PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
29518627-3	2018	Our previous study demonstrated that HDAC inhibitor phenylbutyrate (PB) could induce AML1-ETO positive leukemia cell line Kasumi-1 cells to undergo differentiation and apoptosis accompanied by significant changes in gene expression profile.	Phenylbutyrates	52-66	RUNX family transcription factor 1	Homo sapiens	85-89
30562925-14	2018	However, 3 days of exposure to butyrate (1 to 8 mM) or other HDAC inhibitors such as phenylbutyrate, valproic acid and trichostatin stimulated OPG secretion.	Phenylbutyrates	85-99	TNF receptor superfamily member 11b	Homo sapiens	143-146
29755574-5	2018	Increased BCKD activity is responsible for enhanced oxidation of BCAA in chronic renal failure, trauma, burn, sepsis, cancer, phenylbutyrate-treated subjects, and during exercise.	Phenylbutyrates	126-140	AT-rich interaction domain 4B	Homo sapiens	65-69
29518627-3	2018	Our previous study demonstrated that HDAC inhibitor phenylbutyrate (PB) could induce AML1-ETO positive leukemia cell line Kasumi-1 cells to undergo differentiation and apoptosis accompanied by significant changes in gene expression profile.	Phenylbutyrates	52-66	RUNX1 partner transcriptional co-repressor 1	Homo sapiens	90-93
29518627-3	2018	Our previous study demonstrated that HDAC inhibitor phenylbutyrate (PB) could induce AML1-ETO positive leukemia cell line Kasumi-1 cells to undergo differentiation and apoptosis accompanied by significant changes in gene expression profile.	Phenylbutyrates	68-70	RUNX family transcription factor 1	Homo sapiens	85-89
29518627-3	2018	Our previous study demonstrated that HDAC inhibitor phenylbutyrate (PB) could induce AML1-ETO positive leukemia cell line Kasumi-1 cells to undergo differentiation and apoptosis accompanied by significant changes in gene expression profile.	Phenylbutyrates	68-70	RUNX1 partner transcriptional co-repressor 1	Homo sapiens	90-93
29518627-4	2018	ZFP36L2 was one of the up-regulated genes in Kasumi-1 cells induced by PB treatment.	Phenylbutyrates	71-73	ZFP36 ring finger protein like 2	Homo sapiens	0-7
25601413-0	2015	Differential inhibition of PDKs by phenylbutyrate and enhancement of pyruvate dehydrogenase complex activity by combination with dichloroacetate.	Phenylbutyrates	35-49	pyruvate dehydrogenase kinase 2	Homo sapiens	27-31
28501528-6	2017	And the process above could be inhibited by a BCKDK inhibitor, phenyl butyrate.	Phenylbutyrates	63-78	branched chain keto acid dehydrogenase kinase	Homo sapiens	46-51
27911272-7	2017	Overexpression of FOXO4 was evident in lymphoma cells surviving after phenylbutyrate treatment and refractory patient-derived lymphoma cells.	Phenylbutyrates	70-84	forkhead box O4	Homo sapiens	18-23
27297240-0	2016	Tauopathy induced by low level expression of a human brain-derived tau fragment in mice is rescued by phenylbutyrate.	Phenylbutyrates	102-116	microtubule associated protein tau	Homo sapiens	67-70
26646320-0	2016	Epigenetic regulation of ZEB1-RAB25/ESRP1 axis plays a critical role in phenylbutyrate treatment-resistant breast cancer.	Phenylbutyrates	72-86	zinc finger E-box binding homeobox 1	Homo sapiens	25-29
26646320-0	2016	Epigenetic regulation of ZEB1-RAB25/ESRP1 axis plays a critical role in phenylbutyrate treatment-resistant breast cancer.	Phenylbutyrates	72-86	RAB25, member RAS oncogene family	Homo sapiens	30-35
26646320-0	2016	Epigenetic regulation of ZEB1-RAB25/ESRP1 axis plays a critical role in phenylbutyrate treatment-resistant breast cancer.	Phenylbutyrates	72-86	epithelial splicing regulatory protein 1	Homo sapiens	36-41
26646320-7	2016	Thus, PB sensitivity is influenced by epigenetic expression alteration of ZEB1.	Phenylbutyrates	6-8	zinc finger E-box binding homeobox 1	Homo sapiens	74-78
28450154-0	2017	Phenyl butyrate inhibits pyruvate dehydrogenase kinase 1 and contributes to its anti-cancer effect.	Phenylbutyrates	0-15	pyruvate dehydrogenase kinase, isoenzyme 1	Mus musculus	25-56
28450154-1	2017	Phenyl butyrate (PB) has been proved to decrease pyruvate dehydrogenase (PDH) phosphorylation level and increase PDH activity by inhibiting pyruvate dehydrogenase kinase 1 (PDK1) in fibroblast cells, PDH deficiency zebrafish and wild type mice.	Phenylbutyrates	0-15	pyruvate dehydrogenase kinase, isozyme 1	Danio rerio	140-171
28450154-1	2017	Phenyl butyrate (PB) has been proved to decrease pyruvate dehydrogenase (PDH) phosphorylation level and increase PDH activity by inhibiting pyruvate dehydrogenase kinase 1 (PDK1) in fibroblast cells, PDH deficiency zebrafish and wild type mice.	Phenylbutyrates	0-15	pyruvate dehydrogenase kinase, isozyme 1	Danio rerio	173-177
28450154-1	2017	Phenyl butyrate (PB) has been proved to decrease pyruvate dehydrogenase (PDH) phosphorylation level and increase PDH activity by inhibiting pyruvate dehydrogenase kinase 1 (PDK1) in fibroblast cells, PDH deficiency zebrafish and wild type mice.	Phenylbutyrates	17-19	pyruvate dehydrogenase kinase, isozyme 1	Danio rerio	140-171
28450154-1	2017	Phenyl butyrate (PB) has been proved to decrease pyruvate dehydrogenase (PDH) phosphorylation level and increase PDH activity by inhibiting pyruvate dehydrogenase kinase 1 (PDK1) in fibroblast cells, PDH deficiency zebrafish and wild type mice.	Phenylbutyrates	17-19	pyruvate dehydrogenase kinase, isozyme 1	Danio rerio	173-177
28450154-4	2017	We hypothesize that the therapeutic effects of PB in cancers might also depend on suppressing PDK1 and promoting PDH activity, in addition to its proposed role as HDAC inhibitor.	Phenylbutyrates	47-49	pyruvate dehydrogenase kinase, isoenzyme 1	Mus musculus	94-98
28450154-5	2017	We showed that PB directly inhibited the kinase activity of PDK1 and increased the activity of PDH in an enzyme assay.	Phenylbutyrates	15-17	pyruvate dehydrogenase kinase, isoenzyme 1	Mus musculus	60-64
28450154-7	2017	In summary, this is the first study indicated that PB could exert its anti-cancer effects through inhibiting PDK1, altering the mitochondrial bioenergetics and inducing apoptosis.	Phenylbutyrates	51-53	pyruvate dehydrogenase kinase, isoenzyme 1	Mus musculus	109-113
28438947-1	2017	We have shown previously that oral treatment with sodium butyrate or phenylbutyrate in an experimental model of shigellosis improves clinical outcomes and induces the expression of the antimicrobial peptide CAP-18 in the large intestinal epithelia.	Phenylbutyrates	69-83	antimicrobial protein CAP18	Oryctolagus cuniculus	207-213
26432617-5	2015	Furthermore, activators of DJ-1 are available in the form of mortalin, phenylbutyrate and NAD(P)H: quinone oxidoreductase 1.	Phenylbutyrates	71-85	Parkinsonism associated deglycase	Homo sapiens	27-31
26218841-0	2015	Phenylbutyrate induces LL-37-dependent autophagy and intracellular killing of Mycobacterium tuberculosis in human macrophages.	Phenylbutyrates	0-14	cathelicidin antimicrobial peptide	Homo sapiens	23-28
23326523-8	2013	It further exhibited a synergistic effect with butyrate and phenylbutyrate on CAMP induction.	Phenylbutyrates	60-74	cathelicidin antimicrobial peptide	Homo sapiens	78-82
24246949-4	2014	We recently observed a synergistic induction of LL-37 expression by stimulating the colonic epithelial cell-line HT-29 with lactose and phenylbutyrate (PBA).	Phenylbutyrates	136-150	cathelicidin antimicrobial peptide	Homo sapiens	48-53
20225233-1	2010	The effects of the selective peroxisome proliferator activated receptor-gamma (PPAR-gamma) inhibitor GW9662 on phenylbutyrate (PB)-induced NMR-detectable lipid metabolites was investigated on DU145 prostate cancer cells.	Phenylbutyrates	111-125	peroxisome proliferator activated receptor gamma	Homo sapiens	29-77
21836606-2	2012	Our previous study showed that the differentiation and apoptosis of Kasumi-1 induced by sodium phenylbutyrate (PB), were accompanied by significant upregulation of PIG7 and AML1b (one of the AML1 isoforms).	Phenylbutyrates	111-113	lipopolysaccharide induced TNF factor	Homo sapiens	164-168
21836606-2	2012	Our previous study showed that the differentiation and apoptosis of Kasumi-1 induced by sodium phenylbutyrate (PB), were accompanied by significant upregulation of PIG7 and AML1b (one of the AML1 isoforms).	Phenylbutyrates	111-113	RUNX family transcription factor 1	Homo sapiens	173-177
21836606-7	2012	Moreover, ectopic expression of PIG7 could sensitize these cell lines to PB or all-trans retinoic acid, respectively, which could then be abrogated by downregulation of PIG7 expression.	Phenylbutyrates	73-75	lipopolysaccharide induced TNF factor	Homo sapiens	32-36
21270237-3	2011	Here we examined the efficacy of the chemical chaperone, sodium phenylbutyrate (PBA), a drug with known capacity to reduce ER stress in animal models and in vitro, on lipid-induced insulin resistance and beta-cell dysfunction in humans.	Phenylbutyrates	80-83	insulin	Homo sapiens	181-188
23141465-0	2012	Evidence for involvement of medium chain acyl-CoA dehydrogenase in the metabolism of phenylbutyrate.	Phenylbutyrates	85-99	acyl-CoA dehydrogenase medium chain	Homo sapiens	28-63
23141465-12	2012	The results are consistent with MCAD playing a key role in phenylbutyrate metabolism.	Phenylbutyrates	59-73	acyl-CoA dehydrogenase medium chain	Homo sapiens	32-36
22845560-7	2012	These processes required both PB-induced hyperacetylation of histone H4 and trimethylation of histone H3 at lysine 4, indicating the cooperative action of histone modifications and DNA methylation/demethylation in derepression of E-cadherin.	Phenylbutyrates	30-32	cadherin 1	Homo sapiens	230-240
22042554-2	2012	In addition to its apoptotic effect, phenylbutyrate (PB), a carboxylic acid HDACI, inhibited an anaplastic (ATC) thyroid cancer cell line ARO from penetrating a matrigel coated transwell with concomitant suppression of a metastasis-associated gene, matrix metalloproteinase-7 (MMP-7) and stimulation of a transformation suppressor protein, reversion-inducing- cysteine-rich protein with Kazal motifs without affecting MMP-2 expression levels.	Phenylbutyrates	37-51	matrix metallopeptidase 7	Homo sapiens	249-275
22042554-2	2012	In addition to its apoptotic effect, phenylbutyrate (PB), a carboxylic acid HDACI, inhibited an anaplastic (ATC) thyroid cancer cell line ARO from penetrating a matrigel coated transwell with concomitant suppression of a metastasis-associated gene, matrix metalloproteinase-7 (MMP-7) and stimulation of a transformation suppressor protein, reversion-inducing- cysteine-rich protein with Kazal motifs without affecting MMP-2 expression levels.	Phenylbutyrates	37-51	matrix metallopeptidase 7	Homo sapiens	277-282
22042554-2	2012	In addition to its apoptotic effect, phenylbutyrate (PB), a carboxylic acid HDACI, inhibited an anaplastic (ATC) thyroid cancer cell line ARO from penetrating a matrigel coated transwell with concomitant suppression of a metastasis-associated gene, matrix metalloproteinase-7 (MMP-7) and stimulation of a transformation suppressor protein, reversion-inducing- cysteine-rich protein with Kazal motifs without affecting MMP-2 expression levels.	Phenylbutyrates	37-51	matrix metallopeptidase 2	Homo sapiens	418-423
22042554-2	2012	In addition to its apoptotic effect, phenylbutyrate (PB), a carboxylic acid HDACI, inhibited an anaplastic (ATC) thyroid cancer cell line ARO from penetrating a matrigel coated transwell with concomitant suppression of a metastasis-associated gene, matrix metalloproteinase-7 (MMP-7) and stimulation of a transformation suppressor protein, reversion-inducing- cysteine-rich protein with Kazal motifs without affecting MMP-2 expression levels.	Phenylbutyrates	53-55	matrix metallopeptidase 7	Homo sapiens	249-275
22042554-2	2012	In addition to its apoptotic effect, phenylbutyrate (PB), a carboxylic acid HDACI, inhibited an anaplastic (ATC) thyroid cancer cell line ARO from penetrating a matrigel coated transwell with concomitant suppression of a metastasis-associated gene, matrix metalloproteinase-7 (MMP-7) and stimulation of a transformation suppressor protein, reversion-inducing- cysteine-rich protein with Kazal motifs without affecting MMP-2 expression levels.	Phenylbutyrates	53-55	matrix metallopeptidase 7	Homo sapiens	277-282
22042554-2	2012	In addition to its apoptotic effect, phenylbutyrate (PB), a carboxylic acid HDACI, inhibited an anaplastic (ATC) thyroid cancer cell line ARO from penetrating a matrigel coated transwell with concomitant suppression of a metastasis-associated gene, matrix metalloproteinase-7 (MMP-7) and stimulation of a transformation suppressor protein, reversion-inducing- cysteine-rich protein with Kazal motifs without affecting MMP-2 expression levels.	Phenylbutyrates	53-55	matrix metallopeptidase 2	Homo sapiens	418-423
22042554-4	2012	In addition, H-89, a protein kinase A inhibitor, remarkably restored the down-regulaed MMP-7 level treated by PB.	Phenylbutyrates	110-112	matrix metallopeptidase 7	Homo sapiens	87-92
22042554-5	2012	Thus, the suppressive effect of PB on MMP-7 was partially carried out through H3 phosphoacetylation.	Phenylbutyrates	32-34	matrix metallopeptidase 7	Homo sapiens	38-43
22042554-6	2012	To conclude, our findings suggest PB inhibits MMP-7 expression epigenetically through phosphoacetylation of histone proteins, and thereby, reduced invasive ability of an ATC thyroid cancer cell line.	Phenylbutyrates	34-36	matrix metallopeptidase 7	Homo sapiens	46-51
21610752-8	2011	Furthermore, we investigated the response of these cell lines to hydroxyurea, valproate and phenylbutyrate, drugs previously reported to upregulate SMN2.	Phenylbutyrates	92-106	survival of motor neuron 2, centromeric	Homo sapiens	148-152
21632108-5	2011	Histone deacetylation (HDAC) inhibitors sodium phenylbutyrate (PB) and valproic acid (VPA) block AML1-ETO.	Phenylbutyrates	63-65	RUNX family transcription factor 1	Homo sapiens	97-101
21632108-5	2011	Histone deacetylation (HDAC) inhibitors sodium phenylbutyrate (PB) and valproic acid (VPA) block AML1-ETO.	Phenylbutyrates	63-65	RUNX1 partner transcriptional co-repressor 1	Homo sapiens	102-105
21372141-8	2011	After screening a number of small molecules, we have found that the histone deacetylase inhibitor phenylbutyrate increases DJ-1 expression by 300% in the N27 dopamine cell line and rescues cells from oxidative stress and mutant alpha-synuclein toxicity.	Phenylbutyrates	98-112	Parkinson disease (autosomal recessive, early onset) 7	Mus musculus	123-127
21372141-8	2011	After screening a number of small molecules, we have found that the histone deacetylase inhibitor phenylbutyrate increases DJ-1 expression by 300% in the N27 dopamine cell line and rescues cells from oxidative stress and mutant alpha-synuclein toxicity.	Phenylbutyrates	98-112	synuclein, alpha	Mus musculus	228-243
21372141-9	2011	In mice, phenylbutyrate treatment leads to a 260% increase in brain DJ-1 levels and protects dopamine neurons against 1-methyl 4-phenyl 1,2,3,6-tetrahydropyridine (MPTP) toxicity.	Phenylbutyrates	9-23	Parkinson disease (autosomal recessive, early onset) 7	Mus musculus	68-72
21372141-10	2011	In a transgenic mouse model of diffuse Lewy body disease, long-term administration of phenylbutyrate reduces alpha-synuclein aggregation in brain and prevents age-related deterioration in motor and cognitive function.	Phenylbutyrates	86-100	synuclein, alpha	Mus musculus	109-124
20864248-3	2011	We found that sodium phenyl butyrate alone and 6h-pretreatment with phenyl butyrate or FK228 before the induction of differentiation with all-trans-retinoic acid in the presence of vitamin B3 effectively accelerated and enhanced differentiation to granulocytes in HL-60 but not in NB4 cells as detected by NBT test and the expression of CD11b and CD114 (G-CSFR) using flow cytometric analysis.	Phenylbutyrates	21-36	integrin subunit alpha M	Homo sapiens	337-342
20864248-3	2011	We found that sodium phenyl butyrate alone and 6h-pretreatment with phenyl butyrate or FK228 before the induction of differentiation with all-trans-retinoic acid in the presence of vitamin B3 effectively accelerated and enhanced differentiation to granulocytes in HL-60 but not in NB4 cells as detected by NBT test and the expression of CD11b and CD114 (G-CSFR) using flow cytometric analysis.	Phenylbutyrates	21-36	colony stimulating factor 3 receptor	Homo sapiens	347-352
20864248-3	2011	We found that sodium phenyl butyrate alone and 6h-pretreatment with phenyl butyrate or FK228 before the induction of differentiation with all-trans-retinoic acid in the presence of vitamin B3 effectively accelerated and enhanced differentiation to granulocytes in HL-60 but not in NB4 cells as detected by NBT test and the expression of CD11b and CD114 (G-CSFR) using flow cytometric analysis.	Phenylbutyrates	21-36	colony stimulating factor 3	Homo sapiens	354-360
20962230-8	2010	HDAC (histone deacetylase) inhibitors, SAHA (suberoylanilide hydroxamic acid) and PBA (phenylbutyrate), that upregulated NR1 partially rescued the learning disturbance.	Phenylbutyrates	87-101	Histone deacetylase 1	Drosophila melanogaster	0-4
20962230-8	2010	HDAC (histone deacetylase) inhibitors, SAHA (suberoylanilide hydroxamic acid) and PBA (phenylbutyrate), that upregulated NR1 partially rescued the learning disturbance.	Phenylbutyrates	87-101	Histone deacetylase 1	Drosophila melanogaster	6-25
20962230-8	2010	HDAC (histone deacetylase) inhibitors, SAHA (suberoylanilide hydroxamic acid) and PBA (phenylbutyrate), that upregulated NR1 partially rescued the learning disturbance.	Phenylbutyrates	87-101	NMDA receptor 1	Drosophila melanogaster	121-124
20516253-5	2010	The expression of CYP2B6 mRNA was induced in HepG2 cells stably expressing mouse CAR (Ym17) by HDAC inhibitors including valproic acid, phenylbutyrate, and trichostatin A.	Phenylbutyrates	136-150	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	18-24
20516253-5	2010	The expression of CYP2B6 mRNA was induced in HepG2 cells stably expressing mouse CAR (Ym17) by HDAC inhibitors including valproic acid, phenylbutyrate, and trichostatin A.	Phenylbutyrates	136-150	nuclear receptor subfamily 1, group I, member 3	Mus musculus	81-84
20225233-1	2010	The effects of the selective peroxisome proliferator activated receptor-gamma (PPAR-gamma) inhibitor GW9662 on phenylbutyrate (PB)-induced NMR-detectable lipid metabolites was investigated on DU145 prostate cancer cells.	Phenylbutyrates	111-125	peroxisome proliferator activated receptor gamma	Homo sapiens	79-89
20225233-1	2010	The effects of the selective peroxisome proliferator activated receptor-gamma (PPAR-gamma) inhibitor GW9662 on phenylbutyrate (PB)-induced NMR-detectable lipid metabolites was investigated on DU145 prostate cancer cells.	Phenylbutyrates	127-129	peroxisome proliferator activated receptor gamma	Homo sapiens	29-77
20225233-1	2010	The effects of the selective peroxisome proliferator activated receptor-gamma (PPAR-gamma) inhibitor GW9662 on phenylbutyrate (PB)-induced NMR-detectable lipid metabolites was investigated on DU145 prostate cancer cells.	Phenylbutyrates	127-129	peroxisome proliferator activated receptor gamma	Homo sapiens	79-89
20225233-4	2010	In addition, pre-incubation with GW9662 significantly reduced PB-induced caspase-3 activation, reversed the G(1) block as measured by flow cytometry, and otherwise had little effect on cell survival as measured by MTT assay.	Phenylbutyrates	62-64	caspase 3	Homo sapiens	73-82
20225233-5	2010	These results suggest that the NMR visible lipid accumulation and apoptosis induced by PB treatment occurs through a mechanism that is mediated by PPAR-gamma.	Phenylbutyrates	87-89	peroxisome proliferator activated receptor gamma	Homo sapiens	147-157
19818596-8	2009	Histone acetylation was also found to be a critical regulator of EP expression, with the histone deacteylase inhibitors trichostatin A, phenylbutyrate and suberoylanilide hydroxamic acid inducing increased expression of EPs2-4.	Phenylbutyrates	136-150	prostaglandin E receptor 2	Homo sapiens	220-226
20350531-2	2010	We show here that human promyeloblastic leukemia KG-1a cells exposed to the histone deacetylase inhibitor phenylbutyrate resemble many characteristics of leukemia stem cells, including expression of functional ABC transporters such as P-glycoprotein, BCRP and MRP8.	Phenylbutyrates	106-120	ATP binding cassette subfamily B member 6 (Langereis blood group)	Homo sapiens	210-213
20350531-2	2010	We show here that human promyeloblastic leukemia KG-1a cells exposed to the histone deacetylase inhibitor phenylbutyrate resemble many characteristics of leukemia stem cells, including expression of functional ABC transporters such as P-glycoprotein, BCRP and MRP8.	Phenylbutyrates	106-120	BCR pseudogene 1	Homo sapiens	251-255
20350531-2	2010	We show here that human promyeloblastic leukemia KG-1a cells exposed to the histone deacetylase inhibitor phenylbutyrate resemble many characteristics of leukemia stem cells, including expression of functional ABC transporters such as P-glycoprotein, BCRP and MRP8.	Phenylbutyrates	106-120	ATP binding cassette subfamily C member 11	Homo sapiens	260-264
18971205-9	2009	We identified histone deacetylase (HDAC) inhibitors including vorinostat and romidepsin which are able to bypass SMN2 gene silencing by DNA methylation, while others such as valproic acid and phenylbutyrate do not, due to HDAC isoenzyme specificities.	Phenylbutyrates	192-206	histone deacetylase 9	Homo sapiens	14-33
19723072-5	2009	Chromatin immunoprecipitation analysis has revealed phenyl butyrate and its combinations with RA and vitamin B3 cause histone H4 acetylation in the p21 promoter regions corresponding to p53 and/or Sp1 sites.	Phenylbutyrates	52-67	H3 histone pseudogene 16	Homo sapiens	148-151
19723072-5	2009	Chromatin immunoprecipitation analysis has revealed phenyl butyrate and its combinations with RA and vitamin B3 cause histone H4 acetylation in the p21 promoter regions corresponding to p53 and/or Sp1 sites.	Phenylbutyrates	52-67	tumor protein p53	Homo sapiens	186-189
18971205-9	2009	We identified histone deacetylase (HDAC) inhibitors including vorinostat and romidepsin which are able to bypass SMN2 gene silencing by DNA methylation, while others such as valproic acid and phenylbutyrate do not, due to HDAC isoenzyme specificities.	Phenylbutyrates	192-206	histone deacetylase 9	Homo sapiens	35-39
18633133-8	2008	Increases in SMN levels of 50% were demonstrable by ELISA after 24 hours treatment of 10(5) SMA fibroblasts with valproate or phenylbutyrate.	Phenylbutyrates	126-140	survival of motor neuron 1, telomeric	Homo sapiens	13-16
18345520-5	2008	METHODS: In this preliminary study, we investigated the effect of phenylbutyrate, a histone deacetylase (HDAC) inhibitor, on SMN2 expression in two SMA type III Epstein-Barr virus (EBV)-transformed lymphoblastoid cell lines to understand the suitability of lymphoblastoid cell lines in drug screening.	Phenylbutyrates	66-80	survival of motor neuron 2, centromeric	Homo sapiens	125-129
18322101-8	2008	HDAC1 siRNA or other HDAC inhibitors (phenylbutyrate, sodium butyrate or trichostatin A) also caused synergistic neuroprotection together with lithium.	Phenylbutyrates	38-52	histone deacetylase 1	Homo sapiens	0-5
18322101-8	2008	HDAC1 siRNA or other HDAC inhibitors (phenylbutyrate, sodium butyrate or trichostatin A) also caused synergistic neuroprotection together with lithium.	Phenylbutyrates	38-52	histone deacetylase 9	Homo sapiens	0-4
19014694-5	2008	We observed that the HDAC inhibitors, MS-275, trichostatin-A, phenylbutyrate, LAQ824 and depsipeptide, enhanced the antineoplastic action of 5AZA-CdR on EWS cells.	Phenylbutyrates	62-76	histone deacetylase 9	Homo sapiens	21-25
18345520-7	2008	Quantitative analysis of SMN2 mRNA was performed on established cell lines treated with various concentrations of phenylbutyrate and for a range of incubation periods using real-time polymerase chain reaction.	Phenylbutyrates	114-128	survival of motor neuron 2, centromeric	Homo sapiens	25-29
17256134-8	2007	PB + CRA induced p21 expression and cell-cycle arrest in G1 phase, while TX and DOXO induced G2/M arrest.	Phenylbutyrates	0-2	H3 histone pseudogene 16	Homo sapiens	17-20
17707275-0	2007	Phenylbutyrate sensitizes human glioblastoma cells lacking wild-type p53 function to ionizing radiation.	Phenylbutyrates	0-14	tumor protein p53	Homo sapiens	69-72
17707275-14	2007	There was no radiopotentiating effect in two cell lines with wild-type p53, but knockdown of wild-type p53 resulted in radiosensitization by PB.	Phenylbutyrates	141-143	tumor protein p53	Homo sapiens	103-106
17707275-16	2007	This suggests the potential application of combined PB and radiotherapy in glioblastoma harboring mutant p53.	Phenylbutyrates	52-54	tumor protein p53	Homo sapiens	105-108
16875574-8	2006	After Kasumi-1, U937 and NB4 cell lines exposed to PB, the expression of p21WAF1/CIP1 gene was increased by (2.06 +/- 0.27), (2.78 +/- 0.40) and (1.78 +/- 0.20) times at its maximum, respectively.	Phenylbutyrates	51-53	cyclin dependent kinase inhibitor 1A	Homo sapiens	81-85
17123441-3	2006	In this study the combination of the HDAC inhibitor phenylbutyrate (PB) and the nucleoside analogue gemcitabine (GEM) was evaluated and the mechanisms underlying increased cell death were analyzed.	Phenylbutyrates	52-66	histone deacetylase 9	Homo sapiens	37-41
17123441-3	2006	In this study the combination of the HDAC inhibitor phenylbutyrate (PB) and the nucleoside analogue gemcitabine (GEM) was evaluated and the mechanisms underlying increased cell death were analyzed.	Phenylbutyrates	68-70	histone deacetylase 9	Homo sapiens	37-41
17123441-17	2006	CONCLUSION: Therapy combining GEM and the HDAC inhibitor PB initiates a spectrum of apoptosis-inducing mitochondrial and further JNK-dependent events, thereby overcoming the therapeutic resistance of NSCLC tumor cells.	Phenylbutyrates	57-59	histone deacetylase 9	Homo sapiens	42-46
17123441-17	2006	CONCLUSION: Therapy combining GEM and the HDAC inhibitor PB initiates a spectrum of apoptosis-inducing mitochondrial and further JNK-dependent events, thereby overcoming the therapeutic resistance of NSCLC tumor cells.	Phenylbutyrates	57-59	mitogen-activated protein kinase 8	Homo sapiens	129-132
16508748-4	2006	Several clinical trials with drugs that increase the SMN2 expression such as valproic acid and phenylbutyrate are in progress.	Phenylbutyrates	95-109	survival of motor neuron 2, centromeric	Homo sapiens	53-57
16875574-9	2006	PB could stimulate p21WAF1/CIP1 promoter activity (by luciferase-reporter assay) and the effect was dose dependent.	Phenylbutyrates	0-2	cyclin dependent kinase inhibitor 1A	Homo sapiens	27-31
16085712-5	2005	In vivo application of the chromatin-modifying agents 5-azadeoxycytidine and phenylbutyrate as well as local damage by cardiotoxin injections caused a small increase in dystrophin-positive fibers without abolishing the appearance of "silent" nuclei.	Phenylbutyrates	77-91	dystrophin	Homo sapiens	169-179
17076267-5	2006	Drugs such as valproic acid, phenylbutyrate, sodium butyrate, M344 and SAHA that mainly act as histone deacetylase inhibitors can mediate both: they stimulate the SMN2 gene transcription and/or restore the splicing pattern, thereby elevating the levels of FL-SMN2 protein.	Phenylbutyrates	29-43	survival of motor neuron 2, centromeric	Homo sapiens	163-167
17076267-5	2006	Drugs such as valproic acid, phenylbutyrate, sodium butyrate, M344 and SAHA that mainly act as histone deacetylase inhibitors can mediate both: they stimulate the SMN2 gene transcription and/or restore the splicing pattern, thereby elevating the levels of FL-SMN2 protein.	Phenylbutyrates	29-43	fms related receptor tyrosine kinase 3 ligand	Homo sapiens	256-258
17076267-5	2006	Drugs such as valproic acid, phenylbutyrate, sodium butyrate, M344 and SAHA that mainly act as histone deacetylase inhibitors can mediate both: they stimulate the SMN2 gene transcription and/or restore the splicing pattern, thereby elevating the levels of FL-SMN2 protein.	Phenylbutyrates	29-43	survival of motor neuron 2, centromeric	Homo sapiens	259-263
15494404-5	2005	Phenylbutyrate increased mRNA for components of the ubiquitin-proteosomal pathway and down-regulated caspases implicated in apoptotic cell death, and active caspase 3 immunoreactivity in the striatum.	Phenylbutyrates	0-14	caspase 3	Mus musculus	157-166
15934930-4	2005	Phenylbutyrate administration ameliorated histone hypoacetylation observed in G93A mice and induced expression of nuclear factor-kappaB (NF-kappaB) p50, the phosphorylated inhibitory subunit of NF-kappaB (pIkappaB) and beta cell lymphoma 2 (bcl-2), but reduced cytochrome c and caspase expression.	Phenylbutyrates	0-14	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	114-135
15934930-4	2005	Phenylbutyrate administration ameliorated histone hypoacetylation observed in G93A mice and induced expression of nuclear factor-kappaB (NF-kappaB) p50, the phosphorylated inhibitory subunit of NF-kappaB (pIkappaB) and beta cell lymphoma 2 (bcl-2), but reduced cytochrome c and caspase expression.	Phenylbutyrates	0-14	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	137-146
15934930-4	2005	Phenylbutyrate administration ameliorated histone hypoacetylation observed in G93A mice and induced expression of nuclear factor-kappaB (NF-kappaB) p50, the phosphorylated inhibitory subunit of NF-kappaB (pIkappaB) and beta cell lymphoma 2 (bcl-2), but reduced cytochrome c and caspase expression.	Phenylbutyrates	0-14	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	148-151
15934930-4	2005	Phenylbutyrate administration ameliorated histone hypoacetylation observed in G93A mice and induced expression of nuclear factor-kappaB (NF-kappaB) p50, the phosphorylated inhibitory subunit of NF-kappaB (pIkappaB) and beta cell lymphoma 2 (bcl-2), but reduced cytochrome c and caspase expression.	Phenylbutyrates	0-14	B cell leukemia/lymphoma 2	Mus musculus	241-246
15934930-7	2005	Phenylbutyrate acts to phosphorylate IkappaB, translocating NF-kappaB p50 to the nucleus, or to directly acetylate NF-kappaB p50.	Phenylbutyrates	0-14	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	60-69
15934930-7	2005	Phenylbutyrate acts to phosphorylate IkappaB, translocating NF-kappaB p50 to the nucleus, or to directly acetylate NF-kappaB p50.	Phenylbutyrates	0-14	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	70-73
15934930-7	2005	Phenylbutyrate acts to phosphorylate IkappaB, translocating NF-kappaB p50 to the nucleus, or to directly acetylate NF-kappaB p50.	Phenylbutyrates	0-14	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	115-124
15934930-7	2005	Phenylbutyrate acts to phosphorylate IkappaB, translocating NF-kappaB p50 to the nucleus, or to directly acetylate NF-kappaB p50.	Phenylbutyrates	0-14	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	125-128
14585280-9	2003	The synergistic effect of histone deacetylase inhibitors, including phenylbutyrate (PB), in reactivating silenced genes encouraged clinical studies on the combination of PB and demethylating agents in hematological diseases, characterized by p15 silencing.	Phenylbutyrates	68-82	cyclin dependent kinase inhibitor 2B	Homo sapiens	242-245
15026552-4	2004	We found that the antitumor agents known as histone deacetylase (HDAC) inhibitors (phenylbutyrate, trichostatin A, and valproic acid) could suppress cutaneous radiation syndrome.	Phenylbutyrates	83-97	histone deacetylase 9	Homo sapiens	44-63
15026552-4	2004	We found that the antitumor agents known as histone deacetylase (HDAC) inhibitors (phenylbutyrate, trichostatin A, and valproic acid) could suppress cutaneous radiation syndrome.	Phenylbutyrates	83-97	histone deacetylase 9	Homo sapiens	65-69
15634569-9	2004	The expression of CD11b and CD13 antigen of the tumor cells was increased in xenografted mice model treated with PB when compared with the control \[(12.08 +/- 1.02)% and (54.91 +/- 2.72)%\], respectively (P < 0.01), and tumor cells showed a cell cycle arrest with increased G(0)/G(1)-phase cells and decreased S-phase cells.	Phenylbutyrates	113-115	integrin subunit alpha M	Homo sapiens	18-23
15634569-9	2004	The expression of CD11b and CD13 antigen of the tumor cells was increased in xenografted mice model treated with PB when compared with the control \[(12.08 +/- 1.02)% and (54.91 +/- 2.72)%\], respectively (P < 0.01), and tumor cells showed a cell cycle arrest with increased G(0)/G(1)-phase cells and decreased S-phase cells.	Phenylbutyrates	113-115	alanyl aminopeptidase, membrane	Homo sapiens	28-32
14560316-0	2004	Phenylbutyrate increases SMN expression in vitro: relevance for treatment of spinal muscular atrophy.	Phenylbutyrates	0-14	survival of motor neuron 1, telomeric	Homo sapiens	25-28
15171260-2	2004	A number of structural classes of HDAC inhibitors have been developed of which several are in clinical trials, including phenylbutyrate (PB) and related compounds; the hydroxamic acids, suberoylanilide hydroxamic acid (SAHA) and depsipeptide (FK-228); and the benzamides, MS-275 and C1-994.	Phenylbutyrates	121-135	histone deacetylase 9	Homo sapiens	34-38
15171260-2	2004	A number of structural classes of HDAC inhibitors have been developed of which several are in clinical trials, including phenylbutyrate (PB) and related compounds; the hydroxamic acids, suberoylanilide hydroxamic acid (SAHA) and depsipeptide (FK-228); and the benzamides, MS-275 and C1-994.	Phenylbutyrates	137-139	histone deacetylase 9	Homo sapiens	34-38
14585280-9	2003	The synergistic effect of histone deacetylase inhibitors, including phenylbutyrate (PB), in reactivating silenced genes encouraged clinical studies on the combination of PB and demethylating agents in hematological diseases, characterized by p15 silencing.	Phenylbutyrates	84-86	cyclin dependent kinase inhibitor 2B	Homo sapiens	242-245
12859874-1	2003	OBJECTIVE: To explore the blockade effect of phenylbutyrate (PB), a histone deacetylase inhibitor, on the in vitro biological function of AML1/ETO to reverse its transcription repression and induce Kasumi-1 cells to differentiate and apoptosis.	Phenylbutyrates	45-59	RUNX family transcription factor 1	Homo sapiens	138-142
14599803-4	2003	We found that the histone deacetylase (HDAC) inhibitors (phenylbutyrate and trichostatin A) causing histone hyperacetylation to modulate multiple gene expression not only induced the expression of p21(Cip1) and p16(INK4) in synovial cells but also inhibited the expression of tumor necrosis factor-alpha in affected tissues in adjuvant arthritis, an animal model of RA.	Phenylbutyrates	57-71	histone deacetylase 9	Homo sapiens	18-37
14599803-4	2003	We found that the histone deacetylase (HDAC) inhibitors (phenylbutyrate and trichostatin A) causing histone hyperacetylation to modulate multiple gene expression not only induced the expression of p21(Cip1) and p16(INK4) in synovial cells but also inhibited the expression of tumor necrosis factor-alpha in affected tissues in adjuvant arthritis, an animal model of RA.	Phenylbutyrates	57-71	histone deacetylase 9	Homo sapiens	39-43
14599803-4	2003	We found that the histone deacetylase (HDAC) inhibitors (phenylbutyrate and trichostatin A) causing histone hyperacetylation to modulate multiple gene expression not only induced the expression of p21(Cip1) and p16(INK4) in synovial cells but also inhibited the expression of tumor necrosis factor-alpha in affected tissues in adjuvant arthritis, an animal model of RA.	Phenylbutyrates	57-71	cyclin dependent kinase inhibitor 1A	Homo sapiens	197-200
14599803-4	2003	We found that the histone deacetylase (HDAC) inhibitors (phenylbutyrate and trichostatin A) causing histone hyperacetylation to modulate multiple gene expression not only induced the expression of p21(Cip1) and p16(INK4) in synovial cells but also inhibited the expression of tumor necrosis factor-alpha in affected tissues in adjuvant arthritis, an animal model of RA.	Phenylbutyrates	57-71	cyclin dependent kinase inhibitor 1A	Homo sapiens	201-205
14599803-4	2003	We found that the histone deacetylase (HDAC) inhibitors (phenylbutyrate and trichostatin A) causing histone hyperacetylation to modulate multiple gene expression not only induced the expression of p21(Cip1) and p16(INK4) in synovial cells but also inhibited the expression of tumor necrosis factor-alpha in affected tissues in adjuvant arthritis, an animal model of RA.	Phenylbutyrates	57-71	cyclin dependent kinase inhibitor 2A	Homo sapiens	211-214
14599803-4	2003	We found that the histone deacetylase (HDAC) inhibitors (phenylbutyrate and trichostatin A) causing histone hyperacetylation to modulate multiple gene expression not only induced the expression of p21(Cip1) and p16(INK4) in synovial cells but also inhibited the expression of tumor necrosis factor-alpha in affected tissues in adjuvant arthritis, an animal model of RA.	Phenylbutyrates	57-71	cyclin dependent kinase inhibitor 2A	Homo sapiens	215-219
14599803-4	2003	We found that the histone deacetylase (HDAC) inhibitors (phenylbutyrate and trichostatin A) causing histone hyperacetylation to modulate multiple gene expression not only induced the expression of p21(Cip1) and p16(INK4) in synovial cells but also inhibited the expression of tumor necrosis factor-alpha in affected tissues in adjuvant arthritis, an animal model of RA.	Phenylbutyrates	57-71	tumor necrosis factor	Homo sapiens	276-303
12859874-1	2003	OBJECTIVE: To explore the blockade effect of phenylbutyrate (PB), a histone deacetylase inhibitor, on the in vitro biological function of AML1/ETO to reverse its transcription repression and induce Kasumi-1 cells to differentiate and apoptosis.	Phenylbutyrates	45-59	RUNX1 partner transcriptional co-repressor 1	Homo sapiens	143-146
12859874-1	2003	OBJECTIVE: To explore the blockade effect of phenylbutyrate (PB), a histone deacetylase inhibitor, on the in vitro biological function of AML1/ETO to reverse its transcription repression and induce Kasumi-1 cells to differentiate and apoptosis.	Phenylbutyrates	61-63	RUNX family transcription factor 1	Homo sapiens	138-142
12859874-1	2003	OBJECTIVE: To explore the blockade effect of phenylbutyrate (PB), a histone deacetylase inhibitor, on the in vitro biological function of AML1/ETO to reverse its transcription repression and induce Kasumi-1 cells to differentiate and apoptosis.	Phenylbutyrates	61-63	RUNX1 partner transcriptional co-repressor 1	Homo sapiens	143-146
12859874-7	2003	PB induced a time- and dose-dependent increase in expression of myeloid cell surface protein CD(11b) and CD(13).	Phenylbutyrates	0-2	integrin subunit alpha M	Homo sapiens	93-99
12393583-2	2002	Short-chain fatty acids (SCFAs) of 2 to 6 carbons in length induce gamma globin expression in animal models, and butyrate, phenylbutyrate, and valproate induce gamma globin in human patients.	Phenylbutyrates	123-137	hemoglobin subunit gamma 1	Homo sapiens	160-172
12669235-4	2003	Consistent with the cell cycle block, only PB, but not PA, induced the cyclin-dependent kinase inhibitors p21(CIP1) and p27(KIP1).	Phenylbutyrates	43-45	cyclin dependent kinase inhibitor 1A	Homo sapiens	106-109
12669235-4	2003	Consistent with the cell cycle block, only PB, but not PA, induced the cyclin-dependent kinase inhibitors p21(CIP1) and p27(KIP1).	Phenylbutyrates	43-45	cyclin dependent kinase inhibitor 1A	Homo sapiens	110-114
12669235-4	2003	Consistent with the cell cycle block, only PB, but not PA, induced the cyclin-dependent kinase inhibitors p21(CIP1) and p27(KIP1).	Phenylbutyrates	43-45	zinc ribbon domain containing 2	Homo sapiens	120-123
12669235-4	2003	Consistent with the cell cycle block, only PB, but not PA, induced the cyclin-dependent kinase inhibitors p21(CIP1) and p27(KIP1).	Phenylbutyrates	43-45	cyclin dependent kinase inhibitor 1B	Homo sapiens	124-128
12481425-3	2002	The aim of this study was to determine the in vivo effects of PB in the normal mammary gland on epithelial cell proliferation, estrogen receptor alpha (ER alpha) expression, and cyclin D1 expression.	Phenylbutyrates	62-64	estrogen receptor 1 (alpha)	Mus musculus	127-150
12481425-3	2002	The aim of this study was to determine the in vivo effects of PB in the normal mammary gland on epithelial cell proliferation, estrogen receptor alpha (ER alpha) expression, and cyclin D1 expression.	Phenylbutyrates	62-64	cyclin D1	Mus musculus	178-187
11855750-0	2002	Phenylbutyrate-induced apoptosis is associated with inactivation of NF-kappaB IN HT-29 colon cancer cells.	Phenylbutyrates	0-14	nuclear factor kappa B subunit 1	Homo sapiens	68-77
12394273-6	2002	Phenylbutyrate (PB), an inhibitor of histone deacetylase (HDAC), increases histone acetylation, neutralizing its positive charge and resulting in DNA with a more open structure, which favors transcription.	Phenylbutyrates	0-14	histone deacetylase 9	Homo sapiens	37-56
12394273-6	2002	Phenylbutyrate (PB), an inhibitor of histone deacetylase (HDAC), increases histone acetylation, neutralizing its positive charge and resulting in DNA with a more open structure, which favors transcription.	Phenylbutyrates	0-14	histone deacetylase 9	Homo sapiens	58-62
12394273-6	2002	Phenylbutyrate (PB), an inhibitor of histone deacetylase (HDAC), increases histone acetylation, neutralizing its positive charge and resulting in DNA with a more open structure, which favors transcription.	Phenylbutyrates	16-18	histone deacetylase 9	Homo sapiens	37-56
12394273-6	2002	Phenylbutyrate (PB), an inhibitor of histone deacetylase (HDAC), increases histone acetylation, neutralizing its positive charge and resulting in DNA with a more open structure, which favors transcription.	Phenylbutyrates	16-18	histone deacetylase 9	Homo sapiens	58-62
11830487-4	2002	Of the 5 RA + PB-treated patients, 4 had PML-RARalpha mutations.	Phenylbutyrates	14-16	PML nuclear body scaffold	Homo sapiens	41-44
11830487-4	2002	Of the 5 RA + PB-treated patients, 4 had PML-RARalpha mutations.	Phenylbutyrates	14-16	retinoic acid receptor alpha	Homo sapiens	45-53
11830487-8	2002	These results indicate that PML-RARalpha mutations occurred with high frequency after multiple RA treatment relapses, indicate that the functional potential of PML-RARalpha was not correlated with clinical response to RA + PB treatment, and suggest that the response to RA + PB therapy in one patient was related to the ability of PB to circumvent the blocked RA-regulated gene response pathway.	Phenylbutyrates	275-277	PML nuclear body scaffold	Homo sapiens	28-31
11830487-8	2002	These results indicate that PML-RARalpha mutations occurred with high frequency after multiple RA treatment relapses, indicate that the functional potential of PML-RARalpha was not correlated with clinical response to RA + PB treatment, and suggest that the response to RA + PB therapy in one patient was related to the ability of PB to circumvent the blocked RA-regulated gene response pathway.	Phenylbutyrates	275-277	retinoic acid receptor alpha	Homo sapiens	32-40
11830487-8	2002	These results indicate that PML-RARalpha mutations occurred with high frequency after multiple RA treatment relapses, indicate that the functional potential of PML-RARalpha was not correlated with clinical response to RA + PB treatment, and suggest that the response to RA + PB therapy in one patient was related to the ability of PB to circumvent the blocked RA-regulated gene response pathway.	Phenylbutyrates	275-277	PML nuclear body scaffold	Homo sapiens	160-163
11830487-8	2002	These results indicate that PML-RARalpha mutations occurred with high frequency after multiple RA treatment relapses, indicate that the functional potential of PML-RARalpha was not correlated with clinical response to RA + PB treatment, and suggest that the response to RA + PB therapy in one patient was related to the ability of PB to circumvent the blocked RA-regulated gene response pathway.	Phenylbutyrates	275-277	retinoic acid receptor alpha	Homo sapiens	164-172
11830487-8	2002	These results indicate that PML-RARalpha mutations occurred with high frequency after multiple RA treatment relapses, indicate that the functional potential of PML-RARalpha was not correlated with clinical response to RA + PB treatment, and suggest that the response to RA + PB therapy in one patient was related to the ability of PB to circumvent the blocked RA-regulated gene response pathway.	Phenylbutyrates	275-277	PML nuclear body scaffold	Homo sapiens	28-31
11830487-8	2002	These results indicate that PML-RARalpha mutations occurred with high frequency after multiple RA treatment relapses, indicate that the functional potential of PML-RARalpha was not correlated with clinical response to RA + PB treatment, and suggest that the response to RA + PB therapy in one patient was related to the ability of PB to circumvent the blocked RA-regulated gene response pathway.	Phenylbutyrates	275-277	retinoic acid receptor alpha	Homo sapiens	32-40
11830487-8	2002	These results indicate that PML-RARalpha mutations occurred with high frequency after multiple RA treatment relapses, indicate that the functional potential of PML-RARalpha was not correlated with clinical response to RA + PB treatment, and suggest that the response to RA + PB therapy in one patient was related to the ability of PB to circumvent the blocked RA-regulated gene response pathway.	Phenylbutyrates	275-277	PML nuclear body scaffold	Homo sapiens	160-163
11830487-8	2002	These results indicate that PML-RARalpha mutations occurred with high frequency after multiple RA treatment relapses, indicate that the functional potential of PML-RARalpha was not correlated with clinical response to RA + PB treatment, and suggest that the response to RA + PB therapy in one patient was related to the ability of PB to circumvent the blocked RA-regulated gene response pathway.	Phenylbutyrates	275-277	retinoic acid receptor alpha	Homo sapiens	164-172
11855750-6	2002	RESULTS: Exposure of HT-29 colon cancer cells to PB resulted in growth inhibition and induction of apoptosis as measured by annexin V staining.	Phenylbutyrates	49-51	annexin A5	Homo sapiens	124-133
11855750-9	2002	After PB treatment, NF-kappaB-DNA binding was markedly decreased and specifically, this decreased DNA binding was observed in the p50:p65 heterodimer.	Phenylbutyrates	6-8	nuclear factor kappa B subunit 1	Homo sapiens	20-29
11855750-9	2002	After PB treatment, NF-kappaB-DNA binding was markedly decreased and specifically, this decreased DNA binding was observed in the p50:p65 heterodimer.	Phenylbutyrates	6-8	nuclear factor kappa B subunit 1	Homo sapiens	130-133
11855750-9	2002	After PB treatment, NF-kappaB-DNA binding was markedly decreased and specifically, this decreased DNA binding was observed in the p50:p65 heterodimer.	Phenylbutyrates	6-8	RELA proto-oncogene, NF-kB subunit	Homo sapiens	134-137
11855750-10	2002	The decreased NF-kappaB DNA binding was observed as early as 3 h after PB treatment, while no apparent changes in annexin V binding were detected until 12 h after PB treatment.	Phenylbutyrates	71-73	nuclear factor kappa B subunit 1	Homo sapiens	14-23
11855750-12	2002	CONCLUSION: These results suggest that PB-induced apoptosis may be partly regulated through the inactivation of NF-kappaB.	Phenylbutyrates	39-41	nuclear factor kappa B subunit 1	Homo sapiens	112-121
11485828-2	2001	We demonstrate that HT-29 colon cancer cells exposed to PB and TB result in growth inhibition associated with an induction of apoptosis mediated through the activation of caspase-3 activity.	Phenylbutyrates	56-58	caspase 3	Homo sapiens	171-180
11391852-1	2001	INTRODUCTION: Phenylbutyrate (PB) and its metabolite phenylacetate (PA) demonstrate anticancer activity in vitro through promotion of cell differentiation, induction of apoptosis through the p21 pathway, inhibition of histone deacetylase, and in the case of PB, direct cytotoxicity.	Phenylbutyrates	14-28	H3 histone pseudogene 16	Homo sapiens	191-194
11571633-4	2001	We show that PB attenuates the expression of the apoptosis antagonist Bcl-X(L), the double-strand break repair protein DNA-dependent protein kinase, the prostate progression marker caveolin-1, and the pro-angiogenic vascular endothelial growth factor.	Phenylbutyrates	13-15	BCL2 like 1	Homo sapiens	70-78
11571633-4	2001	We show that PB attenuates the expression of the apoptosis antagonist Bcl-X(L), the double-strand break repair protein DNA-dependent protein kinase, the prostate progression marker caveolin-1, and the pro-angiogenic vascular endothelial growth factor.	Phenylbutyrates	13-15	protein kinase, DNA-activated, catalytic subunit	Homo sapiens	119-147
11571633-4	2001	We show that PB attenuates the expression of the apoptosis antagonist Bcl-X(L), the double-strand break repair protein DNA-dependent protein kinase, the prostate progression marker caveolin-1, and the pro-angiogenic vascular endothelial growth factor.	Phenylbutyrates	13-15	caveolin 1	Homo sapiens	181-191
11391852-1	2001	INTRODUCTION: Phenylbutyrate (PB) and its metabolite phenylacetate (PA) demonstrate anticancer activity in vitro through promotion of cell differentiation, induction of apoptosis through the p21 pathway, inhibition of histone deacetylase, and in the case of PB, direct cytotoxicity.	Phenylbutyrates	30-32	H3 histone pseudogene 16	Homo sapiens	191-194
11391852-13	2001	CONCLUSIONS: These data indicate that PA and PB penetrate well into the CSF after i.v.	Phenylbutyrates	45-47	colony stimulating factor 2	Homo sapiens	72-75
11164382-0	2001	Direct block of the cystic fibrosis transmembrane conductance regulator Cl(-) channel by butyrate and phenylbutyrate.	Phenylbutyrates	102-116	CF transmembrane conductance regulator	Homo sapiens	20-71
11558827-8	2001	Multiple agents, including uridine triphosphate (UTP), genistein, phenylbutyrate and CPX (cyclopentyl dipropylxanthine), have been demonstrated in cell culture to at least partially correct the primary defect of ion transport related to mutations in the cystic fibrosis transmembrane conductance regulator (CFTR).	Phenylbutyrates	66-80	CF transmembrane conductance regulator	Homo sapiens	254-305
11558827-8	2001	Multiple agents, including uridine triphosphate (UTP), genistein, phenylbutyrate and CPX (cyclopentyl dipropylxanthine), have been demonstrated in cell culture to at least partially correct the primary defect of ion transport related to mutations in the cystic fibrosis transmembrane conductance regulator (CFTR).	Phenylbutyrates	66-80	CF transmembrane conductance regulator	Homo sapiens	307-311
10450755-4	1999	ATRA augmented PB induction of the myelomonocytic marker CD11b at all doses of ATRA tested (0.0025-1 microM).	Phenylbutyrates	15-17	integrin subunit alpha M	Homo sapiens	57-62
10914745-3	2000	The mechanism of this last effect is related to a PB-induced increase in p27Kip1, leading to a decrease in the activity of cyclin-dependent kinase 2 (CDK2), a positive regulator of the G1-S-phase cell cycle transition.	Phenylbutyrates	50-52	cyclin dependent kinase inhibitor 1B	Homo sapiens	73-80
10914745-3	2000	The mechanism of this last effect is related to a PB-induced increase in p27Kip1, leading to a decrease in the activity of cyclin-dependent kinase 2 (CDK2), a positive regulator of the G1-S-phase cell cycle transition.	Phenylbutyrates	50-52	cyclin dependent kinase 2	Homo sapiens	123-148
10914745-3	2000	The mechanism of this last effect is related to a PB-induced increase in p27Kip1, leading to a decrease in the activity of cyclin-dependent kinase 2 (CDK2), a positive regulator of the G1-S-phase cell cycle transition.	Phenylbutyrates	50-52	cyclin dependent kinase 2	Homo sapiens	150-154
10696460-2	2000	STUDY DESIGN: We analyzed the differential expression of different apoptosis modulators, Bcl-2, Bax, p53 and Fas, for their potential role in PB-induced apoptosis using relative quantitative flow cytometry (FCM).	Phenylbutyrates	142-144	BCL2 apoptosis regulator	Homo sapiens	89-94
10696460-2	2000	STUDY DESIGN: We analyzed the differential expression of different apoptosis modulators, Bcl-2, Bax, p53 and Fas, for their potential role in PB-induced apoptosis using relative quantitative flow cytometry (FCM).	Phenylbutyrates	142-144	BCL2 associated X, apoptosis regulator	Homo sapiens	96-99
10696460-2	2000	STUDY DESIGN: We analyzed the differential expression of different apoptosis modulators, Bcl-2, Bax, p53 and Fas, for their potential role in PB-induced apoptosis using relative quantitative flow cytometry (FCM).	Phenylbutyrates	142-144	tumor protein p53	Homo sapiens	101-104
10696460-7	2000	FCM revealed a heterogeneous stimulatory effect on the expression of Bax and Bcl-2 in PC3-PF cells at 0.5-2.5 mM PB.	Phenylbutyrates	113-115	BCL2 associated X, apoptosis regulator	Homo sapiens	69-72
10696460-7	2000	FCM revealed a heterogeneous stimulatory effect on the expression of Bax and Bcl-2 in PC3-PF cells at 0.5-2.5 mM PB.	Phenylbutyrates	113-115	BCL2 apoptosis regulator	Homo sapiens	77-82
10696460-7	2000	FCM revealed a heterogeneous stimulatory effect on the expression of Bax and Bcl-2 in PC3-PF cells at 0.5-2.5 mM PB.	Phenylbutyrates	113-115	chromobox 8	Homo sapiens	86-89
10696460-8	2000	In a p53-positive cell line (DU145), p53 was repressed by 70% and Fas elevated sixfold with 10 mM PB.	Phenylbutyrates	98-100	tumor protein p53	Homo sapiens	5-8
10696460-8	2000	In a p53-positive cell line (DU145), p53 was repressed by 70% and Fas elevated sixfold with 10 mM PB.	Phenylbutyrates	98-100	tumor protein p53	Homo sapiens	37-40
10696460-9	2000	CONCLUSION: Our data show that PB-induced PCa apoptosis is associated with the relative repression of Bcl-2 and with up-regulation of Bax and Fas proteins and that this PB-induced apoptosis is independent of p53 and androgen-dependency status of PCa cell lines.	Phenylbutyrates	31-33	BCL2 apoptosis regulator	Homo sapiens	102-107
10696460-9	2000	CONCLUSION: Our data show that PB-induced PCa apoptosis is associated with the relative repression of Bcl-2 and with up-regulation of Bax and Fas proteins and that this PB-induced apoptosis is independent of p53 and androgen-dependency status of PCa cell lines.	Phenylbutyrates	31-33	BCL2 associated X, apoptosis regulator	Homo sapiens	134-137
10696460-9	2000	CONCLUSION: Our data show that PB-induced PCa apoptosis is associated with the relative repression of Bcl-2 and with up-regulation of Bax and Fas proteins and that this PB-induced apoptosis is independent of p53 and androgen-dependency status of PCa cell lines.	Phenylbutyrates	31-33	tumor protein p53	Homo sapiens	208-211
10696460-9	2000	CONCLUSION: Our data show that PB-induced PCa apoptosis is associated with the relative repression of Bcl-2 and with up-regulation of Bax and Fas proteins and that this PB-induced apoptosis is independent of p53 and androgen-dependency status of PCa cell lines.	Phenylbutyrates	169-171	BCL2 associated X, apoptosis regulator	Homo sapiens	134-137
10450753-4	1999	At comparable doses, PB induced expression of CD11b, indicating myeloid differentiation.	Phenylbutyrates	21-23	integrin subunit alpha M	Homo sapiens	46-51
10450753-8	1999	Consistent with their effects on cell cycle, PB and BA, but not PA, induced the cyclin-dependent kinase inhibitor, p21(WAF1/CIP1), and led to the appearance of hypophosphorylated Rb, suggesting a role for p21(WAF1/CIP1) in PB-induced cytostasis.	Phenylbutyrates	45-47	cyclin dependent kinase inhibitor 1A	Homo sapiens	115-118
10450753-8	1999	Consistent with their effects on cell cycle, PB and BA, but not PA, induced the cyclin-dependent kinase inhibitor, p21(WAF1/CIP1), and led to the appearance of hypophosphorylated Rb, suggesting a role for p21(WAF1/CIP1) in PB-induced cytostasis.	Phenylbutyrates	45-47	cyclin dependent kinase inhibitor 1A	Homo sapiens	119-123
10450753-8	1999	Consistent with their effects on cell cycle, PB and BA, but not PA, induced the cyclin-dependent kinase inhibitor, p21(WAF1/CIP1), and led to the appearance of hypophosphorylated Rb, suggesting a role for p21(WAF1/CIP1) in PB-induced cytostasis.	Phenylbutyrates	45-47	cyclin dependent kinase inhibitor 1A	Homo sapiens	124-128
10450753-8	1999	Consistent with their effects on cell cycle, PB and BA, but not PA, induced the cyclin-dependent kinase inhibitor, p21(WAF1/CIP1), and led to the appearance of hypophosphorylated Rb, suggesting a role for p21(WAF1/CIP1) in PB-induced cytostasis.	Phenylbutyrates	45-47	cyclin dependent kinase inhibitor 1A	Homo sapiens	205-208
10741718-4	2000	The ability to bind and activate PPARgamma was common to biologically active analogues of phenylacetate and corresponded to their potency as antitumor agents (phenylacetate < phenylbutyrate < p-chloro-phenylacetate < p-iodo-phenylbutyrate), whereas an inactive derivative, phenylacetylglutamine, had no effect on PPARgamma.	Phenylbutyrates	178-192	peroxisome proliferator activated receptor gamma	Homo sapiens	33-42
10450753-8	1999	Consistent with their effects on cell cycle, PB and BA, but not PA, induced the cyclin-dependent kinase inhibitor, p21(WAF1/CIP1), and led to the appearance of hypophosphorylated Rb, suggesting a role for p21(WAF1/CIP1) in PB-induced cytostasis.	Phenylbutyrates	45-47	cyclin dependent kinase inhibitor 1A	Homo sapiens	209-213
10450753-8	1999	Consistent with their effects on cell cycle, PB and BA, but not PA, induced the cyclin-dependent kinase inhibitor, p21(WAF1/CIP1), and led to the appearance of hypophosphorylated Rb, suggesting a role for p21(WAF1/CIP1) in PB-induced cytostasis.	Phenylbutyrates	45-47	cyclin dependent kinase inhibitor 1A	Homo sapiens	214-218
10450755-5	1999	Although ATRA did not significantly affect the ED50 of PB, the combination of ATRA (1 microM) and PB (0.5 mM) augmented PB-induced CD11b expression eight-fold.	Phenylbutyrates	98-100	integrin subunit alpha M	Homo sapiens	131-136
10450755-5	1999	Although ATRA did not significantly affect the ED50 of PB, the combination of ATRA (1 microM) and PB (0.5 mM) augmented PB-induced CD11b expression eight-fold.	Phenylbutyrates	98-100	integrin subunit alpha M	Homo sapiens	131-136
10450755-8	1999	ATRA combined synergistically with PB to augment CD11b expression and inhibit colony formation.	Phenylbutyrates	35-37	integrin subunit alpha M	Homo sapiens	49-54
9815560-7	1997	Expression of the monocytic marker CD14 was increased in monocytic and myelomonocytic leukemias in response to PB, and to a lesser extent, PA.	Phenylbutyrates	111-113	CD14 molecule	Homo sapiens	35-39
9796984-4	1998	The inhibition of cell growth in FUdR-treated cells by PB was more sustained in U4 than U9 cells and was associated with an increased and sustained expression of p21waf1 protein, secretion of transforming growth factor beta1, mediators of p53-dependent or -independent G1 cell cycle arrest, and an increase in the alkaline phosphatase activity as well, considered a marker of differentiation in colon carcinoma cells.	Phenylbutyrates	55-57	tumor protein p53	Homo sapiens	239-242
10383127-4	1999	Both the potent inhibitor, trichostatin (TSA), and the well-known but less specific inhibitor, phenylbutyrate (PB), could partially reverse ETO-mediated transcriptional repression.	Phenylbutyrates	95-109	RUNX1 partner transcriptional co-repressor 1	Homo sapiens	140-143
10383127-4	1999	Both the potent inhibitor, trichostatin (TSA), and the well-known but less specific inhibitor, phenylbutyrate (PB), could partially reverse ETO-mediated transcriptional repression.	Phenylbutyrates	111-113	RUNX1 partner transcriptional co-repressor 1	Homo sapiens	140-143
10383127-5	1999	PB was also able to induce partial differentiation of the AML1-ETO cell line, Kasumi-1.	Phenylbutyrates	0-2	RUNX family transcription factor 1	Homo sapiens	58-62
10383127-5	1999	PB was also able to induce partial differentiation of the AML1-ETO cell line, Kasumi-1.	Phenylbutyrates	0-2	RUNX1 partner transcriptional co-repressor 1	Homo sapiens	63-66
10383127-7	1999	In summary, transcriptional repression mediated by AML1-ETO appears to play a mechanistic role in the t(8;21) AML, and relief of repression using agents such as PB (alone or in combination) may prove to be therapeutically useful.	Phenylbutyrates	161-163	RUNX family transcription factor 1	Homo sapiens	51-55
10383127-7	1999	In summary, transcriptional repression mediated by AML1-ETO appears to play a mechanistic role in the t(8;21) AML, and relief of repression using agents such as PB (alone or in combination) may prove to be therapeutically useful.	Phenylbutyrates	161-163	RUNX1 partner transcriptional co-repressor 1	Homo sapiens	56-59
9269314-8	1997	Modulation of tumour radiobiology by PA and PB was tightly correlated with early rise followed by decline in intracellular glutathione levels and the activity of antioxidant enzymes such as catalase, superoxide dismutase, glutathione reductase, glutathione peroxidase and glutathione S-transferase.	Phenylbutyrates	44-46	glutathione-disulfide reductase	Homo sapiens	222-243
9269314-8	1997	Modulation of tumour radiobiology by PA and PB was tightly correlated with early rise followed by decline in intracellular glutathione levels and the activity of antioxidant enzymes such as catalase, superoxide dismutase, glutathione reductase, glutathione peroxidase and glutathione S-transferase.	Phenylbutyrates	44-46	glutathione S-transferase kappa 1	Homo sapiens	272-297
33369803-3	2021	We hypothesised that PB would induce muscle protein catabolism by forcing BCAA degradation away from muscle protein synthesis and mTOR inhibition.	Phenylbutyrates	21-23	mechanistic target of rapamycin kinase	Homo sapiens	130-134
9816181-8	1996	Prostate cancer cell lines overexpressing P-glycoprotein or possessing heterogeneous molecular alterations, including p53 mutations, are also sensitive to the effects of PB.	Phenylbutyrates	170-172	tumor protein p53	Homo sapiens	118-121
7578983-0	1995	Transcriptional upregulation of TGF-alpha by phenylacetate and phenylbutyrate is associated with differentiation of human melanoma cells.	Phenylbutyrates	63-77	transforming growth factor alpha	Homo sapiens	32-41
7578983-3	1995	Treatment of human melanoma 1011 cultures with either PA or PB caused over 40-fold increase in TGF-alpha biosynthesis and secretion into the media.	Phenylbutyrates	60-62	transforming growth factor alpha	Homo sapiens	95-104
7578983-8	1995	Like PA and PB, other differentiation inducers such as all-trans-retinoic acid, dimethyl sulfoxide, and 5-aza-2"-deoxycytidine, all induced TGF-alpha expression in the melanoma cells.	Phenylbutyrates	12-14	transforming growth factor alpha	Homo sapiens	140-149
7578983-9	1995	The close association between enhanced TGF-alpha production and melanoma cell differentiation suggests that this growth factor, often linked to mitogenesis, may play a novel role in tumour differentiation by PA and PB.	Phenylbutyrates	215-217	transforming growth factor alpha	Homo sapiens	39-48
35064074-0	2022	Phenylbutyrate rescues the transport defect of the Sec61alpha mutations V67G and T185A for renin.	Phenylbutyrates	0-14	SEC61 translocon subunit alpha 1	Homo sapiens	51-61
35064074-0	2022	Phenylbutyrate rescues the transport defect of the Sec61alpha mutations V67G and T185A for renin.	Phenylbutyrates	0-14	renin	Homo sapiens	91-96
35064074-6	2022	Treatment with the molecular chaperone phenylbutyrate reversed the defective protein transport of renin and the imbalanced calcium homeostasis.	Phenylbutyrates	39-53	renin	Homo sapiens	98-103
34656124-4	2021	METHODS: We employed the HDAC inhibitor (HDACi) sodium phenylbutyrate (PBA) to address this question in an in vitro RT4 SC inflammation model and an in vivo sciatic nerve transection injury model to examine the effects of HDAC inhibition on the expression of pro-inflammatory cytokines.	Phenylbutyrates	71-74	histone deacetylase 9	Homo sapiens	25-29
34094947-10	2021	We evaluated cell death and apoptosis upon Salubrinal and phenylbutyrate treatment in healthy and IBC cells by caspase-3 activity and cleaved poly (ADP-ribose) polymerase (PARP) protein assay.	Phenylbutyrates	58-72	caspase 3	Homo sapiens	111-120
34094947-10	2021	We evaluated cell death and apoptosis upon Salubrinal and phenylbutyrate treatment in healthy and IBC cells by caspase-3 activity and cleaved poly (ADP-ribose) polymerase (PARP) protein assay.	Phenylbutyrates	58-72	poly(ADP-ribose) polymerase 1	Homo sapiens	142-170
34094947-10	2021	We evaluated cell death and apoptosis upon Salubrinal and phenylbutyrate treatment in healthy and IBC cells by caspase-3 activity and cleaved poly (ADP-ribose) polymerase (PARP) protein assay.	Phenylbutyrates	58-72	poly(ADP-ribose) polymerase 1	Homo sapiens	172-176
35296712-6	2022	Pre-treatment of in vitro corneal epithelial cultures or bone marrow-derived dendritic cells (BMDCs) with phenylbutyrate (PBA) reduces lipopolysaccharide-induced pro-inflammatory Tnf expression.	Phenylbutyrates	106-120	tumor necrosis factor	Mus musculus	179-182
35296712-6	2022	Pre-treatment of in vitro corneal epithelial cultures or bone marrow-derived dendritic cells (BMDCs) with phenylbutyrate (PBA) reduces lipopolysaccharide-induced pro-inflammatory Tnf expression.	Phenylbutyrates	122-125	tumor necrosis factor	Mus musculus	179-182
33369803-5	2021	We found that accelerated BCAA catabolism using PB resulted in adverse effects related to mTOR signalling and muscle protein metabolism in skeletal muscle cells, which may limit its application in conditions where muscle wasting is a risk.	Phenylbutyrates	48-50	mechanistic target of rapamycin kinase	Homo sapiens	90-94
33369803-7	2021	In skeletal muscle cells, we hypothesised that PB would induce muscle protein catabolism due to forcing BCAA degradation away from muscle protein synthesis and downregulating mTOR.	Phenylbutyrates	47-49	mechanistic target of rapamycin kinase	Homo sapiens	175-179
33369803-9	2021	Regulators of anabolic pathways mammalian target of rapamycin (mTOR) and its downstream components were impaired with PB treatment.	Phenylbutyrates	118-120	mechanistic target of rapamycin kinase	Homo sapiens	32-61
33369803-9	2021	Regulators of anabolic pathways mammalian target of rapamycin (mTOR) and its downstream components were impaired with PB treatment.	Phenylbutyrates	118-120	mechanistic target of rapamycin kinase	Homo sapiens	63-67
33369803-10	2021	The present results indicate that accelerated BCAA catabolism using PB resulted in adverse effects related to mTOR signalling and muscle protein metabolism, which may limit its application in settings where muscle wasting is a risk.	Phenylbutyrates	68-70	mechanistic target of rapamycin kinase	Homo sapiens	110-114
33026831-2	2020	Using skeletal muscle cells, we aimed to determine whether continued exposure of high extracellular BCAA would result in impaired insulin signalling, and whether the compound sodium phenylbutyrate (PB), which induces BCAA metabolism, would lower extracellular BCAA, thereby alleviating their potentially inhibitory effects on insulin-mediated signalling.	Phenylbutyrates	198-200	AT-rich interaction domain 4B	Homo sapiens	217-221
33277262-0	2020	Standalone or combinatorial phenylbutyrate therapy shows excellent antiviral activity and mimics CREB3 silencing.	Phenylbutyrates	28-42	cAMP responsive element binding protein 3	Homo sapiens	97-102
33026831-5	2020	Continued exposure of high BCAA resulted in impaired intracellular insulin signalling and glycogen synthesis, and while forcing BCAA catabolism using PB resulted in increases in proteins important for regulating glucose uptake, PB did not prevent the impairments in glycogen synthesis with BCAA exposure.	Phenylbutyrates	150-152	AT-rich interaction domain 4B	Homo sapiens	128-132
33026831-5	2020	Continued exposure of high BCAA resulted in impaired intracellular insulin signalling and glycogen synthesis, and while forcing BCAA catabolism using PB resulted in increases in proteins important for regulating glucose uptake, PB did not prevent the impairments in glycogen synthesis with BCAA exposure.	Phenylbutyrates	150-152	AT-rich interaction domain 4B	Homo sapiens	128-132
33026831-2	2020	Using skeletal muscle cells, we aimed to determine whether continued exposure of high extracellular BCAA would result in impaired insulin signalling, and whether the compound sodium phenylbutyrate (PB), which induces BCAA metabolism, would lower extracellular BCAA, thereby alleviating their potentially inhibitory effects on insulin-mediated signalling.	Phenylbutyrates	198-200	AT-rich interaction domain 4B	Homo sapiens	217-221
33026831-4	2020	PB significantly reduced media BCAA and branched-chain keto acid (BCKA) concentrations, and increased phosphorylation of AKT (+20+-2%; P<0.05 vs. Ctl) and AS160 (+24+-2%; P<0.05 vs. Ctl), however insulin-stimulated glycogen synthesis was further reduced upon PB treatment.	Phenylbutyrates	0-2	AT-rich interaction domain 4B	Homo sapiens	31-35
33026831-4	2020	PB significantly reduced media BCAA and branched-chain keto acid (BCKA) concentrations, and increased phosphorylation of AKT (+20+-2%; P<0.05 vs. Ctl) and AS160 (+24+-2%; P<0.05 vs. Ctl), however insulin-stimulated glycogen synthesis was further reduced upon PB treatment.	Phenylbutyrates	0-2	AKT serine/threonine kinase 1	Homo sapiens	121-124
33026831-4	2020	PB significantly reduced media BCAA and branched-chain keto acid (BCKA) concentrations, and increased phosphorylation of AKT (+20+-2%; P<0.05 vs. Ctl) and AS160 (+24+-2%; P<0.05 vs. Ctl), however insulin-stimulated glycogen synthesis was further reduced upon PB treatment.	Phenylbutyrates	0-2	TBC1 domain family member 4	Homo sapiens	155-160
33026831-4	2020	PB significantly reduced media BCAA and branched-chain keto acid (BCKA) concentrations, and increased phosphorylation of AKT (+20+-2%; P<0.05 vs. Ctl) and AS160 (+24+-2%; P<0.05 vs. Ctl), however insulin-stimulated glycogen synthesis was further reduced upon PB treatment.	Phenylbutyrates	0-2	insulin	Homo sapiens	196-203
33026831-4	2020	PB significantly reduced media BCAA and branched-chain keto acid (BCKA) concentrations, and increased phosphorylation of AKT (+20+-2%; P<0.05 vs. Ctl) and AS160 (+24+-2%; P<0.05 vs. Ctl), however insulin-stimulated glycogen synthesis was further reduced upon PB treatment.	Phenylbutyrates	259-261	AKT serine/threonine kinase 1	Homo sapiens	121-124
32531811-0	2020	Phenylbutyrate ameliorates prefrontal cortex, hippocampus and nucleus accumbens neural atrophy as well as synaptophysin and GFAP stress in aging mice.	Phenylbutyrates	0-14	synaptophysin	Mus musculus	106-119
30706227-7	2019	On microarray analysis, among the PB resistance-related genes, the expression of the genes ASCL2, LEF1, and TSPAN8 was clearly associated with PB resistance.	Phenylbutyrates	34-36	achaete-scute family bHLH transcription factor 2	Homo sapiens	91-96
30706227-7	2019	On microarray analysis, among the PB resistance-related genes, the expression of the genes ASCL2, LEF1, and TSPAN8 was clearly associated with PB resistance.	Phenylbutyrates	34-36	lymphoid enhancer binding factor 1	Homo sapiens	98-102
30706227-7	2019	On microarray analysis, among the PB resistance-related genes, the expression of the genes ASCL2, LEF1, and TSPAN8 was clearly associated with PB resistance.	Phenylbutyrates	34-36	tetraspanin 8	Homo sapiens	108-114
30706227-7	2019	On microarray analysis, among the PB resistance-related genes, the expression of the genes ASCL2, LEF1, and TSPAN8 was clearly associated with PB resistance.	Phenylbutyrates	143-145	achaete-scute family bHLH transcription factor 2	Homo sapiens	91-96
30706227-7	2019	On microarray analysis, among the PB resistance-related genes, the expression of the genes ASCL2, LEF1, and TSPAN8 was clearly associated with PB resistance.	Phenylbutyrates	143-145	lymphoid enhancer binding factor 1	Homo sapiens	98-102
30706227-7	2019	On microarray analysis, among the PB resistance-related genes, the expression of the genes ASCL2, LEF1, and TSPAN8 was clearly associated with PB resistance.	Phenylbutyrates	143-145	tetraspanin 8	Homo sapiens	108-114
30706227-8	2019	PB-sensitive cells transfected with one of these three genes exhibited significant (P &lt; 0.001) augmentation of PB resistance; ASCL2 induced expression of both LEF1 and TSPAN8, while neither LEF1 nor TSPAN8 induced ASCL2.	Phenylbutyrates	0-2	achaete-scute family bHLH transcription factor 2	Homo sapiens	129-134
30706227-8	2019	PB-sensitive cells transfected with one of these three genes exhibited significant (P &lt; 0.001) augmentation of PB resistance; ASCL2 induced expression of both LEF1 and TSPAN8, while neither LEF1 nor TSPAN8 induced ASCL2.	Phenylbutyrates	0-2	lymphoid enhancer binding factor 1	Homo sapiens	162-166
30706227-8	2019	PB-sensitive cells transfected with one of these three genes exhibited significant (P &lt; 0.001) augmentation of PB resistance; ASCL2 induced expression of both LEF1 and TSPAN8, while neither LEF1 nor TSPAN8 induced ASCL2.	Phenylbutyrates	0-2	tetraspanin 8	Homo sapiens	171-177
30706227-8	2019	PB-sensitive cells transfected with one of these three genes exhibited significant (P &lt; 0.001) augmentation of PB resistance; ASCL2 induced expression of both LEF1 and TSPAN8, while neither LEF1 nor TSPAN8 induced ASCL2.	Phenylbutyrates	0-2	achaete-scute family bHLH transcription factor 2	Homo sapiens	217-222
30706227-8	2019	PB-sensitive cells transfected with one of these three genes exhibited significant (P &lt; 0.001) augmentation of PB resistance; ASCL2 induced expression of both LEF1 and TSPAN8, while neither LEF1 nor TSPAN8 induced ASCL2.	Phenylbutyrates	114-116	achaete-scute family bHLH transcription factor 2	Homo sapiens	129-134
30706227-9	2019	RNA interference via ASCL2 knockdown made PB-resistant cells sensitive to PB and inhibited both genes.	Phenylbutyrates	42-44	achaete-scute family bHLH transcription factor 2	Homo sapiens	21-26
30706227-9	2019	RNA interference via ASCL2 knockdown made PB-resistant cells sensitive to PB and inhibited both genes.	Phenylbutyrates	74-76	achaete-scute family bHLH transcription factor 2	Homo sapiens	21-26
30706227-10	2019	ASCL2 knockdown also played a critical role in sensitivity to treatment by 5-fluorouracil and radiotherapy in addition to PB.	Phenylbutyrates	122-124	achaete-scute family bHLH transcription factor 2	Homo sapiens	0-5
32073132-11	2020	The newest reports say that phenylbutyrate increases level of PDC in brain, because reduced level of inactive form of PDH.	Phenylbutyrates	28-42	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	118-121