.58 kg (m3 d)-1, and NAPa could reach 95% with the increase in anaerobic denitrification capacity.	Acecainide	254-258	natriuretic peptide receptor 1	Homo sapiens	192-196
30845766-3	2019	The primary objective of this study was to construct a physiological model that describes pharmacokinetic interactions between PA/NAPA and cimetidine, an inhibitor of rat organic cation transporter 2 (rOCT2) and rat multidrug and toxin extrusion proteins (rMATE1), by performing extensive in vivo and in vitro pharmacokinetic studies for PA and NAPA performed in the absence or presence of cimetidine in rats.	Acecainide	130-134	solute carrier family 22 member 2	Rattus norvegicus	171-199
30845766-3	2019	The primary objective of this study was to construct a physiological model that describes pharmacokinetic interactions between PA/NAPA and cimetidine, an inhibitor of rat organic cation transporter 2 (rOCT2) and rat multidrug and toxin extrusion proteins (rMATE1), by performing extensive in vivo and in vitro pharmacokinetic studies for PA and NAPA performed in the absence or presence of cimetidine in rats.	Acecainide	130-134	solute carrier family 22 member 2	Rattus norvegicus	201-206
30845766-3	2019	The primary objective of this study was to construct a physiological model that describes pharmacokinetic interactions between PA/NAPA and cimetidine, an inhibitor of rat organic cation transporter 2 (rOCT2) and rat multidrug and toxin extrusion proteins (rMATE1), by performing extensive in vivo and in vitro pharmacokinetic studies for PA and NAPA performed in the absence or presence of cimetidine in rats.	Acecainide	130-134	solute carrier family 47 member 1	Rattus norvegicus	256-262
30845766-3	2019	The primary objective of this study was to construct a physiological model that describes pharmacokinetic interactions between PA/NAPA and cimetidine, an inhibitor of rat organic cation transporter 2 (rOCT2) and rat multidrug and toxin extrusion proteins (rMATE1), by performing extensive in vivo and in vitro pharmacokinetic studies for PA and NAPA performed in the absence or presence of cimetidine in rats.	Acecainide	345-349	solute carrier family 22 member 2	Rattus norvegicus	201-206
30845766-8	2019	Moreover, sensitivity analyses of the pharmacokinetics of PA and NAPA showed the inhibitory effects of cimetidine via rMATE1 were probably important for the renal elimination of PA and NAPA in rats.	Acecainide	65-69	solute carrier family 47 member 1	Rattus norvegicus	118-124
30845766-8	2019	Moreover, sensitivity analyses of the pharmacokinetics of PA and NAPA showed the inhibitory effects of cimetidine via rMATE1 were probably important for the renal elimination of PA and NAPA in rats.	Acecainide	185-189	solute carrier family 47 member 1	Rattus norvegicus	118-124
27836674-2	2017	The ability of N-acetyl phenylalanine derivative (NAPA) to increase cartilage matrix components and to reduce inflammatory cytokines, inhibiting IKKalpha kinase activity, has been observed in vitro.	Acecainide	50-54	conserved helix-loop-helix ubiquitous kinase	Mus musculus	145-153
27836674-6	2017	RESULTS: The injection of NAPA significantly improved cartilage thickness (CT) and reduced Chambers and Mankin modified scores and fibrillation index (FI), with weaker MMP13, ADAMTS5, MMP10 and IKKalpha staining.	Acecainide	26-30	matrix metallopeptidase 13	Mus musculus	168-173
27836674-6	2017	RESULTS: The injection of NAPA significantly improved cartilage thickness (CT) and reduced Chambers and Mankin modified scores and fibrillation index (FI), with weaker MMP13, ADAMTS5, MMP10 and IKKalpha staining.	Acecainide	26-30	a disintegrin-like and metallopeptidase (reprolysin type) with thrombospondin type 1 motif, 5 (aggrecanase-2)	Mus musculus	175-182
27836674-6	2017	RESULTS: The injection of NAPA significantly improved cartilage thickness (CT) and reduced Chambers and Mankin modified scores and fibrillation index (FI), with weaker MMP13, ADAMTS5, MMP10 and IKKalpha staining.	Acecainide	26-30	matrix metallopeptidase 10	Mus musculus	184-189
27836674-6	2017	RESULTS: The injection of NAPA significantly improved cartilage thickness (CT) and reduced Chambers and Mankin modified scores and fibrillation index (FI), with weaker MMP13, ADAMTS5, MMP10 and IKKalpha staining.	Acecainide	26-30	conserved helix-loop-helix ubiquitous kinase	Mus musculus	194-202
27836674-8	2017	CONCLUSIONS: NAPA markedly improved the physical structure of articular cartilage while reducing catabolic enzymes, extracellular matrix (ECM) remodeling and IKKalpha expression, showing to be able to exert a chondroprotective activity in vivo.	Acecainide	13-17	conserved helix-loop-helix ubiquitous kinase	Mus musculus	158-166
28154142-6	2017	Consistently, the equivalent residue to K305 in human NHA2 has been replaced with arginine, which is a mutation that makes NapA electroneutral.	Acecainide	123-127	solute carrier family 9 member B2	Homo sapiens	54-58